Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Antihypertensives > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

Thiazide

A
  • loop diuretic (Na+ and K+ in for 2 Cl- out)

- inhibit Na+ absorption in DCT by blocking the NCC transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Toxicity of Diuretics

A
  • low K+ (hypokalemia)
  • metabolic alkalosis (increased delivery of K to the collecting ducts facilitates the exchange of K for H by the H/K exchangers on the intercalated alpha cells, resulting in loss of H [metabolic alkalosis])
  • hyponatremia
  • hypotension and decreased GFR
  • metabolic alkalosis also due to increased proximal HCO3 reabsorption
  • increased UA/gout
  • hyperglycemia (inhibition of insulin release)
  • hypercalemia (increased proximal calcium reabsoprtion)
  • K-sparring agents –> hyperkalemia
  • gynecomastia/sexual dysfunction (steroid receptor antagonism (spironolactone))
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Prazosin

A
  • adrenoreceptor antagonist
  • alpha1 blockage in peripheral arterioles and venules
  • useful for symptoms of BPH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Doxazosin

A
  • adrenoreceptor antagonist
  • alpha1 blockage in peripheral arterioles and venules
  • useful for symptoms of BPH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Toxicity of Adrenoreceptor Antagonists

A
  • dizziness
  • headaches
  • lassitude (a state of physical or mental weariness, lack of energy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hydralazine

A
  • vasodilator
  • given both PO and IV
  • dilates arterioles, no veins
  • effective in severe hypertension
  • Toxicity: reflex increase in HR can cause myocardial ischemia; potential for lupus syndrome with pericarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clonidine

A
  • vasodilator
  • centrally-acting
  • alpha-2 agonist
  • onset in 30-60 min
  • useful in hypertensive urgencies
  • very useful for treatment-resistant HTN
  • decreases HR and PVR
  • Toxicity: sudden withdrawal can result in sudden hypertensive crisis; sedation, dry mouth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Amlodipine

A
  • vasodilator
  • calcium-channel blocker
  • can have cardiac depressant effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Captopril

A
  • ACE inhibitor
  • inhibit peptidyl dipeptidase - affects RAAS and Kallikrein-kinin system
  • Toxicity: ARF in pts with bilateral renal artery stenosis; dry cough; angioedema
  • contraindicated in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Enalapril

A
  • ACE inhibitor
  • inhibit peptidyl dipeptidase - affects RAAS and Kallikrein-kinin system
  • Toxicity: ARF in pts with bilateral renal artery stenosis; dry cough; angioedema
  • contraindicated in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Losartan

A
  • angiotensin-R blocker
  • AT1 inhibitors; no effect on bradykinin
  • Toxicity: similar effects to ACE inhibitor; less cough and angioedema
  • contraindicated in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Valsartan

A
  • angiotensin-R blocker
  • AT1 inhibitors; no effect on bradykinin
  • Toxicity: similar effects to ACE inhibitor; less cough and angioedema
  • contraindicated in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Propranolol

A
  • beta blocker
  • non-selective
  • decreased CO to decreased BP
  • Benefits: reduce mortality post-MI; inhibits stimulation of renin release by catecholamines
  • Toxicity: increased airway resistance; reduce IO pressure; impair recovery from hypoglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Metoprolol

A

cardiac selective beta blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Atenolol

A

cardiac selective beta blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pindolol

A
  • partial agonist beta blocker
  • decreased SVR (systemic vascular resistance)
  • Benefits: does not change SVR and CO as much
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Acebutaol

A
  • partial agonist beta blocker
  • decreased SVR (systemic vascular resistance)
  • Benefits: does not change SVR and CO as much
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Labetolol

A
  • beta-blocking and vasodilating effects
  • has both beta and alpha blocking action
  • Benefits: reduced SVR without change in HR or CO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Carvedilol

A
  • beta blocking and vasodilating effects
  • has both beta and alpha blocking action
  • Benefits: reduced SVR without change in HR or CO
  • Toxicity: carvediol is effective in CHF and HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Esmolol

A
  • beta-1 selective
  • very rapid; given IV
  • short half-life (~10 min)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Hydrochlorothiazide

A
  • most common diuretic and antihypertensive prescribed (initial or add-on Rx)
  • especially effective in patients with volume expanded/salt dependent/low-renin hypertension - including the elderly, diabetics, and blacks; pts w/ edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Chlorthalidone

