Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharm > Anti-hypertensives > Flashcards

Anti-hypertensives Flashcards

1
Q

Clonidine

A

centrally acting alpha 2 agonist

MOA: activate alpha 2 receptor–>decrease central sympathetic outflow–>decrease NE release

Effect:–>decrease TPR

Uses:

  1. HTN
  2. Clonidine used in withdrawal from abused drugs

Advantages of using:

  1. No change in lipids
  2. used in nicotine dependence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Clonidine Toxicities

A
  1. dry mouth
  2. sedation
  3. rebound HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Methyldopa Toxicities

A
  1. positive Coombs test (hemolytic anemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

DOC to treat anti hypertension in pregnancy

A

Clonidine; also doesn’t cause a change in lipids

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

Methyldopa

A

centrally acting alpha 2 agonist

MOA: activate alpha 2 receptor–>decrease central sympathetic outflow–>decrease NE release

Effect:–>decrease TPR

Uses:
1. HTN in pregnancy–DOC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Reserpine

MOA; Effects & Uses

A

Sympathetic nerve terminal blocker

MOA: blocks vesicular uptake & depletes transmiter stores

Hemodynamic effects: Decrease TPR & CO

Uses: rarely used to treat HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Reserpine Toxicities

A

Toxicities: sedation & depression

Disadvantages/Contraindicated: depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Guanethidine toxicities & disadvantages/contraindications

A

Toxicities:
1. Orthostatic Hypotention
2. Fluid retention
Disadvantages/Contraindicated: CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Guanethidine MOA, Effects & Uses

A

Sympathetic nerve terminal blocker

MOA: interferes with amine release & replaces NE in vesicles

Hemodynamic effects: Decrease TPR & CO

Uses: rarely used to treat HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Use of Alpha 1 blockers to treat Hypertension

A

MOA:

  1. selectively block alpha1A receptors
  2. reduce prostatic SM tone

Hemodynamic effects: Decrease TPR

Uses: 1. HTN 2. BPH

Toxicities: orthostatic hypertension

Disadvantages/contraindications: none

Advantages: Decreases VLDL & LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Alpha 1 blockers used to treat HTN

A
  1. prazosin
  2. terazosin
  3. doxazosin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Use of Beta blockers to treat Hypertension

A

MOA:

  1. Block B1 receptors
  2. decrease renin secretion

Hemodynamic effects–> Decrease CO

Clinical Uses: 1. HTN 2. HF

Toxicities/interactions: Bronchoconstriction

Contraindication:

  1. Bronchial asthma
  2. Heart Block

Advantages: Prolong survival
***labetalol is DOC in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Beta Blockers used to treat Hypertension

A
  1. metoprolol
  2. atenolol
  3. carvedilol (blocks B1 & alpha receptors)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Drugs used to treat HTN that work by decreasing CO

A
  1. beta blockers

2. calcium-channel blockers (work by decreasing HR & FOC)

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

Vasodilators used to treat HTN that work by decreasing systemic vascular resistance

A
  1. alpha blockers
  2. direct-acting vasodilators
  3. Angtiotensin-converting enzyme inhibitors (ACE inhibitors)
  4. angiotensin receptor blockers (ARBs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Antihypertensives that work at the vasomotor center

A
  1. methyldopa
  2. clonidine
  3. guanabenz
  4. guanfacine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Antihypertensives that work at sympathetic ganglia

A

Trimethaphan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Antihypertensives that work at sympathetic nerve terminals

A
  1. guanethidine
  2. guanadrel
  3. reserpine (not used bc it depletes MO–>depression)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Antihypertensives that work at beta receptors of heart

A

beta blockers ie propranolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Antihypertensives that work at angiotensin receptors of vessels

A
  1. losartan

2. other angiotensin receptor blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Antihypertensives that work at alpha receptors of vessels

A
  1. prazosin

2. and other alpha 1 blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Antihypertensives that work at vascular smooth muscle

A
  1. hydralazine
  2. minoxidil
  3. nitroprusside
  4. diazoxide
  5. verapamil & other CCB
  6. Fenoldopam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Antihypertensives that work at kidney tubules

