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HLB > Drugs for IHD and Heart Failure > Flashcards

Drugs for IHD and Heart Failure Flashcards

1
Q

Core Drug: Digoxin: Mechanism of Action:

A
  • inhibits the Na+/K+ ATPase channel
  • binds to the extracellular K+ binding site
  • increases intracellular Na+
  • Na+ and Ca2+ exchange through
    exchanger (Na+ out, Ca2+ in)
  • increased intracellular Ca2+
  • increased ionotropy
  • increases force of contraction and
    contractility of the heart
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2
Q

Core Drug: Digoxin: What tissues/organs it acts on?

A
  • SA node
  • AV node
  • cardiac muscle
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3
Q

Core Drug: Digoxin: Physiological effects:

A
  • slows the heart rate
  • increases contractility
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4
Q

Core Drug: Digoxin: side effects:

A
  • DOES NOT DECREASE BP
  • arrhythmias especially with hypokalaemia
  • xanthopsia = colour vision deficiency,
    mostly see yellow
  • anorexia
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5
Q

Core Drug: Digoxin: Interactions:

A
  • many drugs increase toxicity
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6
Q

Core Drug: Digoxin: Pharmacokinetics:

A
  • orally active
  • requires loading dose
  • half life c. 36 hours
  • narrow therapeutic window
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7
Q

Core Drug: Digoxin: Clinical Use:

A
  • end stage heart failure sometimes
  • to slow heart rate in atrial fibrillation, very
    commonly
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8
Q

Core Drug: “Digoxin Effect”:

A

reverse tick on ECG
not necessarily toxic

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9
Q

Core Drug: Digoxin: specific antidote:

A

Digibind
for too much digixin causing toxicity

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10
Q

Digoxin is from which plant

A

foxglove

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11
Q

Core Drug: digoxin: Mechanism of action diagram:

A
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12
Q

Heart Failure Pathophysiology:

A

INSERT DIAGRAM

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13
Q

Therapeutic Targets for heart Failure Drugs:

A

insert slide

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14
Q

Therapeutic Targets for angina drugs:

A

insert slide

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15
Q

Core Drug: Furosemide: Mechanism of action:

A
  • blocks Na+/K+/Cl co transporter in the thick ascending limb of the loop of henle
  • blocks the Cl- channel of the cotransporter
  • increased loss of: Na+, K+, Cl- and WATER
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16
Q

Core Drug: Furosemide: clinical uses:

A
  • much more powerful than other diuretics
  • used to clear peripheral oedema
  • used intravenously for acute pulmonary
    oedema
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17
Q

Core Drug: Furosemide: Pharmacokinetics:

A
  • “Lasix” = lasts for 6 hours
  • route of administration?
  • therapeutic window?
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18
Q

Core Drug: Furosemide: Side Effects:

A
  • dehydration
  • renal impairment
  • hypokalaemia
  • hyponatraemia
  • hypomagnesaemia
  • hyperuricaemia (high uric acid, causes
    gout)
  • auditory nerve damage (especially high
    doses and renal impairment)
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19
Q

Core Drug: Ramipril: mechanism of action:

A
  • ACE inhibitors (improves prognosis,
    mortality and quality of life)
  • blocks conversion of angiotensin I to
    angiotensin II
  • and blocks break down of Bradykinin
    (vasoactive peptide)
  • hence decrease in angiotensin II and increase in bradykinin peptide
20
Q

Core Drug: Ramipril: Physiological effects:

A
  • arteriolar dilation:
    - decreases after load, left
    ventricle has to pump more, increases
    speed of contraction
  • venodilation:
    - decreases preload
    - descending LA pressure
  • decrease in aldosterone and ADH, hence
    decrease in fluid retention
21
Q

Core Drug: Ramipril: clinical uses:

A
  • most commonly used drug to treat heart
    failure
  • also used for hypertension
22
Q

Core Drug: Ramipril: side effects:

A
  • dry cough (bradykinin accumulation in
    lungs)
  • renal impariment
  • hyperkalaemia: commonly given with a
    diuretic
23
Q