A
  • diuretic
  • more potent than HCTZ
  • reduction in stroke, heart failure, coronary events
  • more expensive to manufacture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Loop Diuretics

A
  • reserved for CHF or resistant edema

- Na+ and K+ in for 2 Cl- out

24
Q

K-sparing agents

A
  • helpful for hypokalemic patients
  • Na+ in for K+ out
  • aldosterone antagonists
  • may have heart failure benefits
25
Direct Vasodilators
- least frequently used for HTN - most useful in severe or refractory HTN - hypertensive emergencies like in pulmonary edema - reflex increased SNS activity, increased HR and CO - counters CO effect on HTN, so need to use in combination with beta-blocker - BP lowering effect is non-renin dependent - decreased renal perfusion leads to increased plasma renin activity and increased sodium-volume retention and edema - "pseudotolerance" - almost always requires combination with loop diuretics and beta blockers
26
Minoxidil
- direct vasodilator - very potent oral agent - Adverse Effects: hypertrichosis (abnormal amount of hair growth), PEs, massive fluid retention, tachycardia
27
Nitroprusside
- direct vasodilator - releases NO - dilates arterioles and venules (decreased cardiac afterload and preload) - Adverse Effect: structure of thiocynate is similar to cyanide and can result in cyanide toxicity
28
Alpha Adrenergic Receptors
- agonists (norepi>epinephrine) - alpha-1 receptor (post-synaptic; mediates vasoconstriction) - alpha-2 receptor (mostly pre-synaptic; inhibits norepinephrine release at peripheral and CNS sympathetic nerve terminals)
29
Alpha Receptor Antagonists
- inhibit the vasoconstrictor effects of norepi - hemodynamic action (decreased TPR) similar to vasodilators, but with less tachycardia - usually most effective in combination Rx - may increase the sxs of HF as monotherapy - Adverse Effects: postural hypotension, headache, edema
30
CNS-acting Sympathetic Inhibitors
- alpha-2 receptor AGONISTS in the medullary brainstem | - act in the CNS to decrease outflow of the SNS
31
Alpha Methyldopa
- CNS-acting sympathetic inhibitor - alpha-2 agonist - decreases outflow of the SNS - given oral and IV - used most commonly in pregnancy-associated HTN - Adverse Effects: sedation; hepatitis and coombs pos hemolytic anemia
32
beta-1 Adrenergic Receptors
- increase cardiac SA node (increase heart rate) - increase cardiac muscle contractility - increase renin release (renal JGA cells)
33
beta-2 Adrenergic Receptors
- vascular smooth muscle (dilate) - bronchial smooth muscle (bronchodilation) - hepatocytes (glycogenolysis) - pancreatic islet cells (insulin release)
34
Non-Selective Beta-Receptor Antagonists
- increases rick of bronchospasm, worsening diabetes, hyperlipidemia, risk of prolonged hypoglycemia, symptoms of PVD - increased CNS adverse effects (fatigue, depression, ED) due to high lipid solubility - may be superior for migraine prevention
35
beta-1 Selective Antagonists
- atenolol, metoprolol, bisoprolol - inexpensive, may have fewer adverse effects - most common type prescribed today
36
Vasodilatory Beta Blockers
- may have faster onset of BP reduction than other beta-blockers - non-selective beta/alpha - labetalol - carvedilol - RCT w/ carvedilol show long-term survival benefit in patients w/ CHF - Nebivolol: beta-1 selective agent, releases NO
37
ISA (intrinsic sympathomimetic activity)
- pindolol, acebutolol - may prevent extreme decreases HR at rest - agonist and antagonist effects - some pts on other antihypertensive meds have unusual degrees of bradycardia, so with a drug like pindolol you will have control of BP due to beta-blocker effect, but at night the heart rate will rise to normal levels
38
Indications for Beta Blockers (hypertension)
- often more effective in younger pts, those with signs of greater adrenergic activity or elevated plasma renin - less BP reduction in low renin patients - blacks, elderly - may have less stroke prevention in the elderly
39
Indications for Beta Blockers (cardiac disorders)
- tachyarrhythmias - chronic LV dysfunction (metoprolol XL/carvedilol/bisoprolol) - CAD: angina, acute coronary syndrome (ACS), post-MI - hypertrophic subaortic stenosis
40
Indications for Beta Blockers (non-cardiac disorders)
