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Pharm test 3 > antiHTN > Flashcards

antiHTN Flashcards

1
Q

what effects BP

A

CO and SVR

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2
Q

What effects CO

A

HR and SV

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3
Q

what effects SVR

A

direct innervation
circulating regulators
local regulators

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4
Q

what effects SV

A

contractility and preload

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5
Q

what effects preload

A

venous tone

intravascular volume

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6
Q

what de/increased HR

A 
D: PSNS
I: SNS, catecholamines
HTN drugs that effect here:
B-antagonists
CCB
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7
Q

Catecholamines effect

A 
contractility
HTN drugs that effect here: B-antagonists, CCB
venous tone
HTN drugs that effect here:
alpha 1 antagonist
ACEI
ARB
Nitroprusside
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8
Q

what effects intravascular volume

A 
Na/H2O retention
I: by SNS, aldosterone, ADH
D: natriuretic peptide
HTN drugs that affect here: 
Diuretics
ACEI
ARB
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9
Q

what causes Direct innervation of SVR

A

Alpha 1
so then for HTN drugs would want
alpha 1 antagonist or alpha 2 agonists

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10
Q

what Circulating regulators effect SVR

A 
Increased by catecholamines, ATII 
HTN drugs that effect this would be 
alpha 1 antagonist
alpha 2 agonist
ACEI
ARB
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11
Q

what Local regulators effect SVR

A 
Decreased by NO, prostacyclin, adenosine, H 
Increased by endothelin, ATII
HTN drugs that effect this would be:
endothelin antagonist
Nitroprusside
ACEI
ARB
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12
Q

tx guidelines
normal
tx thresholds

A

> 120/80 than than should initiate “lifestyle modifications”
Tx when
140/90 without DM or kidney d
130/80 with DM or kidney disease (bc of end organ damage)

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13
Q

first-line therapy is

A

thiazide diuretic UNLESS “compelling indication”

most pts will requires at least 2 meds to reach this goal

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14
Q

Compelling indications 7

A
  • Heart Failure: Thiazide and either bblocker, ACEI, (those 2 first pick) or ARB, aldosterone antagonist
  • MI:?no thiazide? bblocker (first choice) ACEI, aldosterone antagonist
  • High CVD risk: Thiazide, bblocker, ACEI, CCB
  • DM: Thiazide, then 1st choice ACEI, then bblocker, ARB, CCB
  • chronic kidney disease:? thiazide? ACEI or ARB
  • recirrent stroke prevention: Thiazide, ACEI
  • Isolated systolic HTN; Thiaside, CCB
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15
Q

HTN emergency 2 types

A

HTN urgency or Crisis

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16
Q

HTN Urgency

A

DPB >120 with evidence of progressive end organ Damage
BUN and creat increasing
Goal: decreased DBP to 100-105 within 24hrs: Clonidine

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17
Q

HTN Crisis

A

DBP> 120 with evidence of end organ FAILURE

Goal: decreased DBP 100-105 ASAP: nitroprusside, NTG, Labetalol, Fenoldapam

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18
Q

Renin secreted by

A

Juxaglomerular apparatus

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19
Q

Renin results in

A

vasoconstriction, Na retention–increased intravascular volume

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20
Q

goal of renin

A

is aimed at maintaining tissue perfusion through increased extracellular fluid volume

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21
Q

Renin-angiotensin system is synergistic with…

A

SNS by increasing the release of NE from sympathetic nerve terminals

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22
Q

Renin-angiotensin system pathway

A

BP falls stimulates kidney to release renin
renin converts angiotensinogen (from liver) to angiotensin I
ACE converts angiotensin I to angiotensin II
ATII causes vasoconstriction (increased afterload) and stimulates the secretion of aldosterone
**Aldosterone increased Na and H2O retention causing an increase in Preload

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23
Q

Angiotensin II acts where (4) which each cause what?

A

Adrenal cortex: aldosterone–increased Na reabsorption
Renal proximal tubule: increased Na reabsorption
Renal efferect arterioles: vasoconstriction
Hypothalamus: thirst, increased ADH secretion

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24
Q

ACE inhibitors
first line therapy for?
more effective in… bc..

A

renin-angiotensin system blockers
first line therapy: HTN, CHF, Mitral regard
More effective in DM pts
Delay progression of renal disease

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25
Q

main action of ATII are at what receptors? which has stronger effects?

