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HLTH 2511 > Module C: 10-13 > Flashcards

Module C: 10-13 Flashcards

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1
Q

The majority (~95%) of hypertension is classified as _______ (primary / secondary) hypertension

A

Primary

this is hypertension that can not be attributed to a specific cause.

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2
Q

normal ranges for SBP are _______ for normal, _________ for prehypertension, _________ for stage 1 hypertension, and _________ for stage 2 hypertension

A

Normal: <120

Prehypertension: 120-139

Stage 1 HT: 140-159

Stage 2 HT: 160+

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3
Q

The diuretics that are most frequently used in the treatment of hypertension are:

A

Thiazide diuretics

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4
Q

The 5 common classes of diuretic and their site of action are:

A
  1. Thiazide and thiazide-related
    • NaCl Symporter in DCT
  2. Loop
    • NaK2Cl costransporter in thick ascending limb of loop of henle
  3. Potassium sparing
    • Aldosterone receptors or Na channels in CD
  4. Osmotic
    • Cause osmotic diuresis
  5. Carbonic anhydrase inhibitors
    • Carbonic anhydrase near PCT
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5
Q

Describe the effects of thiazide diuretics on electrolyte balance

A

Increased excretion of sodium, potassium, and magnesium. Retention of Calcium

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6
Q

The hypokalemia caused by thiazide and loop diuretics may cause a secondary ___________ (blood pH imbalance)

A

Hypokalemic metabolic alkalosis

body cells exchange H+ ions for potassium in an attempt to preserve serum potassium

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7
Q

Explain why thiazide diuretics may be used in treatment of nephrolithiasis

A

thiazides reduce calcium excretion and thereby reduce calcium concentration of the filtrate

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8
Q

Apo-Hydro (Hydrochlorothiazide)

A
  • thiazide diuretic
  • Acts on NaCl symporter in DCT, causing natriuresis, kaliuresis, and Calcium retention
  • First line diuretic for treatment of hypertension and edematous states.
  • Also used in treatment of nephrolithiasis, diabetes insipidus, and renal disorders
  • Common side effects: hypokalemia, hyperglycemia, hyperlipidemia, hyperuricemia
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9
Q

_______ diuretics are called “high-ceiling” diuretics because they produce a __________ (dose - dependent / flat) dose-response curve.

A

loop** diuretics are called “high-ceiling” diuretics because they produce a **dose-dependent dose-response curve.

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10
Q

Describe the effects of loop diuretics on electrolyte balance

A

Increased excretion of sodium, potassium, magnesium, and calcium

contrast this with the calcium-sparing effects of the thiazide diuretics

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11
Q

Common non-electrolyte side effects of thiazide diuretics include:

A

Hyperuricemia, hyperglycemia, and hyperlipidemia. May also cause a hypokalemic metabolic alkalosis

result of inhibition of uric acid secretion from the PCT and decreased insulin sensitivity

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12
Q

The preferred diuretics for treatment of edematous states (CHF, pulmonary edema, cirrhosis, nephrotic syndrome, etc.) are:

A

loop diuretics

especially due to their dose-dependent response across the therapeutic range

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13
Q

Lasix (Furosemide)

A
  • Loop diuretic
  • Inhibits the Na/K/2Cl cotransporter in thick ascending limb of loop of henle
  • high-ceiling dose-dependent diuretic
  • Preferred first line diuretic for edematous states
  • Adverse effects: hypokalemia, hypomagnesemia, hypocalcemia, hyperglycemia, hyperuricemia, ototoxicity
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14
Q

_______ is a diuretic that has an anti-androgenic effect and is therefore used in treatment of PCOS

A

spironolactone

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15
Q

The two classes of potassium-sparing diuretics are:

A

sodium-channel blockers and aldosterone receptor antagonists

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16
Q

Treatment of edematous states that causes hypokalemia may be supplemented with:

A

a potassium-sparing diuretic like spironolactone

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17
Q

Aldactone (Spironolactone)

