Patho Week 2 Flashcards by mohamed osama1 osama1

3 places at which the deposition of amyloid happen

1- wall of blood vessels
2- reticulin fibers
3- basement membrane

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2 methods of detecting of fresh tissue and 5 of histological section

1- Dark brown with lugol iodine
2- blue with iodine + 1% sulphoric acid

1- H&E : pale red homogeneous material
2- congo red : orange red with green birefringence when observed under polarized light microscopy
3- methyl violet ( metachromatic ) stain rose red
4- immunohistochemistry
5- EM

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Dioagnosis in systemic form of amyloidosis can be established with biopsy of 3 places

1- rectal mucosa
2- gingiva
3- abdominal fat pad

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How do amyloid proteins injury the tissues (4)

1- pressure causes atrophy
2- accumulation in blood vessels cause ischemia and increase permeability
3- cause direct cytotoxicity e.g light chain protein is toxic to cardiac cells
4- perifibrillar oligomers -> are found to be more injurious than actual fibrils as in Alzheimer disease

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3 examples of localised amyloidosis

1- laryngal nodules
2- in brain in case of Alzehimer
3- in neoplasm : stroma in many endocrine glands e.g : medullary carcinoma of thyroid gland

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Primary amyloidosis 6 elements

1- rare
2- occur in old people
3- in plasma cell disorder ( multiple myeloma)
4- diagnosed by serum and urinary electrophoresis
5- death may occur due to cardiac and renal failure
6- in heart , tongue, GIt , skeletal muscle

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5 Secondary ( reactive systemic amyloidosis)

In AA disease

1- rheumatoid arthritis
2- chronic suppurative inflammation ( bronchectasis, chronic osteomyelitis)
3- infective granuloma ( TB, leprosy , syphilis)
4- inflammatory bowel disease
5- malignant tumor ( Hodgkin disease)

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3 other types of amyloidosis

1- heredofamilial amyloidosis ( familial Mediterranean fever)
2- amyloidosis of old age ( senile amyloidosis for over 70 years and may cause heart failure

3- haemodialysis associated amyloidosis ( B2 micro globulin)

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Renal amyloidosis . Amyloid are deposited where (3) and what does that cause

1- wall of arterioles and venules : thick wall and narrow lumen , fatty change of tubules and tubular atrophy, hypertension, renal failure

2- BM of glomerular capillaries: hypoproteinemia and edema ( nephrotic syndrome)

3- BM of collecting tubules : diabetus insipidus

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3 places of deposition of amyloid in liver

1- wall of hepatic arterieoles -> thick wall and narrow lumen

2- wall of sinusoids ( space of disse) -> pressure atrophy on adjacent hepatocyte

3- total replacement of large area of liver cells by amyloid material

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2 types of amyloidosis in spleen

1- focal ( sago spleen )
Deposition in wall of central arterioles , spleen is moderately enlarged

2- diffuse
Deposition in red pulp and wall of sinusoids
Spleen is markedly enlarged

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Where is the deposition of amyloid in adrenal gland and what happen if bilateral affection

1- in cortex
2- addison disease

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2 examples of amyloidosis in GIT and 4 clinicals

1- tongue -> macroglossia
2- intestine -> mucosal atrophy

Malabsorption, intestinal obstruction, haemorrhage, diarrhea

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2 clinical of cardiac amyloidosis

1- arrhythmia
2- heart failure

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5 cellular hyalinosis

1- Islet cells of pancreas in DM
2- corpora amylacea in senile hyperplasia in prostate
3- plasma cell in chronic inflammation eg Rhinoscleroma ( Russel bodies)
4- zenker degeneration( hyalinosis in voluntary muscle diseases)
5- Liver cells in Alcoholic cirrhosis ( Mallory hyaline bodies )

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Connective tissues hyalinosis

1-Wall of blood vessels (5)
1- Atherosclerosis
2- Benign hypertension
3- glomeruli of kidney in chronic diffuse glomerulonephritis
4- central arterioles in spleenic lymphoid follicles in old age
5- ovary in female ( corpus albicans)

2- old scars and keloid
3- mesodermal tumor ( leiomyoma)

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3 causes of dystrophic calcification

1- Alkalinity of necrotic tissue
2- increases phosphatase activity
3- Release the phosphate of nucleolprotein breakdown

What is the color of calcium salt and what will happen due to lamellation of calcium salts on necrotic focus

1- Dark blue

Psmmoma bodies

Examples of dystrophic calcification (7)

1- Degenerated tissue
1- atheroma
2- chronic rheumatic valvulitis
3- degenerated tumor

2- necrotic tissue
1- fat necrosis
2- TB necrosis
3- old thrombi
4- dead parasite

6 causes of metastatic calcification

1- increase calcium absorption from intestine ( hypervitaminosis D)
2- increase calcium mobilization from bone
1- hyperparathyroidism or parathyroid adenoma
2- prolonged immobilization
3- destructive disease ( paget disease)
4- malignant tumors of bone ( multiple myeloma )
5- diffuse skeletal metastases