A
  1. thiazides, etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Antihypertensives that work at beta receptors of juxtaglomerular cells that release RENIN

A

Propranolol & other beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Angiotensinogen is converted to angiotensin 1 by _____ which is inhibited by _______

A
  1. renin

2. alskiren

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

angiotensin 1 is converted to angiotensin II by _________ which is inhibited by ___________

A
  1. Angiotensin-converting enzyme (ACE)

2. Captopril & other ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How do diuretics treat HTN?

A
  1. they reduce venous pressure & CO by reducing blood volume
  2. HOW? They act on the kidney to enhance Na & water excretion
  3. Reducing blood volume not only reduces central venous pressure, but also CO!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What group of diuretics are preferred for HTN? WHY? Ex?

A

Thiazides, bc maximum antihypertensive action is at LOWER doses than the diuretic dose!

Ex) hydrochlorothiazide

Added BONUS: they reduce SVR with long-term use

Loss of Na–>decreased vessel stiffness–>decreased TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Toxicity of Thiazides

A
  1. hypokalemia
  2. decrease glucose tolerance and may unmask latent DM
  3. increase plasma LDL, cholesterol & triglycerides (TG)
  4. increase plasma uric acid & may precipitate acute gout
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

MOA for beta blockers as anti-HTN drugs

A
  1. decrease in CO by blocking cardiac Beta 1 receptors

2. inhibition of renin release by blocking beta 1 receptors on JG cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Hemodynamic effects of beta blockers in HTN

A

a) Decreased:
1. HR
2. CO
3. PVR

b) Unchanged: venous tone
c) Negligable: postural hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

all beta blockers are equally effective in lowering BP in??

A

mild to moderate HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

in severe HTN, beta blockers are useful???

A

in preventing the reflex tachycardia that often results from treatment with direct vasodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

beta blockers have shown to reduce mortality after

A

MI & heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Propranolol

a) type
b) toxicities
c) prolonged use warning

A

a) non-selective comound
b)
1. bradycardia or cardiac conduction disease
2. asthma
3. peripheral vascular insufficiency
4. diabetes
c) DO NOT discontinue abruptly after prolonged regular use bc can result in reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Cardio-selective beta 1 drugs

b) benefits?

A
  1. atenolol
  2. metoprolol

b) cause less bronchoconstriction than propranolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

beat blockers with additional alpha blocking activity

b) when would you use them?

A
  1. labetalol
  2. carvedilol

b) tumor in adrenal medulla (pheochromocytoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Calcium channel blockers act on

A

L type calcium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

CCB effective in lowering BP

A
  1. verapamil
  2. diltiazem (has intermediate actions)
  3. DHP (amlodipine, felodipine, isradipine, nicardipine, nifedipine, nisoldipine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

DHP

a) examples
b) selectivity
c) can cause

A
  1. amlodipine
  2. felodipine
  3. isradipine
  4. nicardipine
  5. nifedipine (not for HTN bc too short acting!!)
  6. nisoldipine

b) more selective as vasodilators
c) can cause slight reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Verapamil

A
  1. has the greatest depressant effect on the heart
  2. may decrease HR & CO
  3. How? L-type Ca channels–>decrease FOC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

DHP not used for HTN bc too short acting

A

nifedipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How do calcium channels lead to muscle contraction?

A
  1. calcium comes in

2. binds to myosin light chain kins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Inhibitors of Renin Angiotensin Aldosterone System (RAAS)

A
  1. ACE inhibitors: end in “-pril” (captopril, Enalapril, Ramipril, Benazepril, fosinopril, lisinopril, quinapril)
  2. Angiotensin Receptor Blockers (ARBs): end in “-sartan” (Losartan, Valsartan, Candesartan, sprosartan, irbesartan, telmisartan, olmesartan)
  3. Renin antagonist: aliskiren
  4. Aldosterone Receptor inhibitors: end in “-one” (spironolactone, elprenone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

ACE Inhibitors

A

end in “-pril”

  1. captopril
  2. Enalapril
  3. Ramipril
  4. Benazepril
  5. fosinopril
  6. lisinopril
  7. quinapril
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

end in “-pril”

A

ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Angiotensin Receptor Blockers (ARBs) (Losartan, Valsartan, Candesartan, sprosartan, irbesartan, telmisartan, olmesartan)

A
  1. Losartan
  2. Valsartan
  3. Candesartan
  4. sprosartan
  5. irbesartan
  6. telmisartan
  7. olmesartan)
48
Q

End in “-sartan

A

Angiotensin Receptor Blockers (ARBs)

1. Losartan, Valsartan, Candesartan, sprosartan, irbesartan, telmisartan, olmesartan

49
Q

Aldosterone Receptor inhibitors

A

end in “-one”

  1. spironolactone
  2. elprenone
50
Q

end in “-one”

A

Aldosterone Receptor inhibitors:

  1. spironolactone
  2. elprenone
51
Q

Effects of ATII on the myocardium & kidney

A
  1. mitogenic for vascular & cardiac muscular cells

Remodeling:

52
Q

Remodeling effects of ATII

A
  1. increased wall-to lumen ratio in bv
  2. concentric & eccentric hypertrophy
  3. fibrosis & stenosis of intimal surface of bv
  4. due to increased migration & hyperplasia of vascular sm cells, myocytes & fibroblasts
    * *slowed, prevented & even reversed by ACE inhibitors
53
Q

Effects of angiotensin II

b) inhibited by

A
  1. vasoconstriction–>increased peripheral vascular resistance–>increased BP
  2. aldosterone secretion–>increased Na & water retention–>increased BP

b) Angiotensin receptor blockers (ARBs)

54
Q

Effects of aldosterone secretion

b) inhibited by

A

aldosterone secretion–>increased Na & water retention–> increased BP

b) inhibited by spironolactone, eplerenone (aldosterone receptor inhibitor

55
Q

Effects of bradykinin

A

Bradykinin is an important vasodilator: normally it stimulates release of NO & prostacyclin–> decreases PVR

  1. increased prostaglandin synthesis–>vasodilation
  2. release of NO–> vasodilation–>decreased PVR–> decreased BP

**causes dry cough in ACEI (MC ADR w ACEI)

56
Q

Role of ACE inhibitors

A
  1. act by inhibiting the ACE converting enzyme (peptide dipeptidase)
  2. enzyme normally hydrolyzes angiotensin I–>II
  3. also inactivates bradykinin (an important vasodilator: normally it stimulates release of NO & prostacyclin–> decreases PVR)
  4. ACEI lower BP principally by DECREASING PVR
57
Q

How do ACE inhibitors treat HTN?

A

They lower BP principally by DECREASING PVR

58
Q

When are ACEI DOC?

A
  1. Diabetic nephropathy, bc they diminish proteinuria & stabilize renal function
  2. They improve internal hemodynamics with DECREASED glomerular EFFERENT arteriolar RESISTANCE & a resulting REDUCTION of intraglomerular capillary pressure

Don’t use concurrently with K+ sparing diuretics bc can result in HYPERkalemia

59
Q

ACEI ADR

A
  1. Severe HYPOtension can occur after initial doses in pots who are HYPOVOLEMIC
  2. DRY COUGH = MC!!
    * due to increased levels of BRADYKININ
  3. Acute renal failure in patients with bilateral renal artery stenosis
    * *in renovascular HTN, glomerular filtration pressures are maintained by vasoconstriction of the post-glomerular arterioles, an effect mediated by AGII–>ACEI can therefore ppt a significant reduction in GFR & cause acute renal failure
  4. Angioedema is rare but may be potentially fatal; more common in blacks
  5. PREGNANCY CATEGORY D: DO NOT USE IN PREGNANCY bc can cause SEVERE renal pathology in fetus
  6. DRUG interactions: HYPERkalemia: if K+ sparing diuretics & ACEI are concurrently used
60
Q

Angiotensin Receptor Blockers (ARBs) uses & MOA

A
  1. Block the ATII type 1 (AT1) receptor
  2. have NO effect on bradykinin metabolism & are therefore MORE SELECTIVE blockers of angiotensin effects than ACEI
  3. ARBS provide benefits similar to those of ACEI in patients with heart failure & chronic kidney disease
61
Q

ARB ADR

A
  1. Noticeably lower incidence of cough (bc no effect on bradykinin metab)
  2. hyperkalemia
  3. renal effects
  4. pregnancy category D: DO NOT use in pregnancy! (bc can cause renal pathology in fetus)
62
Q

Alpha Blockers

A
  1. alpha 1 selective drugs produce their antihypertensive effects by selectively blocking alpha 1 receptors in arterioles & venues
  2. postural hypotension can be seen
  3. used in men with concurrent HTN & BPH
  4. nonselective alpha blockers work by blocking both the presynaptic and postsynaptic receptors–> tachycardia
63
Q

Men with concurrent HTN & BPH should use

A

alpha 1 selective blockers

  1. prazosin
  2. terazosin
  3. doxazosin
64
Q

alpha 1 selective blockers

A
  1. prazosin
  2. terazosin
  3. doxazosin

used primarily in men with concurrent HTN & BPH

65
Q

Used in diagnosis & treatment of pheochromocytoma

A

nonselective alpha blockers:

  1. phentolamine
  2. phenoxybenzamine

work by blocking both the presynaptic and postsynaptic receptors–> tachycardia

66
Q

nonselective alpha blockers

A
  1. phentolamine
  2. phenoxybenzamine

work by blocking both the presynaptic and postsynaptic receptors–> tachycardia

67
Q

4 MOA Vasodilators use

A

dilate vessels by acting directly on SM cells through NONAUTONOMIC mechanisms

  1. Release of NO
  2. Blockade of Ca Channels
  3. Opening of K+ Channels
  4. Activation of D1 receptors
68
Q

Vasodilators that act by releasing NO

A
  1. Nitroprusside
  2. Hydralazine
    Other drugs that act by this mechanism are
  3. Nitrates
  4. Histamine
  5. ACh
69
Q

Vasodilators that act by Blockade of Ca channels

A
  1. Verapamil
  2. diltiazem
  3. DHP like nifedipine, amlodipine
70
Q

Vasodilators that act by Activation of D1 receptors

A

Fenoldopam

71
Q

Vasodilators that act by Opening K+ Channels

A
  1. minoxidil

2. diazoxide

72
Q

MOA by which Vasodilators that act by Opening K+ Channels WORK

A
  1. intercellular K ion concentration (150mM) > extracellular K ion concentration (3-4 mM)
  2. K channel opening–> outflow of K ions —> hyper polarization –> a series of cellular responses like smooth muscle relaxation
73
Q

vasodilators that act on the venous bed

A
  1. nitrates (more V>A)
  2. ACEI (both venous & arterial beds)
  3. alpha 1 antagonists (both venous & arterial beds)
  4. Nitroprusside Sodium (both venous & arterial beds)
74
Q

vasodilators that act on the arterial bed

A
  1. ACEI (both venous & arterial beds)
  2. alpha 1 antagonists (both venous & arterial beds)
  3. Nitroprusside Sodium (both venous & arterial beds)
  4. Ca-antagonists (almost entirely act on arterial bed)
  5. hydralazine
  6. minoxidil
  7. nitrates (more V>A)
75
Q

Hydralazine

A
  1. acts by release of NO
  2. arteriolar vasodilator
  3. used in low doses bc of toxicities
  4. combo of hydralazine w nitrates is approved for patients with both BPH & heart failure–esp blacks!
  5. major route of metabolism = acetylation
    a) rapid acetylators = reduced bioavailability (30%)
    b) slow acetylators = 50% bioavailability
  6. Toxicities: Compensatory respones:
  7. tachycardia
  8. salt & water retention
  9. Drug induced REVERSIBLE lupus erythematous like syndrome, characterized by:
  10. arthralgia
  11. myalgia
  12. skin rashes
  13. fever (in slow acetylators)
76
Q

Combo approved for patients with BPH & heart failure, especially blacks

A

Combo of hydralazine + nitrates

77
Q

Toxicities assoc with Hydralazine

A

Toxicities:
Compensatory respones:
1. tachycardia
2. salt & water retention

Drug induced REVERSIBLE lupus erythematous like syndrome, characterized by:

  1. arthralgia
  2. myalgia
  3. skin rashes
  4. fever (in slow acetylators)

*Used in low doses bc of toxicities

78
Q

Minoxidil

A
  1. reserved for severe HTN
  2. arteriolar vasodilator
  3. acts as a K+ channel opener–> hyper polarization –> relaxes vascular smooth muscle
    * after activation of a KATP channel, K+ efflux occurs from the vascular cell membrane–>hyperpolarization–> smooth muscle relaxation –> decreased BP
  4. Toxicities:
    a) Severe compensatory responses:
  5. tachycardia
  6. palpitations
  7. angina
  8. edema
    b) hypertrichosis/hirsutism (increased hair growth)
  9. Other use: topical minoxidil (as rogaine) is used as a stimulant of hair growth for correction of baldness
79
Q

Reserved for severe HTN

80
Q

Arteriolar vasodilators

A
  1. Minoxidil

2. Hydralazine

81
Q

Toxicities assoc with Minoxidil

A

a) Severe compensatory responses:
1. tachycardia
2. palpitations
3. angina
4. edema

b) hypertrichosis/hirsutism (increased hair growth)

82
Q

Rogaine

A

topical minoxidil used as a stimulant for hair growth to correct baldness

83
Q

parenteral vasodilators (act on both arteries & veins) used in hypertensive emergencies

A

Sodium Nitroprusside & Diazoxide

84
Q

Sodium Nitroprusside

A
  1. Parenteral vasodilator (acts on both arteries & veins)
  2. used in hypertensive emergencies
  3. Structure: grease iron center complex w 5 cyanide moieties & a nitrosyl group (44% cyanide by weight)
  4. SHORT acting drug (few minutes)–> so given by IV infusion
  5. MOA: release of NO from the drug molecule (NO donor) stimulates GC & increases cGMP in smooth muscle
  6. Toxicities:
  7. Excessive hypotension
  8. tachycardia
  9. causes accumulation of cyanide (cyanide toxicity)
  10. manifests as lethargy, disorientation, muscle spasms & convulsions
  11. cyanide toxicity treated by Na thiosulfate or hydroxocobalamine
85
Q

lethargy, disorientation, muscle spasms & convulsions

a) diagnosis
b) treatment

A

a) Cyanide toxicity

b) cyanide toxicity treated by Na thiosulfate or hydroxocobalamine

86
Q

Toxicities associated with Sodium Nitroprusside

A
  1. Excessive hypotension
  2. tachycardia
  3. causes accumulation of cyanide (cyanide toxicity)
    - ->manifests as lethargy, disorientation, muscle spasms & convulsions
    - ——->cyanide toxicity treated by Na thiosulfate or hydroxocobalamine
87
Q

Diazoxide

A
  1. Given by IV infusion, DOA several hours
  2. acts by opening K+ channels (hyper polarization)
  3. prevents/reduces smooth muscle contraction
  4. also reduces insulin release–>used to treat hypoglycemia produced by insulinomas
  5. ADR:
  6. hypotension
  7. hyperglycemia
  8. salt & water retention
88
Q

Used to treat hypoglycemia produced by insulinomas

A

Diazoxide bc it reduces insulin release

89
Q

ADR of Diazoxide

A
  1. hypotension
  2. hyperglycemia
  3. salt & water retention
90
Q

Fenoldopam

A
  1. peripheral arteriolar dilator
  2. used for hypertensive emergencies
  3. and postoperative hypertension
  4. agonist @ D1 receptors
  5. causes vasodilation particularly in RENAL VESSELS
  6. 1/2 life = 10 minutes
  7. administered by continuous IV infusion
91
Q

alpha 2 selective agents

A
  1. clonidine

2. methyldopa

92
Q

alpha 2 selective agents: MOA

A
  1. activates alpha 2 receptors in the CNS (bc readily enter CNS)
  2. cause decrease in sympathetic outflow
  3. –>decrease in BP ( bc decreases CO &/or TPR)
  4. –>major compensatory response is SALT RETENTION
93
Q

Clonidine

A
  1. reduces BP by reduction in CO due to DECREASED HR & Relaxation of capacitance vessels, with a REDUCTION in peripheral vascular resistance

Toxicities:

  1. Dry mouth
  2. Sedation
  3. Sudden withdrawal–>rebound HTN (this is treated with alpha blockers i.e. phentolamine)
94
Q

How do you treat the rebound hypertension associated with sudden withdrawal of clonidine

A

alpha blockers ie phentolamine

95
Q

Methyldopa

A
  1. prodrug (converted into active metabolite methylnorepinephrine in the brain)
  2. —–>this stimulates central alpha 2 adrenoceptors
  3. widely used in the past but is now used primarily for HTN DURING PREGNANCY

Toxicity:

  1. Sedation
  2. methyldopa causes HEMATOLOGIC IMMUNE TOXICITY (POSITIVE Coomb’s test)
    - ->may progress to hemolytic anemia
96
Q

primarily used for HTN during pregnancy

A

methyldopa

97
Q

Ganglion blocking drugs used to treat hypertension

A
  1. Hexamethonium
  2. trimethaphan
    a) these are nicotinic blockers acting in the ganglion
    b) cause a severe reduction in BP
    * No longer used clinically
    * *Major compensatory response = salt retention
98
Q

Hexamethonium & trimethaphan

A
  1. Ganglion blocking drugs used to treat hypertension
  2. these are nicotinic blockers acting in the ganglion
  3. cause a severe reduction in BP
  4. No longer used clinically
  5. Major compensatory response = salt retention
99
Q

Toxicity associated with ganglion blockers

A

a) symptoms associated with parasympathetic blockade:
1. blurred vision, dizziness, syncope
2. constipation*
3. urinary hesitancy–particularly with BPH
* remember parasympathetic carried via vagus!

b) symptoms associated with sympathetic blockade:
1. sexual dysfunction
2. orthostatic hypotension

THIS IS WHY WE NO LONGER USE GANGLION BLOCKERS TO TREAT HTN

100
Q

Adrenergic neuron blockers used to treat HTN

A
  1. drugs depleting NE stores in the adrenergic nerve terminal (reserpine)
  2. Drugs depleting & blocking the release of stored NE (guanethidine)
  3. both lead to decrease in SNS activity–>decrease in BP
  4. compensatory response = salt retention
101
Q

Reserpine

A

drugs depleting NE stores in the adrenergic nerve terminal

  1. Reserpine blocks the vesicular uptake & storage of biogenic amines
  2. by interfering w an uptake mechanism (vesicular membrane associated transporter-VMAT) –>depletion of NE, serotonin & dopamine
  3. both very effective as antihypertensive, but has more toxicities
  4. Reserpine READILY CROSSES BBB–>depletion of cerebral amine stores–>sedation, mental depression & parkinsonism symptoms
102
Q

Guanethidine

A

Drugs depleting & blocking the release of stored NE

  1. Inhibits the release of NE from sympathetic nerve endings
  2. guanethidine is transported across the nerve membrane by the same mechanism that transports NE (NET)
    - –>uptake is essential for the drug’s action
  3. Once it has entered the nerve it’s concentrated in transmitter vesicles, where it replaces NE–>causes gradual depletion of NE stores
103
Q

ADR of reserpine

A

mental depression

104
Q

ADR of guanethidine

A
  1. orthostatic hypotension (bc lost sympathetic regulation)
  2. sexual dysfunction (bc loss of sympathetic effects)
  3. diarrhea (unopposed PNS activity)
  4. If used with cocaine & TCAs–> can BLOCK the effect of guanethidine bc G uses the catecholamine repute pump that is inhibited by cocaine & TCAs!
105
Q

