PHARMACOLOGY FINAL EXAM STUDY GUIDE AND PRACTICE QUESTIONS | LATEST VERSION 2021, Assignments of Pharmacology

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JNC-8 (2014)

AHA/ACC

Guidelines (2017) Definitions Normal: <120/< Pre-hypertension: 120-139/80-89Stage 1: 140-159/90- Normal: <120/ Elevated: SBP 120- 129 Stage 1: 130- 139/80-

60 yo: >150/ Thresholds for initiating treatment <60 yo or comorbid conditions (DM, CKD): >140/ 130 SBP or > DBP if history ofCVD or 10% ASCVD risk. 140/90 if no clinical CVD and <10% ASCVD risk Treatment goals <140/90 if <60 yo or comorbid conditions (DM, CKD); (Grade E recommendation) <130/ <150/90 if >60 yo (Grade A recommendation)

PHARMACOLOGY FINAL EXAM STUDY GUIDE AND PRACTICE QUESTIONS |

LATEST VERSION 2021

Thiazide diuretics include:

• HCTZ (hydrocholorothiazide) 12. to 25 mg PO daily
• Hygroton (chlorthalidone) 12.5 to 25mg PO daily
• Lozol (indapamide) PO daily preferred agent for treating stage 1 hypertension, and the preferred initial therapy for treating African Americans with hypertension. All diuretics decrease blood volume, venous pressure, and preload. More specifically, thiazide diuretics block the sodium- chloride channel in the kidney, decreasing the cross of sodium over the luminal membrane, which in turn decreases the action of the sodium-potassium pump and sodium and water passage to the renal interstitium. These changes increase urinary output and require the monitoring of potassium and other electrolytes to prevent adverse effects. All thiazides contain sulfa compounds; therefore, these medications should be avoided in patients allergic to sulfa. Thiazide diuretics are also used to manage osteopenia or osteoporosis, as they slow calcium loss in bones. SE: Hyper o (^) Hyperglycemia (evidence unclear about interactions o (^) Hyperuricemia (can precipitate gout) o (^) May cause hyperlipidemia

Hypo o (^) Hypokalemia (potentiates digoxin toxicity and increases risk of arrhythmias) o (^) Hyponatremia (hold diuretic, restrict water intake, replace K+ loss) o (^) Hypomagnesemia Contraindications: Allergy to SULFA or thiazide Angiotensin-converting-enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) Action: Block conversion of angiotensin I to II o (^) Results in vasoconstriction o Drug of choice for DM and/or CKD due to renal protection Pregnancy: Category C and D o (^) Category C during first trimester o (^) Category D during second and third trimester o Cause fetal kidney malformations and fetal hypotension Side Effects: Dry cough (up to 10% with ACEI; less with ARBs) o (^) Hyperkalemia risk

o Angioedema is rate bue can be life threatening Contraindications: Moderate to severe kidney disease; monitor GFR o (^) Renal artery stenosis o (^) Acute renal failure is precipitated if given ACEI or ARB o (^) Additive effect of hyperkalemia Calcium channel blockers (CCBs) are also used to treat hypertension Action: Create vasodilation by blocking voltage-gated calcium channels in both cardiac smooth muscles as well as in blood vessels. o (^) CCBs have both an inotropic and chronotropic effect, meaning the heart gets both depressed and slowed down. Side Effects: Mainly due to vasodilation o (^) Headaches o (^) Ankle edema o (^) Heart block or bradycardia (due to depressed muscle and AV node) o Reflect tachycardia Contraindications: Due to the inotropic and chronotropic effects o (^) 2nd and 3rd degree heart block

o (^) Bradycardia o Congestive heart failure Examples: "pine" ending o (^) nifedipine (Procardia XL) o (^) amlodipine (Norvasc) o (^) felodipine (Plendil)

• avoid with African-Americans ORDER in which HTN meds are preferred for Rx Thiazide Diruetics ACE-Inhibitors

Angiotensin-II Receptor Antagonists

• preferred for African-Americans Calcium Channel Blockers

Beta blockers

HTN Treatment Plan ACEI or ARB as first line, plus beta blockers, diuretics, and others as needed DM Treatment Plan ACEI or ARB as first line; if African American, start with CCB or thiazide diuretic CKD Treatment Plan ACEI or ARB as first line; can add CCB or thiazide diuretic Pregnancy Treatment Plan Labetolol Anda presents to the clinic for monitoring. She has been diagnosed with heartfailure and has been taking an angiotensin-converting enzyme inhibitor (ACEI), thiazide diuretic, and beta blocker for several months. Which of the following diagnostic tests are required to ensure Anda is not developing any

adverse effects from her medication regimen? serum electrolyte levels C o r r e c t a n s w e r. LaMar reports a family history of hypertension and cardiovascular disease but has no other risk factors. Current blood pressure is 126/82 mm Hg; normal weight and body mass index for height and age are noted. Which of the following treatment plans is the primary focus for educating LaMar about his cardiovascular health?

