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

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

Function
Damage severity-amount of tissue, intensity-decides inflammation-local systemic
al
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
continues-long.
Loss of units
change in the structure of system, organ(lumen),tissue(cell cell, cell matrix interaction),
cell, organelle,molecule(chemical).
Accumulation
No damage-no inflammation function
Size
kept.
increase
Cell infiltration-re cells, neoplasia organ,
tissue
Calcification- dystrophic, metastatic
Decompensation-dependent cell affected,compensation,response-local,systemic,short long,
receptor irritation, structure (depending on ease to see feel) have to cross a threshold to cause
symptom/sign/lab change.
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.
Same system/organ localization-Variation in functional/local.systemic response/receptor irritationlocalises further.
Different system/organ localized- multisite disease, or tissue/organelle/cell/metabolic step
common
Age,Presenting complain with duration.
Events since asymptomatic
Exact duration,symptoms
Initiating event
Cause
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.
Severity depends on site, tissue,structural change & damage[tissue response/receptor
irritation/function]
trend(progressive/regressive)/rate of change gives cause.
Symptom severity-mild moderate severe.increase, same, less.fast,slow.Sudden recover-allergy
fast recover- vascular
Continous, intermittent-duration, Process of
cyclic
symptom
precipitating,increasing relieving Process
Ex ischemic threshold reached as peristalsis
factor
increase in inflamed gall bladder.
Frequency
Degree of damage
Interval behavior
Process intermittent vs contionus with
exacerbations
sequenc
e

Expecte
d
not

Same organ
localisation
Other organ

Increased severity
New process
Spread
Organelle,cell,metaolic
New lesion- ferile conv

Unreported symptom- bladder, bowel

illness in contacts
similar/other past episodes,pre inter post illness systemic response- behavior,activity(low tired,
early fatige) ,appetite.growth(short limited illness-even if recurrent-normal, abn in chronic-chronic
persistent,chr with exacerbations)
recurrent-allergy metabolic.
disease in family
Summary (pattern)-logical or empirical interpretation
Odp
SeqPer-diet dev
Signs
ex, not imm
Ph fh growth
Site
y-loc diff
Contact
Sst
Y
Pre/interepiso
Genesi
Y
Y

s
Path

dic
Y-loc demarcated/not,
diffuse.type

Cause
Y
Comp
Y
Resp/d
Y
ys
Provisional diagnosis
Signs- pathology specific- not etiology specfic
Chemica discomf Structu Response Dysfuncti
l
ort
re
on
Signs-see feel hear
Y
Y
Y
smell
Dysfunction-rs cvs pa-distention, cns,hem-purpura
Response- rr :pr =rs vs cvs. Pr more than for T=cvs.
Dysmorphic
vitals,proportion of vitals change-rs vs cvs.
Disease in consideration.clinical availability.sensitivity(not miss-single,usually early), specificity(not
overdiagnose-group, sst,sequence speed ) of finding/person.pathognomic.Valid/Reliable measure.
Risk of waiting for specific-evoulution(neo,low imm)-counsel look fordanger signsreport,unanticipated new symptom ,necessary inv-those altering diagnosis/rxpossibilistic,probabilistic,pragmatic.
Inv-for rx, prog-dysfunction,spread complication sequlae-significant,permenant.
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
process
functional

Abc
Antiinf
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.
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,