NR 508 Final Exam Study Guide
, NR 508 Final Exam Study Guide
Cardiovascular management:
1. Know Initial treatment choices for HTN
1st line options: ACE Inhibitors OR ARB, Calcium Channel Blocker, thiazides
Black people 1st line: CCB and/or thiazides preferred (better outcomes)
CKD (regardless of ethnicity): ACE Inhibitor OR ARB (but not together)
For someone with gout: thiazides increase uric acid (Do NOT use); CCBs and
Losartan (but not other ACEIs decrease the risk)
ALL other antihypertensives are 2nd line
Could consider BB if indicated for a comorbidity (eg arrhythmia, tremor, need
for migraine prophylaxis) but no longer considered 1 st line
2. Diuretics:
Loop diuretics; Thiazide-type diuretics; Potassium-Sparing Diuretics
The loop diuretics inhibit sodium reabsorption in the ascending loop of Henle. These
drugs are short-acting and cause a large natriuresis. The thiazide-type diuretics act on
the distal renal tubule to inhibit sodium reabsorption. Their effect is generally longer-
lasting, and they cause less brisk diuresis. Both classes increase potassium excretion.
The potassium-sparing diuretics include aldosterone antagonists and agents like
amiloride that inhibit excretion of potassium distally. These agents are weak diuretics,
often used in combination with thiazides to reduce potassium loss.
Diuretics may also be used as adjunct therapy for disease processes in which the
treatment itself may contribute to fluid retention—for example, use of some CCBs and
antiarrhythmics. Spironolactone blocks the mineral corticosteroid receptor that
aldosterone binds to; *Aldosteronism. It is also useful in ventricular remodeling and
decreasing the inflammatory cascade that can occur in the days following an MI.
Amiloride's potassium-sparing characteristics are used to counter any chronic
potassium losses that cannot be reliably corrected with diet or supplements.
Uses
Diuretics are first-line therapy in the treatment of HF & HTN through their reduction in
ECF volume. Ones most commonly used in primary care are the distal tubular (thiazides
and aldosterone antagonists) & loop diuretics.
, Side effects
All - hypokalemia, arrhythmia, metabolic alkalosis, fatigue, postural hypotension,
hyperlipidemia
K+-sparing - hyperkalemia, gynecomastia, peptic ulcer
Thiazides - hyperglycemia & hypercalcemia
Loop- hypocalcemia
Drug Interactions
All diruetics- a) digoxin (hypokalemia/toxicity risk); b) NSAIDs (reduce diuresis),
c) lithium (toxicity risk), d) corticosteroids (enhance hypokalemia), e) anti-diabetic
drugs (decrease anti-diabetic levels)
Thiazides & Beta blockers increase hyperglycemia/ hyperlipidemia
Loops & aminoglycosides cause ototoxicity & nephrotoxicity
Spironolactone – Aldactone
Furosemide-Lasix
Metolazone- Zaroxolyn
Hctz- Apo-Hydro; Aquazide; BPZide; Dichlotride; Esidrex; Hydrochlorot; Hydrodiuril;
HydroSaluric; Microzide; Oretic
Amiloride (Midamor)
Triamterene (Dyrenium)
3. Preferred diuretic with renal impairment
Loop diuretics are the best Tx for renal impairment generally (GFR <30); Amiloride
is contraindicated in diabetic neuropathy patients, pts c a BUN > 30 or a creatinine
>1.5mg. Metolazone is the only thiazide effective in stage 3 or 4 CKD. Potassium
sparing diuretics are absolutely contraindicated in patients with severe renal
impairment.
4. Post diuretic sodium retention
Loop diuretics cause a post-effect, a compensatory sodium-retention process that
begins as the diuretic action wanes.
The effect of loop diuretics dissipates rapidly, after which the kidneys immediately begin
to reabsorb sodium and nullify the diuretic effect. This process is called post-diuretic
sodium chloride retention. If sodium chloride intake is high and the half-life of the
diuretic is short (as with a loop diuretic), post-diuretic sodium chloride retention
compensates entirely for the sodium loss.7 Therefore, sodium restriction is important
when a patient is taking loop diuretics.