A
  • Potassium-sparing diuretic, aldosterone receptor antagonist
  • inhibits binding of aldosterone in the late DCT and collecting duct, which prevents expression of sodium channels.
  • Used in combination with other diuretics to prevent hyperkalemia, in treatment of primary hyperaldosteronism, and in PCOS as an anti-androgenic
  • Adverse effects; gynecomastia and infertility in men, hyperkalemia.
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18
Q

Osmotic diuretics are primarily used to manage: (list 2)

A

glaucoma and cerebral edema

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19
Q

Mannitol

A
  • osmotic diuretic
  • increases filtrate osmolarity, drawing additional fluid into urine and causing diuresis
  • Used in treatment of cerebral edema, increased intraocular pressure (glaucoma), and to icrease urine volume
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20
Q

Diamox (Acetazolamide)

A
  • Carbonic anhydrase inhibitor, diuretic
  • Inhibits Carbonic anhydrase at the PCT, which causes increased bicarbonate excretion and a weak diuretic effect
  • may cause a secondary metabolic acidosis
  • used in treatment of glaucoma, acute mountain sickness, and epilepsy
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21
Q

Common non-electrolyte side effects of loop diuretics include:

A

Hyperuricemia, hyperglycemia, and ototoxicity

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22
Q

Name the preferred first-line class of diuretic for treatment of each of the following states:

  1. Edematous states (cirrhosis, CHF, etc.)
  2. Hypertension
  3. Hypokalemia
  4. Renal impairment
  5. Glaucoma
  6. Nephrolithiasis
  7. High altitude sickness
  8. Cerebral edema
A
  1. Edematous states (cirrhosis, CHF, etc.)
    • Loop diuretics
  2. Hypertension
    • Thiazides
  3. Hypokalemia
    • K+ - sparing
  4. Renal impairment
    • Loop
  5. Glaucoma
    • CAIs
  6. Nephrolithiasis
    • thiazides
  7. High altitude sickness
    • CAIs
  8. Cerebral edema
    • osmotic diuretics
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23
Q

Carbonic anhydrase inhibitors cause increased excretion of _________ and may therefore cause a matabolic ________

A

Carbonic anhydrase inhibitors cause increased excretion of bicarbonate** and may therefore cause a metabolic **acidosis

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24
Q

Suggest two ways in which thiazide diuretics provide a therapeutic effect in hypertension

A

in early treatment they lower BP through natriuretic diuresis. With prolonged treatment there is a decrease in sodium in arteriolar smooth muscle cells, causing vasodilation and decreased PVR