- vascular (migraine) headache prevention | - essential tremor and performance anxiety
41
Calcium Channel Antagonists
- Ca channel antagonists bind the alpha-1 subunit of the L channel - produce relaxation of VSM/myocardium; and slows SA and AV nodal transmission - broad effectiveness as a single or combination Rx - metabolically neutral: no effects on glucose, electrolytes, uric acid, lipids - no renal, CNS, or pulmonary AEs
42
Diltiazem Hydrochloride
- calcium channel antagonist - decreases heart rate - decreases myocardial contractility - decreases nodal conduction - increases peripheral vasodilation
43
Verapamil Hydrochloride
- calcium channel antagonist - decreases heart rate - greatly decreases myocardial contractility (and CO) - greatly decreases nodal conduction - increases peripheral vasodilation
44
Nifedipine
- calcium channel antagonist - increases heart rate - slightly decreases or no effect at all on myocardial contractility - NO EFFECT on nodal conduction - greatly increases peripheral vasodilation
45
Nicardipine Hydrochloride
- calcium channel antagonist - increases heart rate - no effect on myocardial contractility - no effect on nodal conduction - greatly increases peripheral vasodilation
46
Calcium Channel Antagonist AEs
- edema, flushing, lightheadedness, constipation - bradycardia and HF (uncommon) - skin rash uncommon but can be serious - diltiazem and verapamil (but not DHP) inhibit hepatic P450 isozymes
47
AT1 receptor
- vasoconstriction - increased aldosterone levels - proximal nephron increased Na+ retention - JGA cells (inhibits renin release) - cardiac and vascular tissue (profibrotic/remodeling)
48
Renin
- synthesis and release by the JGA cells, which are under feedback control - decreased renal perfusion pressure leads to increased renin release - increased renal SNS stimulation (JGA cell surface beta-1 receptors) leads to increases renin release (why we use beta blockers to help with HTN) - angiotensin II negative feedback (JGA AT1 receptors) leads to decreases renin release (so we don't release too much) - increased distal tubular sodium content leads to increased renin release
49
Direct Renin Inhibitors
- inhibition of renin proteolytic action on its substrate and the formation rate of angiotensin I - decreased PRA, angiotensin I, angiotensin II, aldosterone - increases plasma renin level
50
ACE Inhibitors
- inhibition of the formation of angiotensin II from angiotensin I - decrease angiotensin II and aldosterone levels - increase levels of vasodilatory pepties (e.g. bradykinin) - increase plasma renin levels - increase plasma renin activity (PRA)
51
ARBs (angiotensin receptor blockers)
- blockage of angiotensin II (AT1) receptors at tissue sites - decrease aldosterone levels - increase plasma renin level, PRA, and angiotensin II levels
52
Aldosterone Antagonists
- blockage of mineralocorticoid/aldosterone receptors in the kidney and other sites - Adverse Effect: hyperkalemia
53
Potential Adverse Effects of ACEi, ARB, DRI
- hyperkalemia (aldosterone inhibition) - hypotension - worsen renal insufficinecy (disproportionate glomerular efferent arterial vasodilation) - fetal injury (angiotensin II important for fetal cell differentiation)... all inhibitors of RAA are contraindicated in pregnancy! - ACEi - cough (5-10%) and angioedema (<1%)... ACE has many substrates (angiotensin I, bradykinin, substance P, neuropeptide Y, etc.)
54
Conditions that May Worsen with Certain Drug Therapies
- Pregnancy (RAA agents absolutely contraindicated!) - Depression (beta blockers, central inhibitors) - Sexual Dysfunction (beta blockers, central inhibitors, spironolactone) - Asthma (beta blockers... especially non-selective) - Gout (diuretics) - Constipation (verapamil)
55
Conditions that May have Favorable Effects From BP Rx
- BPH (alpha blockers) - essential tremor; performance anxiety; cardiac awareness (beta blockers) - migraine headache (beta blockers, CCBs) - osteoporosis (thiazides) - kidney stones (thiazides) - Raynaud's Syndrome (DHP, CCBs) - Chronic Diarrhea (verapamil... causes constipation) - Hyponatremia/Hypercalcemia (loop diuretics (+IV saline)

Antihypertensives (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions