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PHRM 5001 > 10. Antihypertensive Medications > Flashcards

10. Antihypertensive Medications Flashcards

1
Q
  1. What are the 3 mechanisms to controlling blood pressure?
  2. Crisis is present when a patients blood pressure rises greater than ____________.
  3. Which anatomical sites are responsible for BP control in the human body?
A
  1. Changes in CO, Changes in vasomotor tone and Changes to plasma volume
  2. 180/120 mmHg.
  3. Kidneys, Heart, Precapillary arterioles, Postcapillary venules and Adrenal cortex
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2
Q
  1. What are the 5 different drug therapies that can be used for treating hypertension?
  2. What is the definition of a Hypertensive Crises?
  3. What are the two classifications of this type of crises?
A
  1. Diuretics, Sympatholytics, Vasodilators, Angiotensin-converting enzyme (ACE) inhibitors and Angiotensin II receptors blockers (ARBs)
  2. Systolic BP >180mmHg and/or a Diastolic BP >120mmHg
  3. Hypertensive urgency and Hypertensive emergency
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3
Q
  1. When managing a hypertensive urgency, when is this considered an urgent situation?
  2. The hypertension is corrected over how many hours?
  3. What are the 4 manifestations of a hypertensive urgency?
A
  1. when BP is elevated but there are no signs/symptoms of acute organ compromise
  2. 24-48 hours
  3. Severe headaches, Shortness of breath, Nosebleeds, and Severe anxiety
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4
Q
  1. What is the definition of a hypertensive emergency?
  2. What are the 6 manifestations of a hypertensive emergency?
  3. What is the first step (goal) in treating hypertensive emergencies? second step? third step?
A
  1. ↑ BP accompanied by acute progressing target organ injury requiring immediate treatment
  2. Encephalopathy, Intracranial hemorrhage, Severe retinopathy, Renal failure, Unstable angina, and Acute LV failure
  3. ↓ MAP by no more than 25% within first hour, THEN BP further ↓ to ~ 160/100 mmHg over 2-6 hrs, THEN BP gradually normalized over 24-48 hrs
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5
Q
  1. Adrenergic drugs interfere with? which 4 components?

2. Where can the effects be seen on the body?

A
  1. neurotransmission –> Central nervous system, Autonomic ganglia, Sympathetic nerve endings, and Adrenergic receptors
  2. centrally or peripherally
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6
Q
  1. What is the other drug name for Methyldopa?
  2. What type of drug is Methyldopa? What does this treat?
  3. What is required by the body in order for this drug to produce an effect? What is the end product called after this process?
  4. What are the two MOA of this drug?
A
  1. Aldomet
  2. Centrally acting a2- agonist prodrug; treats mild to moderate HTN
  3. Metabolic activation –> a-methylnorepinephrine
    • ↓ sympathetic outflow from medullary vasomotor centres (tricks body into thinking there is lots of circ. epi/norepi)
      - Binding at a2-adrenergic receptors on pre-synaptic membranes of peripheral neurons (fully saturated receptors = stops prod. epi/norepi)
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7
Q
  1. What are the precautions for Methyldopa? (4)
  2. What is the other drug name for Clonidine?
  3. What type of drug is Clonidine?
  4. What are the 3 net results when taking this drug?
A
  1. Risk of orthostatic hypotension*, Gradual withdrawal when stopping agent to minimize rebound HTN, Na+ retention with long-term use, and Anticholinergic-like side effects
  2. Catapres
  3. Mechanism similar to methyldopa –> centrally acting a2- adrenergic agonist (Depresses medullary vasomotor centres)
  4. ↓ HR, ↓ CO, and ↓ tone of capacitance vessels
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8
Q
  1. When is the use of Clonidine specifically indicated?
  2. What are this drugs 2 off- label uses?
  3. What is needed when considering stopping this drug?
A
  1. for moderate to severe hypertension (Second-line treatment due to side effects)
  2. Nicotine symptom withdrawal and Pain management
  3. Tapered withdrawal needed
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9
Q
  1. What are the 5 anti-cholinergic side effects of centrally acting agents?
  2. What are the 5 CNS side effects of centrally acting agents?
  3. Peripherally acting sympatholytic drugs interfere with? Which 3 components are involved with this?
A
  1. Sedation, Blurred vision, Dry mouth, Constipation, Urinary retention
  2. Drowsiness, Headaches, Depression, Psychosis, Nightmares
  3. neuronal activity at various sites of action –> Autonomic ganglia, Postganglionic neurons, and Adrenergic receptors*
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10
Q
  1. What is the other drug name for Propranolol?
  2. What type of drug is this?
  3. MOA?
  4. 4 net effects of this drug?
