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PHA4107 > Cardiovascular pharmacology > Flashcards

Cardiovascular pharmacology Flashcards

1
Q

Normal human heart

  • A ______-chambered muscular organ
  • Chambers are: _______
  • A ______________ pump
  • Cardiomyocytes: ______________ cells in heart
A
  • Four
  • Left atrium (LA); Right atrium (RA); Left ventricle (LV); Right ventricle (RV)
  • Mechanical
  • Contractile
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2
Q

Normal heart: concept of cardiac output

  • Function of heart is to ________________________ which causes _________ pressure and tissue ___________
  • Cardiac output (CO): and index of cardiac __________. Defined as the amount of blood ______________ per unit time
  • CO = Stroke volume x HR
A
  • Pump blood into the circulation; blood; perfusion

- Activity; ejected

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3
Q

Normal heart: determinants of stroke volume

Stroke volume (volume of blood ejected in each heart ___________) is determined by:

  1. Contractility: the intrinsic strength of muscle __________
  2. Preload: initial ______ of muscle fibres prior to contraction
  3. Afterload: the load _______ which the heart must contract to eject blood
    - ________ pressure is a major component of after load for the _______
A

Contraction

  1. Contraction
  2. Stretching
  3. Against
    - Aortic; LV
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4
Q

Heart failure:

  • Heart is unable to maintain a normal cardiac ______
  • Common causes (n=4): _______
  • 2 types
A 
- Output
Causes:
- Ischemic Heart disease
- Cardiomyopathy
- Valvular disease
- Hypertension
  • Systolic heart failure
    Diastolic heart failure
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5
Q

Symptoms of heart failure

LV failure:

  • Pulmonary ___________ leading to dyspnea
  • Insufficient tissue ____________ leading to fatigue

RV failure:
- Systemic congestion leading to peripheral _______ (ankles), abdominal __________ (liver), _________ (GI tract)

A
  • Congestion
  • Perfusion
  • Edema; discomfort; nausea
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6
Q

Compensatory mechanisms of heart failure

  • In short term: they’re ___________
  • In long term: ________ load on heart which _________ heart failure
A
  • Beneficial

- Increases; accelerates

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7
Q

Cardiac remodelling in heart failure

Heart disease (_________ CO) leads to:
1. Increase in _________ nervous system, _____________ system (RAS) and inflammatory ______________
which lead to
2. Early stage: cardiac ___________
- Increase in mass/thickness of ___________ (increase in _________ of myocytes and no change in _______ of myocytes)
leading to
3. Late stage: heart _________
- Dilation; wall ___________; fibrosis; myocyte __________ (death of muscle cells)

A

Reduced
1. Sympathetic; renin-angiotensin; cytokines

  1. Hypertrophy
    - Ventricle; size; number
  2. Failure
    - Thinning; apoptosis
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8
Q

Drugs for heart failure (DHF)

Goals of therapy:

  • To improve __________
  • To slow or _________ adversity cardiac remodelling
  • To prolong ________ and reduce ___________
A
  • Symptoms
  • Reverse
  • Survival; mortality
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9
Q

Drugs for heart failure: calcium is a key determinant of cardiac ____________
- Digoxin, dobutamine, milrinone cause an ______ of calcium which causes _______ in contractility

A

Contractility

  • Increase; increase
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10
Q

(DHF)
Positive inotropic drugs: ________
- Drugs that increase cardiac ___________

Cardiac glycosides

  • Isolated from leaves of ___________ plant
  • Used for over 200 years in treatment of ____________

Digoxin:

  • The most extensively used _____________
  • Readily absorbed ___ tract
  • Excreted by __________
  • Rapid _________
  • __________ = 1.5 days
A

Digoxin
- Contractility

  • Foxgloves
  • Heart failure
  • Glycosides
  • GI
  • Kidney
  • Onset
  • Half-life
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11
Q

Digoxin:
- Increases ___________ in heart failure
- Increases activity of the __________ nervous system which inhibits sinoatrial node (SAN) and _______ HR
Mechanism of inotropic effect
1. Inhibition of ___________
2. Increase cytosolic ____
3. Inhibition of ____ export via Na+/Ca2+ exchanger
4. Increased intracellular _____ and ______

