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Pharmaco > Cardiovascular + diuretics > Flashcards

Cardiovascular + diuretics Flashcards

1
Q

What is the effect of vasopressors on a hypovolemic patient

A
  • Venoconstricton -> decreased venous return due to increased resistance to venous flow (and no volume to “push forward”)
  • Arterioconstriction -> increased afterload

=> decreased CO and tissue perfusion despite improved BP

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2
Q

Catecholamine table :)

A

See picture

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3
Q

What is the effect of vasopressors causing venoconstriction on cardiac output

A

Depends on the balance between venous capacitance and venous resistance -> will increase venous return by decreasing venous capacitance but will decrease venous return by increasing venous resistance. Will improve CO in volume-loaded patients vs hypovolemic patients.

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4
Q

What are the actions of dopamine? At what doses?

A
  • Direct alpha- and beta-agonist
  • Precursor of norepinephrine -> other way to stimulate alpha- and beta-adrenergic receptors
  • Stimulation of D1 receptors (post-synaptic) -> vasodilation
  • Stimulation of D2 receptors (pre-synaptic) -> inhibition of norepinephrine release
  • Low dose (1-4 mcg/kg/min) -> mostly vasodilatory dopaminergic effects
  • Medium dose (5-10 mcg/kg/min) -> beta effects predominating
  • High dose (> 10 mcg/kg/min) ->alpha effects predominating

(But overall causes a modest vasoconstriction and increase in BP with little increase in CO)

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5
Q

What is a potential adverse effect of dobutamine in cats

A

Seizures -> use lower range of doses (5-10 mc/kg/min)

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6
Q

What is the mechanism of action of ephedrine

A
  • Increases release of norepinephrine from sympathetic nerve endings
  • Has some direct beta-agonist effects
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7
Q

What is the risk with repeated / prolonged use of ephedrine

A

Exhaustion of stores of endogenous norepinephrine -> decreased efficiency

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8
Q

What catecholamine has the longest duration of action and can be used as a “push-dose” (= bolus)

A

Phenylephrine

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9
Q

List and explain 3 metabolic / electrolytic effects of catecholamines

A
  1. Hyperglycemia
    - Alpha effects -> decreased insulin production, increased glycogenolysis
    - Beta effects -> increased glucagon and cortisol synthesis + stimulation of lipolysis
  2. Hypokalemia
    - Stimulation of Na/K ATPase -> K entry into cells
  3. Hyperlactatemia
    - Increased glycolysis
    +/- Mitochondrial dysfunction
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10
Q

What is the effect of catecholamines on the immune system

A

Mostly immunosuppressive effect

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11
Q

What is the mechanism of action of vasopressin on vascular smooth muscle

A
  • Stimulation of Gq receptors -> activation of phospholipase C -> IP3 pathway -> increased intracellular iCa -> contraction
  • Inhibition of K-ATPase in vascular smooth muscle cells -> prevents hyperpolarization and allows depolarization
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12
Q

List all the receptors of vasopressin and their locations

A
  • V1: vascular smooth muscle (-> contraction) + platelets (->activation via calcium entry)
  • V2: basolateral membrane of distal tubule cells and in principal cells (-> AQP2 synthesis and expression + urea transporter expression) + vascular endothelium (-> release of vWF and fVIII) + bone marrow (-> release of platelets)
  • V3: anterior pituitary (-> release of ACTH) + CNS (memory, BP, temperature, sleep)
  • Oxytocin receptor (-> uterine contraction + mammary contraction + vasodilation of umbilical vein, aorta, pulmonary artery)
  • P2 class of purinoreceptors (-> NO-mediated and prostacyclin-mediated vasodilation + positive inotropy)
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13
Q

Name 2 selective V1 receptor agonists and 1 selective V2 receptor agonist

A

V1: Terlipressin, selepressin

V2: Desmopressin

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14
Q

What are the different indications of vasopressin therapy and associated doses

A

See picture

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15
Q

Name 3 effects of ACE inhibitors contributing to their anti-hypertensive effect

A
  • Vasodilation due to decreased angiotensin II (venodilation and arteriodilation)
  • Decreased aldosterone -> less retention of Na and water
  • Decreased metabolism of bradykinin -> further vasodilation
  • Decrease proteinuria (ATII promotes glomerular protein loss through preferential efferent constriction)
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16
Q

Why is amlodipine not recommended as a sole agent for management of hypertension due to glomerular disease

