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.
- Which outcome characterizes the resolution phase of inflammation?
a) Scar tissue formation
b) Complete restoration of tissue structure
c) Formation of granulomas
d) Persistent fibrosis.
Answer: b) Complete restoration of tissue structure
Explanation: Resolution restores tissues to their normal state without lasting damage,
- How do fibroblasts promote healing?
a) By enhancing neutrophil recruitment
b) By secreting collagen to form the extracellular matrix
c) By inhibiting macrophage activity
d) By preventing capillary growth
Answer: b) By secreting collagen to form the extracellular matrix
Explanation: Fibroblasts deposit collagen, providing structural support for regenerating
tissue.
- Why does acute inflammation sometimes progress to chronic inflammation?
a) The initial injury resolves quickly.
b) Persistent infection or irritants remain at the site.
c) Neutrophil activity subsides too carly.
d) Excessive collagen deposition inhibits tissue repair.
Answer: b) Persistent infection or irritants remain at the site.
Explanation: Ongoing injury or infection sustains the inflammatory response, leading to chronie inflammation.
- Which cells are involved in the formation of granulomas?
a) Neutrophils
b) Macrophages
c) Lymphocytes
d) Both band e
Answer: d) Both b and e
Explanation: Macrophages and lymphocytes collaborate to form granulomas, isolating persistent pathogens..
- Which phase of wound healing involves fibroblast proliferation?
a) Hemostasis phase
b) Proliferative phase
c) Inflammatory phase
d) Remodeling phase
Answer:
b) Proliferative phase
Explanation: Fibroblasts multiply during the proliferative phase, aiding tissue repair.
- Which inflammatory mediators promote vasodilation?
a) Histamine
b) Nitric oxide
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Both histamine and nitric oxide relax vascular smooth muscles, increasing blood flow.
- How does chronic inflammation affect tissue structure?
a) It reduces immune cell activity.
b) It promotes fibrosis through…..
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c) It enhances tissue regenerati
d) It prevents angiogenesis.
Answer: b) It promotes fibrosis through collagen deposition.
Explanation: Persistent inflammation stimulates fibroblasts to deposit collagen, leading
to scar formation
- Why are fibroblasts essential for wound healing?
a) They seerete histamine to reduce inflammation.
b) They produce collagen, forming new tissue.
c) They prevent macrophage activation.
d) They inhibit vascular permeability.
Answer: b) They produce collagen, forming new tissue.
Explanation: Fibroblasts generate collagen, supporting tissue repair and regeneration.
d) Both b and e
Answer: d) Both b and e
Explanation: Eosinophils and mast cells play roles in allergic reactions and parasitic
defenses.
- What marks the transition from acute to chronic inflammation?
a) Resolution of infection
b) Persistent macrophage activity
c) Neutrophil dominance
d) Formation of scar tissue
Answer: b) Persistent macrophage activity
Explanation: Chronic inflammation is characterized by prolonged macrophage involvement and tissue remodeling.
- A dog presents with sudden respiratory distress after long-distance travel. Which condition should be suspected first?
a) Pulmonary edema
b) Pulmonary thromboembolism
c) BOTH a and b
d) NEITHER of the two
Answer: b) Pulmonary thromboembolism
Explanation: Pulmonary embolism is a common complication following prolonged inactivity or stress.
- A cat presents with pale mucous membranes, tachycardia, and lethargy. What diagnostic approach should be prioritized?
a) Check for dehydration levels.
b) Perform a complete blood count (CBC)
c) BOTH a and b
d) NEITHER a nor b
Answer: b) Perform a complete blood count (CBC)
Explanation: These signs suggest anemia or blood loss, requiring a CBC for
confirmation.
- A veterinarian observes a thrombus in a cow’s jugular vein post-venipuncture.
What is the most likely cause?
a) Blood stasis
b) Endothelial injury
c) BOTH a and b
d) NEITHER of the two
Answer: c) BOTH a and b
Explanation: Thrombosis often results from blood stasis and vessel wall injury.
- Which intervention is most appropriate for a dog with left-sided heart failure presenting with pulmonary edema?
a) Administer loop diuretics
b) Increase dietary sodium
c) BOTH a and b
d) NEITHER of the two
Answer: a) Administer loop diuretics
Explanation: Diuretics help reduce fluid accumulation in pulmonary edema.
- What condition could develop from injecting a solution containing bubbles into a vein?
a) Thromboembolism
b) Air embolism
c) BOTH a and b
d) NEITHER of the two
Answer: b) Air embolism
Explanation: Air embolism can occur when air bubbles obstruct blood flow in a vessel.
- A horse presents with jugular vein distention and ascites. What is the most likely
diagnosis?
a) Right-sided heart failure
b) Left-sided heart failure
c) Pulmonary edema
d) Anemia
Answer: a) Right-sided heart failure
Explanation: Right-sided heart failure often leads to systemic venous congestion and ascites.
- Which of the following best describes the process of infarction?
a) Tissue necrosis due to infection
b) Necrosis resulting from vascular obstruction
c) Tissue inflammation without neerosis
d) Hemorrhagic diathesis leading to necrosis
Answer: b) Necrosis resulting from vascular obstruction
Explanation: Infarction refers to tissue death due to blocked blood supply.
- A dog with chronic liver disease shows signs of generalized edema. What is the most likely cause?
a) Hypoalbuminemia
b) Hyperkalemia (Potassium K-kalium)
c) Increased plasma oncotic pressure
d) BOTH a and b
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Answer: a) Hypoalbuminemia
Explanation: Chronic liver disease reduces albumin production, leading to generalized
edema.
- What is the primary mechanism involved in septic shock?
a) Blood volume loss
b) Vasodilation and increased vascular permeability
c) Deerea
d) Hyperc
Answer: b) Vasodilation and increased vascular permeability
infection.