, NR 508 Final Exam Study Guide
Cardiovascular management:
1. Know Initial treatment choices for HTN
1st line options: ACE Inhibitors OR ARB, Calcium Channel Blocker, thiazides
Black people 1st line: CCB and/or thiazides preferred (better outcomes)
CKD (regardless of ethnicity): ACE Inhibitor OR ARB (but not together)
For someone with gout: thiazides increase uric acid (Do NOT use); CCBs and
Losartan (but not other ACEIs decrease the risk)
ALL other antihypertensives are 2nd line
Could consider BB if indicated for a comorbidity (eg arrhythmia, tremor, need
for migraine prophylaxis) but no longer considered 1 st line
2. Diuretics:
Loop diuretics; Thiazide-type diuretics; Potassium-Sparing Diuretics
The loop diuretics inhibit sodium reabsorption in the ascending loop of Henle. These
drugs are short-acting and cause a large natriuresis. The thiazide-type diuretics act on
the distal renal tubule to inhibit sodium reabsorption. Their effect is generally longer-
lasting, and they cause less brisk diuresis. Both classes increase potassium excretion.
The potassium-sparing diuretics include aldosterone antagonists and agents like
amiloride that inhibit excretion of potassium distally. These agents are weak diuretics,
often used in combination with thiazides to reduce potassium loss.
Diuretics may also be used as adjunct therapy for disease processes in which the
treatment itself may contribute to fluid retention—for example, use of some CCBs and
antiarrhythmics. Spironolactone blocks the mineral corticosteroid receptor that
aldosterone binds to; *Aldosteronism. It is also useful in ventricular remodeling and
decreasing the inflammatory cascade that can occur in the days following an MI.
Amiloride's potassium-sparing characteristics are used to counter any chronic
potassium losses that cannot be reliably corrected with diet or supplements.
Uses
Diuretics are first-line therapy in the treatment of HF & HTN through their reduction in
ECF volume. Ones most commonly used in primary care are the distal tubular (thiazides
and aldosterone antagonists) & loop diuretics.
, Side effects
All - hypokalemia, arrhythmia, metabolic alkalosis, fatigue, postural hypotension,
hyperlipidemia
K+-sparing - hyperkalemia, gynecomastia, peptic ulcer
Thiazides - hyperglycemia & hypercalcemia
Loop- hypocalcemia
Drug Interactions
All diruetics- a) digoxin (hypokalemia/toxicity risk); b) NSAIDs (reduce diuresis),
c) lithium (toxicity risk), d) corticosteroids (enhance hypokalemia), e) anti-diabetic
drugs (decrease anti-diabetic levels)
Thiazides & Beta blockers increase hyperglycemia/ hyperlipidemia
Loops & aminoglycosides cause ototoxicity & nephrotoxicity
Spironolactone – Aldactone
Furosemide-Lasix
Metolazone- Zaroxolyn
Hctz- Apo-Hydro; Aquazide; BPZide; Dichlotride; Esidrex; Hydrochlorot; Hydrodiuril;
HydroSaluric; Microzide; Oretic
Amiloride (Midamor)
Triamterene (Dyrenium)
3. Preferred diuretic with renal impairment
Loop diuretics are the best Tx for renal impairment generally (GFR <30); Amiloride
is contraindicated in diabetic neuropathy patients, pts c a BUN > 30 or a creatinine
>1.5mg. Metolazone is the only thiazide effective in stage 3 or 4 CKD. Potassium
sparing diuretics are absolutely contraindicated in patients with severe renal
impairment.
4. Post diuretic sodium retention
Loop diuretics cause a post-effect, a compensatory sodium-retention process that
begins as the diuretic action wanes.
The effect of loop diuretics dissipates rapidly, after which the kidneys immediately begin
to reabsorb sodium and nullify the diuretic effect. This process is called post-diuretic
sodium chloride retention. If sodium chloride intake is high and the half-life of the
diuretic is short (as with a loop diuretic), post-diuretic sodium chloride retention
compensates entirely for the sodium loss.7 Therefore, sodium restriction is important
when a patient is taking loop diuretics.
