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4. HF Flashcards

1
Q

What are the co-morbidities that can contribute to HF?

A
  1. Hyperthyroidism
  2. Anemia
  3. AF
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2
Q

Which drugs can ⬇️ mortality in patients with LVSD ?

A
  1. ACEi
  2. Bb’s
  3. Sporonolactone
    4 ARB’s
  4. Hydralazine or nitrate combs
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3
Q

What does digoxin do in morbidity and mortality?

A

⬇️ morbidity
⬇️hospital admissions
🚫 benefit on mortality

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4
Q

What is used for the T of acute HF?

A
  1. IV opiates : reduce anxiety & preload
  2. High flow of O2 with IV furosemide / IV GTN & nesiritide: Treat breathlessness
  3. Digoxin : control AF
  4. Amiodarone : Ventricular arrhythmias
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5
Q

What is the MoA of digoxin ?

A
  1. Inhibition of Na+/K+ ATPase : ( in HF )
    A. ⬆️ Na+ intracellular levels and ⬇️ K+ intracellular levels
    B. The conc gradient on the Na+/Ca+2 exchanger ⬇️ —> Na is ⬆️ in the cells so no Na+ enters —> as a result no Ca+2 goes out in exchange with Na+ —> free Ca+2 and SER get loaded with Ca+2
    C. If there is impulse to the muscle —> massive release of Ca+2 —> more interaction between actin and myosin —> ⬆️ contractility
    D. +ve inotropic effect
    E. Generally, this happens bcz digoxin and K+ compete for the Same bonding site so, if the patient with HF is has ⬆️ levels of K+ he will overcome digitalis effect but if he is hypokalemic digoxin will have toxic effects
  2. Inhibition of SNS & ⬆️ PS vagal tone leading to : ( in supra ventricular arrhythmias )
    A. -ve chronotropic effect —> bradycardia
    B. Suppresses AV nodal activity
  3. Autonomic effects : ⬆️ vagal tone —> posses PNS activity
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6
Q

What are the autonomic effects of digoxin on the SA node, AV node , atrial muscle , and ventricular muscle & purkinje?

A

SA node: ⬇️ automaticity ⬇️HR - ⬆️RR

AV node: ⬇️ conduction velocity and ⬆️ refractory period- ⬆️PR

Atrial muscle: ⬇️ refractory period

Ventricular & purkinje: slight ⬇️ of refractory period - ⬆️QR

At ⬆️⬆️ doses —> ⬆️ sympathetic activity which causes
A. Atrial arrhythmia
B. DAD —> ventricular tachycardia & fibrillation

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7
Q

When digoxin I’s a 1st line drug?

A

In patients with congestive HF with AF

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8
Q

What are the indications & effects of digoxin ?

A
  1. adjunct therapy in patients with moderate to severe HF who remain symptomatic with LVSD despite adequate doses of ACEI & diuretic treatment.
  2. No effect on survival improvement ( mortality )
  3. improvement of functional status
  4. reduction of hospitalization.
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9
Q

What are the doses of digoxin?

A
  1. Target 0.5 - 2 ng/ml
  2. Initiated & maintained at 0.125 - 0.25 mg/day
  3. In AF patients —> higher doses -0.8-2 ng/ml
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10
Q

What are the pharmacokinetics of digoxin?

A
  1. Narrow therapeutic index —> 2!
    Therapeutic levels 0.5-2 ng/ml.
    Toxic signs seen at Cp > 3 ng/ml.
  2. Good absorption
    bioavailability ~75%
    T1/2 36 hrs.
  3. Elimination by kidney (90%)
    needing dose reduction in RF patients (substitute with digitoxin bcz have longer onset of action & drug life )
  4. Metabolism partially attributed to bacterial flora in GIT (interactions with antibacterial drugs).
  5. Levels are affected in hypo/hyperkalemic patients.
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11
Q

What are the cardiac & extra cardiac effects of digoxin?

