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Spring 22 PT HTN > Oyekan HTN > Flashcards

Oyekan HTN Flashcards

1
Q

HTN increases the risk for _______

A

MI, kidney disease, and stroke

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2
Q

Causes of Secondary HTN

A 
Disease States 
• Kidney disease 
• Adrenal gland tumors 
• Thyroid disease 
• Congenital blood vessel disorders
• Alcohol abuse or chronic alcohol use
• Obstructive sleep apnea

Drugs and Other Products

  • NSAIDS
  • Oral contraceptives
  • Decongestants
  • Cocaine
  • Amphetamines
  • Corticosteroids
  • Foods
  • Alcohol
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3
Q

RF for HTN regarding gender

A

Gender: Female >70 years of age; male <55 years of age

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4
Q

Primary hypertension

A

Overactivity of sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS), and alterations in natriuretic peptides

Inflammation, endothelial dysfunction, obesity-related hormones, and insulin resistance

Genetics interact with diet, smoking, age, and other risk factors to cause chronic changes in vasomotor tone and blood volume.

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5
Q

Genetic factors like insulin resistance causes what affect in hypertension and what does it lead to?

A

Genetic factors like insulin resistance leads to VASOCONSTRICTION which increases systemic vascular resistance(^ SVR) and ultimately results and sustained hypertension

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6
Q

Environmental factors like inflammation leads to Reno salt and water with tension which increases the blood volume and ultimately result in sustained hypertension

A

Environmental factors like inflammation leads to renal salt and water retension which increases the blood volume and ultimately result in sustained hypertension

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7
Q

BP= CO * SVR

A

TX= Diuretics * Vasodilators

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8
Q

Stroke volume=

A

Stroke volume = EDV – ESV i.e. dependent on loading (pre-and afterload) and contractility

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9
Q

cardiac dysfunction i.e. pump-based hypertension requires what antiHTN medication?

A

cardiac dysfunction i.e. pump-based hypertension (↑ CO, normal SVR) in the younger patients. Calls for use of β- antagonists (BETA BLOCKERS)

Beta blockers cause the heart to beat more slowly and with less force, which lowers blood pressure. Beta blockers also help widen veins and arteries to improve blood flow.

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10
Q

vascular dysfunction i.e. vascular resistance-based hypertension requires what antiHTN medication?

A

vascular dysfunction i.e. vascular resistance-based hypertension (normal CO, ↑ SVR) in the elderly. Calls for use of DIURETICS

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11
Q

renal dysfunction i.e. volume-based Hypertension (↑ CO, ↑SVR), and neuroendocrine dysfunction involving excessive secretion of

A
  • catecholamines (pheochromocytoma)
    •aldosterone (primary aldosteronism)
    •thyroid hormones (hyperthyroidism)
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12
Q

SYMPATHOLYTICS (SNS outflow blockers) consists of

A
  • Ganglionic Blockers
  • Postganglionic adrenergic nerve terminal antagonists

•a1-adrenergic antagonists

  • B1-adrenergic antagonists
  • Mixed a/B adrenergic antagonists
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13
Q

Vasodilators:

A
  • CCB
  • Minoxidil

+

*Hydralazine sodium

= K Channel openers

*Nitroprusside

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14
Q

What antiHTN medications affect HR?

A
  • B-blockers (Beta blockers cause the heart to beat more slowly and with less force, which lowers blood pressure. Beta blockers also help widen veins and arteries to improve blood flow.)
  • CCB (Calcium channel blockers are medications used to lower blood pressure. They work by preventing calcium from entering the cells of the heart and arteries. Calcium causes the heart and arteries to squeeze (contract) more strongly. By blocking calcium, calcium channel blockers allow blood vessels to relax and open.)
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15
Q

Stroke/blood volume is controlled by contractility and preload, what antiHTN medications tx contractility?

A

Bblockers

CCBs

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16
Q

Stroke/blood volume is controlled by contractility and preload(amount of VOLUME of blood in veins), what antiHTN medications tx preload(Vol)?

