AntiHTN Flashcards by Tatiana ose

What are the main reasons that Diuretics are used:

to decrease HTN (lowers bld pressure), decreases edema (peripherally and pulmonary) in pts w/HF or renal/liver disorders.

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Elevated blood pressure is defined as:

HTN

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How do diuretics increase urine flow:

Diuresis occurs by the inhibition of Na and H2O reabsorption from the kidney tubules.

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What drugs are considered to be the first-line meds for HTN:

diuretics (can be used alone or in combination w/other antiHTN)

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Where does the reabsorption of Na and H2o occur throughout the renal tubular segments:

Na and H2o reabsorption typically occurs in the proximal tubule, Loop of Henle (both descending and ascending loops), and collecting tubules.

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What diuretics act on the proximal tubule:

Osmotics (mannitol), mercurial, and carbonic anhydrase inhibitor diuretics act on the proximal tubule

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What diuretics act on the loop of Henle:

High-ceiling (loop) diuretics act on the loop of Henle

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What diuretics act on the distal convoluted tubule:

thiazide diuretics act on the distal tubule

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What diuretics act on the collecting tubules:

k-sparing diuretics act on the collecting tubules

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Every 1.5 hrs, the glomeruli filters out what from the ECF (extra cellular fluid)-process for beginning process of urine formation:

electrolytes, Na, H20, drugs, glucose, waste products from protein metabolism are filtered through the glomeruli

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Where of the renal tubules can diuretics have the greatest effect (where the effects of diuretics are the fastest) in causing natriuresis (loss of Na in urine):

Greatest diuretic effect in natriuresis occurs at the tubules closest to the glomeruli: proximal tubule

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Why do diuretics have an anti-HTN effect:

There’s an anti-HTN effect when taking diuretics due to the blocking of Na and Cl reabsorption (thus promoting Na and water loss thru urine). This blockage decreases fluid volume=lower BP; decrease in fluid volume=decrease in edema

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What are the most commonly used diuretics effective i the removal water and sodium:

thiazides (or thiazides-like diuretic), high-ceiling (loop), osmotic (mannitol), k-sparing, carbonic anhydrase inhibitors are all the diuretics commonly used for HTN (minus the last diuretic)

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This type of diuretic should not be used on pts w/renal insufficiency or DM, can be combined with ace-inhibitors and beta-blockers; acts on the distal convoluted tubule to promote Na, Cl, K, H2O excretion

HydrochloroTHIAZIDE or HydroDiuril

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What are some common effects of thiazides:

hyperglycemia, hypercalcemia, hypokalemia (potentiates digoxin), hyperuricemia, and hyponatremia, (should be given in the morning to avoid nocturia

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What can the herbs: aloe, ginko, and licorice cause when taking diuretics:

aloe and licorice can cause hypokalemia and ginko can increase BP

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This type of diuretic id considered extremely potent in the cause of rapid diuresis and rapid decrease in BP; its effects are dose dependent; should not be Rx if some other diuretic could alleviate bofy fluid excess; not an effective HTN med; used primarily on end-stage renal pts; acts on the ascending loop of Henle by inhibiting Cl transport of Na into the circulation

Furosemide (Lasix) and Bumetanide (Bumex-more potent then Lasix)

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This “potassium wasting diuretic will cause hypokalemia (muscle weakness, abd distension, leg cramps, cardiac dysrhythmias), orthostatic hypotension, digoxin toxicity, should not be combined with another loop diuretic but can be combined with thiazide:

Furosemide (Lasix) and Bumetanide (Bumex)

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Why is Furosemide (Lasix) and Bumetanide (Bumex), both of which are Loop or high-ceiling dieretics, considered to be potent in the cause of rapi diuresis and rapid decrease in BP:

Loop diuretics have a great saluretic (Na-Cl-losing) or natriuretic (Na-losing) effect that causes rapid diuresis, which decreases CO and BP

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This diuretic increases the concentration and Na reabsorption in the proximal tubule and the loop of Henle by pulling fluid from the interstitial tissue spaces into vascular; used in emergency cases such as ICP (intracranial pressure) and IOP (intraocular pressure), to prevent kidney failure, and used often in cancer therapy; diuresis occurs w/in 1-3 hrs after IV