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25
Describe how potassium-sparing diuretics are used in the management of hypertension
Potassium-sparing diuretics are highly effective anti-hypertensives, but also have a relatively high rate of adverse events, so they are used in hypertension not already managed with 3 other drugs.
26
The four major classes of antihypertensive agents are:
1. Diuretics 2. Sympatholytics 3. Angiotensin inhibitors (ACEIs or ARBs) 4. Vasodilators (CCBs, minoxidil)
27
Blood Pressure = ______ X \_\_\_\_\_\_
Blood Pressure = **_C_****_ardiac Output (CO)_** X **_Systemic Vascular Resistance (SVR)_**
28
An advantage of using thiazides in the management of hypertension is they protect against \_\_\_\_\_\_\_
osteoporosis ## Footnote *thiazide diuretics reduce the rate of calcium excretion*
29
Loop diuretics are preferred for treating hypertension in individuals with _______ (normal / reduced) kidney function
reduced
30
α1 - blockers used in management of hypertension may cause "first dose" \_\_\_\_\_\_\_
syncope
31
**Minipress** (Prazosin)
* α1 - blocker, sympatholytic, anti-adrenergic * used to manage hypertension by decreasing SVR * Generally a second-line treatment, used in combination with a diuretic (diuretic required due to RAAS activation) * may cause **reflex sympathetic activation** (resulting in increased CO), **orthostatic hypotension**, or **"first dose" syncope**
32
**Aldomet** (Methyldopa)
* centrally-acting sympatholytic antihypertensive, selective α2 - agonist * inhibit sympathetic outflow from the CNS, causing vasodilation and some reduction in CO * too many side effects compared to other drugs, especially immunologic effects. Used only when other options are ineffective. Also used in **pregnancy**
33
**Inderal** (Propranolol)
* Non-selective β-antagonist (beta-blocker) * Primarily given orally but may be given parenterally * One of the first developed and thus has the ridest range of approved clinical uses * hypertenion, angina, cardiac dysrhythmias, migraine, AMI, pheochromocytoma * Has more CNS side effects than other non-selective beta-blockers
34
**Tenormin** (Atenolol)
* Selective β1-antagonist (beta-blocker) * oral or parenteral * good antihypertensive, antianginal, antiarrhythmic * Low rate of CNS side effects due to poor lipid solubility
35
**Brevibloc** (Esmolol)
* Selective β1-antagonist (beta-blocker) * IV-only! * good antihypertensive, antianginal, antiarrhythmic * very short half-life compared to other beta-blockers, used in emergent settings (check out that trade name!)
36
**Lopressor** (Metoprolol)
* Selective β1-antagonist (beta-blocker) * oral or parenteral * good antihypertensive, antianginal, antiarrhythmic * relatively short half-life (3-4hr)
37
Under what conditions are Beta-blockers (beta-antagonists) the preferred drugs in the management of hypertension
hypertension in the context of cardiovascular disease, otherwise CCBs or angiotensin inhibitors are preferred
38
Calcium channel blockers are better ________ (arteriole / venous) vasodilators
arteriole ## Footnote *they therefore decrease SVR without decreasing preload as much*
39
**Nipride** (Nitroprusside)
* Nitric Oxide donor, vasodilator, antihypertensive * Causes smooth muscle relaxation in arterioles and veins * short half-life and time of onset * Used in hypertensive emergencies * Prolonged use may lead to cyanide and thiocyanate toxicity
40
Suggest a treatment strategy for a patient with stage 1 hypertension (SBP 140-159)
* lifestyle modifications * Drug monotherapy (likely Angiotensin inhibitor or CCB due to low side-effect risk)
41
Suggest a treatment strategy for a patient with stage 2 hypertension (SBP \>160)
* lifestyle modifications * Drug therapy with at least 2 medications, often starting with CCBs and angiotensin inhibitors, perhaps adding a thiazide diuretic or beta-blocker * Trial new drug combinations for several weeks before switching treatment
42
Centrally-acting sympatholytics are rarely used to treat hypertension, but may be useful in: (list 2)
* hypertensive emergencies in an outpatient setting (one dose provides lasting effect) * **pregnancy** (methyldopa does not harm the fetus)
43
identify the differences between the various classifications of angina
* **Typical** angina involves narrowing of coronary artery lumens by atherosclerotic plaques and is seperated into **stable** and **unstable** * **Stable** angina occurs with exertion/sympathetic activation * **Unstable** angina occurs at rest and varies in intensity, frequency, and duration. Caused by thrombotic occlusion and may lead to MI * **Variant/Prinzmetal** angina is due to coronary artery spasm and is prolonged and cyclic
