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Pharm II > Lecture 4 (HTN)-Exam 3 > Flashcards

Lecture 4 (HTN)-Exam 3 Flashcards

1
Q

ESSENTIAL (PRIMARY) HYPERTENSION (HTN)
* What are the factors that may implicate? (6)

A
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2
Q

SECONDARY HYPERTENSION (5-10% OF CASES)
* What are the common and uncommon causes?

A
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3
Q

What are some medications that can cause HTN?(12)

A
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4
Q

Screening-USPSTF (BP)
* When do you start?
* What is the frequency?

A
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5
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6
Q
  • What needs to happen if patients fall within two categories based on SBP and DBP?
  • BP indicates BP based on what?
A
  • Individuals with SBP and DBP in 2 categories should be designated to the higher BP category.
  • BP indicates blood pressure (based on an average of ≥2 careful readings obtained on ≥2 occasions
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7
Q

Calculate 10-year atherosclerotic cardiovascular disease risk:
* What does the calculator help you predict? (3)

A

This calculator helps predict the 10-year risk of the following hard ASCVD events:
* First occurrence of nonfatal myocardial infarction
* Coronary heart disease death
* Fatal or nonfatal stroke

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8
Q

CALCULATE 10-YEAR ATHEROSCLEROTIC CARDIOVASCULAR DISEASE RISK

This calculator may overestimate risk and a discussion with the patient needs to ensue if there are any questions.
* Risks estimates were developed by what?
* Risk may be underestimated in who?
* Risk may be overestimated in who?
* This calculator has only been validated for what ages?

A
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9
Q

What is the the low, borderline, intermediate and high risk for ASCVD

A
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10
Q

What are the treatment goals for HTN? (4)

A

Reduce mortality and morbidity from cardiovascular events:
* Coronary events
* Cerebrovascular events
* Heart failure
* Kidney disease

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11
Q
A
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12
Q

lab testing:
* baseline testing to help establish what?
* Serum electrolytes should be monitored when?

A
  • Baseline testing to help establish ASCVD risk and organ function prior to pharmacotherapy initiation
  • Serum electrolytes should be monitored 2 to 4 weeks after initiation of a diuretic, ACEI or ARB
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13
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A
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14
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15
Q

What are modifiable risk factors?

A
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16
Q

What are the fixed risk factors?

A
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17
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18
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19
Q

What is the first line therapy if not compelling indication?

A
  • ACEI or ARBS
  • Calcium channel blockers: DHP or Non-DHP
  • Thiazide diuretics: Hydrochlorothiazide or chlorthalidone
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20
Q

First line pharm:
* What does it reduce?

A

Reduce CV mortality when used for hypertension compared to other agents

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21
Q

Fill in

A
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22
Q

Combination Therapy
* What do the accomplish trial show about Benazepril plus HCTZ vs benazepril plus amlodipine?

A
  • Both equal BP lowing benefit
  • Benazepril plus amlodipine 20% lower CV events – study terminated after 36 months
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23
Q

Combination therapy:
* Low dose combo therapy does greater what?
* Multiple what?

A
  • Low-dose combination therapy greater BP reduction with less adverse effects
  • Multiple fixed-dose combination products available
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24
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25
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26
Q

What are the sulfonamide and not sulfonamide thiazide diuretics? where is the site of action?

A
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27
Q

What is the MOA of thiazide diuretics?

A
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28
Q

What are the indications of thiazide? (4)

A
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29
Q

What are the SE of thiazides?

A
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30
Q

What are the CI of thiazide?

A
  • Anuria
  • Sulfonamide allergy
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31
Q

Hydrochlorothiazide vs chlorthalidone
* Both agents are recommended as what?
* 2017 American College of Cardiology / American Hear Associated guidelines recommend what?

A
  • Both agents are recommended as first-line therapies for the treatment of hypertension
  • 2017 American College of Cardiology / American Hear Associated guidelines recommend chlorthalidone because it has a longer half-life and proven trial reduction of cardiovascular disease
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32
Q

Hydrochlorothiazide vs chlorthalidone: Hripsak G et al Jama Internal Medicine 2020
* Retrospective, observational comparative cohort study; Jan 2001 to Dec 2018; first-time antihypertensive monotherapy with what/
* what were the results?
* What did chlorthalidone have an increase of?(5)

A
  • Retrospective, observational comparative cohort study; Jan 2001 to Dec 2018; first-time antihypertensive monotherapy with hydrochlorothiazide or chlorthalidone
  • 730,225 subjects; no significant difference associated with myocardial infarction, hospitalized heart failure or stroke
  • Chlorthalidone had significantly higher risk of hypokalemia, hyponatremia, acute renal failure, CKD, and type 2 diabetes
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33
Q
A
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34
Q

What are the second line agents for HTN?(6)

A
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35
Q

Central Alpha-2 agonists (clonidine)
* What does presynaptic vesicles contain?
* NE released into what?
* What will NE stimulate? What will it cause?

