Ruggles Lecture 1 Flashcards

1
Q

The ____ reflex is important in the control of BP. Pressure sensors, located in large arteries of the thorax and neck, monitor changes in blood pressure and heart rate. If they sense a drop in blood pressure, the information is relayed to the brainstem. The brainstem then signals an increase in [sympathetic/ parasympathetic] discharge to the heart and peripheral vasculature and [sympathetic/ parasympathetic] outflow to the heart is decreased.

A

baroreceptor; sympathetic; parasympathetic

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2
Q

What are the (5) responses when Alpha-1 receptors are stimulated?

A
  1. Vascular sm. m. contraction
  2. Intestinal sm. m. relaxation
  3. Increased motility in ureters
  4. Urinary sphincter contraction
  5. Spleen capsule contraction
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3
Q

What are the (5) responses when Alpha-2 receptors are stimulated?

A
  1. Decreased sympathetic discharge from CNS
  2. Decreased NE release
  3. Decreased motility and secretion in GI tract
  4. Decreased insulin secretion from pancreas
  5. Vasoconstriction in some arterioles (sk. m., liver, kidney)
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4
Q

What are the (3) responses when Beta-1 receptors are stimulated?

A
  1. Increase HR and contractility of cardiac m.
  2. Increased renin secretion from kidney
  3. Increased lipolysis in fat cells
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5
Q

What are the (6) responses when Beta-2 receptors are stimulated?

A
  1. Relaxation of bronchiole sm. m.
  2. Vasodilation of some arterioles (sk. m., liver)
  3. Decreased motility of GI sm. m.
  4. increased cellular metabolism in sk. m. and liver cells
  5. relaxation of uterus
  6. relaxation of gallbladder
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6
Q

What are the (3) responses when Beta-3 receptors are stimulated?

A
  1. Increased lipolysis in fat cells
  2. decreased contraction of detrusor muscle in bladder
  3. decreased contractility of the heart
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7
Q

What are the systolic/ diastolic values considered to be prehypertensive? Stage 1 HTN? Stage 2 HTN?

A

Pre-hypertension = 120-139/ 80-89
Stage 1 = 140-159/ 90-99
Stage 2 = ≥160/ ≥100

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8
Q

What are common factors that likely are the cause of primary HTN?

A
  1. Diet
  2. stress
  3. smoking
  4. alcohol abuse
  5. metabolic syndrome
  6. genetic predisposition
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9
Q

What are the substances produced by cells lining the peripheral vasculature that cause vasodilation?

A
  1. Nitric oxide
  2. Bradykinin
  3. Prostaglandin L2
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10
Q

What are the substances produced by cells lining the peripheral vasculature that cause vasoconstriction?

A
  1. Angiotensin II

2. Endothelin-I

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11
Q

work on the kidney to increase the excretion of sodium and water; ADRs = fluid depletion, electrolyte imbalance, impaired glucose and lipid metabolism, GI disturbances, weakness/fatigue, orthostatic hypotension

A

Diuretics

- don’t take a diuretic before therapy or leaving home – will have to pee a lot

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12
Q

What are the 3 types of diuretics?

A
  1. Thiazide
  2. Loop
  3. potassium-sparing
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13
Q

Type of diuretic that works in the distal tubule to block sodium reabsorption; Osmotic forces causes the nephron to retain more water and both are excreted from the body

A

Thiazide diuretics

  • Hydrochlorothiazide (HCTZ)
  • Metolazone
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14
Q

Type of diuretic that works in the loop of Henle blocking sodium and chloride reabsorption

A

Loop diuretics

  • Furosemide
  • Torsemide
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15
Q

Type of diuretic that interferes with the exchange of sodium and potassium in the distal tubule. Sodium is then excreted and potassium loss is reduced

A

Potassium-sparing diuretics

  • Spironolactone (can cause gynecomastia and hyperkalemia)
  • Triamterene
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16
Q

Drug that reduces the workload of the heart and are used after a myocardial infarction to help the heart recover; ADRs = bronchoconstriction, excessive depression of HR and cardiac contractility, orthostatic hypotension, depression, fatigue, and GI disturbances

A

Beta-blockers

  • end in -olol
  • first couple weeks are hard for pts; feel sluggish
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17
Q

What are the beta-1 selective beta blockers?