A

AT1 and AT2 receptors which belong to gprotein coupled receptors
AT1effects> AT2 effects

26
Q

AT1 receptor effects

A

generalized vasoconstriction- especially in the afferent arterioles of renal glomeruli
Increased NE release
Proxima tubular reabsorption of Na
Secretion of aldosterone from adrenal cortex

27
Q

AT2 receptor effects

A

are subtle

28
Q

ACEI MOA and site of action

A

block the conversion of ATI to ATII through an interaction with the zinc ion of ACE (peptidyl-dipeptidase), preventing conversion of ATI to II
Site of action: ACE endothelium

29
Q

ACE inhibitors drugs 9

A 
Captopril- capoten
Enalapril- vasotec
Ramipril- altace
Benazepril- lotensin
Lisinopril- zestril, prinivil
Moexipril- univasc
Quinapril- accupril Fosinopril- monopril
Trandorapril- mavik
30
Q

ACE inhibitors pharm effects and uses

A

fall in arterial pressure, reduced cardiac load
(more arterial than venous)
For: HTN, Cardiac failure, postMI, diabetic neuropathy, CRI

31
Q

ACE inhibitors SE

A 
*Prolonged hypotension intra-op
(prohibit taking on the A.M of surgery
Granulocytopenia
*Angioedema
Proteinuria
*Persistent Cough (increased bradykinin which causes vasodilation) 
Hyperkalemia
32
Q

ACE inhibitors contraindications

A

renal artery stenosis

Renal artery stenosis patients may develop Renal failure due to efferent arteriole constriction

33
Q

Captopril, dose, kinetics, SE

A

ACEI prototype
Dosage 12.5-25mg q 8hrs
Onset 15mins
Short plasma half-life (E1/2 time 2hrs)
Decreases SVR, does not interfere with sympathetic outflow.
Side effects: rash, loss of taste, NSAID antagonize its effects, hyperkalemia, angioedema.

34
Q

Enalapril

A

ACEI
IV preparation
Compared to captopril it lacks a sulfhydryl group (H-S-CH2) thus does not cause the rash and renal insufficiency caused by captopril

35
Q

Lisinopril

A

ACEI

Administered in a active form and excreted unchanged in the kidney

36
Q

Angiotensin II Receptor Blocker (ARBs) MOA

A

Competitive binding to inhibit the action of angiotensin II at its receptor
By blocking the vasoconstrictive actions of angiotensin II without effecting ACE activity
results in decreased peripheral vasoconstriction
At the AT1 receptor

37
Q

ARBs SE

A

Side effects similar to ACE inhibitors
less cough noted
No effect on ACE
No significant bradykinin accumulation

38
Q

ARB contraindications

A

renal art stenosis

pregnancy

39
Q

ARB drugs 8

A 
Losartan-hyzaar, cozaar
Valsartan- diovan
Irbesartan- avalide, avapro
Candesartan- atacand
Telmisartan- micardis
Eprosartan- teveten
Olmesartan- benicar
Tasosartan- verdia
40
Q

arterial vasodilators

A

minoxidil

hydralazine

41
Q

Hydralazine MOA, dose, peak

A

arterial vasodilator
phthalazine derivative
activates guanylate cyclase (which synthesized cGMP to GTP, which signal to relax)
produces Direct relaxant effecy on vascular smooth muscle
arteries>veins
Calcium ion transport in vascular smooth muscle
Dosage 2.5-10mg IV
peaks 10-20m, can last up to 6 hrs

42
Q

Hydralazine kinetics

A 
Extensive hepatic first
pass metabolism
Onset 15 minutes give slowly
Elimination 1⁄2 time 3 hours
After IV < 15% appears unchanged in the kidney
43
Q

Hydralazine SE

A 
Reflex tachycardia
DBP reduced >SBP
Decreased SVR
Increase HR, SV, CO
Tolerance and Tachyphylaxis
Sodium and H20 retention
Angina with EKH changes
Clinically used in combination with BB and diuretic- Limits the increased SNS activity
44
Q

Minoxidil MOA, use

A

arterial vasodilator
Directly relaxes the arteriolar smooth muscle little effect on venous capacitance
increase influx of K into vascular smooth resulting in hyperpolarization and vasodilation
orally activated
Use: tx most severe forms of HTN due to:
renovascular disease
renal failure
transplant rejection
-also used in combo with BB and diuretics

45
Q

Minoxidil kinetics

A

90% oral dose absorbed from GI tract
peak levels in 1 hr
e1/2t 4hrs
10% unchanged in urine

46
Q

Minoxidil SE

A

Marked increase in
heartrate CO
Increased plasma concentration of NE and Renin
Compensatory retention of Na and H20
Weight gain
Edema
hypertrichosis
Pulmonary HTN
Pericardial effusion or cardiac tamponade
Can have abnormal EKG
flat or inverted T wave, increased voltage of the QRS complex

47
Q

Peripheral vasodilators

utilized for

A

facilitate forward LV in AR, MR, or HF
controlled hypotension in OR- a techinque, will have less bleeding, goal MAP<70, however must avoid myocardial ischemia, cerebral ischemia-blindness (ex, used for ENT, near clips)
Tx HTN crisis

48
Q

Peripheral vasodilators drug names 8

A 
Nitroglycerin (NTP)
Nitroprusside (SNP)
Isosorbid
Dipyridamole
Papaverine
Trimethaphan
Diazoxide
Adenosine
49
Q

Sodium Nitroprusside (SNP) MOA

A

Direct acting , nonselective peripheral
vasodilator
Relaxation of arterial and venous vascular smooth muscle
Lacks significant effects on nonvascular smooth muscle and cardiac muscle
SNP interacts with oxyhemoglobin
– dissociates immediately to form Methemoglobin Releasing Nitric Oxide (NO)
Nitric Oxide activates guanylate cyclase (in the vascular muscle) thus increasing cGMP
cGMP inhibits calcium entry into vascular smooth muscle but increases uptake of Ca into the sER
** Results in vasodilation via NO

50
Q

Nitroprusside metabolism

A

Transfer of an electron from the Iron (Fe) of
oxyhemoglobin to SNP yields
metHGb and an unstable SNP radical where all 5 cyanide ions are released.
One of these cyanide ions reacts with metHGb to form cyano-methemoglobin (nontoxic)
the remainder are metabolized In the liver and kidney converted to thiocyanate

51
Q

Nitroprusside toxicity

A

Toxicity: occurs due to the effects of high plasma concentrations of thiocyanate
– Cyanide Toxicity
can occur at rates >2ug/kg/min for long periods
Suspect when the pt starts demonstrating resistance to hypotensive effects or a previous responsive patient who is unresponsive (tachyphylaxis) at rates >2-10 ug/kg/min
May precipitate tissue anoxia, anaerobic metabolism, and lactic acidosis (if lactate levels >10 – see CNS dysfunction, mental status changes-sz)
Caution in pregnancy

52
Q

Cyanide levels

SNP

A

plasma lactate concentrations of >10 mM, which correlates with blood cyanide concentra- tions of > 40 mcgM
clinical toxicity appear to exceed 40 mcgM, and deaths have been reported with cyanide concentrations of > 77mcgM

53
Q

SNP toxicity tx

A

Immediate discontinuation of SNP
100%02 administration despite normal oxygen saturation
Sodium bicarbonate to correct metabolic acidosis
Sodium thiosulfate 150mg/kg over 15 minutes
Sodium thiosulfate Acts as a sulfur donor to convert cyanide to thiocyanate
– Sodium nitrate 5mg/kg if severe toxicity
Converts hemoglobin to metHgb which coverts cyanide to cyanometHemoglobin

54
Q

Thiocyanate toxicity SNP

A

Rare as thiocyanate is cleared by the kidney in 3-7 days
Less toxic than cyanide
Symptoms include:
– N/V, tinnutis, fatigue, CNS hyperreflexia, confusion, psychosis, miosis
seizure and coma

55
Q

SNP methomoglobinema

A

Rare
Should be considered as a differential diagnosis in patients with impaired oxygenation despite adequate cardiac output and arterial oxygenation

56
Q

SNP phototoxicity

A

SNP should be mixed with 5% glucose in water and be protected
◆ With continuous exposure to light SNP is converted to aquapentacyanoferrate in the presence of light and the release of hydrogen cyanide
◆ Wrap the solution and tubing in foil or dark plastic bag

57
Q

SNP dose

A

.3ug/kg/min - 10ug/kg/min IV
– Max dose: should not be infused for greater that 10 minutes
– Immediate onset
– Short duration of action
– Requires continuous IV administration to maintain therapeutic effect
– Extremely potent: use A-line

58
Q

SNP cv effects

A

Direct venous and arterial vasodilation, decreased venous capacitance due to venous return
Baroreceptor mediated reflex responses increased HR
↓SBP, ↓SVR,↓PVR, ↑contractility, causes an intracoronary steal in areas of damage associated with MI

59
Q

SNP: CNS, pulm and blood effects

A

increase CBR, ICP
attenuation of hypoxic vasoconstriction?
increased in intracellular GMP- inhibit platelet aggregation and bleeding time.

60
Q

SNP clinical uses

A

Controlled hypotension:
0.3-0.5ug/kg/min not to exceed 2 ug/kg/min
– Hypertensive crises:
infusion 1-2ug/kg IV can be given as bolus
– Cardiac disease:
decreases LV afterload, benefits management of MR or AR, CHF, and heart failure.
Consider coronary steal

Pharm test 3 (6 decks)

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