A
  • Presynaptic vesicles contain NE
  • NE released into the synaptic cleft from the hypothalamic ganglia in the CNS brain Spinal cord
  • Released NE will stimulate post synaptic neuron and stimulate alpha-2 receptors
  • Stimulation of alpha-2 receptors inhibit further release of NE into the synaptic cleft
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36
Q

Central Alpha-2 agonists (clonidine)
* What does it oppose the effects of?
* Clonidine primary agent in this class used to what? how?

A
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37
Q

Central Alpha-2 agonists (clonidine)
* What is the route (2)?
* What are the se?

A
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38
Q

Methydopa:
* Preferentially gets converted to what? What does that cause?

A
  • Preferentially gets converted to methylnorepinephrine
  • Methylnorepinephrine builds up in the presynaptic ganglia and pushes NE into the synaptic cleft where it gets degraded by monoamine oxygenase
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39
Q

Methyldopa:
* When stimulating signal comes, what is released instead?
* What can it not activate?
* What can it stimulate?

A

When stimulating signal comes – methyl NE released instead
* CANNOT activate post synaptic adrenergic receptors
* CAN stimulate alpha-2 receptors – further decreases NE release

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40
Q

What are the se of methyldopa?(7)

A
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41
Q

What is the normal pathophysio of normal vasodilation?

A
  • Tunica intima – endothelial cells that produce nitric oxide (NO)
  • NO produced in tunica intima moves to tunica media and activates guanylyl cyclase that converts GTP to cGMP
  • cGMP induces vascular smooth muscle relaxation
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42
Q

Vasodilators - antihypertensives (hydralazine)
* What is the MOA?
* What are the indications (3)

A
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43
Q

Vasodilators - antihypertensives (hydralazine)
* What are the SE?

A
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44
Q

Vasodilators - antihypertensives (nitroprusside)
* What is the MOA?

A
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45
Q

What are the indications of nitroprusside?

A
  • Short-term management of severe HF
  • Hypertensive crisis
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46
Q

What are the SE of nitropursside?

A
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47
Q

HTN

Heart failure with reduced eiection fraction:
* What is first line?
* What is Add on?

A

First line
* ACEi or ARB then add beta blocker #
* Diuretic if edema present

Add on:
* Mineralocorticoid receptor antagonist

(#) in HFrEF only, use bisoprolol, carvedilol or metoprolol succinate, titrated to the evidence based dose

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48
Q

HTN

Heart failure with preserved ejection fraction
* What is first line?

A
  • ACEi or ARB then add beta blocker
  • diuretic if edema present
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49
Q

HTN

Stable ischemic heart disease:
* What is first line?
* What is add on?

A
  1. Beta blocker
  2. Add ACEi or ARB
  3. Add CCB if angina
  4. Add thiazide or mineralocorticoid receptor antagonist
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50
Q

HTN

Diabetes mellitus
* What are the different choices for txt?

A

ACEi, ARB, CCB, or thiazide
* If albuminuria present in diabetes, treat like chronic kindey disease and use an ACEi or ARB titrated to the max tolerated dose

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51
Q

HTN

Chronic kidney disease
* What is first line?

A

ACEi or ARB

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52
Q

HTN

Secondary stroke prevention:
* What is the first line?

A

Thiazide or thiazide with ACEi

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53
Q

If a patient has HTN and one of these, what is the first line:
* BPH:
* Migraine:
* Raynaud phenomenon:

A
  • BPH: alpha blocker
  • Migraine: beta blocker, CCB
  • Raynaud phenomenon: dihydropyridine CCB
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54
Q

What antihypertensive meds cannot be used in pregnancy?

A

ACRi, ARB, renin inhibitor

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55
Q

DM:
* What is the primary cause of mortality in patients with DM?
* What is first line with and without albuminuria?