A 
1. Cardiac 
A. Arrthymia 
B. Sinus bradycardia
C. AV block
D. Atrial arrhythmia
E. Ventricular tachycardia
F. Ventricular fibrillation
  1. Extra cardiac:
    A. GI: N / V / D ( + anorexia = early syms of toxicity )
    B. CNS : Diorientation and hallucination
    C. Visual: blurred and yellow- green
    D. Endocrine: gynecomastia at therapeutic doses
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12
Q

How to treat digoxin toxicity?

A
  1. Restoring K+ levels to normal (KCl administration)
  2. Lidocaine (ventricular arrhythmia) & atropine (bradycardia)
  3. Anti-digoxin antibodies (Digiband in Emergency) —> in hospital setting
  4. Withdrawals: cause deterioration of clinical status and exercise capacity and increased hospitalization. But dose reduction is possible instead of complete cessation
  5. Digitalis competes for K binding at Na/K ATPase
  6. Hypokalemia: increase toxicity (loop diuretics)
  7. Hyperkalemia: decrease toxicity
  8. Hypercalcemia: increases toxicity
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13
Q

What are the conds that lead to enhanced potential for digitalis cardiotoxicity/ interaction with digoxin ?

A 
1. Drugs that ⬆️ digitalis levels 
A. Amiodarone
B. Erythromycin
C. Quinidine 
D. Tetracycline
E. Verapamil 
F. Propafone
G. CCB
H. 
( A/E/F —> related to renal clearance & mycins are related to absorption bcz they inactivate the metabolic enteric bacteria )
2. Drugs that ⬇️ K levels 
A. Corticosteroids
B. Loop & thiazides diuretics 
C. B2 agonists 
D. Amphotericin B
  1. BB —> cause heart block
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14
Q

What is the MoA of PDEi?

A
  1. ⬆️ cAMP levels —> +ve inotropic effect
  2. Mixed arterial and venous dilation
  3. Inodilators —> both inotropic and vasoD effects
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15
Q

What are the types if PDEi?

A

Different PDE’s, with PDE-3 isoenzyme having the most beneficial
effect on both cardiac and smooth muscle.

  1. Selective PDE-3 i —> amrinone & milrinone ( suffix is none but they are selective )
  2. Non-selective —> theophylline
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16
Q

What is the indication of using PDEi?

A

Short-term management of severe HF not resp to other therapies

Short-term bcz they are not disease modifying agents

Used only IV bcz of ⬆️ in mortality after oral dose and thrombocytopenia

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17
Q

What are the BB and what is their MoA?

A

Only carvedilol, bisoprolol, nebivolol, and metoprolol SR are used.

Ø Acts primarily by inhibiting the sympathetic nervous system.
Ø Up-regulation of b1-receptors.
Ø Decrease cardiotoxicity of catecholamines (apoptosis).
Ø Reduce cellular morphology and myocardial modeling.
Ø Decrease neurohormonal activation.
Ø Anti-arrhythmic properties.
Ø Anti-oxidant properties.
Ø Reduce mortality by 30% or more in patients with HF
Ø reduce hospitalization

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18
Q

What are the ACEi and what is their MoA?

A

End with pril

* improve :
mortality
morbidity
exercise tolerance
left ventricular ejection fraction.
  • ⬇️ preload & afterload
  • Beneficial effects on HF may be also related to kinin-mediated PG production —> modify cardiac remodeling more favorably than ARB
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19
Q

What are the indications of ACEi?

A
  1. First line treatment for all grades of HF due to LVSD, including asymptomatic patients.
  2. Can alleviate symptoms, improve clinical status, quality of life, and survival in mild to severe LV dysfunction patients (16-40%), with or without CAD.
  3. Normally used with BB & diuretics (if fluid retention exist), as ACEI efficacy and side effects depend on fluid retention.
  4. All ACEIs are efficacious, even though enalapril is mostly studied in trials.
  5. They reduce morbidity & mortality in HF or post-MI populations.
  6. Clinical response is usually delayed for weeks or months
  7. ⬆️ doses are more eff than ⬇️ doses in relation to mortality ⬇️
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20
Q

What is used with ACEi and what Can’t be used?

A

Can : BB & diuretics —> if fluid retention

add BB before target dose of ACEi is reached

Can’t (C/I) :
A. Previous exposure to angiodema
B. Anuric renal failure
C. Pregnant women

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21
Q

Cautions of ACE I?

