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N550 Pharm > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

Joint Nat. Committee says we should treat what BP for someone with DM/kidney disease and what BP without? What do they say is first-line therapy?

A

Over 140/90 without DM/kidney disease
Over 130/80 with DM/kidney disease
First line therapy = thiazide diuretic

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2
Q

What antihypertensives are these patients on..

  1. HF
  2. MI
  3. High CVD risk
A
  1. HF: Thiazide diuretic, B-blocker, ACEI, ARB, aldosterone antagonist
  2. MI: B-blocker, ACEI, aldosterone antagonist
  3. High CVD risk: Thiazide, B-blocker, ACEI, CCB
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3
Q

What antihypertensives are these patients on..

  1. DM
  2. CKD
  3. Stroke prevention
  4. Isolated systolic HTN
A
  1. DM: Thiazide diuretic, B-blocker, ACEI, ARB, CCB
  2. CKD: ACEI or ARB
  3. Stroke prevention: Thiazide diuretic, ACEI
  4. Systolic hypertension: Thiazide, CCB
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4
Q

Hypertensive urgency vs. crisis?

A

DBP over 120
Urgency with evidence of organ damage (BUN/creat inc)
Crisis with evidence of organ failure

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5
Q

Why wouldn’t we want a pt to take ACEI before surgery?

A

ACEI decrease preload leading the patient to be hypovolemic

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6
Q

Angiotensinogen, secreted by the ____ -> (Renin, secreted by the ____) -> AT1 -> (ACE) -> AT2 -> Aldosterone
What effects Do AT2 and Aldosterone have on preload/afterload?

A

Angiotensinogn by liver
Renin by kidney’s juxtaglomerular cells
Aldosterone INC preload
AT2 INC afterload (potent vasoconstrictor)

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7
Q

ACEI uses?

A

HTN, CHF, mitral regurgitation, post MI, diabetic neuropathy, CRI
More effective in DM patients
Reduces BP and cardiac load

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8
Q

What are some Angiotensin-1 receptor effects (belong to G-protein coupled receptors)?

A

Vasoconstriction (especially in afferent arterioles of glomeruli)
Increase NE release
Proximal tubular reabsorption of Na
Secretion of aldosterone from adrenal cortex

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9
Q

ACEI MOA? Name a few.

A

Block conversion of AT1 to AT2 through interaction with zinc ion of ACE (in endothelium)
Prevents vasoconstriction, sodium retention and SNS stimulation
PRILS! Lisinopril, captopril (capoten), ramipril, enalapril (vasotec), fosinopril, quinapril, benazepril

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10
Q

What’s the major difference between ACEI? Captopril vs. enalapril vs. lisinopril

A

Captopril onset 15-30 min, DOA 6-10h, E1/2t 2h (more redosing)
Enalapril onset 1-2h, DOA 18-30h (no rash/renal insufficiency bc lacks sulfhydryl group)
Lisinopril onset 1h, DOA 18-30h

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11
Q

ACEI side effects?

Note: in general, they are mild, good compliance

A

Prolonged hypotension intra-op!!! (Don’t have them take it before surgery!!)
Granulocytopenia, angioedema, proteinuria, persistent cough, hyperkalemia
Captopril: rash, loss of taste

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12
Q

ACEI contraindication?

A

Renal artery stenosis (bc patients may develop renal failure due to efferent arteriole constriction)

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13
Q

ARB MOA? Name some.

A

Competitive binding to inhibit AT2 at its receptor, blocks AT2 without effecting ACE activity, results in decreased peripheral vasoconstriction
SARTAN! Losartan (cozaar), valsartan (diovan), irbesartan, candesartan, telmisartan, eprosartan

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14
Q

ARB side effects and contraindication?

A

SE: similar to ACEI but less cough and no bradykinin accumulation
CI: renal artery stenosis, pregnancy

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15
Q

Hydralazine is a ____ derivative, what does this do? Does it work more on arteries or veins?

A

Arterial vasodilator. Phthalazine derivative which activates gaunylate cyclase producing relaxant effect on vascular smooth muscle.
ARTERIES > VEINS

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16
Q

Hydralazine dose? When does it peak?

A

2.5-10 mg IV

10-20 min peak (this is a LONG time in surgery), lasts up to 6h

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17
Q

Hydralazine pharmacokinetics?

A

Extensive hepatic first pass metabolism
Onset 15 min, give slow
E1/2t 3h
15% unchanged in kidney

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18
Q

Hydralazine side effects?

A 
Reflex tachycardia! Tachyphylaxis, tolerance
DBP reduced more than SBP
Dec SVR
Inc HR, SV, CO
Na/ H2O retention, EKG changes, angina
Drug induced lupus- rash, joint pain
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19
Q

Minoxidil MOA, uses?

A

Directly relaxes ARTERIAL smooth muscle (little effect on venous) by increasing influx of K into smooth muscle, hyperpolarize, vasodilate
Used to treat HTN due to renovascular disease, renal failure, transplant rejection

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20
Q

Minoxidil pharmacokinetics?