A

Cardiovascular disease is the primary cause of mortality in patients with DM
* All four first-line agents decrease cardiovascular events in patients with DM
* ACEI or ARBs recommended as first-line for patients with persistent albuminuria

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56
Q

CKD
* HTN damages what?
* Usually presents as what?
* BP control can slow down what?

A
  • HTN damages renal tissues and arteries
  • Usually presents as albuminuria (urine albumin to creatinine ratio of 30 to 299 mg/g with spot check)
  • BP control can slow the decline of kidney function
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57
Q

CKD
* What is first line?

A

ACEI and ARBS can decrease intraglomerular pressure which can further decrease kidney function decline
* First-line for patients with CKD / albuminuria

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58
Q

Special populations-African american
* Why is the HTN pathophysiolgy different?
* Harder to do what?

A

Pathophysiology of hypertension in AA population different from that of other ethnicities
* Low renin HTN
* MC associated with abnormal sodium reabsorption

Harder to control – usually requires 2 or more agents to reach the goal of < 130/80 mmHg

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59
Q

SPECIAL POPULATIONS – AFRICAN AMERICANS
* What is inital therapy without compelling indications?

A
  • Calcium channel blocker: MC amlodipine or nifedipine (ER formulations) OR
  • Thiazide diuretics
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60
Q

SPECIAL POPULATIONS – AFRICAN AMERICANS
* Initial therapy with compelling indication?
* What is the combo therapy?

A

Initial therapy with compelling indication:
* Treat as per recommendations for indication

Combination therapy
* Thiazide or CCB with ACEI or ARB

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61
Q

SPECIAL POPULATIONS AFRICAN AMERICANS
* In studies, what drugs (2) had the highest response?
* Lowest (1)

A
  • Highest response with diltiazem and HCTZ
  • Lowest with captopril
62
Q

SPECIAL POPULATIONS – ELDERLY (≥ 60 YEARS)
* Hypertension prevalences increases with what?
* Isolated systolic hypertension common; associated with what?
* Often not what?

A
63
Q

SPECIAL POPULATIONS – ELDERLY (≥ 60 YEARS)
* What did the SHEP and syst-Eur studies show?

A
64
Q

SPECIAL POPULATIONS - ELDERLY
* What is the BP goal?
* Improved what?
* Increased what?
* Relaxed goals in who?

A
65
Q

SPECIAL POPULATIONS - ELDERLY
* What medication is preferred?
* What do you need to be careful about with elderly? What should you do?

A
66
Q

HYPERTENSIVE URGENCY
* What is the definition?

A

Acute increase in BP > 180 systolic or 120 diastolic NOT associated with acute or progressing end organ injury
* Encephalopathy, intracranial hemorrhage, acute LV failure with pulmonary edema, dissecting aortic aneurysm, unstable angina, acute renal failure

67
Q

What is the txt of hypertensive urgency? (list the drugs)

A

Oral antihypertensives – decrease BP to stage 2 over several hours to days
* Increase maintenance medications
* Add new agent
* Treat anxiety

68
Q

What is the issues with captopril, clonidine and IR nifedipine?

A
69
Q

Fill in

A
70
Q

HTN emergencies:
* What are the 3 major exceptions to BP lowering over the first 24 hours?

A
71
Q

HTN emergency:
* All pts should be treated where?
* What route?
* Specific medication depends on what?
* What should be monitored?

A
72
Q

Hypertensive Emergency:
* What drugs can you use? What are the comments? (4-> red boxes only)

A
73
Q

HTN retinopathy (malignant htn)
* Characterized by what?
* If untreated, what can happen?
* What is the first line agents?

A
  • Characterized by DBP > 140 mmHg with papilledema plus either encephalopathy or nephropathy
  • If untreated, progressive renal failure occurs
  • First-line agents: sodium nitroprusside or clevidipine
74
Q

She skipped this slide, so I just placed it all in one card

Fenoldopam
* What is the MOA
* Indications?
* Administration?
* SE?

A
75
Q

Factors that reduce adherence to antihypertensive therapy
* What are the patient and disease chacteristics? (6)

A
  • Asymptomatic
  • Chronic condition
  • No immediate consequences to stopping therapy
  • Social isolation
  • Disrupted home situation
  • Psychiatric illness
76
Q

Factors that reduce adherence to antihypertensive therapy
* What are the txt characteristics? (7)

A
  • Long duration of therapy
  • Complicated regimens
  • Expensive medications
  • Side effects
  • Lack of follow-up
  • Long waiting times in office
  • Lack of patient education
77
Q

What are the factors that improve medication compliance (10)

A
78
Q

A 63 year-old female with history of diabetes mellitus presents for blood pressure follow-up. At her last two visits her blood pressure was 150/92 and 152/96. Today in the office her blood pressure is 146/92. Recent blood work shows a Sodium 140 mEq/L, Potassium 4.2 mEq/L, BUN of 23 mg/dL, and Creatinine of 1.1 mg/dL. Which of the following is the most appropriate initial medication in this patient?
A. Clonidine
B. Metoprolol
C. Ramipril
D. Hydrochlorothiazide
E. Hydralazine

A

C. Ramipril

79
Q

Acute rebound hypertensive episodes have been reported to occur with the sudden withdrawal of
A. Lisinopril
B. Amlodipine
C. Clonidine
D. Nitroprusside
E. Hydrochlorothiazide

A

C. Clonidine

80
Q

A 55 year-old diabetic female presents for a 3 month blood pressure follow-up. At the last visit the BP was 160/90 for the third consecutive visit. She was placed on an ACE inhibitor and educated regarding lifestyle modifications. At today’s visit the patient complains of persistent annoying dry cough that has been going on since the last visit. BP today is 120/70. What is the best recommendation to control her BP?
A. No change
B. Stop ACE inhibitor, start amlodipine
C. Switch to losartan
D. Stop ACE inhibitor, continue lifestyle changes
E. Switch to carvedilol

A

C. Switch to losartan

81
Q

What are the 7 classes of dyslipidemia medical therapy?

A
  • Statins
  • Bile Acid sequestrants
  • Fibrates
  • Cholesterol Absorption inhibitors
  • Lipid-Regulating Agents (Omega-3-Fish Oils)
  • Nicotinic Acid derivatives
  • Proprotein convertase subtilisin kexin 9 (PCSK9) Inhibitors
  • Microsomal triglyceride transfer protein inhibitor
82
Q

Cholesterol metabolism: Lipoproteins available in four main subtypes
* Chylomicron: produced where? Mostly what?
* VLDL: Produced in what? Mostly what? More what?

A
83
Q

Cholesterol metabolism: Lipoproteins available in four main subtypes
* LDL: primarily composed of what? Delivers cholesterol to cells to be used for what? (3)

A

Primarily composed of cholesterol

Delivers cholesterol to cells used for:
* Cell membrane formation
* Synthesis of steroid hormones
* Taken up by liver – used for bile acid synthesis

84
Q

Cholesterol metabolism: Lipoproteins available in four main subtypes
* HDL: Produced where? Primarily what? What does it do?

A

Produced in liver and small intestine

Primarily protein with a small amount of lipids
* Transports excess cholesterol back to the liver

85
Q

Cholesterol metabolism
* Chylomicrons produced where? Consist mostly of what?
* VLDL is produced where? Consist mostly of what?
* Chylomicrons and VLDL function to do what?

A
  • Chylomicrons produced in the gut from dietary lipids; consist mostly of TG
  • VLDL is produced in liver and consist mainly of TG and some cholesterol – more than chylomicrons
  • Chylomicrons and VLDL function to deliver energy rich TG to cells throughout the body
86
Q

Cholesterol metabolism:
* TG reduced by what? What happens after that?
* LDL=

A

TG reduced by lipoprotein lipase to free fatty acids (FFA) in the blood stream
* FFA are taken up by the tissues
* Transforms VLDL into LDL

LDL = higher cholesterol content

87
Q

Cholesterol metabolism
* LDL delivers what? Why?
* More than half of the LDL is taken up by what?
* Excess cholesterol is what?

A
  • LDL delivers cholesterol to cells where it is used for cell membrane formation and the synthesis of steroid hormones
  • More than half of the LDL is taken up by the liver and used to synthesize bile acids
  • Excess cholesterol is transported back to the liver by HDL
88
Q

When LDL is a problem
* High levels of LDL accumulate where?
* Plaque rupture stimulates what?

A
  • High levels of LDL accumulate in the artery wall – atherosclerotic lesions
  • Plaque rupture stimulates primary hemostasis – recruiting platelets, further decreasing size of artery lumen
89
Q

HDL
* Prevents the formation of what?
* Suppresses what?