A

Venous tone:

  • a1 antagonists
  • sodium nitroprusside
  • ACEI
  • ATII antagonists

Intravascular VOLUME: (Na+/H20 retention):

  • diuretics
  • ACEI
  • ATI antagonists
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17
Q

SVR is affected by direct innervation, circulator regulators, and local regulators, what anti-hypertension medications are used to treat direct innervation?

A
  • a1 antagonists (The alpha-1 adrenergic receptor antagonists (also called alpha-blockers) are a family of agents that bind to and inhibit type 1 alpha-adrenergic receptors and thus inhibit smooth muscle contraction)
  • central a2 AGONISTS
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18
Q

SVR is affected by direct innervation, circulator regulators, and local regulators, what anti-hypertension medications are used to treat circulating regulators?

A
  • a1 antagonists
  • central a2 agonists
  • ACEI
  • AT1 antagonists
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19
Q

SVR is affected by direct innervation, circulator regulators, and local regulators, what anti-hypertension medications are used to treat local regulators?

A

Endothelin antagonists

Sodium nitroprusside

ACE inhibitors

AT1 antagonists

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20
Q

TorF: Diuretics target Na+ reabsorption along every segment of the nephron

A

True

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21
Q

JNC7 recommends thiazide diuretics as the 1st line of treatment unless dictated otherwise such as patients with ______

A

JNC7 recommends thiazide diuretics as the 1st line of treatment unless dictated otherwise e.g. start with ACEIs in patients with diabetes.

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22
Q

__________ are effective in patients with volume-based hypertension characterized by renal dss and in African Americans.

A

Thiazide diuretics

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23
Q

SE of Thiazide diuretics

A

hypercalcemia, hyperuricemia, hyperglycemia, hyperlipidemia, HYPOkalemia

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24
Q

Major difference between different loop diuretics is:

A

Major difference between different loop diuretics is potency and incidence of allergies.

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25
Q

SE of loop diuretics

A

hypocalcemia, hypomagnessemia, metabolic alkalosis

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26
Q

volume-contraction alkalosis is often seen with what class of medications?

A

Loop diuretics

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27
Q

Loop diuretic uses:

A

1st line therapy for acute relief of edema in heart failure

Increase in Ca2+ diuresis in hyperparathyroidism and malignancy-associated hypercalciuria of parathyroid gland

Counteract hyperkalemia due to K+-retaining adverse effects of other drugs

ARF – useful to counteract decrease GFR of ARF

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28
Q

Which diuretic has the longest duration of action? Which diuretic has the shortest duration of action?

A

Loop diuretics are characterized by short duration of action (4-6 hrs) very potent diuresis, moderate antihypertensive effect

Thiazide diuretics have high oral bioavailability and long duration of action

e.g.
Chlorothiazide 6-12 hrs
Chlorthalidone 48-72 hrs
HCTZ 16-24 hrs.

29
Q

Which diuretic is preferred in patients with chronic kidney disease? 

A

Loop diuretics are preferred over thiazides in the management of malignant hypertension and volume-based hypertension in patients with advanced CKD.

30
Q

SE of Loop diuretics

A

Hypokalemia

Ototoxicity: deafness (most common with ethacrynic acid)

• Others 
- Metabolic (hypokalemic) alkalosis
- Acute hypovolemia 
– possibility of hypotension, shock,  arrythmias
- Hypomagnesemia
31
Q

MOA of K-sparing diuretics

A
  • Aldosterone receptor antagonism - Spironolactone & Eplerenone
  • Competitive inhibition epithelial Na+ transporter (ENaC) activity –Amiloride, Triamterene
  • ENaC is controlled by aldosterone. Aldosterone binding to mineralocorticoid receptor (MR), increases ENaC activity, increases Na+ reabsorption, increases intravascular volume
32
Q

SE of k-sparing diuretics:

A
  • Hyperkalemia → main danger
  • Androgenic/estrogenic effects – due to binding to androgen receptor resulting in Hirsutism, menstrual irregularity, gynecomastia, impotence
  • Gynecomastia – Eplerenone (more selective), t/4 less adverse effect
  • Nephrotoxicity( Triamterene)
  • OhypoTN
33
Q

Which class of diuretics causes gastric upset and peptic ulcers?

