patomorph cycle 1 inflammation PUM 3rd year

signs of inflammation

rubor (redness); calor (heat); tumor (swelling); dolor (pain); loss of function

4 types of inflammation

acute, chronic, specific and non specific

inflammation can be

with cell damage; Exudative and productive

exudative inflammation can be

serous; fibrinous; suppurative; catarrhal; hemorrhagic

location of exudative serous inflammation

peritoneal/ pleural/ pericardial cavities and mucosal surfaces;

serous pericarditis is found in

rheumatic heart

disease, lupus erythematosus, tumours,

scleroderma, uremia, viral myocarditis

location of exudative fibrinous inflammation

peritoneal/ pleural/ pericardial cavities and mucosal surfaces; synovium

fibrous pericarditis is found in

myocardial infarction,

s. Dresler, uremia, rheumatic heart disease,

lupus erythematosus, trauma, radiation

serofibrinous pleuritis are

tuberculosis, pneumonia,

abscess, bronchiectases, rheumatic heart

disease, lupus erythematosus, uremia,

tumors

remember about Lobar pneumonia

congestion Red/ gray and yellow hepatization

exudative suppurative inflammation can be

superficial and deep

superficial exudative suppurative inflammations are

pyorrhoe (on mucosa) and empyema (on serous)

depp localised exudative suppurative inflammations are

abscesses (immature and mature)

depp diffuse exudative suppurative inflammations are

phlegmone (panaritium and paronychia)

bacteria causing Exudative suppurative inflammation

staphylococcus; streptococcus; Neisseria gonorrhoeae; actinomyces israeli

Exudative suppurative inflammation caused by actinomyces are located

head and neck (most common); lung, abdomen; pelvis

sepsis with the formation of

metastatic abscess

Pyemia

Pyemia can be found in

lungs, myocardium, liver,

brain, spleen, skin,

subcutaneous tissue, kidneys

Mucosal inflammation with large amount of mucus

exudative catarrhal infection

chronic catharral infections

atrophic and hypertrophic catarrh

Exsudative haemorrhagic inflammation can cause

hemorrhagic pleuritis/pericarditis

examples for Acute productive inflammation

acuter proliferative glomerulonephritis; membranoproliferazive glomerulonephritis

Chronic productive inflammation with hyperplasia of epithelial cells is found in

hyperplastic gastritis; polypoid rhinitis; condylomata acuminata

Chronic productive inflammation with fibrosis is found in

liver cirrhosis

Chronic productive inflammation with exudation is found in

chronic arthritis

a systemic autoimmune disease (or autoimmune connective tissue disease) causing major changes I'm skin, kidney, joint, serous membrane, heart

systemic Lupus erytheatosus (SLE)

SLE is more common

in women

Antinuclear antibodies (ANA) act against

DNA, histones, rna related proteins, nucleolar Ag

hematologic manifestation of SLE

decrease in RBC; WBC and PLT

found in 40-50% of SLE patients

anti-phospholipid (lupus anticoagulant)

function of anti phospholipid

in vitro prevent clotting; in vitro initiate clotting

clinical manifestations of antiphospholipid antibody syndrome

arterial/ vein/ capiallary thrombosis; foetal loss

genetic factos of SLE

more common in monozygotic twins (25%)

environmental factors causing SLE

drugs (Procainamide; Hydralazine); UV; estrogens; smoking

in blood vessels SLE causes

acute necrotising vasculitis (in capillaries, arterioles and small arteries)

fragments of vessel wall with necrotic characteristics

fibrinoid necrosis

deposit in fibrinoid necrosis

immune complexes, complement

in about 50% of people SLE causes

lupus nephritis

in lupus nephritis immune complex deposit in

mesangium, sub endothelial, subepithelial glomeruli

in lupus nephritis proliferation of glomeruli happens in

mesangium; intracappilary; extracapillary

lupus nephritis type I

normal

lupus nephritis type II

mesangial GN

lupus nephritis type III

focal proliferative GN

lupus nephritis type IV

diffuse proliferative GN (35-60%)