A
  • Prevents the formation of atherosclerotic lesions
  • Suppresses LDL oxidation and vascular inflammation
90
Q

HMG-coA reductase inhibitors (Statins)
* Inhibits what?

A

Inhibits the conversion of HMG-CoA to mevalonic acid
* Rate-limiting step in endogenous cholesterol biosynthesis

91
Q

Statins also increase what?

A

Increases HDL levels – mechanism unknown

92
Q

HMG-CoA REDUCTASE INHIBITORS (STATINS)
* The liver identifies the decreased cholesterol production
and begins to compensate, how? (3)

A
  • ­ Increases LDL receptors on the cell membrane
  • ­ Bind and internalize circulating LDL
  • ­ Low LDL triggers decreased release of VLDL which lowers triglyceride levels
93
Q

What are the hydrophillic and lipophillic statins?

A
94
Q

What is the short and long half life statins?

A
95
Q

What are the interacting medications of statins?

A
96
Q

What are the high and moderate intensity statins?
* What are they meatbolized by?

A
97
Q

What are the SE and baseline labs of statins?

A
98
Q

When are statins CI? (3)

A
  • Previously in pregnant women
  • New evidence supports use in women at high risk of ASCVD when benefits > risk
  • Use of hydrophilic statins (rosuvastatin, pravastatin) recommended
99
Q

What are SAMS? (common and rare)

A
  • Myalgias – bilateral muscle aches of larger muscle groups including thighs and back
  • Rhabdomyolysis most serious – RARE
100
Q

What are the RFs of SAMS(7)

A
101
Q

What is the prevention of SAMS?

A
  • Start with low dose for high-risk patients
  • Avoid drug interactions
102
Q

What is the management of SAMS?

A
103
Q
A
104
Q

Bile acid sequestrants
* bile acids are excreted where?

A

Excreted into gut and facilitate digestion and absorption of lipids

105
Q

What is the MOA of bile acid sequestrants?

A
  • Bind negatively charged acids and salts
  • Form insoluble complex with bile acid
  • Increased excretion of bile acids – increased demand for production
  • Bile acids made of cholesterol
  • Liver senses decreased cholesterol and increases LDL receptors on surface
  • Brings in more LDL and decreases cholesterol levels
106
Q

Bile Acid sequestrants
* MC used as what?
* DOC in what?
* What are the SE?

A
107
Q

What are the CI with bile acid sequestrants?

A

CI: bowel obstruction, history of TG > 500

108
Q

What are the different types of bile acids?

A
109
Q

fibrates
* What is the MOA?

A

Bottomline: good at decreasing TG by 50% compliciated MOA (had this in my notes)

110
Q

What does fibrates decrease and increase?

A

Highest efficacy for hypertriglyceridemia
* Decrease TG 20 to 50 %
* Increase HDL 10 to 15%

111
Q

What the two types of drugs for fibrates? What are the SE? and comments?

A
112
Q

How does normal cholesterol absorption work?

A
  • Free cholesterol binds to NP1L1 receptor on cell membrane of intestinal enterocytes
  • Binding results in endocytosis of cholesterol/NP1L1 complex
  • Supported by a protein complex Clathrin AP2
  • Following endocytosis cholesterol is released and NP1L1 returns to cell membrane
113
Q

How do Cholesterol absorption inhibitors work? What does it not impact

A
  • Bind to NP1L1 and inhibits its ability to interaction with Clathrin AP2 which is necessary for endocytosis
  • Decrease delivery of intestinal cholesterol to the liver
  • Decreased LDL
  • Do NOT impact absorption of TG or fat-soluble vitamins
114
Q

Cholesterol absorption inhibitor - Ezetimibe (Zetia)
* Only what?
* Most often used in what?
* Decreases what?
* What are the SE (2)?

A
115
Q

Omega 3 polyunsaturated fatty acids:
* Primarily does what?
* What does it decrease (2)

A

Primarily TG lowering – up to 50%
* Decrease ischemic events by 25% when added to statin therapy
* Decrease synthesis and delivery of VLDL and triglycerides

116
Q

Omega 3 polyunsaturated fatty acids:
* What agents are in the class?

A
  • Omega-3 ethyl ester of DHA and EPA (Lovaza)
  • Omega-3 carboxylic acid of EPA and DHA (Epanova)
  • Icosapent ethyl (Vascepa)
117
Q

omega 3 ethyl ester of DHA and EPA (Lovaza)
* What are the SE?
* What does it decrease?
* May poteniate what?

A
118
Q

Omega-3 carboxylic acid of EPA and DHA (Epanova)
* What is the SE?
* What does it decrease?

A
  • Arthralgias
  • decrease TG 45%
  • No effect on LDL
119
Q

Icosapent ethyl (Vascepa)
* What are the SE?
* What does it decrease?
* What can it reduce?
* May potentiate what?

A
120
Q

Niacin:
* where does it work?
* What is the MOA?

A
121
Q

Niacin
* What is the major SE?
* What can you do to help?

A

Flushing and itching – niacin induced prostaglandin release
* Give with ASA 325 mg 30 min prior or ibuprofen 200 mg 60 minutes prior to niacin dose
* Titrate dose slowly
* Improves with time
* Extended-release formulations – may have increased risk of elevated liver enzymes

122
Q

What are other SE besides flushing for niacin? (5)

A
  • Elevated liver enzymes
  • Hyperuricemia
  • Hyperglycemia
  • Hypotension – patients on vasodilators
  • Bleeding – patients with underlying bleeding disorder
123
Q

Proprotein convertase subtilisin/kexin type 9 (PCSK9) Inhibitors
* How does it work?

A
124
Q

PCSK9 Inhibitors
* Indicated for what?
* Lower what?
* Reduce risk of what?

A
  • Indicated for add-on therapy to statin therapy or monotherapy in patients with familial hypercholesterolemia syndromes
  • Lower LDL by as much as 60% in patients on statin therapy
  • Reduce risk of recurrent stroke or myocardial infarction following initial acute coronary event
125
Q

What are the two examples of PCSK9 Inhibitors? What are the SE and comments?

A
126
Q
A
127
Q
A
128
Q

Treatment goals of lipids (5)

A
129
Q
A
130
Q

Inital approach: ID of at risk patients:
* What are the first 3 steps?

A
131
Q

Inital approach: ID of at risk patients:
* What is step 4 and 5

A
132
Q

ACC ASCVD Risk Estimator Plus Calculator
* Estimate what?
* Used for what?
* what are the ages?

A
133
Q

10-YEAR RISK FOR ASCVD IS CATEGORIZED AS:
* What is low, borderline, intermediate and high risk?

A
134
Q

Lifestyle modifications-all patients:
* Physical activity
* Weigh management
* Dietary modifications

A
135
Q

Lifestyle modifications-all patients:
* BP management?
* Diabetes management?

A
136
Q
A
137
Q

Primary prevention:
* What are the three higher risk groups and their txt?

A

Patients with LDL ≥ 190 mg/dL
* high intensity statin

Adults 40 to 75 with DM
* moderate intensity unless additional risk factors

Adults 40 to 75 without DM
* obtain ASCVD score

138
Q

Baseline LDL-C ≥ 190 mg/dL
* What is the txt?
* What are the goals? What do you add if you do not hit the goals?

A
139
Q
A
140
Q

What are patient discussion points?

A
141
Q

What are the major ASCVD events?(4)

A
142
Q

secondary prevention

Very high risk ASCVD event OR ≤ 75 years NOT at very high risk
* What is first, second and third add on therapy?
* What is the goal?

A
  • First-line therapy: High intensity statin
  • Second-line add on therapy: Ezetimibe
  • Third-line add on therapy: PCSK9-I
  • LDL goal: LDL < 70 mg/dL
143
Q

Secondary prevention:

NOT at very high risk ASCVD and age > 75
* What is first line therapy?

A

Moderate or high intensity statin

144
Q
A
145
Q

Evaluation of therapeutic outcomes:
* What do you need to do short term?

A
146
Q

Evaluation of therapeutic outcomes: long term
* Lipid panel when?
* Non-fasting lipid panel is generally acceptable except for what?
* What is not recommended?
* LFTs should be monitored when?

A
147
Q

Hypertriglyceridemia:
* Moderate (175 to 499 mg/dL): What do you need to do, evaluate?

A
  • Lifestyle modifications
  • Evaluate for underlying causes including
  • Disease states (DM, CKD)
148
Q

What is the txt for moderate and severe hypertriglyceridemia?

A
149
Q

Primary focus:
* What reduces ASCVD event rates?
* Suggest that for each 38 mg/dL reduction in LDL = what?
* Select agents with

A
150
Q

Hypertriglyceridemia –
* What is inital txt? What is the other?
* Low HDL: What is the txt?

A

Pharm II (14 decks)

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