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Pathology>>>>>>

Post by mandible on Sat Feb 12, 2011 9:54 pm

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Re: Pathology>>>>>>

Post by mandible on Sat Feb 12, 2011 10:04 pm

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Re: Pathology>>>>>>

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PATHOLOGY AND IMMUNOLOGY MCQS 85 STEM

Post by mandible on Sat Feb 12, 2011 10:40 pm





27 √ Metastatic calcification may be seen in the following conditions: 1
F Old pulmonary tuberculosis. A
√ F Degenerationg leiomyomata. B
T Multiple myeloma. C
T Hyperparathyroidism. D
T Sarcoidosis. E
Comment
Metastatic calcification is the deposition of calcium salts in normal tissues and always reflects some derangement in calcium metabolism (hypercalcemia). Hypercalcemia causes by: 1\ increase secretion of parathyroid hormone. 2\ destruction of bone (Paget disease, immobilization, multiple myeloma and leukemia. 3\ vitamin D intoxication and sarcoidosis. 4\ renal failure.
TISSUE CALCIFICATION *****
• DYSTROPHIC - calcium deposition in tissues in the presence of normal plasma calcium and phosphate levels
• Occurs in old infarcts, fat necrosis, site of dead parasites, previous TB granulomas, scarred heart valves
• METASTATIC *- occurs in normal tissues in the presence of hypercalcaemia
• Associated with hyperparathyroidism, hypervitaminosis D, sarciodosis, milk-alkali syndrome, bone metastases associated with malignant disease and multiple myeloma
√ Metastasis to lymph nodes are commonly associated with: 2
F Fibrosarcoma. A
√ T Malignant melanoma. B
F Medullablastoma. C
T Seminoma of the testis. D
F Basal cell carcinoma of the skin. E
Comment 2:
Lymph node metastases are frequent in lymphomas and carcinomas but are less typical of sarcomas. BCC seldom metastasizes, whereas fibrosarcoma would metastasise more commonly to specific organs. Medulloblastoma seldom metastasizes beyond the brain. Seminoma may metastasize first to the para-aortic lymph nodes.
√ Early blood-borne dissemination is characteristic feature of: 3
F Carcinoma of the endometrium. A
T Osteosarcoma. B
F Basal cell carcinoma. C
F Carcinoma of the cervix. D
T Choriocarcinoma. E

A metaplastic process is involved in the histogenesis of the following tumors: 4
F Squamous cell carcinoma of the vulva. A
T Squamous cell carcinoma of the bronchus. B
F Scirrhous carcinoma of the breast. C
T Squamous cell carcinoma of the cervix. D
T Adenocarcinoma of the oesophagus. E
Comment:
METAPLASIA *****
• Reversible change in which one adult cell type is replaced by another adult cell type
• May be an adaptive response, for instance, squamous metaplasia in the respiratory tract in response to chronic irritation
• In smokers, the normal ciliated columnar epithelium is often replaced by focal areas of stratified squamous epithelium
• The influences that cause metaplasia, if persistent, may induce malignant transformation in metaplastic epithelium - thus the commonest form of cancer in the respiratory tract is squamous cell carcinoma *
• In patients with persistent oesophageal reflux, the distal oesophagus may become lined with columnar secretory epithelium instead of stratified squamous epithelium – Barrett’s oesophagus. This may undergo malignant transformation into an adenocarcinoma *
• In the ovary, the coelomic epithelium can undergo metaplasia into serous, mucinous or endometroid types which undergo malignant transformation into serous, mucinous or endometroid adenocarcinomas*
• Metaplasia may also occur in mesenchymal cells, for instance, bone being formed in areas of soft tissue injury
A metaplastic process is involved in the histogenesis of the following tumors: 5
F Squamous cell carcinoma of the vulva. A
T Squamous cell carcinoma of the bronchus. B
F Scirrhous carcinoma of the breast. C
T Squamous cell carcinoma of the cervix. D
F Adenocarcinoma of the ovary. E
Comments 2:
A metaplastic process may be found preceding the development of many overt carcinomas, particularly cervical, carcinoma of the oesophagus and gastric (Barrett's Oesophagus) and bronchial carcinoma.

Comment:
METAPLASIA *****
• Reversible change in which one adult cell type is replaced by another adult cell type
• May be an adaptive response, for instance, squamous metaplasia in the respiratory tract in response to chronic irritation
• In smokers, the normal ciliated columnar epithelium is often replaced by focal areas of stratified squamous epithelium
• The influences that cause metaplasia, if persistent, may induce malignant transformation in metaplastic epithelium - thus the commonest form of cancer in the respiratory tract is squamous cell carcinoma *
• In patients with persistent oesophageal reflux, the distal oesophagus may become lined with columnar secretory epithelium instead of stratified squamous epithelium – Barrett’s oesophagus. This may undergo malignant transformation into an adenocarcinoma *
• In the ovary, the coelomic epithelium can undergo metaplasia into serous, mucinous or endometroid types which undergo malignant transformation into serous, mucinous or endometroid adenocarcinomas*
• Metaplasia may also occur in mesenchymal cells, for instance, bone being formed in areas of soft tissue injury
√ The following agents are correctly paired with the named tumors: 6
F Androgenic steroids: vaginal clear cell adenocarcinoma. A
T Aflatoxins: liver cell carcinoma. B
F β-naphthylamine: bronchial carcinoma. C
√ T Asbestos: peritoneal mesothelioma. D
T Vinyl chloride: hepatic angiosarcoma. E
Comment
Clear cell carcinoma is associated with synthetic steroid (diethylstilbestrol). β-naphthylamine causes bladder cancer.
CARCINOGENIC CHEMICALS *****
• Include synthetic and natural compounds
• May act directly or require metabolic conversion in vivo to produce the ultimate carcinogen
• Most carcinogens are metabolised by cytochrome P-450 dependent enzymes
1) Direct-acting alkylating agents: used for chemotherapy and treatment of auto-immune disorders. Drugs like cyclophosphamide increase the risk of induced cancer
2) Polycyclic aromatic hydrocarbons - cause a wide range of cancers including skin cancer, sarcomas and organ-specific cancers. The ultimate carcinogen is dihydrodiol epoxide
3) Aromatic amines and Azo dyes - mainly affect the liver where the ultimate carcinogen is formed by P450 dependent enzymes. Beta-naphthylamine is the exception - associated with increased risk of BLADDER cancer in workers in aniline dye and rubber industries *
4) Aflatoxin B1 *- naturally occurring, produced by some strains of Aspergillus flavus which grows in poorly stored grains and peanuts. Causes hepatocellular carcinoma following activation in the liver to produce dihydrodiol epoxide
5) Nitrosamines and amides may be involved in gastric cancer
6) Asbestos - *bronchial carcinoma, mesothelioma and GI cancers
7) Vinyl chloride - 8hemangiosarcoma of the liver

Cool Inhaled chromium and nickel - lung cancer
9) Arsenic - skin cancer
Growth of the following tumors is hormone dependent: 7
F Squamous cell carcinoma of the cervix. A
T Breast adenocarcinoma. B
T Uterine leiomyoma. C
T Prostatic adenocarcinoma. D
F Testicular carcinoma. E
Comment:
HORMONE-DEPENDENT TUMOURS *****
• Endometrial adenocarcinoma - oestrogen
• Breast cancer - oestrogens and progestogens
• Prostate cancer - androgens
• Some melanomas - oestrogen
• Fibroids - oestrogen
Uterine fibroids: 8
T Are defined histologically as fibromyxomas. A
T Arise from endometrial stroma. B
T May be associated with polycythaemia. C
F Predispose to endometrial hyperplasia. D
F Are liable to sarcomatous change in about 5% of cases. E
Comment
Sarcomatous change in 0.2%. may be associated with polycythaemia , iron deficiency anaemia is more common as a result of menorrhagia. Not pre-malignant.
UTERINE LEIOMYOMAS (FIBROIDS) *****
• Benign tumours of the uterine smooth muscle
• Not encapsulated but the compressed surrounding myometrium may give a capsulated appearance
• May be sessile or pedunculated
• May be sub-serosal (sub-peritoneal), intramural or sub-mucosal (immediately beneath the endometrium)
• Sub-serosal fibroids may become attached to the omentum or pelvic peritoneum, forming parasitic leiomyomas
• Present with an irregularly enlarged uterus and are a recognised cause of menorrhagia. Other symptoms include abdominal discomfort, frequency of micturiction, dysmenorrhoea
• Histologically consist of bundles of smooth muscle fibres with varying degrees of fibrous connective tissue *
• Oestrogen sensitive. Atrophy after the menopause and increase in size during pregnancy and may obstruct labour
• May undergo calcification, hyaline degeneration, torsion, & infarction. Red degeneration typically occurs in association with pregnancy
• Not pre-malignant *
• May be associated with polycythaemia *although iron deficiency anaemia is more common as a result of menorrhagia
√ The following pairs indicate correct pathological association: 9
T Epstein-Barr virus: Burkett's lymphoma. A
T Peutiz-Jeghers syndrome: intestinal carcinoma. B
F Wood dust: pleural mesothelioma. C
F Progestagens: endometrial carcinoma. D
T Aniline dyes: bladder carcinoma. E
Comment
Wood dust causes nasal sinuses
The following tumors produce characteristic blood markers: 10
F Clear cell carcinoma. A
T Choriocarcinoma. B
F Osteogenic sarcoma. C
T Yolk sac tumor. D
F Transitional cell tumor. E
Comment:
TUMOUR MARKERS *****
Hormones
• Human chorionic gonadotrophin - trophoblastic tumours, non-seminomatous testicular tumours *
• Calcitonin - medullary carcinoma of the thyroid
• Catecholamines and metabolites - phaeochromocytoma
Onco-fetal antigens
• Alpha-fetoprotein - hepatocellular carcinoma, non-seminomatous germ cell tumours of testis, ovarian endodermal sinus / yolk sac tumour *
• Carcino-embryonic antigen - carcinoma of the colon, pancreas, lung, stomach, breast
Enzymes
• Prostatic acid phosphatase - prostatic carcinoma.
• Neuron-specific enolase - small cell carcinoma of the lung, neuroblastoma
Specific proteins
• Immunoglobulins - multiple myeloma
• Prostate specific antigen - prostate cancer
Glycoproteins
• CA-125 - ovarian cancer *
√ Concerning the adrenal gland: 11
F The cortex is derived from neural crest cells. A
F The zona fasciculate secretes aldosterone. B
T Cortical adenomas may cause Cushing syndrome. C
T Neuroblastomas arise in the medulla. D
T Addison's disease may result from autoimmune destruction of the cortex. E