A
  • CO
  • Parasympathetic; decreases
  1. Na+/K+ ATPase
  2. Na+
  3. Ca2+
  4. Ca2+ and contractility
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12
Q

Adverse effects of Digoxin

  • Cardiac ________________
    1. Digoxin increases _____
    2. Overload of calcium in the _______
    3. Afterdepolarizations
    4. Cardiac arrhythmias: premature ______/______ beats and __________

Digoxin has low __________ index

Adverse effects and toxicity:

  • ____________: nausea and vomiting
  • _______________: blurred visions and seizures
  • ____________: arrhythmias (worsened by low K+)

Treatment of digoxin toxicity:

  • Antidote: Digoxin __________ (Fab)
  • ____ supplements
A

Arrhythmias

  1. Calcium
  2. SR
  3. Atrial/ventricle; tachycardias

Therapeutic

  • GI tract
  • Neurologic reactions
  • Heart
  • Antibody
  • K+
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13
Q

Interaction of digoxin w/ other drugs

Digoxin toxicity can be increased by:

  • Diuretics that reduce ______ in plasma which ________ binding of digoxin to Na+/K+ ATPase which further increases ___________
  • Drugs that interfere with renal ____________ of digitoxin leads to __________ serum digoxin levels
  • ___________ dysfunctions
A
  • K+; increases; toxicity
  • Clearance; increased
  • Renal
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14
Q

Other positive inotropic drugs

A

Dobutamine

Milrinone

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15
Q

Stimulation of cardiac contraction by B-adrenergic signalling:

  1. Greater influx of ________
  2. Higher ___________ Ca2+
  3. Enhanced _________
A
  1. Ca2+
  2. Cytosolic
  3. Contraction
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16
Q

Dobutamine

A synthetic ________ receptor agonist which leads to increase in cardiac _______

  • Acts on B1 receptor in heart to ________ contractility
  • Acts on B2 receptor to relax _________ and decrease _____________

Clinical use:

  • Can _________ symptoms of heart failure which is used for __________ management of acute heart failure and cardiogenic shock
  • No improvement of patient ______________
A

Beta; output

  • Increase
  • Blood vessels; after load
  • Improve; short-term
  • Survival
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17
Q

Milrinone

Increases __________ levels by inhibiting PDE which can cause 2 things that will lead to increased __________

  • Increased cardiac ___________
  • Decrease ___________

Clinical use:

  • Used for ____________ management of heart failure patients not responsive to other drugs
  • Used for __________ awaiting cardiac transplantation

Adverse effects (long-term use):

  • Ventricular ____________-
  • Increased ____________
A

cAMP; cardiac output

  • Contractility
  • After load
  • Short-term
  • Infants
  • Arrhythmias
  • Mortality
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18
Q

Vascular smooth muscle : Blood vessel

3 layers:

  • _________ layer: endothelial cells
  • _________ layer: SM cells
  • _________ layer: collagen + fibroblast

Fibroblast secrete _________

Vascular SM cells:
- Contraction of smooth muscle affects vessel _______ which affects blood _______ rate

A
  • Inner
  • Middle
  • Outer

Collagen

Diameter; flow

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19
Q

Vascular SM: mechanisms of SM contraction

SM contraction:

  1. Initiated by increase of ______
  2. Ca2+ binds to ___________
  3. Ca2+/calmodulin complex activates _________ (MLCK)
  4. MLCK will then phosphorylate __________
  5. Phosphorylated myosin binds to actin forming _________, hence triggering ___________

SM relaxation:
- There needs to be a decrease in _________ or activation of _______________ to remove phosphate from myosin

A
  1. Ca2+
  2. Calmodulin
  3. Myosin Light Chain Kinase
  4. Myosin
  5. Cross-bridge; contraction
  • Ca2+; MLC phosphatase
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20
Q

Coronary arteries:

  • First to branch off the ________
  • Two of them : _________ and _________
  • Supply blood to ________muscle (the heart takes up ___% of total CO and uses about ____% of total body O2 consumption

O2 supply rate to heart = (Coronary flow rate) x (O2 content)

A
  • Aorta
  • Left and Right coronary arteries
  • Heart; 5; 11
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21
Q

Coronary arteries: balance between O2 supply and demand (in normal heart)

