VIVA CHECKLIST 101

Success is counted sweetest

By those who ne'er succeed.

To comprehend a nectar

Requires sorest need.

- Emily Dickinson
1. Difference between sarcoma and carcinoma

Sarcomas and carcinomas are types of malignant tumors that can affect bones. They are derived
from different types of cells. Sarcomas are derived from mesodermal (mesenchymal cells) and
carcinomas are derived from epithelial types of cells. Sarcomas and carcinomas grow and spread
differently. Sarcomas grow like "ball-like" masses and tend to push adjacent structures like arteries,
nerves, veins away. The compress adjacent muscles into a pseudocapsule that contains microscopic
projections of the tumor referred to as satellite nodules. The local growth of sarcomas like a ball
enables resection in most instances. Sarcomas tend to arise primarily (directly) from bone as
opposed to spreading to bone from another site. Sarcomas spread most commonly to the lungs.
They can also spread to other bones (ie. arise from a bone and spread to other bones) and to the
liver. These are the most common sites of spread. Sarcomas rarely spread to lymph nodes.
Carcinomas grow in an infiltrative manner and grow through infiltration or invasion of adjacent
structures. They more easily invade adjacent nerves, blood vessels and muscles. They do not form a
pseudocapsular layer and therefore it is difficult to determine its exact anatomic extent during
surgery. This makes it more difficult to remove entirely with surgery. Carcinomas spread to lymph
nodes, lungs, bones and many other organs depending on the type of carcinoma. Carcinomas
involve bone secondarily, that is by spreading from another site such as the breast to the bone.

2. Vitamin D Deficiency

1. Nutrional
2. X-linked hyperphosphatemia
3. Vitamin D resistance – receptor type 1, absent of alpha hydroxylase type 2
4. Renal osteodystrophy – inability to convert to active forms

Pathophysiology of tumour cachexia

About half of all cancer patients show a syndrome of cachexia, characterized by anorexia and loss
of adipose tissue and skeletal muscle mass. Numerous cytokines have been postulated to play a
role in the etiology of cancer cachexia. Cytokines can elicit effects that mimic leptin signaling and
suppress orexigenic ghrelin and neuropeptide Y (NPY) signaling, inducing sustained anorexia and
cachexia not accompanied by the usual compensatory response. Furthermore, cytokines have been
implicated in the induction of cancer-related muscle wasting. Cytokine-induced skeletal muscle
wasting is probably a multifactorial process, which involves a protein synthesis inhibition, an
increase in protein degradation, or a combination of both.

Or simplified:

1. Loss of appetite
2. TNF production by activated macrophages
3. Proteolysis inducing factor (PIF), increase catabolism muscle and adipose tissue
Definition of neoplasia, grading and staging

Neoplasia – aberrant autonomous growth despite removal of external stimuli. The neoplastic
grading is a measure of cell anaplasia (reversion of differentiation) in the sampled tumor and is
based on the resemblance of the tumor to the tissue of origin.

Grading in cancer is distinguished from staging, which is a measure of the extent to which the
cancer has spread.

Bone healing

Bone healing, or fracture healing, is a proliferative physiological process in which the body
facilitates the repair of a bone fracture. Phases: Hematoma, inflammation, repair (soft and hard
callus), remodeling. Fracture stability dictates the type of healing that will occur the mechanical
stability governs the mechanical strain; when the strain is below 2%, primary bone healing will
occur; 2% and 10%, secondary bone healing will occur

1. Hematoma and inflammation phase;

 Hematoma forms and provides source of hemopoieitic cells capable of secreting growth
factors.
 Macrophages, neutrophils and platelets release several cytokines
o this includes PDGF, TNF-Alpha, TGF-Beta, IL-1,6, 10,12
o they may be detected as early as 24 hours post injury
o lack of TNF-Alpha (ie. HIV) results in delay of both enchondral/intramembranous
ossification
 Fibroblasts and mesenchymal cells migrate to fracture site and granulation tissue forms
around fracture ends
o During fracture healing granulation tissue tolerates the greatest strain before

failure
 Osteoblasts and fibroblasts proliferate
o Inhibition of COX-2 (ie NSAIDs) causes repression of runx-2/osterix, which are
critical for differentiation of osteoblastic cells

2. Repair

 Primary callus forms within two weeks. If the bone ends are not touching, then bridging
soft callus forms.
o the mechanical enviroment drives differentiation of either osteoblastic (stable
enviroment) or chondryocytic (unstable environment) lineages of cells
 Enchondral ossification converts soft callus to hard callus (woven bone). Medullary callus
also supplements the bridging soft callus
o Cytokines drive chondocytic differentiation.
o cartilage production provides provisional stabilization
  Type II collagen (cartilage) is produced early in fracture healing and then followed by type I
collagen (bone) expression
 Amount of callus is inversely proportional to extent of immobilization
o primary cortical healing occurs with rigid immobilization (ie. compression plating)
o enchondral healing with periosteal bridging occurs with closed treatment

3. Remodeling

 Begins in middle of repair phase and continues long after clinical union
o chondrocytes undergo terminal differentiation
 complex interplay of signaling pathways including, indian hedgehog (Ihh),
parathyroid hormone related peptide (PTHrP), FGF and BMP
 these molecules are also involved in terminal differentiation of the
appendicular skeleton
o type X collagen types is expressed by hypertrophic chondrocytes as the
extraarticular matrix undergoes calcification
o proteases degrade the extracellular matrix
o cartilaginous calcification takes place at the junction between the maturing
chondrocytes and newly forming bone
 multiple factors are expressed as bone is formed including BMPs, TGF-
Betas, IGFs, osteocalcin, collagen I, V and XI
o subsequently, chondrocytes become apoptotic and VEGF production leads to new
vessel invasion
o newly formed bone (woven bone) is remodeling via organized
osteoblastic/osteoclastic activity
 Shaped through
o Wolff's law: bone remodels in response to mechanical stress
o piezoelectic charges : bone remodels is response to electric charges: compression
side is electronegative and stimulates osteoblast formation, tension side is
electropostive and simulates osteoclasts

Factors that promote bone remodeling

Fracture healing influenced by these factors:

1. Local – extent of injury, blood supply (internal / periosteal- thickness in children), fixation
technique
2. External – LIPUS, NSAIDS, bone stimulators, radiation
3. Patient – nutrition status, co morbid, age
4. Remodeling follows the above laws.

Difference malunion and non-union

Malunion – healing occurred in sub-anatomical position. Nonunion is arrest of healing process and
usually non tender. Perkins table indicates: A spiral fracture in the upper limb unites in 3/52
double it for consolidation, double it again for the lower limb, double it again for a transverse
fracture.

Type of non-union: 1) septic nonunion 2) aseptic non union

 septic nonunion
 hypertrophic nonunion
o caused by inadequate immobilization with adequate blood supply
o type 2 collagen is elevated
o typically heal once mechanical stability is improved
 atrophic nonunion
o caused by inadequate immobilization and inadequate blood supply
 oligotrophic nonunion
o produced by inadequate reduction with fracture fragment displacement

Definition of Abscess

An abscess is an enclosed collection of liquefied tissue, known as pus lined by granulation tissue or
fibrosis. It is the result of the body's defensive reaction to foreign material. It contains
PMN/macrophages and lymphocytes

Process of gram stain

1. Stained with crystal violet (all will be purplish colored)

2. Application iodine based solution (KI) – fixed the stained

3. de staining with alcohol

4. Counter stain with safranin – red or pink

*Gram positive showed purplish discoloration

Osteoporosis

Osteoporosis is defined as age related decrease in bone mass. WHO defines as L2-L4 density level at
least 25 standard deviations below the peak bone mass of 25-year-old individual.

Mechanical compensation for osteoporosis

Definition of hemostasis
Hemostasis is a physiological process by which bleeding is controlled. It consists of four
components:
1. vasoconstriction
2. platelet activation
3. coagulation mechanism
4. fibrinolytic system

Coagulation cascade
Cell cycle

The cell cycle is an ordered set of events, culminating in cell growth and division into two daughter
cells.

Chemotherapy

Medical treatment in cancer management which alter cell’s DNA to induce cell apoptosis. It can be
used as primary treatment (Lymphoma), adjuvant (after debulking) or neoadjuvant (pre-operative)
therapy.

Function: cure, control, palliation

Complications of chemotherapy

1. Short term: actively dividing cells (skin, mucosa GIT, hair follicles, pancytopenia)
2. Long term: lung fibrosis, liver hepatitis, infertility.
Tumor follows gompertzian growth: debulk to stimulate angiogenic switch

Types:
1. alkylating agents - cyclosphamide
2. antitumor antibiotic – both RNA / DNA synthesis non phase dependent
doxorubicin
3. antimetabolites - > S phase (mtx)
4. Mitotics inhibitor -> M phase vincristine
5. Nitroureas inhibit enzyme for DNA repair – carmostine (non phase
dependent)
Stages of Hemorrhagic shock

Shock is defined as hypo perfusion to an organ, which in this case caused by blood loss.

Compensation of hemorrhagic shock

Hypoxia will lead to acidosis due to lactic acid accumulation.

Lungs: As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of
carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the body is
attempting to raise the pH of the blood.
CVS: The baroreceptors in the arteries detect the resulting hypotension, and cause the release of
epinephrine and norepinephrine. Norepinephrine causes predominately vasoconstriction with a
mild increase in heart rate, whereas epinephrine predominately causes an increase in heart rate
with a small effect on the vascular tone; the combined effect results in an increase in blood
pressure.
Renal: The renin–angiotensin axis is activated, and arginine vasopressin (Anti-diuretic hormone;
ADH) is released to conserve fluid via the kidneys. These hormones cause the vasoconstriction of
the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain.
The lack of blood to the renal system causes the characteristic low urine production.
How a diathermy works

Diathermy is a medical device used for surgical instruments utilizing electro current wave. Heat is
used to destroy tissues, to cut and to cauterize blood vessels. Waves normally 200-3.3mghz
1. Monopolar – using exit pad
2. Bipolar – current flow through from tip end to another, (pacemaker advantage)

Coagulation/Fulguration: Produced by interrupted pulses of current (50-100 per second), square

wave-form. Tissue cells contract to increase normal clotting

Cutting : Produced by continuous current, sinus wave-form

Generation of heat destroys tissue cell.
Desiccation: Cell walls destroyed through dehydration

How an audit works

Audit is part of clinical governance, quality improvement process to ensure current practices are in-
line with standard / recommendation of treatment. Retrospective process. Data presented to
distinguished between normal variation between surgeons or institutions and significant
divergence.

Keloid formation

A sharply elevated, irregularly shaped, progressively enlarging scar, due to excessive collagen
formation in the corium during connective tissue repair. Exceeding scar size (difference with
hyperthropic scarring)
Histologically, keloids are fibrotic tumors characterized by a collection of atypical fibroblasts with
excessive deposition of extracellular matrix components, especially collagen, fibronectin, elastin,
and proteoglycans. Generally, they contain relatively acellular centers and thick, abundant collagen
bundles that form nodules in the deep dermal portion of the lesion. Treatment: Cryotherapy,
Steroids, and Radiotherapy. Surgical removal not recommended.

Techniques to reduce formation of keloid:

Align incisions with natural skin creases to lessen tension.
Don’t make incisions across joints, which are a high-stress area for the skin.
Don’t make tight sutures to minimize tension at wound site.
Use all necessary precautions to avoid further inflammation by infection or foreign material left
under the skin (e.g., sutures)
What is biofilm?

A thin coating containing biologically active agents, which coats the surface of structures affecting
implanted or indwelling device. It contains viable and nonviable microorganisms that adhere to the
surface and are trapped within a matrix of organic matter (for example, proteins, glycoproteins,
and carbohydrates). It consists of 15% cells and 85% polysaccharide layer (glycocalyx) also known as
exopolysaccharide. Glycocalyx allows biofilm to adhere to prosthesis and sealoff infection and
protect bacteria from host immune system.

Five stages of biofilm development: (1) Initial attachment, (2) Irreversible attachment (secrete
sticky extraceullular polysaccharide), (3) Maturation I (first colonist fasciliate arrival other cells by
providing more diverse adhesion site, and build the polysaccharide matrix: nutrients accumulate,
cells divide), (4) Maturation II (fully mature biofilm, matrix act as protective layer), and (5)
Dispersion. Each stage of development in the diagram is paired with a photomicrograph of a
developing P. aeruginosa biofilm. All photomicrographs are shown to same scale.

Quorum sensing

Bacteria constitutively produce and secrete certain signaling molecules (called autoinducers or
pheromones). These bacteria also have a receptor that can specifically detect the signaling
molecule (inducer). When the inducer binds the receptor, it activates transcription of certain genes,
including those for inducer synthesis. As the population grows, the concentration of the inducer
passes a threshold, causing more inducer to be synthesized. This forms a positive feedback loop,
and the receptor becomes fully activated. Activation of the receptor induces the up-regulation of
other specific genes, causing all of the cells to begin transcription at approximately the same time.
These processes will triggers specific behavioral response.
TB appearance on HPE

Granulomatous appearance, presence of langhans giant cell with or without caseous necrosis at the
centre. This granuloma surrounded by epitheloid cell, macrophage, fibroblasts and lymphocytes,
implifies chronic infections.
Tuberculosis cell wall is waxy and contains components that confer acid-fastness; that is, the
retention of carbol fuchsin after rinsing with acid alcohol

ZIehl Neelsen staining:

1. Carbol Fuhsin to stained all cell wall (red), heated till dry and wash off under tap water
2. Destaining using alcohol
3. Methelyne blue application (cell which do not have acid fast thick waxy later, will take this
up)
4. AFB is stained Red

Sites of action anti TB

Peak bone mass curve

*sharp decline post menopausal period

Desribe how body Balance and caloric reflex

1. Semicircular canal has vestibules – small dilatation is ampulla. This contains kinociullium
and stereocillium (hair cell cells wilth layer of gel like material = cupula, and attached to
nerve endings)
2. kinicilium longest, stereocillium shorter
3. moving head to right will displaced fluid to left, fluid moves towards kinocillium on right
side. – k channels open and enters cell, causing action potentials. Passive electrochemical
gradient
4. generation of AP on right side – brain noted right movement
5. once the kinocillium catches up with movement, K channel no longer open, no AP, brain
notices head not moving.
Caloric reflexes : COWS
Cold opposite, warm same
1. push cold water inside auditory canal, tympanic membrance -> middle ear cavity
2. fluid will move away from stimulus
3. stimulating nystagmus on contralateral side
4. warm water = nystagmus same side
Action potential

Graded potential can occur to all membrane – depending on the strength of stimulus
Action potential only occurs at excitable membranes.
Follows electronegative charge course. One-way route. Consists of Na and K channel to maintain -
70mv membrane charge.
Na channel fast: K channel slow (cause hyperpolarization)
All or none character
Refratory periods
Absolute refractory: no second potential produce
- Cardiac muscle has long refractory period = hence no tetani.
Relative refractory: able to fire second AP if a stimulus is strong enough
Myelin is an insulator to promote salutatory conduction – leaping current = faster

Muscle structure and contractions

Epimysium – surrounds muscle bundles

Perimysium – Surrounds muscles fascicles
Endomysium – Surrounds individual fibers

Myofibrils -> collection of sarcomeres, which consists of:

Thin actin and thick myosin filaments.
Ach at neuromuscular junction _> Na/K channels open -> depolarization -> DHP (dihyropyridine
receptor bind with ca channel at sarcoplasmic) -> Ca in sarcoplasmic reticulum to be released -> Ca
binds to troponin and alter its configuration -> exposed actin -> crosslinked actin and myosin with
consumption of ATP

Draw a sarcomere
A band unchanged
I band reduced
H zone reduced

Action of Botox

Botolinum toxin is a competitive inhibitor of presynaptic cholinergic receptor, which lasted about 2-
3 months.

Describe Cardiac cycle

1. Rapid ventricular filling

2. Reduced ventricular filling
3. Atrial systole
4. Isovolumetric contraction
5. Rapid ventricular ejection
6. Reduced ventricular ejection
7. Isovolumetric relaxation

Calcium metabolism

Calcium is controlled mainly by PTH hormones (which response to hypocalcemia) and calcitonin
(which response to hypercalcemia)

In order to understand calcium hemostasis, the understanding of calcium absorption is

fundamental.

Vitamin D3 is produced photochemically from 7-dehydrocholesterol in the skin. The UV lights will
help convertion of vitamin D in the skin or ingested orally, and subsequently added 25-
hydrocholecalciferol in liver. This in turn will be further hydrolyses in the kidney by alpha hydrolase,
to give 1,25 dihydrochelocalciferol. This activated version of vitamin D will promote calcium
absorption in the intestines, promoting bone mineralization, maintaining calcium and phosphate
levels for bone formation, and allowing proper functioning of parathyroid hormone to maintain
serum calcium levels.

In response to hypocalcemia PTH will be released by parathyroid hormones and will act in
according manner:
↑ serum Ca2+ and ↓ serum phosphate in response to hypocalcemia/hypomagnesemia via
↑ bone resorption of calcium and phosphate (bone is destroyed)
PTH receptor is on the osteoblasts which secretes IL-1 to activated osteoclasts
↑ kidney resorption of calcium in distal convoluted tubule
↓ kidney resorption of phosphate
↑ 1,25-(OH)2 vitamin D production
PTH indirectly stimulates osteoclasts by binding to its receptor on osteoblasts, inducing RANK-L and
M-CSF synthesis . Excessive PTH leads to over-stimulation of bone resorption. cortical bone affected
more than cancellous

Difference Osteomalacia and Osteoporosis

Osteoporosis Osteomalacia
Reduced bone mass, normal
Definition Bone mass variable, reduced mineralization
mineralization
Post menopausal (Type I) or elderly (Type
Age Any age
II)
Vit D deficiency or abnormal vit D pathway,
Endocrine abnormality, age, idiopathic,
Etiology hypophosphatemia, hypophosphatasia, renal
inactivity, alcohol, calcium deficiency
tubular acidosis
Symptoms
Pain and tenderness at fracture site Generalized bone pain and tenderness
and signs
Appendicular fracture predominance,
Xray Axial fracture predominance symmetric, includes pseudofractures (Looser
zones)
Serum Ca Normal Low or normal
Serum PO4 Normal Low or normal
ALP Normal Elevated (except hypophosphatasia)
Urinary Ca High or normal Normal or low (high in hypophosphatasia)
Bone biopsy Tetracycline labeling normal Tetracycline labeling abnormal

What is composition of bone

Bone is made up of
organic component - 40% of dry weight
inorganic component - 60% of dry weight

Organic – type 1 collagen, proteoglycans (compressive str), matrix proteins (promote bone
formation: osteocalcin – produce by mature osteoblast, osteonectin, osteopontin) and cytokines
and growth factors. Other cells: osteoblast and osteoclast

Inorganic – Calcium hydroxyapatite and osteocalcium phosphate (brushite)

How we can measure blood pressure

Measurement using sphygmamometer. At level of heart. Adequate cuff width. Too small will cause
false high reading. First sound (korotkoff) is the systolic value and when the sounds disappear is the
diastolic value.
Diastolic value is determine by the compliance of aorta, as the pressure in diastolic ventricles
would be 0-5mmhg.

Poiseulles’s law

Poiseuille's Law. In the case of smooth flow (laminar flow), the volume flowrate is given by the
pressure difference divided by the viscous resistance. This resistance depends linearly upon the
viscosity and the length, but the fourth power dependence upon the radius is dramatically different.
Flow rate

Flow rate = Pressure difference / resistance

Resistance = 8 L Viscosity / Pie Radius4

* biggest determinant is the radius of the vessels

Describe glucose metabolism

Types of dehydration

Physiological changes in sepsis

Sepsis is defined as SIRS with evident source of infection. It is results when an infectious insult
triggers a localized inflammatory reaction with released toxin (endo or exotoxin), in which
stimulates the body response by exhibiting;
1. tachycardia >90
2. fever >38 or hypothermia <36
3. leukocytosis >12 or leukopenia <4
4. hypocapnia <32mmhg

These clinical symptoms are called the systemic inflammatory response syndrome. Severe sepsis is
defined by dysfunction of one of the major organ systems or unexplained metabolic acidosis. The
inflammatory reaction is mediated by the release of cytokines, including tumor necrosis factor-
alpha, interleukins, and prostaglandins, from neutrophils and macrophages. It will also promote
capillary leakage and causing reduced in blood pressure, which causes ischemia, and fluid
accumulation in third space. Body will react by activating baroreceptor, causing the increase of
heart rate. The inadequacy of blood supply will resort the tissue to utilizing anerobic pathway with
will produce lactate acid. This in turn will decrease the body pH, stimulating the peripheral
chemoreceptors and causing the compensatory mechanism of the respiratory system. Kidney
function is most likely inefficient due to insufficient blood supply received. The cytokines also
activate the extrinsic coagulation cascade and inhibit fibrinolysis. This will lead to DIVC, a condition
whereby the consumption of coagulation factors and causing increase in bleeding tendency, as
result of widespread coagulate pathway activation. This thrombosis event will cause further
ischemia, and causing vicious cycle.