√ In tumors of bone: 12
√ F Primary malignancy is more common than secondary malignancy. A
F Osteoma rarely present in skull bones. B
T Osteosarcoma is associated with paget's disease of bone. C
T Lymph node metastases are unusual. D
T Simple bone cysts have a strong tendency to recur. E
Comment
The commonest tumor in bone is secondary carcinoma. The commonest sites are the proximal bones: the skull, spine, pelvis and the proximal ends of humerus and femur.
TUMOURS *****
• The commonest malignant tumour in bone is a secondary deposit *
• In adults, malignant primary bone tumours are more common than benign tumours. Osteosarcoma is commonest, followed by chondrosarcoma and Ewing's tumour. The peak incidence of osteosarcoma is the second decade*
• In the first decade of life, only 15-20% of primary bone tumours are malignant
• Patients with retinoblastoma have a 500 fold increased risk of osteosarcoma. Risk also increased in Paget's disease of bone. *
• All osteosarcomas are aggressive tumours and metastasise rapidly via the bloodstream to the lungs. Lymph node involvement is unusual *
• Osteomas are sessile tumours composed of sclerotic, well-formed bone projecting out from cortical surfaces, most often of skull and facial bones. Often protrude into one of the air sinuses *. Only need to be excised if they cause obstruction or pose a cosmetic problem.
The following are premalignant conditions: 13
F Diverticular disease of the large bowel. A
T Ulcerative colitis. B
T Pulmonary asbestosis. C
T Paget's disease of the bone. D
F Condylomata lata of the vulva. E
Comment
HPV, HSV infections, vulvar dysplasia, low socioeconomic class and history of vulvar dystrophies are associated with increased incidence of vulvar carcinoma. Vulvar condylomas are not precancerous.
Pre-neoplastic conditions
• Neurofibromatosis - autosomal dominant, gliomas of the brain and optic nerve, acoustic neuromas, meningioma, phaeochromocytoma

• Tuberous sclerosis - autosomal dominant, glial tumours, harmatomas
• Xeroderma pigmentosa -autosomal recessive, basal and squamous cell carcinoma of the skin, malignant melanoma
• Fanconi’s anaemia - autosomal recessive, acute leukaemias
• Ataxia telangiectasia - autosomal recessive, acute leukaemia, lymphoma and breast cancer in females
ACQUIRED PRE-NEOPLASTIC CONDITIONS ****
• Endometrial hyperplasia, especially atypical hyperplasia
• Cervical intra-epithelial neoplasia *
• Vulval intra-epithelial neoplasia
• Bronchial squamous metaplasia
• Pulmonary asbestosis *
• Cirrhosis of the liver *
• Chronic atrophic gastritis
• Chronic ulcerative colitis *
• Solar keratosis of the skin
• Leukoplakia of the oral cavity, penis and vulva
• Paget's disease of bone
• Pulmonary asbestosis
Adenocarcinoma of the large bowel: 14
√ T Most common originates in the ascending colon. A
T May develop as a single polyp. B
T May show signet ring features histologically. C
F Characteristically metastasis to the liver before the lymph nodes. D
T Is a recognized complication of long-standing ulcerative colitis. E
Comment:
MALIGNANT COLONIC TUMOURS *****
• 60-70% located in the rectum and sigmoid colon. However, the incidence of carcinoma of the right colon is increasing *
• Over 95% are adenocarcinomas *
• May arise from a single polyp of from multiple polyps in patients with familial polyposis coli *
• Associated with dietary factors such as low vegetable fibre, high fat and high refined carbohydrate content. Oestrogen and NSAIDs may be protective
• Peak incidence in the 7th decade. Male : female = 2 : 1
• May be fungating, ulcerating or infiltrating. Right sided tumours tend to be fungating but because of the wide diameter of the caecum, rarely cause obstruction while left sided tumours tend to be infiltrating and cause annular constriction of the bowel
• Spread is to regional lymph nodes. Haematogenous spread to liver, lungs and brain is late *
• Associated with increased levels of CEA (Carcino-embryonic antigen) in 19-40% of patients. Mucinous carcinomas produce mucin which may accumulate within the cells, pushing the nucleus to one side and giving the cell a signet ring appearance *
May be the primary in a woman with a Kruken
The following statements relate to embryonic tumors: 15
F An ovarian teratoma is usually malignant. A
F A nephroblastoma may be benign. B
T A neuroblastoma can arise in the adrenal medulla. C
F A hamartoma is usually malignant. D
T Choriocarcinoma may arise in a teratoma. E
Comment:
GERM CELL TUMOURS
• 15-20% of all primary ovarian tumours
• May be benign (mature terratomas, gonadoblastoma) or malignant
TERRATOMAS
• Result from the differentiation of germ cell tumours into embryonic tissue
MATURE TERRATOMA - DERMOID CYST *****
• Tissues are microscopically similar to those seen in adult tissue
• Benign
• Most are cystic. The mature cystic terratoma or dermoid cyst accounts for 15-20% of all ovarian neoplasms
• Large thick walled cyst with hair and sebaceous material. Typically lined by stratified squamous epithelium. May contain teeth, cartilage, thyroid tissue or respiratory epithelium
• Malignant change supervenes in 1% of dermoid cysts and is usually a squamous cell carcinoma
IMMATURE TERRATOMA *****
• Make up ~5% of all terratomas. Contain immature tissue of either ectodermal, mesodermal or endodermal origin with immature neural tissue being the most common
• Only germ cell tumour for which histological grade is of prognostic significance
• Contra-lateral ovary contains mature terratoma in 10-15% of cases
OVARIAN CHORIOCARCINOMA *****
• Usually a secondary from a uterine tumour
• Primary ovarian choriocarcinoma is rare and develops from germ cells
• Solid tumours, typically unilateral with cytotrophoblasts and syncytiotrophoblasts on histological examination. Produce HCG
HAMARTOMAS
• Local malformations in which normal cells are present in abnormal proportions - such as moles.
• Usually present from birth and growth is not progressive
• Neither malignant nor pre-malignant.
√ The following tumors are correctly paired with likely causative agents: 16
F Angiocarcinoma of the liver: vinyl chloride. A
F Carcinoma of the colon: dietary fiber. B
T Hepatoma: aflatoxins. C
F Carcinoma of the bronchus: coal dust. D
T Carcinoma of the bladder: beta naphthylamine. E
Comment:
CARCINOGENIC CHEMICALS *****
• Include synthetic and natural compounds
• May act directly or require metabolic conversion in vivo to produce the ultimate carcinogen
• Most carcinogens are metabolised by cytochrome P-450 dependent enzymes
1) Direct-acting alkylating agents: used for chemotherapy and treatment of auto-immune disorders. Drugs like cyclophosphamide increase the risk of induced cancer
2) Polycyclic aromatic hydrocarbons - cause a wide range of cancers including skin cancer, sarcomas and organ-specific cancers. The ultimate carcinogen is dihydrodiol epoxide
3) Aromatic amines and Azo dyes - mainly affect the liver where the ultimate carcinogen is formed by P450 dependent enzymes. Beta-naphthylamine is the exception - associated with increased risk of BLADDER cancer in workers in aniline dye and rubber industries *
4) Aflatoxin B1 *- naturally occurring, produced by some strains of Aspergillus flavus which grows in poorly stored grains and peanuts. Causes hepatocellular carcinoma following activation in the liver to produce dihydrodiol epoxide
5) Nitrosamines and amides may be involved in gastric cancer
6) Asbestos - *bronchial carcinoma, mesothelioma and GI cancers
7) Vinyl chloride - hemangiosarcoma of the liver
Cool Inhaled chromium and nickel - lung cancer
9) Arsenic - skin cancer
Adenocarcinoma is the commonest type of primary malignant tumor to occur in the: 17
F Bladder. A
F Lung. B
T Oesophagus. C
T Fallopian tube. D
F Testis. E