A

Amlodipine causes vasodilation of afferent arteriole preferentially -> increased glomerular pressure and GFR -> risk of worsening glomerulopathy

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17
Q

Name 2 non-selective beta-blockers and 2 selective beta-blockers

A

Non-selective:
- Propranolol
- Timolol
(- Sotalol)

Selective (b1):
- Esmolol
- Atenolol

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18
Q

Mechanism of action of hydralazine

A

Alteration of smooth muscle intracellular calcium metabolism -> decreased vascular resistance

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19
Q

Mechanism of action of sodium nitroprusside

A

Releases NO -> NO activates guanylyl cyclase in endothelial cells -> increased cGMP -> decreases intracellular iCa -> relaxation

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20
Q

What vessels (arterioles vs veins) are dilated by nitroprusside / nitroglycerin / hydralazine

A
  • Nitroprusside: both arteries and veins
  • Nitroglycerin: both but mostly veins
  • Hydralazine: almost exclusively arteries
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21
Q

True or false: Sodium nitroprusside and nitroglycerin can cause cyanide toxicity

A

False.
Nitroprusside only.

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22
Q

What potentially anti-hypertensive drug category should never be used as a sole agent in dogs with pheochromocytoma

A

Beta-blockers (will lead to worse hypertension due to un-opposed vasoconstriction from alpha effect)

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23
Q

Mechanism of action of fenoldopam

A

Selective agonist of dopamine-1 receptor -> peripheral and renal vasodilation (due to Gs receptor effect: increase in cAMP -> myosin light chain phosphatase ->vasodilation)
+ increased GFR
+ decreased Na reabsorption

24
Q

Name one mixed alpha- and beta-antagonist

A

Labetalol
(-> decreases BP due to decreases vascular resistance and prevents reflex tachycardia)

25
Q

Mechanism of action of pimobendan

A
  1. Calcium sensitizer:
    Increases the affinity of the regulatory site on troponin C for calcium -> increased calcium binding -> increased interaction between actin and myosin -> increased cardiomyocyte contraction -> positive inotropy + lusitropy
  2. Phosphodiesterase III inhibitor -> increased cAMP and cGMP

cAMP -> activation of protein kinase in cardiomyocytes leading to increased calcium influx during systole and increased calcium sequestration during diastole -> positive inotropy

cAMP and cGMP -> increased calcium uptake in vascular smooth muscle -> decreased intracellular calcium -> relaxation
(+ cAMP activates MLCP -> relaxation)

Suppresses production of NO –> increase cardiac contractility

26
Q

What is the benefit of pimobendan vs. catecholamines to increase cardiac contractility

A

Pimobendan does not increase myocardial oxygen consumption and does not cause arrhythmias.

27
Q

What are the overall effects of pimobendan

A
  • Positive inotropy
  • Positive lusitropy
  • Arterial and venous vasodilation
    +/- platelet inhibitor (nothing proven at clinical doses)
28
Q

What is the metabolism / elimination of pimobendan

A
  • Metabolized to an active metabolite in the liver
  • Eliminated mostly in the feces (minimal renal excretion)
29
Q

Indicate on which phases of the action potential the different classes of anti-arrhythmics work

A
  • Class IA -> inhibit phase 0 + prolong phase 3
  • Class IB -> inhibit phase 0 + shorten phase 3
  • Class II -> inhibit phase 2 + inhibit phase 4 in nodes
  • Class III -> inhibit phase 3
  • Class IV -> mostly inhibit phase 0 in nodes
30
Q

What is the effect on the duration of action potential of anti-arrhytmics of class IA, IB, II, III, IV

A

IA: prolongs
IB: shortens
II: no change
III: prolongs
IV: no change

31
Q

What is a proposed anti-arrhythmic mechanism of MgSO4

A

Blocks Na, Ca, and K channels
Cofactor of Na/K ATPase

32
Q

What are the 2 currents inhibited by beta-blockers responsible for their anti-arrhythmic properties

A
  • Funny Na current (If)
  • L-Ca current
33
Q

What is the only diuretic that does not reach its site of action through the urinary space

A

Spironolactone

34
Q

Why is the efficiency of most diuretics decreased in case of severe proteinuria

A

Most diuretics except mannitol are highly protein-bound -> hypoproteinemia leads to lower plasma concentration of diuretic + the small portion that does get secreted in the urine binds proteins in the urine and get neutralized

35
Q

Name a few effects of mannitol that are theoretically beneficial for the kidneys

A
  • Prostaglandin-mediated renal vasodilation
  • Decreased renal vascular congestion
  • Decreased hypoxic cellular edema
  • Protection of mitochondria and decreased oxidative damage
36
Q