Hypertensive Emergency/Crisis Causes

A
  1. ingestion of tyramine-rich goods in patients taking MAOIs (use labetalol)
  2. pre-eclampsia
  3. Recreational drug use (cocaine, amphetamines)–>need to use alpha and beta blockers)
  4. Pheochromocytoma (massive release of endogenous catecholamines)
  5. Thyrotoxicosis (hyperthyroidism)
  6. sudden withdrawal of beta blockers, clonidine
106
Q

Symptoms of thyrotoxicosis (hyperthyroidism)

A
  • Sudden weight loss, even when your appetite and the amount and type of food you eat remain the same or even increase
  • Rapid heartbeat (tachycardia) — commonly more than 100 beats a minute — irregular heartbeat (arrhythmia) or pounding of your heart (palpitations)
  • Increased appetite
  • Nervousness, anxiety and irritability
  • Tremor — usually a fine trembling in your hands and fingers
  • Sweating
  • Changes in menstrual patterns
  • Increased sensitivity to heat
  • Changes in bowel patterns, especially more frequent bowel movements
  • An enlarged thyroid gland (goiter), which may appear as a swelling at the base of your neck
  • Fatigue, muscle weakness
  • Difficulty sleeping
  • Skin thinning
  • Fine, brittle hair
107
Q

Symptoms of pheochromocytoma

A

-episodic and sudden onset of severe headaches.
sweating.
-abdominal pain.
-hypertension (high blood pressure) which may be resistant to conventional medications.
-rapid heart rate.
-irritability and anxiety.

108
Q

symptoms of pre-eclampsia

A
  1. High BP

2. Protein in urine

109
Q

Drugs used to treat Hypertensive Emergencies

A
  1. Parenteral antihypertensive medications are used to lower BP RAPIDLY
  2. MC used drug to treat = Sodium Nitroprusside
    Also used:
    -fenoldopam
    -nitroglycerine
    -labetalol
    -calcium channel blockers
    -diazoxide
    -hydralazine
110
Q

MC drug used to treat hypertensive emergencies

A

Sodium Nitroprusside

111
Q

Drug used to manage intraoperative & postoperative hypertension

112
Q

Drugs used to treat angina pectoris & contraindicated drugs

A

Used: 1. beta blockers, CCB
Contraindicated: direct vasodilators

113
Q

Drugs contraindicated to treat bradycardia, heart block, sick sinus syndrome

A
  1. beta blockers. labetalol, verapamil, diltiazem
114
Q

ADR associated with clonidine & methyldopa

A

CNS: sedation & drowsiness (up to 50%); nightmares; decreased REM sleep (up to 40% with clonidine)

Cardio: Clonidine–> can cause hypertensive crisis when drug is withdrawn, may –> tachycardia, sweating, nausea, tremor, restlessness, apprehension & can be life threatening

GI: xerostomia (clonidine up to 50%, methyldopa up to 10%, centrally mediated

Other Symptoms:
sexual dysfunction
skin eruption
+ coombs test w methyldopa (up to 30% w long-term therapy)
hemolytic anemia occurs in 1-5% of cases with methyldopa

115
Q

Stimulation of alpha 2 adrenoreceptors results in

A
  1. DECREASES sympathetic outflow & INCREASES vagal outflow
  2. stimulation of alpha 2 receptors on NE terminals DECREASES NE release
116
Q

What effect will reserpine have on the content of NE within the nerve terminal? Why?

A
  1. the consequence of reserpine = that dopamine & any NE present in the cytoplasm are decimated by MAO–>so the vesicular content of NE falls
  2. bc of the depletion of NE in adrenergic nerves–> fall in BP & a pictures of PNS dominance with nasal stuffiness & diarrhea
  3. bc of the central depletion of amines patient s may complain of
    a) depression–due to depletion of dopamine
    b) Parkinsonism
    c) galactorrhea

Pharm (32 decks)

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