Carcinoma in situ in epithelium (intraepithelial neoplasia) is characterized by: 18
T Increased mitotic activity. A
T Loss of polarity. B
F Increased adhesiveness to the underling stroma. C
T Pyknosis. D
T Increased thickness of the epithelium. E
Comment:
CERVICAL INTRA-EPITHELIAL NEOPLASIA ****
• Histological diagnosis made following cervical biopsy. The abnormality originates at the squamo-columnar junction
• Pre-malignant although CIN I and probably CIN II regresses spontaneously
• Associated with HPV 16, 18, 31, 33 *
• Atypical cells are characterised by:
1) Loss of cell polarity
2) Loss of maturation
3) Increased nuclear : cytoplasmic ratio with nuclear and cytoplasmic pleomorphism
4) Increased number of mitotic figures and the presence of abnormal mitotic figures
• CIN I - dysplastic cells are confined to the lower third of the epithelium
• CIN II - dysplastic cells are confined to the lower two thirds of the epithelium
• CIN III - the entire thickness of the epithelium is involved
√ The parathyroid glands: 19
F Originate from the pharyngeal cleft ectoderm. A
T Secrete parathyroid hormone via the chief cells. B
F Secrete calcitonin via the oxyphil cells. C
T May become hyperplastic in the presence of intestinal malabsorption. D
T May develop adenomas in association with islet cell tumours of the pancreas. E

√ The following conditions may lead to hydronephrosis: 20
F Mercury poisoning. A
T Cervical carcinoma. B
T Renal calculi. C
F Renal vein thrombosis. D
T Posterior urethral valves. E

Acquired diverticular disease of the colon: 21
T Is present in at least 15% of Caucasians over the age of 50 years. A
T Is due to a congenital abnormality of the bowel wall. B
T Is associated with increased intra-luminal pressure. C
F Is associated with muscular thickening. D
T May result in intestinal obstruction. E
Comment:
DIVERTICULAR DISEASE *****
• Saccular out-pouchings of the colon that develop in the recto-sigmoid with advancing age. Herniations of the mucosa and sub-mucosa at points of muscular weakness *
• Asymptomatic in the majority of cases
• Commoner in developed countries. Rare in those < 30 years old. Present in over 50% of those aged over 60 years *
• Arises as a result of increased intra-luminal pressure (constipation, low fibre diet) and foci of muscular weakness in the colonic wall *
• 95% located in the sigmoid colon. There is hypertrophy of the musculature*of the affected segment and the taeniae coli are more prominient with 0.5-1cm flask-like out-pouchings at their margins. The walls of the diverticula are composed of flattened mucosa, compressed sub-mucosa and thin or absent muscularis.
• Complications include acute inflammation, abscess formation, fistulas and strictures with obstruction following recurrent inflammation
• Not pre-malignant
Obstruction of the lower end of the common bile duct is suggested by: 22
T An elevated serum conjugated bilirubin concertration. A
F A reduced serum alkaline phosphatase concentration. B
T The presence of urobilinogen in the urine. C
√ T Increased conjugated bilirubin in the urine. D
√ T A reduced serum cholesterol concentration. E

Apoptosis: 23
F Causes necrotic cell death. A
T Is involved in embryonic remodeling. B
F Releases pro-inflammatory mediators. C
T Is characterized by condensation of nuclear chromatin. D
T Is associated with endonuclease activity. E
Comment:
APOPTOSIS *****
• Programmed cell death *
• Affects single cells surrounded by unaffected viable cells
• Characterised with shrinkage of cell volume and chromatin condensation
• Energy dependent process *
• Endonucleases *are activated and break down chromatin. Cytosolic proteins are cross-linked, converting the cell into a shrunken shell with intense basophilic staining
• Apoptotic cells are phagocytosed by macrophages, forming apoptotic bodies -secondary lysosomes containing cellular debris
• Not associated with inflammation *
• Occurs during organogenesis - mechanism by which fingers / toes are separated *
• May be pathological and occur in irradiated or atrophic tissue and following exposure to cytotoxic T cells.
• May be prominent in malignant tissue.
Neutrophil polymorphs at the site of inflammation are capable of the following: 24
T Phagocytes. A
T Production of oxygen free radicals. B
F Replication. C
F Fusion to form giant cells. D
F Antibody production. E

Chemical mediators concerned in the production of an inflammatory response include: 25
T 5-hydroxytryptamine. A
F Aldosterone. B
F Glucocorticoids. C
T Bradykinin. D
T Leukotrienes. E
Comment:
The chemical mediators of acute inflammation include *****
• Vaso-active amines - histamine and serotonine
• Plasma proteases - kinin system (bradykinin & kallikrein), complement system
• Coagulation -fibrinolytic system
• Arachidonic acid metabolites - prostaglandins and leukotrienes
• Lysosomal components
• Cytokines
• Growth factors such as EGF, FGF
• Platelet activating factor
• Oxygen free radicals
Granulomatous inflammation occurs in: 26
F Lobar pneumonia. A
T Pulmonary tuberculosis. B
T Sarcoidosis. C
F Staphylococcal. D
F Temporal arteritis. E
Comment:
• Granulomatous inflammation occurs in: *
1) TB and leprosy
2) Syphilis - gumma
3) Cat scratch disease
4) Schistosomiasis
5) Cryptococcus and coccidiodes infections
6) Sarcoidosis
7) Silicosis and berylliosis
Granulation tissue contains the following: 27
F Elastin fibres. A
T Inflammatory cells. B
T Capillaries. C
√ F Epithelioid cells. D
T Fibroblasts. E
Comment:
• Granulation tissue formation: * Granulation tissue consists of inflammatory cells, fibroblasts and new vasculature in a hydrated matrix of glycoproteins, collagen and glycosaminoglycans. Its formation begins within 3-5 days after wounding and overlaps with the preceding inflammatory phase. Wound contraction and neovascularisation occur at this stage. Contraction is maximal between 5 and 15 days after wounding and is mediated to a great extent by the myofibroblast and its specialized connections with the surrounding extracellular matrix
The following cells may be phagocytic: 28
T Neutrophils. A
T Kupffer cells. B
T Monocyte cells. C
T Hofbauer cells. D
F Plasma cells. E

White cell migration from blood vessels in areas of inflammation involves: 29
T Cell migration occurring between endothelial cells. A
T A passive loss of fluid blood elements. B
F Cell migration independent of endothelial cell motion. C
T Initial emigration of polymorphonuclear neutrophils. D
F More polymorphs than monocytes after 2 days. E