4 sites of metastatic calcification

1- renal tubules ( nephrocalcinosis)
2- mucosa of stomach
3- wall of lung alveoli
4- media of blood vessels

3 examples of physiological atrophy

1- fetal structures ( thyroglossal duct )
2- atrophy of thymus gland after puberty
3- atrophy of breast and ovary after menopause

3 examples of general pathological atrophy

1- increase catabolism in TB, thyrotixicosis, malignant tumour
2- decrease anabolism in malnutrition and starvation
3- senile atrophy of old age

2 examples of local disuse atrophy

Decrease functions
1- muscles limb due to prolonged immobilization
2- renal tubules after fibrosis of glomeruli in chronic diffuse glomerulonephritis

2 examples of pressure atrophy

Long continued pressure on a tissue often cuts its blood supply 1- aortic aneurism cause atrophy in sternum and vertebral and not intervertebral disc ( avascular ) 2- liver atrophy in amyloidosis

2 examples Vascular ( ischemic atrophy)

1- coronary atherosclerosis cause atrophy of heart muscle 2- atherosclerosis of renal artery cause renal atrophy

Neurogenic atrophy and endocrine atrophy

When a motor nerve supplying a muscle is cut the muscle undergoes atrophy e.g : in poliomyelitis Atrophy of female genital organ after removal of the ovary

2 examples of physiological hypertrophy , 5 pathological hypertrophy ( adaptive, compensatory)

1- myometrium ( uterine smooth muscle) of the pregnant 2- skeletal muscles of the athletes 1- aortic stenosis and aortic incompetence -> hypertrophy of left ventricle in hypertension 2- pyloric stenosis -> hypertrophy of stomach 3- chronic intestinal obstruction-> hypertrophy in intestine 4- bladder neck obstruction-> hypertrophy of bladder 5- after nephrectomy

2 examples of physiological hyperplasia ( one is compensatory)

1- in breast and genital organ after puberty, during pregnancy and lactation 2- compensation : hyperplasia of bone marrow after haemorrhage and hyperplasia of liver after partial hepatectomy

Pathological hyperplasia Hormonal 2 examples Irritation 2 examples

Hormonal : 1- mamary cystic hyperplasia cause endometrial and breast hyperplasia 2- androgenic hormones cause nodular hyperplasia of prostate Irritation hyperplasia 1- hyperplasia of lymphoid tissue in case of infection and toxemia 2- hyperplasia of epithelium in bilharzial and viral infection

What is squamous metaplasia and mention 2 examples

Transitional of columnar , transitional epithelium to the more resistant stratified squamous type 1- chronic inflammation of bronchi , gall bladder, endocervix and in bilharzial 2- chronic infection or stones of urinary bladder

Glandular ( columnar ) metaplasia 3 examples

1- gastric epithelium around peptic ulcer transform to intestinal type 2- lower part of esophagus in reflux esophagitis 3- cystitis glandularis in bilharziasis of urinary bladder

Explain traumatic myositis ossification

Trauma to muscle lead to hematoma formation, the hematoma undergoes organization , the fibroblast invading hematoma change to osteoplast which lay down osteoid tissue

3 places at which bone may develop

1- scars 2- athematous lesion 3- calcified tuberculous lesion

What is serosal or mesothelial metaplasia and say example

Irritation of serosal cells may change them to cubical , columnar , glandular or stratified squamous Peritoneum may develop endometrial tissue ( endometriosis) due to sever serosal metaplasia

2 tumor metaplasia examples

1- adenocarcinoma with squamous metaplasia in endometrium 2- transitional carcinoma with squamous differentiation in urinary bladder

Why inflammation is protective response

1- eliminates the initial cause of cell injury 2- remove necrotic cells and tissue 3- initiate the process of repair

4 steps of local vascular reactions

1- vasoconstriction ( for seconds) by the direct effect of the irritant 2- vasodilation : associated with increase arterial blood flow ( active hyperemia ) by action of histamine 3- increases vascular permeability: histamine cause endothelial cells to contract and wide the inter endothelial gaps 4- slowing of blood flow ( stasis) due to A- increase vascular viscosity B- swelling of vascular endothelium which becomes sticky and offer resistance to blood flow

3 Mechanism of formation of Inflammatory fluid exudate

1- arterial vasodilation lead to increase volume of blood flow lead to increase hydrostatic pressure 2- increase vascular permeability 3- reduction of intra vascular osmotic pressure

4 functions of inflammatory fluid exudate

1- dilute bacterial toxin 2- bring the chemicals mediator derived form plasma e.g complement 3- bring antibodeis from blood 4- contains fibrinogen which is converted to fibrin

3 functions of fibrin in acute inflammation

1- localize inflammation 2- form network to bring the polymorphic, macrophage to the inflammed are 3- allows movement of proliferation fibroblast during the process of repair