Patho Week 2 Flashcards
3 places at which the deposition of amyloid happen
1- wall of blood vessels
2- reticulin fibers
3- basement membrane
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
Dioagnosis in systemic form of amyloidosis can be established with biopsy of 3 places
1- rectal mucosa
2- gingiva
3- abdominal fat pad
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
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
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
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)
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)
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
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
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
Where is the deposition of amyloid in adrenal gland and what happen if bilateral affection
1- in cortex
2- addison disease
2 examples of amyloidosis in GIT and 4 clinicals
1- tongue -> macroglossia
2- intestine -> mucosal atrophy
Malabsorption, intestinal obstruction, haemorrhage, diarrhea
2 clinical of cardiac amyloidosis
1- arrhythmia
2- heart failure
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 )
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)
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