  • At rest, O2 supply and O2 demand are the _________
  • During exercise, the _________ nervous system is activated, increasing O2 supply which consequentially increases O2 demand (so O2 supply and demand are still the __________)
A
  • Same

- Sympathetic; same

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22
Q

Coronary artery diseases

  1. Artery is ________
  2. Coronary blood flow rate is _______
  3. O2 _____________ increases and so there’s an __________ between O2 supply and demand

Angina pectoris (________ block):

  • Crushing ________ pains
  • Ischemia and metabolites accumulation
Myocardal infraction (\_\_\_\_\_\_\_\_\_\_\_\_\_ block)
- Abbreviation: MI
A
  1. Blocked
  2. Limited
  3. Demand; imbalance

Partial
- Chest

Complete

23
Q

Angina pectoris

  1. Typical Angina (caused by ______ changes in blood vessel):
    - Stable Angina
    - Formation of plaque in wall of _______ and ______constriction
    - Similar _______ every time it occurs (pain, triggers)
    - Unstable Angina
    - Rupture of ______, aggregation of ______ and ________ formation (blood clots)
    - Sudden _________ in frequency and duration/severity of angina
    - Precursor of Myocardal Infraction (MI)
  2. Variant Angina (no structural change but ______ change):
    - Intense ___________
    - Can occur at _________
A
  1. Structural
    - Artery; vaso
    - Characteristics
    - Plaque; platelets; thrombosis
    - Increase
  2. Functional
    - Vasospasms
    - Rest
24
Q

Antiangenal/anti-ischemic agents:

  • Vasodilators (organic nitrates/nitrites and Ca2+ channel blockers)
    - __________ O2 supply
  • Beta blockers
    - __________ O2 demand

Goal of these therapies: to restore the ___________

A
  • Increase
    - Decrease
  • Balance
25
Q

Vasodilators
Organic nitrates and nitrites: mechanisms of action

  • Nitrates and nitrites can dilate __________ by releasing ___________ (NO) which is normally generated by the ____________ cells
A
  • Blood vessels; nitric oxide; endothelial cells
26
Q

Vasodilators: Organic nitrates and nitrites

Amyl nitrite

  • Volatile __________; inhalation
  • Onset: almost _________ (about 30 sec)
  • Very _________ duration of action (3-5 min)
  • Used for treatment of acute ________ attacks

Nitroglycerin

  • _______: well absorbed by gut but rapidly metabolized by liver; sustained release for prevention
  • _________: rapid absorption and used for treatment of acute angina attacks
  • __________: slow release and used for prevention of angina attacks
  • _________: reduces pre and after load in patients with MI or acute heart failure
A
  • Liquid
  • Immediately
  • Short
  • Angina
  • Oral
  • Sublingual
  • Transdermal (ex: patches or ointments)
  • Intravenous (IV)
27
Q

Vasodilators: organic nitrates and nitrites

Antianginal actions

  • Nitrates and nitrites cause the release of _____ which can lead down 2 pathways
    1. Dilation of _____ -> _____ in venous return preload -> _________ in contraction and O2 demand
                                          or
  1. Dilation of large epicardial vessels of the _______ -> _________ in blood flow to ischémie areas -> _____ O2 supply
A
  • NO
    1. Veins; decrease; decrease
    2. Heart; increase; increase
28
Q

Vasodilators: organic nitrates and nitrites

Clinical uses

  • To relieve _______ of an already established attack
  • To prevent an ______ prior to activity/exercise
  • To provide __________ prophylaxis
A
  • Pain
  • Attack
  • Long-term
29
Q

Vasodilators: organic nitrates and nitrites
Side effects and tolerance

  • Excessive vasodilation -> decrease in blood pressure -> side effects (n=3): ________

Tolerance of nitrates:
- _________ administration -> decrease in vasodilation effect

Prevention of tolerance:
- _________ dose and frequency

Mechanism of tolerance:
- When nitrates/nitrites release _____, causes release of oxygen ______ radicals which _________ aldehyde dehydrogenase causing a further reduction of NO release

A
  • Hypotension, headache, reflex tachycardia
  • Continuous
  • Decreasing
  • NO; free; inhibit
30
Q

Vasodilators: calcium channel blockers (CCBs)

