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Pharm 1 - SP19 > 29 - CHF drugs > Flashcards

29 - CHF drugs Flashcards

1
Q

_ heart failure occurs when the heart muscle cannot efficiently pump blood out of the heart

A

systolic

weakened heart muscle, can’t squeeze as well - less blood pumped out of ventricles

ventricles still fill, but only 40-50% of blood pumped out compared to normally 60%

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2
Q

_ heart failure occurs when the heart muscles are stiff, the hearts chambers do not properly fill up with blood

A

diastolic

stiff heart muscle can’t relax normally - less blood fills the ventricles

ventricles fill with less blood than normal - ventricles still pump out 60% of blood - but 60% of a lesser volume

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3
Q

Heart failure is a condition in which the heart can’t _ to meet the body’s needs. In some cases, the heart can’t fill with enough blood. In other cases, the heart can’t
pump blood to the rest of the body with enough
force. Some people have both problems.

A

pump enough blood

Much of the tx is superficial

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4
Q

causes of heart failure

MI, coronary artery disease, valve disease, idiopathic, viral/bacterial, myocarditis, pericarditi, arrhytmias, chronic hypertension, thyroid, pregnancy, septic shock

big picture?

A

big picture is that some of these causes are choices/preventable some we have no say over can’t do anything about

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5
Q

An action potential in skeletal or cardiac muscle triggers
muscle contraction.
This is called _.

In cardiac muscle, contraction is the result of _ from
depolarization causing the release of more Ca++ from the
sarcoplasmic reticulum. The liberated Ca++ binds to troponin
leading to a change in the interaction between actin and
tropomyosin, exposing sites on the actin filament for myosin.
Myosin pulls on the actin as it hydrolyzes ATP, contracting the
muscle.

A

excitation-contraction coupling

cardiac - Ca++ influx

Ca++ induced Ca++ release

  • Ca exposes binding sites
    Different than sketal and SM
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6
Q

Depolarization of the cardiac myocyte leads to opening of

_ channels

A

voltage gated Ca++

Skeletal muscle
and cardiac
muscle similar,
but things happen
much faster in
skeletal muscle
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7
Q

cardiac muscle

Ca++ influx from the voltage gated Ca++ channel activates
_ receptors on the sarcoplasmic reticulum, leading to
more Ca++ release.

A

ryanodine

in skeletal muscle depolarization activates a protein
that is linked to the sarcoplasmic reticulum, directly
causing Ca++ release

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8
Q

cardiac or skeletal muscle

Ca++
binding to
troponin alters
the interaction
between
tropomyosin and
actin, exposing
myosin binding
sites on the actin

ATP-hydrolysis fueled movement of the actin-myosin complex
produces contraction.

A

both

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9
Q

Factors that contribute to how well the heart pumps blood

deals with 1 ion

A
  1. Sensitivity of contractile proteins to Ca++
  2. Amount of Ca++ that is released
  3. Amount of Ca++ that is stored
    in the sarcoplasmic reticulum
  4. Amount of Ca++ that enters
    the cell upon depolarization
  5. Activity of the Na+/Ca++ Exchanger
  6. Intracellular Na+
    concentration and activity of
    the Na+/K+ ATPase (affects
    Ca++ via 5.
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10
Q

_ drugs alter the force or energy of muscular

contractions.

A

Inotropic

Negative inotropes weaken the force of
muscular contractions.

Positive inotropes increase the
strength of muscular contraction.

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11
Q

_ drugs may change the heart rate by

affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node.

A

Chronotropic

Positive chronotropes increase heart rate;

negative
chronotropes decrease heart rate.

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12
Q

_ drugs

Cardiac glycosides (inhibit Na+/K+ ATPase; Ca++) - digoxin

β-adrenergic receptor agonists

Bipyridines

A

positive inotropic

increase the
strength of muscular contraction.

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13
Q

Drugs without positive inotropic effects used to treat _

β adrenergic receptor blockers
diuretics
angiotensin converting enzyme inhibitors
Angiotensin receptor blockers
Aldosterone receptor antagonists
Vasodilators
A

to tx heart

failure

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14
Q

a positive inotropic drug

blocks Na+/K+ ATPase

Internal Na+ increases. This slows the Na+/Ca++
exchanger, slowing removal of Ca++.

A

Cardiac glycosides:

(in the US) digoxin only one
used
Digitalis (name for any of the cardiac glycosdes

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15
Q

Cardiac glycosides
blocks Na+/K+ ATPase
Internal Na+ increases. This slows the Na+/Ca++
exchanger, slowing removal of Ca++

_ condition increases the effect of the drug

A

hypokalemia - low potassium

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16
Q

Cardiac glycosides

the increase in contractility results in reversal of the compensatory responses to heart failure:

_ ventricular ejection
_end diastolic and end systolic cardiac size
_CO
_renal perfusion

A

increase ventricular ejection

decrease end diastolic and end systolic cardiac size

increase CO
increase renal perfusion

the above effects lead to a decrease in sympathetic and renal responses - increase renal perfusion - no renin release no angiotensin

the decrease in sympathetic tone is benefical, decrease HR, preload and after load improve the efficiency of heart

17
Q

positive inotropic drugs to tx heart failure

The effect of _ is cardiac stimulation, such as increased heart rate, heart contractility, heart conduction velocity and heart relaxation.

