Why-gene,metabolic storage,physical chemicalpoison,toxin,biologic,allergy,multiple,deficiency,excess,unknown

Damage-adapt,cell degeneration/necrosis-inflamation, repair-------------structure.

Damage severity-amount of tissue, intensity-decides inflammation-local systemic
response,receptor irritation
Systemic-T,behavior,activity,appetite.catabolic.Receptor irritation-reflex(cough vomit), pain.
Cause resolved, eliminated,damage stopped-resolve-short.Cause persist, damage continueslong.
Loss of units-bleeding
change in the structure of system, organ(lumen),tissue(cell cell, cell matrix interaction),cell,
organelle,molecule(chemical).

F
u
n
ct
io
n
al
.

Accumulation
No damage-no inflammation function kept until
Si
late.
z
Cell infiltration-re cells, neoplasia organ,
e
tissue
Calcification- dystrophic, metastatic
Functional-when damage erodes reserve, when need>functional limit due to structural
issue.structure blocks-in/out roads.
Disease results in a processeach identified by,
Decompensation-dependent cell affected,compensation,response-local,systemic,short long,
receptor irritation, structure (depending on ease to see feel) which have to cross a threshold
to cause symptom/sign/lab change.
Each process-initially reflex irritation dominates clinically-than systemic response-local responsecompensation-decompensation.
Our job is to find evaulate each process-same or other location-synthesise a link to a disease.
Major Symptoms sign-localise to a organ-process-other symptom same process or not-new
process same or other site-link to a disease.
Defining process.
Localization.
Organ/system decides symptom-so Symptom localise to system/organ.
Systemic responses, non localizing reflexes-low localizing value-but tell degree of damage.
Some symptoms are common to organs- ex vomit-reflex- receptor irritation- digestive tract,
meninges, urinary tract.
So associated symptom(even a minor one)- ie group localizes better.
Multiple symptoms.
Localise to same(disease,tissue cell organelle step) /other processsame /other site.
Variation in functional/local.systemic response/receptor irritation-localises further.
Chart.
Age,Presenting complain duration.events since all well(exact duration, symptoms),initiated
by(cause).
Contino
Odp
Inc relieving
us
Episode Odp of episode-ppt/eventsInterval behavior(int vs cont with exac),
releiving
Odp of symptom-freq(severity),cyclic
Origin- time to reach symptom threshold- speed of damage-site/tissue specfic
Origin-in minutes/hours/days/weeks. Mild /moderate/severe-(initial severity).
minutes(sudden severe , critical path.reflex-vasogenic,neurogenic ,spasmogenic.type 4, mech,
toxin
hours-damage in hours. chronic with acute decompensation may appear acute.
Duration.
trend/rate gives cause.symptom severity depends on site,tissue,structural change &
damage.
(trend)increase, same, less.(rate)fast,slow.mild moderate severe. Sudden recover-allergy fast
recover- vascular
Sequen Expecte
Summary.
ce
d
See symptoms of same or
Not
Same organ
Increased severity
different process-same other sitelocalization
link to form a disease.
New process
Other organ
Spread
Organelle,cell,meta
olic
New lesion- febrile
conv
New process suspected if reappearance of receptor irritation, systemic response.
Ex. Reappearance of fever in a child with meningitis- possible abcess.
Link may be available from,
Unreported symptom- bladder, bowel.development. illness in contacts immunization.
Disease limited to the illness presented or otherwise.
See these episode same disease(same /other site) or new.

1. similar/other past episodes,

2. pre inter post illness systemic response- behavior,activity(low tired, early fatige)
appetite.growth
1. short limited illness or recurrent-interillness/growth normal. Recurrent- allergic/metabolic.
2. chronic-persistent/with exacerbations.
disease in family.
Summary.
Link to a disease.logical or empirical interpretation-Provisional diagnosis
Signs( pathology specific- not etiology specific).
Decompensation, compensation(valid reading), response,structure(localised/diffuse
demarcated/not-).
Response- rr :pr =rs vs cvs. Pr more than for T=cvs.
Disease in consideration.clinical availability,sensitivity(not miss-single,usually early), specificity(not
overdiagnose-group, sequence speed.100 % specific=pathognomic ) of finding/person.
Risk of waiting specificity-evolution(neo,low imm)-counsel look fordanger signsreport,unanticipated new symptom ,necessary inv-those altering diagnosis/rx
inv-possibilistic,probabilistic,pragmatic(inv for treatable). For rx,prognosis-morbodity sequlaesignificant,permanent.
Lab- Chemical-fluid tissue . Structure-Available tissue/fluid,Imaging.Function study chemical.
rx options-limit damage
to curtail/eliminate cause and process of damage,
limit damage and
restore anatomical/functional integrity.
Cause
Abc
Process
Antiinf
functional
Rehab
Replacement
rx
Prognosis.
response -cause, site, severity,spread/complication/nutrition/comorbid conditions
reversibility- inflammation resolve-chronic,necrosis-regnerate/scar, sequelae-anatomical functional
risk to life.
Pattern
Functional unit