Dihydropyridine class (-dipine)
- n=2
A
  • Amlodipine (longest half-life at 40hrs) and Felodipine (14 hrs)
31
Q

Vasodilators: calcium channel blockers (CCBs)
Mechanism of action

L-type Ca2+ channels:

  • Expressed in cell membrane of: vascular ____ cells, cardio_________, SAN and AV node cells
  • Allow _____ influx into cells
  • Blockage by CCB -> _______ Ca2+ influx -> vaso____

T-type Ca2+ channels:

  • Expressed in ______ and _______ tissue
  • Is not blocked by ______
A
  • SM; myocyte
  • Ca2+
  • Reduced; dilation
  • Heart; vascular
  • CCBs
32
Q

Vasodilators: calcium channel blockers (CCBs)
Antiangenial actions

Dihydropyridine drugs cause ______ of coronary artery which ________ O2 supply

Non-dihydropyridine drugs can do dihydropyridine action or they can cause _________ in HR and contractility which leads to _________ in O2 demand

A

Dilation; increase

Decrease; decrease

33
Q

Vasodilators: calcium channel blockers (CCBs)

Clinical uses:

  • ___________ of variant angina
  • ___________ of typical angina
  • ___________ of exercise endurance
  • Used for atrial _____cardia

Adverse affects:

  • Vaso______ and ____tension are associated with: headaches, peripheral edema, dizziness
  • Relaxation of gut _____ is associated with constipation
A
  • Prevention
  • Treatment
  • Improvement
  • Tachy
  • Dilation; hypo
  • SM
34
Q

Vasodilators: B blockers (-olol)

B blockers used for angina (n=4)

A
  1. Atenolol
  2. Metoprolol
  3. Nadolol
  4. Propanolol
35
Q

Selective B1 blockers (atenolol, metoprolol): block B1 receptors in _______ which ________ HR and contractility, leading to ______ O2 demand

  1. Prevents _______ angina
  2. Prevention of _____cardia induced by vasodilators

Non-selective (nadolol, propanolol): Block B1 receptors, but also block B2 receptor in ________ leading to smooth muscle _________

  • _____________: in airways of lungs
  • ___________________: in arteries of skeletal muscle

B blockers have no direct effect on coronary _______

A

Heart; reduces; reduced

  1. Typical
  2. Tachy

SM; contraction

  • Bronchoconstriction
  • Reduced blood flow during exercise

Arteries

36
Q

New drugs for angina:

Ivabradine:

  • _______ funny currents (determine HR) in SAN pacemaker cells
  • selectively _______ HR which ______ O2 demand of heart
  • Used for treatment of _______ angina and heart failure

Ranolazine:

  • ________ late Na+ currents in cardiomyocytes
  • _________ diastolic wall tension (reduces O2 demand, and improves blood supply)
  • Treatment of _______ stable angina (increases exercise capacity and reduces anginal frequency)

Trimetazidine:
- _________ B-oxydation and reduces FA metabolism
Leads to
- __________ in glucose metabolism
Leads to
- __________ O2 consumption/demand of the heart

A
  • Inhibits
  • Decreases; reduces
  • Chronic
  • Inhibits
  • Reduces
  • Chronic
  • Inhibits
  • Increases
  • Reduces
37
Q

Blood pressure

  • Pressure of circulating ________ on blood vessel wall
  • Not stable, it fluctuates
    1. ___________: peak pressure (during contraction)
    2. ___________: lowest pressure (during relaxation)
A
  • Blood
  1. Systolic pressure
  2. Diastolic pressure
38
Q

Hypertension:

  • Systolic pressure (>___ mmHg) or Diastolic pressure ( > ___ mmHg)
  • Is a risk factor for other _____ diseases: coronary heart disease, stroke, heart/renal failure
  • 2 types:
    1. _______ hypertension
    2. ________ hypertension
  • Chronic kidney disease
  • Aldosterone-secreting tumors
A
  • 140; 90
  • Heart
  1. Primary
  2. Secondary
39
Q

Short-term regulation of blood pressure (fast response)