In acute tubular necrosis of the kidney: 30
T The lesion is reversible. A
F The kidney is small. B
T 25% of deaths occur in the diuretic phase. C
F The distal convoluted tubules are mainly affected in mercury poisoning. D
T Proteinaceous casts are found in the collecting ducts. E
Comment:
ACUTE TUBULAR NECROSIS (ATN) *****
• Major cause of acute reversible renal failure
• Associated with destruction of tubular epithelial cells
• Two types:
1) Ischaemic or tubulorrhectic - associated with hypotension, severe renal hypoperfusion and ischaemia: ante / post-partum haemorrhage or septic shock. Pigmented ATN is a form of ischaemic ATN associated with massive haemoglobinuria or myoglobinuria *
2) Nephrotoxic - toxic agents that direct damage the tubes including gentamicin, cephalosporins, contrast media, cyclosporine; lead, mercury and arsenic poisoning, organic solvents like carbon tetrachloride, methyl alcohol, ethylene glycol and other poisons like mushrooms, insecticides and herbicides. Injury is most obvious in the proximal convoluted tubule *
• There is focal tubular necrosis at multiple points with skip areas in between and tubular occlusion with casts
• The straight portion of the proximal tubule and the thick ascending limb of the loop of Henle are most commonly affected
• Eosinophilic hyaline casts and pigmented granular casts are common and contain Tamm-Horsfall protein* (a specific glycoprotein normally secreted by tubular epithelial cells), haemoglobin, myoglobin and other plasma proteins. There is usually evidence of epithelial regeneration
• The disorder progresses through initiation, maintenance and recovery phases.
• Initiation phase is dominated by the underlying injury
• Maintenance phase characterised by sustained oliguria, salt and water retention, electrolyte imbalance and increased serum urea and creatinine
• Recovery phase - increased urine out-put with eventual polyuria and loss of fluid and salt. Risk of hypokalaemia. There is increased vulnerability to infection
• Up to 50% of patients with ATN may not have oliguria and may have increased urine out-put.
The development of tissue necrosis: 31
F Can be identified by light microscopy within 1 hour of myocardial infarction. A
T Is recognized by the presence of karyorrhexis. B
F Is of colliguative type in the kidney. C
T Occurs in tertiary syphilis. D
T Is associated with rupture of lysosomes. E
Comment:
NECROSIS *****
• Death of cells or tissues which are still part of living organisms
• Caused by anoxia = infarction
• May be caused by infection, extremes of temperature, chemicals
• Rapid freezing and the use of cryoprotectants prevents the formation of ice crystals in tissues, minimising cellular damage and preventing necrosis
• Microscopically characterised by cytoplasmic eosinophilia. Some nuclei undergo dissolution (karyolysis), break-up into distinct fragments (karyorrhexis) or shrink and appear as densely staining masses (pyknosis) *
• There is vacoulisation of the mitochondria, swelling of lysosomes and development of amorhous densities in the mitochondrial matrix. These changes are visible in the myocardium as early as 30-60min after ischaemia
• However, unmistakable light microscopic changes characteristic of cell death do not occur in the myocardium until 10-12h after total ischaemia *
• Using routine staining, coagulative necrosis is not detectable in the myocardium for the first 4-8h *
• The lysosomes eventually rupture and their enzymes leak into the cytoplasm*
• Coagulative necrosis - thromboplastin deposition results in dead tissue becoming swollen and firm with bright eosinophylic staining - occurs typically in the heart / kidneys/stromal malignancies *
• Colliquative necrosis - associated with autolysis with eventual cyst formation - typically occurs in the brain *
• Necrosis associated with bacterial infection and polymorphonuclear cell infiltration forms an abscess
• Caseation - typically occurs in TB infection *
• Necrosis + bacterial infection = gangrene: colliquative necrosis forms wet gangrene while coagulative necrosis forms dry gangrene
• Fat necrosis occurs in breast tissue after trauma. Also occurs in pancreatitis due to release of lipase into the abdomen
Wound healing is delayed by: 32
F Insulin. A
√ F Ultraviolet light. B
T Zinc deficiency. C
T Low temperature. D
T Glucocorticosteroids. E
Comment:
Wound healing is impaired by: *****
• Local factors:
• Infection
• Surgical technique - crushing of tissue with blunt instruments impairs healing. Excessive tension at wound edges impairs healing
• Ischaemia - foreign bodies, infection or strangulating tissue
• Haematoma
• Foreign body reaction - wounds with foreign bodies are characterised by low pH and low pO2 and these impair healing
• Topical medications and dressings - Occlusive or semi-occlusive dressings promote faster re-epithelization. They may also alter certain aspects of dermal repair. They also provide the moist environment needed for optimal wound repair, they may also help to prevent bacterial invasion and wound infection
• Low temperature: *The relatively low tissue temperature in the distal aspects of the upper and lower extremities (a reduction of 1-1.5C [2-3F] from normal core body temperature) is responsible for slower healing of wounds at these sites
• Systemic factors
• Metabolism*: Abnormal carbohydrate and fat metabolism slows wound repair. Glucose may be unavailable or fail to enter cell properly. Insulin deficiency leads to suppress collagen deposition in the wound
• Protein deficiency may occur after major trauma or during sepsis. Fibroplasia and matrix formation are delayed, wound remodelling is impaired. Protein deficiency may lead to an increased risk of infection
• Vitamins: Vitamin A deficiency associated with slowed re-epithelization, decreased collagen synthesis and stability and an increased risk of infection.
• Vitamin C (Ascorbic acid) is an essential cofactor during collagen biosynthesis. In scurvy, the collagen formed is unhydroxylated, relatively unstable - wound healing is poor
• Vitamin K deficiency results in a deficiency in the production of vitamin K dependent clotting factors - bleeding diathesis, hematoma formation and poor wound healing
• Trace elements and minerals - Required as cofactors for various enzymes during wound healing.
• Zinc deficiency* important clinically, as it is a constituent of multiple important metalloenzymes including collagenase and DNA and RNA polymerases. Its deficiency results in impaired immune responses, decreased protein and collagen synthesis, decreased lysyl oxidase activity and interfere with vitamin A transport
• Wound healing impaired in the elderly. Mechanism behind lack of scarring in fetal wounds unknown
• Systemic conditions
Hereditary

Ehlers-Danlos syndrome
Coagulation disorders
Hemophilia, Von Willebrand’s disease, Factor XIII deficiency
Vascular disorders
Congestive heart failure, Atherosclerosis, Vasculitis
Venous stasis
Lymphoedema
Metabolic
Chronic renal failure
Diabetes mellitus
Malnutrition
Cushing’s syndrome
Hyperthyroidism
Others
Chronic pulmonary disease
Chronic liver disease (cirrhosis)
Malignancy
Myelofibrosis and other chronic hematologic disorders associated with thrombocytopenia
Drugs *****
Glucocorticoids
Anticoagulants
Antineoplastic drugs
Cyclosporin A
Colchicine
Penicillamine
** Ultraviolet light improves wound healing *
In healing by primary intention, the following events occur: 33
F Formation of fibrin-free haematoma. A
T An acute inflammatory reaction. B
F Migration of epithelial cells within 6 hours. C
T Phagocytosis. D
T Invasion by capillary buds within three days. E
Comment:
HEALING BY PRIMARY INTENTION *****
• Wound associated with minimal loss of tissue and is without significant bacterial contamination
• The incision space is immediately filled with blood clot containing fibrin and blood cells *
• Dehydration of the clot forms a scab that seals the wound from the environment.
• Vascular and inflammatory phase:* An initial 5-10 minutes period of vasoconstriction is followed by more persistent vasodilatation. Within 24h: neutrophils appear at the margins of the incision. Their prime function is the phagocytosis and killing of contaminant bacteria. By day 3, neutrophils have largely been replaced by macrophages. They become activated and release proteases and vasoactive peptides as well as growth and chemotactic factors for fibroblasts and endothelial cells.
• Re-epithelisation: *Within 24-48h, spurs of epithelial cells from the edges grow along the cut margins of the dermis and beneath the surface of the scab to fuse in the mid-line forming a continuous thin epithelial layer. Proliferation is maximal at 48 to 72 hours after wounding and is reflected by a 17 fold increase in mitosis and epithelial hyperplasia at the wound edges
• Granulation tissue formation: * Granulation tissue consists of inflammatory cells, fibroblasts and new vasculature in a hydrated matrix of glycoproteins, collagen and glycosaminoglycans. Its formation begins within 3-5 days after wounding and overlaps with the preceding inflammatory phase. Wound contraction and neovascularisation occur at this stage. Contraction is maximal between 5 and 15 days after wounding and is mediated to a great extent by the myofibroblast and its specialized connections with the surrounding extracellular matrix
• Fibroplasia and matrix formation: * Collagen deposition begins by day 3 but is initially vertically oriented and do not bridge the wound. By day 5, collagen fibres are more abundant and begin to bridge the incision. Fibroblasts and epithelial cells proliferate and by day 5, the epidermis recovers its normal thickness with surface keratinisation
• Matrix and collagen remodelling: * During the second week, there is continuous accumulation of collagen and proliferation of fibroblasts and there is regression of vascular channels with blanching. Type I collagen becomes the major collagen present in the remodelled scar, reversing the earlier type III collagen predominance. The process of remodelling may continue for up to a year and maximal tensile strength is regained.
Collagen: 34
F Has a double helical structure. A
T Shows a regular banding pattern on electron microscopy. B
T Is not formed normally in the absence of ascorbic acid. C
F Is not found within basement membranes. D
T Synthesis is inhibited by glucocorticoids. E
Comment
Trihelical structure.
Concerning cells: 35
√ F Glycosylation takes place in the smooth endoplasmic reticulum. A
T Low density Lipoproteins attach to cell membrane receptors. B
F Glycoproteins are present on the cytosol surface of the plasma membrane. C
T Centrioles are composed of tubulin. D
T Nuclear heterochromatin is genetically inactive. E

√ The following tissues are capable of cellular regeneration: 36
F Spinal cord. A
T Liver. B
T Epidermis. C
F Myocardium. D
T Bone marrow. E
Comment 2:
Skin and bone marrow are particularly active in cellular turnover and capable of regeneration. The liver is also capable of regeneration as is often seen in cirrhosis with regenerating nodules amongst the cirrhotic tissue. Myocardium nor spinal cord do not regenerate.
The following provide conclusive evidence of pregnancy in uterine curettings: 37
F Decidua compacta. A
F Arias-stella changes in endometrial glands. B
F Spiral arterioles. C
F Plasma cell infiltration. D
T Chorionic villi. E
Comment:
THE ARIAS-STELLA REACTION *****
• Secondary to a direct effect of progesterone on the endometrium *
• Endometrial epithelial cells become increasingly vacuolated and thrown into pseudo-papillary folds giving a hyper-secretory impression
• There is evidence of decidualisation around spiral arteries and under the surface of the epithelium
• Complete decidualisation is however, not evident until pregnancy is well established
• The cell nuclei are pleomorphic and there is glandular hyperplasia, intra-nuclear cytoplasmic invaginations which may resemble viral inclusions
• The Arias-Stella occurs in normal intra-uterine pregnancy, ectopic pregnancy, progestogen therapy and can also occur in the endocervix *
• The presence of chorionic villi on endometrial currettings provide conclusive evidence of an intra-uterine pregnancy *
In anaphylactic shock in humans: 38
T IGE is a mediator. A
T There is degranulation of mast cells. B
F Complement is required. C
T Histamine release occurs. D
F The principle response is in the gastrointestinal tract. E
Comments 2:
Anaphylaxis is a type I hypersensitivity reaction and occurs within minutes or hours. As well as bronchoconstriction, vasodilatation and circulatory collapse with pharyngeal swelling with possible airway obstruction, anaphylaxis may be associated with urticaria and pruritis.
Comment:
IMMEDIATE (TYPE I) HYPERSENSITIVITY *****
• Rapid IgE and mast cell dependent vascular and smooth muscle reaction that is usually followed by an inflammatory reaction in an individual who has been previously exposed to an antigen (sensitized) *
• Antigen binds to IgE on mast cells, cross-linking receptors and inducing mast cell degranulation *
• Released mast cell granules contain histamine, heparin, neutral proteases and cytokines typical of TH2 responses - IL-3 and IL-4 *
• Cyclo-oxygenase and lipoxygenase are also activated with the production of vasodilator prostaglandins, leukotrienes and thromboxanes *
• In the skin is characterized by a wheal and flare reaction *
• The result is increased capillary permeability, smooth muscle contraction and this manifests as wheezing, oedema, hypotension - this is the acute phase and occurs within minutes *
• The latent phase peaks after 3-5 hours and is caused by cytokine mediated inflammatory infiltration by neutrophils and eosinophils - this is responsible for tissue damage that occurs after repeated episodes of immediate hypersensitivity *
• Typical disease processes include asthma, hay fever, drug and insect bite induced anaphylaxis, penicillin allergy, food allergy, atopic dermatitis *

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PATHOLOGY AND IMMUNOLOGY

Post by mandible on Sat Feb 12, 2011 10:41 pm

Amyloid: 39
F Is predominantly intracellular. A
T Contains fibrils. B
F Is enzymatic. C
T Can be found in nerve tissue. D
T Deposits occur with chronic sepsis. E
Comment:
AMYLOIDOSIS *****
• Process characterised by extracellular* tissue deposits of amyloid in one or many organs
Amyloid is characterised by
• Homogenous pink extracellular material on H & E staining
• Orange colour by light microscopy and green birefringence by polarising microscopy in sections stained with Congo red
• Fine non-branching 7.5 - 10nm on electron microscopy
• Beta-pleated sheet *structure of fibrils by x-ray diffraction

Amyloid deposition may be either a primary (idiopathic) or secondary to some other condition and may be localized to one specific site or generalized throughout the body (systemic)
• Primary amyloidosis tends to involve mesodermal tissues, most frequently affecting peripheral nerves, skin, tongue, joints, heart, and liver while secondary amyloidosis mainly affects parenchymatous organs, such as spleen, kidneys, liver, and adrenals.
• Systemic forms of amyloid are derived from circulating protein precursors by conversion from soluble into insoluble (fibrillar) form.

Classification

• Based upon the tissue distribution (local or systemic), the absence or presence of preexisting disease (primary or secondary), and the chemical type of amyloid protein fibril.

Classification
Disease association


Amyloid precursor






Systemic amyloidosis















Primary / secondary





Multiple myeloma*





Immunoglobulin lambda / kappa chain






Secondary





Chronic inflammation*
TB, rheumatoid, lung abscess, chronic pyelonephritis, chronic osteomyelitis





Non-immunoglobulin amyloid associated protein






Secondary





Hodgkin's disease





Non-immunoglobulin amyloid associated protein






Secondary





Chronic renal failure / dialysis





Beta-2-microglobulin







Localised amyloidosis


























Medullary carcinoma of thyroid*





Calcitonin














Senile cardiac amyloidosis





Transthyretin














Senile cerebral amyloidosis, Alzheimer’s disease*





Amyloid precursor protein


• Amyloidosis Related to Monoclonal Ig Light Chains - usually lambda chain produced by abnormal clones of Ig-secreting plasma cells (B cells) *
• Amyloidosis occurs in about 5-10% of patients who have pre-existing or coexisting multiple myeloma. *
• Amyloidosis associated with Inflammatory or Infectious Diseases *- deposits have a systemic distribution and contain AA (amyloid-associated) fibrils which are related to the nonimmunoglobulin AA protein and its serum protein precursor (SAA), an acute phase reactant synthesized by hepatic cells. Associated with rheumatoid arthritis (5-10% of rheumatoid patients) and also dermatomyositis, scleroderma, Crohn’s disease, ulcerative colitis, chronic pyelonephritis, chronic osteomyelitis
• Reactive-type amyloidosis may also occur in association with cancer, such as Hodgkin's disease and renal cell carcinoma.
• Endocrine-related - *Localized amyloid deposits are associated with hormones produced by certain endocrine tumours and endocrine glands, such as medullary carcinoma of the thyroid gland (procalcitonin), islet cell tumors of the pancreas, and the islets of Langerhans (islet associated polypeptide, IAPP) in patients with type II diabetes mellitus.
• Age-related. Amyloid deposits of transthyretin occur in the heart of elderly patients with senile cardiac amyloidosis.
• Beta amyloid protein is deposited in the cerebral blood vessels and plaques of patients with senile cerebral amyloidosis and Alzheimer's disease *
• Organs extensively infiltrated by amyloid are enlarged and have a pale, waxy appearance and tough consistency.
• The iodine test for amyloid is done by applying iodine solution to the washed cut surface of the organ: amyloid typically stains mahogany-brown, and this changes to blue ( a "starch-like" reaction) after the application of dilute sulphuric acid.

SYMPTOMS & SIGNS
• Nonspecific, determined by organ or system affected, and often obscured by the underlying disease.
• Nephrotic syndrome is the most striking early manifestation with anasarca, hypoproteinemia, and massive proteinuria.
• Hepatic amyloidosis - hepatomegaly but rarely jaundice. Liver function test usually normal
• Cardiac amyloidosis - cardiomegaly, intractable heart failure, or any common arrhythmia.
• GI amyloid - oesophageal motility abnormalities, gastric atony, motility abnormalities of the small and large intestine, malabsorption, bleeding, or pseudo-obstruction. Macroglossia is common in primary and myeloma-related amyloidoses.
• A firm, symmetric, nontender goiter resembling Hashimoto's or Riedel's struma may result from amyloidosis of the thyroid gland.
TREATMENT

• Treat underlying condition
Amyloid deposition is part of the pathological process in the following diseases: 40
√ F Medullary carcinoma of the thyroid. A
T Plasmacytoma. B
√ F Diabetes mellitus. C
T Chronic pyelonephritis. D
F Bronchial asthma. E

In tissue pigmentation, the following are associated: 41
F Kernicterus and conjugated bilirubin. A
T Addison's disease and increased cutaneous melanin. B
F Melanosis coli and bile pigments. C
T Wilson's disease and copper deposition in the cornea. D
T Corpusluteum and carotenoids. E

In sarcoidosis: 42
F Lesions are confined to the lung. A
F The Mantoux test is strongly positive. B
T Caseation is not present. C
T The lesions contain giant cells. D
F The Kveim test is a useful adjunct to diagnosis. E
Comment:
SARCOIDOSIS *****
• Multi-system granulomatous disorder *
• Affects young adults (peak incidence 30-40years) and presents with bilateral hilar lymphadenopathy, pulmonary infiltration, skin and eye lesions
• Wide-spread non-caseating granulomas with epitheloid cells *
• Differential diagnosis is berylliosis
• Common in USA and more severe in Blacks than Whites
• There is depressed cell-mediated reactivity to tuberculin - negative in 80% of patients
• Lymphopaenia is present - T-lymphocytes low, B-lymphocytes normal
• Commonest cause of erythema nodosum
• Eyes - anterior uveitis and kerrato-conjunctivitis sicca
• Hypercalcaemia in 10% due to increased circulating 1, 25 dihydroxyD3. Increased risk of calculi
• CNS involvement rare but may cause severe disease
• Arthralgia, hepato-splenomegaly and cardiac involvement
• Serum levels of angiotensin converting enzyme are elevated
• Raised ESR with normochromic, normocytic anaemia
• The Kveim test is of very limited value and is very rarely used for diagnosis. CT / CXR and biopsy / bronchial lavage are used.
In cystic fibrosis, abnormalities are seen in the: 43
T Pancreas. A
T Salivary glands. B
T Brain. C
F Kidneys. D
T Ileum. E

The following are consequence of pulmonary embolism: 44
T Pulmonary infarction. A
T Fibrinous pleurisy. B
T Right ventricular hypertrophy. C
T Sudden death. D
T Haemoptysis. E
Comment:
PULMONARY EMBOLISM (PE) *****
• An embolus is a detached intravascular solid, liquid or gas which is carried by blood to a site distant from its site of origin
• PE is one of the commonest preventable causes of death in hospital patients, especially following pregnancy or pelvic surgery
• Over 95% of all PE arise from thrombi in large veins of the lower limbs - popliteal, femoral, iliac veins
• Venous thrombosis is only identified in 20-70% of patients with confirmed PE. A patient who survives a PE has a 30% risk of developing another one
• 60-80% of PE are clinically silent
• Obstruction of > 60% of the pulmonary vasculature causes sudden death, acute right heart failure (acute cor pulmonale) or cardiovascular collapse *
• Obstruction of small pulmonary arteries which function as end arteries causes pulmonary infarction
• Obstruction of larger branches which are not end arteries causes pulmonary haemorrhage as the bronchial circulation maintains tissue viability. Patients present with SOB and / or haemoptysis but rarely pleurytic chest pain as the pleura is not involved *
• Multiple emboli lead to pulmonary hypertension with right ventricular hypertrophy *
• Only 10% of PE cause infarction which is typically haemorrhagic. The infracted area is wedge shaped with the apex pointing towards the lung hilum. The pleural surface is covered by a fibrinous exudates *
Features of disseminated intravascular coagulation include: 45
F Thrombocythaemia. A
T Petechiae. B
T Haemorrhage. C
F Reduced circulating fibrin degradation products. D
T Small-vessel thrombosis. E
Comment:
DISSEMINATED INTRA-VASCULAR COAGULATION *****
• Acute, sub-acute or chronic thrombo-haemorrhagic disorder secondary to a variety of diseases
• Coagulation system is activated, leading to the formation of micro-thrombi *
• There is consumption of platelets and clotting factors and secondary activation of fibrinolysis with increased concentration of fibrin degradation products *
• May therefore present with signs / symptoms of tissue ischaemia secondary to thrombi or haemorrhage *
• There is thrombocytopaenia, decreased fibrinogen concentration, increased concentration of fibrin degradation products, evidence of red cell fragmentation on blood film and haemoglobinuria in severe cases. Hyperbilirubinaemia is unconjugated *
• Associated with;
1) Obstetric complications such as placental abruption, pre-eclampsia, amniotic fluid embolism, fetal death in-utero, septic miscarriage
2) Infection - gram negative septicaemia, malaria, meningococcal septicaemia
3) Massive tissue injury including burns and extensive surgery
4) Malignant disease - carcinoma of the pancreas, prostate, lung
The following are adverse effects of blood transfusion: 46
T Hypothermia. A
√ T Haemoglobinuria. B
T Hypocalcaemia. C
F Hypocalaemia. D
F Thrombocytosis. E

