Cpharmdrugs That Reduce Pr

Front 1

List three uses of drugs that reduce TPR?

Back 1

-CHF
-Hypertension
-Anti-ischemic vasodilators

Front 2

Sympatholytics
1) common adverse side effects

Back 2

1) a)Decreased SNS activity --> orthostatic hypotension, failure of ejaculation, nasal congestion
b) Due to increased PNS activity relative, when organ is dually innervated: bradycardia, abdominal cramps, diarrhea, exacerbation of peptic ulcer

Front 3

alpha methyl dopa
1) Drug class
2) Mechanism of action
3) Use
4) Administration

Back 3

1) Sympatholytic that acts on CNS
2) Metabolite, alpha-methylNE, activates alpha 2 receptor in CNS (primary sympatholytic effects). Peripherally, acts as false transmitter
3) Used in pregnant women w/ HT where ACEI use is counterindicated
4) CNS: sedation, drowsiness, allergic.
Normal sympatholytic
4) Oral, tough to dose, great 1st pass met. Increases kidney perfusion.

Front 4

Prazosin
1) Drug class
2) Mechanism of action
3) common side effects
4) Use

Back 4

1) Sympatholytic
2) alpha 1 selective blocker --> does not couse alpha 2 blocking effects including tachycardia, increase in CO or renin
3) NL: orthostatic hypotension, nasal congestion, dry mouth from alpha blockade. *** Some fluid retention due to alpha blockade)
4) Used for mild HT b/c not very potent and does not affect lipid met.

Front 5

Phentolamine
1) Drug class
2) Mechanism of action
3) Use

Back 5

1) Sympatholytic
2) non selective alpha R competitive antagonist
3) used for hypertensive crisis

Front 6

Propanolol
1) Drug class
2) Mechanism of action
3) Adverse effects
4) Admin, met

Back 6

1) Sympatholytic
2) Non specific beta receptor competitive antagonist
3)

Front 7

Actions of beta blockers
1) CV effects
2) Bronchiolar effects
3) Metabolic effects
4) RAS effects

Back 7

1) Decrease HR, slow AV conduction, decrease contractility, increase TPR due to reflex, decrease BP, these effects are more apparent under conditions of normal SNS activation
2) Non selective block bronchodilation effects in airways due to B2 receptor activity. B1 selective drugs at high levels can also block bronchodilation
3) blocks Epi induced FFA release --> exercise fatigue
-can induce hypoglycemic shock in diabetics since Epi is needed to release glucose
4) Decreases renin release via JG cells

Front 8

Untoward effects of Beta blockers
1) CV
2) Withdrawal
3) Lung
4) Diabetics
5) Systemic
6) CNS

Back 8

1) Decreased myocardial contractility trouble in patients that rely on SNS to maintain CO
2) Propanolol withdrawal rebound: MI after cessation
3) inhibition of bronchodilation in asthmatics
4) hypoglycemic shock
5) Fatigue, depression
6) calming effect with lipid soluble blockers but can lead to nightmares

Front 9

Beta blocker therapeutic uses

Back 9

-arrhythmias
-angina pectoris
-essential hypertension
-migraine prophylaxis
-thyroidtoxicosis
-CHF potentially

Front 10

Mechanism of action of beta blockers in txt of HT:

Back 10

1) Decrease Plasma Renin activity
2) adaptation of vascular resistance to chronic decrease in CO
3) Reduced SNS activity due to block of presynaptic B1 receptors (the positive feedback loop).
4) Increase in prostacyclins
5) Modulation of gene expression of inflammatory cytokines, ie NO

Front 11

Metoprolol
1) Drug class
2) Mechanism of action
3) lipid solubility
4) Admin/Metabolism

Back 11

1) Sympatholytic
2) Selective B1 blocker at low doses
3) Moderate --> calming effect
4) low doses, hepatic

Front 12

Atenolol
1) Drug class
2) Mechanism of action
3) lipid solubility
4) Excretion

Back 12

1) Sympatholytic
2) Selective B1 blocker, long lasting
3) low
4) Renal excretion

Front 13

Labetalol
1) Drug class
2) Mechanism of action
3) Advantages
4) Half life

Back 13

1) Sympatholytic
2) selective alpha 1, non selective beta blocker with some b2 sympathomimetic activity
3) Fast onset, vasodilating, blunting of rise in heart rate and BP in response to stress.
4) Short acting