If prolonged, this condition will cause distributive shock, whereby the loss in third space is greater
than circulating blood + resuscitation.

Endotoxin: lipopolysaccharide moiety contained in the outer membrane of gram negative bacteria.

Septic shock is severe sepsis plus persistently low blood pressure despite the administration of
intravenous fluids.

Sequence:
Primay precipitating event -> inflammatory response -> SIRS -> MODS -> Multiorgan failure
MODS: Multi organ dysfunction - > evidence of death of tissue cell in two or more organ.

Stage I: local wound : inflammatory response, promote wound repair

Stage 2: cytokines release to enhance local response: macrophage and platelet recruited. Acute
phase response (inflammatory + endogenous antagonist) keeping check
Stage 3: occurs if hemostasis not restored. SIRS sets in. Leading to loss of microcirculation integrity.
Mediators: endotoxin, TNF, IL-1=6

Types of hypoxia:

A state of oxygen deprivation at cellular level

1. anemia – low oxyhemoglobin

2. ischemia – blockage and causes reduction in blood supply
3. hypoxemia hypoxic – low oxygen
4. carbon monoxide – high affinity of oxygen, competitive binding
5. histotoxic hypoxia – cyanide poisoning

What an abg measures

ABG measures Ph, paO2, pco2, bicarbonate, and base excess. Useful to measure the causes of
alkalosis and acidosis.
Difference between artheroma and thrombosis

Artheroma ; slow progression of lipid plaque deposition into the tunica intima layer (beneath
endothelial layer), stimulating macrophages and form foam cell.

Thrombosis : abnormal clot formation inside the blood vessels characterized by line of zahn (fibrin
and platelet product overlapped with RBC)
Types of shock

Blood composition

Whole blood – consists of packed cell, plasma, and platelet, added with citrate
- Packed cell 45-60% – leukocyte depleted, gamma irradiate, stored in
3celcius with 35/7 days
- 1g Hb increment per packed
Platelet – 5 days, agitator machine, 10-20-platelet increment per packed
Plasma – frozen, at -30celcius, thaw water bath and to be used within 2hours
- Centrifuge becomes cryoprecipitate (factor 8, vwF and fibrinogen) /
cryosupernatant
Transfusion depends on body weight
Complications:
1. Acute: <24h
a. In acute hemolytic transfusion reactions, there is a destruction of the donor's RBCs
within 24 hours of transfusion. Hemolysis may be intravascular or extravascular.
The most common type is extravascular hemolysis, which occurs when donor RBCs
coated with immunoglobulin G (IgG) or complement are attacked in the liver or
spleen.17 Intravascular hemolysis is a severe form of hemolysis caused by ABO
antibodies.
b. Urticarial allergic reactions are defined by hives or pruritus.20 Patients
experiencing allergic transfusion reactions have been sensitized to the antigens in
the donor unit. These antigens are soluble, and the associated reaction is dose-
dependent. Allergic transfusion reactions occur in 1 to 3 percent of transfusions
c. Transfusion-related acute lung injury (TRALI) is noncardiogenic pulmonary edema
causing acute hypoxemia that occurs within six hours of a transfusion and has a
clear temporal relationship to the transfusion
d. An FNHTR is defined as a rise in body temperature of at least 1.8°F (1°C) above
98.6°F (37°C) within 24 hours after a transfusion; it may involve rigors, chills, and
discomfort
e. Fluid overload
 2. Chronic: >24h
a. Graft vs host disease: Transfusion-associated graft-versus-host disease is a
consequence of a donor's lymphocytes proliferating and causing an immune attack
against the recipient's tissues and organs.
b. Infections

Mechanics of breathing

2 centers in medulla;
Dorsal Respiratory Group – passive breathing
Ventral Respiratory Group – when additional volume required, eg exercise.
Breathing centre in medulla -> impulse to phrenic nerve -> diaphragm contract and external
intercostal muscle contract -> intrapleural space sub atmospheric level -> draw of lung due to
surface tension inside -> lung expand -> subatmospheric level -> air breathe in
 In force inspiration -> abdominal muscle, and neck muscle help to contract and further
increase force inspiratory volume.

Expiration cause by inhibition of phrenic stimulation, diaphragm to relax -> increase intrapleural
pressure -> lung muscle recoil -> increase transpulmonary pressure -> alveoli compression -> air
flows out
In force expiration internal intercostal will contract to further decrease space
intrapulmonary

Role of surfactant:

Produce by type 2 pneumocyte, a mixture of lipid and protein, increase production by stretching.
Produce in late gestation phase.
Helps to overcome law of laplace:

P = 2T/R

T = tension over alveoli.

P pressure
R radius

Since alveoli are interconnected, provide all factors are equal; the smaller alveoli will tend to
collapse due to higher pressure intraalveoli, and air moves to other connected alveoli. Surfactant
will reduce the surface tension of this, in tandem with smaller radius and will provide equal
pressure to both smaller and bigger alveoli, preventing to collapse and helps with alveoli
compliance.
Describe lung volumes and capacities

Tidal volume; normal inspiration

Inspiratory reserve volume; force inspiration
Expiratory reserve volume; force expiration
Residual volume; air remaining after force expiration

Vital capacity: ER + TV + IR
Inspiratory capacity: TV + IR
Functional Residual capacity: RV + ERV
Total lung capacity; RV + VC

Describe dead space

Air inhaled but does not participate in gaseous exchange; also known as physiological dead space.
1. anatomical dead space – air left in previous ventilation, in respiratory tract eg trachea
2. alveoli dead space – new air inhaled reached alveoli, but lack of blood supply or due to
disease, the alveoli not participating in gaseous exchange.

Difference mechanical and normal ventilations

1. machine controlled vs medullary controlled

2. larger dead space in mechanical ventilations
3. mechanical mostly using positive pressure ventilations – from inside to expand lung whilst
the normal ventilations using negative pressure
 4. Complications of prolonged mechanical ventilations: overinflation, pneumothorax,
infections, and effects on hemodynamic controlled of preload and afterload.

Describe Osteomyelitis

Infection of bone characterized by progressive inflammatory destruction and apposition of new

bone

Can be divided into:

Acute – less than 2 weeks
Subacute – 2 weeks to months
Chronic – months to years

Mechanism of spread:
1. hematogenous
2. direct inoculation (trauma)
3. contiguous focus (adjacent surgery)

Bacteria ability to form biofilm – reducing ability of penetration of antibiotics

Recurrent rate 30%.

Classification:
Tcherne Mader classification;
1. intramedullary
2. superficial
3. focal
4. diffuse

Host;
Type A: normal, Type B: immunocompromised, Type C: treatment is worse

The anatomical classification of osteomyelitis is important for understanding and localizing the
infection.
Type I (medullary osteomyelitis) diffusely involves the intramedullary cavity, usually after medullary
nailing. The entire medullary canal is involved, and will require surgical clearance (nail removal and
reaming).
Type II osteomyelitis is superficial, may be present under a plate, but is rarely, if ever, seen with
fracture-site infection.
Type III osteomyelitis (localized full-thickness cortical involvement), will require excision of all
necrotic bone. During the excision, the full extent of the necrotic area becomes evident. This may
weaken the bone, or produce significant dead space. Soft-tissue cover may be inadequate and
therefore require reconstruction. Fracture healing may be a problem requiring additional
treatment.
Type IV osteomyelitis diffusely involves the entire circumference of a segment of the bone. The
entire bone segment must be removed to eliminate necrotic tissue and persistent bacteria.

Necrotising Fascitis and Gas gangrene

Necrotizing fasciitis is a life threatening infection that spreads along fascia soft tissue planes

Type 1 Polymicrobial • Most common (80-90%)

Typical 4-5 aerobic and anaerobic species • Seen in immunosuppressed (diabetics and cancer
cultured: patients)
• non-Group A Strep • Postop abdominal and perineal infections
• anaerobes including Clostridia
• facultative anaerobes
• enterobacteria
• Synergistic virulence between organisms
Type 2 Monomicrobial • 5% of cases
• Group A β-hemolytic Streptococci is most • Seen in healthy patients
common organism isolated • Extremities
Type 3 Marine Vibrio vulnificus • Marine exposure
(gram negative rods)
Type 4 MRSA

LRINEC score:
Score > 6 have PPV of 92% of having necrotizing fasciitis
CRP (mg/L) ≥150: 4 points
WBC count (×103/mm3): <15: 0 points 15–25: 1 point >25: 2 points
Hemoglobin (g/dL) >13.5: 0 points 11–13.5: 1 point <11: 2 points
Sodium (mmol/L) <135: 2 points
Creatinine (umol/L) >141: 2 points
Glucose (mmol/L) >10: 1 point
 Gas Gangrene
Also known as clostridal myonecrosis.
gram-positive obligate anaerobic spore-forming rods that produce exotoxins (e.g. C. perfringens
alpha toxin) causes muscle necrosis and vessel thrombosis , hemolysis and shock
incubation period <24h
gas produced by fermentation of glucose: main component is nitrogen

OE: blebs, hemorrhagic bullae, tenderness and crepitus

Both NF and GG mainstay of treatment would be:

Extensive wound debridement
IV antibiotics
Hyperbaric oxygen therapy in GG

Difference between endotoxin and exotoxin

S.N. Exotoxins Endotoxins

1 Excreted by organisms, living cell Integral part of cell wall
2 Found in both Gram positive and Gram Negative bacteria Found mostly in Gram Negative Bacteria
3 It is polypeptide It is lipopolysaccharide complex.
4 Relatively unstable, heat labile (60°C) Relatively stable, heat tolerant
5 Highly antigenic Weakly immunogenic
6 Toxoids can be made by treating with formalin Toxoids cannot be made
7 Highly toxic, fatal in µg quantities Moderately toxic
8 Usually binds to specific receptors Specific receptors not found
9 Not pyrogenic usually, Toxin Specific Fever by induction of interleukin 1 (IL-1)
production, Shock
10 Located on extrachromosomal genes (e.g. plasmids) Located on chromosomal genes
11 Filterable Not so
12 It has no enzymatic activity It has mostly enzymatic activity
13 Its molecular weight is 10KDa Its molecular weight is 50-1000KDa
14 On boiling it get denatured. On boiling it cannot be denatured.
15 Detected by many tests (neutralization, precipitation, Detected by Limulus lysate assay
etc)
16 Examples: Toxins produced by Staphylococcus aureus, Examples: Toxins produced by E.coli,
Bacillus cereus, Streptococcus pyogenes, Bacillus Salmonella Typhi, Shigella, Vibrio
anthrcis(Alpha-toxin, also known as alpha-hemolysin cholera(Cholera toxin- also known as
(Hla)) choleragen)
17 Diseases: Tetanus, diphtheria, botulism Diseases: Meningococcemia, sepsis by gram
negative rods

Antibiotics and mechanism of actions

Anatomy:

Compartments of the thigh

Compartments of the calf

Course of vertebral artery:

The vertebral arteries arise from the subclavian arteries, one on each side of the body, then enter
deep to the transverse process of the level of the 6th cervical vertebrae (C6), or occasionally (in
7.5% of cases) at the level of C7. They then proceed superiorly, in the transverse foramen (foramen
transversarium) of each cervical vertebra. Once they have passed through the transverse foramen
of C1 (also known as the atlas), the vertebral arteries travel across the posterior arch of C1 and
through the suboccipital triangle before entering the foramen magnum.
Herniated Nucleo Pulposus
Herniation to posterolaterally due to thick PLL
Disc consists of:
Annulus fibrosus (type1 collagen, oblique orientation fibers – resist tensile)
- inner annulus is type 2 collagen
Nucleus pulposus (gelatinous mass, type2 collagen – resist compression)

the disk is avascular with capillaries terminating at the end plates

nutrition reaches nucleus pulposus through diffusion through pores in the endplates
annulus is not porous enough to allow diffusion

Posterior triangle of neck

Apex: Union of the sternocleidomastoid and the trapezius muscles at the superior nuchal line of the
occipital bone

Anterior: Posterior border of the sternocleidomastoideus

Posterior: Anterior border of the trapezius
Base: Middle one third of the clavicle
Roof: Superficial layer of the deep cervical fascia

Divided into two:

an upper or occipital triangle
a lower or subclavian triangle (or supraclavicular triangle)

Contents:
A) Nerves and Plexuses:
Spinal accessory nerve (Cranial Nerve XI)
Branches of cervical plexus
Roots and trunks of brachial plexus
Phrenic nerve (C3,4,5)

B) Vessels:
Subclavian artery (Third part)
Transverse cervical artery
Suprascapular artery
Terminal part of external jugular vein

C) Lymph Nodes:
Occipital
Supraclavicular

D) Muscles:
Inferior belly of omohyoid muscle
Anterior Scalene
Middle Scalene
Posterior Scalene
Levator Scapulae Muscle
Splenius
What is Horner’s syndrome?

Horner syndrome (Horner’s syndrome) results from an interruption of the sympathetic nerve
supply to the eye and is characterized by the classic triad of miosis (ie, constricted pupil), partial
ptosis, and loss of hemifacial sweating (ie, anhidrosis).

Causes: Pancoast tumor, Trauma, infections, Carotid artery ischemia

Types of joints

1. Ball and socket joint – Hip

2. Hinge joint – elbow / knee
3. Gliding joint – AC joint (flat surface)
4. Saddle joint – Thumb carpometacarpal

Risk factors of hip dislocation

1. Bony – coxa valga, shallow acetabulum

2. Soft tissue – weak soft tissue restraining, weakened iliofemoral ligaments, systemic disease

Adductor canal

From apex of femoral triangle until adductor hiatus at middle third of thigh
Borders:
1. Anteromedial: subsortrial fascia
2. Lateral : medial border of vastus medialis
3. Posterior: adductor longus and part of adductor magnus

Contents: Saphenous nerve and nerve to vastus medialis, femoral artery, femoral vein

Blood supply to femoral head

2 anastamosis contributed blood supply to femoral head

1. Trochanteric anastomosis (contributed by: sup gluteal, Lat circumflex, med circumflex,
inferior glut)

2. Cruciate anastomosis (contributed by: lat circumflex. Infr glut, medial circumflex, first
perforating branch of deep femoral artery)
a. The cruciate anastomosis is clinically relevant because if there is a blockage
between the femoral artery and external iliac artery, blood can reach the popliteal
artery by means of the anastomosis.
And also obturator artery.

Retrograde blood supply, ascend through retinacular fibers

Blood supply to scaphoid

1. major blood supply is dorsal carpal branch (branch of the radial artery)
enters scaphoid in a nonarticular ridge on the dorsal surface and supplies proximal 80% of
scaphoid via retrograde blood flow
2. minor blood supply from superficial palmar arch (branch of volar radial artery)
enters distal tubercle and supplies distal 20% of scaphoid
Blood supply to talus

1. Tarsal sinus – laterally – DPA and perforating peroneal branch

2. Tarsal canal – Medially - PTA
3. Deltoid artery
4. Direct branch from dorsalis pedis artery

Appendics

Mc burney line
Average in 9cm, 2cm below at ileocecal junction.
Most common is retrocecal 60%,
Connected to mesentery by mesoappendics -> appendicular artery from terminal branch of
ilieocolic artery -> SMA
Difference in appearance small and large bowel

Small vs large
1. Small is long – 7m meters. Large comparatively shorter at 1.5m
2. Small has 3 parts: duodenum, jejunum and ileum. : large has four parts; cecum, colon,
rectum and anal canal
3. Small: internal surface has circular folds, large are abscent
4. Small: present of villi , absent in large
5. Small: Peyers patches present, absent in large
6. Absent of tenia coli in small, present in large
7. Haustra abscent in small, present in large
8. Doesn’t have epiploic appendages, present in large
9. Absorb digested nutrients, mainly water absorption in large
10. Small : relatively small movements, large largely fixed.

Course of radial artery

Brachial artery divides into radial & ulnar artery at the level of neck of radius. Radial artery is
usually the continuation, ulnar a. is usually (90%) larger and branch at an angle – ulnar
dominant. Upper part of foream it is deep to brachioradialis. Medial to superficial branch of
radial nerve. Distal part of radial artery covered only by skin & superficial and deep fascia. It
enters hand by crossing anatomical snuffbox

Course of radial nerve. PIN

Radial nerve arises from posterior cord, emerged from triangular interval. From there it goes down
posterior to arm, and winds around radial groove at distal midhsaft of humerus while piercing
lateral intermuscular septum. It then descends in between brachioradialis and brachialis muscle
and pierce the supinator and bifurcates, giving posterior interrouseous nerve, and superficial radial
nerve.

PIN runs past vascular leash of henry, and ERCB though the arcade of frohse of the supinator ( 2
common places for entrapment syndrome). It then goes posteriorly and supply muscle of extensor
of hand and ends at dorsal capsule of wrist joint.

Meanwhile superficial branch descends beneath brachioradialis, making its way to dorsally at 5 cm
proximal to wrist joint. It then supplies sensory at lateral 3rd of dorsal of hand.
Brachial plexus
Roots (anterior rami of C5 – T1) – between scalene muscles
Trunks – in posterior triangle
Divisions – behind clavicle
Cords – according to position in the second part of axillary artery (beneath pec minor)

*axillary artery division depends on pectoralis minor position

* division of axillary artery: She (1) Taste Like (2) Sweet Apple Pie (3)

*subclavian artery depends on anterior scalene division

* Vitamin (vertebral, internal thoracic, and Thyrocervical trunk- contribute to scapula
anaestomosis) Costocervical, Dorsal scapular
*site of scapula anastomosis. (Transverse cervical + suprascapular artery: first part of subclavian ) +
(subscapular artery- thoracodorsal / circumflex scapular : third part of axillary artery)

Acromial anastomosis: thoracoacromial + acromial branch of suprascapular artery + ascending

branch from circumflex artery

Blood supply to breast: internal thoracic, lateral thoracic

Base of skull and Cranial Nerves

** Foramen lacerum : internal carotid artery

** Foramen magnum : spinal cord, vertebral artery
** Foramen spinosum : middle meningeal artery and vein (branch from external carotid)

Branch of external carotid artery

Bifurcate from common carotid at level of C4 (thyroid cartilage)

In the carotid triangle

Sup thyroid artery
Ascending pharyngeal artery
Lingual artery
Facial
Occipital (post)
Lingual (supply tongue)

Posterior auricular artery

Superficial temporal artery (terminal branch)
Maxillary artery (terminal branch – divided into 3 main branches : mandibular, pterygoid,
pterygopalatine)

Bones of skull

Sinuses of brain
Brain

Blood supply to brain:

Posterior portion:
Vetebral artery -> vetebrobasillar artery (given off branch to cerebellum on way up: anterior
inferior and superior cerebellar artery -> posterior cerebral artery
Anterior Portion:
Internal carotid -> Middle cerebral artery and anterior cerebral artery
Both portions connected by posterior comminucating artery and anterior comminucating artery =
circle of willis

Middle supply lateral fronto-parietal-temporal lobe

Anterior supply fronto – falx cerebri – 2cm from midline (lowerlimb more affected)
Posterior cerebral -> temporo-occipital lobe
CSF route

CSF is produced by choroid plexus in ventricles; mostly at lateral ventricles

Function: cushions, immunology and cerebral autoregulation
500mls per day
Ependymal cells actively secrete sodium into the lateral ventricles. This creates osmotic pressure and
draws water into the CSF space. Chloride, with a negative charge, moves with the positively charged
sodium and a neutral charge is maintained. As a result, CSF contains a higher concentration of
sodium and chloride than blood plasma, but less potassium, calcium and glucose and protein

Route: lateral ventricles -> interventricular foramina (foramen of Monroe) -> third ventricle ->
cerebral aquaduct -> fourth ventricle -> foramen of magendi (to cisterna magna – median aperture
and foramen of luschka (lateral aperture))
Vocal cords

The vocal folds are located within the larynx at the top of the trachea. They are attached posteriorly
to the arytenoid cartilages, and anteriorly to the thyroid cartilage. They are part of the glottis,
which includes the rima glottidis. Their outer edges are attached to muscle in the larynx while their
inner edges, or margins are free, forming the opening called the rima glottidis. They are
constructed from epithelium, but they have a few muscle fibres in them, namely the vocalis muscle
which tightens the front part of the ligament near to the thyroid cartilage. They are flat triangular
bands and are pearly white in color. Above both sides of the glottis are the two vestibular folds or
false vocal folds which have a small sac between them.

Situated above the larynx, the epiglottis acts as a flap which closes off the trachea during the act of
swallowing to direct food into the esophagus. If food or liquid does enter the trachea and contacts
the vocal folds it causes a cough reflex to expel the matter in order to prevent pulmonary
aspiration.

Nerve supply: recurrent laryngeal nerve

Femoral Sheath

The femoral sheath (crural sheath) is formed by a prolongation downward, behind the inguinal
ligament, of the fasciae which line the abdomen, the transverse fascia being continued down in
front of the femoral vessels and the iliac fascia behind them.

It’s about 4 cm below the inguinal ligament.

The lateral compartment contains the femoral artery and femoral branch of genitofemoral nerve,
and the intermediate the femoral vein, while the medial and smallest compartment is named the
femoral canal, and contains some lymphatic vessels and a lymph gland embedded in a small
amount of areolar tissue.

** Femoral nerve does not include in femoral sheath as it descends lateral to this structure.
Femoral canal

The femoral canal is conical and measures about 1.25 cm. in length. Its base directed upward and
named the femoral ring, is oval in form, its long diameter being directed transversely and
measuring about 1.25 cm.
Borders:
anterosuperiorly by the inguinal ligament
posteriorly by the pectineal ligament lying anterior to the superior pubic ramus
medially by the lacunar ligament
laterally by the femoral vein
Contains: lymph node of cloquet
** site of indirect inguinal hernia

Femoral Triangle

Borders;
Sup; inguinal ligament
Lateral: medial aspect of Sartorius
Medial: medial aspect of adductor longus
Roof: Superficial fascia
Base; pectineus and adductor longus

Femoral nerve

Arises from lumbar plexus L2-L4 (posterior division of plexus, anterior is obturator nerve)
It descends through the fibers of the psoas major muscle, emerging from the muscle at the lower
part of its lateral border, and passes down between it and the iliacus muscle, behind the iliac fascia;
it then runs beneath the inguinal ligament, into the thigh, and splits into an anterior and a posterior
division. Under the inguinal ligament, it is separated from the femoral artery by a portion of the
psoas major.

Divided into anterior and posterior

Anterior give rise to: nerve to pectineus and Sartorius and sensation at medial aspect of thigh
Posterior: muscular branch to quadriceps and iliacus and knee joint

Sciatic nerve

Arises from lumbosacral plexus L4-S3

The nerve passes beneath piriformis and through the greater sciatic foramen, exiting the pelvis.
From here, it travels down the posterior thigh to the popliteal fossa. The nerve travels in the
posterior compartment of the thigh deep behind long head of biceps and underlying adductor
magnus. At apex of popliteal fossa (about handbreath above knee joint) it divides into:

Anterior division: tibial

Posterior division: common peroneal

Supplies all compartment of leg and its anterolateral aspect of cutaneous innervation.
Thigh: Long head biceps femoris, Semitendinosous, Semimembranosous, and hamstring part of
adductor magnus (by tibial division of sciatic nerve)

Compartment Hand
Kidney

Lies behind peritoneum

Measures about 3x6x12cm and weighs 130-150g
Hilum lies just below the transpyloric plane, over psoas muscle
 Separated by peritoneum by: Right: second part duodenum, left: body of pancreas
Upper pole left kidney = 11th rib
Upper pole right kidney = 12th rib
Posteriorly: diaphragm and quadratus lumborum
The lateral part of lower pole : bound by hepatic and splenic flexure of transverse colon
 Hence splenomegaly grow inferomedially

Each moves 2cm vertically during respiration

Layers; Renal fascia of gerota -> Perinephric fat -> renal capsule -> kidney

Blood supply: Renal artery (1 litres per minute), behind pancreas n renal vein
 Has 5 segments (4 ant, 1post), with no collaterals
 Renal vein communicate to one another -> renal vein
 Front to back: vein artery ureter.
Lymph : Para-aortic nodes at L2

Nerve : Sympathethic – T12- L1, afferent fibres accompanies.

Heart

Heart is muscular pump responsible for blood circulation. Comprises of four chambers.
Lies oblique in thorax, apex towards left side.

Borders:
Right = right atrium
Inferior border = right ventrile mainly
Left border = left ventricles
Sternocostal surface; right ventricle
Diaphragmatic surface; mainly left ventricles.

Surface markings; lower border of 3rd to 6th intercostal space

Apex: 5th intercostal space

Blood supply:
2 coronary artery;
both will supply conducting system.

Right
1. ventricular artery
2. marginal artery
3. posterior interventricular artery
Left
1. left main stem;
a. circumflex artery – marginal artery -
b. anterior descending – diagonal artery - anterior interventricular

Vein:
Coronary sinus at posterior interventricular groove opens into right atrium
Middle and great cardiac vein; open into coronary sinus
Anterior cardiac veins drains into right atrium
Venae cordis minimae opens into respective chambers
Lungs

1. 2 Lobes on left, 3 lobes on right

2. surface is mottled depending on environment
3. Lung surface conforms to shape of cavity : costal convex surface, concave diaphragmatic surface
Posterior surface rounded to fit paravertebral gutter.
Impressions ; aorta, subclavian at apex, cardiac, trachea
4. bronchus of right upper lobe divide before hilum

5. Surface markings:
a. hilum behind 3rd and 4th intercostal cartilage at the level of t5 vetebra
b. upper costal – lung = pleural
c. inferior surface - 2 ribs higher than in pleural at inferior surface; ie; midclavicular 6th,
midaxillary 8th and lateral border of erectae spinae at 10th rib.
d. fissures – oblique at line at 5th rib with abducted scapula above head; horizontal at fourth
costal cartilage.

5. Bronchus:
a. Right : 2.5cm long, shorter wider and more vertical : 3:2:5
b. Left: 5cm : 5:5 – both lung have 10 bronchopulmonary
c. Smooth hyaline cartilage
d. Pseudostratified columnar ciliated cell

6. Blood supply
a. Bronchial tree – bronchial artery (direct branches from aorta)
b. Alveoli – pulmonary artery deoxygenated blood
c. Vein – right to azygos, left into accessory hemiazygos
7. Nerves
a. Autonomic from cardiac plexus direct from thorcacic n sympathetic chain feeds into
pulmonary plexus
b. Parasympathetic helps clear secretions; bronchoconstricor and vasodilation
c. Sympathetic: bronchodilator and vasoconstrictor
Osteology of thorax

1. Sternum: manubrium, sternum and xiphoid process. Joint by secondary cartilaginous joint.
a. Manubrium; flat four sided. Upper margin = jugular notch. Investing layer deep
cervical fascia attached to it. Lateral border attached to first costal cartilage by
primary cartilaganoeus joint. Inferior angle has articular surface for second
cartilage. Anterior surface covered by pec major attachment.
b. Body of sternum; articular facet till 7th cartilage – synovial joints. Pectoralis major
arises from anterior to midline; laterally anterior and internal intercostal cartilage
c. Xiphoid process attachment of linea alba – ossifies at mid age.

2. Ribs;
a. Ossifications at 8th week anterior – posterior. Fused at 20years.
b. Typical (3-10): head has two articular facet, upper facet articulate with above
vertebra. Neck is flattened. Tubercle has two components. Articulating facet
attached to own transverse process of vertebra while rough tubercle site of
attachment of lateral costotransverse ligament. Shaft slopes down. External
intercostal arises from sharp lower border whilst the internal interostal is attached
to the costal groove.
c. Atypical (1,2,11,12): First rib: strongest broadest. Neck slopes upwards hence the
anterior surface and head lies same plane. Head is single facet. It is crossed by
(medial to lateral) : sympathetic trunk, intercostal vein, superior intercostal artery,
and T1 root. -> dome of cervical pleural hold these structure in place. Going further
anterior, neck broadens and prominent tubercle noted at lateral side. Structures
across Posterior to anterio: subclavian artery, anterior scalene muscle, subclavian
vein. Anteriorly attachments of subclavius and costoclavicular ligaments
d. 11th rib: head with single facet, short neck with no tubercle
e. 12th rib: single facet no tubercle.

3. Costal cartilage
a. First is short and thick. Articulates with clavicle and costoclavicular ligament.
Spleen

Largest lymphoid organs

1x3x5 inches measurement, weight 7oz, lies deep to 9-11th rib.
Hilum is at angle of stomach and kidney, lies within the splenorenal ligaments
Have impressions of; stomach, kidney, colonic, and diaphragm
Enlarges towards RIF due to splenic flexure colon which rather fixed.

Blood supply – splenic artery from abdominal aorta, vein drain into portal system (together w
mesenteric)
Nerves – celiac provides sympathetic nerves

Level of vertebra:
1. T12 – celiac trunk
2. L1 – splenic vein, SMA, pyloric of stomach, fundus of gallbladder, hilum left kidney, neck of
pancreas
3. L2 – renal artery and vein, pancreas w uncinate process
4. L3 – IMA
5. L4 – intercrestal line, bifurcation of aorta

‘
Pancreas

Function as exocrine and endocrine organ.

Neck of pancreas at transpyloric plane
Head moulded in C shaped concavity of duodenum (L2), lies over IVC and right and left renal vein.
Posterior surface extension hook shaped – uncinate process
Neck: narrow band of pancreatic tissue infront of portal vein, transverse mesocolon attached at its
lower border
Body: sloping upwards, across left renal vein and aorta, crus of left diaphragm, posas muscle and
lower part of suprarenal gland. Triangular in cross section. Superior border cross at celiac trunk.
Inferior border crosses the origin of SMA. Transverse mesocolon attached anteriorly.

Tail: lies within the splenorenal ligaments.

Pancreatic duct: at the hepatopancreatic ampula, joined at angle of 60’. Drains most of pancreas
except uncinate process that drain by the accessory pancreatic duct. Opens at second part of
duodenum. Surrounded by sphincter of oddi.

Blood supply: The superior pancreaticoduodenal artery and inferior pancreaticoduodenal artery
Lesser sac boundaries

The quadrate lobe of the liver, the stomach, lesser omentum and gastrocolic ligament, demarcates
it anteriorly. Posteriorly the pancreas marks it. Its left lateral margin is made by the left kidney and
adrenal gland. Its boundary on the right is made by the omental foramen and lesser omentum.If
these structures rupture they may leak into the lesser sac. For the stomach, which lies anterior to
the lesser sac, the rupture must be on the posterior side; if it were anteriorly located, the leak
would collect in the greater sac.

Stomach

At the left hypochondriac region, a muscular portion of alimentary system

Outer longitudinal, inner circular and innermost obliquely oriented muscle.
Cardia = gastroesophageal junction at level of T10, 2.5cm to the left midline, behind 7th costal
cartilage
Pylorus = gastroduodenal junction (L1)
Invested by peritoneum
- lesser omentum from lesser curvature
- greater omentum from greater curvature
angular incisura – curvature in body with lesser curvature.
Pyloric sphincter anterior indicated by prepyloric vein of mayo. Pyloric canal lies on head and neck
of pancreas.

Stomach bed:
1. left crus of diaphragm
2. splenic artery
3. body of pancreas
4. transverse mesocolon
5. upper part of left kidney
6. left suprarenal gland
7. spleen
8. and left colic flexure.

Blood Supply:
Lesser curvature
 1. celiac trunk – common hepatic – right gastric
2. left gastric artery

Greater curvature
3. splenic artery – short gastric
4. common hepatic – right gastroduodenal -> right gastroepiploic
5. splenic artery -> left gastroepiploic artery.

Veins follows artery into SMA or splenic -> portal system

Nerve supply:
Parasympathetic: vagus nerve
Sympathetic: direct fibres accompany the artery

Describe the structure of Penis

Part of male urogenital organ

Root of penis is attached to inferior surgace of the perineal membrane.
Bulb, surrounded by crus bilaterally.

3 main structures;
a. corpus spongiosum contains penile urethra
b. 2 corpus cavernosum which divides by septum of penis, surrounds
by tunica albuinea

Blood supply from branches of internal pudendals:

1. artery to the bulb of penis -> corpus spongiosum
2. Deep artery of penis -> corpus cavernosum
3. Dorsal artery -> skin (also receives supply from superficial external pudendal)

Nerve supply:
Pudendal nerves
Ilioinguinal nerve – small area proximal penis
Sympathetic from hypogastric plexus (L1)
Parasympathetic by pelvic splanchnic nerves
How to set up an operation theatre

i. Must not be at busy place (1st floor)

ii. Adjacent to intensive care unit; ICU, PICU
iii. Easy access to radiology department
iv. Consist of dirty, clean, sterile area (induction, theatre)
v. Air flow is laminar and air changes are positive pressure
vi. HEPA (high efficiency particulate arressantace) Filter which able to filter :
0.3 miumeter
vii. Adequate size for and plug point for ventilator and other equipment’s, xray
box
viii. Floor: seemless polyvinyl chloride
ix. Ceiling height: 100 feet
x. Lighting: 27-127000 lux
xi. Humidity: 30-60
xii. Temp: 18-24’c

Operation Room Hazard

1. Staff
2. Environment
3. Equipment

Electrical hazards – diathermy faulty placement

Thermal hazards – low temperature for neonates
Radiation hazards – usage of I/I
Infective hazards- poor asepsis control, risk Hep B and AIDS
Chemical hazards – hypersensitivity
Anesthesia gas pollution
Physical hazard during transfer
Positioning of patients – neuropraxia

Tell me about sterilization:

Process of destruction of all forms of microbial life including spores, cysts and viruses.

1. Heat – autoclave – steam heated to 121’c for lb/in 15 mins, or 134’c at pressure of 30lb/in
for 3 mins. Test using Bowie-Dick test (heat sensitive)
a. Moist heat helps penetrate material better
Dry Heat: 160’c for 2hours – not suitable for all surgical materials
2. Irradiation – industrial, large batch, useful for plastics materials
3. Chemicals – useful for heat labile items
a. Ethylene oxide: useful for heat labile, electrical equipment (rubber n plastic)
b. Glutraldehyde: 2% for endoscopic equipments. Longer time for TB (60minutes)
c. Formaldehyde: 73’c at 2 hours, lowest sterilization temperatures
4. Filtration
a. Drugs – large, industrial usage. Determine by pore size.
What about Disinfectant:

Process to reduce the number of viable micro-organism. Unable to inactivate some if not all spores
and virus.
Cleaning: physical removes contamination but does necessary inactivate organism.

Efficicency depends on: length of exposure and presence of foreign body/ blood

1. Hypochloride; wide spectrum, includes virus

2. Povidone – broad spectrum bacteria -> virus, bacteriocidal, may induce allergy
3. Chlorhexidine – quaternary ammnonium compound, bacterial cell wall disruption. 6
hours duration. Non toxic to skin
4. Alcohol – denatures protein, broadest spectrum at 70%. Relatively inactive against
spores and fungi.
5. Cetrimide – active against gram positive, not pseudomonas, weak disinfectant
6. Formaldehyde – wide antibacterial including spores.usage in 10% aqueous.
7. Boiling water – kills bacteria including TB – for items, not patient.
8. Pasteurisation – 63-66’c for 30mins. Inactivate non-spore forming including
mycobacterium n salmonella.

Massive blood transfusion

In adults, as a transfusion of half of one blood volume in 4 hours, or more than one blood volume in
24 hours (adult blood volume is approximately 70 mL/kg)

In children, as a transfusion of more than 40 mL blood/kg (blood volume of children older than
neonates is approximately 80 mL/kg)

Complications:
Hypothermia: The prevention of hypothermia during massive transfusion is critical as the morbidity
and mortality is significantly increased in the presence of hypothermia. Many of the complications
associated with massive transfusion are a consequence of decreased core body temperature

Hypocalcemia: The citrate used as the anticoagulant in transfusion products binds calcium resulting
in hypopcalemia, of which the most common clinical symptom is hypotension. Arrhythmias and
myocardial depression can further lead to hemodynamic instability.

Hypomagnesemia is also a complication of citrate toxicity and thus the likelihood is increased in the
presence of hypothermia.

Hyperkalemia: Potassium is gradually released from stored red blood cells resulting in hyperkalemia
in 5% of massively transfused patients.

Acidosis: The addition of storage media to red blood cells lowers the PH to 7.0. After 21 days of
storage it is further reduced to 6.9, secondary to the accumulation of lactate and pyruvic acids as
well as CO2 from RBC metabolism
Postoperative fever

the lungs, i.e. pneumonia, aspiration, and pulmonary

Wind POD1-2 embolism. Once attributed to atelectasis, but a recent review
suggests that is not supported by existing clinical evidence.
urinary tract infection, related to indwelling catheter (during
Water POD3-5
surgery or currently i.e. Foley catheter )
Walking (or VEINS, which
POD4-6 deep vein thrombosis or pulmonary embolism
then sounds like "Weins")
surgical site infection, which in obstetrics or gynaecology,
Wound POD5-7
may refer to the uterus.
Wonder drugs or “What drug fever, infections related to intravenous lines or reaction
POD7+
did we do?” to blood products

Describe the differential diagnosis of a patient with postoperative fever. Discuss clinical
manifestations, diagnostic work-up, and management:
• Within 24 hours - response to surgical trauma; atelectasis; necrotizing wound infections.
• Between 24 and 72 hours:
o pulmonary disorders (atelectasis, pneumonia)
o catheter related complications (IV-phlebitis, Foley-UTI)
• After 72 hours:
o infectious (UTI, pneumonia, wound infection, deep abscess, anastomotic leak,
prosthetic infection, acalculous cholecystitis, parotitis)
o noninfectious (deep vein thrombosis)

• Intraoperative - malignant hyperthermia

Malignant hyperthermia (MH) or malignant hyperpyrexia is a rare life-threatening condition
that is usually triggered by exposure to certain drugs used for general anesthesia — specifically the
volatile anesthetic agents and succinylcholine, a neuromuscular blocking agent. In a large
proportion (50–70%) of cases, the propensity for malignant hyperthermia is due to a mutation of
the ryanodine receptor (type 1), located on the sarcoplasmic reticulum (SR), the organelle within
skeletal muscle cells that stores calcium. RYR1 opens in response to increases in intracellular Ca2+
level mediated by L-type calcium channels, thereby resulting in a drastic increase in intracellular
calcium levels and muscle contraction

The end result of these alterations is greatly increased Ca2+ release due to a lowered activation and
heightened deactivation threshold. The process of sequestering this excess Ca2+ consumes large
amounts of adenosine triphosphate (ATP), the main cellular energy carrier, and generates the
excessive heat (hyperthermia) that is the hallmark of the disease. The muscle cell is damaged by the
depletion of ATP and possibly the high temperatures, and cellular constituents "leak" into the
circulation, including potassium, myoglobin, creatine, phosphate and creatine kinase.
Post-operative hypoxia

Can be divided into:

1. Lack of alveolar ventilation – obstructive airway, drugs, atelectasis lobar pneumonia,
pneumothorax, bronchospasm
2. V/Q perfusion mismatch – pulmonary embolism
3. Decreased alveolar diffusion – pneumonia, pulmonary embolism, ARDS

Post-operative analgesia
*Lateral spinothalamic tract carries pain upwards.

** Pain gate theory

A Theory that pain pathway controlled regulated by – inhibitory neuron

And that the larger afferent fibres will overcome the slower pain fibres.

Example:
1. Iniitial pain; A delta fibres, fast -> signal to brain, then rubbing effect will induce a larger
than C fibres (small- (aching pain) to be evoked, and thus overlapped the response to C
fibres. It will also activate the inhibitory neuron and blocked the pain stimulation. These
occurs at dorsal horn ganglia, substantia gelatinosa.