The following cause platelet aggregation: 47
T ADP(adenosine diphosphate). A
F Prostacyclin. B
√ F Serotonin. C
F Antithrombin III. D
T Thromboxane A2. E
Comments 2:
Platelets are membrane encapsulated fragments of megakaryoctes. Although platelets have no nucleus, they are metabolically active and are able to express membrane receptors and release stored substances when triggered. However, because they have no nucleus they are unable to produce new proteins and therefore aspirin and other drug effect function for the remainder of the platelet lifespan. Platelet life span is approximately 9-10 days in normal individuals. Platelets are capable of producing Nitric oxide, prostaglandins and thromboxane, but not the vasoconstrictor prostacyclin.
Stored blood which is to be used for transfusion: 48
T Is kept at -4 C. A
F Must be used within 1 week. B
F Is tested for complement content before transfusion. C
F May be used for platelet replacement. D
T Contains an acid anticoagulant. E

Platelets: 49
T Are approximately 50 micrometers in diameter. A
T Contain myosin. B
T Release a growth factor. C
T Are formed from myeloblasts. D
F Are prevented from aggregating by thromboxane A2. E
Comment:
PLATELETS *****
• Attach to sites of endothelial injury, where sub-endothelial elements, particularly fibrillar collagen are exposed. Von Willebrand’s factor is necessary for adhesion *
• Secretion - platelets release the contents of their granules: alpha granules contain fibrinogen, fibronectin, platelet-derived growth factor, anti-heparin and cationic proteins. Dense bodies contain ADP, ionised calcium, histamine, adrenaline and serotonine *
• Aggregation - formation of platelet-platelet inter adherence promoted by the formation of thromboxane A2 which is also a vasoconstrictor. Activated platelets also produce ADP which is a platelet activator. The platelet aggregate forma the primary haemostatic plug. *
• Platelet activation also results in thrombin formation, a powerful platelet agonist and activates the clotting system. A secondary haemostatic plug is formed
In the pathogenesis of thrombosis: 50
F Prostacyclin induces platelet aggregation. A
T Platelets synthesis thromboxane A2. B
T Thromboxane A2 induces vasoconstriction. C
T Contact with subendothelial collagen causes platelet aggregation. D
F Thrombin inhibits platelet aggregation. E
Comment:
THROMBOSIS
Three influences pre-dispose to thrombosis
1) Endothelial injury
2) Alterations in normal blood flow - turbulence or stasis
3) Alterations in the blood - hypercoagulability
• A thrombus is formed by the interaction of the vessel wall; blood cells particularly platelets and clotting factors. A blood clot only involves the clotting system
• Thrombi formed within rapidly moving arterial and cardiac circulations are composed largely of fibrin and platelets and differ from blood clots
• Vascular injury results in a brief period of vasoconstriction which may reduce / stop blood loss in small vessels
• Injury to endothelial cells exposes highly thrombogenic sub-endothelial connective tissue to which platelets adhere and become activated - occurs within minutes: primary haemostasis *
• Tissue factors and platelet factors released at the site of injury activate the clotting system forming fibrin
The following factors present on the normal endothelium prevent thrombus formation:
1) Thrombomodulin - binds thrombin and converts it into an activator of protein C, a plasma protein which is a potent anti-coagulant *
2) Protein S synthesised by the endothelial cells is a cofactor for the anti-coagulant activities of protein C *
3) Heparin-like molecules on endothelial cells accentuate the effects of anti-thrombin III, a plasma protein which binds and inactivated thrombin and other clotting factors such as XII a, XIa, Xa, IXa
4) Conversion of ADP (potent platelet activator) to adenine nucleotide by endothelial cells
5) Production of prostacyclin (PGI2), potent inhibitor of platelet aggregation and a vasodilator *
6) Tissue plasminogen activator - promotes fibrinolytic activity.
Comments 2:
Prostacyclin is thought to have a role in inhibiting platelet aggregation. TBX A2 is synthesized by platelets and its effects are to induce vasoconstriction and procoagulant. Other factors mediating platelet aggregation include contact with the subendothelium, thrombin, fibrin, exposed collagen etc.
Complications of myocardial infarction include: 51
T Fibrous pericarditis. A
F Aortic aneurysm. B
T Ventricular mural thrombi. C
F Coronary atherosclerosis. D
T Ventricular aneurysm. E
Comment:
• Complications of acute MI include: *****
a) Sudden death
b) Arrhythmias
c) Mitral incompetence following infarction +/- rupture of a papillary muscle
d) Fibrinous or fibrinohaemorrhagic pericarditis - develops on day 2-3. May be localised or generalised
e) Mural thrombosis with risk of peripheral embolism
f) Ventricular aneurysm
g) Myocardial rupture causing cardiac tamponade or left-to-right shunt
Osteoporosis is associated with: 52
√ F An increase in uncalcified bone matrix. A
F Prolonged oestrogen therapy. B
T Long term heparin treatment. C
T Bone fractures. D
F Irregularity of epiphyseal plates. E
Comment:
OSTEOPOROSIS *****
• Reduction in bone mass sufficient to render bone fragile and liable to fracture
• Peak bone mass attained at the age of ~ 30 years
• Rate of bone loss thereafter is greater in women because bone loss increases significantly after the menopause - 'senile osteoporosis'
• Bone loss also occurs secondary to increased corticosteroid exposure (exogenous / endogenous), hypogonadism, thyrotoxicosis, pregnancy, hypo-pituitarism, mal-nutrition, mal-absorption, chronic heparin therapy, prolonged weightlessness *
• The condition is systemic, although the vertebrae, femoral neck and metacarpals are more affected than the skull and mid-shaft of long bones *
• Additional target sites are the distal radius, proximal humerus, proximal tibia and pelvis
• Resorption begins at the cortico-endosteal surface, resulting in enlargement of the medullary cavity and thinning of the cortex
• Cancellous bone is also affected and trabeculae may be completely resorbed
• The blood concentration of calcium / phosphate remains normal
Osteoporosis is associated with: 53
√ F An increase in uncalcified bone matrix (osteoid tissue). A
F Prolonged oestrogen therapy. B
T A normal histological bone structure. C
T Bone fractures. D
F Irregularity of epiphyseal plates. E

The following are causes of hypokalaemia: 54
F Angiotensin-converting enzyme(ACE) inhibitors. A
F Addison's disease. B
T Diarrhea. C
F Digoxin overdose. D
√ T Metabolic alkalosis. E

Osteomalacia is characterized by: 55
F Mineralization of the periosteum. A
T Deposition of uncalcified bone matrix. B
F Normal osteoblastic activity. C
T Increased capillary fragility. D
F Normal calcification of bone. E
Comment:
RICKETS & OSTEOMALACIA *****
• Rickets occurs in children while osteomalacia occurs in adults
• Caused by vitamin D deficiency *
• Dietary deficiency, inadequate exposure to sun light, malabsorption, derangements in vitamin D metabolism (for instance, chronic renal failure), end-organ resistance or hereditary abnormalities of vitamin D metabolism
• There is a failure in bone mineralization resulting in excess un-mineralised matrix and abnormally wide osteoid seams *
• Rickets results in skeletal deformity with defective mineralization of the epiphyseal cartilage necessary to control cartilaginous growth while in the adult, there is a pre-disposition to fracture *
Rickets is characterized by the following: 56
F Mineralization of the periosteum. A
T Deposition of uncalcified osteoid. B
T Abnormal osteoblastic activity. C
T Increased capillary fragility. D
√ T Overgrowth of cartilage. E

Tetany may occur as a complication of: 57
F Osteoporosis. A
F Hypercapnia. B
F Respiratory acidosis. C
F Peripheral neuropathy. D
F Untreated hyperparathyroidism. E