Explanation:
- A veterinarian notices petechial hemorrhages on a cow’s mucosal surfaces. Which condition should be considered first?
a) Coagulopathy
b) Hyperemia
c) BOTH a and b
d) NEITHER of the two
Answer: a) Coagulopathy
Explanation: Petechial hemorrhages often indicate an underlying coagulopathy.
- Which of the following factors would likely exacerbate chronic inflammation despite the removal of the initial offending agent?
a) Fibroblast overactivation
b) Persistent cytokine release
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Even if the offending agent is removed, fibroblast overactivation can lead to fibrosis, and persistent eytokine release can prolong the inflammatory response.
- How would impaired neutrophil diapedesis affect inflammation?
a) Pathogen clearance would be delayed.
b) Granuloma formation would be accelerated.
c) Both a and b
d) Neither a nor b
Answer: a) Pathogen clearance would be delayed.
Explanation: Neutrophils are essential in the early phase of inflammation. Without disck this site ofisfaction to slane sathanasi
- What would happen if macrophages failed to transform into epithelioid and giant cells?
a) Chronic inflammation would accelerate.
b) Granulomatous inflammation would fail to develop.
c) Both a and b
d) Neither a nor b
Answer: b)
Granulomatous inflammation would fail to develop.
Explanation: Epithelioid and giant cells are essential for forming granulomas, a hallmark of chronic inflammation.
- Why would excessive fibroblast activation during healing be detrimental?
a) It can cause excessive scar formation.
b) It can lead to contractures, impairing tissue movement.
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Overactive fibroblasts deposit excessive collagen, leading to scar tissue and contractures, reducing tissue flexibility.
- What would be the consequence of unchecked complement activation (C5-C9) during inflammation?
a) Formation of the membrane attack complex (MAC)
b) Increased tissue damage
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Uncontrolled complement activation can result in MAC formation, which directly damages host tissues.
- How would blocking arachidonic acid metabolism impact the inflammatory response?
a) Prostaglandin synthesis would decrease.
b) Leukotriene production would be inhibited.
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Arachidonic acid metabolism is required for the synthesis of both prostaglandins and leukotrienes, critical mediators of inflammation.
- Which of the following would happen if vascular permeability were left unchecked during a severe inflammatory response?
a) Persistent edema formation
b) Development of hypovolemic shock
Answer: c) Both a and b
Explanation: Excessive vascular permeability leads to fluid leakage, causing edema and, in severe cases, hypovolemic shock.
- What is the primary consequence of macrophages failing to secrete TNF-a during
inflammation?
a) Impaired fever induction
b) Reduced apoptosis of infected cells
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: TNF-a plays a crucial role in inducing fever and promoting the apoptosis of infected cells, limiting pathogen spread.
- Why would failure of the kinin system impair the inflammatory response?
a) It would reduce vasodilation.
b) It would inhibit pain perception.
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: The kinin system, especially through bradykinin, promotes vasodilation and pain, which are essential features of inflammation.
- Which condition would most likely result from an abnormal increase in cosinophils?
a) Chronic allergic reaction
b) Parasitic infection
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Eosinophils are elevated in allergic reactions and parasitic infections,
- What would happen if lymphocytes failed to transition from acute to chronic
inflammation?
a) Persistent neutrophil infiltration
b) Lack of granuloma formation
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Without lymphocyte involvement, neutrophil-dominated acute
- Which of the following would likely develop if fibrosis became excessive during the
healing process?
a) Contracture deformity
b) Impaired tissue remodeling
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Excessive fibrosis leads to contractures and disrupts normal tissue architecture, impairing function.
- Why would failure to clear fibrin impair healing?
a) Persistent exudate formation
b) Delayed tissue remodeling
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Fibrin must be cleared for tissue remodeling to proceed. If not, exudate persists, and healing is delaved.
- What would be the consequence of excessive anti-inflammatory activity?
a) Increased susceptibility to infections
b) Chronic inflammation
c) Both a and b
d) Neither a nor b
Answer: a) Increased susceptibility to infections
Explanation: Suppressing the immune response too much leaves the body vulnerable to infections.
- Which symptom would most likely result from overproduction of leukotrienes?
a) Bronchoconstriction
b) Increased vascular permeability
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Leukotrienes cause bronchoconstriction and increase vascular permeability, leading to edema.
- Which of the following would happen if prostacyclin (PGI2) production is
impaired?
a) Increased platelet aggregation
b) Reduced vasodilation
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Prostacyclin inhibits platelet aggregation and promotes vasodilation, so its absence results in clotting and reduced blood flow.
- What is the most immediate effect if reactive oxygen species (ROS) production is
blocked during phagocytosis? a) Impaired bacterial killing
b) Reduced chemotaxis.
c) Both a and b
d) Neither a nor b
Answer: a) Impaired bacterial killing
Explanation: ROS are essential for killing bacteria inside phagocytic cells.
- How would impaired lymphocyte proliferation affect chronic inflammation?
a) Granuloma formation would be impaired.
b) Antibody production would decrease.
e) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Lymphocyte proliferation is essential for granuloma formation and
antibody production during chronic inflammation.
- What happens if mast cells fail to degranulate during an allergic response?
a) Histamine release decreases.
b) Vascular permeability decreases.
e) Both a and b
d) Neither a nor b
Answer: c) Both a and b
- Which outcome would result from prolonged cytokine release during chronic
inflammation?
a) Tissue destruction
b) Fibrosis
c) Both a and b
d) Neither a nor b
Answer: c) Both a and b
Explanation: Persistent cytokine release contributes to tissue destruction and fibrosis, hallmark signs of chronic inflammation.