44
The cause of angina is \_\_\_\_\_\_\_\_
myocardial hypoxia
45
Drugs to treat angina generally work by: (list 2)
* decreasing myocardial oxygen demand * increasing myocardial oxygen supply
46
Use the provided chart to organize the antianginal drugs
47
Use the provided chart to organize the antihypertensive drugs
48
Organic nitrites and nitrates are useful in which forms of angina?
All forms of angina
49
CCBs are useful in which forms of angina?
Stable typical angina and variant angina. CCBs are not useful in MI or unstable angina
50
β - blockers are useful in which forms of angina?
all forms of typical angina, especially in MI. Not useful in atypical/prinzmetal angina
51
**Nitrostat** (Nitroglycerin)
* Nitrate antianginal * Increases NO concentrations near vascular smooth muscle, which leads to increased cGMP production and **venous** vasodilation. * Causes a decrease in preload and myocardial oxygen demand. In higher doses has arteriolar effects, resulting in decreased afterload * May cause drop in SBP and reflex tachycardia
52
Explain how nitrates reduce myocardial workload and oxygen demand
nitrates primarily cause venous vasodilation which reduces preload and myocardial wall tension
53
A danger of prolonged administration of nitrates is \_\_\_\_\_\_\_\_\_
development of tolerance
54
nitrates are primarily ________ (arteriolar / venous) vasodilators
venous
55
which CCBs have the greatest vasodilatory effect relative to cardiac effect?
the dihydropyridine (those that end in -pine) CCBs. For example; amlodipine, felodipine, nifedipine
56
How do CCBs help relieve angina?
* All CCBs cause smooth muscle relaxation and therefor **increase coronary blood flow**, and also may decrease cardiac workload. * Diltiazem and verapamil also have a higher affinity for cardiac calcium channels and are **negative inotropes and chronotropes**, so they must be used with cuation in heart failure
57
Which CCBs must be used with caution in heart failure and why?
Diltiazem and especially Verapamil, due to their negative inotropic and chronotropic effects.
58
**Adalat** (Nifedipine)
* Calcium channel blocker (CCB), antianginal, antihypertensive * dihydropyridine CCB, therefore has primarily vasodilatory effects * may cause reflex tachycardia * As an antianginal, increases coronary perfusion and reduces afterload * Short half-life, but may be given as a sustained-release formulation once daily
59
**Isoptin** (Verapamil)
* Calcium-channel blocker, antianginal, antiarrhythmic * Has the strongest cardiac effect of the CCBs * Useful in stable and variant angina * Must be used with caution in **heart failure** due to its negative inotropic and chronotropic effect
60
**Cardiazem** (Diltiazem)
* Calcium-channel blocker, antianginal, antiarrhythmic * Has an intermediate cardiac effect (more than nifedipine, less than verapamil) * Useful in stable and variant angina * Must be used with caution in heart failure due to its negative inotropic and chronotropic effect
61
CCBs act on _________ (arterial / venous / both) smooth muscle
**arterial only!!**
62
How do CCBs provide an antianginal effect? (list 3 ways)
* they increase coronary blood flow (arteriolar vasodilation) * they decrease afterload (arteriolar vasodilation), thereby reducing cardiac wall tension and oxygen demand * The non-dihydropyridines (diltiazem, verapamil) have negative chronotropic and inotropic effects which reduce workload
63
How do β1-blockers provide their anti-anginal effect?
They reduce cardiac ischemia by preventing exercise-induced tachycardia and may prevent reflex tachycardia caused by other antianginals (esp. nitrates and dihydropridine CCBs)
64
Why should β1-blockers be used in caution in patients with heart failure? What drugs might potentiate this effect?
because they are negative inotropes. This could be potentiated by verapamil, and to a lesser degree, diltiazem.
65
The hallmark of heart failure is \_\_\_\_\_\_\_\_\_
reduced stroke volume and cardiac output
66
List common changes that occur as a result of cardiac/ventricular remodelling
* Wall thickening (hypertrophic) or thinning (dilated) * Cardiac narrowing (hypertrophic) or dilatation (dilated) * Interstitial fibrosis * Cardiac wall stiffening
67
Describe how neuroendocrine responses can exacerbate heart failure
* SNS activation, RAAS, Inflammatory cytokines attempt to restore CO by Frank-Starling mechanism * Leads to an increase in cardiac remodelling (incr. wall stiffness, fibrosis, hypertrophy/thinning, dilation/narrowing) * RAAS activation leads to incr. PVR and blood volume, incr. workload on myocardium
