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Pathophys 121-150
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Questions in this quiz (30)
1121. What is one of the immediate compensatory cardiac responses in heart failure?
- Aincreased cardiac lusitropic effect
- Bincreased erythropoiesis
- Cmyocardial hypertrophy
- Dincreased cardiac chronotropic effect
- Eincreased cardiac bathmotropic effect
2122. What are the immediate compensatory cardiac responses in heart failure?
- Aheterometric compensation in resistance overload
- Bheterometric compensation in volume overload
- Cheterometric compensation in resistance and volume overload
- Dhomeometric compensation in resistance overload
- Ehomeometric compensation in volume overload
3123. What is one of the late compensatory cardiac responses in heart failure caused by aortic valve stenosis?
- Aincrease in cardiac inotropic effect
- Bincrease in cardiac dromotropic effect
- Cconcentric myocardial hypertrophy
- Deccentric myocardial hypertrophy
- Eincrease in cardiac bathmotropic effect
4124. What is one of the late compensatory cardiac responses in heart failure caused by mitral valve insufficiency?
- Aincreased cardiac inotropic effect
- Bincreased cardiac dromotropic effect
- Cconcentric myocardial hypertrophy
- Deccentric myocardial hypertrophy
- Eincreased cardiac bathmotropic effect
5125. What is one of the immediate extracardiac compensatory mechanisms in heart failure?
- Ahomeometric hyperfunction with increased cardiac output
- Bincreased amplitude and frequency of respiration mediated by baroreceptors
- Cperipheral vasodilation with redistribution of blood to vital organs
- Dheterometric hyperfunction with increased cardiac output
- Eincreased amplitude and frequency of respiration mediated by chemoreceptors
6126. What is one of the immediate extracardiac compensatory mechanisms in heart failure?
- Ashift of the oxyhemoglobin dissociation curve to the left
- Bhomeometric compensation occurs when there is a resistance overload
- Cperipheral vasodilation with redistribution of blood to vital organs
- Dheterometric hyperfunction with increased cardiac output
- Eshift of the oxyhemoglobin dissociation curve to the right
7127. What late extracardiac compensatory mechanisms are involved in heart failure?
- Aabsolute primary erythrocytosis
- Bhypotonic hyperhydration
- Chypertonic hyperhydration
- Drelative erythrocytosis
- Eabsolute secondary erythrocytosis
8128. How does the structure of hypertrophied myocardium change?
- Aabsolute coronary insufficiency develops
- Brelative coronary insufficiency develops
- Cincrease in the number of cardiomyocytes caused by hypertrophy
- Dhyperplasia of cardiomyocytes with an increased number of cells
- Ehypertrophy of cardiomyocytes with a constant number
9129. How do stroke volume and cardiac output change in heart failure?
- Acardiac output increases and stroke volume decreases
- Bcardiac output decreases and stroke volume increases
- Ccardiac output decreases and stroke volume decreases
- Dcardiac output increases and stroke volume increases
- Ecardiac output decreases stroke volume unchanged
10130. What are the causes of hypervolemia in chronic heart failure?
- AInhibition of the renin-angiotensin-aldosterone system
- BPrimary absolute erythrocytosis
- CRelative erythrocytosis
- DSecondary absolute erythrocytosis
- EActivation of the renin-angiotensin-aldosterone system
11131. What factors determine hypervolemia in chronic heart failure?
- AADH hyposecretion
- Bprimary hyperaldosteronism
- Crelative erythrocytosis
- Dsecondary absolute erythrocytosis
- Ehypersecretion of ADH
12132. What factors determine hypervolemia in chronic heart failure?
- APrimary hyperaldosteronism
- BLow blood renin level
- CRelative erythrocytosis
- DHigh blood renin level
- ESecondary hyperaldosteronism
13133. What consequences does venous stasis induce in circulatory failure?
- Adevelopment of hypooncotic edema with hyperalbuminemia
- Bshift of the oxyhemoglobin dissociation curve to the right
- Cshift of the oxyhemoglobin dissociation curve to the left
- Ddevelopment of osmotic edema due to reduced ADH secretion
- Edevelopment of lymphostatic edema
14134. What are the consequences of venous stasis in circulatory failure?
- Adevelopment of hypooncotic edema due to hypoalbuminemia
- Bdevelopment of hypooncotic edema due to hyperalbuminemia
- Cdevelopment of osmotic edema due to RAAS activation
- Ddevelopment of osmotic edema due to reduced ADH secretion
- Edevelopment of lymphostatic edema due to reduced ADH secretion
15135. What is one of the consequences of portal hypertension in heart failure?
- AVenous hyperemia in the abdominal organs
- BIschemia of the abdominal organs
- CVaricose dilatation of the veins of the legs
- DArterial hyperemia in the abdominal organs
- EDevelopment of cava-caval anastomose
16136. What are the pathogenetic factors of cardiac edema?
- Arenin hypersecretion and secondary hyperaldosteronism
- Brenin hyposecretion and secondary hyperaldosteronism
- Crenin hypersecretion with primary hyperaldosteronism
- Dvasopressin hyposecretion and water retention
- Eatrial natriuretic peptide hypersecretion
17137. What is one of the pathogenetic factors of cardiac edema?