A

90% oral dose absorbed from GI
Peak in 1 h
E1/2t 4h
10% unchanged in urine

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21
Q

Minoxidil side effects?

A

Inc HR, CO
Inc plasma concentration of NE, renin (retains Na/H2O, weight gain, edema, hypertrichosis, pulm HTN, pericardial effusion)
Abnormal EKG (flat/inverted T wave)

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22
Q

What are peripheral vasodilators used for? Name some.

A

Facilitates forward LV flow in AR, MR, HF
Controlled hypotension in OR
Treat hypertensive crisis
Nitroglycerine, nitroprusside, isosorbid, dipyridamole, papverine, trimethaphan, diazoxide, adenosine

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23
Q

SNP (sodium nitroprusside, nipride) class? In general, what does it do?

A

Nonselective peripheral vasodilator, direct acting
Relaxes arterial and venous vascular smooth muscle
Lacks effects on nonvascular smooth/cardiac muscle

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24
Q

SNP MOA?

A

Interacts with oxyhemoglobin, dissociates immediately to form methemoboin and releases NO and cyanide
NO activates guanylate cyclase, increasing cGMP
cGMP inhibits calcium entry to vessels, increases uptake of Ca into ER resulting in vasodilation

25
Q

SNP metabolism?

A

Transfer an electron from Fe of oxyhemoglobin to SNP yields metHGb and SNP radical where all 5 cyanide ions are released, one of these ions reacts with metHGb to form cyano-methemoblobin (nontoxic), the remainder is metabolized in liver and kidney converted to thiocyanate (if they are on it too long, this leads to cyanide toxicity)

26
Q

Cyanide toxicity: signs and treatment?

A

Can occur at over 2 mcg/kg/min for long periods
Pt is resistant to hypotensive effects, tachyphylaxis, this may precipitate tissue anoxia, anaeorobic metabolism, and lactic acidosis (get lactic level drawn)
Treat by stopping SNP, 100% O2, sodium bicarb, sodium thiosulfate, sodium nitrate for severe toxicity

27
Q

Signs of SNP-induced thiocyanate toxicity or methemoglobinemia?

A

Thio toxicity: rare, less toxic than cyanide, s/s: N/V, tinnitus, fatigue, CNS hyperreflexia, consfusion, physchosis, miosis, seizure, coma
Methemoglobinemia: rare, impaired O2 with adequate CO
Phototoxicity is also possible, comes in dark bag so light doesn’t convert the SNP to hydrogen cyanide

28
Q

SNP dose

A

0.3 mcg/kg/min - 10 mcg/kg/min
0.3-0.5 for controlled hypotension, 1-2 mcg/kg for hypertensive crisis
Max should not be given for more than 10 min, immediate onset, short duration of action, put in an A-line for close monitoring!!

29
Q

SNP cardiac, CNS, pulmonary, and blood effects?

A

CV: venous/art dilation, dec venous capacitance (due to venous return), baroreceptor reflex inc HR, dec SBP/SVR/PVR, inc contractility, does NOT dilate coronary artery so consider coronary steal
CNS: inc CBF/ICP
Pulm: stops hypoxic vasoconstriction
Blood: inc intracellular GMP which inhibits platelet aggregation and bleeding time

30
Q

Nitroglycerin (NTG) class, in general what does it do?

A

Organic nitrate that acts on venous capacitance vessels and large coronary arteries
Peripheral vasodilator

31
Q

NTG MOA?

A

Generates NO through a glutathione-dependent pathway (that involves glutathione and glutathione S-transferase)
It requires the presence of thio-containing compound to generate NO
NO generation stimulates cGMP to cause peripheral vasodilation (like SNP)

32
Q

How does NTG form metHGb? How is methemoglobinemia treated?

A

Nitrite metabolite oxidizes ferrous ion in Hgb to ferric form that leads to formation of metHgb (makes pulse ox go down)
Methemoglobinemia can be treated with methylene blue 1-2 mg/kg IV over 5 min

33
Q

Tolerance to NTG starts after how long?

A

24 hours of sustained treatment

34
Q

NTG effects of CV?

A

Venodilation, dec venous return, dec preload, dec L/R EDP, dec CO, so REDUCES myocardial oxygen requirements
(No change in HR/SVR)
Increase in coronary blood flow to subendocardial areas (opposite of SNP)
Good for angina, cardiac failure, and controlled hypotension (4-5 mcg/kg/min)

35
Q

NTG effects on CNS, pulmonary, blood, GI?

A

CNS: vasodilation, increased ICP headache
Pulmonary: dec PVR, bronchial dilation, inhibits hypoxic pulmonary vasoconstriction
Blood: dose related prolonged bleeding time, inhibits platelet aggregation
GI: relaxes smooth muscles of GI (good for biliary spasm)

36
Q

Isosorbid key points?

A

Oral nitrate, not used over NTG; just know it exists
Works on venous circulation, improves regional distribution of myocardial blood flow in pt with CAD
SE orthostatic hypotension
Active metabolite isosorbid-5-mononitrate

37
Q

Trimetaphan key points?