Rs
Awupp,large,
sm
Alv

Cvs
Hypo

Upper mot

Liver
Cellular

Distrib

Lower motar

Cholestatic

Pleural

Cardio
Obs

Extrapyrami
dal
Cerebellar

Path

Inter-infilt

Infil,it is

Encephalitis

Etio

autoimmu
ne

Anaphy

Toxogenic
Traumatic
Degenerativ
e
Encephalopa
thy
Ischemic
Vascular
venous

Duration
Pathophy

Ph

Ccf
Neurog
Vasoge
nic

Sm
all

Glo
m

larg
e

Tub
Upp
er
lowe
r

Infiltr,itis,Fa
tty
Alf clf

Arf
crf

Tissue
Myopathi
c
Connecti
ve
Neuroge
nic
Vascular
Bleed
Emb
Throm
Vasculitis
-t
Spasm
Ext obn

hemody
Ph
ccf
Hypoperfusion
cns
Git
kid
inj
Life and function of a group of cell depends on,
In roads and out roads.vascular/non vascular.
Luminal field of function can be overlapping or demarcated.
The roads work if the lumen is patent- get obstructed if the angle of orientation of the lumen
changes with respect to the anchoring point(twist) or if there is a luminal or extraluminal mass.
cell interaction with extracellular matrix.cell cell-cell size affected,signal path damaged. In
luminal cells this damages the
lumen tissue barrier-ex blood brain barrier,endotheial damage-blood tissue barrier.vessel
lumen barrier.
intracellular process- metabolism, organelle functional
The problem with these tend to cause characteristic symptom pattern.
lumin Speed and nonvascul In
Resource
Pattern of damage
al
degree of
ar
deprivatio decompensation,compensation,local systemic
block.
n
responses, receptor irritation.

Ou
t
In
ou
t

Vascular

Renal
Glomerula
r
tubular
tract

Effuluent
builtup
Ischemia
Stasis

Hemat prot

Major lumen blocks-muscle tissue ischemia,

reflex vomiting

Rbc cola no pain bp

End-redu urine,oed bp
Ep-massive oed, no
rbc
Interst-no oed, no bp

Red urine pain

Upper-more systemic
Lower-local-dysuria
freq

Ftt polyuria h+ bone

crf
Growth hb bp bone metabolic
arf
Reduced urine
Small int chronic-infreq stool distent ftt large-tenesmus mucus
Vomit-gi-oes stom int drug cough ctz-met(ren hep iem) ict ans-myocard, vertigo
----associated.timing in reln to illness
Persistant without illhealth-psycho. Decreasing-gi
later-comp major illness
Diarr-malabn inc app, inflm-reduced tb-block-sec diarr
Dominant vomit-liver pain-append t-uti
Sequence-t-v-diarage
diarr-vomit=ileus distention,intusse(cry)
drug=vom later-complic
Multiple- each sym, back in time
Abd dist 2wks- organ fluid gas(wx wane) tumor---------2wks short----vasogenic-cap
Ge- look oed-sick acute cap leak, ang chr-liver comfort
t-onset parectmol inter trend d3 4 accom
vomit>24 hrs-worry
tc
inc
inc
++

p
inc
inc
+
+

low

+-

+-

e
0

=
+
inc

+
Hb
less

+-

Plt
n
inc
re
d

0
O
in
c
n

Low plt-

uti

Vir mal typ

bact
Inf
Viral
Ent-inc
mon
Chr

re
Mal
d
++
inc n
re
leuk
+
d
inc
+
re
d
T drowsy sim=enceph
tdrowsy laterunanticipated
Intersymp period tired-chr
n-rec/partial rx
Cough chief- aw, assoc-paren inter pleura gerd cardiac
Upp-str bark low-wet smaller-less cough-more breathless
ronchiolotis high coughviral hrperactive
Upp low---largecough>dist sm dist>cough
Bronchiolitis-no retrat paren- grunt intercostals T ----demarcated to lobes
Rt ant up mid, post
left ant post
asthama-trap-no ic ,sc
Pleural- unilat pain non lobar tb , empyema-need penumon
Interst-inc rr mild cough sat less fine crac
Gen aw paren int-myco viral
Coughpredaw seq past,atopy fh, accom-t cold breathless growth
Cough pred-----T-viral
bact-pertusis myco tb no T asth
Breathless sudden pneumoth fb=mech
hrs- allergy 2-3d pneum
upp ic-paren sc asth-aw

