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Cardiology M2 > 11 05 2014 Anti-hypertensive drugs > Flashcards

11 05 2014 Anti-hypertensive drugs Flashcards

1
Q

what are the 4 classes of drugs used to treat hypertension

A
  • Diuretics
  • Sympatholytics
  • Vasodilators
  • Drugs that interfere with renin-angiotensin system
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2
Q

what are factors that increase cardiac output

A
  1. Excess sodium intake – could be due to an altered renal sodium retention
    - this increases fluid – increases preload – increases CO
  2. Renin - RAAS – Increase sodium retention
  3. SNS increases HR and contractility

CO = HR X BP

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3
Q

What are the targets of Antihypertensive drugs

A
  1. sodium/ Plasma volume
  2. RAAS
  3. SNS
  4. Vascular Smooth muscle
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4
Q 
Thiazide diuretics
(mechanism)
A

target Na+ -Cl- exchanger (NCC) symporter – inhibit reabsorption of Na+ in distal tuble

Affects Na+/K+ pump and now K+ is excreted
= hypokalemic statuses

Hydrochlorothiazide
Chlorthalidone

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5
Q

Loop Diuretic

A

Target Na+ K+ 2Cl- symporter in thick ascending limb of nephron

Block reabsorption of Na+

Very potent but very short lived

Ex. Flurosemide

  • reserved for CHF or resistant edema
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6
Q

Adverse effects of Thiazide/ Loop Diuretic Therapy

A
  1. Volume depletion (hypotension and decrease GFR)
  2. Hypokalemia ( increase in distal Na+/K+ exchanger)
  3. Hyponatremia
  4. Metabolic Alkalosis
  5. Increase in uric acid — Gout
  6. Hyperglycemia
  7. K- sparing agents : hyperkalemia
  8. Gynecomastia/ sexual dysfunction ( spironolactone –potassium sparing diuretic)
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7
Q

Hydrochlorthiazide

A

most common drug used – thiazide

Good for volume-overloaded/ salt depedent/ low renin HTN

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8
Q

Direct Vasodilators

A
  • calcium channel blockers
  • Hydralazine and minoxidil

Adverse effects: fluid retention, tachycardia
-reflex increase in SNS so pair with beta-blocker

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9
Q

Calcium channel blockers

  1. target
  2. any AE?
  3. names of drugs
  4. interesting fact about two drugs?
A

Target voltage-sensitive L-Type canals
- affect Ca2+ in smooth muscle, AV and SA node
= relaxation

Metabolically neutral : no effects on glucose

No renal, CNS or pulmonary AE.

AE: edema, flushing, lightheadedness, CONSTIPATION at all doses.

  • Bradycardia
  • Skin rash is common

Diltiazem
Verapamil
Nifedipine ( Amlodipine)
Nicardipine

  • Diltiazem and verapamil inhibit hepatic P450 enzymes
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10
Q

Hydralazine

A

Oral and IV
Short acting

Directly relaxes vascular smooth muscle of pre capillary resistance vessels

Potential for lupus syndrome w/ pericarditis

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11
Q

Minoxidil

A

Very potent oral agent
AEs include hypertrichosis, pericardial effusions, massive fluid retention

Directly relaxes vascular smooth muscle of pre capillary resistance vessels

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12
Q

Nitroprusside

A

Release NO = dilates arterioles and venues (decrease preload and after load)

Cyanide toxicity

Useful in severe or refractory HTN – pulmonary edema emergency

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13
Q

Alpha receptor Antagonist

A

Inhibit vasoconstriction of NE

Decrease total peripheral resistance (TPR) but with LESS tachycardia

Adverse effects: postural hypotension, headache, edema

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14
Q

Phentolamine

A

(IV)
Nonselective alpha receptor antagonists

Adverse Effects: postural hypotension, headache, edema

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15
Q

Phenoxybenzamine

A

Oral
Nonselective alpha receptor antagonist

Adverse Effects: postural hypotension, headache, edema

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16
Q

Prazosin, terazosin, doxazosin

A

Alpha 1 selective antagonists
oral

Also used for symptoms of prostatic hypertrophy.

Blockade of peripheral arterioles and venues

Toxicity: Dizziness, headaches,lassitude

17
Q

CNS- acting Sympathetic inhibitor

A

Alpha 2 receptor antagonists in the medullary brainstem

Act in CNS to decrease outflow

Clonidine
Alpha methyldopa

18
Q

Clonidine

A

Oral and transdermal (patch)
Onset 30-60 min – useful for HTN urgencies

AE: sedation, dry mouth, rebound BP (increase)

Sudden withdrawal can result in sudden hypertensive crisis

19
Q

Alpha methyldopa

A

Oral and IV

AE: sedation ,hepatitis, and coombs pos hemolytic anemia

*** PREGNANCY ASSOCIATED HTN

20
Q

Effects of a beta blocker

- target organs and their effects on them

A
  1. heart
    - slowing of heart range and negative inotropic effect
    = reduction in CO
  2. Kidney
    - Inhibition of Renin release (mostly B1)
  3. brain
    - possible central action
21
Q

Nonselective Beta Blockers

A

B1 and B2 receptor antagonists
- propranolol

AE: bronchospasms, worsening of diabetes, hyperlipidemia, prolonged hypoglycemia

May also have fatigue, depression, erectile dysfunction

22
Q

Beta 1 selective agents

A

Atenolol, metoprolol, bisoprolol
-may enhance Co, contractility and sA node firing.

