patomorph cycle 1 degenerative and proliferative changes PUM 3rd year

pathologic prooien deposited between cells in various tissues and organs

Amyloid

group of diseases in which amyloid is deposited

Amyloidosis

accumulation of amyloid causes

pressure atrophy (shrinkage) of cells

Amyloid light chain causing multiple myeloma and malignant B cell proliferation

primary systemic amyloidosis

chronic inflammation/ tissue destruction and tumors that are amyloid associated

secondary systemic amyloidosis

tumors associated with amyloid

renal cell carcinoma and Hodgkin disease

amyloidosis affected organs appear

enlarged; waxy; firm

sites of primary amyloidosis

heart; GIT; peripheral nerves; skin; tongue

sites of secondary amyloidosis

kidneys; liver; spleen; lymph nodes; adrenals; thyroid

clinical symptoms of Amyloidosis

no clinical manifestation; nonspecific symptoms (weakness, syncope, weight loss); depending on affected organ

median survival of amyloidosis after diagnosis is

poor, 2 years

types of hereditary amyloidosis

familial mediterranean fever; familial amyloidotic neuropathies; senile Amyloidosis

types of reversible cell injury

cellular swelling and fatty change

types of irreversible cell injury

necrosis and apoptosis

morphologic changes that follow

sudden cell death in living tissue

necrosis

type of necrosis in which protein denaturation dominates

coagulative necrosis

type of necrosis in which enzyme digestion of cell dominates

liquefactive necrosis

lysosomal enzymes from dead cell causing necrosis is

autolysis

lysosomal enzymes from leukocytes causing necrosis

heterolysis

morphological feature of cytoplasm of necrotic cell

increase of eosinophilia; vacuolisation; calcification

morphological feature of nucleus of necrotic cell

Karyolysis; Pycnosis; Karyorrhexis

enzymatic digestion of necrosis with phagocytosis by neutrophils and

macrophages causes

cavity, scar

necrosis found in association with Mycobacteria

caseous (cheesy) necrosis tuberculosis must be ruled out

fat necrosis (statonecrosis) is caused by

acute pancreatic injury; hemorrhagic pancreatitis

pathway of gangrene (liquefactive necrosis)

artery occlusion -> coagulative necrosis -> bacterial infection -> liquefactive necrosis (gangrene)

characteristics of fibrinoid necrosis

necrotic fragments on vessel wall; immune complex/ complement deposit; plasma proteins

cellular consituents of intracellular accumulation

H2O; lipids; proteins; glycogen

process describing the abnormal

retention of lipids within a cell

steatosis

steatosis reflects an impairment of the normal

processes of

synthesis and elimination of triglyceride fat

in steatosis excess lipid accumulates in

vesicles displacing cytoplasm

steatosis can occur in

heart, liver, muscle, kidney

cause of liver steatosis

alcohol; Ischaemia; malnutrition; diabetes; obesity; toxins

diffuse steatosis of heart is caused by

diphtheria; Reys syndrome; severs ischaemia

focal (cor tigrinum) steatosis of heart is caused by

mild ischaemia

accumulation of cholesterol causes

atherosclerosis; xanthomas; inflammation/ necrosis; choleserolosis; Nieman Pick type C

liver cirrhosis is replacement of the normal lobular architecture by

parenchymal NODULES separated by fibrous septa

liver cirrhosis is a

diffuse, chronic, irreversible process

patomorphology of liver cirrhosis

loss of fenestration; BM; collagen I and III deposition; decrease of albumin clotting factor secretion (by hepatocytes)

stellate cells (Ito cells) in liver cirrhosis get activated causing

transformation to myofibroblasts; proliferation; chemotaxis; collagen synthesis

characteristics of cirrhotic liver

loss of fenestration; basement membrane; proliferation/. transformation into myofibroblasts; abundant collagen (I and III)

vascular hemodynamic of portal trace in cirrhotic liver

increase in presinusoidal resistance (by fibrosis); increase in portal vein pressure (HA to PV shunts)

vascular hemodynamic of sinusoids in cirrhotic liver

increase in sinusoidal resistance; septal shunts bypassing parenchyma

vascular hemodynamic of terminal hepatic vein in cirrhotic liver

increase in postsinusoidal resistance (by fibrosis)

liver cirrhosis causes

hepatic failure and portal hypertension

consequences of hepatic failure

jaundice; decrease of albumin/ clotting factor synthesis; inactivation of estrogens

inactivation of estrogens caused by hepatic failure causes

palmar erythema; spider angiomas; hypogonadism; gynecomastia

consequences of portal hypertension

portosystemic shunt; congestive splenomegaly

congestive splenomegaly increases breakdown of RBC; WBC and PLT causing

anemia; infections; diathesis

symptoms of liver cirrhosis

portal hypertension; renal failure; anorexia; osteoporosis; dupuytren contracture; gastritis; peptic ulcers; hepatorenal syndrome

causes death in liver cirrhosis

progressive lifer failure; rupture of oesophageal varicose; hepatocellulr carcinoma (HCC)

liver cirrhosis with radius < 3mm

micro nodular

liver cirrhosis with radio < 3mm

macro nodular

alcoholi liver cirrhosis more often occurs in

males; 50-60 years (symptoms are only present in 10-15% of alcoholics

characteristics of liver in early stage liver cirrhosis

> 2kg; large; yellow; micro nodular

characteristics of liver in late stage of liver cirrhosis

< 1kg; small and firm; micro and macro nodular

post inflammatory liver cirrhosis is cases hy

HBV; HCV, HDV

decrease of hepatocyte secretion of bile and bile flow through canaliculi

cholestasis

cells that bile accumulates in in cholestasis

hepatocytes; Kupfer cells; bile canaliculi

causes of cholestatsi

obstruction of biliary tree by stones (extra hepatic) or primary biliary cirrhosis; familial intrahepatic cholestasis

consequences of cholestasis

bile stasis -> proliferation of bile duct epithelium -> ductular proliferation

characteristics of primary biliary cirrhosis

autoimmune; intrahepatic bile duct damage; autoantibodies in serum (more common in women age 20-60)

characteristics of secondary billiary cirrhosis

prolonged extra hepatic biliary obstruction

secondary billiary cirrhosis causes

cholelithiasis; scars; pancreatic head cancer; Atresia; cystic fibrosis

characteristics of Hemochromatosis

Fe accumulation; HFE gene mutation; more common in men; starts 5-6 day of life

in hemochromatosis deposition of hemosiderin happens in the following organs

liver, pancreas, myocardium, pituitary, adrenal, thyroid, parathyroid, joints, skin

in Wilsons dies cu accumulates in

liver (cirrhosis); brain (atrophy of basal ganglia); eye (kaiser fleischer rings)

histological changes in liver caused by Wilsons disease

acute/ chronic hepatitis; massive liver necrosis; cirrhosis

a1-ANTITRYPSIN DEFICIENCY causes

liver cirrhosis and pulmonary epmhysema

hepatic failure happens when

only 10-20% of liver are retained

causes of Fulminant hepatitis (massive hepatic necrosis)

acetaminophen; halotan; isoniazid;CCL4, mushrooms

decrease in cell size

atrophy

increase in cell size

hypertrophy

increase in cell number

hyperplasia

A reversible change in which one adult cell

type is replaced by another adult cell type

metaplasia

causes of atrophy

disuse; compression; inadequate nutriton; loss of innervation; loss of endocrine stimulation; aging; decrease in blood supply

causes of hypertrophy

increase in workload; hormonal stimulation

causes hypertrophy in heart

stretch and activation of alpha adrenergic receptor

consequences of hypertrophy

increase in protein synthesis and myofilaments; reexpression of fetal protein in myocytes

in myocardial hypertrophy cardiac myocytes increase from 15 to 25µm causing

increase in distance between capillaries and ct between myocytes

myocardial hypertrophy can be

concentric and excentric

causes of hyperplasia

hormonal (e.g. puberty/pregnancy); compensatory (e.g. partial hepatectomy); viral (HPV); wound healing

both hyperplasia and hypertrophy happen in

uterus in pregnancy and kupffer cells in acute hepatitis

metaplasia happens with

epithelial and mesenchymal cells