Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal II > Antihypertensive Pharm Lecture > Flashcards

Antihypertensive Pharm Lecture Flashcards

1
Q

Hypertension and CardioVascular Disease

A
  • Hypertension affects roughly 70 Million individuals in the USA and 1 Billion Worldwide
  • HIGH BP is associated with an INCREASED RISK of MI, HEART FAILURE, STROKE and KIDNEY DISEASE

** In the General Population less than 60 y/o, initiate Pharmacologic treatment to LOWER BP at DBP Greater than 90 mmHG and treat to a GOAL DBP Less than 90 mmHg

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

The Blood Pressure Equation

A

** Mean Arterial Pressure = CO x TPR !!!!!

***** Cardiac Output = HR x SV !!!!!!!!!!!!!!

Drug Strategies:
- REDUCE CARDIAC OUTPUT and BLOOD PRESSURE is REDUCED!!!!!

Compensatory Responses May Include:

  • REFLEX TACHYCARDIA (INCREASED Sympathetic Activity)
  • Edema (Increased Renin Activity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Four Major Categories of Drugs according to Mechanism of Action

A

1) Diuretics
2) Agents that BLOCK the PRODUCTION or ACTION of ANGIOTENSIN
3) DIRECT VASODILATORS
4) SYMPATHOPLEGIC Agents (Those that alter Sympathetic Function)

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

Diuretics: A Preview

A
  • INCREASE the RATE OF URIEN FLOW and SODIUM EXCRETION
  • Used to adjust the Volume and/ or Composition of BODY FLUIDS in a Variety of Clinical Situation including (but not limited to):
    a) EDEMATOUS STATES: Heart Failure, Kidney Disease and Renal Failure, Liver Disease (Cirrhosis)

b) NONEDEMATOUS STATES: Hypertension, Nephrolithiasis (Kidney Stones), Hypercalcemia, and Diabetes Insipidus

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

Diuretics: Molecular Targets

A

1) Specific Membrane Transport Proteins
a) Sodium/ Potassium/ Chloride Cotransporter (LOOP DIURETICS)

b) Sodium/ Chloride Cotransporter (THIAZIDE DIURETICS)
c) Sodium Channels (POTASSIUM-SPARING DIURETICS)

2) ENZYMES:
a) Carbonic Anhydrase (CARBONIC ANHYDRASE INHIBITORS)

3) HORMONE RECEPTORS:
a) Mineralocorticoid Receptor (POTASSSIUM-SPARING DIURETICS)

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

Drug List: CARBONIC ANHYDRASE INHIBITORS

A
  • ACETAZOLAMIDE!!!!!!
  • Brinzolamide
  • Dorzolamide
  • Methazolamide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Drug List: LOOP DIURETICS

A
  • Bumetanide
  • ETHACRYNIC ACID ( This is the NON- SULFA DRUG!!!!!)
  • FUROSAMIDE (Lasix)
  • Torsemide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Drug List: THIAZIDE DIURETICS

A
  • Bendroflumethiazide
  • Chlorothiazide
  • CHLORATHALIDONE
  • HYDROCHLOROTHIAZIDE
  • Hydroflumethiazide
  • Indapamide
  • Methyclothiazide
  • Metolazone
  • Polythiazide
  • Trichlormethiazide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Drug List: K+ SPARING DIURETICS

A

1) ALDOSTERONE ANTAGONISTS:
• Eplerenone

• SPIRONOLACTONE!!!!!!

2) EPITHELIAL SODIUM CHANNEL INHIBITORS:
• AMILORIDE!!!!!

• Triamterene

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

Drug List: OSMOTIC DIURETICS

A
  • Mannitol

* Isosorbide

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

Drug List: ADH ANTAGONISTS

A
  • Conivaptan

* Tolvaptan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Carbonic Anhydrase Inhibitors

A

** Prototype: ACETAZOLAMIDE!!!!!!

1) MOA: INHIBITS the Membrane-Bound and Cytoplamis forms of CARBONIC ANHYDRASE

2) Results in:
- DECR H+ Formation INSIDE PCT Cell

  • DECR Na+/ H+ Antiport
  • INCREASE Na+ and HCO3- in LUMEN!!!!!!!!
  • INCR DIURESIS!!!!!!!
    3) Urine pH is INCREASED and Body pH is DECREASED!!!!!
    4) Other Agents: Brinolamide, Dorzolamide, Methazolamide

5) Clinical Indications:
- Rarely used as ANTIHYPERTENSIVES due to LOW EFFICACY as a Single Agents and Development of METABOLIC ACIDOSIS!!!!!

  • Used for GLAUCOMA, ACUTE MOUNTAIN SICKNESS, and METABOLIC ALKALOSIS!!!!!
    6) Adverse Effects include ACIDOSIS, HYPOKALEMIA, RENAL STONES, PARATHESIAS (with High Doses) Sulfonamide Hypersensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Loop Diuretics

A

*** Prototype: FUROSEMIDE and ETHACRYNIC ACID (Only one that is Non-Sulfa)!!!!!!

1) MOA: INHIBIT the Luminal Na+/ K+/ 1Cl- Cotransporter (NKCC2) in the THICK ASCENDING LIMB of the LOOP OF HENLE

2) RESULTS IN:
- DECR Intracellular Na+, K+, Cl- in TAL

  • DECR back Diffusion of K+ and POSITIVE POTENTIAL
  • DECR Reabsorption of Ca2+ and Mg2+!!!!!!!!
  • INCR DIURESIS
    3) Ion transport is Virtually NONEXISTENT
    4) Among the MOST EFFICACIOUS DIURETICS available

5) Diuretic activity tied to SECRETION RATES (Act at LUMINAL SIDE of Tubule)
a) Half Lide correlated to Kidney Function

b) 0.5 to 2 Hours (HEALTHY vs 9 hrs (END STAGE RENAL DISEASE) for FUROSEMIDE
6) Used for EDEMA, HEART FAILURE, HYPERTENSION, ACUTE RENAL FAILURE, ANION OVERDOSE, HYPERCALCEMIC STATES
7) ADVERSE Effects Include HYPOKALEMIA, ALKALOSIS, HYPOCALEMIA, HYPOMAGNESEMIA, HYPERURICEMIA, OTOTOXICITY, Sulfonamide Hypersensitivity (Not All)

** Causes OTOTOXICITY so LOSS of HEARING!!!!!!!!**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Thiazide Diuretics

A

** Prototype: HYDROCHOLOTHIAZIDE (HCTZ)

1) MOA: Cause INHIBITION of the Na+/ Cl- Cotransport (NCC) and BLOCK NaCl Reabsorption in the DISTAL CONVOLUTED TUBULE

2) Results in:
- INCR Luminal Na+ and Cl- in DCT

  • INCR Diuresis
    3) Enhance the REABSOPTIONof Ca2+ in BOTH DCT
    4) Largest Class of DIURETIC AGENTS!!!!!!
    5) Used for HYPERTENSION, Mild Heart Failure, NEPHROLITHIASIS (Calcium Stones), NEPHROGENIC DIABETED INSIPIDUS!!!!!!
    6) ADVERSE EFFECTS include HYPOKALEMIA, Alkalosis, Hypercalcemia, Hyperuicemia, HYPERGLYCEMIA, HYPERLIPIDEMIA, Sulfonamide Hypersensitivity

** HYPERGLYCEMIA and HYPERLIPIDEMIA!!!!!!**

7) MORE HYPONATREMIC EFFECTS THAN Loop Diuretics!!!!!!!!!!!!!
8) Use with Caution in patients with DIABETES MELLITUS

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

K+ Sparing Diuretics

Overview

A
  • The MOST IMPORTANT SITE of K+ Secretion by the Kidney!!!!!
  • Site at which ALL DIURETIC-INDUCED changes in K+ Balance occur, more Na+ DELIVERED to COLLECTING TUBULE LEADS to MORE K+ SECRETION!!!!!!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

K+ Sparing Diuretics

A

1) MINERAL CORTICOID RECEPTOR (MR) ANTAGONISTS:
a) SPIRONOLACTONE and Eplerenone

b) Uses include HYPERALDOSTERONISM, adjunct to K+ Wasting Diuretics, Antiandrogenic uses (Female Hirsutism), Heart Failure (REDUCES MORTALITY)
c) DO NOT require ACCESS to the Tubular Lumen to INDUCE Diuresis
d) Adverse Effects include HYPERKALEMIA, ACIDOSIS, and ANTIANDROGENIC!!!!

2) Na+ CHANNEL (ENaC) INHIBITORS:
a) AMILORIDE and Triamterene

b) Uses include adjunct to K+ Wasting Diuretics and LITHIUM INDUCED NEPHROGENIC DIABETES INSIPIDUS (AMILORIDE)
c) Adverse Effects include HYPERKALEMIA and ACIDOSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Mineralocorticoid Receptor (MR)

A
  • NUECLEAR HORMONE RECEPTOR responsible for REGULATING the Expression of MULTIPLE GENE PRODUCTS
  • Natural AGONISTS include Mineralocorticoids, a Class of Steroid hormones that INFLUENCE SALT and WATER BALANCE
  • Examples include ALDOSTERONE, DEOXYCORTICOSTERONE, and GLUCOCORTICOIDS (Cortisol)
  • Also known as the ALDOSTERONE RECEPTOR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Drug List: Angiotensin Converting Enzyme (ACE) Inhibitors

A
  • Benazepril
  • CAPTOPRIL!!!!! (t1/2 = 2 Hours)
  • ENALAPRIL!!!!! (t1/2 = Less than 2 Hours or 12 Hours by IV)
  • Enalaprilat
  • Fosinopril
  • LISINOPRIL!!!!! (t1/2 = 12 Hours)
  • Moexipril
  • Perindopril
  • Quinapril
  • Ramipril
  • Trandolapril
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Angiotensin Receptor Blockers (ARBs)

A
  • Azilsartan
  • Candesartan
  • Eprosartan
  • Irbesartan
  • LOSARTAN!!!!!!!
  • Olmesartan
  • Telmisartan
  • VALSARTAN!!!!!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Other Modulators

A

1) Drugs that BLOCK RENIN SECRETION:
• Clonidine

• Propranolol

2) RENIN INHIBITORS:
• ALISKIREN!!!!!

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

Pharmaceutical Strategies for Inhibition of the Renin- Angiotensin- Aldosterone System

A

1) Aldosterone Receptor (MR) Antagonists
2) ACE Inhibitors (ACEIs)
3) Angiotensin II Receptor Blockers (ARBs)
4) Beta Blockers

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

Angiotensin Converting Enzyme Inhibitors

A

** Prototypes: CAPTOPRIL and ENALAPRIL

1) MOA: INHIBIT the CONVERSION of ANG I to the more active ANG II; also PREVENT DEGRADATION OF BRADYKININ and other Vasodilator Peptides
2) Clinical Indications: HYPERTENSION, Heart Failure, Left ventricular Dys, Prophylaxis of Future Cardiovascular Events (Ex MI, CAD, Stroke) and Nephropathy (+/- Diabetes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Benefits of ACE Inhibitors in HTN

A

1) LOWERS TPR and Mean, Diastolic, and Systolic BP

2) Cardiac function in patients with UNCOMPLICATED HYPERTENSION is little changed
- STROKE VOLUME and CARDIAC OUTPUT may INCREASE Slightly with sustained Treatment

3) Baroreceptor Function and CARDIOVASCULAR REFLEXES are NOT COMPROMISED
- Responses to POSTURAL CHAGNES and EXERCISE are Little Impaired

4) Evidence that ACEIs are SUPERIOR in treating HTN in patients with DIABETES!!!!!!
- Improve Endothelial function and reduce CV events more so thanCCBs or Diuretic and Beta Blocker Combo

24
Q

Adverse Effects of ACEIs

A
  • Hypotension
  • COUGH!!!!!!
  • ANGIOEDEMA!!!!!!
  • HYPERKALEMIA!!!!!! (Avoid K+ Sparing Diuretics)
  • ACUTE RENAL FAILURE, Particularly in patients with RENAL ARTEYR STENOSIS!!!!
  • Fetopathic Potential (Teratogen)- CONTRAINDICATED IN PREGNANCY!!!!!!!!
  • Drug Interactions: Antacids, Capsaicin, NSAIDs, K+ Sparing Diuretics, Digoxin, Lithium, Allopurinol
25
Q

Renal Consideration with ACEIs

A

1) ACEIs prevent/ delay the progression of Renal Disease in Type 1 DIABETICS and in patients with NONDIABETIC Nephropathies (Results MIXED in Type 2 Diabetics)

2) ACEIs Vasodilator EFFERENT ARTERIOLES GREATER THAN Afferent Arterioles
- Reduces BACK PRESSURE on the Glomerulus and REDUCES Protein Excretion

3) ACEIs usually IMPROVE RENAL BLOOD FLOW and Na+ EXCRETION RATES in CHF!!!!!
4) In Rare Cases, ACEIs can cause a RAPID DECREASE in GFR

26
Q

Risk Factors of ACEI- Induced ARF

A

1) MAP insufficient for adequate RENAL PERFUSION
- Poor Cardiac Output
- Low Systemic Vascular Resistance

2) Volume Depletion (Diuretic Use)

3) Renal Vascular Disease
- Bilateral Renal Artery STENOSIS

  • Stenosis of Dominant or Single Kidney
  • Afferent Arteriolar Narrowing (HTN, Cyclosprorin A)
  • Diffuse ATHEROSCLEROSIS in Smaller Renal Vessels
    4) VASOCONSTRICTIR Agents (NSAIDS, Cyclosporine)
    5) All cause RENAL HYPOPERFUSION
27
Q

Angiotensin II Receptors

A

1) G Protein Coupled Receptors
2) Tw Receptor Subtypes (AT1 and AT2)

3) AT1 RECEPORS!!!!!:
- Major Subtype in ADULTS!!!!
- Gq —> PLC —> IP3 + DAG —-> Smooth Muscle CONTRACTION!!!!!!

4) AT2 Receptors:
- Activation causes production fo NITRIC OXIDE and BRADYKININ
- Smooth Muscle DILATION!!!!!!!!

28
Q

Angiotensin II Receptor Blockers (ARBs)

A

** Prototypes: LOSARTAN (t1/2 = 2 Hours) and VALSARTAN (t1/2 = 6 to 9 Hours)!!!!**

1) MOA: Selectively BLOCK AT1 Receptors, which leads to:
- DECR CONTRACTION of Vascular Smooth Muscle

  • DECR ALDOSTERONE Secretion
  • DECR Pressure Responses
  • DECR Cardiac Cellular Hypertrophy and Hyperplasia
    2) NO EFFECT on BRADYKININ METABOLISM!!!!!
    3) Therapeutic Uses: Hypertension, Diabetic Nephropathy, HF, HF or Left Ventricular Dys after AMI, and Prophylaxis of Cardiovascular Events
    4) ADVERSE effects Similar to ACEIs but LESS COUGH and EDEMA; CONTRAINDICATED DURING PREGNANCY!!!!!!!
29
Q

ACEIs vs ARBs

A

1) ARBs REDUCE ACTIVATION of AT1 Receptors MORE EFFECTIVELY than do ACEIs
2) ARBs permit activation of AT2 Receptors!!!!
3) ACE Inhibitors INCREASE the levels of a Number of ACE Substrates, including BRADYKININ!!!!!!!**
4) Unknown whether or not these Pharmacological differences result in significant differences in Therapeutic Outcomes

30
Q

Aliskiren: A Direct RENIN Inhibitor

A

1) MOA: INHIBITS RENIN and BLOCKS the conversion of Angiotensinogen to ANG I
2) DOES NOT INCRASE BRADYKININ
3) Rise in Plasma RENIN LEVELS but DECREASED PLASMA Renin Activity (ACEIs, ARBs, and Diuretics RAISE PLASMA RENIN LEVELS and Activity via Feedback Loop)
4) Studies show effectiveness comparable to ACEIs and ARBs
5) AEs similar to ACEIs and ARBs; Contraindicated in PREGNANCY!!!!!!

31
Q

Drug List: Calcium Channel Blockers (CCBs)

A

1) DIHYDROPYRIDINES (DHPs):
• AMLODIPINE!!!!!

  • Clevidipine
  • Felodipine
  • Isradipine
  • Nicardipine
  • NIFEDIPINE
  • Nisoldipine

2) NON- DIHYDROPYRIDINES:
• DILATIAZEM

• VERAPAMIL

32
Q

Drug List: Potassium Channel Openers

A
  • Diazoxide

* Minoxidil

33
Q

Drug List: Dopamine Agonist

A

• Fenoldopam

34
Q

Drug List: Nitric Oxide Donors

A
  • HYDRALAZINE
  • NITROPRUSSIDE (Nitropress)
  • Organic Nitrates

a) Isosorbide dinitrate
b) Nitroglycerin

35
Q

Calcium Channel Blockers (CCBs): MOA

A
  • L Type Ca++ Channels also regular Calcium flux into CARDIAC Monocytes and SA and AV Nodal Cells
36
Q

CCBs: Two Major Subclasses

A
  • All CCBs bind to L-Type Ca++ Channels. But the Two Classes bind to DIFFERENT SITES, resulting in DIFFERENT EFFECTS on VASCULAR vs CARDIAC TISSUE

1) NON- DIHYDROPYRIDINES:
- Prominent CARDIAC EFFECTS (At SA and AV NODES), but also act at Vascular Tissues

** VERAPAMIL is GREATER THAN DILATIAZEM!!!!!!! ))))))

2) DIHYDROPYRIDINES (DHPs):
- Predominantly Arteriolar VASODILATION Effects

  • AMLODIPINE, Clevidipine, Felodipine, Isradipine, Nicardipine, NIFEDIPINE!!!!!
37
Q

CCBs: Adverse Effects and Toxicity

A

1) Generally VERY WELL TOLERATED!!!!!
2) Excessive Vasodilation, Dizziness, Hypotension, Headaches, Flushing, Nausea; diminished by Long-acting Formulation and Long Half-Life Agents
3) CONSTIPATION (Esp VERAPAMIL), PERIPHERAL EDEMA, Coughing, Wheezing, Pulmonary Edema
4) Use of VERAPAMIL/ DILTIAZEM with a BETA BLOCKER is CONTRAINDICATED because of the Potential for AV Block!!!!!!!
5) Verapamil. Diltiazem SHOULD NOT be used in Patients with Ventricular Dys, SA or AV Nodal Conduction DEFECTS and SYSTOLIC BP Less than 90 mmHg

38
Q

CCBs: Clinical Use

A

1) Hypertension
- Most useful when COMBINED with Another Agent to counteract the REFLEX Cardiovascular Responses

2) HYPERTENSIVE EMERGENCIES
- Parenteral Formulations

3) ANGINA
- Reduction of O2 demand makes Particularly USEFUL

39
Q

Potassium Chanel Openers: MOA

A
  • Increased Potassium PERMEABILITY STABILIZES the Smooth Muscle Cell Membrane at RESTING POTENTIAL, reducing the Probability of CONTRACTION!!!!!
40
Q

Potassium Channel Openers:

A

1) DIAZOXIDE:
- Arteriolar Vasodialtion

  • Diminishing use in HYPERTENSIVE EMERGENCIES due to Adverse Effects:
    a) Excessive Hypotension can CAUSE STROKE and MI

b) Hyperglycemia

2) MINOXIDIL:
- Arteriolar Vasodilation

  • Clinical uses INCLUDE SEVER HYPERTENSION and BALDNESS (Topical)
  • ADVERSE Effects:
    a) Headache, Sweating

b) Hypertrichosis!!!!

C) Reflex Tachycardia and Edema, must be used with BETA BLOCKER and DIURETIC TO AVOID THESE EFFECTS!!!!!!!

41
Q

Fendolopam

A

1) D1 Dopamine Recepto AGONIST!!!!!
2) Renal AFFERENT Arteries contain Dopamine Receptors, activation INCREASES BLOOD FLOW TO THE KIDNEYS
3) For HTN Emergencies and Post-Operative HTN
4) Adverse Effects include Tachycardia, Headache, and Flushing
5) Should be AVOIDED in Patients with GLAUCOMA due to INCREASES in INTRAOCULAR PRESSURE!!!!!!!!!

42
Q

Nitric Oxide Modulators

A
  • Hydralazine
  • Nitroprusside
  • Nitroglycerine, Isosorbide Denigrate
  • Synergistic interaction with PDE5 Inhibitors!!!!
43
Q

Hydralazine

A

1) MOA: RELEASES NITRIC OXIDE form Endothelium
- DILATES ARTERIOLES, but NOT VEINS!!!!

2) Clinical Uses
- FIRST LINE ORAL Therapy for HYPERTENSION in PREGNANCY, with METHYLDOPA!!!!!!!!

  • Combination with NITRATES is EFFECTIVE in Patients with HEART FAILURE!!!!!
  • Parenteral Formulation useful in Hypertensive Emergencies

3) Adverse Effects:
- Can INDUCE Fluid and SODIUM RETENTION

  • Headache, Nausea, Anorexia, Sweating, Flushing, Palpitations
  • REFLEX TACYCARDIA can provoke ANGINA in patients with ISCHEMIC HEART DISEASE!!!!!!
  • LUPUS- like Syndrome (REVERSIBLE on Drug Withdrawal!!!!)
44
Q

Nitroprusside and Organic Nitrates

A

1) Used to TREAT HYPERTENSIVE EMERGENCIES, Heart Failure, and Angina (Nitrates)
2) Prototype Organic Nitrate: NITROGLYCERINE!!!!!

3) PHARMACODYNAMIC EFFECTS:
- DILATES BOTH ARTERIAL AND VENOUS VESSELS ————> DECREASES TPR and VENOUS RETURN

  • DECREASE BOTH PRELOAD and AFTERLOAD
  • Mainly RELAXATION of Large Veins ——> DECR Venous Return —–> DECR PRELOAD —-> DECR O2 Demand (MAJOR EFFECT), SMALLER DECR in AFTERLOAD

4) ADVERSE EFFECTS:
- NITROPRUSSIDE: EXCESSIVE HYPOTENSION, CYANIDE POISONING

  • NITRATES: ORTHOSTATIC HYPOTENSION, Syncope, Throbbing Headache
45
Q

Drug List: Beta Adrenergic Antagonists (Beta Blockers)

A
  • Acebutolol
  • ATENOLOL
  • Betaxolol
  • Bisoprolol
  • Carteolol
  • CARVEDILOL
  • Esmolol
  • LABETALOL
  • METOPROLOL
  • Nadolol
  • Nebivolol
  • Penbutolol
  • Pindolol
  • PROPRANOLOL
  • Timolol
46
Q

Drug List: Alpha 1 Adrenergic Antagonists (Alpha 1 Blockers)

A
  • Doxazosin
  • PRAZOSIN
  • Terazosin
47
Q

Drug List: Centrally Acting Sympathoplegics

A
  • CLONIDINE
  • Guanabenz
  • Guanfacine
  • METHYLDOPA
48
Q

Beta Blockers Selective vs Non Selective

A

NON-SELECTIVE:

1) Non- Intrinsic Sympathomimetic Activity:
- PROPRANOLOL
- Carvedilol
- Nadolol
- Timolol

2) Intrinsic Sympathomimetic Activity:
- LABETALOL
- Carteolol
- Penbutolol
- Pindolol

Beta 1 SELECTIVE:

1) NON- Intrinsic Sympathomimetic Activity:
- METOPROLOL
- ATENOLOL
- Esmolol
- Bisoprolol
- Betaxolol

2) Intrinsic Sympathomimetic Activity:
- Acebutolol
- Nebivolol

49
Q

Beta Blockers in Hypertension

A
  • NO LONGER 1st line treatment for Hypertension, except when concomitant with a compelling indication
    a) Heart Failure
    b) Recent MI
    c) Reduced Left Ventricular Function
  • Predispose to DIABETES, particularly when combined with THIAZIDE
  • Relative CONTRAINDICATION: ASTHMA!!!!!!!!
  • LESS STROKE PROTECTION than other Antihypertensives
50
Q

Beta Blockers with ALPHA BLOCKING ACTIVITY

A

1) LABETALOL:
- Selective ALPHA 1 BLOCKER!!!!