B1 mediates renin release!!

Inexpensive and have fewer AE

23
Q

Labetalol, carvedilol

A
  • vasodilitary beta blockersnon-selective B/alpha

primarily beta 3:5

24
Q

Nebivolol

A

B1 selective agent

Release of NO

25
Q

Pindolol, acebutolol

A

ISA - intrinsic sympathomimetic activity
( beta agonis and antagonist effect)

Prevents dangerous bradycardia at night (due to other beta blockers)

26
Q

Adverse Side Effects of Beta Blockers

A
  1. heart
    - Contradicted during acute heart failure
    - Intensification of AV block
    - Arterial insufficiency
    - bradycardia
  2. CNS
    - depression
    - confusion
    - fatigue
  3. Pulmonary
    - Dyspnea
    - Bronchospasm
27
Q

Indications for use of Beta blocker in HTN

A

younger patients (greater adrenergic activity or elevation of plasma renin)

May have less stroke prevention in the elderly

28
Q

Indications for use of Beta Blocker in Cardiac Disorders

A
  • tachycardia
  • Chronic LV dysfunction
  • CAD - coronary artery disease
  • Hypertrophic subaortic stenosis
29
Q

Indications of beta blocker in non-cardiac disorders

A

Vascular (migraine) headache prevention

Essential tremor and performance anxiety

30
Q

Diltiazem Hydrochloride

A

Calcium Channel Antagoinst
- used in atrial fibrillation

  • decreases HR
  • decreases Myocardial contractility
  • decreases nodal conduction
  • increases peripheral vasodilation
31
Q

Verapamil Hydrochloride

A

Calcium channel antagonists

  • decreases HR
  • decreases Myocardial contractility
    (better than other)
  • decreases nodal conduction
    (better than others)
  • increases peripheral vasodilation
32
Q

Nifedipine/ Amlodipine

A

Calcium channel antagonists

  • increase/ no change to HR
  • decreases/no change to Myocardial contractility
  • no effect on nodal conduction
  • increases peripheral vasodilation (way better than Diltiazem and verapamil)
33
Q

Nicardipine hydrochloride

A

Calcium channel antagonists

  • increase/ no change to HR
  • no change to Myocardial contractility
  • no effect on nodal conduction
  • increases peripheral vasodilation (way better than Diltiazem and verapamil)
34
Q

Renin- Physiological Regulation

A
  1. decrease in renal perfusion = renin release from JG cells
  2. Increase SNS via B1 receptors = increase in renin
  3. Angiotensin II production and negative feedback = decrease in renin
  4. Increase distal tubular Na content = increase in renin release
35
Q

Differences among ACE inhibitor, ARB and Direct Renin inhibitor:

A

ACE Inhibitor:

  • decrease AII and Aldosterone
  • Increase plasma renin level
  • increase plasma renin activity (PRA)
  • increase vasodilitary peptides ( bradykinin)

ARB:

  • decrease aldoserone level
  • Increase plasma Renin level, PRA, and AII levels

DRI

  • decrease PRA
  • decrease in AI, AII, Aldosterone
  • Increase Plasma renin LEVEL
36
Q

Potentinal adverse Effects of ACEi, ARB, DRI

A
  1. hyperkalemia (aldosterone inhibition)
  2. Hypotension
  3. Worsen renal insufficiency ( disproportionate glomerular efferent arterial vasodilation)
  4. Fetal injury
    - ALL INHIBITORS OF RRA ARE CONTRAINDICATED IN PREGNANCY
  5. ACE-I Cough
37
Q

What drugs will worsen the following situations of HTN:

  1. Pregnancy
  2. Depression
  3. sexual dysfunction
  4. Asthma
  5. Gout
  6. Constipation
A
  1. ALL RRA agents
  2. beta blockers, central inhibitors
  3. beta blockers, central inhibitors, spironolactone (potassium sparing diuretic)
  4. Asthma: Beta blocker (non selective)
  5. Gout - Diuretic
  6. Verapamil
38
Q

Captopril, Enanalapril

A

ACE inhibitors

Inhibit peptdyl dipeptdase – affects RAAS
and Kallikrein-­‐kinin system

Toxicity: ARF in pts wi/bilateral renal artery
stenosis; dry cough; angioedema:

39
Q

Losartan, Valsartan

A

AT1 inhibitors; no effect on bradykinin

Similar effects to ACE-­‐I; less cough and angioedema

Cardiology M2 (25 decks)

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