2-3 wks-interst

ss-

Cough episode sig T---adenoid ton sin

cold cough-viral lower-cough T --growthcilia tb
imm cf
No T/occ-episodic nocturnal-hyperactive atopy ph fh , aspir prem l to right fb
Slured speech- bell 7
Upper cranialless sign sym

subtensigns sym lot

emotional-frontal

Art
to begin

cort-seiz sensory aphasis-write read

subcor-no seiz no sensory

ic-dense

Is disease sensitive finding present (chances of it being positive in those with disease).
interpersonal variation in the symptom presentation by patient or observation by physician.
Sureity of diagnosis (specific finding-chances of it being negative in those without disease)pathognomic is not found in any other disease.interpersonal variation in a observers specificity
also matters.
Vomiting is sensitive but not specific to detect meningitis.
Not to miss- use sensitive test.
Not to overdiagnose- use specific finding
If a process is to be measured use a valid measure-ex rr is a valid measure lung damage.
Reliable measure- same on repetation.
gcs is valid but may not be reliable.
Single findings increase the sensitivity. Group of findings,sequence- pattern increse specificity.
A disease more prevelant in the settings considered-positive finding-increase likelyhood of
disease
More prevelance- finding negative more likely to be false negative-so value of negative test
saying that disease absent decreases with prevalence.
Clinical Availability, sensitivity, specificity of a finding- decide chance and confidence of
diagnosis.
Hidden, deep structures not visible, felt late
Degree/ease- of Availability of a finding-ex redness of colon is specific to colitis-but not available
easily.
Clinician has to depend on the available findings use the ones sensitive or specific according to
the purpose of evaluation.
early in course of signs are not specific-clinical diagnosis can be made after specif ic signs
appear or by following a pattern.Specfic lab test turnaround time
Waiting for confirmed clinical finding/specific lab test may result in irreversible damage /serious
sequlae,treatment on presumptive diagnosis is necessary.
Risk of waiting for diagnosis,risk of rx,community implications decide approachpossibilistic,probabilistic,
pragmatic(directed at the diseases which can cause damage and for which a remedy is
available).
Disease life cycle- non specific findings(discomfort),structural functional changes(mid
life),response-compensated/decompensated-mortality.
Point of presentation vs point of origin of disease same or different.
If different the relation between two should be deduced.
Chapter 1.localisation
1)systems,Organs Rs ,digestive,renal,endocrine,reproductive,special senses-visual,auditory.
circulatory - epi myo endocardium.elastic/muscular arteries,arterioles.Veins-small med
large.
Capillaries -continous fenestrated sinusoidal.Lymph caps, vessels.
Lymphoid =collection of lymphocytes- various sites, encapsulated thymus node tonsils
spleen.
Skin epidermis-epithelium(keratinocytes melanocytes merkel langerhan=basal spinosum
granulosum lucidum corneum, dermis-connectice(papillary reticular sweat gland, hair
follicles)
3)Tissue.
Epithelium.simple squamous,columnar, cuboidal. Pseudostratified columnar, stratifiedsquamous cuboidal transitional.
Connective-loose,dense irr, dense reg,reticular,adipose(fibrocytes, mast , fat,
macrophages plasma leucocytes.collagen reticular elastin ground)