Mannitol osmotic (and Urea) diuretic

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Mannitol should not be given to pts w/HF or renal failure. Some s/s of mannitol are:

Fluid and electrolyte imbalances (due to rapid fluid shifts), tachycardia, and pulmonary edema

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What diuretic is usually given to pts tin the prevention of AKI, oliguria (low output of urine), IOP in glaucoma, and ICP:

Mannitol (osmotic diuretics) or Urea

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What diuretic is typically used on pts with chronic (open-angle) glaucoma, management of epilepsy, pts w/metabolic alkalosis, and may cause metabolic acidosis w/prolonged use:

Carbonic anhydrase inhibitors

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How do carbonic anhydrase inhibitors work:

This diuretic blocks the action of the carbonic anhydrase enzyme (needed to maintain H+ and bicarbonate ion-acid base balance-balance) to increase Na,K, and bicarbonate secretion

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What diuretic is primarily Rx for pts w/chronic cardiac problems, blocks the action of aldosterone in the sodium-potassium pump, it's main side effect is hyperkalemia if taken w/and ACE or angiotensin II bc of increased K levels, acts primarily on the collecting duct of the renal tubules:

Spironolactone (Aldactone) potassium-sparing diuretics (can be use with a HCTZ or loop-potassium wasting diuretics-to enhance diuretic effect and prevents K-loss)

What are the S/S of hyperkalemia that can be caused when taking ACE inhibitors (or angiotensin II) along with Spironolactone (Aldactone):

tachycardia which could lead to bradycardia, EKG irregularities, numbness/tingling of hands and feet, N/V and abd cramps

Thiazides (hydrochlorothiazide or HydroDiuril ) is commonly combined w/what types of drugs:

Spironolactone (aldactone) potassium-sparing diuretic, BBs, ACE inhibitors, and Angiotensin II antagonists

A pt is taking hydrochlorothiazide 50 mg a day along w/digoxin 0.25 mg a day. What type of electrolyte imbalance would you expect to occur: A: hypocalcemia, B: hypokalemia, C: hyperkalemia, D: hypermagnesemia

B: digoxin and thiazides taken together can cause hypokalemia (same with loop diuretics and digoxin)

The nsg is teaching a pt who's has DM and is taking hydrochlorothiazide 50 mg/day. The teaching should include the importance of monitoring which levels: A: Hgb &HCT, B: BUN, C: arterial blood gases, D: Serum glucose

C: thiazides (hydrochlorothiazide or HydroDiuril) increase glucose levels

A pt has HF and is Rx Lasix. The nurse is aware that Lasix (furosemide) is what kind of drug: A: Thiazide diuretic, B: Osmotic diuretic, C: High-ceiling diuretic (loop), D: K-sparing diuretic

C: High-ceiling (loop) diuretic

The nurse acknowledges that which condition can occur when taking a loop diuretic such as furosemide: A: hypokalemia, B: Hyperkalemia, C: hypoglycemia, D: hypermagnesemia

A: hypokalemia

For a pt taking a diuretic, a combination such as hydrochlorothiazide is taken with a Spironolactone may be Rx. The nurse realizes that this combination is ordered for which purpose: A: decrease potassium level, B: increase potassium level, C: decrease glucose level, D: increase glucose level

A: to decrease potassium levels

The pt is taking spironolactone for HF. The nurse should closely monitor the pt for which condition: A: hypokalemia, B: hyperkalemia, C: hypoglycemia, D: hypermagnesemia

B: aldactone is a potassium sparing diuretic

The increase in BP such as >140/90 is defined as:

HTN

The most common type of HTN that affects 90% of people with high BP is defined as:

essential HTN

Risk factors for essentil HTN are:

family h/o HTN, hyperlipidemia, African american, DM, obesity, stress, old age

HTN that's r/t renal and endocrine disorders are defined as:

secondary HTN (in 10% of HTN pts)

What are the three BP regulators of the body:

Renin-angiotensin-aldosterone system (regulated via kidneys), baroreceptors in the aorta/carotid sinus and vasomotor center in the medulla, and the ADH (antidiuretic hormone) regulates BP

Explain how the renin-angiotensin-aldosterone regulates BP:

When BP decreases, Renin is released from the kidneys--> renin stimulates production of angiotensin II (potent vasoconstrictor) from angiotensin I--> peripheral vasoconstriction occurs and Aldosterone hormone is released to promote Na retention-->BP becomes stabilized as Na/H2O is retained causing fluid volume increase-->increased BP

Explain how ADH affects BP

Antidiuretic hormone is produced by the hypothalamus ans it's stored/released by the pituitary gland. The ADH hormone stimulates the kidneys to conserve or excrete water thus affecting BP

How does a diet high in carbs and fats, alcohol intake, obesity all affect HTN:

Diets high in fat and carbs affect the sympathetic nervous system (releases norepinephrine=vasoconstriction), alcohol increases renin activity=production of angiotensin II, obesity affects sympathetic and cardiovascular systems=increasing CO/stroke volume/L ventricular filling,

What are some non-pharmacologic controls of HTN:

Stress reduction, exercise, diet, weight reduction, lifestyle modifications can manage HTN

What are some stress reductions techniques for HTN management:

Laughter, meditation, relaxation, yoga

What are some diet restrictions in the management of HTN:

Salt restriction (2gm Na diet), decrease in fat/caloric intake, and increase in fiber

What are some excercise and weight reduction recommendations in HTN management:

exercise increases high-density lipoprotein, Reduce weight, walking/bicycling, aerobic, resistance training

What are some Lifestyle modifications in the management of HTN:

smoking cessation, decrease amount in EtOH consumption of about 1 drink/day, red wine and grape juice have polyphenolic compounds that have an antioxidant effect=relaxes bld vessels

What's the BP of stage-2 HTN

>160/100

What are the six classifications of anti-HTN:

Diuretics, sympatholytics, diuretic-acting arteriolar vasodilators, ACEI (ace inhibitors), ARBs (angiotensin II receptor blockers), CCB (calcium blocker channels)

Which ethnicity is most likely to develop HTN and the effect of what anti-HTN are less effective for that ethnicity group:

African american (some Native Americans); BB and ACE inhibitors

What anti-HTN drugs are most effective to the ethnicity group that has a higher incidence to HTN and mortalities r/t HTN:

alpha 1 blockers, and CCB

What ethnicity is sensitive to BBs and other anti-HTN and may need to have the dosage reduced:

Asians

What is a serious side effect of the use of anti-HTNs in older adults and what should use instead to prevent HTN:

orthostatic hypotension; lifestyle modifications should be done: 2 g sodium reduction diet, avoiding tobacco, exercise

When is anti-HTN drugs ordered when nonpharmocological control of HTN are not effective:

When the SBP is greater than 140mmHg.

With pts >50 yo, which BP (SBP or DBP) is of more concern:

SBP with a 20mmHg above goal should be intervened w/meds

Drugs that are first RX for HTN pts are defined as;

initial agents

What first line of drugs in the Tx of HTN promote Na depletion which decreases ECFV thus decreasing HTN:

diuretics; HCTZ are most commonly given

Which of these diuretics (hydrochlorothiazide or furosemide is best used in pts w/renal failure:

Thiazides depresses renal blood flow. High-ceiling are commonly recommended

If HTN is the direct result of renin-angiotensin-aldosterone system, will diuretics be Rx:

No, diuretics are not prescribed in this case as they tend to elevate the serum renin level.