Barorecetpro reflex

  1. Pressure _________
  2. __________ of vessel wall stretch and baroreceptor input
  3. ___________ symp. NS and ______ of parasymp. NS (vagal nerve)
  4. _____________ in HR, contractility, vascular contraction
A
  1. Increases
  2. Increase
  3. Decrease; Increase
  4. Decrease
40
Q

Long-term regulation of blood pressure (slow response)

Angiotensin II

  • Generated by _________________ enzyme (ACE) from ______________
  • Causes vaso____________
  • Stimulates secretion of ___________
A
  • Angiotensin-converting; angiotensin I
  • Constriction
  • Aldosterone
41
Q

Antihypertensive drugs: Diuretics

  1. ___________ renal sodium excretion
  2. ___________ blood volume
  3. ___________ filling pressure
  4. ___________ preload
  5. ___________ stroke volume
A
  1. Increase
  2. Decreases
  3. Decreases
  4. Decreases
  5. Decreases
42
Q

Antihypertensive drugs: Urine formation

  • ____________ of water, ions and other small molecules into tubular fluid
  • ____________ of substances back to the blood
  • ____________ of substances into tubular fluid

Diuretics ________ reabsorption of Na+ -> _________ osmolarity of tubular fluid -> ____________ urine volume
-> _____________ blood volume and blood pressure

A
  • Filtration
  • Reabsorption
  • Secretion
  • Inhibit; Increase; increase; decrease
43
Q

Antihypertensive drugs (diuretics): Thiazide Diuretics

Drugs: Hydrochlorothiazide and indapamide
Most commonly used diuretics for ______________
Economic

Mechanism of action:

  1. _________ Na+/Cl- cotransporter in early distal tubule
  2. __________ Na+ and osmolarity of tubular fluid causing _______ of urine volume (diuresis)
  3. ____________ of K+ secretion (hypokalemia - loss from blood)

Adverse effects:

  • Hypokalemia: low serum _____ which causes cardiac arrhythmias and skeletal muscle weakness
  • __________ blood levels of glucose, lipids and uric acid in some patients
A

Hypertension

  1. Inhibits
  2. Increases; Increase
  3. Stimulation
    - K+
    - Increased
44
Q

Antihypertensive drugs: Loop diuretics

Drug: furosemide

  • ____________ Na/K/Cl cotransporter into ascending limb of Loop of Henle
  • Has powerful _________ effect
  • Side effect: _____________

Clinical uses:

  • Used when intensive ___________ is required
  • Used in __________ patients when thiazides aren’t effective
A
  • Inhibits
  • Diuretic
  • Hypokalemia
  • Diuresis
  • Hypertension
45
Q

Antihypertensive drugs: potassium-sparing diuretics

Drug: amiloride
- _________ Na+ channels in distal tubule and collecting duct which __________ Na+ reabsorption and causes _________

Effects:

  • Has mild natriuretic effects
  • ________ K+ secretion so often used for prevention of ________________
A
  • Blocks; reduces; diuresis

- Reduces; hypokalemia

46
Q

Antihypertensive drugs: Renin-Angiotensin-Aldosterone system

Renin:

  • A protease that generates ______________
  • Secreted by ____________ cells in kidneys
  • Its secretion is stimulated by:
    • _______ pressure in renal afferent arteriole
    • _______ NaCl content in distal tubule
    • _______ outflow of symp. NS

3 types of angiotensin inhibitors:

  1. ACE: _________________ inhibitor
  2. ARB: _________________
  3. Renin __________
A
  • Angiotensin I
  • Juxtaglomerular
    • Reduced
    • Reduced
    • Increased
  1. Angiotensin-converting enzyme
  2. Angiotensin receptor blockers
  3. Inhibitors
47
Q

Antihypertensive drugs: ACE inhibitors

Mechanism of action:
1. Ace inhibitors ________ angiotensin II levels which causes:
- ____________ vasoconstriction which leads to ___________ blood pressure
OR
- __________ aldosterone, leading to __________ sodium retention and blood volume which causes _________ in blood pressure

A
  1. Decrease
    • Decrease; decreased
    • Decreased; decrease; decrease
48
Q

Antihypertensive drugs: ACE inhibitors

Captopril:

  • ________ ACE inhibitor ever developed
  • _________ absorption in gut
  • Side effects: dry ________, rash, _____ taste sensation