A
  1. Inderal
  2. peripherally acting b-blocker
  3. non-selective catecholamine antagonist causing b-adrenergic blockade
  4. ↓ HR, ↓ CO, ↓ SVR, ↓ renin release
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11
Q
  1. What are the 3 indications for taking Propranolol?
  2. What are the 4 contraindications for taking this drug?
  3. What are the 3 precautions?
A
  1. HTN management as part of a combination therapy, Unstable angina, and Control of cardiac arrhythmias
  2. Variant angina, classic angina, Asthma, and Acute CHF
  3. Transient rise in BP –> unopposed a-response , ↑ airway resistance, and Upregulation of b receptors with prolonged use
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12
Q
  1. b-blockers cannot be ____ ___________.
  2. Asthma and COPD patients should use what type of b-blocker?
  3. patients with liver failure should use what type of b-blocker?
  4. Patients with PIH (pregnancy induced hypertension) need what type of b-blocker? example?
A
  1. used interchangeably
  2. cardio-selective
  3. one that is NOT metabolized in the liver
  4. one that WON’T compromise fetal BF –> Labetalol
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13
Q
  1. What is the other drug name for Metoprolol?
  2. What type of drug is this?
  3. Dominant effects at which receptors in the body?
  4. Indicated for patients with which 2 conditions? Can also be used to control what?
A
  1. Betaloc
  2. Peripherally acting, cardio-selective b-blocker
  3. b1 receptors in the heart
  4. asthma and peripheral vascular disease (PVD), can be used to control cardia arrhythmias
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14
Q
  1. What is the other drug name for Nadolol?
  2. What type of drug is this?
  3. NOT metabolized in the ______.
  4. How do we get rid of this drug in the body?
  5. This drug is ideal for patients with?
A
  1. Corgard
  2. peripherally acting b-blocker
  3. body
  4. excreted in the urine
  5. hepatic dysfunction
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15
Q
  1. What is the other drug name for Labetalol
  2. What type of drug is this?
  3. This drug has ____ ________ effects. Can you describe the two effects?
  4. This drug is primarily used to treat which condition? Why? (3 reasons)
A
  1. Normodyne
  2. peripherally acting b-blocker
  3. dose dependent –> low dose = b-blockade, high dose = a-blockade
  4. pregnancy induced HTN (PIH) because…..
