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Pharmacology for APRN > HTN + Dyslipidemia > Flashcards

HTN + Dyslipidemia Flashcards

1
Q

What is Blood Pressure

A

BP = HR x SV x PVR

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2
Q

Age Related Changes in BP

A

PVR increases (loss of arterial elasticity)
SV decreases (reduced CO)
HR slows down (reduced CO)

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3
Q

How do you measure the most accurate BP?

A

Empty Bladder
Correct Size Cuff
Cuff on Bare Arm
Support arm at heart level
Support back and feet
Uncrossed Feet

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4
Q

What is the definition of Hypertension?

A

Sustained elevated blood pressure (over several visits/weeks of measurement) of systolic blood pressure (BP) ≥ 130mm Hg and/or a diastolic BP ≥ 80 mm Hg.

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5
Q

What is White Coat HTN?

A

Elevated BP in the clinician’s office but normal BP at home

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6
Q

What is masked HTN?

A

Elevated BP at home but normal BP in the clinic

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7
Q

Describe a properly fitting BP Cuff

A

Covers 80% of upper arm; cuff’s bladder ~40% of arm circumference
Too Small = Falsely high!

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8
Q

What is the target for BP treatment?

A

<140/90
<130/80 for those at risk for CV disease
Geriatric Consideration: Relax tight BP control when balancing polypharmacy and lifestyle risk concerns such as dizziness, risk of falls, etc

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9
Q

Lifestyle modifications for HTN management

A

diet (reduced sodium intake) and increased activity to >150min per week, quitting smoking, reduced alcohol intake

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10
Q

Name triggers for screening for Secondary HTN

A

Occurring before 30
Accelerated or malignant HTN
Onset of Diastolic HTN in older adults >65
Drug resistant / induced HTN
Abrupt onset
Exacerbation of previously controlled HTN
Disproportionate target organ damage (TOD) for degree of HTN
Unprovoked or excessive hypokalemia

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11
Q

What is a normal GFR?

A

90-120

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12
Q

What are Predictors of resistant HTN?

A

Presence of CKD with creatinine of > or equal to 1.5mg/dL
DM
Residing in southeastern USA
African Ancestry
Age >75yrs
Presence of LVH
Obesity (BMI >30 kg/m)

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13
Q

1st Line HTN Tx Diuretic Class: Hydrochlorothiazide (HCTZ) MOA

A

Inhibits sodium and chloride reabsorption in the distal convoluted tubule resulting in low volume low volume sodium depletion- alongside K+, and Mg+ leading to decreased PVR.

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14
Q

1st Line HTN Tx Diuretic Class: Chlorthalidone MOA

A

Chlorthalidone (Thiazide-Like) is useful when HCTZ isn’t yielding goal - it is more potent and has a longer half life. Monitor K+ closely especially w initiation. Same properties but lacking the benzothiadiazine molecular structure.

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15
Q

1st Line HTN Tx Diuretic Class for Renal Impairment: Furosemide (Lasix)

A

Can be used to tag onto HR with resistant LLE.

Used in patients with chronic renal disease

Loops when <30ml/min for volume and BP. furosemide and bumetanide (Bumex) BID, torsemide QD

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16
Q

1st Line HTN Tx: ACEi MOA

A

Inhibits angiotensin converting enzyme which functions to convert angiotensin I to Angiotensin II
Causes vasodilation, reduced aldosterone secretion, and decreased sodium and water retention
Reduces afterload and preload

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17
Q

1st Line HTN Tx: ACEi SE

A

Cough: Due to accumulation of bradykinin.
Hyperkalemia
Angioedema
Contraindicated in pregnancy (teratogenic)

CXN: Contraindicated in patients with bilateral renal artery stenosis (can cause renal impairment)

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18
Q

1st Line HTN Tx: ARBs MOA

A

Block the angiotensin II receptor, preventing vasoconstriction and aldosterone secretion without affecting bradykinin levels
This leads to vasodilation, decreased sodium and water retention, and reduced blood pressure.

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19
Q

1st Line HTN Tx: ARBs SE

A

Hyperkalemia
Dizziness
Angioedema (less common than with ACE inhibitors)
Contraindicated in pregnancy

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20
Q

CCB Class Dihydropyridine (DHP) Amlodipine MOA

A

Work on arterial smooth muscle causing vasodilation reducing PVR

Works on isolated systolic HTN

Used for Angina, lowers afterload

Relieve vasospasm in peripheral vasculature in Raynauds

Minimal effect on heart and contractility

Modest Inhibitor: CYP450 3A4

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21
Q

CCB Class Dihydropyridine (DHP) Amlodipine SE

A

Peripheral edema is common with dihydropyridines and may require dose adjustment or combination with a diuretic.