Name the 6 classes of diuretics, their site of action, and their effect on electrolytes and minerals

A

See table

37
Q

What is the mechanism of action of acetazolamide and its indiction

A

Carbonic anhydrase inhibitor (cytosolic and membrane) in the proximal tubule -> inhibits reabsorption of HCO3- and Na+ in proximal tubule
Limited effect because HCO3- quickly gets less filtered and Na gets reabsorbed more distally

Indicated in management of glaucoma because decreases production of aqueous humor

38
Q

Name 2 mechanisms of resistance to furosemide

A
  • Increased Na reabsorption in distal tubule and collecting duct
  • Short half life of furosemide -> rebound Na reabsorption between doses
39
Q

What are the mechanisms of diuresis induced by furosemide

A
  • Inhibition of Na-K-2Cl transporter ->decreased reabsorption of Na and Cl ->decreased reabsorption of water
  • Inhibition of Na-K-2Cl transporter -> decreased osmolarity of interstitium -> loss of cortico-medullary gradient
  • Inhibition of Cl flux to macula densa -> decreased tubuloglomerular feedback
40
Q

Mechanism of action and indications of thiazide diuretics

A
  • Inhibition of Na-Cl transporter in distal tubule
  • Indicated for prevention of urolithiasis (decrease calciuresis) + can have a paradoxical anti-diuretic effect in diabetes insipidus (by decreasing circulating volume)
41
Q

Name 3 potassium-sparing diuretics

A
  • Spironolactone
  • Amiloride
  • Triamterene
42
Q

Name a new class of aquaretic diuretics

A

Vaptans = V2 receptor inhibitors

43
Q

Name indications of diuretic therapy and their associated diuretics

A

See table

44
Q

List 2 adverse effects of ACE inhibitors

A
  1. Worsening GFR and renal function through dilation of efferent arteriole in dehydrated patients (or if diuretics on board)
  2. Hyperkalemia (inhibition of aldosterone) - unlikely clinically relevant
45
Q

What is the mechanism of action of spironolactone?

A

Selective aldosterone antagonist, blocks its effects in distal convoluted tubule and collecting duct

May block detrimental effects of aldosterone on the vasculature and cardiac remodeling

46
Q

What is the mechanism of action of amlodipine?

A

Calcium channel blocker –> decreases calcium flux into vascular smooth muscle cells –> vasorelaxation and reduces SVR

47
Q

Name 2 selective alpha-1 receptor antagonists

A

Prazosin
Phenoxybenzamine

48
Q

What is the mechanism of action of atenolol?

A

Selective beta-1 antagonist –> decreases HR an contractility + decreases renin release and PVR

49
Q

List 5 categories of oral antihypertensives

A
  1. ACE inhibitors
  2. Angiotensin receptor blockers
  3. Aldosterone antagonists
  4. CCB
  5. Alpha-1 blockers
  6. Beta-1 blockers
  7. Arteriol vasodilators
50
Q

If injectable antihypertensives are not available, what medications can be considered to address a hypertensive crisis?

A

Oral hydralazine or amlodipine as they have rapid onset of action

51
Q

What physiological conditions enhance lidocaine’s mechanism of action?

A
  • Acidosis
  • Hyperkalemia
52
Q

List 3 contraindications of using beta-blockers

A
  • Evidence of sinus node dysfunction
  • AVN conduction disturbances
  • CHF
  • Pulmonary disease
53
Q

What is the mechanism of action of stall and how does it vary with dose?

A

Beta-blocker + sinus and AVN depression at lower doses

Inhibition of depolarization (I kr)

54
Q

Why is sotalol’s negative inotropic effect less than expected?

A

Prolongs action potential duration –> can result in enhanced Ca entry during action potential plateau

55
Q

What are adverse effects of amiodarone?

A
  • Vomiting
  • Anorexia
  • Hepatopathies
  • Thrombocytopenia
  • Effects of vasoactivee solvent of IV formulation –> hypotension, anaphylaxis, bradycardia, acute hepatic necrosis, death
56
Q

Why is lidocaine not effective in SVT?

A

Atrial myocytes lack plateau phase –> fewer inactivated Na channels blocked by lidocaine (which works by inhibiting Na channels)

57
Q

With which drug should digoxine be combined in order to adequately slow the ventricular rate?

A

Diltiazem

Pharmaco (7 decks)

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