• the DASH diet, sodium restriction, and exercise C o r r e c t a n s w e r. Anda is taking a thiazide diuretic and may develop hypokalemia, which increases the risk for dysrhythmias. Therefore, serum electrolyte levels are required to ensure she is not developing any adverse effects from her medication regimen. At this time, a CBC is not recommended. Anda is taking the medications recommended for patients with StageC heart failure. Although her quality of life and ability to participate in activities should bemonitored, routine measurement of the ejection fraction and maximal exercise capacity is not warranted at this time. LaMar patient has elevated hypertension without other risk factors; therefore,lifestyle changes are indicated rather than pharmaceutical agents.

Dislipidemia pressure rises to hypertensive levels, other measures, including drug therapy, may be initiated. Calcium and potassium supplements are not indicated at thistime for LaMar. Lifestyle Changes

• (^) weight loss
• (^) exercise
• (^) improved diet
• (^) smoking cessation DASH Diet
• low sodium, low saturated fat Increase Dietary Soluble Fiber
• (^) lowers LDL by blocking absorption in the GI tract LDL is first priority to lower unless triglycerides are >

• 500 triglycerides= risk for pancreatitis Low HDL alone is a risk factor for heart disease.

*simvastatin and lovastatin should not be taken with grapefruit juice or macrolides. NONstatin meds

Heart Failure

Loop Diuretics

Diuretic therapy, particularly loop diuretics, are the mainstay of treatment for heart

failure; management targets relieving the acute symptom of congestion.

o Mechanism of Actions

o volume management by inhibiting the absorption of sodium-

chloride in proximal/distal tubules, and the thick ascending

loopof Henle. Loop diuretics are not permeated through the

glomerulus but undergo active transport into the tubular

lumen by way of the organic acid route (Chisholm-Burns et al.,

2019).

o Commonly Used Agents

o Furosemide (Lasix®), Bumetanide (Bumex®), Torsemide

(Demadex®)

o Side Effects

o dry mouth

o tinnitus

o hypotension

o blurred vision

o headache

o Special Considerations

o severe liver disease because of risk of hepatic coma,

therefore,concurrent use of a potassium sparing diuretic may

be necessary

o electrolyte depletion

o diabetes mellitus

o hypoproteinemia, increases the risk of ototoxicity

o hypotension and electrolyte imbalances in older adults

o Contraindications

o cross-sensitivity with thiazide diuretics and sulfonamides

mayoccur

o hepatic coma

Angiotensin Receptor Neprilysin Inhibitors (ARNIs)

Angiotensin receptor neprilysin inhibitors (ARNIs) play a critical role in reducing the

risk for cardiovascular deaths and hospitalizations in heart failure patients (NYHA II-

IV) with low ejection fractions. Examine the table below to learn more about ARNIs.

o Sacubitril/Valsartan (Entresto®) Sacubitril (neprilysin inhibitor)

enhances the natriuretic peptides which results in:

o increased diuresis

o increased vasodilation

o increased aldosterone suppression

o increased inhibition of fibrosis

o Valsartan (angiotensin receptor blocker) inhibits the renin-

angiotensin-aldosterone system (RAAS) which results in:

o decreased sodium and water retention

o decreased vasoconstriction

o decreased hypertrophy

o decreased fibrosis

o Entresto is often administered in conjunction with other heart failure

therapies, in place of an ACEIs or other ARB

o May cause angioedema, hypotension, hyperkalemia,

andimpaired renal function

o Contraindicated with concomitant use of ACEIs

o Should not be administered within 36 hours of switching from

orto an ACEIs

Aldosterone Receptor Antagonists/Mineralocorticoid

Receptor Antagonists (MRAs)

Aldosterone Receptor Antagonists/Mineralocorticoid Receptor Antagonists also

playa role in managing heart failure as demonstrated below.

o Mechanism of Action

o Blocks the effects of aldosterone by attaching to

mineralocorticoid receptors (Chisholm-Burns et al., 2019).

o Commonly Used Agents: Spironolactone (Aldactone®), eplerenone

(Inspra®)

o Enhances the action of thiazide and loop diuretics and

counteract potassium loss by these types of medications.