HA, Flushing, Dizziness, Reflex tachycardia

CXN: not in Pt’s with HF, CYP3A4 inhibitors and inducers. Red Flags:
CTN in HF, renal or hepatic impairment 2/2

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22
Q

CCB Class Non-DHP Diltiazem, Verapamil: MOA

A

Act on both the heart and vascular smooth muscle

Reduces HR, Contractility, and BP

Used for tachyarrhythmias

Mild Vasodilation

Rate Control in AF and SVT by decreasing rate conduction through AV node

Hypertrophic Cardiomyopathy to reduce contractility

Modest Inhibitor: CYP450 3A4

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23
Q

CCB Class Non-DHP Diltiazem, Verapamil: SE

A

Non-dihydropyridines should be used cautiously in patients with heart failure or bradycardia.

Constipation (verapamil), fatigue, bradycardia

CXN: not in those HB, Sick Sinus Syndrome, CYP3A4 inhibitors and inducers.

Red Flags: CTN in HF, renal or hepatic impairment 2/2 MOA; negative inotropes lending to reduction in contractility of the heart

24
Q

HTN Tx Considerations in the Elderly

A

Target 140/90

Thiazide Diuretics and CCB’s First choice

BB and ACEi - NOT TOLERATED!

Instruct: slow position changes, dangle p/t standing

25
Q

HTN Tx Consideration in CKD

A

Target less than 130/80

Early Tx is key

First line Tx: ACEi and ARB. Slows progression of CKD by decreasing glomerular pressure

26
Q

HTN Tx Consideration in DM

A

Target less than 130/80

First Line: ACEi and ARB

Caution: BB can mask the symptoms of hypoglycemia

27
Q

HTN Tx Consideration in Pregnancy

A

First Line: Labetalol, alpha agonist methyldopa, CCB Nifedipine

Contraindication: ACEi, ARB

28
Q

HTN Tx Consideration in HF

A

First Line: ACEi

29
Q

Dyslipidemia Defined

A

Umbrella term for lipid disorders e.g. familial hypercholesterolemia, hypertriglyceridemia, mixed hypercholesterolemia, diabetic dyslipidemia

30
Q

Aldosterone Antagonist (Spironolactone, eplerenone) MOA:

A

Block effects of aldosterone, regulating sodium and water homeostasis and maintenance of intravascular volume

31
Q

What are recommendations for lipid screening?

A

Complete lipid profile starting at age 20 (then every 5 years)
Older than age 40 years, screen every 2-3 years
Preexisting hyperlipidemia: screen annually or more frequently

EXCEPTION: Homozygous Familial Hypertension (HoFH)

32
Q

HMG-COA Reductase Inhibitors / STATINS: MOA

A

Primarily block the conversion of HMG-CoA to mevalonate, which is the rate-limiting step in the production of cholesterol in the liver.

Maximum effects: usually are seen after 4 to 6 weeks of therapy. For this reason, dosage adjustments should not be made more frequently than q 4 weeks.

33
Q

Aldosterone Antagonist (Spironolactone, Eplerenone) Indications

A

Good for HTN resistance or primary aldosteronism
Spironolactone: Higher dose (150-300mg), androgen blocking effect.
Eplerenone: Aldosterone antagonist wo anti-estrogen effect 25mg/d

34
Q

Aldosterone Antagonist (Spironolactone, Eplerenone) SE’s

A

Hyperkalemia, especially when combined with ACEi or ARB or in excessive diuresis
CXN: Renal Impairment

35
Q

Triglyceride Target value

A

Triglycerides: less than 150

36
Q

LDL target value

A

Want LOW.

Optimal: less than 100 mg/dL

Less than 130 mg/dL for low-risk patients with fewer than two risk factors

Very high: greater than 190

Heart disease or DM: less than 100

37
Q

HDL Target Value

A

Want HIGH = Healthy for the HEART

Men: Greater then 40 mg/dL

Women: Greater than 50 mg/ dL

38
Q

HMG-CoA Reductase Inhibitors: STATINS MOA

A

Action: primarily block the conversion of HMG-CoA to mevalonate, which is the rate-limiting step in producing cholesterol in the liver.

39
Q

HMG-CoA Reductase Inhibitors: STATINS Indications

A

Individuals who have clinical ASCVD (highest risk group)

Individuals who do not have ASCVD but have severe hyperlipidemia defined as LDL-C >190 and are 20-75 yrs old

Individuals who are 40-75 yrs old with Type I or Type II DM and have LDL-C values of 70-189mg/dL

Individuals who are 40-75 yrs old with LDL-C values of 70-189mg/dL and have a 10 year risk of ASCVD of 7.5% or more

40
Q

HMG-CoA Reductase Inhibitors: STATINS Efficacy

A

Maximum effects are usually seen after 4-6 weeks of therapy.
Dose adjustments made every 4 weeks

41
Q

HMG-CoA Reductase Inhibitors: STATINS Contraindications

A

pregnant and lactating women

active liver disease

unexplained elevated aminotransferase levels

heavy alcohol use.