A

B1 - adrenergic receptor agonist \NOT FIRST LINE OF DEFENSE

18
Q

positive inotropic drugs to tx heart failure

phosphodiesterase - 3 inhibitors

this enzyme is responsible for the degradation of cAMP, inhibitory this raises cAMP levels - leading to contractility and vasodilation

A

Bipyridines

19
Q

Drugs without positive inotropic effects used
to treat heart failure
β-adrenergic receptor antagonists

Decreased _-mediated remodeling

A

Decreased catacholamine-mediated remodeling

excessive stimulation of B1 leads to activation of Bcl-2 ( anti-apoptotic protein because it inhibits the activity of Bax)

This leads
to Bax-mediated
cytochrome c release
and cell death by
apoptosis and is
thought to be
significant in heart
failure. Blockade of β1
adrenergic receptors is
thought to lead to Bcl2 mediated survival
20
Q

β blockers might provide effective
treatment of heart failure

Proteases called _ do the dirty
work of Apoptosis

A

Caspases

Proteases with an active site cysteine
that cleave at aspartic acid residues
(about 10 of them)
Proenzymes that require proteolytic
cleavage for activation
Some act as initiators (initiation phase)
Some act as effectors (aka executioners, execution phase)

21
Q

β blockers might provide effective
treatment of heart failure

Activation of something called the Intrinsic Pathway of
Apoptosis leads to activation of an _
(and therefore initiation of apoptosis)

A

Initiator Caspase

22
Q

beta blockers

Initiation Phase of the Intrinsic Pathway Depends on
_ and _
1. Stress signals leads to release of cytochrome c
2. Cytochrome c in cytoplasm binds to
apoptotic protease activating factor 1 (apaf
1)
3. This leads to formation of an apoptosome
(hexamer of cytochrome c and apaf 1)
4. This leads to binding of the initiator
procaspase 9. Putting them in proximity leads to
their activation. Activated caspase 9 activates
downstream executioner caspases

A

Mitochondria and Cytochrome c

23
Q

beta blockers

The _family of proteins regulates the intrinsic pathway by
regulating cytochrome c release from the mitochondrion

A

Bcl 2

The antiapoptotic proteins bind to
proapoptotic proteins and inhibit
them
When activated, these aggregate
on mito outer membrane and
promote cyto c release
The BH3-only proteins are
proapoptoic and produced or are
activated in response to an
apoptotic signal. The promote
apoptosis by binding and inhibiting
the antiapoptoic proteins
24
Q

_ is a pro-apoptotic protein because it enhances
cytochrome c release from the mitochondrion

_ is an anti-apoptotic protein because it inhibits
the activity of Bax

A

Bax - proapoptotic

Bcl-2 anti-apoptotic

25
Q

Drugs without positive inotropic effects used
to treat heart failure
_
This is a mainstay in treatment of congestive heart failure.

A

Diuretics

Try thiazide, then
move on to a loop
diuretic

26
Q 
Drugs without positive inotropic effects used
to treat heart failure
ACE inhibitors and Angiotensin receptor
antagonists
Aldosterone receptor antagonists
Direct vasodilators

more than just blood pressure, also cardiac _

A

remodeling

MOA not sure - decreased catacholamine mediated remodeling - finely tuned specialized cells of tissue not good -still present but not as good as once was

27
Q

_Americans disproportionately affected by heart failure. Clear evidence
that the _ help as supplements to other treatment strategies.

A

African-

vasodilators

28
Q

the medications for CHF can cause dry mouth and gingivitis

people with more severe heart failure should not lie down in the dental chair too far because _

they should also take it slow when moving from standing position to the chair, and when from standing up from the chair. because they can become dizzy and light-headed easily

A

the fluid buildup in their lungs may affect breathing

29
Q

Cardaic - electrical signals are telling heart to contract - moving from _ to _ - atrial first contract then ventricles - slow wave that comes thru the heart

Arrithmias - electrical signals are not in sync wave

100msec for cardaic
1msec - for skeletal muscle

A

atria to ventricles

30
Q

pain or discomfort in the chest that happens when some part of the heart does not receive enough oxygen from the blood

A

angina

classical/typical stable/ exertional - due to fixed or stable plaque

prinzmetal/variant - due to spasm of coronary artery

unstable - due to unstable plaque and thrombus

31
Q 
Drugs used to treat _
nitrates/nitrites
β-adrenergic receptor blockers
calcium channel blockers
aspirin, antiplatelet, and anticoagulant drugs
ranolazine
A

Angina

32
Q

drugs used to treat Angina

are esters of nitrous or nitric acid or prodrugs that spontaneously produce nitric oxide

NO - is the vasodilator - lowers BP

A

nitrates/nitrites

33
Q

which drugs to treat immediate angina

A

nitrates/nitrites

organic - extremely volatile, crushed, inhaled, rapid effects

34
Q

drugs to tx Angina

rapidly absorbed from oral mucosa
well absorbed from the GI and thru skin

extension first-pass metabolism

1-3 min sublingual tabslets

adverse effects?

A

nitroglycerine -

taking L=arginine as supplement doesn’t do anything

most common side effect is headaches

high doses of organic nitrates can calso cause postural hypotension, facial flushing, and tachycardia

35
Q

Sildenafil (viagra) - potentiates the action of the _, to preclude the danergous hypotension that may occur - this combo is contraindicated

A

nitrates

36
Q

drugs to tx Angina

Verapramil

A

Ca++ channel blocker

blocks contraction

37
Q

most common drugs used in tx of Angina Pectoris

2 classes
3 MOAs

A

Vasodilators - Nitrates and Ca blockers

Cardiac Depressants - Beta-Blockers and Ca blockers

Pharm 1 - SP19 (26 decks)

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