Aldosterone treatment for heart failure was based on the

premisethat ACE Inhibitors do not control the chronic

production and aldosterone release (Chisholm-Burns et al.,

2019).

o Side Effects

o hyperkalemia

o arrhythmias

o amenorrhea

o gynecomastia

o deepening voice and increased hair

o muscle cramps

o agranulocytosis

o Special Considerations

o hepatic dysfunction

o diabetes mellitus because there is an increased risk

forhyperkalemia

o Contraindications

o anuria

o acute renal insufficiency

o renal impairment CrCL < 30 mL/min in heart failure patients

o hyperkalemia

o Addison disease

o concurrent use of Eplerenone (Inspra®)

Thiazide Diuretics

Thiazide diuretics can also be used to treat heart failure; however, loop diuretics

maintain diuretic action in the presence of impaired renal function, whereas thiazide

diuretics do not (Chisholm-Burns et al., 2019).

o Mechanism of Actions

o Volume management by blocking sodium and chloride

reabsorption in the distal convoluted tubule. Thiazide

diureticsare most effective when treating mild congestive

heart failure (Chisholm-Burns et al., 2019).

o Commonly Used Agents

o Chlorthalidone (Hygroton®), Hydrochlorothiazide

(HydroDiuril®),Indapamide (Lozol®) and Metolazone

(Zaroxolyn®)

o Side Effects

o hypokalemia

o hypotension

o dizziness

o muscle cramps

o hyperglycemia

o photosensitivity/rash

o Special Considerations

o renal or hepatic impairment

o gouty arthritis

o Contraindications

o cross-sensitivity with thiazide diuretics and sulfonamides

mayoccur

o intolerance to tartrazine

o anuria

Prescribing Pearls to Maximize Patient Outcomes

• hydrochlorothiazide (HCTZ) (25 mg/d or equivalent) may negatively impactdyslipidemia and glucose control
• higher dose thiazide diuretics lower insulin resistance
• monitor for sodium (Na+), potassium (K+), magnesium (Mg++) depletion
• calcium sparing (good for osteoporosis)
• less effective with advancing renal impairment, with GFR less than 30 mL/ minuteper 1.73 m2. (change to loop diuretics at this point).
• metolazone (Zaroxolyn®) can be administered in patients with renal impairment, creatinine clearance (CrCL) < 30 mL/min because the mechanism of action remains potent. Metolazone (Zaroxolyn®) is often used in combination with loopdiuretics with patients who have edema that does not respond to monotherapy loop diuretics, also classified as diuretic resistance (Chisholm- Burns et al., 2019).

• Volume management by inhibiting the absorption of sodium-chloride in proximal/distal tubules, and the thick ascending loop of Henle and undergoactive transport into the tubular lumen by way of the organic acid route. Thiazide diuretics:
• Volume^ management^ by^ blocking^ sodium^ and^ chloride^ reabsorption^ in^ the distalconvoluted tubule. Sacubitril/Valsartan (Entresto®) Sacubitril (neprilysin inhibitor)
• enhances the natriuretic peptides which result in:
• Increased diuresis
• Increased vasodilation
• Increased aldosterone suppression
• Increased inhibition of fibrosis Valsartan (angiotensin receptor blocker)
• inhibits the renin-angiotensin-aldosterone system (RAAS) which results in:
• decreased sodium and water retention
• decreased vasoconstriction
• decreased hypertrophy

• decreased fibrosis Aldosterone Receptor Antagonists
• blocks^ the^ effects^ of^ aldosterone^ by^ attaching^ to^ mineralocorticoid^ receptors Case Study: William’s EF is estimated at 30%, which suggests systolic heart failure. <40% EFis reflective of systolic heart failure, whereas >40% EF is reflective of diastolic heart failure. The current treatment plan is to introduce an ACE inhibitor. Once a reasonable dose of ACE inhibitor is achieved the plan is to then introduce a β-blocker. ACEIs dilate the blood vessels to improve blood flow, thus reducing the force needed bythe heart. Additionally, ACEIs help block angiotensin that is made as a result of heart failure and causes narrowing of blood vessels. Therefore, this drug is a priority over beta-blockers. Beta-blockers are helpful through their inhibition of chronotropic and inotropic effects of beta1 receptors of smooth cardiac muscle. It is important for patients to take medications as prescribed and notify healthcare providers of changes in symptoms so medications can be titrated and managed in a controlled and well-communicated fashion. However, collaboration with the patient andfamily can create a self-management plan if well documented and adhered to. For example, it could be decided that if the patient weighs himself daily and gains a certainnumber of pounds from one day to the next, he could take two furosemide