    • Does not ↓ uterine/fetal BF
    • Does not inhibit uterine contraction
    • Compatible with breast feeding
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16
Q
  1. What is the other drug name for Prazosin?
  2. What type of drug is this?
  3. When is this drug typically given with treating HTN?
  4. This drug selectively blocks which receptors?
  5. What are the 3 net results of this drug?
A
  1. Minipress
  2. peripherally acting a- adrenergic blocker
  3. typically in combination
  4. post synaptic a1-receptors
  5. ↓ SVR through arterial and venous dilation, ↓ preload , and ↓ afterload
17
Q
  1. Can you describe the “first dose” phenomenon with Prazosin?
  2. What are the 6 side effects associated with this phenomenon?
  3. How can this phenomenon be avoided?
  4. What are the 2 precautions when using this drug?
A
  1. sudden severe drop in BP after given the first does of the medication
  2. Orthostatic hypotension, Palpitations, ↑ HR,
    Dizziness, headaches, and syncope
  3. doses should be slowly increased
  4. Na+ retention leads to expansion of plasma volume (concurrent diuretic therapy needed) and
    Compensatory mechanisms contribute to observed first dose phenomenon
18
Q
  1. What is the other drug name for Doxazosin?
  2. What type of drug is this?
  3. This drug has a favorable effect on _________ profile. What 3 effects does this lead to?
  4. This drug has a minimal effect on? Especially?
A
  1. Cardura
  2. peripherally acting a-blocker
  3. lipoprotein profile leading to –> ↓ triglycerides and LDL, ↑ HDL, and Enlarged prostates/urinary issues in men
  4. electrolytes, especially Na+
19
Q
  1. Vasodilators should be which line of treatment when treating HTN?
  2. Vasodilators act on which muscle in the body? What does this prevent? What effect does this have and how does it do this?
  3. What other vessels in the body can vasodilators act on? what does this lead to?
A
  1. second line therapy
  2. vascular smooth muscle preventing contraction –> decreases SVR by arteriolar vasodilation
  3. capacitance vessels and thereby decreasing venous return
20
Q
  1. Vasodilator therapy triggers which 3 compensatory mechanisms? What can help to reduce these effects?
  2. What is the other drug name for Hydralazine?
  3. What type of drug is this?
  4. Which vessels are the effects of this drug seen? What 2 net effects does this lead to?
A
  1. Baroreceptor reflex, ↑ HR, and RAAS (used in combination to help reduce these effects)
  2. Apresoline
  3. vasodilator
  4. resistance vessels (after the load/precapillary vessels) –> ↓ SVR with no change in venous return, and C.O. may not change as much
21
Q
  1. Hydralazine is very potent, what does this mean? What 3 effects does this lead to?
  2. This drug is typically given with which 2 other drugs?
  3. What are the 3 MOA’s of this drug?
  4. What 2 formulations are available for taking this drug?
A
  1. leads to profound activation of baroreceptors –> reflex tachycardia, renin release, and ↑ in cardiac output
  2. b- blockers and diuretics
  3. ↓ SVR by a direct action on vascular smooth muscle, ↑ intracellular concentrations of cGMP, and Leads to vascular smooth muscle relaxation
  4. PO and IV
22
Q
  1. What is the other drug name for Nitroprusside?
  2. What type of drug is this?
  3. What is this drug typically used to treat?
  4. Which vessel(s) does this drug dilate?
  5. What are the 4 net effects of this drug? What severe result can this ultimately lead to in a patient?
A
  1. Nipride
  2. Vasodilator (Nitrate)
  3. hypertensive emergencies
  4. arterioles and veins
  5. ↓ afterload, ↓SVR, ↓ venous return, and ↓ preload–> can lead to severe hypotension
23
Q
  1. Calcium channel blockers act just like which type of drug?
  2. What vessel(s) does this drug dilate to decrease BP?
  3. MOA?
  4. What is the prototype drug calcium channel blocker?
A
  1. vasodilators
  2. peripheral arterioles
  3. Inhibit Ca2+ influx into vascular smooth muscle to block contraction
  4. verapamil
24
Q
  1. What is the other drug name for Diltiazem?
  2. What type of drug is this?
  3. Where are the effects of this drug primarily exerted?
  4. This drug has sympathetic antagonism effects, what does this cause compared to other drugs of this class?
  5. This drug does NOT alter which 2 profiles? Therefore, this drug is well suited for which 2 patient populations?
A
  1. Cardizem
  2. Calcium channel blocker
  3. on capacitance vessels
  4. Less reflex tachycardia than other Ca2+ blockers
  5. lipid or carbohydrate profiles –> good for diabetes and/or hyperlipidemia
25
Q
  1. What is the other drug name for Nicardipine?
  2. What type of drug is this? What does this drug cause?
  3. From the previous question, what are the 3 net effects of this drug?
  4. This drug has fewer ____ __________.
A
  1. Cardene
  2. 2nd generation calcium channel blocker causing arteriolar vasodilation
  3. ↑ blood flow, ↓ myocardial oxygen demands, and ↓ cardiac depression than diltiazem