A

K-sparing diuretic

34
Q

Metabolic alkalosis is most commonly seen what class of diuretics?

Metabolic acidosis is most commonly seen and what class of diuretics?

A

Metabolic alkalosis is most commonly see in loop diuretics. Clinical consequences are often described as volume contraction alkalosis.

Metabolic acidosis is the most commonly seen in potassium sparing diuretics, due to the decrease Na+ uptake accompanied by decrease H+ secretion

35
Q

Liddle’s Syndrome

A

 Amiloride(MIDAMOR) and triamterene are drugs of choice for treatment of liddle’s syndrome, a rare form of hypertension resulting from gain-of-function mutations in the beta or gamma subunits of the ENaC sodium channel.

36
Q

When are k-sparing diuretics contraindicated?

A

Anuria

Hyperkalemia

Acute renal insufficiency

37
Q

When are loop diuretics contraindicated?

A
  • Hypersensitivity to sulfonamides (contraindicated for furosemide, bumetanide, and torsemide)
  • Anuria
  • Coadministration with aminoglycosides increases ototoxicity and nephrotoxicity



38
Q

What two MOAs does Sympatholytics aka down regulators of sympathetic tone have?

A
  • Decrease SVR and/or CO
  • a and b antagonists
  • Centrally–acting sympatholytics
39
Q

TorF: atenolol is a non selective bblocker?

A

False. Propranolol (nonselective), metoprolol and atenolol (β 1selective)

40
Q

The INITIAL antihypertensive effect of beta blockers/beta antagonists is due to what?

A

negative chronotropism + inotropism —> ↓HR, ↓SV, ↓CO.

41
Q

Subsequent antihypertensive effect of bblockers is due to

A

decrease vasomotor tone—> decrease SVR.

42
Q

TorF: Beta antagonists can cause decreased TG levels and increase HLDL?

A

False. Therapy is associated with INCREASE↑TG and DECREASED↓HLDL

43
Q

TorF: beta blockers cause a decrease in blood sugar?

A

False. INCREASE ↑glucose intolerance (hyperglycemia)

44
Q

Bblockers SE:

A

Sedation, impotence, depression, bronchoconstriction (less with cardioselective ones)

45
Q

TorF: Labetalol and carvedilol are useful in hypertensive emergencies, however a side effect is rebound increased heart rate and increased cardiac output?

A

False.

•No reflex ↑HR or CO seen with pure vasodilators (because of concomitant β
1blockade)

•No effect on serum lipids

46
Q

a-antagonists incl:

A

a1 selective

a1 nonselective

Prazosin, Terazosin, Doxazosin

47
Q

TorF: a-antagonists have no effect on serum lipids

48
Q

TorF: Prazosin have an increase incidence of heart failure

A

False. Doxazosin - ↑ incidence of heart failure

49
Q

Non-selective antagonists e.g. phenoxybenzamine (PBZ), phentolamine are not useful for long term treatment because of

A

excessive compensatory responses

50
Q

Central Sympatholytics: a2 AGONISTS MOA

A

methyldopa, clonidine, guanabenz

•↓ sympathetic outflow from the medulla =↓ HR, ↓ contractility, ↓vasomotor tone

51
Q

Central Sympatholytics: Ganglion blockers MOA & SE

A

Trimethaphan, Hexamethonium

  • Inhibit nicotinic receptors at sympathetic ganglia
  • SE: Constipation, blurred vision, sexual dysfunction, postural hypotension
52
Q