instead of one. However, clear instructions should also include at what point the healthcare provider should be notified. Additionally, it is important that William understands the need to monitor his kidney function. When the heart is not pumping efficiently it can create an increase in pressurein the vascular system going to the kidneys resulting in congestion of blood in the kidneys and impact renal function. Heart failure is characterized by the decreased ability of the ventricle to meet the metabolic demands of the body. Decreased perfusion of the kidneys occurs as a result of reduced cardiac output, resulting in the activation of the renin-angiotensin– aldosterone system to compensate for the decreased renal perfusion. However, this contributes to the pathology of the disease by increasing the release of aldosterone. Aldosterone has been shown to cause coronary inflammation, cardiac hypertrophy, myocardial fibrosis, ventricular arrhythmias, and ischemia. Spironolactone is a nonselective aldosterone antagonist that helps prevent the mentioned disease-related outcomes. Angina Prevention of myocardial infarction and death

• (^) antiplatelet drugs
• (^) cholesterol-lowering drugs
• (^) angiotensin-converting enzyme inhibitors Reduction of cardiac ischemia and the associated pain
• (^) nitrates
• (^) beta-blockers
• (^) calcium channel blockers
• (^) ranolazine Cost of Treatments - (^) CCBs& ACEIs most expensive

Organic Nitrate

- Prototype Drug: Nitroglycerin - Therapeutic Action: Acts directly on vascular smooth muscle (VSM) to promote vasodilation - Beta^ Blockers - Prototype Drug: Propranolol; Metoprolol - Therapeutic Action: Decreases cardiac oxygen demand through blockade of specific receptors in the heart . - Drugs^ that^ Increase^ Myocardial^ Efficiency - Prototype^ Drug:^ Ranolazine - Therapeutic Action:^ Reduces the accumulation of sodium and calcium in myocardial cells, which helps the myocardium use energy more efficiently. - Calcium Channel Blockers - Prototype Drug: Verapamil; Nifedipine - Therapeutic Action: Promotes relaxation of peripheral arterioles resulting in a decreased afterload which reduces cardiac oxygen demand. Anticoagulants

• (^) decrease formation of fibrin
• (^) used primarily to prevent thrombosis in veins and the atria of the heart Antiplatelet Drugs
• suppress platelet aggregation
• used primarily to prevent thrombosis in arteries

clinical practice guideline objective. Thrombolytics

• (^) promote lysis of fibrin
• (^) used for the dissolution of thrombi A patient is taking warfarin and presents to the clinic stating they misunderstood the directions and have been taking twice as much as was prescribed. The patient does nothave any obvious hematomas or petechiae and denies complaints of pain. What diagnostic test will the provider order to assess the patient's current condition?
• (^) Protamine sulfate
• (^) An activated partial thromboplastin (aPTT)
• (^) *CORRECT A prothrombin time (PR) and in international normalized ratio (INR)
• (^) Vitamin K This patient does not exhibit any signs of bleeding from a warfarin overdose. There areno hematomas or petechiae, and the patient does not have pain. A PT and INR shouldbe drawn to evaluate the anticoagulant effects. Vitamin K may be given if laboratory values indicate overdose. Protamine sulfate is given for heparin overdose. Heparins Warfarin Direct Oral Anticoagulant s(DOAC) Antiplatelet Medications Prevention ofthrombosis Prevention ofthrombosis Prevention andtreatment of thrombosis P r e v e n t b l o c k a g e o f coronary artery s t e n t s a n d

required baseline data type of monitoring Anticoagulant s(DOAC) Medications Partial thromboplastin time(PTT), platelets, complete blood count (CBC) PT, CBC. Genetic testing for variantsof CYP2C9 and VKORC1 may be done to identify patients who may require a

PTT, CBC,

renalfunction CBC, consider testing for variantsof the CYP2C19 gene when initiating clopidogrel Heparins Warfarin Direct Oral Antiplatelet Heparins Warfarin Direct Oral Anticoagulants Antiplatelet Medications Use of unfractionated heparin for treatment of venous thromboembolism (VTE) requires frequent monitoringof PTT or anti-Xa levels. PT/INR should be monitored frequently at the onset of therapy (daily to every fewdays). Once the INR goal has beenobtained and is stable on a weeklybasis, monthly No routine monitoring is No routine required with these monitoring