A
  1. Atenolol
  2. Bisoprolol
  3. Metoprolol
  4. Nebivolol
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18
Q

What are the nonselective beta blockers?

A
  1. Carvedilol

2. Propranolol

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19
Q

Drugs that decrease vascular resistance; ADRs = reflex tachycardia, orthostatic hypotension, increased risk of cardiac disease

A

Alpha blockers

- also used to treat benign prostatic hypertrophy and allow men to void urine more easily

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20
Q

What are types of alpha blockers?

A
  1. Alfuzosin & Tamsulosin – selective for alpha-receptors on smooth muscle in the prostate and lower urinary tract
  2. Doxazosin – highly alpha-1 selective, promotes relaxation of smooth muscle in the vasculature decreasing PVR
  3. Prazosin – also used for HTN
    * *-osin
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21
Q

What are the drug families used to treat HTN?

A
  1. Diuretics
  2. Beta blockers
  3. Alpha blockers
  4. Vasodilators
  5. Calcium Channel Blockers
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22
Q

What are the drug families used to treat angina pectoris?

A
  1. Nitrates
  2. Beta blockers
  3. Calcium Channel Blockers
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23
Q

What are the drug families used to treat arrhythmia?

A
  1. Class I – Sodium Channel Blockers
  2. Class II – Beta blockers
  3. Class III – Drugs that prolong repolarization
  4. Class IV – Calcium channel blockers
24
Q

Inhibit sympathetic discharge from the brainstem; Stimulation of alpha-2 receptors cause a decrease in sympathetic discharge to the heart and vasculature; ADRs = dry mouth, dizziness, sedation

A

Centrally Acting Agents (Clonidine)

- can be used for sleeping pill in low dose

25
Q

inhibit smooth muscle contraction by increasing the intracellular production of cGMP and other messengers. Increased cGMP inhibits contraction of smooth muscle leading to vasodilation; ADRs = reflex tachycardia, dizziness, orthostatic hypotension, weakness, nausea, fluid retention, and headache

A

Vasodilators

26
Q

What are the types of vasodilators?

A
  1. Hydralazine
  2. minoxidil
  3. Nitroprusside
    - Hydralazine and minoxidil can be used as add of therapy for resistant hypertension. Nitroprusside is reserved for patients in hypertensive crisis
    - minoxidil causes an increase in hair growth (Rogaine)
27
Q

Prevent the conversion of Angiotensin I to Angiotensin II; don’t have a lot of ADRs, which is why they are used first; End in -pril

A

ACE inhibitors

- Enalapril, Ramipril, Lisinopril Benazepril, Moexipril, Captopril, Perindopril, Quinapril, Fosinopril, Trandolapril

28
Q

Block Angiotensin II from binding to receptors; Can cause dry, hacky cough; End in -sartan

A

Angiotensin II Receptor Blockers (ARBs)

29
Q

Prevents renin from converting angiotensinogen to angiotensin I

A

Direct Renin inhibitor

  • Only one = Aliskiren (Tekturna)
  • not often used since ACEs and ARBs are cheap and work well
30
Q

What are the ADRs of renin-angiotensin system inhibitors (ACEs, ARBs, Direct Renin Inhibitors)?

A
  1. Dry cough (not ARB’s)
  2. Hematological effects (neutropenia, agranulocytosis)
  3. Renal problems (glomerulonephritis, renal failure)
  4. Angioedema (welts, burning/itching skin, swelling of the face, difficulty breathing)
    - Emergency! Can happen at any time, but most likely to occur within first month
    - side effects are rare
31
Q

What are the types of calcium channel blockers?

