Anti-hypertensives Flashcards
(116 cards)
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:
- HTN
- Clonidine used in withdrawal from abused drugs
Advantages of using:
- No change in lipids
- used in nicotine dependence
2
Q
Clonidine Toxicities
A
- dry mouth
- sedation
- rebound HTN
3
Q
Methyldopa Toxicities
A
- positive Coombs test (hemolytic anemia)
4
Q
DOC to treat anti hypertension in pregnancy
A
Clonidine; also doesn’t cause a change in lipids
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
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
7
Q
Reserpine Toxicities
A
Toxicities: sedation & depression
Disadvantages/Contraindicated: depression
8
Q
Guanethidine toxicities & disadvantages/contraindications
A
Toxicities:
1. Orthostatic Hypotention
2. Fluid retention
Disadvantages/Contraindicated: CHF
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
10
Q
Use of Alpha 1 blockers to treat Hypertension
A
MOA:
- selectively block alpha1A receptors
- reduce prostatic SM tone
Hemodynamic effects: Decrease TPR
Uses: 1. HTN 2. BPH
Toxicities: orthostatic hypertension
Disadvantages/contraindications: none
Advantages: Decreases VLDL & LDL
11
Q
Alpha 1 blockers used to treat HTN
A
- prazosin
- terazosin
- doxazosin
12
Q
Use of Beta blockers to treat Hypertension
A
MOA:
- Block B1 receptors
- decrease renin secretion
Hemodynamic effects–> Decrease CO
Clinical Uses: 1. HTN 2. HF
Toxicities/interactions: Bronchoconstriction
Contraindication:
- Bronchial asthma
- Heart Block
Advantages: Prolong survival
***labetalol is DOC in pregnancy
13
Q
Beta Blockers used to treat Hypertension
A
- metoprolol
- atenolol
- carvedilol (blocks B1 & alpha receptors)
14
Q
Drugs used to treat HTN that work by decreasing CO
A
- beta blockers
2. calcium-channel blockers (work by decreasing HR & FOC)
15
Q
Vasodilators used to treat HTN that work by decreasing systemic vascular resistance
A
- alpha blockers
- direct-acting vasodilators
- Angtiotensin-converting enzyme inhibitors (ACE inhibitors)
- angiotensin receptor blockers (ARBs)
16
Q
Antihypertensives that work at the vasomotor center
A
- methyldopa
- clonidine
- guanabenz
- guanfacine
17
Q
Antihypertensives that work at sympathetic ganglia
A
Trimethaphan
18
Q
Antihypertensives that work at sympathetic nerve terminals
A
- guanethidine
- guanadrel
- reserpine (not used bc it depletes MO–>depression)
19
Q
Antihypertensives that work at beta receptors of heart
A
beta blockers ie propranolol
20
Q
Antihypertensives that work at angiotensin receptors of vessels
A
- losartan
2. other angiotensin receptor blockers
21
Q
Antihypertensives that work at alpha receptors of vessels
A
- prazosin
2. and other alpha 1 blockers
22
Q
Antihypertensives that work at vascular smooth muscle
A
- hydralazine
- minoxidil
- nitroprusside
- diazoxide
- verapamil & other CCB
- Fenoldopam
23
Q
Antihypertensives that work at kidney tubules
A
- thiazides, etc
24
Q
Antihypertensives that work at beta receptors of juxtaglomerular cells that release RENIN
A
Propranolol & other beta blockers
25
Angiotensinogen is converted to angiotensin 1 by _____ which is inhibited by _______
1. renin
| 2. alskiren
26
angiotensin 1 is converted to angiotensin II by _________ which is inhibited by ___________
1. Angiotensin-converting enzyme (ACE)
| 2. Captopril & other ACE inhibitors
27
How do diuretics treat HTN?
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!
28
What group of diuretics are preferred for HTN? WHY? Ex?
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
29
Toxicity of Thiazides
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
30
MOA for beta blockers as anti-HTN drugs
1. decrease in CO by blocking cardiac Beta 1 receptors
| 2. inhibition of renin release by blocking beta 1 receptors on JG cells
31
Hemodynamic effects of beta blockers in HTN
a) Decreased:
1. HR
2. CO
3. PVR
b) Unchanged: venous tone
c) Negligable: postural hypotension
32
all beta blockers are equally effective in lowering BP in??
mild to moderate HTN
33
in severe HTN, beta blockers are useful???
in preventing the reflex tachycardia that often results from treatment with direct vasodilators
34
beta blockers have shown to reduce mortality after
MI & heart failure
35
Propranolol
a) type
b) toxicities
c) prolonged use warning
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
36
Cardio-selective beta 1 drugs
b) benefits?
1. atenolol
2. metoprolol
b) cause less bronchoconstriction than propranolol
37
beat blockers with additional alpha blocking activity
b) when would you use them?
1. labetalol
2. carvedilol
b) tumor in adrenal medulla (pheochromocytoma)
38
Calcium channel blockers act on
L type calcium channels
39
CCB effective in lowering BP
1. verapamil
2. diltiazem (has intermediate actions)
3. DHP (amlodipine, felodipine, isradipine, nicardipine, nifedipine, nisoldipine)
40
DHP
a) examples
b) selectivity
c) can cause
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
41
Verapamil
1. has the greatest depressant effect on the heart
2. may decrease HR & CO
3. How? L-type Ca channels-->decrease FOC
42
DHP not used for HTN bc too short acting
nifedipine
43
How do calcium channels lead to muscle contraction?
1. calcium comes in
| 2. binds to myosin light chain kins
44
Inhibitors of Renin Angiotensin Aldosterone System (RAAS)
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)
45
ACE Inhibitors
end in "-pril"
1. captopril
2. Enalapril
3. Ramipril
4. Benazepril
5. fosinopril
6. lisinopril
7. quinapril
46
end in "-pril"
ACE inhibitors
47
Angiotensin Receptor Blockers (ARBs) (Losartan, Valsartan, Candesartan, sprosartan, irbesartan, telmisartan, olmesartan)
1. Losartan
2. Valsartan
3. Candesartan
4. sprosartan
5. irbesartan
6. telmisartan
7. olmesartan)
48
End in "-sartan
Angiotensin Receptor Blockers (ARBs)
| 1. Losartan, Valsartan, Candesartan, sprosartan, irbesartan, telmisartan, olmesartan
49
Aldosterone Receptor inhibitors
end in "-one"
1. spironolactone
2. elprenone
50
end in "-one"
Aldosterone Receptor inhibitors:
1. spironolactone
2. elprenone
51
Effects of ATII on the myocardium & kidney
1. mitogenic for vascular & cardiac muscular cells
| Remodeling:
52
Remodeling effects of ATII
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
Effects of angiotensin II
b) inhibited by
1. vasoconstriction-->increased peripheral vascular resistance-->increased BP
2. aldosterone secretion-->increased Na & water retention-->increased BP
b) Angiotensin receptor blockers (ARBs)
54
Effects of aldosterone secretion
b) inhibited by
aldosterone secretion-->increased Na & water retention--> increased BP
b) inhibited by spironolactone, eplerenone (aldosterone receptor inhibitor
55
Effects of bradykinin
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
Role of ACE inhibitors
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
How do ACE inhibitors treat HTN?
They lower BP principally by DECREASING PVR
58
When are ACEI DOC?
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
ACEI ADR
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
Angiotensin Receptor Blockers (ARBs) uses & MOA
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
ARB ADR
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
Alpha Blockers
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
Men with concurrent HTN & BPH should use
alpha 1 selective blockers
1. prazosin
2. terazosin
3. doxazosin
64
alpha 1 selective blockers
1. prazosin
2. terazosin
3. doxazosin
used primarily in men with concurrent HTN & BPH
65
Used in diagnosis & treatment of pheochromocytoma
nonselective alpha blockers:
1. phentolamine
2. phenoxybenzamine
work by blocking both the presynaptic and postsynaptic receptors--> tachycardia
66
nonselective alpha blockers
1. phentolamine
2. phenoxybenzamine
work by blocking both the presynaptic and postsynaptic receptors--> tachycardia
67
4 MOA Vasodilators use
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
Vasodilators that act by releasing NO
1. Nitroprusside
2. Hydralazine
Other drugs that act by this mechanism are
1. Nitrates
2. Histamine
3. ACh
69
Vasodilators that act by Blockade of Ca channels
1. Verapamil
2. diltiazem
3. DHP like nifedipine, amlodipine
70
Vasodilators that act by Activation of D1 receptors
Fenoldopam
71
Vasodilators that act by Opening K+ Channels
1. minoxidil
| 2. diazoxide
72
MOA by which Vasodilators that act by Opening K+ Channels WORK
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
vasodilators that act on the venous bed
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
vasodilators that act on the arterial bed
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
Hydralazine
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:
1. tachycardia
2. salt & water retention
7. Drug induced REVERSIBLE lupus erythematous like syndrome, characterized by:
1. arthralgia
2. myalgia
3. skin rashes
4. fever (in slow acetylators)
76
Combo approved for patients with BPH & heart failure, especially blacks
Combo of hydralazine + nitrates
77
Toxicities assoc with Hydralazine
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
Minoxidil
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:
1. tachycardia
2. palpitations
3. angina
4. edema
b) hypertrichosis/hirsutism (increased hair growth)
5. Other use: topical minoxidil (as rogaine) is used as a stimulant of hair growth for correction of baldness
79
Reserved for severe HTN
Minoxidil
80
Arteriolar vasodilators
1. Minoxidil
| 2. Hydralazine
81
Toxicities assoc with Minoxidil
a) Severe compensatory responses:
1. tachycardia
2. palpitations
3. angina
4. edema
b) hypertrichosis/hirsutism (increased hair growth)
82
Rogaine
topical minoxidil used as a stimulant for hair growth to correct baldness
83
parenteral vasodilators (act on both arteries & veins) used in hypertensive emergencies
Sodium Nitroprusside & Diazoxide
84
Sodium Nitroprusside
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:
1. Excessive hypotension
2. tachycardia
3. causes accumulation of cyanide (cyanide toxicity)
4. manifests as lethargy, disorientation, muscle spasms & convulsions
5. cyanide toxicity treated by Na thiosulfate or hydroxocobalamine
85
lethargy, disorientation, muscle spasms & convulsions
a) diagnosis
b) treatment
a) Cyanide toxicity
| b) cyanide toxicity treated by Na thiosulfate or hydroxocobalamine
86
Toxicities associated with Sodium Nitroprusside
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
Diazoxide
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:
1. hypotension
2. hyperglycemia
3. salt & water retention
88
Used to treat hypoglycemia produced by insulinomas
Diazoxide bc it reduces insulin release
89
ADR of Diazoxide
1. hypotension
2. hyperglycemia
3. salt & water retention
90
Fenoldopam
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
alpha 2 selective agents
1. clonidine
| 2. methyldopa
92
alpha 2 selective agents: MOA
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
Clonidine
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
How do you treat the rebound hypertension associated with sudden withdrawal of clonidine
alpha blockers ie phentolamine
95
Methyldopa
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
primarily used for HTN during pregnancy
methyldopa
97
Ganglion blocking drugs used to treat hypertension
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
Hexamethonium & trimethaphan
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
Toxicity associated with ganglion blockers
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
Adrenergic neuron blockers used to treat HTN
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
Reserpine
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
Guanethidine
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
ADR of reserpine
mental depression
104
ADR of guanethidine
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
Hypertensive Emergency/Crisis Causes
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
Symptoms of thyrotoxicosis (hyperthyroidism)
- 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
Symptoms of pheochromocytoma
-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
symptoms of pre-eclampsia
1. High BP
| 2. Protein in urine
109
Drugs used to treat Hypertensive Emergencies
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
MC drug used to treat hypertensive emergencies
Sodium Nitroprusside
111
Drug used to manage intraoperative & postoperative hypertension
Esmolol
112
Drugs used to treat angina pectoris & contraindicated drugs
Used: 1. beta blockers, CCB
Contraindicated: direct vasodilators
113
Drugs contraindicated to treat bradycardia, heart block, sick sinus syndrome
1. beta blockers. labetalol, verapamil, diltiazem
114
ADR associated with clonidine & methyldopa
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
Stimulation of alpha 2 adrenoreceptors results in
1. DECREASES sympathetic outflow & INCREASES vagal outflow
2. stimulation of alpha 2 receptors on NE terminals DECREASES NE release
116
What effect will reserpine have on the content of NE within the nerve terminal? Why?
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