- ADevelopment of hydrostatic edema caused by venous hyperemia
- BDevelopment of osmotic edema caused by primary hyperaldosteronism
- CDevelopment of hydrostatic edema caused by hypoalbuminemia in hepatic congestion
- DDevelopment of osmotic edema caused by hypotonic hyperhydration
- EDevelopment of osmotic edema caused by secondary hyperaldosteronism
18138. What is the impact of decreased NO in vascular remodeling?
- AActivates fibroblasts
- BActivates extracellular matrix metalloproteinases
- CDegranulates mast cells in the intima-muscular media of the vascular wall
- DDegranulates mast cells in the muscular media-adventitial zone of the vascular wall
- EInhibits the transformation of fibroblasts into myofibroblasts
19139. What is the impact of decreased NO in vascular remodeling?
- AIncreases the production of endothelin 1 (ET-1) by stimulating the expression of the ET1 converting enzyme
- BIncreases the amount of endothelin 1 (ET-1) by inhibiting the degradation of ET-1
- CDecreases the expression of ET-1 ETB receptors on the endotheliocyte
- DIncreases the expression of ET-1 ETB receptors on the endotheliocyte
- EFacilitates the storage of ET1 in the extracellular matrix granules of the vascular wall
20140. What is the impact of decreased NO in vascular remodeling?
- AIncreases the expression of angiotensin converting enzyme type 1 (ACE)
- BIncreases the expression of angiotensin converting enzyme type 2 (ACE2)
- CIncreases expression of AT2 receptors to angiotensin II (Ang II)
- DDecreases endothelial NADH oxidase activity
- EIncreases the rate of secretory vascular smooth myocyte
21141. What is the impact of excess endothelin-1 (ET-1) in increasing peripheral vascular resistance?
- AStimulates hypertrophy of the muscular media of the vessel
- BIncreases NO production with vasoconstriction
- CDecreases NO production with vasoconstriction
- DIncreases alpha-2 receptor sensitivity to acetylcholine
- EIncreases alpha-1 receptor sensitivity to acetylcholine
22142. What is the impact of excess angiotensin II (Ang II) in increasing peripheral vascular resistance?
- AStimulates the proliferation of vascular smooth myocytes with a contractile phenotype
- BStimulates the proliferation of vascular smooth myocytes with a secretory phenotype
- CInhibits extracellular matrix metalloproteinases
- DIncreases collagen III production
- EIncreases the sensitivity of the alpha-1 receptor to acetylcholine
23143. What impact does aldosterone have in the pathogenesis of essential arterial hypertension?
- AIncreases the production of oxygen free radicals by activating endothelial receptors
- BIncreases the production of oxygen free radicals by activating myocyte receptors
- CDecreases arginase expression
- DIncreases arginase expression
- EIncreases homocysteine level
24144. What factors induce hyperhomocysteinemia?
- ACastle factor deficiency
- B5-deoxyadenylcobalamin deficiency
- CVitamin B12 deficiency
- DHydrogen peroxide deficiency
- ECalcitriol deficiency
25145. What is the impact of angiotensin 1-7 deficiency in the pathogenesis of essential arterial hypertension?
- AProduces vasoconstriction via mass receptors
- BDecreases the affinity of alpha-1 receptors for norepinephrine
- CDecreases the affinity of AT1 receptors for angiotensin II (Ang II)
- DDecreases NOS3 expression with vasoconstriction
- EIncreases acetylcholine release from parasympathetic axon
26146. What is the role of Ang II in the pathogenesis of essential arterial hypertension?
- AAng II → hyperaldosteronism → plasma hyperosmolarity → ADH secretion → vasoconstriction
- BAng II → hyperaldosteronism → plasma hyperosmolarity → ADH secretion → vasodilation
- CAng II → hyperaldosteronism → plasma hypo-osmolarity → ADH secretion → vasodilation
- DAng II → hyperaldosteronism → hypernatremia → hypervolemia → hypertension
- EAng II → hyperaldosteronism → hypernatremia → hypovolemia → hypotension
27147. What is the main pathogenetic link in renovascular hypertension?
- AActivation of the renin-angiotensin-aldosterone system
- BActivation of the endothelin system
- CExcessive synthesis of vasoconstrictors
- DInactivation of NOSe
- ERenal ischemia
28148. What are the compensatory mechanisms involved in diastolic heart failure?
- AIncreased activity of sarcoplasmic reticulum ATPase (SERCA2)
- BPhospholamban phosphorylation
- CPhospholamban dephosphorylation
- DTroponin I phosphorylation
- EDecreased SERCA2 pump activity
29149. Which hypertrophy is the consequence of the heterometric compensatory mechanism?
- AEccentric hypertrophy
- BConcentric hypertrophy
- CHypertrophy due to cardiomyocyte hyperplasia
- DHypertrophy due to cardiomyocyte hypoplasia
- EHypertrophy cannot be the consequence of the compensatory heterometric mechanism
30150. Which hypertrophy is the consequence of the homeometric compensatory mechanism?
- AEccentric hypertrophy
- BConcentric hypertrophy
- CHypertrophy due to cardiomyocyte hyperplasia
- DHypertrophy due to cardiomyocyte hypoplasia
- EHypertrophy cannot be the consequence of the compensatory heterometric mechanism
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- Quiz on Pathophys 121-150, created by Gin Gin on 11/03/2026.
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- Gin Gin
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