A

Peripheral vasodilator, rapid onset
Lowers BP, CO, SVR
Inc HR due to PSNS blockade
Not better than NTG or SNP; Just know it exists

38
Q

What do phosphodiesterase inhibitors do?

A

Isoenzymes that inhibit the breakdown of intracellular cAMP and cGMP causing vascular smooth muscle relaxation (vasodilation) and positive inotropy

39
Q

What are phosphodiesterase inhibitors used for? Which drugs are contraindicated? Name a couple phosphodiesterase inhibitors.

A

Used for heart failure
Avoid nitrates or ED meds
Amrinone, milrinone

40
Q

How do calcium channel blockers work?

A

CCB bind to receptor on voltage-gated Ca ion maintaining the channel in a inactive or closed state

41
Q

Where are calcium ion channel present?

A 
Cell membranes of skeletal muscle
Vascular smooth muscle
Cardiac muscle
Mesenteric muscle
Neurons
Glandular cells
42
Q

CCB with phenyl-alkyl-amines or benzothiazepines structure will block the _____. CCB with 1,4-dihydropyridines will block _____.

A

phenyl-alkyl-amines or benzothiazepines structure block AV node
1,4-dihydropyrides block arterial beds

43
Q

What effects do CCB have?

A

Dec contractility (ionotropy)
Dec HR (chronotropy)
Dec activity of SA node
Dec rate of conduction of impulses via AV node (dromotropy)
Dec SVR and BP (vascular smooth muscle relax, art > venous)

44
Q

CCB side effects?

A

Prolonged bleeding
GI constipation
Cardiac problems
CAncer

45
Q

CCB uses?

A 
Systemic and pulmonary HTN
Cerebral arterial spasm
Raynaud's disease
Migraine
Bronchial asthma, esophageal spasm, dysmenorrhea, premature labor
46
Q

CCB drug interactions?

A

Inhalational agents, B-blockers- myocardial depression, vasodilation
Potentiate NM blockers
LA toxicity (verapamil)
Dantrolene with verapamil can cause hyperK
Interacts with platelet function (causes prolonged bleeding)
Digoxin plasma conc inc with CCB
H2 antagonists (ranitidine and cimetidine) inc CCB plasma levels

47
Q

Toxicity of CCB reversed with what?

A

IV calcium or dopamine

48
Q

What is verapamil, where does it primarily work?

A

Derivative of papaverine, specific for slow calcium channel
Primary site of action: AV node; Depress AV node, neg chonotropic, neg inotropic, moderate vasodilation on coronary and systemic arteries

49
Q

Verapamil uses?

A

SVT, vasospastic angina, HTN
Hypertropic cardiomyopathy
Maternal and fetal tachydysrhythmias
Premature onset of labor

50
Q

Verapamil pharmacokinetics?

A

Highly protein bound (presence of agents like lidocaine/diazepam inc its activity)
Orally almost completely absorbed, extensive hepatic first pass metabolism, almost none of the drug appears unchanged in the urine (limited bioavailability)
Oral peaks in 30-45 min, IV in 15 min
E1/2t 6-12h

51
Q

What is nifedipine? What is it used for? What effects does it have?

A

Dihydropyridine derivative used for angina
Primary site of action is peripheral arterioles (vasodilates more than verapamil, little/no effect on SA/AV node)
Dec SVR/BP
Reflex tachycardia
Myocardial depression on pts with LV dysfunction or on B-blockers

52
Q

Nifedipine and nicardipine mostly work where?

A

Coronary and peripheral artery vasodilation

53
Q

Diltiazem works where? Uses?

A

Benzothiazepine derivative; principle site of action is AV node
Uses: (similar to verapamil but less potent) SVT, HTN, vasospastic angina, hypertrophic cardiomyopathy, maternal/fetal tachydysrhythmias

54
Q

What is the only CCB with an active metabolite?

A

Verapamil

55
Q

Clonidine MOA

A

It is a centrally acting agent; reduces sympathetic outflow from vasomotor centers in the brainstem
Centrally acting selective partial alpha-2 adrenergic agonist
(200:1 A1 over A2)

56
Q

Clonidine uses?

A

Hypertension (it dec BP from dec CO due to dec HR/PVR)
Induce sedation, analgesia
Dec anesthetic requirements (DEC your MAC by 50%!!)
Improve peri-op hemodynamics

57
Q

Clonidine SE and what happens if it is stopped abruptly?

A

If stopped abruptly, rebound HTN. Withdrawal after 18 hours of no use, lasts 24-72 hours if pt on doses over 1.2 mg/day, treat with clonidine
SE: bradycardia, sedation, xerostomia (dry mouth), nightmares, depression, vertigo, EPS, lactation in med

58
Q

Should a patient continue using B-blockers, CCB, or ACE pre-op?

A

B-blocker: YES, if not they care at risk of peri-operative MI
CCB: YES unless severe LV dysfunction
ACEI: NO (hypovolemia intra-op)

N550 Pharm (14 decks)

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