Front 14

Carvedilol
1) Drug class
2) Mechanism of action
3) Effect
4) Use

Back 14

1) Sympatholytic
2) selective alpha 1, nonselective beta blocker
3) alpha 1 --> rapid vasodilation
beta--> long term benefits
4) Used in patients with CHF in combination with other drugs. Especially in cases associated with catecholamine excess.

Front 15

Hydralazine
1) Drug class
2) Mechanism of action
3) Use
4) Adverse effects

Back 15

1) Vasodilator
2) Direct sm vasodilation via EDRF
3) used in lower doses with other drugs as antiHT. Very potent vasodilator but with many adverse effects --> use with beta blocker. Also decreases supine and standing BP because does not constrict veins.
4) -Hyperdynamic state: palpitation, tachycardia, increased CO via increased sympathetic activity. --> use with beta blocker to minimize cardiac stimulation
-Na and water retention
-HD ache, dizziness, acute psychosis
-Acute rheumatoid or LE effect in slow acetylators, especially women

Front 16

Nifedipine
1) Drug class
2) Mechanism of action
3) Effects on PR and BP
4) Adverse effects
5) Use

Back 16

1) Vasodilator
2) L type Ca channel blocker, neutral --> tonic block --> vasodilation
3) Decreases PR, but only lower BP in HT pts. Fast acting and drop is related to pre txt diastolic P, higher the P the bigger the drop.
4) Some reflex tachy but less than hydralazine (still use of beta blocker reduces this)
-hypotension, flushing, HD ache, edema, burning sensation on face.
5) Monotherapy in mild HT

Front 17

Chlorothiazide/Hydrochlorothiazide
1) Drug class
2) Mechanism of Actions
3) Effects
4) Uses
5) Adverse effects

Back 17

1) Saluretic
2) Blocks Na/Cl reuptake in distal tubule --> H20 and Na excretion
3) Decreases blood volume and BP on in HT pts. Effect decreased in high Na diet. Na depletion decreases SM sensitivity to AII
4) Heart failure, mild HT alone, moderate and up in combo

Front 18

Chlorothiazide/Hydrochlorothiazide
5) Adverse effects
6) Administration/plasma levels
7) Bonuses

Back 18

5) Hypokamia --> long QT --> must give lowest dose with K supplement
-Glucose intolerance due to decreased insulin secretion
-Hyperuricemia --> gout
-NSAID decreases drug effect
-Erective dysfunction
6) Plateau effect, only up to certain concentration do therapeutic effects increase.
7) No hemodynamic effects, no tolerance with chronic use

Front 19

What are four methods of renin release?

Back 19

Released by JG cells in afferent arterioled in response to
1) decreased BP
2) decreased Na
3) B adrenergic stimulation
4) Prostaglandin secreation

Front 20

AII
1) Cardiovascular actions
a) Direct
b) Indirect

Back 20

Fast pressor response
1) a) Vasoconstriction (precapillary vessels). 10x more potent than NE, affects all vasculature. Vasoconstriction is directly related to Na levels. AII receptors on vasculature works through G protein.
-Positive weak inotropy and chronotropy
b) Activation of SNS. AII does this directly, likely in the medulla. Facilitates NE release from adrenergic endings.

Front 21

AII Renal actions

Back 21

---> Slow pressor response
1) Increased Na reabsorption in proximal tubule
2) Simtulates aldosterone secretion by adrenal ctx.
3) Direct constriction of renal SM
4) stimulates drinking in CNS at high doses

Front 22

AII effects on cardiovascular remodeling

Back 22

---> hypertrophy, apoptosis, HF
1) disease induced changes of myocytes, fibroblasts inhibited by ACEI
2) Increases
-expression of proto-oncogenes
-growth factor production
-ECM proteins in increased migration proliferation, and hypertrophy of myocytes and ECM

Front 23

Angiotensin receptors and involvement in BP?