A
  1. Dihydropyridine agents

2. non-dihydropyridine

32
Q

Block calcium entry into vascular smooth muscle inhibiting contraction and leading to vasodilation; Ends in -pine

A

Dihydropyridine agents

  • Amlodipine, Nifedipine, Felodipine, etc.
  • more useful for arrhythmias than HTN
33
Q

Have a greater effect on calcium influx into myocardial cells and a primary effect of decreased heart rate and myocardial contraction

A

Non-dihydropyridine

- Diltiazem, Verapamil

34
Q

What are the ADRs of calcium channel blockers?

A
  1. excessive vasodilation (swelling)
  2. orthostatic hypotension
  3. abnormal heart rate
  4. reflex tachycardia
  5. dizziness
  6. headache
  7. nausea
35
Q

What are non pharmacological interventions for HTN?

A
  1. Dietary modifications (DASH diet) – sodium restriction, fruits, vegetables, low-fat dairy
  2. Decreased use of alcohol and tobacco
  3. Decrease in body weight
  4. Regular exercise
  5. Stress management
36
Q

How do drugs that treat angina pectoris work?

A

drugs help restore or maintain the balance between myocardial oxygen supply and demand
- increase O2 supply or decrease demand

37
Q

Dilate the vascular smooth muscle by increasing the production of cGMP which decreases the oxygen demand of the heart; cGMP inhibits smooth muscle contraction; work by decreasing preload and after load; ADRs = headache*, dizziness, orthostatic hypotension, tolerance

A

Organic nitrates

- Taking this with viagra will result in massive vasodilation, causing BP to plummet

38
Q

What are the types of organic nitrates?

A
  1. Nitroglycerin can be used as treatment or prophylaxis; Many formulations: IV, oral, sublingual, transdermal ointment, transdermal patches
  2. Isosorbide Dinitrate – long-acting, also used for treatment or prophylaxis
  3. Isosorbide Mononitrate – long-acting, for prevention only
39
Q

Why are calcium channel blockers used to treat angina pectoris?

A

CCB block entry of calcium into coronary artery smooth muscle, which vasodilates the coronary blood vessels and results in an increased supply of oxygen to the myocardium
- Concerns about an increased risk of MI due to rapid changes in PVR and blood pressure and increased risk of cancer

40
Q

Decreases the concentration of calcium in heart muscle cells. This results in a reduced contraction force, which reduces cardiac workload, oxygen demand, and symptoms of angina; Does not promote arrhythmias or reduce blood pressure; Not used first line

A

Ranolazine (Ranexa)

41
Q

Angina pectoris is associated with some degree of coronary artery occlusion. Drugs that reduce platelet activity are essential in preventing platelet-induced clotting so the arteries do not become completely occluded and cause a myocardial infarction. What are the drugs used in for this?

A
  1. Aspirin
  2. Clopidogrel (Plavex) and Prasugrel (effient)
  3. Heparin and LMWH - enoxaparin (Lovenox)
    - decrease morbidity and mortality in pts with ischemic heard disease
42
Q

Classification of angina: myocardial oxygen demand exceeds oxygen supply; usually brought on by physical exertion

A

stable angina

- Nitroglycerin at onset, beta-blower or long-acting nitrate for prevention

43
Q

Classification of angina: myocardial oxygen supply decreases due to coronary vasospasm; ay occur at rest

A

variant angina

-CCB used

44
Q

Classification of angina: myocardial oxygen supply decreases at the same time oxygen demand increases; can occur at any time

A

Unstable angina

  • combo therapy (CCB + BB) and anticoagulants
  • dangerous form of angina
45
Q

What are the options for nonpharmacological management of angina pectoris?

A
  1. Lifestyle changes (exercise, weight control, smoking cessation, stress management)
  2. Surgical techniques: Coronary artery bypass, Coronary artery angioplasty
46
Q

What are the phases of the cardiac action potential?

A

Phase 0 – Rapid depolarization; sudden influx of Na+ ions
Phase 1 – brief period of repolarization; specific K+ channels in the cell membrane open and allow K+ to leave
Phase 2 –The AP undergoes a plateau because Ca channels open (influx of Ca); no net change in charge bc the efflux of K+; plateau allows the heart to rest and fill with blood
Phase 3 – Repolarization is complete; no more Ca entering the cell
Phase 4 – Slow, spontaneous depolarization in certain cardiac pacemaker cells; continuous leak of Na+ ions into the cells with a decr. in K+ exiting from the cell; progressive accumulation of (+) charge within the cell, which causes it to become more (+) until it reaches threshold and phase 0 is initiated again

47
Q

Drugs for arrhythmias: Normalize the rate of sodium entry into cardiac tissues and thereby help control cardiac excitation and conduction

A

Sodium channel blocker

48
Q

Subdivision of Na channel blocker; slow phase 0 depolarization, slow action potential propagation, and prolong repolarization of the cardiac cell; Can be used for atria or ventricular arrhythmias

A

Class IA

- Quinidine, procainamide, disopyramide

49
Q

Subdivision of Na channel blocker; shorten cardiac repolarization; Used to treat ventricular arrhythmias

A

Class IB

- Lidocaine and mexiletine

50
Q

Subdivision of Na channel blocker; decrease the rate of phase 0 depolarization and slow cardiac conduction; Used to treat ventricular arrhythmias

A

Class IC

- Flecainide and propafenone

51
Q

What drugs are these ADRs a result of:

  • proarrhythmic effect
  • Dizziness
  • Visual disturbances
  • GI problems (nausea, vomiting, diarrhea)
  • May signal the presence of arrhythmias
A

Class I antiarrhythmics

  • Tendency to increase rhythm disturbances (proarrhythmic effect) – most common reason why these aren’t used
  • While controlling one type of arrhythmia, these medications can aggravate/initiate other cardiac rhythm abnormalities
  • Patients with heart failure, myocardial ischemia, and structural heart disease are especially prone to class-I induced arrhythmias and should avoid these medications
52
Q

Drugs for arrhythmias: Decrease excitatory effects of the sympathetic nervous system and related catecholamines (NE and epinephrine) on the heart; decreases cardiac automaticity and prolongs the refractory period, slowing the heart rate;
Effective in treating atrial fibrillation but can also be used for ventricular arrhythmias; ADRs = bronchoconstriction (non-selective agents), excessive slowing of cardiac conduction

A

Class II: Beta blockers

  • ends in -olol
  • usually first line antiarrhytmic
53
Q

Drugs for arrhythmias: These medications delay repolarization of cardiac cells which slows and stabilizes the heart rate; Used to treat ventricular and atrial arrhythmias

A

Class III: Drugs that prolong repolarization

  • Amiodarone, Dronedarone, Dofetilide, Ibutilide
  • ADRS: Proarrhythmic effect, especially torsades de pointes (fatal ventricular tachycardia) - seen with dofetilide
  • ADR of Amiodarone (Used most often, fairly common; needs frequent monitoring due to severe side effects) – pulmonary toxicity, thyroid problems, liver damage
54
Q

Drugs for arrhythmias: Inhibit calcium influx into myocardial cells altering excitability and conduction of cardiac tissues.
Most effective treating atrial dysfunction; ADRs = Bradycardia, Dizziness, Headache

A

Class IV: Calcium Channel Blocker
- Only the non-dihydropyridines (verapamil and diltiazem) are effective, the CCB’s ending in –pine do not have substantial effects on cardiac rhythm

55
Q

What are the non pharmacological treatment options of treating arrhythmias?

A
  1. Implantable devices (pacemakers, cardioverter defibrillators)
  2. Surgical interventions (electrode catheter ablation)