The MT4L4 ELHM Pathology Course (Exam 1) assesses key concepts in pathology, focusing on inflammation mechanisms, chemical mediators, and cellular responses. It is designed to enhance understanding of disease processes and repair, crucial for medical students and professionals.
Increased vascular permeability
Chemolaxis
Fever
All of the above
None of the above
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Lt is mainly induced by vasoconstriction.
Lt mainly occurs after emigration of leucocytes
Lt may lead to thrombosis
AII of the above
None of the above
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Opsonins play an important role in the process of pavementing
Neutrophils and monocytes emigrate at the same time.
Emigration of leucocytes is followed by Ieucopenia
Giant cells are formed by fusion of neutrophils
Bacilli are more chernotactic to macrophages while cocci mainly attract neutrophils
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Deposition of fibrin in inflammatory conditions is known as fibrosis
Fibrin plays important functions in inflammation & repair
Cellulitis is characterized by excess fibrin deposition
All of the above
None of the abovE
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This is diversion cf Ieucocytes out of the axial column of blood prior to their emigration
Typhoid bacilli are strongly chemotactic to neutrophils.
Complement components are important chemotactic factors
AlI of the above
None of the above
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They are the first cells to emigrate in acute inflammation
They are the most predominant cells in chronic inflammation.
The most important chemotactic factors for neutrophiis are derived from bacilii.
They efficiently engulf foreign bodies
They can give rise to giant cells
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Persistent vasoconstriction
Vasodilatation
Lncreased vascular permeability
Emigration of leucocytes
Vascular stasis.
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Opsonization
Sealing of bleeding vessels
Facilitation of movement of inflammatory cells
Localization of inflammatory fields
Facilitation of movement of fibroblasts during repair
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Neutrophils
Eosinophils
Macrophages
Lymphocytes
Plasma cells
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Lt provides the phagocytic cells with phospholipids
Lt provides the phagocytic cells with energy
Lt hydrolyses the release of calcium and enhances cell Mobility.
AIl of the above
None of the above.
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May be caused by alcohol intake
May occur in cases of hepatitis C
May be followed by cirrhosis.
All of the above
None of the above
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Lt is always caused by irritànts such as anoxia, bacteriai infections and alcohol.
Lt is characterized by fragmentation of nuclear DNA.
It is characterized by formation of cell membrane blebs.
Lt is characterized by transformation cf the affected cell into apoptotic bodies.
Phagocytosis of the apoptotic bodies is common.
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Cheese-like material
Commonly seen in tuberculous Iesions.
The structural outlines of the necrotic cells are preserved.
Lt represents partially iiquified coagulative necrosis.
Microscopically appears as amorphous eosinophilic granular debris.
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Pyknosis
Karyorrhexis
Mitosis
Karyolysis
Cytomegaly
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Lung infarction
Cerebral infarction
Pulmonary tuberculosis
AlI of the above
None of the above
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It is due to hypercalcemia
Lt affects healthy tissues
Lt can be seen in tubeculosis.
Lt cormmonly occurs in teeth and bone
Lt is more common in arterial lhan venous thrombi
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Lt may occur in cases of hyperparathyroidism.
It is seen in metastatic tumors.
Calcified thrombi represent a type of metastatic calcitication
All of the above
None of the above
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Amyloid is predominantly a fibril protein.
Macrophages may play an important role in systemic amyloidosis
Sudan lll and osmic acid can specifically stain amyloid
Amyloid is mainly deposited within the walls of small blood vessels
Amyloidosis may Iead to Addison's disease.
Acute suppurations
Tuberculosis
Ulcerative colitis.
Rheumatoid arthritis
Mlultiple myeloma.
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Amyloid sago spleen
Hepatic amyloidosis
Renal amyloidosis
Amyloid diffuse spleen
Cutaneous amyloidosis
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Ulcerative colitis
Multiple myeloma
Tuberculosis
Chronic Iung abscess
Hodgkin's disoase.
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The amyloid protein is secreted by macrophages within the thyroid gland.
The amyloid protein is produced by tumor cells .
Lt may be accompanied by renal or hepatic amyloidosis.
The amyloid protein is AL
None of the above
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Neurofibromatosis
Brown atrophy of the heart
Melanosis coli
Leukoderma
All of the above
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Arteriolar contraction
Blood flow slows.
Dilatation of arterioles.
Emigration of leucocytes from blood vessels.
Protein rich fluid escapes from blood vessels.
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Glycogen stores are depleted
Cytoplasmic sodium increases
Nuclei undergo karyorrhexis
Intracellular pH diminishes
Blebs form on cell membranes
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Lipofuscin
Bilirubin
Melanin
Hemosiderin
Glycogen
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Cytoskeletal intermediate filament loss
Decreased intracellular pH from anaerobic glycolysis
Increased free radicals
Reduced protein synthesis
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Dysplasia
Hyperplasia
Carcinoma
Metaplasia
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Liquefactive necrosis
Atrophy
Coagulative necrosis
Apoptosis
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Stromal hypertrophy
Epithelial dysplasia
Steatocyte atrophy
Lobular hyperplasia
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Hemosiderin from iron overload
Lipochrome from 'wear and tear
Glycogen from a storage disease
Cholesterol from atherosclerosis
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Ovarian follicles
Small intestinal epithelium
Erythropoietic cells of bone marrow
Spermatogonia of testicular tubules
Neurons of cerebral cortex
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Elevated troponin I
Increased sodium
Elevated lactate
Increased hematocrit
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Steatosis in hepatocytes
Bilirubin in canaliculi
Hemosiderin in hepatocytes
Glycogen in hepatocytes
Amyloid in portal triads
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Coagulative necrosis
Dry gangrene
Fat necrosis
Liquefactive necrosis
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Dysplasia
Hyperplasia
Neoplasia
Metaplasia
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Cholestasis
Fatty change
Hemochromatosis
Coagulative necrosis
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Physiologic atrophy
Breast trauma
Radiation injury
Hypoxic injury
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CO2 of 30 mmol/L
Phosphorus of 2.2 mg/dL
Uric acid of 15.1 mg/dL
Sodium of 121 mmol/L
Calcium of 4.5 mg/dL
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