  4. drug interactions
26
Q
  1. In the RAAS, what is renin normally released in response to? (3)
  2. Where is the macula densa located in the kidneys? What does it sense?
A
  1. ↓ renal perfusion pressure, Sympathetic stimulation, and [Na+] in distal tubules
  2. close to distal tubule and senses amount of Na+ there (decreased conc = release of renin)
27
Q
  1. What is the other drug name for Captopril?
  2. What type of drug is this?
  3. How can this drug help to control HTN?
  4. What are the 3 reasons as to why there is no reflex tachycardia when taking this drug?
  5. What does this drug also help to prevent?
A
  1. Capoten
  2. ACE inhibitor
  3. controls HTN caused by excess renin release
  4. ↓ BP due to fall in SVR while HR & CO unchanged
  5. inactivation of bradykinin (powerful vasodilator)
28
Q
  1. If angiotensin II is inhibited by an ACE inhibitor such as Captopril, how does this specifically help treat HTN?
  2. If the enzyme Kininase is inhibited with the drug Captopril, how does this specifically help treat HTN?
  3. What are the 3 indications for using Captopril?
A
  1. we decrease the amount of vasoconstrictor (angiotensin II) which in turn decreases BP
  2. leads to increased amounts of bradykinin which is a vasodilator in turn causing a decrease in BP
  3. HTN caused by ↑ plasma renin, Concurrent ischemic heart disease, and refractory cases when pt unresponsive to –> Sodium restricted diet, Diuretics, Sympatholytics, or Vasodilators
29
Q
  1. What are the 5 adverse reactions when taking Captopril?
  2. What is the other drug name for Enalapril?
  3. What type of drug is this?
  4. This is a _____. Therefore meaning?
A
  1. Bone marrow suppression, Proteinuria, Persistent cough (ACE cough), Angioedema – increased vessel permeability from vasodilation, and Drug interactions with NSAIDs and lithium (treating bipolar)
  2. Vasotec
  3. long acting (24hr) ACE inhibitor taken OD for compliance
  4. Prodrug –> needs to be hydrolyzed into active metabolite once taken
30
Q
  1. Enalapril has a low incidence of?
  2. This drug is suitable for? Can also be used?
  3. What is the other drug name for Ramipril?
  4. What type of drug is this?
A
  1. adverse effects
  2. monotherapy for HTN and can be used in combination for more severe cases
  3. Altace
  4. commonly prescribed long acting (24hr) ACE inhibitor
31
Q
  1. What are the 3 indications for using Ramipril?
  2. What are the 7 adverse effects?
  3. Angiotensin II can be generated via which 2 pathways? What does this mean?
A
  1. Heart failure post-MI, Hypertension, and ↓ risk of stroke, MI and death from CV disease
  2. Angioedema, Cough, Jaundice, Hyperkalemia, Hypersensitivity, Hypotension/syncope, and ↓ renal function
  3. non-renin and non-ACE mediated pathways meaning other substances can mediate angiotensin production therefore ACE inhibitors can NOT completely block vasoconstriction via angiotensin II (considered 2nd line treatment)
32
Q
  1. What is the other drug name for Losartan? For Telmisartan? For valsartan?
  2. What type of drugs are these?
  3. MOA?
  4. What does the MOA prevent with these drugs? What does this decrease? (2)
A
  1. Cozaar, Micardis, and Diovan
  2. Angiotensin II receptor blockers
  3. ARBs competitively antagonize angiotensin II at receptors found on –> Myocardial tissue and Vascular smooth muscle
  4. prevents constriction –> decreasing vascular resistance and BP
33
Q
  1. Why are Losartan, Telmisartan, and Valsartan less potent anti-HTN than ACE inhibitors?
  2. There is less incidence of?
  3. What are the 3 indications for using this class of drugs?
  4. What are the 6 adverse effects when taking either of these drugs?
A
  1. Cannot inhibit bradykinin inactivation to further ↓ BP
  2. Less incidence of a cough
  3. Refractory HTN, refractory heart failure, and
    when adverse effects of other drugs are not tolerated
  4. Orthostatic hypotension, Hyperkalemia , Nephrotoxicity, Fetotoxicity , ↑ serum [digoxin], and Possible drug interactions (NSAIDs & lithium)

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