A

SBP < 80,
increased serum creatinine levels > 3 mg/dL
bilateral renal stenosis
elevated K levels (> 5.5 mmol/L).

Start with small dose then increase

SUDDEN withdrawl should be avoided unless C/I

22
Q

What are the AE of ACEi?

A

§ Dry irritating persistent cough

§ Hyperkalemia (that’s why it is used with caution in patients with elevated K levels ) —> can eliminate the need of K+ supplements

§ Angioedema (5xmore in African populations, due to increased bradykinin) bcz C/I in patients with history of angioedema

§ Fetal toxicity —> teratogenic —> C/I in pregnant

23
Q

What’s are the ARBs?

A

VELOCIT and all end with spartan

24
Q

What is the MoA of ARBs?

A
  1. Block AT1 receptors ( cause vasoconstriction & proliferating action )

and not AT2 ( cause vasodilation & anti-proliferative action )

  1. Competitive antagonist so if you put enough ANGII to this sys you can overcome the effect of AT1 receptor blocker
  2. Hemodynamic & neurohumoral effects similar to ACEI, but much less experience in HF patients
  3. ⬇️mortality & hospitalization in P with LVD
25
Q

What are the indications for ARBs and dose

A

In patients intolerant to ACEi

Same criteria of dose initiation —> Add BB along with ARB

Vallarta’s 20mg BID —> maximal dose of 160mg BID

26
Q

Can we combine ACEi & ARBs ?

A

may produce more reduction of LV size than either agent alone and decrease hospitalization in chronic therapy, but ⬆️ side effects may result.

No 🚫 of ACE

No cough

27
Q

What are the indications for loop diuretics ? And give ex

A

Chronic symptomatic HF patients to relieve pulmonary and peripheral edema and reduce jugular venous pressure & weight

—> RAPIIIIIDDD

Ex:
1. Furosemide most commonly used one

  1. Torsemide favorable also due to
    A. Superior abs
    B. longer duration of action
28
Q

What is the MoA of loop diuretics?

A
  1. Blockage of the Na+ resorption in the loop of the Henley —> ⬆️ Na+ excretion up to 25% of the filtered load of Na+ unless renal function I’s impaired —> High-ceiling agent —> dose dependent
  2. Loop and thiazides Cause hypokalemia —> reduced by K sparing diuretics BUT may produce hypovolemia and postural hypotension at ⬆️ doses
  3. Improve cardiac function, syms, and exercise capacity
  4. Eff on mortality and morbidity are not known
29
Q

What is the diff btwn loop and thiazides diuretics?

A

Loop diuretics increase Na+ excretion up to 25% of the filtered load of Na+ and maintain their efficacy unless renal function is severely impaired.

In contrast, thiazide diuretics increase Na+ excretion to only 5-10% of the filtered Na+ load and lose their efficacy in patients with RF (Cr Cl < 30 ml/min).

Therefore, loop diuretics are more efficacious than thiazide in HF patients.

30
Q

When the dirutic become unresponsive?

A

may occur due to

  1. consumption of large amount of Na+
  2. consumption of large amount or NSAIDs
  3. impaired renal function.

This could be overcome by adding 2 ore more diuretics. E.g. metolazone (a thiazide diuretic).

31
Q

What is special about diuretics compared to ACEi and digitalis?

A

Can adequately control fluid retention of HF

Bcz digitalis and ACEi cannot control Na+ balance

32
Q

Info about loop diuretics?

A
  1. Optimal use of diuretics is a key element in the success of
    other drugs to treat HF.
  2. Clinical progression of HF may require increasing doses of diuretics due to slow absorption and a decline in renal perfusion.
  3. Continued elevation of jugular venous pressure usually suggests a need for more diuretic.
33
Q

What is the MoA aldosterone antagonists AA? Give ex

A

Include spironolactone and eplerenone

ØDecrease Na+/water retention (edema reduction).
ØDecrease K+/Mg+ excretion (prevent arrhythmias)
ØDecrease Collagen deposition (prevent myocardium/vessel fibrosis)

34
Q

When does AA ⬆️ risk of hyperkalemia?

A

When combined with ACEi at a dose > 50 mg

At lower dose —> 25mg it has a little effect on K and provide significant reduction in mortality

35
Q

What are the SE of AA?

A

Fluid depletion
hyperkalemia (counsel patients regarding high K+ food)
worsen renal failure

36
Q

What are nitrates & hydralazine ?

A

Hydralazine ⬇️ afterload to achieve a balanced effect on venous & arterial circulation with nitrate —> ⬇️preload & afterload —> ⬆️CO

Comb is eff in ⬇️ mortality but not as ACEi

37
Q

What up is the dose of nitrates / hydralazine and to whom is it given?

A

Hydralazine 300mg daily

Isosorbide dinitrate 160mg daily

Used only in patients who are intolerant to ACEi or is C/I

38
Q

What is the use of GTN in HF treatment?

A

IV GTN is used with loop diuretics like furosemide to relieve pulmonary congestion

39
Q

What are the hemodynamics effects of nitrates?

A
  1. Venous vasodilation —> ⬇️ preload
    A. ⬇️ pulmonary congestion
    B. ⬇️ ventricular size
    C. ⬇️ ventricular wall stress
  2. Coronary vasodilation —> ⬆️myocardial perfusion
  3. Arterial vasodilation —> ⬇️afterload
    A. ⬆️CO
    B. ⬇️ BP
40
Q

What is nesiritide ?

A

It is a vasodilator

Synthetic analogue of the endogenous peptide BNP

BNP ⬆️ —> in HF patients

41
Q

What is the MoA of nesiritide ?

A

It is a vasodilator —>
A. ⬆️cGMP in the smooth muscle cells ( like nitrates )
B. ⬇️venous and arteriolar tone

42
Q

What are the indications for nesiritide?

A

acute decompensated congestive HF who have dyspnea at rest bcz
A. It reduces pulmonary capillary wedge pressure
B. improves dyspnea and fatigue

NOT USED TO REPLACE DIURETICS

43
Q

What are the SE of nesiritide ?

A

Excessive hypotension

May worsen renal damage

44
Q

What are the inotrotropic agents/vasodilators? And what are it’s indications?

A

Include Digoxin and some NT: dopamine, adrenaline, and noradrenaline.

They are used for acute HF in hospital settings bcz they are not disease modifying agents

Direct-acting vasodilators such as sodium nitroprusside is
rarely used except in acute setting of HF.

45
Q

What are dopamines? What are there effects ?

A

Neurotransmitter that has inotropic and vasodilator effects .

At low doses —> stimulate D1 receptors

At moderate doses —> stimulate B1 receptors

At high doses —> stimulate Alfa-adrenergic

46
Q

What is dobutamine ?

A

It is a predominant B1 agonist effect with modest peripheral vasoD

BEST INODILATORS

47
Q

Inodilators use depends on?

A
  1. Tolerance on prolonged administration

2. ⬆️ risk of arrhythmia

48
Q

What is the MoA of ivabradine and what is the overall effect ?

A

Is a hyperpolarization-activated cyclic nucleotide-gated channel blocker that reduces the pacemaker activity of SA node by inhibiting “If” current —> resp for the ⬆️ in slope in phase 4

If is funny bcz it is opened by hyperpolarization while the others close

⬇️ HR with no effect on ventricular repolarization and no negative inotropic effect —> ⬇️ risk of morbidity but NOT mortality

49
Q

What are the indications for ivabradine ?

A

Reduce hospitalization risk of for worsening HF in stable HF patients

50
Q

What are the pharmacokinetics related to ivabradine?

A

ORALLY

2times/day

1ry metabolized by CYP3A4 in the liver

51
Q

What are the SE of ivabradine?

A
  1. BRADYCARDIA from the name
  2. HTN
    E. Visual impairment
  3. AF
52
Q

What do you know about the comb of Valsartan + sacubitril ? ( ENTRESTO = interesting 🤔)

A

When compared to enalapril —> it was superior in ⬇️ CV death or hospitalization for HF

INDICATIONS: in CHF AND ⬇️ EF

DOSE: orally twice daily

Pharma (5 decks)

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