What are thiazides commonly combined with in the Tx of HTN:

potassium-sparing diuretic (keeps K from being lost); BBs; ACEI (ACE inhibitors tend to increase K levels, K loss in minimal); ARBs

What are the four most commonly used sympatholytics:

1:beta-adrenergic blockers (BAB), 2:centrally acting alpha 2-agonists, 3:alpha-adrenergic blockers; 4: alpha 1 & beta 2 adrenergic blockers (5: there's a fifth in the book=adrenergic neuron blockers)

Which sympatholytic reduce CO by decreasing SNS response & vascular resistance (via continuous use) through the actions of reducing HR/contractility/renin release to lower BP:

(BBs) beta-adrenergic blockers (commonly used w/a diuretic)

Why shouldn't BBs be abruptly stopped:

Rebound HTN, angina, dysrhythmias, & MI can occur (important teaching point)

What are the two types of BBs and what is their common suffix:

Nonselective/noncardioselective BBs and cardioselective BBs; "lols" is the suffix

Which BB inhibits both beta 1 (describe effect on b1) and beta 2 (describe effect it has on B2); inhibits liver's ability to convert glycogen to glucose in hypoglycemia, and should NOT be used on pts w/COPD:

nonselective/noncardioselective (e.g. propranolol); beta 1=decrease in BP as HR slows; beta 2=bronchoconstriction occurs (unopposed parasympathetic tone-which is why cardioselective BBs are preferred)

Which BBs are selected to act mainly on the beta 1 (how is beta 1 effected); and what are the two most commonly used names:

cardioselective BBs acts by blocking beta1 to slow HR, thus decreasing BP; two most common are: atenolol and Lopressor (metoproloL)

When would you hold a BBs from a pt and what are some common side effects of BBs:

Hold on pts if HR <60/min or if they have on pulmonary disease; side effects include bradycardia, markedly decreased BP, impotence, brochospasm

Which of the sympatholytics are used to decrease sympathetic response from the brainstem which decreases epi/norepi/renin release=decreased peripheral vascular resistance due to vasodilation:

Centrally acting alpha2-agonists (CAAA)

What are the two most common CAAAs are used for HTN but may cause edema due to Na/H2O retention (usually prescribed w/a diuretic), bradycardia, drowsiness, and rebound HTN and how are they usually given:

Methyldopa (aldomet) and Clonidine (catapress); transdermal patches

Which of the sympatholytics are commonly used for HTN by blocking the alpha-adrenergic receptor resulting in vasodilation=decreased BP; helps to maintain renal bld flow (treats BPH or benign prostatic renal hypertrophy); does not effect DM or asthmatic pts; used to tx pts w/LIPID ABNORMALITIES (Increases HDL good fats):

Alpha-adrenergic blockers (ABs-alpha blockers)

What are the two most common Abs; why are they both commonly combined with diuretics; what are the main side effects:

Alpha blockers ("osins") Prazosin (minipress) and tamsulosin (flomax); used to vasodilate and decreased BP in Benign Prostatic Hypertrophy and increases HDLs (MINI-mizes prostate and increase urine FLOw)

Which of the 6 anti-HTNs is used as a last resort, only for severe chronic HTN; blocks the norepinephrine to decrease CO=decreasedPVR=decreased BP; causes SEVERE orthostatic hypotension, suicidal ideation, vivid nightmares; and bc of orthostatic hypotension is a drug that's RARELY used:

Adrenergic Neuron blockers

What is the name of the adrenergic neuron blocker (what does it block) that is RARELY used and why is it RARELY used:

Reserpine (serpasil) blocks the release of norepinephrine which decreases CO=decreased PVR=decreased BP, but causes severe orthostatic hypotension and suicidal ideation/vivid nightmares

Which of the sympatholytics is commonly used for HTN that blocks both alpha 1 (what effect occurs w/alpha 1) and beta 1 (what effect occurs w/beta1); has a bigger impact with ALPHA 1 than beta 1; and what are the two most common meds called:

Alpha1 and Beta 1 adrenergic blockers (ABBs) block alpha 1 to decrease PVR=vasodilation and blocks beta 1 by decreasing contractility=MODERATE decreased HR=MODERATE decreased BP; two most common ABBs are Labetalol and Cartrol

What are the side effects of ABBs and why should pts w/asthma AVOID taking LARGE DOSES of Labetalol (Normodyne) and Cartrol:

ABBs can cause orthostatic hypotension, AV block (in lrg doses); asthma pts shouldn't take Labetalol or Cartrol in large dosages bc dual blockage of A1 and B1 can block B2 receptors (in large doses) causing airway resistance.