Cartilage-hyaline elastic fibro

bone-compact cancellous hemopoetic- rbc wbc
platelets plasma
Nervous=neurons neuroglia
Muscular-smooth skeletal cardiac
1
Metabolic step
2)Organe Cytosketelon
Structure maintained
lle
Transport of goods in cell, in out
Membrane
Gate way- control of movement of molecules across
Signal propogation
Cilia
Move mucus
Mitochondria
Energy production.reduces oxygen
Ribosomes
Enzymes steps of daily cell life, damaging molecules to
less or excretable
Lysosomes
Degrade molecules
Perioxosomes
Rna
Signal from nuclei to cytoplasm
Dna
Codes for life and reproduction
Chapter 2.
chemical change
chemical, alteration of molecular structure,loss/excess/change in proportion or change in location
of molecules.
Temp-coag cold-crystal vasoconstriction. Radical/hypoxia/calcium=damagers
chemical change causes alteration in micro and macro structure.Chemical/structural change
causes problem with function.
b)physical change
1)Loss of functioning units ex bleeding causing reduced number of red blood cells
available
2)Block of luminal passage of nutrients-food, gases,excretory or secretory organs.
3)damage to the structure of cell/tissue-ex crush injury-Cell cell, cell matrix interactions
Injury-adaptation-reversible damage-irreversible damage necrosis-autolysis or hetrolysis
a.Adaptations=
Hypotrophy
Atrophy-less use,nutrition blood endo nerve loss
hypertrophy
hyperplasia-physiologic=compensatory ,endo. nonphysiologic
metaplasia dysplasia .
Varying appearance to the damaged tissue depending on the basic chemical nature and type of
chemical change
b.Reversible damage appearance-cell degneration-cloudy hydropic fatty hyaline lipoid mucoid
degeneration.(cell membrane pumps, plasma membrane, mitochondria,cytoskeleton
Cell mitoch er swell, riosomes detach myelin loss of villi blebs chromatin clump lipid
c.Irreversible damage appearance-necrosis
coagulative =even enzyme damaged-solid organ
liquificative enzymes brain, bacteria
gangrenous-dry,wet- black tissue
caseous -tb
fat-saponification,
firinoid, apoptosis-memb disrupted, leak of enzymes,lysosom enz ,prot dig,basophilia nuclear
changes
d.Accumulations,
e.calcification-dystrophic metastatic
f.acute inflammation(redness, swelling,local heat, pain, and loss of function)-resolves, organizesfibrosis,chronic.
acute=exudates-serous, hemorrhagic, fibrinous,memranous, or purulent.
chronic cell+fibroblasts-subtle signs
g.repair-regeneration, scarring
h.neoplasia.
Degenerative-slow progressive loss of function
Infiltration cell/accumulation-no function loss, no pain fever redness -progressive increase in
size.

Chapter 3.
cause
1. Physical-sudden fast slow, external vs internal(ex disc prolapsed-physical damage to
nervous tissue

2. Hypersensitivity type I mediators-vasodilation, smooth muscle spasm,inflamation.

type II -antibodies damage cells-phagocytosis or lysis inflammatory damage. Antibodiesblock cellular functions-disease without tissue injury.
type III- antibodies antigen complex- inflammation directly/complement.wbc-lysosomal
enzymes/free radicals.
type IV-cell mediated-T lymphocytes-cellular injury.
Chapter 4
1.discomfort
Pain cutaneous deep somatic , visceral(distention ischemia contraction), referred
2.Functional change Physiological function of the site damaged determines type of functional loss.
Hence it can be used to know the physiological process affected,anatomical site affected.
cognition,sensations, movement, oxygenation,ventilation,circulation,excretion,secretion,
transport through lumens.
FunctionNervous neurons neuroglia ependy
Generate and propogate signal
Muscle skeletol cardiac smooth
Generate force
Connective loose dense reg irr adipose
Structure, fight microbes
reticular
Epithelium=cell basement
Enzymes, transport molecules across.barrier for
microbes chemicals
The distribution can help the localization of the lesion.
Chance of functional change is proportional to the importance of point of damage in the
overall function.
Can the deficit be compensated-the liver, lung have independent functioning units-the loss
of few units can be compensated by others .loss of part of lung could be compensated by
the remaining.
Neurological cells have designated functions and are clustered according to function
Loss of particular subset of neurons cause loss of function specific to them.
Amount of tissue damage and the functional loss.
Damage should overcome the reserve capacity for the functional loss to perceived.Stress
requiring the escalation of the function in question unfolds the functional loss.
Smaller lesions can cause a significant change in the function
1. if the cells result in a endocrine/paracrine effect.
2. Cause a obstruction to the lumen
3. Dense population of a functionall important tissue.
The time over which the functional loss develops depends on the
amount of tissue damaged
cause and mechanism of damage affect the rate at which tissue change occurs.Hence the
time over which the symptom occur and the severity give a idea of the cause and
mechanism.
Chemical/physical/type 1 hypersensitivity can cause immediate symptoms.
type of tissue affected.
Nervous tissue- more perceptible functional loss-followed by muscle-epithelial-connective
tissue.
This occurs as epithelial and muscle tissue can compensate.
While the perciptable change in the connective tissue function occurs late in the course.
3.Response of body systems to damage-fever, increase stool frequency,pr, rr.
Category of Liver Disease by Predominant Serum Enzyme Abnormality
Liver Disease Category

Test

Hepatocellular

Cholestatic

Infiltrative

AST, ALT higher than alkaline phosphatase level

Typical

Alkaline phosphatase higher than AST, ALT levels

Typical

Elevation of alkaline phosphatase with near-normal AST, ALT levels

Typical

Typical

ALT, alanine aminotransaminase; AST,