Immunology


Tissue macrophages: 58
T Are found in the placental villous stroma. A
F Express HLA class I but not HLA class II surface antigens. B
T Have a role in protection against intracellular pathogens. C
T Are phagocytic. D
F Are derived from circulating plasma cells. E

Natural killer (NK) cells: 59
T Are related to B cells. A
T Have large granular lymphocyte morphology. B
T Have receptors for HLA class I molecules. C
F Are present in large numbers in decidua during the first trimester. D
F Express CD3 (cluster differentiation antigen 3) on their surface. E
Comment:
NATURAL KILLER (NK) CELLS *****
• NK cells a group of cytolytic lymphocytes, distinct from B-lymphocytes and T-lymphocytes, that participate in both innate immunity and adaptive immunity*
• Lack B-cell receptors (surface immunoglobulins) and T-cell receptors (TCR / CD3) *
• Express receptors for the Fc portion of some IgG antibodies *
• Large granular lymphocytes - make up 10% of lymphocytes in blood and peripheral lymphoid tissues and about 2% of lymphocytes in peripheral blood *
• Specialized to kill certain types of target cells, especially cells infected with virus or malignant cells *
Features of NK Cells
• NK cells do not express surface immunoglobulins or TCR/CD3 on their surface. The surface markers that best characterize NK cells are CD2+,CD3-, CD4-, and CD56+ *
• NK receptors are polymorphic so that the repertoire of NK receptors differs from person to person.
• The first NK cell receptor, called the killer-activating receptor recognises stress-induced molecules. This interaction sends a positive signal which enables the NK cell to kill the cell to which it has bound unless the second receptor cancels that signal.
• This second receptor, called the killer-inhibitory receptor (KIR), recognises MHC-I molecules which are usually present on all nucleated human cells.
• If MHC-I molecules are expressed on the cell, the killer-inhibitory receptor sends a negative signal that overrides the kill signal and prevents the NK cell from killing that cell
• This ensures that NK cells are not activated by normal host cells
• Viruses often suppress class I MHC expression in cells they infect, the virus-infected cell becomes susceptible to killing by NK cells.
• Malignant cells have reduced or no class I MHC expression and are susceptible to killing by NK cells.
• NK cells kill cells to which antibody molecules have attached through a process called antibody-dependent cytotoxicity
• The killing is done by the exocytosis of granules containing perforin and granzymes.
• Pre-programmed to recognise their targets and have no need to develop into a clone of identical cells.
• Secrete cytokines such as IFN-γ and TNF-α *
Plasma cells: 60
T Are increased in myeloma. A
F Are characteristic of acute infection. B
F Are phagocytic. C
T Synthesis immunoglobulins. D
T Are derived from B lymphocytes. E
Comment:
LYMPHOCYTES *****
• Make up 20-45% of total leukocyte count
• Only immune cells with specific receptors for antigens
• Count is increased in viral infections, toxoplasmosis, brucellosis, and whooping cough
• Count is decreased in uraemia, Legionnaires disease, corticosteroid treatment, chemotherapy and radiotherapy and HIV infection
• Characterised by their differential expression of CD (cluster of differentiation) antigens.
• Following stimulation by antigen, some lymphocytes differentiate into memory cells which are capable of mounting a rapid response if the same antigen is later encountered
• Most lymphocytes are located in secondary lymphoid tissues - lymph nodes, the white pulp of the spleen, the gut- and bronchial-associated lymphoid tissues.
• The part of the B cell receptor that binds antigen is surface immunoglobulin*
• Subsequent B cell proliferation and maturation generates plasma cells that secrete this immunoglobulin *
• In contrast to B cell receptors, T cell receptors do not bind free antigen. The antigen must be processed into small peptides by antigen presenting cells and these antigen derived peptides are displayed on the antigen presenting cell surface in the clefts of molecules called major histocompatibility molecules (MHC) *
• There are three main types of T cells *
1) T helper cells that facilitate B cell responses to antigen
2) T inflammatory cells that facilitate macrophages in the eradication of intracellular infection
3) Cytotoxic T cells that recognise and destroy virus infected cells.
B-LYMPHOCYTES *****
• Mature in the bone marrow. Develop into antibody producing plasma cells. Only immune cells capable of antibody production *
• Have membrane-bound immunoglobulins which act as antigen receptors *
• Plasma cells migrate to the bone marrow where they produce small quantities of antibodies for long periods of time after the initial infection has been cleared
• B-cell receptors bind soluble antigens
• The bound antigen molecules are engulfed into the B cell by receptor-mediated endocytosis. *
• The antigen is digested into fragments which are then displayed at the cell surface nestled inside a class II histocompatibility molecule. *
• Helper T cells with complementary TCRs bind the B cell and secretelymphokines that *
1) Stimulate the B cell to enter the cell cycle and develop, by repeated mitosis, into aclone of cells with identical BCRs;
2) Switch from synthesizing their BCRs as integral membrane proteins to a soluble version;
3) Differentiate into plasma cells that secrete immunoglobulins.
Lymphocytes in healthy: 61
F Form about 2% of the white cell count. A
√ T Play an essential role in cell mediated immunity. B
T Can change into plasma cells. C
T Have proportionately more nuclear material than cytoplasm. D
F Have a life span of about 30 days. E
Comment:
LYMPHOCYTES *****
• Make up 20-45% of total leukocyte count
• Only immune cells with specific receptors for antigens
• Count is increased in viral infections, toxoplasmosis, brucellosis, and whooping cough
• Count is decreased in uraemia, Legionnaires disease, corticosteroid treatment, chemotherapy and radiotherapy and HIV infection
• Characterised by their differential expression of CD (cluster of differentiation) antigens
• Following stimulation by antigen, some lymphocytes differentiate into memory cells which are capable of mounting a rapid response if the same antigen is later encountered
• Most lymphocytes are located in secondary lymphoid tissues - lymph nodes, the white pulp of the spleen, the gut- and bronchial-associated lymphoid tissues.
• The part of the B cell receptor that binds antigen is surface immunoglobulin*
• Subsequent B cell proliferation and maturation generates plasma cells that secrete this immunoglobulin *
• In contrast to B cell receptors, T cell receptors do not bind free antigen. The antigen must be processed into small peptides by antigen presenting cells and these antigen derived peptides are displayed on the antigen presenting cell surface in the clefts of molecules called major histocompatibility molecules (MHC) *
• There are three main types of T cells *
1) T helper cells that facilitate B cell responses to antigen
2) T inflammatory cells that facilitate macrophages in the eradication of intracellular infection
3) Cytotoxic T cells that recognise and destroy virus infected cells.
B-LYMPHOCYTES *****
• Mature in the bone marrow. Develop into antibody producing plasma cells. Only immune cells capable of antibody production *
• Have membrane-bound immunoglobulins which act as antigen receptors *
• Plasma cells migrate to the bone marrow where they produce small quantities of antibodies for long periods of time after the initial infection has been cleared
• B-cell receptors bind soluble antigens
• The bound antigen molecules are engulfed into the B cell by receptor-mediated endocytosis. *
• The antigen is digested into fragments which are then displayed at the cell surface nestled inside a class II histocompatibility molecule. *
• Helper T cells with complementary TCRs bind the B cell and secretelymphokines that *
1) Stimulate the B cell to enter the cell cycle and develop, by repeated mitosis, into aclone of cells with identical BCRs;
2) Switch from synthesizing their BCRs as integral membrane proteins to a soluble version;
3) Differentiate into plasma cells that secrete immunoglobulins.
B lymphocytes: 62
√ F Produce tumor necrosis factor. A
F Produce complement. B
T Produce antibodies. C
√ F Contribute to delayed hypersensitivity. D
T Produce IgE. E

T lymphocytes: 63
T Differentiate in the thymus. A
T Are involved in the generation of both cell-mediated and immoral Immune responses. B
T Are the predominant lymphoid population in decidua. C
T Are the predominant lymphoid population in peripheral blood. D
F Are the major cell type in the germinal centers of lymph nodes. E
Comment:
T-LYMPHOCYTES *****
• Mature in the thymus gland *
• Can only recognise peptide antigens that are bound to MHC molecules on specialised antigen-presenting cells - MHC-restricted *
• CD4 positive T-cells are helper T-cells - help B cells produce antibodies and help phagocytes destroy ingested organisms *
• CD8 positive T-cells are cytotoxic T-cells - capable of killing host cells infected with intracellular organisms *
• Na-ve T-cells have antigen receptors but do not perform the functions required to eliminate the antigen.
CD8+ T cells
• CD8+ T cells bind that are part of class I histocompatibility molecules. Almost all the cells of the body express class I molecules
• The best understood CD8+ T cells are cytotoxic T lymphocytes - secrete molecules that destroy the cell to which they have bound.
• The role of the CD8+ T cells is to monitor all the cells of the body, ready to destroy any that express foreign antigen fragments in their class I molecules.
CD4+ T cells
• CD4+ T cells bind epitopes that are part of class II histocompatibility molecules. Only specialized antigen-presenting cells express class II molecules
• Essential for both the cell mediated and antibody-mediated branches of the immune system
• Bind to antigen presented by antigen-presenting cells and release lymphokines that attract other cells to the area.
• Bind to antigen presented by B cells, resulting in the development of clones of plasma cells secreting antibodies against the antigenic material.
The following are recognized function of T lymphocytes: 64
F Antibody production. A
T Cell-mediated immunity. B
T Immune suppression. C
√ F Phagocytosis. D
T Cytokine production. E

The following are recognized function of T lymphocytes: 65
F Antibody production. A
T Cell-mediated immunity. B
T Immune suppression. C
√ F Phagocytosis. D
T Lymphokine production. E

Immunodeficiency states may be associated with: 66
T Viral infection of T lymphocytes. A
T B cell lymphomas. B
T Glucocorticoid administration. C
F Haemolytic disease of the newborn. D
T Hodgkin's lymphoma. E

Immunodeficiency states may be associated with: 67
T Viral infection of T lymphocytes. A
T B cell lymphomas. B
T Glucocorticoid administration. C
F Haemolytic disease of the newborn. D
T Untreated Hodgkin’s lymphoma. E

Concerning immunoglobulins: 68
T IgG contains tow heavy chains. A
√ T IgM is produced before IgG in the immune response. B
F IgE is the principal immunoglobulin secreted by mucous membranes. C
F IgA is the principal immunoglobulin involved in allergic reactions. D
√ T IgA is secreted in breast milk. E

Human immunoglobulin M (IGM): 69
F Has a molecular weight of 150 000 Daltons. A
T Contain J chains. B
F Crosses the placenta readily. C
F Fixes complement by the alternative pathway. D
F Is a dimmer in external secretions. E
Comment:
IgM *****
• One type, pentamer - ten antigen binding sites *
• Half-life in serum = 5 days.
• Activates complement and serves as naive B-cell receptor *
• First immunoglobulin to be synthesised during B-cell maturation *
• Molecular weight 970kDa, makes up 5-10% of immunoglobulins *
• Does NOT bind to mast cells, neutrophils or macrophages *
• Does not cross the placenta - the presence of IgM in fetal blood indicates fetal infection and fetal antibody production *
Concerning immunoglobulin in pregnancy: 70
F Maternal IgM is responsible for rhesus isoimmunisation in the fetus. A
F IgA concentration in cord blood is higher than that in maternal blood. B
F IgE crosses the placenta readily. C
T IgG crosses the placenta readily. D
F Fetal IgM is dimeric. E

Immunoglobulin M: 71
F Fixes complement by the alternative pathway. A
F Crosses the placenta readily. B
√ F Fixes to mast cells. C
T Is produced by plasma cells. D
F Is smaller than immunoglobulin E. E
Comment:
IgM *****
• One type, pentamer - ten antigen binding sites *
• Half-life in serum = 5 days.
• Activates complement and serves as naive B-cell receptor *
• First immunoglobulin to be synthesised during B-cell maturation *
• Molecular weight 970kDa, makes up 5-10% of immunoglobulins *
• Does NOT bind to mast cells, neutrophils or macrophages *
• Does not cross the placenta - the presence of IgM in fetal blood indicates fetal infection and fetal antibody production *
The following are examples of type-III hypersensitivity (immune-complex) disease: 72
F Autoimmune haemolytic anaemia. A
T Systemic lupus erythematosus. B
T Glomerulonephritis. C
F Tuberculosis. D
F Sarcoidosis. E
Comment:
IMMUNE COMPLEX MEDIATED (TYPE III) HYPERSENSITIVITY *****
• Caused by immune complex deposition in the blood vessels or tissues *
• These complexes activate macrophages, activate complement and cause the extracellular release of neutrophil granules and tissue damage *
• The inflammatory response is characterised by the Arthus reaction which is characterised by a neutrophilic infiltration and immunoglobulin + complement deposition *
• The inciting antigen may be -self- or -non-self- from infectious organisms
• Disease processes include *
1) Polyarteritis nodosa and SLE
2) Farmer's lung - occurring in patients sensitized to thermophilic actinomycetes; pigeon-fancier's disease - these disorders are generally known as extrinsic allergic alveolitis
3) Post-streptococcal glomerulonephritis
4) Jarisch-Herxheimer reaction+
Type III hypersensitivity: 73
F Is mediated by specifically-sensitized T lymphocytes. A
F Causes myasthenia gravis. B
T Occurs in systemic lupus erythematosus. C
T Is a recognized cause of glomerulonephritis. D
F May cause allergic asthma. E

Type III (immune complex-related) hypersensitivity is: 74
T Damage localized to a particular cell type. A
√ F Decreased vascular permeability. B
T Microthrombus formation. C
T Complement activation. D
F Mediation by IgE antibodies. E

The major histocompatibility complex (MHC): 75
F Resides on chromosome 11. A
T Is composed of human leukocyte antigen (HLA) genes. B
F Codes for three classes of antigens. C
F Will be identical in dizygotic twins. D
F Codes for blood group antigens. E
Comment:
THE MAJOR HISTOCOMPATIBILITY COMPLEX
• Made up of membrane bound proteins on antigen presenting cells that display peptide antigens for recognition by T-cells *
• Play a central role in graft rejection *
• Human MHC molecules are called human leukocyte antigens (HLA) *
• MHC genes are highly polymorphic - there are many different alleles present in different individuals. No two individuals in an outbred population have identical MHC genes or molecules (except identical twins) *
• Human MHC located on chromosome 6 *
• Variations in MHC genes are not due to DNA recombinations
• There are two sets of highly polymorphic HLA genes called class I and class II genes
• The MHC also contains several non-polymorphic genes, some involved in antigen presentation and others with unknown functions
• Inherited in an autosomal co-dominant fashion *
• Class I molecules are expressed by all nucleated cells while class II molecules are expressed by professional antigen-presenting cells only (dendritic cells, macrophages and B-lymphocytes) *
• Each MHC molecule can only present one antigen at a time, but is capable of presenting many different peptides. The binding of peptides to MHC molecules is a low affinity, low specificity interaction. Bound peptides are displayed for several days to enable recognition by T-cells
• Antigenic peptides are acquired during the synthesis and assembly of MHC molecules in the cytoplasm - class I molecules display peptides acquired from cytosolic proteins while class II molecules acquire peptides from intracellular vesicles
• MHC molecules cannot discriminate between self and non-self peptides
• MHC molecules cannot present non-peptide antigens
Antibodies play an important part in the development of: 76
T Phagocytosis. A
F The Mantoux response. B
T Erythroblastosis fetalis. C
F Hyperemesis gravidarum. D
T Anaphylaxis. E

Antibodies: 77
T Are proteins. A
F Are formed in the fetus before 12 weeks of intrauterine life. B
F Have an average molecular weight of around 10 000 Daltons. C
T Of the rhesus type are genetically transmitted. D
T Are produce of the ribosomes of plasma cells. E

The biological effects of complement in the human include: 78
T Opsonisation. A
T Cell membrane lysis. B
F Participation in the blood coagulation process. C
F Promotion of sperm motility. D
F Prevention of immune rejection of trophoblast. E

Autoantibodies are found in: 79
T Systemic lupus erythematosus. A
T Rheumatoid arthritis. B
T Pernicious anaemia. C
F Bronchial asthma. D
T Chronic active hepatitis. E

The following cells are correctly paired with their products: 80
T Endothelial cell: factor VIII related antigen. A
T Plasma cell: IgG. B
T Salivary gland epithelial cell: amylase. C
F Mast cell: IgA. D
T Decidual stromal cell: prolactin. E

In uncomplicated homozygous beta thalassaemia there is: 81
T Hypochromasia. A
F A reductionin haemoglobin A2. B
T An increase in haemogobin F. C
F Megaloblastic erythropoiesis. D
F Red cell sickling. E

In uncomplicated homozygous beta thalassaemia there is: 82
T Hypochromatasia. A
F A reduction in haemoglobin A2. B
T An increase in haemoglobin F. C
T No depletion of iron stores. D
F The presence of megaloblasts in bone marrow. E

In beta thalassaemia: 83
F The erythrocytes will sickle at low oxygen tension. A
F A homozygous fetus is usually anemic. B
F Stainable iron stores in the marrow are usually decreased. C
T Target cells may be found in the peripheral blood. D
F Erythrocyte survival time is increased. E

Characteristic features of addisonian pernicious anemia include: 84
F Leucocytosis. A
F Inheritance as an autosomal dominant trait. B
F A raised mean corpuscular haemoglobin concentration. C
T An increased incidence of gastric neoplasia. D
T An increased incidence of primary hypothyroidism. E

Steps involved in the identification of restriction fragment length polymorphisms (RFLP) include: 85
F Western blotting. A
T Restriction enzyme digestion. B
T Southern blotting. C
T Agarose gel electrophoresis. D
F Thin layer chromatography. E


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Re: Pathology>>>>>>

Post by aiwahsh on Wed Mar 09, 2011 4:08 pm

الف شكر وتسلم ايدك بصراحه مجهود اكتر من رائع
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Re: Pathology>>>>>>

Post by wafyazaz on Sun Oct 23, 2011 2:54 pm

استأذن حضرتك.....هل هذه الاسئله من امتحانات سابقه للزماله...ام هي من مواقع لاسئله؟.....جزاك الله خيرا
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Re: Pathology>>>>>>

Post by drhmada on Mon Nov 14, 2011 6:27 am

thank u
where the answer
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Re: Pathology>>>>>>

Post by omar.faisal on Sun Mar 11, 2012 12:03 am

Thanks
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