Back 23

AT1, mostly found in smooth muscle
AT2, fetal

Front 24

Losartan
1) Drug class
2) Mechanism of action
3) Admin/Metabolism
4) Adverse effects

Back 24

1) ARBs
2) Competitive/high affinity antagonist of AT1
3) Oral/ active metabolite shows indomethacin type activity
4) Hypotension, hyperkalemia (when given with diuretic), URI, dizziness, diarrhea.

Front 25

Enalapril
1) Drug class
2) Mechanism of action
3) Admin/met
4) Adverse effects

Back 25

1) ACEI
2) inhibits ACE
3) Long lasting --> dosed once a day and is a prodrug converted in gut
4) Without sulfur moiety does not cause skin rash, taste disturbance, and proteinuria.
*** increased rate of still births
* general well being
nasal stuffiness
5) Both decreased AII and decreases breakdown of bradykinin (vasodilator) (This is attenuated by indomethacin)

Front 26

Quinapril and Ramipril
1) Drug class
2) Mechanism of action
3) Use
4) Adverse effects

Back 26

1) ACEI
2) lower AII and decrease kinin breakdown, and may modulate PG production
3) CHF b/c AII release from failing hearts, HT, vent dysfunction after MI
4) Skin rash, pruritis, loss of taste, and proteinuria (mostly with catapril), dry cough (chronic use of all ACEI), hyperkalemia when pt takes K sparing diuretics, beta blockers, NSAIDs, or K supplement. Still births rate increase. DDI with diuretics and inomethicin

Front 27

Quinapril and Ramapril
5) Effectiveness
a) dosing
b) most effective in which population
c) positive effect

Back 27

5) a) once a day orally, rapid onset, no tolerance
b) young white people
c) --> general sense of well being

Front 28

Aldosterone
1) Effect
a) on kidney
b) MR, mineral corticoid, dependent sites of action
c) MR independent sites of action

Back 28

1)a) increase Na retention and K excretion
b) sM cells and cardiac tissues --> Na influx in vascular SM cells
c) --> endothelial dysfunction through inhibition of NO and --> fibrosis of heart via fibroblast stim and collagen deposition.

Front 29

Eplerenone/spirolactone
1) Drug class
2) Mechanism of action
3) Effects
4) Uses
5) Adverse effects

Back 29

1) Aldosterone blocker
2) Binds MR
3) restores endothelial function, reduces vascular injury and reduces interstitial fibrosis
4) in HT to reduce LVH, additive with ACEIs (Enalapril)
5) Eplerenone has less hyperkalemic and androgen/progestrin interaction than spirolactone

Front 30

Endothelin
1) Via which receptor does endothelin cause vasoconstriction?
2) What forms of endothelin exist?
3) Cardiovascular effects

Back 30

1) ETa, G protein coupled
2) ET-1, 2, and 3 are inactive intermediates activated by endothelin converting enzymes (ECEs)
3) Vasoconstriction
-stimulation of cytokines, GFs
-induced ECM formation
-promotes cell adhesion and thrombosis --> endothelin markers can be used to determine disease progression

Front 31

Bosentan
1) Drug class
2) Mode of action
3) Effects?

Back 31

1) ETa receptor antagonist
2) used when ET-1 levels increase as in HF
3) Reduces arterial pressure in early L vent/Heart failure
-In CHF pts, --> pulmonary and systemic vasodilation
-In HT pts --> decrease in BP without heart rate increase

Front 32

sodium nitroprusside
1) Mechanism of action
2) Uses

Back 32

1) metabolized to NO which increase cGMP levels to cause vasodilation of all vasculature
2) hypertensive crisis, controlled hypotension in surgical setting, CHF, acute pulmonary edema

Front 33

Fenoldapam
1) Drug class
2) Mechanism of action
3) Uses
4) Adverse effects
5) Administration

Back 33

1) Vasodilator, DA1 receptor agonist
2) vasodilation and renal effects via DA1
3) short term for hypertensive crisis.
4) Does not cross BBB
5) Reduction in BP directly related to infusion rate. Potentiated by ACEIs and ARBs