MID Flashcards
- How does protein deficiency contribute to generalized edema?
a) It raises hydrostatic pressure within arteries.
b) It reduces oncotic pressure, promoting fluid leakage into tissues.
c) It triggers systemic vasodilation.
d) It prevents sodium retention.
Answer: b) It reduces oncotic pressure, promoting fluid leakage into tissues.
Explanation: Protein deficiency lowers plasma oncotic pressure, reducing fluid reabsorption from interstitial spaces
- Which combination of factors would most likely result in venous congestion?
a) Increased arterial inflow and decreased venous outflow
b) Decreased arterial inflow and increased venous drainage
c) Increased lymphatic drainage and reduced vascular permeability
d) Only increased venous drainage
Answer: a) Increased arterial inflow and decreased venous outllow
Explanation: Reduced venous outflow leads to blood accumulation in veins, causing congestion.
- Which statement about pulmonary edema is correct?
a) It occurs when hydrostatic pressure in the pulmonary artery decreases.
b) It is characterized by protein-rich fluid in alveoli.
c) It results from increased capillary permeability in the lungs.
d) It leads to systemic vasoconstriction.
Answer: c) It results from increased capillary permeability in the lungs.
Explanation: Pulmonary edema can result from damage to capillaries, increasing fluid leakage into alveoli.
- Both mural and valvular thrombi can dislodge to cause embolism. Which is more likely to travel to the brain?
a) Mural thrombi
b) Valvular thrombi
c) Neither a nor b
d) Both a and b
Answer: b) Valvular thrombi
Explanation: Thrombi on heart valves are more prone to embolization and can travel to cerebral vessels, causing strokes.
- Why does chronic liver disease increase the risk of ascites?
a) It decreases venous return to the heart.
b) It lowers albumin production, reducing plasma oncotic pressure.
c) It inhibits sodium absorption.
d) It increases lymphatic drainage from the abdomen.
Answer: b) It lowers albumin production, reducing plasma oncotic pressure.
Explanation: Hypoalbuminemia from liver disease promotes fluid accumulation in the abdominal cavity.
- Which mechanism best explains shock lung (congestive atelectasis)?
a) Pulmonary artery dilation.
b) Fluid overload in the alveoli
c) Collapse of alveoli due to prolonged capillary congestion
d) Bronchoconstriction from allergic reactions
Answer: c) Collapse of alveoli due to prolonged capillary congestion
Explanation: In shock, blood pooling in the lungs compresses alveoli, impairing gas exchange.
- Why does disseminated intravascular coagulation (DIC) cause both thrombosis and hemorrhage?
a) It increases platelet production,
b) It simultaneously depletes clotting factors and promotes coagulation.
c) It reduces blood pressure.
d) It affects only venous thrombi.
Answer: b) It simultaneously depletes clotting factors and promotes coagulation.
Explanation: DIC consumes clotting factors, leading to thrombosis and a bleeding tendency,
- Both embolism and thrombosis can cause infarction. How does their mechanism differ?
a) Embolism is always due to air bubbles, while thrombosis involves clots.
b) Embolism involves foreign material traveling to occlude vessels, while thrombosis is the formation of a clot at the site.
c) Thrombosis affects only veins, while embolism affects arteries.
d) Embolism and thrombosis are unrelated to each other.
Answer: b) Embolism involves foreign material traveling to occlude vessels, while thrombosis is the formation of a clot at the site,
Explanation: Thrombi form locally, whereas emboli travel to block distant vessels.
- How does neurogenic shock differ from other types of shock?
a) It involves heart failure.
b) It results from fluid loss.
c) It occurs due to the loss of sympathetic vascular tone.
d) It increases cardiac output.
Answer: c) It occurs due to the loss of sympathetic vascular tone.
Explanation: Neurogenic shock leads to excessive vasodilation from impaired autonomic control.
- Why do prostaglandins play a critical role in pain during inflammation?
a) They increase platelet aggregation.
b) They sensitize nerve endings, amplifying the pain response.
c) They inhibit the release of histamine.
d) They decrease blood flow, causing tissue ischemia.
Answer: b) They sensitize nerve endings, amplifying the pain response.
Explanation: Prostaglandin E2 (PGE2) lowers the pain threshold, increasing the sensitivity of peripheral nerves to inflammatory stimuli.
- How does edema develop during acute inflammation?
a) Vasodilation reduces capillary hydrostatic pressure.
b) Increased vascular permeability allows fluid to leak into tissues.
c) Neutrophil migration draws fluid into tissues.
d) Platelet aggregation promotes water retention.
Answer: b) Increased vascular permeability allows fluid to leak into tissues.
Explanation: Vascular leakage occurs as endothelial cells separate, permitting plasma proteins and fluids to move into the extracellular space.
- Which process ensures that leukocytes accumulate at the site of injury?
a) Diapedesis
b) Chemotaxis
c) Phagocytosis
d) Margination
Answer: b) Chemotaxis
Explanation: Chemotaxis is the movement of leukocytes along a chemical gradient toward the site of infection or injury.
- Which of the following mediators increase vascular permeability?
a) Histamine
b) Leukotrienes
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Histamine and leukotrienes promote vascular leakage, enabling immune cells to infiltrate tissues.
- Why does chronic inflammation result in fibrosis?
a) Neutrophils release collagen-degrading enzymes.
b) Fibroblasts secrete excessive collagen in response to persistent injury.
c) Lymphocytes inhibit tissue repair mechanisms.
d) Vascular permeability decreases over time.
Answer: b) Fibroblasts secrete excessive collagen in response to persistent injury.
Explanation: Prolonged inflammation activates fibroblasts to lay down collagen, leading to scar formation and fibrosis.
- Which cells are primarily responsible for phagocytosis of dead tissue during chronic
inflammation?
a) Eosinophils
b) Neutrophils
c) Macrophages
d) Mast cells
Answer: c) Macrophages
Explanation: Macrophages engulf and digest dead cells, debris, and pathogens during chronic inflammation.
- How does nitric oxide influence blood flow during inflammation?
a) It induces bronchoconstriction.
b) It promotes vasodilation, increasing blood flow.
c) It enhances platelet adhesion.
d) It triggers neutrophil apoptosis.
Answer: b) It promotes vasodilation, increasing blood flow.
Explanation: Nitric oxide relaxes vascular smooth musele, enhancing blood flow to the site of inflammation.
- Which phase of inflammation involves the formation of a phagosome?
a) Adhesion
b) Emigration
c) Phagocytosis
d) Chemotaxis
Answer: c) Phagocytosis
Explanation: Phagocytosis involves the engulfing of pathogens into vesicles called phagosomes for intracellular degradation.
- Why do granulomas form in chronic inflammation?
a) To block vasodilation at the injury site
b) To encapsulate pathogens or foreign material that cannot be destroyed
c) To prevent chemotaxis of neutrophils
d) To inhibit fibroblast activation
Answer: b) To encapsulate pathogens or foreign material that cannot be destroyed
Explanation: Granulomas isolate persistent pathogens or irritants that resist elimination.
- Why do granulomas form in chronic inflammation?
a) To block vasodilation at the injury site
b) To encapsulate pathogens or foreign material that cannot be destroyed
c) To prevent chemotaxis of neutrophils
d) To inhibit fibroblast activation
Answer: b) To encapsulate pathogens or foreign material that cannot be destroyed
Explanation: Granulomas isolate persistent pathogens or irritants that resist elimination.
Which cells are the first responders during acute inflammation?
a) Lymphocytes
b) Macrophages
c) Neutrophils
d) Eosinophils
Answer: c) Neut
Explanation:
- How does histamine promote inflammation?
a) It decreases vascular permeability.
b) It causes vasodilation and vascular leakage.
c) It inhibits leukocyte migration.
d) It triggers fibroblast activity.
Answer: b) It causes vasodilation and vascular leakage.
Explanation: Histamine promotes inflammation by increasing blood flow and vascular
permeability
- How does histamine promote inflammation?
a) It decreases vascular permeability.
b) It causes vasodilation and vascular leakage.
c) It inhibits leukocyte migration.
d) It triggers fibroblast activity.
Answer: b) It causes vasodilation and vascular leakage.
Explanation: Histamine promotes inflammation by increasing blood flow and vascular
permeability
- Which process describes the movement of leukocytes through vessel walls into
tissues?
a) Phagocytosis
b) Diapedesis
c) Opsonization
d) Chemotaxis
Answer: b) Diapedesis
Explanation: Diapedesis is the passage of leukocytes through the endothelial wall into
the tissue
58, Which inflammatory mediators directly induce pain?
a) Bradykinin
b) Prostaglandin E2
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Bradykinin and prostaglandin E2 enhance the sensitivity of pain receptors.
- Which cells dominate during chronic inflammation?
a) Neutrophils
b) Macrophages
c) Mast cells.
d) Basophils
Answer: b) Macrophages
Explanation: Macrophages play a central role in chronic inflammation by phagocytosing debris and secreting cytokines.
- Why is edema a common feature of acute inflammation?
a) Neutrophils release water into tissues.
b) Vascular permeability allows plasma to leak into tissues.
c) Lymphatic drainage increases.
d) Platelets aggregate in tissue spaces.
Answer: b) Vascular permeability allows plasma to leak into tissues.
Explanation: Fluid accumulation in tissues results from increased permeability of blood
vessels.