68
β1-blockers ________ (do / do not) improve mortality in unstable angina
DO
69
Goals of treatment in heart failure are:
1. improve symptoms 2. slow or reverse deterioration 3. prolong survival / reduce mortality
70
The 3 major strategies to treat heart failure, and the classes of drugs used in each are:
1. Increase cardiac output * positive inotropes * vasodilators 2. Reduce pulmonary and systemic congestion * vasodilators * diuretics 3. Slow or reverse cardiac remodelling * angiotensin inhibitors * sympatholytics
71
The three classes of inotrope used in the management of HF are:
1. cardiac glycosides 2. adrenergic agonists 3. PDE3 inhibitors
72
Describe the MOA and role of digoxin in the management of HF
* Digoxin inhibits the action of the Na/K pump, increasing intracellular sodium, which activates the sodium-calcium exchanger. This increases intracellular calcium. Also inihibits sympathetic activity * Decreases AV nodal conduction, positive **inotrope** * Generally used to treat heart failure associated with A Fib
73
Digoxin has a _______ (low / high) therapeutic index
LOW! ## Footnote *adverse effects include arrhythmias, GI disorders, hallucinations, seizures. Antidote is **digoxin-immune Fab.***
74
**Lanoxin** (Digoxin)
* Cardiac Glycoside, antiarrhythmic * used in treatment of A Fib and HF * inhbits Na/K pump and increases intracellular Ca through Ca/Na exchanger * negative **chronotrope** and positive **inotrope** * LOW therapeutic index
75
What is the advantage of using **dobutamine** in treating HF vs. other adrenergic agonists
it improves SV with little to no increase in HR
76
Adrenergics and PDE3 inhibitors are used in __________ (acute / chronic) heart failure
Acute! ## Footnote *these drugs may cause angina, increased myocardial workload, tolerance, and other adverse effects.*
77
**Primacor** (Milrinone)
* type 3 phosphodiesterase inhibitor (PDI), positive inotrope * increases cAMP and therefore Ca2+ concentration in cardiomyocytes * used in acute heart failure **when other inotropes are ineffective**.
78
Describe the roles of Angiotensin inhibitors (ACEIs and ARBs) in the management of heart failure
they reduce both preload (reduces congestion) and afterload (improves SV) while slowing cardiac remodelling. ARBs are generally less effective in HF than ACE inhibitors
79
Common drug types used in the management of acute heart failure are:
* IV vasodilators (nitrates/hydralazine) * Diuretics * Inotropic agents, esp. Dobutamine and Milrinone * Oxygen
80
Common management of **chronic systolic heart failure** generally includes 3 classes of drugs:
A diuretic (loop), an angiotensin inhibitor, and a β - Blocker. Aldosterone antagonists may be added as needed
81
Use the table provided to organize drugs commonly used in managing heart failure
82
Which Beta-blockers have been shown to reduce mortality in heart failure?
carvedilol, metoprolol, bisoprolol
83
Describe the MOA of nitric oxide donors in management of angina and hypertension
NO donors increase local concentrations of NO, which triggers increased intracellular cGMP production. cGMP causes decreased intracellular Ca2+ concentration which brings about smooth muscle relaxation and vasodilation
84
What determines the level of Ca2+ in cells? How does this differ between different cell types?
* cAMP concentration determines Ca2+ level * In cardiomyocytes and pacemaker cells, cAMP levels correlate positively with Ca2+ concentration. The opposite is true in smooth muscle cells explaining how the same types of receptor (Gs GPCRs) can have opposite effects in different cells when stimulated. * Ex: both beta-1 and beta-2 receptors are Gs GPCRs but have opposite effects on calcium levels when stimulated
85
Describe the locations and functions of V1 and V2 receptors for ADH
* V1 receptors are found in vascular smooth muscle. Activation causes vasoconstriction * V2 receptors are found in the basolateral membrane of the kidney tubules. Stimulation leads to aquaporin insertion and increased water retention * The result of V1 and V2 activation is increased circulating volume and vasoconstriction leading to increased BP
86
Which class of diuretics are referred to as "low-ceiling" diuretics?
thiazides
87
Why are beta1-blockers better at reducing BP than alpha1-blockers?
Because alpha1 blockers cause reflex tachycardia, leading to increased CO and BP. Beta1-blockers inhibit reflex tachycardia directly, while alpha1-blockers have no direct cardiac effect.

HLTH 2511 (11 decks)

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