Core Drug: Ramipril: pharmacokinetics:

A
  • route of administration?
  • dosage: once daily dosage
  • therapeutic window?
  • half life?
24
Q

Core Drug: Losarten/Candesarten: mechanism of action:

A
  • blocks action of angiotensin II on the
    angiotensin I receptor
25
Q

Core Drug: Losarten/Candesarten: physiological effects:

A
  • arteriolar dilation:
    - decreases after load, left
    ventricle has to pump more, increases
    speed of contraction
  • venodilation:
    - decreases preload
    - descending LA pressure
  • decrease in aldosterone and ADH, hence
    decrease in fluid retention

SAME AS ACE INHIBITORS

26
Q

Core Drug: Losarten/Candesarten: side effects:

A
  • DECREASE IN DRY COUGH COMPARED TO
    ACE-Is
  • renal impariment
  • hyperkalaemia: commonly given with a
    diuretic

SIMILAR TO ACE INHIBITORS

27
Q

Core Drug: Losarten/Candesarten: pharmacokinetics:

A
  • route of administration
  • dosage
  • half life
  • therapeutic window
  • used in a fixed dose combination
28
Q

Core Drug: Losarten/Candesarten: clinical uses:

A
  • most commonly used for heart failure
  • alternative for patients intolerant of ACE
    inhibitors
29
Q

Core Drug: Spironalactone: Mechanism of action:

A
  • blocks the upregulation of Na+ channels in
    the DCT by aldosterone
30
Q

Core Drug: Spironalactone: physiological effects:

A
31
Q

Core Drug: Spironalactone: side effects:

A
  • impaired renal function
  • hyperkalaemia
  • glynaecomastia (structurally similar to
    oestregen)
  • causes men to grow breasts
32
Q

Core Drug: Spironalactone: clinical uses:

A
  • prognostic benefit in:
    - very poor LV function
    - post MI (esp with acute heart failure)
33
Q

Core Drug: Spironalactone: pharmacokinetics:

A
  • route of administration
  • dosage
  • half life
  • therapeutic window
34
Q

Eplerenone vs spironolactone

A

fewer side effects in eplerenone

35
Q

over activation of sympathetic nervous system in heart failure results in (3) physiological processes

A

insert diagram

36
Q

Positive ionotropes associated with what in heart failure

A

increased mortality

37
Q

Heart failure and the adrenergic system:

A
  • positive inotropes uniformly associated with increased mortality
  • malignant arrhythmias
  • catecholamine cardiotoxicity:
    - structural/functional cardiomyocyte
    changes
    - LV dilation and adverse remodelling
    - some are pressors = cause
    vasoconstriction
  • activate RAAS
38
Q

adrenoreceptor activation

A

insert slide

39
Q

Core Drug: Bisoprolol & Propranolol : Mechanism of action:

A
40
Q

Core Drug: Bisoprolol & Propranolol: physiological effects:

A
  • slow heart rate <70bpm
    - increased diastolic filling time
  • reduced afterload (lower BP)
  • reduced renin release: reduces RAAS
    activation
  • do not affect contractility (once patient is
    stabalised):
    - no effect on contractility in the
    absence of catecholamines (NAdr,
    Adr)
    - unlike calcium channel blockers
  • substantial mortality benefit (35%
    reduction)
41
Q

Core Drug: Bisoprolol & Propranolol: clinical uses:

A
42
Q

Core Drug: Bisoprolol & Propranolol: side effects:

A
43
Q

Core Drug: Bisoprolol & Propranolol: pharmacokinetics:

A
  • route of administration
  • dosage
  • half life
  • therapeutic window
44
Q

Ivabradine used for and how

A
  • heart failure
  • slows the heart by blocking the i (small f)
    channel in the SA node
45
Q

Sacubitril used for, how take, what does it do

A
  • neprilysin inhibitor
  • used with valsartan in fixed dose
    combination
  • slows heart rate?
46
Q

Dapaglifozin used for and what does it do

A
  • heart failure
  • inhibits glucose reabsorption in the kideny

HLB (49 decks)

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