Enalapril

  • _________ sulf-hydril group (doesn’t reduce taste sensation)
  • Is a pro_______ and is metabolized by body into its ________ form
  • Has a longer duration of ________ (24h) than Captopril (6-12hrs)

Clinical effects:

  • Excellent anti_____________ action
  • Used for management of _______ to _______ hypertension

Adverse effects:

  • Dry _______ (ACE inhibitors reduce activity of ACE, increasing bradykinin and causing dry cough)
  • Fetal/neonatal injury and death (not to be used during ____________)
A
  • First
  • Rapid
  • Mouth; reduces
  • Lacks
  • Drug; active
  • Action
  • Hypertension
  • Mild to severe
  • Cough
  • Pregnancy
49
Q

Antihypertensive drugs: Angiotensin receptor blockers (ARBs)

  • Angiotensin II causes __________ of angiotensin receptors which __________ free calcium levels in vascular SM which causes vaso__________
  • Drugs: Losartan and Valsartan

Action and clinical effects:

  • Directly blocks ___________ receptors
  • Similar effects as ______ inhibitors (used for treatment of hyper_________)
  • Rarely cause dry _________

Adverse effects:

  • Fetal and neonatal __________ and death (same as ACE inhibitors)
  • May _________ blood levels of liver aminotransferase enzymes
A
  • Activation; increased; constriction
  • Angiotensin
  • ACE; tension
  • Cough
  • Injury
  • Increase
50
Q

Antihypertensive drugs: Renin inhibitor

Drug: Aliskiren

  • The ___________ renin inhibitor developed
  • ____________ defective

_____________ of renin activity -> ___________ production of angiotensin I and II -> ___________ blood pressure

A
  • First
  • Orally

Inhibition; reduced; reduced

51
Q

Antihypertensive drugs: Drugs on sympathetic nervous system

B1 receptor blockers in heart and kidney:
Action:
- ___________ HR and contractility
- ___________ renin secretion in kidneys

a1 receptor blockers in blood vessels:
Drug: Prazosin
Action:
- Arteriolar ___________ -> __________ vascular resistance -> ___________ blood pressure
Side effect:
- Reflex ____________ sympathetic nervous system causes _____________ HR and contractility
Uses:
- Not used for initial treatment of ______________
- Can be added to other _____________

a2 receptor agonists in vasomotor center in brainstem medulla
Drug: Clonidine
- ____________ sympathetic outflow leads to arteriolar _______________ which causes ___________ blood pressure
Uses:
- Not recommended for chronic treatment of __________
- Can be used for hypertensive ___________ (has a rapid onset, a single dose can reduce BP to normal levels)
Hypertensive urgencies:
- Systolic BP > ___ mmHg or
- Diastolic BP > ___ mmHg w/ no evidence of target organ damage

A
  • Reduce
  • Reduce
  • Dilation; reduced; reduced
  • Activation; increased
  • Hypertension
  • Drugs
  • Reduced; dilation; reduced
  • Hypertension
  • Urgencies
  • 180
  • 120
52
Q

Antihypertensive drugs: Vasodilators
Calcium channel blockers (CCB)
- ______________ of vascular SM -> Arteriolar ____________ -> ____________ of vascular resistance and BP

Uses:

  • Mostly recommended for initial treatment of __________
  • Protects against stroke; coronary ________ disease and kidney __________
A
  • Relaxation; dilation; decrease
  • Hypertension
  • Heart; disease
53
Q

Antihypertensive drugs: Vasodilators
Sodium Nitroprusside
- Releases _______________ (NO) -> vaso___________
- IV infusion for hypertensive ____________; has a ___________ onset
- Action lasts for up to ______ minutes

Side effects:

  • _______tension
  • Cyanide _________
A
  • Nitric oxide; dilation
  • Emergencies; rapid
  • 10
  • Hypo
  • Toxicity
54
Q

4 types of drugs for hypertension:

  1. ____________: increase renal sodium/water excretion
  2. ___________: reduce production of aldosterone (etc.)
  3. ___________: B blockers and a1 blockers
  4. ____________: can directly relax SM in arteries to reduce BP
A
  1. Diuretics
  2. Angiotensin inhibitors
  3. Sympathetic nervous system inhibitors
  4. Vasodilators

PHA4107 (4 decks)

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