Adverse events: Well tolerated by most patients; myopathies, gastrointestinal (GI) complaints, headache may occur

CXN: May increase blood sugar by inhibiting the efficacy of insulin

42
Q

Ezetimibe & Statin Combination (Vytorin): MOA

A

Acts on the brush border of the small intestine and inhibits the absorption of cholesterol, leading to a decrease in the delivery of intestinal cholesterol to the liver. This reduces hepatic cholesterol stores and increases clearance of cholesterol from the bloodstream

Anticipated LDL-C reduction 15-20% (helpful adjunct)

43
Q

Ezetimibe & Statin Combination (Vytorin): Contraindications

A

pregnant
lactating women
active liver disease
unexplained elevated aminotransferase levels
heavy ETOH use

44
Q

PCSK9: Human monoclonal Ab proprotein convertase involved in the degradation of LDL receptors in the Liver: MOA

A

Receptors on our liver cells primarily sweep away excess cholesterol in our body, but a protein called “PCSK9” blocks this action by destroying the receptors on the liver cells, causing the cholesterol levels to go up.
PCSK9 inhibitors attach to this protein and block their action. As a result, more receptors can continue to do their job and this lowers the amount of LDL CHL in the blood.

45
Q

Ezetimibe & Statin Combination (Vytorin): SE’s

A

HA
Diarrhea
ABD Pain
Combination therapy: Myopathy / Rhabdomyolysis

46
Q

PCSK9: Human monoclonal Ab proprotein convertase involved in the degradation of LDL receptors in the Liver: Indications

A

Additional LDL-C ~60% for patients already on an optimized statin therapy

Blocking activity of PCSK9 with monoclonal antibodies reduces the degradation of LDL receptors and increases clearance of LDL cholesterol

47
Q

Bempedoic Acid: Indication

A

Heterozygous familial hyperlipidemia or established ASCVD risk wo goal, max statin tolerated statin therapy

48
Q

Bempedoic Acid: MOA

A

ACL enzyme upstream of HMG CoA reductase in CHL synthesis- Inhibition of ACL reduces CHL biosynthesis in the liver and decreases LDL
Anticipated LDL-C reduction 18% (helpful adjunct)

49
Q

Bempedoic acid & Ezetimibe (Nexlizet) Combination: Indication

A

LDL reduction of 38% when used maximally with statin

50
Q

Bempedoic Acid: SE’s

A

ADE Risk: Monitor uric acid levels /gout flare + tendon rupture risk (older, tendon damage history, concurrent or recent use of FQ).

51
Q

Fibrates (Gemfibrozil, Fenofibrate): Indication

A

Typically used as an adjunct to diet to treat adults with severe hypertriglyceridemia or to elevate high-density lipoprotein cholesterol (HDL-C)

52
Q

Fibrates (Gemfibrozil, Fenofibrate): MOA

A

Unclear stimulation of lipoprotein lipase, enhancing breakdown of VLDL to LDL CHL
Multiple studies (per guidelines) have shown that if TG >500 and low HDL, despite dietary modifications then addition of fibrate to statin may trend toward less CVD events.

53
Q

Fibrates (Gemfibrozil, Fenofibrate): SE’s

A

Contraindicated with h/o cholecystitis, cholelithiasis, and hepatic or renal disease
No studies in pregnant women
GI related (epigastric pain, N/V, dyspepsia, flatulence, constipation)
Myopathy, Rhabdomyolysis
Hepatotoxicity
Cholestatic jaundice
Anemia / thrombocytopenia

54
Q

Niacin (B Vitamin, high dose): MOA

A

Decrease VLDL synthesis in the liver, inhibit lipolysis in adipose tissue, increase lipoprotein lipase activity.

This decreases TG and LDL CHL in the bloodstream

HDL may be increased by up to 35%

55
Q

Niacin (B Vitamin, high dose): Contraindications

A

Hepatic dysfunction
Severe Hypotension
Persistent hyperglycemia
Acute gout
New onset AF
Active peptic ulcers
WORSEN GLUCOSE CONTROL

56
Q

Niacin (B Vitamin, high dose): Adverse Events

A

Pruritus
Flushing of face and neck
Increase uric acid
Worsen glucose control
GI side effects - not in pts with active ulcer
Hepato-toxicity
Acanthosis Nigricans (hyperpigmentation of the skin)

Pharmacology for APRN (11 decks)

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