2. Endogenous opioids by reticular spinal pathway – bleeding solder able to continue to walk
for safety. Endogenous opioid blocks the release of substance P.
Mode of Action Analgesia:

1. Paracetamol
a. NAPQI, act on TRPA1-receptors in the spinal cord to suppress the signal
transduction from the superficial layers of the dorsal horn, to alleviate pain.
b. Central acting reducing prostaglandin within the CNS.

2. NSAIDS
a. Aspirin's ability to suppress the production of prostaglandins and thromboxanes is
due to its irreversible inactivation of the cyclooxygenase (COX; officially known as
prostaglandin-endoperoxide synthase, PTGS) enzyme required for prostaglandin
and thromboxane synthesis.
b. Diclofenac The primary mechanism responsible for its anti-inflammatory,
antipyretic, and analgesic action is thought to be inhibition of prostaglandin
synthesis by inhibition of cyclooxygenase (COX). It also appears to exhibit
bacteriostatic activity by inhibiting bacterial DNA synthesis.
c. A highly selective reversible inhibitor of the COX-2 isoform of cyclooxygenase,
celecoxib inhibits the transformation of arachidonic acid to prostaglandin
precursors. Therefore, it has antipyretic, analgesic and anti-inflammatory
properties.[2] Nonselective NSAIDs (such as aspirin, naproxen, and ibuprofen)
inhibit both COX-1 and COX-2. Inhibition of COX-1 (which celecoxib does not inhibit
at therapeutic concentrations) inhibits the production of prostaglandins and the
production of thromboxane A2, a platelet activator. COX-1 is housekeeping enzyme
whilst COX-2, on the contrary, is extensively expressed in cells involved in
inflammation and is upregulated by bacterial lipopolysaccharides, cytokines,
growth factors, and tumor promoters It binds with its polar sulfonamide side chain
to a hydrophilic side pocket region close to the active COX-2 binding site
 3. Opioids
a. Opioids and non-steroidal anti-inflammatory drugs (NSAIDs) are the commonest
drugs used to treat pain. Opioids mimic the actions of endogenous opioid peptides
by interacting with mu, delta or kappa opioid receptors. The opioid receptors are
coupled to G1 proteins and the actions of the opioids are mainly inhibitory. They
close N-type voltage-operated calcium channels and open calcium-dependent
inwardly rectifying potassium channels. This results in hyperpolarization and a
reduction in neuronal excitability. They also decrease intracellular cAMP, which
modulates the release of nociceptive neurotransmitters (e.g. substance P).

Glucose transport in body:

GLUT (with carrier protein) vs SGLT-1 / -2 (fascilitated diffusion in intestine and kidney)
GLUT -1 RBC, BBB
GLUT-2 kidney, pancreas, intestine, liver

Primary transport : direct ATP

Secondary active: due to pressure gradient, being pumped out.

Osteology

1) Pterion – significance, medial meningeal artery, how patient present SDH vs EDH
The pterion is the region where the frontal, parietal, temporal, and sphenoid join together. The
pterion overlies the anterior branch of the middle meningeal artery on the internal aspect of the
skull, and it corresponds to the stem of the lateral sulcus of the brain.

The center of the pterion is about 4 cm above the midpoint of the zygomatic arch and nearly the
same distance behind the zygomatic process of the frontal bone.

The pterion is identifying as the weakest part of the skull. SDH presented with lucid interval, tear of
bridging veins that cause slow rise in ICP. Occurs more frequent in elderly.

2) Venous drainage in skull – (posterior system) superior sagittal + inferior sagittal (goes to
straight sinus) = confluence of sinus – goes bilaterally to transverse sinus then to sigmoid sinus
and drains into internal jugular vein. Anterior system: cavernous sinus -> inferior petrosal ->
sigmoid

3) Facial nerve injury – Due to its long course, it can be attributed to multiple causes. Most
common is bells palsy. Other causes include trauma, herpes infection, stroke to pons (nucleus is
there) and tumore (acustic neuroma). Bells palsy treated with steroids. Supportive
management of symptoms. Dry eyes.

4) Danger triangle: corners of mouth and bridge of nose. Higher risk of infection to brain due to
cavernous sinus (contains internal carotid and cranial nerves 3,4,5,6 passed through this) ->
superior and inferior petrosal sinus -> sigmoid sinus -> internal jug
5) Mandible – muscle attachments, nerve in mandibular foramen
contains the inferior alveolar nerve, inferior alveolar artery, and inferior alveolar vein.
Muscle attachment : buccinators, pterygoid, mylohyoid, masseter
- inside; genioglossus, geniohyoid, digastric

6) What structures crosses Angle of Louis – at T4

a) Ascending arch of aorta ends, bifurcation of trachea, division of pulmonary trunk below this
level, upper limit of base of heart, cardiac plexus

7) Internal carotid artery course and division

a) It is relatively superficial at its start, where it is contained in the carotid triangle of the neck,
and lies behind and lateral to the external carotid, overlapped by the sternocleidomastoid
muscle, and covered by the deep fascia, the platysma, and integument: it then passes
beneath the parotid gland, being crossed by the hypoglossal nerve, the digastric muscle
and the stylohyoid muscle, the occipital artery and the posterior auricular artery. Higher up,
it is separated from the external carotid by the styloglossus and stylopharyngeus muscles,
the tip of the styloid process and the stylohyoid ligament, the glossopharyngeal nerve and
the pharyngeal branch of the vagus nerve. It is in relation, behind, with the longus capitis,
the superior cervical ganglion of the sympathetic trunk, and the superior laryngeal nerve;
laterally, with the internal jugular vein and vagus nerve, the nerve lying on a plane posterior
to the artery; medially, with the pharynx, superior laryngeal nerve, and ascending
pharyngeal artery. At the base of the skull the glossopharyngeal, vagus, accessory, and
hypoglossal nerves lie between the artery and the internal jugular vein.

b) Unlike the external carotid artery, the internal carotid normally has no branches in the neck

C1: Branches from the cervical portion - none.

C2: Branches from the petrous portion
Caroticotympanic arteries
Artery of pterygoid canal (vidian artery)
C3: Branches from the lacerum portion - none
 C4: Branches from the cavernous portion
Branches of the meningohypophyseal trunk:
Tentorial basal branch
Tentorial marginal branch
Meningeal branch - helps supply blood to the meninges of the anterior cranial fossa
Clivus branches - tiny branches that supply the clivus
Inferior hypophyseal artery
Capsular branches - supplies wall of cavernous sinus
Branches of the inferolateral trunk:
Branches to trigeminal ganglion - provide blood to trigeminal ganglion
Artery of the foramen rotundum
Branches to nerves
C5: Branches from the clinoid portion - none
C6: Branches from the ophthalmic portion
Ophthalmic artery
Superior hypophyseal artery
C7: Branches from the communicating portion
Posterior communicating artery
Anterior choroidal artery
Anterior cerebral artery (a terminal branch)
Middle cerebral artery (a terminal branch)

8) Cervical spine with some embrology C1/C2 - what happen to C1 body, course of vertebral artery,
how much percentage of people does it go through C7 transverse foramen? Show exact location
of vertebral artery when it goes from C2 to C1
a) Both are atypical cervical vertebra. (not bifid)
Atlas:
b) Atlas ossifies at 7th week of fetal life (in centre lateral mass)
c) Unite at 4th year
d) Kidney shaped upper surface, - articulate with occipital condyle
e) Articular facet inline with uncovetebral joint – so anterior rami nerves sent behind
f) Lateral mass bears weight of skull, not dens.
g) Atlanto-occipital is a synovial joint covered with hyaline cartilage.

Axis:
h) has dens and large spinous process
i) Large bifid spinous process.
j) Ligaments for stability:
i) Transverse ligament
ii) Sup and inferior cruciform ligaments
iii) Alar ligaments
iv) Tectorial ligament
Atlanto- axial = rotatory movement
Muscles: SCM, splenius capitis and inferior oblique
Vetebral artery : enters through C6 – C1.
- course from C6-c2 is vertical, while after exiting atlas, it curves laterally
with posterior convexity to allow rotational movement. Then it enters the
 C1 foramen transversarium while going medially and backwards behind
lateral mass of atlas. It lies in the floor of suboccipital triangle before
piercing the lateral angle of posterior atlanto-occipital membrane. It deeply
grooves the posterior arch of atlas before entering through foramen
magnum.

9) Position of hyoid, cricoid and thyroid bone

10) Disc structures and nerve compression

a) Consist of annulus fibrosus – type 1 collagen (strong), oblique orientation to resist tensile
force: inner layer comprises of fibrocartilage – innervation at outer layer
b) Nucleus polposus : consists of water and proteoglycan (age dependent) – resist
compression. Posterolateral herniation due to PLL
 i) Degeneration
ii) Prolapse
iii) Protusion
iv) Extrusion

11) Scapula - suprascapular notch, suprascapular nerve and artery course, structures attached on
coracoid process and acromion
a) Suprascapular artery run above the notch, so suprascapular nerve can be compressed.
b) Coracoid; pec minor, coracobrachialis, short head biceps. Ligament of trapezoid and conoid
c) Acromion: deltoid and trapezius. Ligament of coracoacromial.

12) Humerus – draw where supracondylar # in children occur

a) Most common area is proximal to epicondyles due to thin portion. Most common is
extension type.
b) Gartland classification
c) Complication; cubital varus

13) Clavicle – muscle attachments

a) S shape bone, widens at lateral, weakest at middle third
b) Smooth upper surface, grooves posterior surface
c) Attachment of pec major, subclavius, SCM, deltoid, trapezius
d) Peculiarities: most horizontal bone, first to ossifies, last to fuse, long bone without
intramedullary, long bone with intramembranous

14) Hip bone – greater/lesser sciatic foramen structures

a) Greater sciatic foramen:
7 nerves:
Sciatic Nerve:
Superior Gluteal Nerve:
Inferior Gluteal Nerve:
Pudendal Nerve:
Posterior Femoral Cutaneous Nerve
Nerve to Quadratus Femoris
Nerve to Obturator Internus
3 Vessel Sets:
Superior Gluteal Artery & Vein
Inferior Gluteal Artery & vein
Internal Pudendal Artery & vein
1 Muscle:
Piriformis

Lesser sciatic foramen:

the tendon of the Obturator internus
internal pudendal vessels
pudendal nerve
nerve to the obturator internus
15) Pudendal nerve branch and supply, what is meaning of pudendal.
a) S2-S4, supplies perineum region.
b) Divides into inferior rectal nerves, perineal nerve, dorsal nerve of penis / clitoris
c) Pudendum means part to be ashamed off. (external genitalia)
d) Pudendal canal can be compressed (alcock canal)

16) Fracture subcapital neck VS IT, which affect blood supply to femoral head more?
a) Subcapital will have worse outcome due to retrograde blood supply of head of femur, and
retinacular arteries already formed intracapsularly.
b) IT fractures still have cruciate anastomosis

17) Patella – orientate, its facets, which larger

a) Lateral facet larger, hence lateral subluxation
b) Odd facet at far medial, articulate in extreme flexion.

18) Show how to do knee aspiration

a) Aseptic technique, patient lie supine, knee in 30’ to open joint space
b) Analgesia
c) Palpate joint patellofemoral joint line, laterally insert.

19) Tibial plateau structures (Anterior posterior)

a) Anterior horn of medial meniscus
b) Anterior cruciate ligament
c) Anterior horn of lateral meniscus
d) Posterior horn of lateral meniscus
e) Posterior horn of medial meniscus
f) PCL

20) Knee meniscus – anatomy, mobility of lateral meniscus, what type of cartilage, what attach ot
posterior horn lateral meniscus
a) Fibrocartilage disc interposed in femorotibial joints.
b) Triangular in crossection
c) Made in type 1 collagen : water: proteoglycans : glycoproteins and elastin.
d) 3 layers:
i) superificial ; woven collagen fiber pattern
ii) surface layer: randomly orientated
iii) middle: circumferential / longitudinal; - dissipate hoop stresses
Vascular zone; from superior, inferior medial and lateral geniculate artery.
Red-red – 3mm from capsule – tear will heal
Red-white – 3-5mm – 50% heal
Whit-white – tear will not heal (receives nutrition from synovial fluid)
Medial meniscus – C shaped less mobile attach to tibia (coronary) and capsule MCL
Lateral: circular, more mobile.

Function:
e) Shock absorption
f) Joint congruity and stabily
 g) Lubrication distrbution
h) Nutrition
i) Proprioception

21) McMurray's examination – how to differentiate center and peripheral tear

22) Knee joint – LCL, structures attached to fibula head

a) Biceps femoris, fibular collateral ligament, fabellofibular ligament, popliteofibular ligament
(primary static ER resistant), arcuate ligament

23) Hip joint

a) Ball and socket
b) Static and dynamic stabilisers
i) Static: bone, labrum, capsule –strongest ligament Y bigalow – iliofemoral, pubofemoral
and ischiofemoral, ligament of teres.
ii) Dynamic: muscle and short external rotators

24) Varus/valgus stress test in extension and flexion 30' why?

a) 30’ to alleviate function of function of PCL, ACL. MCL alone stressed at 30’.

25) ACL, PCL – structure, function, attachment, tests for integrity

a) ACL prevent anterior translation (post med lat condyle – anterior tibia)
i) Anteromedial = taut in flexion
ii) Posterolateral = taut in extension
iii) Anterior drawer / Lachmann
b) PCL prevent posterior translation (bigger attachment as more important)
i) Anterolateral bundle = ant condyle – lat tibia – taut in flexion
ii) Posteromedial = post origin – med tibia – taut in extension
iii) Posterior drawer

26) Knee locking mechanism

a) Quadriceps contract, ACL taut bring medial rotation of femur and subsequently maintained
by tensor fascia lata for extension.

27) Popliteus
a) Externally rotate femur on tibia while unlocking the stance to initiate flexion
b) From medial proximal tibia to lateral femoral condyle; it is intraarticular.

28) Syndesmotic joint of ankle – any movement there.

a) Slight movement of ankle. Permits downwards and lateral rotation to allow dorsiflexion of
ankle.
b) Movement; plantar flexion 20’ by gastroc/soleus + long flexion
c) Dorsiflexion : anterior tibia, toes extension
29) Talus
a) Carries all weight of body
b) Articulate with tibia, fibular, calcaneum and navicular.
c) Blood supply intraoasseously from anterior to posterior
d) Branches of: dosalis pedis, PTA and peroneal artery

30) Pas anserinus

a) Anteromedial attachment of muscle at proximal tibia
b) Consist of (AP) : Sartorius, gracilis, semitendinosus

31) Foot arch and tarsal sinus

a) Medial longitudinal arch
i) Calcaneum, talus, navicular, medial cuniforms + base of three metatarsal
ii) Soft tissue; plantar aponeurosis,spring ligament, FHL, FDL, Tibia anterior and posterior
b) Lateral longitudinal arch
i) Calcaenum, cuboid, and lateral two metatarsal
ii) Plantar aponeurosis, FDL
c) Transverse arch;
i) Tarsal bones and base of five metatarsal
ii) Tendon of peroneus longus

32) Veins of upper and lower limb

i) Lower limb:
(1) Dorsal veins – post lat malleolus – short saphenous – popliteal
(2) Dorsal veins – ant med malleolus – greater saphenous – behind medial malleolus –
drains at SFJ

ii) Upper limb:

(1) Palmar digital veins + venae comitantes – cephalic (lateral) and median vein of
forearm – cephalic contributes to median cubital vein at antecubital fossa - +
basilica vein and perforates deep fascia of arm form the axillary vein
(2) Cephalic vein continues superficially lateral to bicep – into deltopectoral goove
intor infrclavicular fossa.

33) Antecubital fossa;

a) Margin – imaginary line between condyles, brachiioradialis and pronator teres
b) Contents medial to lateral: Median nerve, brachial artery, brachial vein (posterior), biceps
tendon, radial nerve.

34) Types of joints in body:

a) Union of bone achieved by:
i) Fibrous joints – sutures skull
ii) Cartilaginous – Primary – bone and hyaline cartilage meet (synchondrosis)
Secondary – bone covered with hyaline cartilage, attached
by fibrous tissue. (symphysis)
 b. Synovial joints – bone ends covered with hyaline + capsule enclosing joint cavity
and lined by synovial embrane, and joint is able for carrying degree movement.
Synovial membrane secretes hyaluronic acid for lubrication.

45. Parotid gland and duct – structures pass through

1. Facial nerve
2. Retromandibular vein
3. External carotid artery
4. Superficial temporal artery
5. Branches of the great auricular nerve
6. Maxillary Artery

Stensen Duct open at second molar, after piercing the buccinators muscle
46. Facial muscles

47. Facial nerve course and branches, supply

1. Upon exiting the internal auditory meatus, the nerve then runs a tortuous course
through the facial canal, which is divided into the labyrinthine, tympanic, and
mastoid segments.
 Labyrinthine – petrosal nerve –lacrimal, sinuses
Tympanic – submandibular, sublingual stapedius , chordae tympanic – special taste of
tongue
Mastoid – exit stylomastoid foramen - post auricular, zygomatic, temporal, buccal,
marginal and cervical branch.

48. Posterior triangle of neck – accessory nerve

The average distance traveled by nerve from base of skull to crossing the internal jugular
vein was 2.38 cm. As it courses caudally, the nerve pierces the sternocleidomastoid muscle
while sending it motor branches, then continues inferiorly until it reaches the trapezius
muscle to provide motor innervation to its upper portion.
Apex: meeting point of SCM + trapezius
Base; middle third clavicle
Ant/post: anterior part of trapezius n post part of scm
Roof; Deep cervical fascia

Divided into: occipital triangle / subclavian triangle by omohyoid muscle.

Occipital; accessory nerve, supraclavicular nerves
Subclavian;
1. Third portion subclavian artery
2. Brachial plexus root and trunks
3. Transverse scapular vessels
 4. Suprascapular artery
5. EJV
6. Nerve to subclavius

49. Sternocleidomastoid
1. Origin: manubrium + clavicle
2. Insertion: mastoid process
3. Innervation: accessory nerve
4. Blood supply: Occipital artery and superior thyroid artery
5. Turn head opposite side with ipsilateral flexion

50. Stab wound to root of neck – depending on which triangles

52. Fascial plane neck

53. Skin

56. Diaphragm – innervation

Front xiphoid process – laterally 6-12 ribs

The left and right crura are tendinous in structure, and blend with the anterior longitudinal
ligament of the vertebral column.

The central tendon of the diaphragm is a thin but strong aponeurosis situated near the
center of the vault formed by the muscle, but somewhat closer to the front than to the
back of the thorax, so that the posterior muscular fibers are the longer.

Nerve: phrenic C3-C5

Blood supply: Direct aorta, internal intercostal, superior and inferior phrenic artery.
57. Thorax muscles
58. Branches of arch of aorta
61. Liver – identify gall bladder bed, what surface marking
1. To concentrate bile. 50mLs. Lies on the visceral surface of the right lobe of the liver,
adjacent to quadrate lobe.
2. Cystic duct 2-3cm, 2-3mm in diameter.
3. Blood supply by cystic artery
4. Lymph drainage into porta hepatis
5. Common hepatic duct 3cm
6. Bile duct: 6-8cm, less than 8mm (anterior to IVC)
7. 60’ joining pancreatic duct, open at posteromedial second part of duodenum, 10cm
from pylorus.

62. What forms portal vein

1. Portal vein : SMA + splenic: infront of IVC and behind pancreas.

63. Sites of portosystemic anastomoses

64. Liver
1. 1500g; receives 1500ml blood per minute
2. 2 surfaces: diaphragmatic and visceral
3. porta hepatis main entry point, VAD – posterior to anterior
4. bare area in contact with diaphragm and right suprarenal gland
5. liver suspended by hepatic and the inferior vena cava
6. falciform ligament anterior: ligamentum teres to visceral area

Surface markings; xiphisternal joint

On left reach 5th intercostal space at midaxillary line
Right side 7-11 ribs at midaxillary line.

Lobes: Right (caudate and quadrate) and left.

Physiologically divided according to blood supply, 8 segments. (anticlockwise)
Caudate has autonomous, receives R and L hepatic / portal vein.

Blood supply: portal vein (main) and hepatic artery

Nerve: sympathetic celiac ganglia.

Structures:

65. Ureters
1. 25cm long,
2. narrowest caliber:
1. pelviureteric junction at pelvic brim
passes down on psoas major, infront of genitofemoral nerve
it is crossed by gonadal vessel.
R Lower down crossed by: ileocolic artery and right colic and root of mesentry
L crossed by left colic, and apex of sigmoid colon
Whitish non pulsatile cord with peristaltic activity upon pinching.