Neuronal blockers MOA & SE

A

Reserpine, Guanethidine

  • These agents are taken up into the terminals of postganglionic adrenergic neurons = depletion of NE from synaptic vesicles = ↓BP
  • SE: initial hypertensive crisis, severe depression (Reserpine), postural hypotension and sexual dysfunction (Guanethidine)
53
Q

Modulators of Vascular Tone aka ARTERIAL VASODILATORS

A

(i) blockade of Ca2+ channels (CCBs) - Verapamil (Verelan PM-extended-release and Verelan-delayed-release and Calan), Diltiazem- Cardizem CD, and Taztia XT, Nifedipine-Adalat, Amilodipine-Norvasc
(ii) opening of K+ channels e.g. Hydralazine-Apresoline, Minoxidil-Rogaine

•arterial vasodilation, negative inotropism and/or negative chronotropism

54
Q

TorF: The DHPs act primarily on vascular tissue as vasodilators

55
Q

TorF: Non DHPs act primarily on cardiac tissue as negative inotropes and chronotropes.

56
Q

Use nonDHPs in caution in pts with

A

(i) impaired LV systolic function (because of ↑ HF)
(ii) conduction system disease (involving SA & AV nodes)
(iii) patients on β-antagonist therapy.

57
Q

K+ channel openers

A
  • hyperpolarization of vascular smooth muscle →↓ response to depolarizing stimuli
  • compensatory retention of Na+ and water, reflex ↑HR (More common with Hydralazine than minoxidil)
58
Q

TorF: minoxidil is largely restricted to patients with severe hypertension that is refractory to other antihypertensive agents.

59
Q

Apresoline + ______ is used as adjunctive therapy (to ACEI + β-antagonist) for management of heart failure in African Americans.

A

lsosorbide dinitrate (ISDN)

60
Q

Any inhibitors of the RAAS sys will cause

A

HYPERkalemia

61
Q

Renin inhibitors e.g. Aliskiren

A
  • Increased BKN(vasodilator) levels
  • Adverse effects – cough, angioedema, precipitate 1st dose hypotension and/or ARF, hyperkalemia (esp with K-sparing diuretics)
62
Q

ACEIs also ↓ ________ degradation =↑ ________ in the circulation =
vasodilation = ↓ SVR

63
Q

TorF: ACEI are equally effective in hypertension as thiazides and β blocker

64
Q

Unique benefits of ACEIs as antihypertensive agents –

A

(i) renoprotective effects in patients with CKD
(ii) relatively few adverse effects e.g. no hypokalemia or effect on serum lipid profile

(iii) they are the preferred antihypertensive agents in the
hypertensive diabetic patent (b/c of renoprotective effect – ie. Slows onset of diabetic glomerular disease).

First dose hypotension and/or acute renal failure are more common in patients with bilateral renal artery stenosis; hyperkalemia is more common in when ACEI are used in combination with potassium sparing diuretics

65
Q

Adverse effects/CI of ACEI

A

use with caution in patients with

(i) intravascular volume depletion as it may cause compensatory ↑ renin/ATII =impaired autoregulation= renal insufficiency
(ii) bilateral or unilateral artery stenosis

66
Q

ARBs

A

MOA – competitive antagonism of AT1 receptors

No effect on BKN metabolism

Minimize incidence of cough and angioedema

ARBs may protect against stroke via DECREASE platelet aggregation, DECREASE serum uric acid, DECREASE incidence of Afib and antidiabetic effects

67
Q

Elderly patients respond better to _________ and __________ while _______ tends to impair cardiac function. 

A

DIURETICS and DHPCCBs while bblockers tends to impair cardiac function

68
Q

African Americans are more responsive to _______ and _______ compared to ________

A

More responsive to diuretics and CCBs than to ACEIs and β-blocker

Exception – Young African Americans do well on β-antagonists

Hypertensive, diabetic African Americans with CKD (use ACEIs & β-blockers

With previous MI, DO NOT USE thiazides

Spring 22 PT HTN (4 decks)

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