Which of the SNS depressor Anti-HTN causes increased airway resistance and shouldn't be taken by pt's w/asthma:

Alpha 1 and beta 1 blockers: labetatol and cartrol

Which of the 6 anti-HTNs are potent HTN meds d/t marked vasodilation caused by the relaxation of sm muscles of bld vessels and are usually used in HTN emergencies or severe HTN:

(ICU) Direct-Acting Arteriolar vasodilators: nipride and apresoline are used in emergencies; are potent vasodilators=decreased BP, NA/H2O retention=peripheral edema

What are some major side effects of nipride and aprelosine:

tacycardia, palpations, edema, confusion, HYPOTENSION=titrate slowly

Which of the 6 anti-HTN block the formation of angiotensin II (vasoconstrictor) and block Aldosterone which has a direct effect of decreasing PVR:

(prils) ACE inhibitors

What are some common side effects of ACE inhibitors:

COUGH, tachycardia, HYPERKALEMIA (when taking spironolactone), FIRST DOSE HYPOTENSION, n/v/d/

Which of the 6 anti-HTNs block the vasoconstrictor effects of angiotensin II to prevent the release of aldosterone for the net effect of vasodilation & decreased PVR:

Angiotensin II blockers ("tans")

What are the common side effects of angiotensin II blockers:

NO COUGH, dizziness, insomnia

What is a commonly combined with angiotensin II blocker:

Losartan + HCTZ = Hyzaar

Which of the 6 anti-HTN decreases Ca levels in the vascular sm muscle for the net effect of vasodilation and decrease in BP; immediate release form can cause sudden cardiac effect which is why a sustained release is preferred; used most commonly on african american pts:

Calcium Channel blockers ("pines")

What are some common side effects of calcium channel blockers:

ankle edema, AV block, flush, HA, bradycardia, reflux tachycardia

A pt's BP is 145/90. According to the guidelines for determining HTN, the nurse realizes that the pt's BP is at what stage:

Stage 1 HTN

The nurse acknowledges that the first-line of drugs for tx of pt/s BP might be which drug: A) diuretic, B)alpha blocke, C) ACE inhibitor, D) alpha/beta blocker:

A: diuretics

The nurse is aware that which group of anti-HTNs drugs are less effective in african-American pts: A) Diuretics, B) CA channel blockers, C) beta blockers and Ace, D) Alpha blockers:

C: ACE and beta blockers

The nurse knows that which diuretic is most frequently combined w/an anti-HTN drug: A) chlorathalidone, B) HCTZ, C) bendroflumethaized, D) K-sparing diuretic

B: HCTZ

The nurse explains that which beta blocker category is preferred for treating HTN: A) B1 blocker, B) B2 blocker, C) B1/B2 blocker, D) B2/B3 blockers

A: B1 blockers

Catopril has been ordered for a pt. The nurse teaches the pt that ACE inhibitors have which common side effects: A) N/V, B) Dizziness and HA, C) upset stomach, D) constant irritating cough

D: constant cough

A pt is prescribed losartan. The nurse teaches the pt that an angiotensin II acts by doing what: A) inhibiting angiotensin converting enzyme, B) blocking angiotensin II from AT receptors, C) prevents release of angiotensin 1, D) promotes the release of aldosterone:

B: blocks angiotensin II from A1 receptors

The pt states that he takes amlodipine (norvasc). The nurse wishes to determine if the pt has any common side effects of a Ca channel blocker. The nurse asks the pt if he has what symptoms. Select all that apply: A) insomnia, B) Dizziness, C) HA, D) angioedema, E) ankle edema, F) hacking cough

B, C, E: dizziness, HA, ankle edema

What is the purpose of combining Anti-HTN drugs:

To obtain increased BP control, to enhance compliance, and to minimize the side effects

Which one of these electrolyte imbalances can cause cardiac arrhythmia and sudden death. Hypokalemia or hyperkalemia:

hyperkalemia

When would you report urin output:

<600 mL/day