Surface markings;
Tip of 9th cartilage to bifurcation common iliac artery ?S1
 Medial to tips of TP, crosses pelvic brim at SIJ, passes and turn medially at ischial
spine

Blood supply:
Upper end: ureteric branch from renal
Middle part: abdominal aorta, gonadal common iliac
Lower end: uterine/vesical artery

Nerve: sympathetic fibre T10-L1, parasymp pelvic splanchnic

69. Shoulder approaches

1. Anterolateral (repair rotator cuff, long head biceps)
1. Coracoid – lateral edge to distal
2. Deltoid sharply divided from coracoid end
3. Acromial branch of throracoacromial artery ligated
4. Coracoacromial ligament split
5. Remove subacromial bursa
 6. Rotator cuff seen
2. Direct lateral (GT, IM nailing, MIPO)
1. 5cm from tip of acromion
2. deltoid split with stay suture inferiorly
3. subacromial bursa removed
4. rotator cuff muscle incised
5. joint capsule entered
3. Deltopectoral (all)
1. Coracoid – deltoid tuberosity
2. Cephalic vein – covered with fat identified
3. Deltoid laterally, pectoral major medially retracted
4. Short head/coracobrachialis medially (MSC nerve 8cm from coracoid
process)
5. External rotate to expose subscapularis
6. Joint line exposed
7. Axillary nerve about 5cm from GT – 7cm from acromion
8. Anterior circumflex humeral artery just above tendon of pec major
9. Ascending branch of anterior circumflex just lateral to long head biceps

70. What pierces clavipectoral fascia

1. Thoraco-acromial artery
2. Cephalic vein
3. Lateral pectoral nerve
4. Lymphatics

71. Deltoid
a. anterior surface of 1/3 clavicle, lateral acromion and scapular spine
b. insertion; deltoid tuberosity v shaped, 3 fibrous
c. fibres from clavicle and scapular to AP insertion not multipennate.
d. Action: abduction
e. Nerve: axillary c5,c6.

72. Supraspinatus by suprascapular nerve c5c6. Initiate abduction 0-15’.

73. Pectoralis major – lateral and medial pectoral nerve

74. Pectoralis minor – medial pectoral nerve
75. Name of the point where C5/C6 roots meet, and what nerve emerges immediately after and
what does that nerve innervate?
- Trunk, suprascapular nerve (supra and infraspinatous), nerve to subclavius
-
76. Upper brachial plexus – which roots involved? What movements compromised?
1. Erbs palsy: C5, C6
2. Movement affected: weak serratus anterior caused winging of scapula, long
thoracic nerve deltoid – axillary (abduction), rotator cuff (suprascapular nerve) –
external and abduction, and radial nerve (weak, not paralyse) – extension
3. End result = adducted, extended and internally rotated and flexion of wrist.

77. Winging of scapula which muscle and innervation

 1. Serratus anterior – lateral aspect of thorax 1-8 ribs
2. Insert into: superior angle, medial border, inferior angle
3. To pull scapula (protracts) to trunk and assist in abduction by rotating the scapula
4. Innervation by long thoracic nerve, (C5, C6, C7)

78. Biceps – nerve supply and from which cord of brachial plexus, origin/attachment
Origin: short head – coracoid process, long head – supraglenoid tubercle, attaches to radial
tuberosity and bicipital aponeurosis
Nerve: Musculocutaneous nerve (C5, C6)
Action: flexes elbow and supination

79. What nerve lies between brachialis and brachioradialis

1. Radial nerve
1. Posterior cord, triangular interval, posterior arm (spiral groove), lateral
intermuscular septum, in between brachialis and brachioradialis, and
anterior to lateral epicondyle
2. In forearm SRN – beneath brachioradialis , PIN in the supinator and winds
around the radial head, accompany by posterior interosseous artery. End at
joint capsule.

80. What nerve emerge btween biceps and brachialis (lateral cutaneous nerve of forearm
branch from musculocutaneous nerve)
81. Triceps innervation – branch of radial nerve, to long head and medial head and posterior
cutaneous nerve of forearm.
82. Radial nerve injury – at groove why still can extend? After repair which muscle function
return first and why? Radial nerve reinnervation
1. Nearest muscle return first – lateral head triceps, wallerian degeneration

83. PIN – why no wrist drop, just weak wrist extension

1. Mobile wards supply by radial nerve not PIN.
2. back of humerus, supplies back the medial and lateral head, and then descend to
supply anconeus, mobile ward and posterior cutaneous nerve of forearm.

84. Humerus medial epicondyle structures attached – common flexor origin

85. Humerus lateral epicondylitis (tennis elbow) – structures effected

1. Overuse injury involving eccentric overload at origin of common extensor tendon
2. leads to tendinosis and inflammation at origin of ECRB

86. Radius approaches

1. Henry approach:
1. Lateral to biceps tendon to radial styloid (modified to in between FCR and
radial artery)
2. Incise fascia
3. Plane between brachioradialis and FCR
4. Identified SRN and RA
5. Retract laterally
 6. Deep dissection
1. Proximal: trace biceps tendon, remove bursa, supinate and cut
along the broad insertion supinator
2. Middle: Pronate arm to see pronator teres insertion and retract
medially
3. Distal: FPL retract medially, PQ cut at laterally
Subperiosteal dissection

87. Ulnar nerve – dorsal cutaneous nerve, how to differentiate wrist and elbow lesion based on
sensation:
1. The dorsal branch of ulnar nerve arises about 5 cm. proximal to the wrist; it passes
backward beneath the Flexor carpi ulnaris, perforates the deep fascia, and, running
along the ulnar side of the back of the wrist and hand, divides into two dorsal
digital branches; one supplies the ulnar side of the little finger; the other, the
adjacent sides of the little and ring fingers.

Course; medial cord, medial to brachial artery, subcutaneously, emerge from

arcade of struthers posterior to medial epicondyle, entered cubital tunnel in
between ligament of Osborne, beneath two heads of FCU, medial to ulnar artery.
Gives rise to dorsal branch of ulnar nerve, and enters guyons canal (divided into 3
zone, mixed, motor and sensation only)

** points of compression at arcade, Osborne ligament, two head FCU and guyons

88. Radial artery

1. Branch from brachial artery. Division occurs at neck of radius level, ulnar forms at
an angle. Continue medially to biceps tendon, over the pronator teres, FDS and in
beneath the brachioradialis proximally, distally by the skin. It disappears at tendon
of APL, and EPB to cross the anatomical snuffbox.

89. FDS and FDP – blood supply (vincula), where does it come from, other blood supply
(diffusion)
1. FDP attaches at base of distal phalanx, pierces thru FDS tendon
2. In flexor sheath, both tendon invested by common synovial sheath
3. Blood vessels from the palmar surface of phalanges
4. Vessels invested by synovial membrane – known as vincula – each tendon has two:
short and long

90. Extensor compartment wrist

1. Six compartment
1. APL, EPB
2. ERCL, ERCB
3. EPL
4. EDC, EI
5. EDM
6. ECU
 91. Median nerve entrapment, distribution, muscles supplied
1. AIN – tendoneous edge pronator teres
2. Pronator syndrome – between ulnar and humeral head, bicipital aponeurosis
(lacertus fibrosus)
3. Carpal tunnel – repetitive stress, OA wrist, sheath thickening and odema

92. Radial tuberosity – biceps attachment

93. Supinator – posterior ulnar to lateral radius: PIN pierces muscle, can be compressed
94. Thenar muscles –
1. Adductor policis
2. Opponens policis
3. Flexor policis brevis (dual innervation)

95. Extensor tendons to index finger – which medial? EI more medial than EDC
1. Use of EI – for tendon transfer to replace EPL tendon

96. DeQuarvain tenosynovitis – why after steroid injection few months later pain will recur?
1. Steroids just reduced inflammation, not treating the cause.

97. A1 A2 pulley and clinical correlation

1. Pulley of fingers consist of flat band and cruciate
2. A1 (mcpj), A2 (prox phalanx), C1 (distal), A3 PIPJ, C2 middle pha, A4 (middle), C3
(end middle), A5 DIPJ
3. A1 – trigger finger
4. A2 and A4 most important to prevent bowing

98. Carpal bones and how flexor retinaculum attached

1. Scaphoid Lunate triquetrium pisiform, trapezium trapezoid capitate hamate
2. Scaphoid + tri – pisiform, base 1st row carpal tunnel, roof palmar aponeurosis

99. Carpal tunnel syndrome– palmar cutaneous branch of median nerve not affected due to
division prior entering the canal

100. Snuff box, contents

1. In between EPL and EPB+APL
1. Contents:
2. Cutaneous branch of radial nerve
3. Radial artery
4. Scaphoid bone, radial styloid, trapezium and base of thumb meta
5. Cephalic vein initiate here

101. FDS tendon – how to identify? Blood supply? Infection in tendon sheath of ring finger can
spread to the hand? Which finger can spread to hand?
 1. Synovial sheath extend about 2.5cm proximally
2. Only FPL and flexor little finger extend to tip of finger
3. Separate sheath for 2,3,4 fingers.
1. Started at distal crease of palm

102. Space of parona

1. Forearm space of parona is a rectangular space situated deep in the lower part of
the forearm just above the wrist. It lies just in front of the pronator quadratus and
deep to the long flexor tendons.
2. Superiorly the space extends upto the oblique origin of the flexor digitorum
superficialis. Inferiorly, it extends up to the flexor retinaculum and communicates
with the midpalmar space; and possibly also with the thenar space.
111. Iliac artery - identify external iliac artery and vein
1. Internal iliac artery

Branch of internal iliac:

Lateral sacral, superior and inferior gluteal artery, middle rectal, superior and
inferior vesical, internal pudendal artery, obturator and uterine artery.

External iliac: gives branch to

inferior and superior epigastric, Deep and superficial circumflex, deep and
supergicial external pudendal and femoral artery

Corona mortis: normal obturator artery runs through the obturator foramen,
whereby 25% aberrant variation, the is anastomosis between external iliac artery
and obturator artery, which commonly seen at 3cm lateral to pubic (the lacunar
ligament)
112. Femoral triangle – contents

1.

113. Inguinal canal

1. Borders:
1. Sup; external oblique aponeurosis
2. Inferior; inguinal ligament
3. Ant; external oblique aponeurosis
4. Post; transversalis fasica

Content
Sperm cord + ilioinguinal nerve
Broad ligament + ilioinguinal

Spermcord content:
3 arteries: artery to vas deferens (or ductus deferens), testicular artery,
cremasteric artery;

3 fascial layers: external spermatic, cremasteric, and internal spermatic

fascia;

3 other structures: pampiniform plexus, vas deferens (ductus deferens),

testicular lymphatics;
 3 nerves: genital branch of the genitofemoral nerve (L1/2), sympathetic
and visceral afferent fibres, ilioinguinal nerve (N.B. outside spermatic cord
but travels next to it)

114. Femoral canal – contains nodes of cloquet draining the clitoris or glans of penis

115. Femoral artery course, branches, what is largest branch? Identify profunda femoris, how
does it supply thigh – superficial and deep system, how does it reach posterior side – through
adductor hiatus
116. Adductor magnus – attached to adductor tubercle, nerve supply from sciatic (hamstring
part) and obturator

117. Popliteal fossa

1. Borders: Semi M, biceps femoris, medial and lateral head of gastroc,
base;popliteus, oblique popliteal ligament
2. Contents;tibial nerve, common peroneal, popliteal vein, popliteal artery,
termination of small saphenous vein

118. Knee joint structures – collaterals, cruciates, meniscus, blood supply of meniscus and
cruciates
Cruciates : Middle genicular arteries
Meniscus: Sup / inf genicular arteries

119. Compartment syndrome – name compartments in leg, which most affected

Acute compartment syndrome occurs when the tissue pressure within a closed muscle
compartment exceeds the perfusion pressure

1. Anterior, lateral, superficial and deep posterior

2. Deep posterior compartment due to vascularized area
120. Gaiters area – clinical significance, why prone to ulcers
1. Less blood supply area, lower venous pressure

121. Venous drainage LL superficial and deep

Superificial: short and great saphenous vein
Deep: medial and plantar vein – posterior tibial vein + peroneal vein +
gastrocnemius vein proximally
Joined by the small saphenous vein at popliteal fossa

Important perforators:
Dodd's perforator at the inferior 1/3 of the thigh
Boyd's perforator at the knee level
Cockett's perforators at the inferior 2/3 of the leg (usually there are three: superior
medium and inferior Cockett perforators)

122. Muscles in anterior compartment of leg

1. Tibialis anterior, EHL, EDL, peroneus tertius

123. LisFranc ligament anatomy and function

1. keystone of lisfranc complex; base of 2nd metatarsal and medial cuneiform = hence
little motion
2. injury occurs in hyperextended foot with axial loads

Function;
critical to stabilizing the second metatarsal and maintenance of the midfoot arch
An interosseous ligament that goes from medial cuneiform to base of 2nd
metatarsal on plantar surface
Lisfranc ligament tightens with pronation and abduction of forefoot
Medial, middle and lateral column
Homolateral, Divergent, Isolated
PATHOLOGY

Immunology
1. Immune system – definitions:
1. Innate: nonspecific immunity, (physical barrier, phagocyte, complements, NK cells:
1. Lacks memory
2. Exterior defense
3. Leukocytes – neut, mono, eosi, baso, mast cell
4. Complement and interferons

NK cell works by having activating and inhibiting receptor. Normal cell have
both. Antigenic cell only has activating receptor.
Phagocyte – ingest bacteria
Consist of neutrophils and monocytes
Neutrophils (PMN) first to defend, has enzyme myeloperoxidase. Dies after
digestion

Monocyte goes periphery = macrophage (to filter residual act of PMN)

Phases:
Recognition
Amplification
Effector phase
Termination
Memory

2. Adaptive: specific immunity and memory: humoral or cell mediated

1. Humoral B cell – mediated by a/b, present as serum globulins
CD4+ induced cytokines to increase production
Antibodies are produced
Primary and secondary antibody response

2. Cell mediated T cell – T lymphocytes

1. APC + helper T cell = Secretion of cytokines, induced CD4, CD8
2. cytotoxic T cells (CD8) lyses the infected cell
Primary and secondary antibody response

Another type of T cell

Natural killer T cells (different type from NK cells innate)
- only kills if MHC class I presented – which is can only be done by
macrophage, lymphocytes (rather specific)
activated by CD1B

*Function of CD4+
- helping B cells produce AB
 activating macrophage
helping CTL to proliferate and destroy viral infected cells
neutrophil recruitment

3. Classification: active or passive

1. Active – self produce
2. Passive – given immunoglobulins

Function of immunoglobulins:
1. attack antigens through agglunitation, neutralizing antigenic
substance, lysing cell wall
2. activate complement system
3. release histamine and activate anaphylaxis and hypersensitivity

2. What is T cell – role and function

3. Cytokines in acute and chronic inflammation, how to classify and devide cytokines
1. Acute phase response: liver production
2. ILN1-IL6, TNF
3. CRP
4. Amyloid Acid

4. Hypersensitivity
1. Immediate, IgE response
2. cytotoxic reactions to self antigens – Ab binds to normal cell, inducing MAC
complex. Eg: body attacks mitral valve as result of group A infections
3. Immune complexes, post infection complexes not cleared, attacked normal
receptor
4. Delay hypersensitivity; cell mediated – antigen processed and presented to T cells –
and macro, mono, lymphocytes activated
 5. Immunoglobulin

1. IgM = first secreted for primary response – agglutination and neutralization

2. igG = for secondary response, carried into tissue – same like IgM, able to cross
placenta
3. IgA = serum and secretions, prevents adherence to mucosa surface
4. IgE = eradication of helminthic parasite, helps trigger mast cell and basophils ->
histamine
5. IgD = as antigen receptor on mature naïve B cells.

Diseases
7. Osteoporosis – what are the lab findings, why use PTH/forteo in osteoporosis
1. Age related bone disease, which defines as 2.5 less standard deviation from normal
population
8. Level of calcium in patients with osteoporotic fracture: normal
9. Osteomyelitis – common organisms

Newborns S. aureus, Enterobacter species, and group A and B Streptococcus

(younger than 4 mo)
Children
(aged 4 mo to 4 y)
Children, adolescents
(aged 4 y to adult)
Adult
species
S. aureus, group A Streptococcus species, Kingella kingae, and
Enterobacter species
S. aureus (80%), group A Streptococcus species, H. influenzae, and
Enterobacter species
S. aureus and occasionally Enterobacter or Streptococcus species
Sickle Cell Anemia S. aureus is typically most common, but Salmonella species is
Patients pathognomonic

10. Septic arthritis - in diabetic patient how to control DM, what antibiotics
1. Gold standard: aspiration; send for gram stained, culture, FEME count, crystals
Serum labs
WBC >10K with left shift
ESR >30 = ESR is often elevated but may be normal early in process
rises within 2 days of infection and can rise 3-5 days after initiation of appropriate
antibiotics, and returns to normal 3-4 weeks
CRP >5 = most helpful. best way to judge efficacy of treatment, as CRP rises within
few hours of infection, and may normalize within 1 week of treatment

Antibioitcs depends on common organism;

Normal adult: S aureus, N. gonorrhea
Immunocompromised: S. Aureus, pseudomonas

In DM suspect polymicrobial

20. FES: Major (1)

1. hypoxemia (PaO2 < 60)::
2. CNS depression (changes in mental status)
3. petechial rash
4. pulmonary edema

Minor (4)
tachycardia
pyrexia
retinal emboli
fat in urine or sputum
thrombocytopenia
decreased HCT

Additional
PCO2 > 55
pH < 7.3
RR > 35
dyspnea
anxiety

11. Osteoarthritis
- degenerative disease
- Articular cartilage – damage to tangential zone, repair produce more
proteoglycan, alter composition, water component
- Damage to tidemark will heal by fibrosis
- Synovium – inflamed – thickened – vascular
12. Thromboembolic diseases and pathogenesis
1. Thrombosis: pathological caused intravascular blood coagulation.
2. Embolus: intravascular material travels to distant site causing blockage to local
perfusion
3. Virchow’s triad: Endothelial injury vs stasis vs hypercoagulability

Prevention:
Mechanical (pump, stocking) vs pharmacological (warfarin, heparin)

13. Acute inflammation – cardinal signs and what occurs to cause signs, sequelae
1. Signs; rubor (red), dolor (pain), functional laesa, calsor (, fumor (swelling)

14. Granuloma – how is it different from granulation tissue, draw a granuloma

1. Granulation tissue forms by collagen type 3 – later replace by type 1, endothelial
cells, macrophages, fibroblast, and lymphocytes. Red beefy appearance.
 2. Granuloma is a chronic inflammation characterized by the granulomatous like
center, with lined by epitheloid cell. Cells are the aggregated macrophages to fend
of infection - PMN (Langerhans or foreign body type), lymphocytes, and fibroblast,
plasma cells

15. What other things can cause caseous necrosis

1. Tuberculosis, Fungi, Syphilis, histoplasmosis, cyrptococcosis

16. Giant cell types

1. Giant cell or langhans– granulomatous infection
2. Foreign body type

17. Gohn's foci, history of Gohn's

1. Primary infection of TB
1. Macrophage eats inhaled TB after opsonisation
2. However TB able to block action of lysosome
3. Within 2-4 weeks T lymphocyte kill via interferon – nitric oxide route
4. 95% asymptomatic
5. 5% will have lobar consolidation, hilar nodes and pleural effusion,
6. rarely can spread to spine (military TB)
7. Gohn complex – lung lesion + hilar node granuloma
2. secondary TB occurs in previously exposed hose
result from immunosuppressive state – causing low grade fever, night sweats, and
weight loss.
May heal spontaneously
Or rupture into vessels and into airways -> spread
18. Mantoux test mechanism and interpretation
A standard dose of 5 tuberculin units (TU - 0.1 ml) (The standard Mantoux test in the UK
consists of an intradermal injection of 2 TU of Statens Serum Institute (SSI) tuberculin RT23
in 0.1 ml solution for injection.) is injected intradermally (between the layers of dermis) and
read 48 to 72 hours later. This intradermal injection is termed the Mantoux technique. A
person who has been exposed to the bacteria is expected to mount an immune response in
the skin containing the bacterial proteins.
19. Wound healing – primary healing, secondary healing, factors affecting it
1. Hematoma and inflammation
2. Repair
3. Remodeling

Primary: wound edges sutured

Secondary: wound left open
Delayed primary healing: granulation tissue presence then sutured

20. Bone healing – factors affecting it, primary and secondary healing, remodeling
1. Hematoma formation
2. inflammation
3. Soft callus formation
4. Remodeling phase

21. Bone healing and strain

1. <2% - primary healing – direct cortical bone healing
2. 2-10% - healing by callus
3. >10% - fibrocartilage predominant –unstable

22. Tendon repair and healing – how long to heal/immobilize, maximum strength attainable,
repair use what suture?
1. Depending on core sutures used.
2. Eg flexor tendon – 2 strands immobilize for 6 weeks, 4 strands active extension
passive flexion by finger bands, 6 strands able to allow limited active motion.
Resistance exercise wait till 8weeks

3. Healing by fibrosis

1. Phases:
1. Inflammatory, fibroblastic, remodeling
4. Use non absorbable sutures

23. Haemorrhage – definition

1. Blood extravasation following vessels rupture

24. Haemostasis - describe 4 phases

1. Involves three main component: endothelium, platelets, coagulation cascade
2. It’s a normal physiological process maintaining blood in a fluid, clot free state in
normal vessels, while inducing rapid localized hemostatic plug at sites of vascular
injury.
1. reflex neurogenic vasoconstriction
2. platelet adhesion and activation
3. activation of coagulation cascade
4. activation of counter regulatory mechanisms
25. Coagulation cascade – PT and aPTT which pathway, normal values, warfarin effect, how to
prep patient for surgery if on warfarin
1. Prepping patient
2. Warfarin 5 days prior, monitor INR then start LMWH once below, stop LMWH 24H
before surgery.
3. Restart LMWH after 24H post surgery once hemostasis secured, overlapped with
warfarin.
4. Monitor INR then stop the LMWH once INR achieved.

26. Thrombosis
1. Inappropriate activation of blood clotting in uninjured vasculature or with relatively
minor injury. Concerning to Virchows triad: stasis, endothelial injury,
hypercoagulabilty

27. Fibrinolysis
1. Mediated by thrombin which induces t-PA release, converting active plasmin from
plasminogen. Plasmin degraded fibrin.
2. Endotheium modulates anticoagulation by releasing plasminogen activatior
inhibitors (PAI) which inhibits t-pa binds to fibrin.

29. DIVC refers to widespread of fibrin microthrombi in the microcirculation, a complication

of diffuse thrombin activation = small infarcts. Consumption of platelets and coagulation of
platelets with fibrinolytic pathway actiation leading to uncontrolled bleeding.

Trigger factors:
1. Release of massive tissue factor or thromboplastic substances
 Eg: gram neg endotoxin activate monocytes to release TNF and IL1 –
increase tissue factor
2. Widespread endothelial injury
- Release of TF, activating intrinsic mechanism

28. Aspirin and action = as described above, bind irreversible to COX 1-2 pathway

29. Platelet half-life = 5 to 7 days

30. Gram stain

1. Crystal violet
2. Potassium iodide
3. Destained with alcohol
4. Safranin

31. Infarction and embolism

1. Infarction is and Area of ischemic necrosis caused by occlusion of either arterial
supply or venous congestion.
1. Divided into white (end artery) or red infarct (double circulation)

2. Embolism is defined as any intravascular solid, liquid, or gaseous mass carried by

the blood flow to distant site from its origin.

32. Shock – types and classes of hypovolumic shock, crystalline or colloid

1. Classes divided into four
2. <15%, 15-30%, 30-40%, >40% blood loss

crystalline stays intravascularly about 45%, needing 3:1 ratio of blood loss
Colloid meanwhile is 1:1 ratio, stays intravascularly about 4hours (depends on
type), but with possible side effects of allergy, coagulopathy.
Stage 3 / 4 requires blood transfusion.

33. Calcium metabolism – which one measured by our labs, PTH and regulation of Ca, calcitonin
1. Ionized calcium + protein bound = corrected calcium value
2. 39-40 is the normal takepoint for correction.

Calcium metabolism involves four main components

Skin – liver and kidney for vitamin D
Intestine - absorption
Bone - storage
PTH and calcitonin for homeostasis – hormonal balance
34. How is calcium being absorbed
1. Absorbed in duodenum (in low calcium) and jejunum and ileum (in normal
condition)
2. Calcium is absorbed across the intestinal epithelial cell's brush border membrane
and is immediately bound to calbindin, a vitamin D-dependent calcium-binding
protein. This will cross the epithelial cytosol.

3. From there TRPV6 and calcium pumps (PMCA1) actively transport calcium into the
body. Active transport of calcium occurs primarily in the duodenum portion of the
intestine when calcium intake is low; and through passive paracellular transport in
the jejunum and ileum parts when calcium intake is high, independently of Vitamin
D level

35. How to manage patient post parathyroidectomy

1. Look out complications
2. Immediate: hematoma causing airway blockage, infection

Delayed: hoarseness, hypocalcemia

Management depends on the possible complications.

36. Pathological compartment syndrome

1. Chronic exertional compartment syndrome
Affect runners, increase in muscle size in tight fascia
Will exacerbate pain and numbness, loss of ankle dorsiflexion. Symptoms resolve
after rest.

37. Red Steinberg cell

1. Reed–Sternberg cells (also known as lacunar histiocytes for certain types) are
different giant cells found with light microscopy in biopsies from individuals with
Hodgkin's lymphoma
2. lacunar histiocyte, whose cytoplasm retracts when fixed in formalin, so the nuclei
give the appearance of cells that lie with empty spaces (called lacunae) between
them
38. Exudate and transudate
Definition:
1. exudate: inflammatory extravascular fluid, that has a high protein concentration
and cellular debri, high specific gravity
2. transudate; extravasation of fluid with low protein content, ultrafiltrate due to high
hydrostatic pressure or dimished osmotic forces

Oncology
42. Carcinogenesis, neoplasia, histological features
1. Carcinogenesis: a process to develop neoplasia
2. Neoplasia abnormal groth with autonomous activity after removal of external
stimuli.
3. Poikilocytosis - shape
4. Anisocytocisis – unequal size
5. Hyperchromasia
6. Loss of polarity

43. Metastasis, explain mechanism, why certain sites more common for metastatic deposits
1. Spread by; transcolemic, lymphatics, hematogenous
2. Metastasis cascade:
 - Clonal expansion, growth, diversification, and angiogenesis
- metastatic subclone
- adhesion to and invasion of basement membrane
- passage through extracellular matrix
- intravasation
- interaction with host lymphoid cell
- tumor cell embolus
- adhesion to membrane basement
- extravasation
- metastatic deposit
- aangiogenesis
- growth

Essential alteration for malignant transformation

a- self sufficiency
b- insensitive to growth inhibitory signals
c- evasion of apoptois
d- defects in DNA repair
e- limitless replicative potential
f- ability to invade and metastasize
g- ability to escape immune recognition and regulation

44. Oncogene and related pathogenesis in cancer

1. Oncogene is genes that promote autonomous cell growth in cancer cells
2. Proto-oncogenes normal cellular genes that affect growth and differentiation
1. 3 mechanism;
point mutations
chromosomal rearrangement
gene amplication

45. Radiotherapy – how does it work?

1. Direct DNA damage by radiation or activation free oxygen radials
2. Given in fractionated because;
1. Reposition cell cycle: G2 most resistance
2. Replenish sub injurious cell
3. Reoxygenation of tumor tissue
4. Repopulation of normal cell tissue

46. Multiple myeloma

1. Cancer of plasma cell – B cell, IgG production, induced local inflammation – bone
lytic, deposition at target site – organ damage
2. Symptoms: CRAB – high calcium, renal, anemia, bone (lytic, bone pain:
overexpression of RANKL over osteoclast by bone marrow stroma stimulate
resorption: classicaly described as punch out lesion

Criteria:
Major Diagnostic Criteria
 1. Plasmacytoma on tissue biopsy
2. Bone marrow plasmacytosis of > 30%
3. M Protein: IgG > 3.5 g/L; IgA > 2.0 g/L
4. Urinary kappa or lambda chain excretion of > 1g / 24 hours in absence of
amyloidosis (bence jones protein of araprotein light chain)

Minor Diagnostic Criteria

1. Marrow plasmacytosis of 10-30%
2. Lytic bone lesions
3. Evidence of a monoclonal protein but lessor amounts than above
4. Hypoglobulinemia of normal proteins: IgM < 500 mg/L, IgA < 1 g/L or IgG
< 6g/L
PRINCIPLES OF SURGERY

49. Surgical site infection – source, how to prevent from before OT, before incision, after
closure, post op
1. Defines as infection within a month in previously surgical wound, or within a year if
involves implant.
2. Sources: endogenous (own), vs exogeneous (colonized worker, operating room)

1. Skin flora, previous injurious site

2. washed with alcohol, shave if needed before cutting, antiobiotics given at 30minutes
before cutting time.

3. Secure hemostasis, wound approximate without tension, local antibiotics

4. Antibiotics continuation depending on intraoperative findings – non mixing between

infected and non-infected wounds. Good nutrition.

50. What happens to surgical site if patient has uncontrolled pain x 3/7
1. Pain will induce sympathetic response -> vasoconstriction -> poor blood supply ->
tissue necrosis -> poor healing -> dehiscence

51. ESR and CRP interpretation

1.
2. ESR – non specific markers, erythrocyte sediments in an hour
1. Age /2 or age +(10 in female)/2
3. CRP – acute inflammatory markers released by liver enzyme
- rather more specific
 - CRP rises within two hours of the onset of inflammation, up to a 50,000-
fold, and peaks at 48 hours. Its half-life of 18 hours is constant, and
therefore its level is determined by the rate of production and hence the
severity of the precipitating cause. CRP is thus a screen for inflammation.
- CRP binds to the phosphocholine expressed on the surface of dead or dying
cells and some bacteria. This activates the complement system, promoting
phagocytosis by macrophages, which clears necrotic and apoptotic cells
and bacteria.
- Plays a role in innate immunity
- Some sort of complements C3b etc

52. Principles of prophylactic antibiotics

1. Antibiotics must be present in wound at time of inoculation of infective agenst
2. Coverage should include all potential infective agents
3. Bactericidal
4. Should not be part of treatment armamentarium
5. Short duration
6. Only given in : clean surgery where implant related, and infection can cause
catastrophy = neurosurgery
: clean contaminated – visceral entered with no spillage
class 3 and 4 – antibiotics as treatment

Recap types of wound:

53. How patient get infection
1. from injury - farm injury / devitilised structures
2. local flora – local flora in different environment
3. systemic risk factors – immunosuppressed

4. surgical technique
5. hospital environment
6. inadequate wound care

53. Antibiotics – therapeutic, empirical, prophylaxis, mode of action, complication of

Aminoglycosides
Principles of therapeutic:
1. full course of at least 5 days (or longer in OM, septic arthritis)
2. Choice should guided by sensitivity studies
3. in-vitro sensitivity may not correlate to in-vivo effectiveness – clinical response
needed
4. antibiotics not substitute for surgical drainage
5. titrated to impairments of renal or liver

54. Tourniquet in surgery – principles, contraindications, what is exsanguinating limb?

ESMACH contraindications
1. Compression device used to control arterial and venous circulation to provide
bloodless surgical field
2. Pneumatic vs non pneumatic (contour – less pressure needed vs cylindrical)
3. Site: good muscle bulk, used of padding to avoid slippage, abrasion, blisters
4. Single - bladder cuff
5. Cuff Shape- cylindrical or conical (contour)
6. Cuff width: as wide a cuff as possible; but cuff edges must not lie close to the joints
of the limb to reduce the risk of nerve injury.
7. Length: Varies depending on cuff manufacturer, cuff type, and limb size but is
typically between ¼ and ½ of the overall cuff length.
8. Cuff application: snugly fit; allows two fingers easily under the cuff at both edges

Limb occlusion pressure (LOP) is the minimum tourniquet pressure required to occlude
blood flow to a specific patient's limb

Pressure: add 50-75 mm Hg and 100-150 mm Hg above the arm systolic blood
pressure, for surgery on the upper limb and lower limb respectively
Or adding 90-100 mm Hg to the pre-operative blood pressure measured in the arm
when operating on the lower limb

Complications of tourniquet:
Local:
1. pain
2. numbness
3. neuropraxia
4. muscle necrosis
 5. compartment syndrome
6. vascular injury

Sytemic:
1. metabolic – reperfusion syndrome – toxic metabolites causing organ damage
2. CVS
3. Brain

Time: 2Hours
Evidence: Venous pH fell to 7.0 at two hours, and resulted in muscle fatigue,
ultrastructural changes and muscle damage.

Serum creatine phosphokinase (CPK) concentration is elevated if the ischaemia time

exceeds 1.5 hours.

If intracellular adenosine triphosphate (ATP) is depleted after three hours of

ischaemia, metabolic recovery of muscle is impaired

Effects of deflation:
Peak embolisation occurs approximately fifty seconds after tourniquet release, but this
may even be inversely proportional to the duration of tourniquet time

CVS: Exsanguination of both lower limbs can account for a 15% increase in circulating
blood volume and cardiorespiratory decompensation and arrest have been reported

Brain: A rise in the pCO2 associated with tourniquet release causes an increase of up
to 50% in the flow to the middle cerebral artery, which usually lasts less than ten
minutes. This may be associated with secondary brain injury in patients with an
increased intracranial pressure

Metabolic: Hyperkalemia associated sudden death

Impairment of perioperative antibiotics = inflate >5 minutes after given

Exsanguination contraindication:
Tumor
Infection

55. Diathermy mehanism of action, why patient does not get electrocuted
1. Electrocurrent waves 200khz-3.3mhz
2. Alternating for coagulation 50-100/min (fulguration / dessication-dry), continuous
for cutting ( and vaporization)
3. Monopolar vs bipolar
4. Receiving end dispersive pad – allow current to flow out from body
1. Must be big, close as possible, not on implanted limb, not cut to fit, hair
free if need.
5. Bipolar current pass between 2 pins
 6. Hazards –
Interfere with pacemaker function
Arcing can occur with metal instruments and implants
Superficial burns if use spirit based skin preparation
Diathermy burns under indifferent electrode if plate improperly applied
Channeling effects if used on viscus with narrow pedicle (e.g. penis or testis)
Fire
Generating smokes -> carcinogenic

56. Principles of disease screening

1. High incidence of disease in population with serious consequences
2. Natural history of is well understood, and can be detected by suitable test
3. Detection and treatment at asymptomatic stage produce significant benefit
4. Method should be:
Simple with high sensitive, specificity and reproducibility
Acceptable to population
Cost effective
Not hazardous to screened population

Drawback
Logistics, compliance, screening schedule, adverse effects (clinical or psychological), cost

Examples: breast and cervical cancer

57. Audit
1. A quality improvement process that seeks to improve patient care and outcomes
through review of car against explicit criteria and the implementation of change.
2. Stages:
3. Preparing for audit / criteria: process or outcome / measuring performance – data
collection / making improvement – identify local barriers, develop pratical
implementation / sustaining improvement – repeating audit – to assess
improvements also closing the audit loop

Difference between audit and research

1. audit to see how close current practice to benchmark, research to establish best
practice
2. specific to one group, result not transferable: research is designed to be
replicated and validated by other group
3. audit aim to improve service, research to generate new evidence
4. audit initiated by service provider, research by researchers
5. audit is practice based: research is theory driven
6. audit is ongoing process: research is one off
7. audit does not involve randomization, research does.
8. audit not involve placebo, research does.
58. Fluid management in pre-op patient calculate requirements
Principles of fluid therapy:
a. maintain daily requirement
b. replace additional loss
c. special case – heart renal and liver failure.
1. First 10kg = 4ml/kg/h then 10kg 2ml/kg/h and subsequently 1ml/kg/h
1. Or 20-30ml/kg in adult
2. Add 500ml per 1celcius feve
2. Sodium 2-3mmol/kg
3. Potassium 1-2mmol/kg
4. Calorie: about 20-40kcal/kg in normal healthy sedentary adult
1. Glucose provide 4kcal/g
2. D5 = 5g/100ml = 20kcal/100ml = 100kcal/500ml
5. protein: 0.5g/kg = 4kval/g
6. fat: 3g/kg = 9kcal/g
7. carbohydrate: 2g/kg = 4kcal/g

Post op
Heart failure: ½ calculate requirement
Renal: previous requirement + 500cc with no K supplements

59. Fluid management in patient starved one month

1. With prolonged starvation there is a gradual decrease in total body energy
expenditure. This decreased metabolic activity is manifested by diminished muscle
activity, increased sleep, and decreased core temperature. In addition to a
decrease in metabolic rate, the need for gluconeogenesis diminishes, mainly as the
result of the conversion of the central nervous system to utilization of ketone
bodies for energy rather than glucose. The stimulus for this adaptation is unknown,
although it may be in part caused by the rise in serum alanine or ketone body
concentrations or by the lowered serum molar ratio of insulin to glucagon. Protein
catabolism falls from 75 to 20 g/day, with a marked decrease in excretion of urea
nitrogen to 3 to 5 g/day. In fully adapted starvation, protein catabolism provides as
little as 5 percent of the total daily calories. With decrease in gluconeogenesis,
adipose tissue becomes even more important as an energy substrate, with 60
percent of the total caloric expenditure derived from metabolism of fat to carbon
dioxide, 10 percent from conversion of free fatty acids to ketone bodies, and 25
percent from metabolism of ketone bodies by peripheral tissues. Serum ketone
body concentrations increase with the increased fat metabolism and eventually
exceed the renal threshold. Metabolic acidosis is not present. The appearance of
ketone bodies in the urine is the hallmark of the physiological response to
prolonged starvation. It is in this adapted state that humans can best tolerate
prolonged fasting, perhaps for 60 to 70 days. Normal total body protein synthesis
occurs at a rate of approximately 18 to 30 g/day.
 Starvation will likely cause:
- hypovolemia
- Hyponatremia
- Hyperkalemia / hypokalemia
- hypoproteinemia with negative nitrogen balance

2. Correction as accordingly. No fast correction of Na – risk of CPM

2. Avoid rapid infusion of glucose – refeeding syndrome

1. Insulin induce glycogen storage -> requires phosphate, will need to be
taken from RBC etc, causing inadequate oxygen supply.

60. What to worry before op if patient CKD

1. Needs to discuss with anaest team reg ICU bed
2. Dialysis should be perform day before surgery
3. RP and FBC pre and post dialysis
4. Reduce dose of drugs with renal exretion (morphine)
5. Site of arteriovenous fistula not to be disturb
6. Predicting problems; hyperkalemia, acidosis and pulmonary edema

61. Prolonged fasting awaiting for op – nutritional requirements in surgical patient

1. As per above

62. Nutritional assessment – patient going for op clinical and lab

1. Anthropometric methods
1. Waist hip ratio
2. Triceps fold
3. BMI

2. Biochemical, laboratory methods

1. Anemia
2. Total protein

3. Clinical methods
1. Hair – spare and thin - protein
2. Angle of mouth – glossitis vit b12
3. Nails – spooning – iron def
4. Bones - vit D
5. Skins – pallor,
6. Eyes – vit A def

4. Dietary evaluation methods

1. 24h evaluation
2. observed food intake
63. What is massive blood transfusion
1. Total blood volume in 24h, or >50% in four hours

64. Management of polytrauma patient and fluid resus – as above

65. Primary survey
1. Airway, breathing, circulation, disability

66. Universal precautions – hand washing, sharps management

1. Handwashing
1. Before seeing patient
2. After touching patient / area
3. Soiled area
4. Before aseptic task

2. clinical waste management

67. Types of sutures and needles, choices in muscle/tendon repair and why

Absorbable

Short term Medium term Long term

Natural Synthetic Braided Monofilament Braided Monofilament

Catgut Vicryl rapide Braided vicryl Monocryl Panacryl PDS II

Non-absorbable

Natural Synthetic

Mersilk Braided Monofilament

Nurolon Ethilon
Ethibond Prolene

Ideal sutures
1.Pliability, for ease of handling
2- Knot security
3- Sterilizable
4- Appropriate elasticity
5- Nonreactivity
6- Adequate tensile strength for wound healing
7- Chemical biodegradability as opposed to foreign body breakdown
Common needle type:
Tapered
Gradually taper to the point and cross-section reveals a round, smooth shaft
Used for tissue that is easy to penetrate, such as bowel or blood vessels

Cutting
Triangular tip with the apex forming a cutting surface
Used for tough tissue, such as skin (use of a tapered needle with skin causes excess trauma
because of difficulty in penetration)

Reverse cutting needle

Similar to a conventional cutting needle except the cutting edge faces down instead of up
This may decrease the likelihood of sutures pulling through soft tissue

**non absorbable sutures used in tendon repair due to healing by fibrosis, and to facilitate
faster rehabilitation regime in order to avoid adhesion.
68. Ebola effect on muscles

1.

After entering the body through mucous membranes, breaks in the skin, or
parenterally, Ebola virus infects many different cell types. Macrophages and
dendritic cells are probably the first to be infected; filoviruses replicate readily
within these ubiquitous "sentinel" cells, causing their necrosis and releasing large
numbers of new viral particles into extracellular fluid

In addition to causing extensive tissue damage, Ebola virus also induces a systemic
inflammatory syndrome by inducing the release of cytokines, chemokines, and
other proinflammatory mediators from macrophages and other cells.

69. Malignant hyperthermia –

1. Malignant hyperthermia (MH) or malignant hyperpyrexia is a rare life-threatening
condition that is usually triggered by exposure to certain drugs used for general
anesthesia — specifically the volatile anesthetic agents and succinylcholine, a
neuromuscular blocking agent. In susceptible individuals, these drugs can induce a
drastic and uncontrolled increase in oxidative metabolism in skeletal muscle, which
overwhelms the body's capacity to supply oxygen, remove carbon dioxide, and
regulate body temperature, eventually leading to circulatory collapse

2. In a large proportion (50–70%) of cases, the propensity for malignant hyperthermia

is due to a mutation of the ryanodine receptor (type 1), located on the sarcoplasmic
reticulum (SR), the organelle within skeletal muscle cells that stores calcium.[6][7] RYR1
opens in response to increases in intracellular Ca2+
level mediated by L-type calcium channels, thereby resulting in a drastic increase in
intracellular calcium levels and muscle contraction. The process of sequestering this
 excess Ca2+ consumes large amounts of adenosine triphosphate (ATP), the main
cellular energy carrier, and generates the excessive heat (hyperthermia) that is the
hallmark of the disease. The muscle cell is damaged by the depletion of ATP and
possibly the high temperatures, and cellular constituents "leak" into the circulation,
including potassium, myoglobin, creatine, phosphate and creatine kinase.

70. Management DM in perioperative

1. Problems DM in surgery:
2. Associated end organ pathology
3. Metabolic decompensation
4. Poorer wound healing
5. Sepsis

Non insulin dependent:

Minor; Omit morning dose
Major convert to insulin

Insulin dependent
Major; serum glucose <6mmol, sub cut insulin 5u / 500mls d10% + kcl 10ml
If >10, double insulin dose

Post op:
>6mmol sub ins 10iu / 500ml d10 + kcl 10mmol
>10, 15iu
>20, 20iu

Hyperglycemia better than hypoglycemia

Hourly monitoring till 3hours last dose of insulin
Continue insulin till taking orally then only convert to previous dose

1iu will lower 1-1.5mmol depending sugar level

71. Level of evidence

72. Prevention of bleeding in surgery

Pre op:
Coagulation status checked
FBC
- identifying cause of defect, and preplan before surgery

Intraoperative bleeding
1. diathermy
direct sutures
hemostatic agent – gelatin, cellulose, fibrin glue, calcium alginate
1. physical stimulation of platelet and coagulation cascada – slow oozing
2.
ligation sutures
endoscopic – laser, adrenaline, sclerotherapy

Post op:
Tamponade
Correct causes of coagulopathy
Transfusion platelet / clotting factors
Steroids, plasmapheresis

Interventional radiology
73. Neurogenic bladder
Neurogenic bladder dysfunction, sometimes simply referred to as neurogenic bladder, is a
dysfunction of the urinary bladder due to disease of the central nervous system or
peripheral nerves involved in the control of micturition (urination).

Bladder overactivity (spastic bladder) is associated with the symptoms of urge

incontinence, while sphincter underactivity (decreased resistance) results in symptomatic
stress incontinence

Detrusor hyperreflexia refers to overactive bladder symptoms due to a

suprapontine upper motor neuron neurologic disorder. External sphincter functions
normally. The detrusor muscle and the external sphincter function in synergy (in
coordination).

Detrusor areflexia is complete inability of the detrusor to empty due to a lower motor
neuron lesion (eg, sacral cord or peripheral nerves).

Overactive bladder refers to symptoms of urinary urgency, with or without urge I

ncontinence, usually associated with frequency and nocturia.

Depending on levels of injury

Brain, pons, spinal cord, peripheral

Also affecting target muscle; Detrusor and external sphincter

BIOMECHANICS AND BIOMATERIALS

78. Newtons law

first law= if there is no net force on an object, its velocity remains constant
second law =force equals mass multiplied by acceleration
F=ma
third law= when a first body exerts a force on a second body, the second body exerts a
force that is equal in magnitude and opposite in direction on the first body
F2=-F1

79. Biocompability and bioinert

1. Biocompatibility: ability of a material to perform with an appropriate host response
in a specific situation
2. Bioinert: materials are ones which do not initiate a response or interact when
introduced to biological tissue. I

80. Definition of stress, strain

1. Stress: intensity of internal force
2. Strain: Relative measure of deformation of an object
3. Load: force acting on body
81. Stress/strain curve

1.

82. Young's modulus

1.Ceramic (Al2O3)
2. Alloy (Co-Cr-Mo)
3. Stainless steel
4. Titanium
5. Cortical bone
6. Matrix polymers
7. PMMA
8. Polyethylene
9. Cancellous bone
10. Tendon / ligament
11. Cartilage
83. What causes material failure?
1. Define as implant which no longer produce adequate function expected of it
2. Broadly can be divided into surgical causes, mechanical causes

Surgical cause: inappropriate implant choice, mixing different metal

Mechanical cause:
1. pure mechanical (overload)
2. pure environmental (corrosion)
3. conjoint

Further divided into types of failure:

Plastic failure – failure to maintain shape -> fail
Brittle failure – effect of design
Fatigue failure – repetitive loading on device -> failure

84. Corrosion – types

Corrosion is define as gradual degradation of metals by electrochemical attack

1. Galvanic: 2 different metals in free ionized condition

2. crevice: affecting oxide covered implant. In a narrow gap (crevice), high
concentration of chloride or hydrogen ions destroy this film. Or area where oxygen
tension is low, causing reactive area. Eg; screw head and plate
3. Pitting: started with defect in passive surface layer, corrosion proceeds into metal,
setting up self-accelerating concentration gradients.
4. Fretting: small oscillation movement/vibration
5. Stress: high mechanical stress alters the activity of metal and rupture a protective
passive surface layer.

85. Fatigue
1. failure at a point below the ultimate tensile strength secondary to repetitive
loading
2. depends on magnitude of stress and number of cycles

86. Viscoelascity
1. a material that exhibits a stress-strain relationship that is dependent on the load
and the rate by which the load is applied.
2. Eg: bone/ligaments

87. Ideal implant material

1. Inert
2. Non toxic to body
3. Absolutely corrosion proff
4. Inexpensive
5. Great strength
 6. High resistance to fatigue
7. Easiy worked

88. Ways to increase plate/implant strength

1. Involving mixture of element through different techniques
1. Casting, forging, cold working, case hardening
2. Surface treatment: polishing (physical and chemically removes scrathes
that could act as local stress) and passivation (immersion int strong nitric
acid solution), nitriding (reaction with ammonia or potassium cyanate)

89. Strength of material

1. Depends on young modulus, higher more brittle, lesser more elastic

90. Stainless steel

1. Primarily a iron-carbon alloy with abit of:
2. chromium
3. molybdenum (decrease rate of dissolution of passivation by 1000x), also protects
again pitting corrosion.
4. manganese
5. nickel

Cheap and strong

Higher stress shielding – prone for failure
Susceptible to corrosion

91. Titanium: advantages

biocompatible
forms adherent oxide coating through self passivation
corrosion resistant
Low modulus of elasticity makes it more similar to biologic materials as cortical bone (half
stainless steel)

Disadvantages
poor resistance to wear (notch sensitivity) (do not use as a femoral head prosthesis)
generates more metal debris than cobalt chrome

91. Bending and torsional rigidity of ILN

1. Bending: proportional to the radius to the 4th power for a nail (solid)
2. Torsional: defined as amount of torque needed to produce torsional (rotational)
deformation. Proportional to the radius to the 4th power. Increase by reaming,
decrease by slotting of nail.

92. Stresses acting on fractures and fracture patterns

1. Bending = transverse – long bone
2. Spiral = torsion – long bone
3. Compression – oblique /compaction – metadiaphyseal region
4. Compression / bending / torsion = oblique, tibfib, forearm
 5. Variable = comminuted
6. Compression + bending = oblique transverse – long bone

93. Strain theory on fracture healing

1. <2% - primary - DCP
2. 2-10% - secondary bone healing – IM nail, exf fix, lcdcp
3. >10% - unstable, fibrous union

94. What Is bone cement – function, what form supplied, complications

Polymethylmethacrylate (PMMA, bone cement)
functions
1. used for fixation and load distribution in conjunction with orthopaedic implants
2. functions by interlocking with bone
3. may be used to fill tumor defects and minimize local recurrence

2 components: powder and liquid

advantages
reaches ultimate strength at 24 hours
strongest in compression
Young's modulus between cortical and cancellous bone

disadvantages
poor tensile and shear strength
insertion can lead to dangerous drop in blood pressure
SE – cement embolism, peripheral vasodilation, allergy reaction
failure often caused by microfracture and fragmentation

gamma irradiation
increases polymer chain cross-linking (improves wear)

Use:
articulating surface components
eg. acetabular component

1. Bone grafts
1. 4 main properties bone graft
1. osteogeniprogenitor – cells present
2. osteoinductive – growth factors present, not cells
3. osteoconductive – scaffolding matrix
4. structural support
2. Drill type and complication
1. Drill bit (twist drill) most common
2. Body has spiral flutes which carry bone chips
3. Cutting performed by two lips at end of drill.
4. Principles
1. Wedge tools progressing at perpendicular surface
2. Process of drilling resuls in deformation of bone
Elastic as tool indents, plastic as failure in shear result materials cut away.

5. Effects of drilling – osteonecrosis at 44.6’celcius – deactivation of alkaline

phosphatase and the degradation of the collagen hydroxyappetite
1. Irrigate with saline
2. Sharp ends
3. Use sleaves
4. Use power drill
5. Avoid over penetration

PILOT HOLE: first step in inserting the bone screw

- 90% of screw thread diameter is optimal

3. Type of metals
1. Common metals
1. Ceramic
Property:
highest Y
typically brittle
low fracture toughness
low tensile strength
poor crack resistance
eg. alumina ceramic (Al2O3)
high compressive & bending strength
better biocompatibility than SS
or cobalt-chromium alloys

2. Cobalt chromium
Components
cobalt
chromium
Molybdenum

Property:
very strong (high Y)
better resistance to corrosion than SS
elastic limit is very close to the breaking load
prevents any possibility of permanent deformation
Low resistance to fatigue
 best for prosthetic femoral heads component.

3. Stainless steel
4. Titanium

Comparison SS vs Ti
SS is stronger, but higher fatigue failure

SS cannot withstand high and low temperatures

SS is magnetic and corrosive

SS is preferred when strength and hardness is needed

Titanium is preferred where a lightweight and strong material is required.

4. Polyethylene Property:
excellent mechanical properties
high impact strength
high fatigue resistance
excellent biocompatibility
Higher molecular weight increases yield and ultimate tensile strength
wear rate - 0.1mm/year
influenced by:
physical activity
weight
femoral head size

4. External fixation principle

Advantage:
• Minimally invasive
• Flexibility (build to fit)
• Quick application
• Useful both as a temporizing or definitive stabilization device
• Reconstructive and salvage applications

Increasing stability:
1. contact of ends of fracture
2. larger diameter pins (most important 1/3 diameter 5mm=144% stronger than 3.
4mm)
Femur – 5 or 6 mm
Tibia – 5 or 6 mm
Humerus – 5 mm
Forearm – 4 mm
 Hand, Foot – 3 mm

4. additional pins
5. decreased bone to rod distance
6. pins in different planes
7. increasing size or stacking rods
8. rods in different planes
9. increased spacing between pins

Complication with the use of the External Fixator include:

Pin-track infection
4 stages:
– Stage I: Seropurulent Drainage
– Stage II: Superficial Cellulitis
– Stage III: Deep Infection
– Stage IV: Osteomyelitis

Treatment:
Stage I: aggressive pin-site care and oral cephalosporin
Stage II: same as Stage I and +/- Parenteral Abx
Stage III: Removal/exchange of pin plus Parenteral Abx
Stage IV: same as Stage III, culture pin site for offending organism, specific IV Abx
for 10 to 14 days, surgical debridement of pin site

**avoid zone of injury within 5cm of injury site, thermal necrosis, bending pins

Pin Loosening
Frame or Pin/Wire Failure
Malunion
Non-union
Soft-tissue impalement
Compartment syndrome

Ring Fixator:
Use full ring if expecting long usage

Definitive= 1-2weeks post trauma

PHYSIOLOGY

Cardio
1. Definition of BP
1. Blood pressure is the strength of your blood pushing against the sides of your blood
vessels.

2. What forms systolic and diastolic BP

1. Systolic is ventricular ejection, whilst diastolic is compliance of aorta

3. BP regulation – what happens if baroreceptor fail

1. Baroreceptor detects fall in blood pressure, thus decrease parasymoathetic signal,
and increase sympathetic, which will cause increase contractility and peripheral
vasoconstriction. Failure will cause hypotension, esp postural, hence frequent
giddiness.

4. Autoregulation
1. Autoregulation is a process within many biological systems, resulting from an
internal adaptive mechanism that works to adjust (or mitigate) that system's
response to stimuli.
2. in CVS = Autoregulation of blood flow denotes the intrinsic ability of an organ or a
vascular bed to maintain a constant perfusion in the face of blood pressure changes

3. For example in cerebral autoregulation: interplay is between 50-150mmhg.

This rapid vascular response occurs within seconds of arterial pressure fluctuations. The
exact mediators of cerebral autoregulation are not completely understood. However,
neurogenic stimuli; metabolic factors, such as adenosine accumulation during low
perfusion; and direct intravascular pressure effects on smooth muscle or mediated via
endothelial-derived relaxation factor (ie, NO) and constriction factor (ie, endothelin-1)
have been implicated
5. Structure of blood vessels, which part cause hypertension in old people

Sustained increase of blood pressure 140/90

Two types morphology hypertension:

1. hyaline arteriolosclerosis – elderly with mild DM and hypertension.microscopically .
Endothelial cell wall injury, smooth muscle cell (SMC) increases extracellular matrix
composition. there is diffuse, pink, hyaline arteriolar thickening

2. hyperplastic arteriosclerosis is for malignant hypertension – onion skin arteriolar

thickening, with reduplicated basement membrane + fibrin deposition at wall.

6. What contributes to diastolic pressure

1. Compliance of aorta / arterial vesslels
Factors contributed:
1. peripheral resistance (arterial)
2. end systolic value
7. Difference between ventricular and aortic pressure
1. Central aortic blood pressure (CAP or CASP) is the blood pressure at the root of
aorta
2. Ventricular pressure is systolic pressure

AORTIC PRESSURE vs VENTRICULAR PRESSURE

8. What sustains blood pressure

1. Compliance of arteries

9. Compliance of vessels
1. Compliance indicates the ability to stretch. Higher compliance means more elastics.

10. Cardiac cycle – draw out the cycle, ventricular pressure

1. Cardiac cycle
1. Rapid ventricular filling
2. Reduced ventricular filling
3. Aortic systole
4. Isovolumetric contraction
5. Rapid ventricular ejection
6. Reduced ventricular ejection
7. Isovolumetric diastole

11. Starling law of heart

1. Ventricular contraction equals to initial stretch of cardiac muscle fibres in end
diastole, up to a certain value.
12. Respond of heart during hypovolaemic state in young and old people
1. During hypovolemic state, body will respond according:
1. Baroceptor: increase sympathetic and decrease sympathetic, which in turn
will increase the heart rate and vasoconstriction
2. Chemoreceptor in responds to increase pCo2, acidic environment
3.
13. Cardiac muscle, type of cardiac cell, draw cardiac AP and SA node AP and explain
1. Cardiac muscle is involuntary striated muscle that is found in the walls and
histological foundation of the heart
2. Comparison:
14. Regulation of heart rate by autonomic system and draw changes in AP if HR changes,
superimpose muscle contraction on AP

15. How long is cardiac AP and why is it long

1. 250msec, to allow ejection of blood to circulation

16. Difference of pulmonary and systemic circulation

Systemic Circulation
Pulmonary Circulation
Definition
Systemic circulation is part of the cardiovascular system which helps carries
oxygenated blood away from the heart to the body, and returns deoxygenated
blood back to the heart. Pulmonary Circulation is the half portion of the
cardiovascular system which helps carry oxygen-depleted blood away from the
heart, to the lungs, and returns oxygenated blood back to the heart.

Function
To carry oxygenated blood to the body vs help carry oxygen-depleted blood to the
lungs and return oxygenated blood to the heart.

Course
In systemic circulation, blood leaves through the left ventricle to the aorta, which is
then sent to smaller arteries, arterioles, and finally capillaries. Waste and carbon in
a cell is replaced by oxygen and the waste and carried away by the blood to venious
capillaries, and then the venae cavae: the lower inferior vena cava and the upper
superior vena cava, through which the blood re-enters the heart at the right
atrium.
 In pulmonary circulation, de-oxygenated blood leaves the heart, goes to the lungs
and then re-enters the heart; de-oxygenated blood leaves through the right
ventricle through the pulmonary artery to the capillaries where carbon dioxide
diffuses out of the blood cell into the alveoli, and oxygen diffuses out of the alveoli
into the blood. Blood leaves the capillaries to the pulmonary vein to the heart,
where it re-enters at the left atrium.

Deals with which side of the heart

Left side of the heart. Vs Right side of the heart.

17. What affects vessel resistence

1. Pousille law;
Resistance = 8 n l / m r4

Flow = Pressure / resistance

18. ECG

1.

19. Valsalva meneuver

The increase in intrathoracic pressure that occurs during the Valsalva maneuver incites a
sequence of rapid changes in preload and afterload stress. During the strain, venous return
to the heart is decreased and peripheral venous pressures become increased.
 Phase 1: increase intrathoracic pressure
Reduce cardiac preload
Increase extrapulmonary pressure of aorta
HR not elevated due to increase of aorta pressure

Phase 2: baroreceptor kicks in; increase heart rate, aortic pressure gradually picking up
Phase 3: sharp decrease in aortic pressure due to reduced external compression, again HR
increased due to baroreceptor
Phase 4: as result of systemic vasoconstriction by baroreceptor, the mean aortic pressure
increases due to increase preload.

Respi
21. RBC and their function
1. Does not have any nucleus, life span 120days.
2. Biconcave disk shape – increase surface area
3. Stimulated production by erythropoeitin
4. Contain haemoglobin for oxygen carrier
5. Contain carbonic anhydrase as carbon dioxide transporter

22. Different environment air and alveolar air

1. Alveoli air has lower partial pressure oxygen, and higher carbon dioxide pressure
2. Alveoli air some of it does not involve with gaseous exchange
3. Higher water vapor content in alveoli air
4. Slightly lesser nitrogen content in alveoli air
23. Mechanics of breathing – all the way to the curves
1. Dorsal group – impulse to phrenic – diaphragm contract + external intercostals –
intrathoracic subatmospheric pressure – surface tension of pleura – ‘pull’ lung to
expand – air flow in – compliance of alveoli – diffusion gas exchange – oxygen
crosses pneumocyte – basement membrane – capillary wall – RBC – heamoglobin –
oxyhemoglobin –pulmonary vein - left atrium – left ventricle – to systemic - arrives
at tissue cell – lower oxygen pao2 – dissociation of oxyghemoglobin – according to
pressure gradient

24. O2 dissociation curve, Bohr, Haldane, factors affecting tissue blood supply, CO poisoning,
how many more times affinity to Hb compared to O2, why painless death, role of 2,3-DPG, HbF,
myoglobin

Sigmoidal due to first binding is hardest, and it alter conformational changes to accept
other 3 oxygen molecules

At pressures above about 60 mmHg, the standard dissociation curve is relatively flat, which
means that the oxygen content of the blood does not change significantly even with large
 increases in the oxygen partial pressure. To get more oxygen to the tissue would require
blood transfusions to increase the hemoglobin count (and hence the oxygen-carrying
capacity)

Right shift: lower ph, high temperature, high 2,3 DPG (product of glycolysis – anerobic)

Bohr effect: stating that hemoglobin's oxygen binding affinity (see Oxygen–haemoglobin
dissociation curve) is inversely related both to acidity and to the concentration of carbon
dioxide

Haldane effect Deoxygenation of the blood increases its ability to carry carbon dioxide.

25. CO2 transport

1. 5% dissolved as gas
2. 10% as carbaminohemoglobin
3. 85% as carbonic acid in plasma
26. Compliance – definition
1. Compliance means elasticity
2. Lung compliance is defined as the magnitude of the change in lung volume,
produced by a given change in transpulmonary pressure.
3. Affected by thickening of lung tissue and surface tension.

27. Acclimatization
1. Body response to change of oxygen pressure (In atmosphere)
2. Peripheral chemoreceptor stimulate ventilation
3. EPO secreted by kidney – increase Hb synthesis
4. DPG increase – curves shift to right, facilitating unloading of oxygen. (also impairs
oxygen loading)
5. Increase in capillary density due to high hypoxia increased. Stimulate mitochondria,
muscle myoglobulin.
6. The peripheral chemoreceptos stimulate an increased loass of sodium and water in
urine. Thus higher concentration of hemoglobin in blood.

28. Respiratory regulation

1. Pneumotaxic – then to apneutic (long deep inspiration)
Inhibiting apneustic center will cause forced expiration by stimulating VRG
 2. DRG – slow quite breathing
3. VRG – force expiration (accessory muscle)
4. Chemoreceptor – po2, pco2, H+
5. Other peripheral receptors – J receptors in lungs interstitium (dry cough eg in heart
failure
1. Cough receptors at pharynx -

Cut off inspiration – by stretch reflex of alveoli sending to impulse to medullary

inspiratory neurons. (hering-breuer reflex)

29. Lung volumes and capacity, normal values – significance of RV, how to measure lung
volumes, significance of FRC in normal breathing and anesthesia, how to measure RV

Tidal volume = normal quite breathing

Residual volume to allow alveoli to in expanded mode – easier to breath
Measuring by lung function test
Measuring RV indirectly TLC - FRC
30. Hypoxia and hypoxaemia
1. Hypoxia is low oxgen at cellular level – can be diveided into hypoxemic hypoxia,
anemic hypoxia, carbon monocide poisiong, ischemic hypoxia, histotoxic hypoxia.
2. Hypoxemia is low oxygen in intravascular

31. Effect of anaesthetic agent

1. Airway obstruction – loss of cilia, and other protecting the airway
2. gaseous exchange
31. Glucose regulation
32. Hypo/hyperglycaemia what happens, hormones involved during DKA, how body
compensate, buffer systems, Kussmaul breathing, central/peripheral chemoreceptors

Ketoacidosis is an extension of normal physiological mechanisms that compensate for

starvation. Normally, in the fasting state, the body changes from metabolism based on
carbohydrate, to fat oxidation. Free fatty acids are produced in adipocytes, and transported
to the liver bound to albumin. There they are broken down into acetate, and then turned
into ketoacids (acetoacetate and beta-hydroxybutyrate). The ketoacids are then exported
from the liver to peripheral tissues (notably brain and muscle) where they can be oxidised.
Note that during ketosis, a relatively small amount of acetone is produced, this giving
ketotic patients their typical smell, often described as 'fruity'.

DKA represents a derangement of the above mechanism. Despite vast amounts of

circulating glucose, this carbohydrate cannot be used owing to lack of insulin. Ketogenic
pathways are maximally "turned on", supply of ketones exceeds peripheral utilisation, and
ketosis results. (There are a few other clinical states where similar keto-acidosis is seen.
One is in alcoholics, who may present with marked ketosis, and a variable degree of either
hypo- or mild hyperglycaemia. Another is in some pregnant women, particularly associated
with hyperemesis gravidarum).

The physiological mechanism of ketoacidosis is interesting. The rate-limiting step in the

manufacture of ketones in the liver is the transfer of fatty acids (acyl groups) from
Coenzyme A to carnitine. Carnitine acyl transferase I is the relevant enzyme, often referred
to as CAT-I. To a certain degree, increased levels of carnitine will drive this transfer, but the
main factor that inhibits CAT-I is the level of malonyl CoA in the liver. High levels of malonyl
CoA effectively turn off the enzyme.

Malonyl CoA is manufactured by another enzyme called Acetyl CoA carboxylase. Acetyl CoA
carboxylase activity is in turn regulated by the amount of citric acid in the cell. The more
the Krebs' cycle is whirling around (and citrate is being produced), the greater the activity
of Acetyl CoA carboxylase, which in turn results in inhibition of ketoacid production. Turn
off the supply of substrate into Krebs' cycle, and ketoacids are formed.

Hepatic gluconeogenesis, glycogenolysis secondary to insulin deficiency, and counter-

regulatory hormone excess result in severe hyperglycemia, while lipolysis increases serum
free fatty acids. Hepatic metabolism of free fatty acids as an alternative energy source (ie,
ketogenesis) results in accumulation of acidic intermediate and end metabolites (ie,
ketones, ketoacids). Ketone bodies have generally included acetone, beta-hydroxybutyrate,
and acetoacetate. It should be noted, however, that only acetone is a true ketone, while
acetoacetic acid is true ketoacid and beta-hydroxybutyrate is a hydroxy acid.

Ketone bodies are produced from acetyl coenzyme A mainly in the mitochondria within
hepatocytes when carbohydrate utilization is impaired because of relative or absolute
insulin deficiency, such that energy must be obtained from fatty acid metabolism

Kussmaul breathing is respiratory compensation for a metabolic acidosis, most commonly

occurring in diabetics in diabetic ketoacidosis. Blood gases on a patient with Kussmaul breathing
will show a low partial pressure of CO2 in conjunction with low bicarbonate because of a forced
increased respiration (blowing off the carbon dioxide). Base excess is severely negative. The patient
feels an urge to breathe deeply, an "air hunger", and it appears almost involuntary.

33. Glucose metabolism – as mentioned above

34. Dumping and short gut syndrome

Gastric dumping syndrome, or rapid gastric emptying is a condition where ingested foods
bypass the stomach too rapidly and enter the small intestine largely undigested. It happens
when the small intestine expands too quickly due to the presence of hyperosmolar (having
increased osmolarity) contents from the stomach. This causes symptoms due to the fluid
shift into the gut lumen with plasma volume contraction and acute intestinal distention.
"Early" dumping begins concurrently within 15 to 30 minutes from ingestion of a meal.
Symptoms of early dumping include nausea, vomiting, bloating, cramping, diarrhea,
dizziness, and fatigue. "Late" dumping happens one to three hours after eating. Symptoms
of late dumping include weakness, sweating, and dizziness. Many people have both types.
The syndrome is most often associated with gastric bypass (Roux-en-Y) surgery.

35. Function of stomach –B12 and intrinsic factor

1. Chief cell - pepsinogen
2. Parietal cell – H+, intrinsic factor B12 (binds to cubulin receptor in terminal ileum)
(this B12 protected by heptocorin from saliva)
1. Pancreatic enzyme cleaves in R receptor in duodenum
2. Absorption of ferum
Endo
36. Ca metabolism, PTH, vit D
1. As above

37. Endocrine – definition, type of hormones

1. Amine hormones – from tyrosine base (adrenaline, dopamine)
2. Peptides
3. Steroids (from medulla adrenal and gonads)
Peptides and catecholamines
1. free in plasma: receptor at plasma membrane: signaling mechanism (1. Second messenger,
enzyme activation by receptor, intrinsic enzymatic activity) : fast acting

Steroids and thyroids hormones

1. Protein bounds, intracellular, signal alters gene transcription, onset slow acting

Splenectomy vaccination; hemophilus influenza, meningococcal and pneumoccocal

38. Effects of various hormones on bone

39. Zones of adrenal cortex and hormone secreted

40. Hypothalamopituitary axis and regulation

41. Function of GH apart skeletal growth, peaks at night – if child does not sleep, how will it
affect GH level?

Increases calcium retention, and strengthens and increases the mineralization of

bone
Increases muscle mass through sarcomere hypertrophy
Promotes lipolysis
Increases protein synthesis
Stimulates the growth of all internal organs excluding the brain
Plays a role in homeostasis
Reduces liver uptake of glucose
Promotes gluconeogenesis in the liver
Contributes to the maintenance and function of pancreatic islets
Stimulates the immune system
Increases deiodination of T4 to T3

** Highest GH release is 2-3hours after sleeping

42. Stress response

43. Thyroid hormone synthesis, how they're transported in blood, danger of hyperthyroidism,
life threatening conditions
Thyroid storm or thyrotoxic crisis is a rare but severe and potentially life-threatening complication
of hyperthyroidism. It is characterized by a high fever (often above 40°C/104°F), fast and often
irregular heartbeat, vomiting, diarrhea and agitation. Heart failure may occur, and myocardial
infarction is encountered. Death may occur despite treatment. Most episodes occur either in those
with known hyperthyroidism whose treatment has been stopped or become ineffective, or in those
with untreated mild hyperthyroidism who have developed an inter current illness (such as an
infection)
Renal
44. Renal countercurrent mechanism – exchange and multiplier
1. Ascending Loop Of Henle only permeable to Na+, active ATP transport.
2. This will increase medullary interstitium osmolarity level
3. Permeable to water in descending limb, water free moves across the osmolarity
gradient.

4. Vasa recta minimizes the loss of solutes in interstitium by diffusion.

5. Urea helps to increase hyperosmlarity by readily filtered through glomerulus –
reabsorb at proximal tubule, and then diffused back into lumen, at loop of henle.

45. GFR – what determines GFR

1. GFR depends on pressure differences between afferent and efferent and bowman
capsule (permeability and surface area)
2. With this anything that will increase afferent diameter and decrease efferent
diameter.
3. Glomerular filtration pressure – (fluid pressure in bowmans capsule + osmotic
pressure at efferent)

Example as below:
46. Renal glucose clearance
1. Glucose is filtered and reabsorbed 98% in PCT, and another 2% in collecting duct.
2. Transport using co transport (down gradient) of sodium through SGLT2 apical
membrane – actively pump Na+ requires ATP
3. GLUT-2 transport to blood.

47. Function of kidney

1. Regulation of water and inorganic ion balance
2. Removal of toxic metabolic waste products
3. Removal of foreign body material
4. Gluconeogenesis
5. Hormones production
1. EPO
2. Renin
3. 1,25-dihydroxyvitamin D

48. Hormones that breakdown in kidney

49. How is urine concentrated

1. Urine concentrated using counter current multiplier – exchanger system.
1. Multiplier – to establish concentration
2. Exchanger – maintain of gradient, by closely related vessels (limbs + vasa
recta)
Fluid/Electrolyte/Acid Base
50. Cations and anions in body

51. Starling's equation on capillaries

Starling’s hypothesis states that the fluid movement due to filtration across the wall of a
capillary is dependent on the balance between the hydrostatic pressure gradient and the
oncotic pressure gradient across the capillary.

Net Driving Pressure = [ ( Pc - Pi ) - ( pc - pi ) ]

hydrostatic pressure in the capillary (Pc)

hydrostatic pressure in the interstitium (Pi)
oncotic pressure in the capillary (pc )
oncotic pressure in the interstitium (pi )

52. Role of plasma protein and albumin

Plasma protein and albumin helps to maintain oncotic pressure in particular vessels

53. Define homeostasis, buffers, osmosis

1. Homeostasis: A property of cells, tissues, and organisms that allows the maintenance and
regulation of the stability and constancy needed to function properly.

2. By definition, a buffer system is a solution that contains weak acids or base, which act to
resist a change in pH when acids or bases are added.
 3. By definition, a buffer system is a solution that resists a change in pH when acids or bases
are added.

54. Buffer system, intracellular and extracellular buffers

*** PROTEIN BUFFER IS INTRACELLULAR AND INTRACELLULAR

*** PHOSPHATE BUFFER SYSTEM IS INTRACELLULAR

*** CARBONIC ANYHYDRASE IS EXTRACEULLAR

** NOTE THAT PROTEIN HAS AMINO ENDS AND ACIDIC ENDS – ABOUT 70% OF BUFFER SYSTEM IN
BODY

2. Phosphate buffer system

Example of bicarbonate buffer systems. The bicarbonate component will bind to h+ and carried
away as water. Opposite occurs at lungs.

55. Acid base balance, anion gap.

1. Henderson hesselbach equation to determine PH
2. Kidney requires hours to days to work
3. Brain is ph sensitive, only Co2 can cross BBB. This will stimulate hyperventilation.
4. In Acidic environment: Renal acts by increase H+ excretion and increase bicarb
absorption at PCT.

Anion Gap
Sum of anion and cation must be in equilibrium.
Na+K – (bicarb+chloride)
Renal control in acidic environment:
H20 + CO2 breaks down to H+ and HCO3-, H+ moves out via H+atpase pump and Na/H+ exchanger.
HCO3- moves into interstitial fluids and bind with tissue H+
H+ will bind to phosphate instead if the HCo3- used up in body.

Bicarbonate can be made using:

H20+ CO2 = H+ and HCO3-
Glutamine metabolise = Ammonium (excreted out) and bicarbonate

Important acid base cells:

The principal cell (mainly water absorption) mediates the collecting duct's influence on sodium
and potassium balance via sodium channels and potassium channels located on the cell's apical
membrane. Aldosterone determines expression of sodium channels. Increases in aldosterone
increase expression of luminal sodium channels. Aldosterone also increases the number of Na⁺/K⁺-
ATPase pumps that allow increased sodium reabsorption and potassium secretion. Vasopressin
determines the expression of aquaporin channels that provide a physical pathway for water to pass
through the principle cells. Together, aldosterone and vasopressin let the principal cell control the
quantity of water that is reabsorbed.
Intercalated cell – in collecting duct

Neuro/Muscle/MISC
56. How do you diagnose death/brainstem death
Irreversible loss of brain + brainstem
Patient must be in deep coma, without external stimuli (drugs)

1. Two consultant / senior registrar

2. at 6-12hours apart (twice)
3. Absence of spontaneous breathing – pco2 >50mmhg or more than 20mmhg rise in 8
minutes
4. absence of cornea reflex
5. absence of gag reflex
6. absence of vestibule-ocular-reflex (30’ flexion, 50cc iced saline turn 90 degree) – normal
response is the eye will deviate towards contralateral side
7. absence of pupil reflex
8. absence cough response

Midbrain = CN3 eye and pupillary function

Pons = CN4,5,6 – eye conjugate movement and corneal reflex (ophthalmic branch
trigeminal and facial nerve)
Medulla = CN9,10 – gag and cough reflex
 Other conditions that needs to be considered:
1. persistent vegetative state – normal sleep wake pattern but no response to external
stimuli
2. locked in syndrome – eye movement and consciousness preserved
3. minimally responsive state – variable response to external stimuli

57. Underlying mechanism to death - explain all brainstem pathways

1. Nuclei present as above

58. Pain pathway, receptors, modulation, gate control theory, tracts - as described above
Pain pathway – impulse to dorsal root ganglion - anterolateral spinothalamic tract,
decussation at same level, or one above then synapse at reticular formation (pons) and
somatosensory cortex

Receptors pain – nociceptive, free nerve endings lies in epidermis layer (most superficial)
Gate theory indicates that pain AP transmission can be override by stimulating sensation,
which uses bigger fibers. Pain also can be suppressed by reticular formation – stimulating
endogenous morphine – blocking the release of substance P.

59. Peripheral nerve injury classify, Wallerian degeneration and regeneration

 Wallerian degeneration; 2 main components
- axon immediately degenerate within 30 minutes
- myelin clearance 24h – till days

By 48-96 hours post-injury, axonal continuity is lost and conduction of impulses is no longer
possible. Myelin disintegration lags slightly behind that of axons, but is well advanced by
36-48 hours. Axonal and myelin debris is removed by the phagocytic action of macrophages
and Schwann cells, a process which can take from 1 week to several months. By 5-8 weeks,
the degenerative process is usually complete, and the nerve fiber is composed of Schwann
cells within an endoneurial sheath.

Wallerian Regeneration depends on severity of injury, endoneural tubes diameter or

fibrosis, roughly ~1mm/day.

60. Neuromuscular junction – drugs/toxins that act on NMJ, MEPP, EPP

Neuromuscular blocker can be divided into
Depolarising – succinylcholine – bind like AcH causing NA+ influx, AP generated, but more
persistent – hence the twitching and relaxation phase.

Non-depolarizing – competitively binds at AcH site, but does not triggers action potential.
This drug needs to block about 70–80% of the ACh receptors for neuromuscular conduction
to fail, and hence for effective blockade to occur. At this stage, end-plate potentials (EPPs)
can still be detected, but are too small to reach the threshold potential needed for
activation of muscle fiber contraction.
Example: Roccuronium, Atracurium
61. Excitation – contraction coupling

62. Draw sarcomere – actin/myosin, sliding filament theory

63. Bone cells and their functions
1. Osteoblast – mesenchymal linage
1. Function to form bone by non mineralized matrix
2. Regulate osteoclast function by osteoprotegrin

2. Osteoclast – hematopeitic linage

1. Structure – MNG cell, with ruffles border
2. Function to reabsorb bone
1. Via ruffles border, howship lacunae is where brushite meets bone
surface.
2. Secrete tartarate acid phosphate
3. Stimulated by RANKL / inhibited by calcitonin, IL10, bisphophate
alters the ruffles border.

3. Osteocytes – trapped osteoblast in matrix, to maintain regulation of calcium and

phosphorus
4. osteoprogenitor cells
64. Types of muscles
1. Striated muscle
2. Smooth muscle
3. Cardiac muscle

65. Types of skeletal muscles

66. Types of spinal cord reflex
1. Stretch reflex (monosynaptic)
2. Inverse Stretch reflex (poly)
3. Withdrawal reflex (poly)

Other reflex: tone maintaining – intrafusal gamma (from cerebellum) via reticulospinal
tract-> small stretch of muscle fibres due to contraction of muscle spindle-> alpha
motor neuron activated via 1a -> contraction -> increase tone

Stepped on sharp object Relieve muscle cramp Ankle jerk

Withdrawal reflex Inverse stretch reflex Stretch reflex

Stimulus Pain Excessive stretching of Passive stretching

cramped muscle
Receptor Pain receptor Golgi Tendon Organ Muscle spindle/intrafusal
fibres
Afferent Type A delta & C Ib Ia/ II (Static response)
neuron
Integration at Polysynapse Disynapse/polysynapse Monosynapse
spinal cord
Efferent neuron Alpha motor neuron Alpha motor neuron Alpha motor neuron

Response Contraction of flexor Relaxation of stimulated Contraction of

muscles muscle stimulated muscle
Function Protect from pain Maintain tension of muscle Maintain length of
muscle, posture
67. Anticoagulant – mechanism on coagulation pathway

68. Cell –definition, cell division (mitosis,meiosis,binary fusion)

The smallest structural and functional unit of an organism, typically microscopic and
consisting of cytoplasm and a nucleus enclosed in a membrane.
69. Metabolic response to trauma

** during EBB PHASE resuscitation is vital, if inadequate, may proceed to necrobiosis -> cell death
70. Blood and composition
71. Nutritional supplement
1. Enteral = Delivery of all necessary nutrition via GIT tract, or surgically created ones
Normal oral, ryles tube, gastrostomy and jejunostomy
1. Cheap and easy
2. More physiological
3. Reduce risk bacteria translocation
4. Maintain GIT structures
5. Enhance immune response
6. Decrease electrolyte imbalance risks

2. Parenteral = delivery substrate through central vein (subclavian, internal jugular)

Parenteral combinations with enteral is no better than enteral alone

Complications from – insertion of CVL, electrolytes imbalance, osmolarities

Believe you can and you’re halfway there.
–Theodore Roosevelt