lupus nephritis type V

membranous GN

lupus nephritis type VI

glomerulosclerosis

morphology of skin in SLE

erythema facial butterfly area

SLE in skin causes

vacuolar degeneration in basal epidermis; oedema in dermoepidermal junction; perivascular/ periadnexal mononuclear inflammation

causes leading to angiopathy in CNS in SLE

anti-phospholipid syndrome and arteriosclerose

consequences of angiopathy ins CNS

multiple small infarct foci

Libman Sacks endocarditis charcacteristics

verrucae (1-3mm); on any valve (most common mitral); on either surface of leaflets

morphology of SLE in spleen

follicular hyperplasia; perivascular fibrosis - onion skin lesion

5 year survival prognosis of SLE

95%

main causes of death in SLE

renal failure; intercurrent infections, myocardial infarct

eleven criteria for SLE of which at least 4 must be fullfilled

malar rash; Discoid rash; photosensitivity; mouth/ nose ulcers; arthritis; cardio-pulmonary involvement; neurological disorders; renal disorder; hematologic disorder; immunologic disorder; antinuclear antibodies

organ specific autoimmune diseases with humoral mechanism

autoimmune haemoltic anemia/ thrombocytopenia; Myasthenia gravis; graves disease, good pasture syndrome

organ specific autoimmune diseases with cellular mechanism

type I diabetes; multiple sclerosis; hashimoto; Crohn disease

systemic autoimmune diseases with humoral mechanism

SLE

systemic autoimmune diseases with cellular mechanism

sjörgen syndrome, systemic sclerotis; rheumatoid arthritis

Primary biliary cirrhosis, Autoimmune hepatitis, Nodular arteritis, Inflammatory miopaties can be of

autoimmune origin

general symptoms of autoimmune diseases

non specific; fever; fatigue; muscular/ joint pain

symptoms of Sjörgens syndrome

dry eyes/ oral cavity

Mechanism of silencing autoreactive T and B

cells in peripheral tissue

anergy; apoptosis; suppression

Fas receptor activation

by FAS ligand

apoptosis mechanism

rheumatic fever is

acute, multi system, autoimmune disease

rheumatic fever occurs 10days to 6 weeks after

beta hemolytic group A streptococcus pharyngitis or skin infection

found in acute rheumatic heart disease (pancarditis)

Aschoff body (endocarditis; myocarditis; pericarditis)

pathogenesis of Verrucous endocarditis

Aschoff bodies causing erosion of endocardium leading to fibrin formation at site

hsitological characteristics of Verrous endocarditis

vegetations (1-2mm) around lines of closure

in rheumatic myocarditis Aschoff bodies are found

near bv and in interstitial connective tissue

chronic changes of endocardium in rheumatic fever

fibrosis and calcification; leaflet thickening/shortening; commissural fusion; thickening/ fusion of tendinous cords

chronic changes of valves in rheumatic fever of endocardium in order

stenosis or mitral; aortic; tricuspid; pulmonic

irregular thickening of the endocardium of the LA caused by mitral stenosis

MacCallum Plaques

CHRONIC CHANGES of the

ENDOCARDIUM that are valvular

mitral stenosis

CHRONIC CHANGES of the

ENDOCARDIUM that are parietal

Maccallum plaques

complications of rheumatic fever

mitral stenosis; chronic left sided heart failure; arrhythmias; infective endocarditis

symptoms of rheumatic fever

migratory polyarthritis; pancarditis; erythema marginatum of skin; subcutaneous nodules; Sydenham, chorea

erythematous lesions with pale centers and rounded or serpiginous margins on trunk and proximal extremities

erythema marginatum

major jones criteria

pancarditis, polyarthritis; chorea minor; erythema, marginatum; subcutaneous nodules

minor jones criteria

CLIN, LAB, evidence of streptococcus infection

jones criteria that must be fulfilled for rheumatic fever

2 major or 1 major + 2 minor

Libman sack endocarditis can be found on

any side of leaflet on any valve with most common mitral valve

NONBACTERIAL THROMBOTIC ENDOCARDITIS

Marantic endocarditis