  • NONSELECTIVE Beta 1 and Beta 2 Blocker
  • Partial AGONIST at Beta 2
  • Clinical Uses:
    a) IV for HYPERTENSION
    b) Acceptable option for HYPERTENSION during Pregnancy

2) CARVEDILOL:
- NONSELECTIVE Beta Blocker + Alpha 1 Blocker

  • Also have ANTIOXIDANT Properties
51
Q

Beta Blockers with VASODILATING Activity

A

1) NON-Selective Vasodilating Beta Blockers:
a) Carteolol
b) CARVEDILOL
c) LABETALOL

2) Beta 1 Selective Vasodilating Beta Blockers:
a) Betaxolol
b) Nebivolol

3) These drugs produce PERIPHERAL VASODILATION through a Variety of Mechanisms
1. ↑NO
2. Activate Beta 2 receptors
3. Block of Alpha 1 receptors
4. Block Ca++ entry
5. Open K+ channels
6. Antioxidant activity
7. Antiproliferative effects

52
Q

Esmolol (Brevibloc)

A

** VERY RAPID ONSET and SHORT DURATION OF ACTION

  • Beta 1 Selective
  • Used in IV INFUSION for PERI-OPERATIVE TACHYCARDIA and Hypertension, Hypertensive Emergencies, Arrhythmias
  • Used in Electroconvulsive Therapy
53
Q

Alpha 1 Selective Receptor Blockers

A

1) CLINICAL USE:
- 3rd and 4th LINE Treatment for ESSENTIAL HYPERTENSION; added to other agents from different classes in Refractory Cases; also use in Men with Concurrent HTN and BPH

2) PHARMACODYNAMIC EFFECTS:
- Precent Vasoconstriction of BOTH Arteries and VEINS

  • DECR TPR, DECR Venous Return, DECR PRELOAD!!!!!
  • Usually DO NOT INCR HR or Cardiac Output
  • DO NO INCR NE Release (No Alpha 2 Block)
  • Favorable Effects on Lipids (DECR LDL and Triglycerides; INCR HDL)
  • Relaxes Smooth Muscle in the PROSTATE

3) ADVERSE EFFECTS:
- Postural Hypotension and Syncope, Especially with INITIAL DOSES

  • Usually Given at Bedtime to MINIMIZE Hypotensive Effects

PHENTOLAMINE: Blocks ALPHA 1 and ALPHA 2

PRAZOSIN: Blocks ALPHA 1 ONLY!!!!

54
Q

Clonidine

A

1) AN ALPHA 2 AGONIST!!!
- IV: INCR BP (Peripheral Alpha2B) followed by DECR BP (Central Alpha2B)

  • Oral: DECR BP (Decreased C.O., Preload)
  • Patch: Same as ORAL

2) Clinical Use:
- ESSENTIAL HYPERTENSION (Rarely Used)!!!!!!!!!!!!!

  • Adjunct for Narcotic, Alcohol, and Tobacco Withdrawal (Unlabeled)

3) SIDE EFFECTS:
- Dry Mouth, Sedation, Impotence, Depression

  • SUDDEN WITHDRAWAL CAUSES HYPERTENSIVE CRISIS!!!!!!!!!!
55
Q

Methyldopa

A

1) False Neurotransmitter Concept
- Converted to Methyl-NE

  • Stored in Vesicles INSTEAD OF NE
  • Released and acts as a CENTRALLY Acting Alpha 2 AGONIST
  • DECR CENTRAL SYMPATHETIC OUTFLOW and DECR BLOOD PRESSURE
    2) MANY SIDE EFFECTS: Sedation, Dry Mouth, Sexual Dysfunction, Postural Hypotension, Anemia
    3) Now ONLY USED to TREAT HYPERTENSION IN PREGNANCY because of its safety!!!!!!!!!!!!!!!!!!!!

Renal II (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions