Ch12: HTN, HLD, CHF Flashcards

1
Q

(3) components of BP

A
  • heart rate
  • stroke volume
  • peripheral vascular resistance
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2
Q

as we age, what happens to CO and PVR

A

cardiac output goes down (decrease in HR and SV)

PVR goes up

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3
Q

(4) primary target organs damaged with uncontrolled HTN

A
  • brain
  • cardiovascular system
  • kidneys
  • eyes
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4
Q

target organ damage from HTN: brain (2)

A

stroke, vascular (multi-infarct) dementia

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5
Q

target organ damage from HTN: cardiovascular system (4)

A
  • atherosclerosis
  • myocardial infarction
  • left ventricular hypertrophy
  • heart failure
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6
Q

1 cause of kidney failure in the US

A

hypertensive nephropathy

3x more common than diabetic nephropathy, the second cause

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7
Q

target organ damage from HTN: kidneys

A
  • hypertensive nephropathy

- renal failure

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8
Q

target organ damage from HTN: eyes

A
  • hypertensive retinopathy

- risk for blindness

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9
Q

Grade 1 & 2 hypertensive retinopathy (LOW GRADE)

A
  • narrowing of the terminal arteriolar branches (grade 1) or severe local constriction (grade 2)
  • no vision change or permanent findings
  • reversible when HTN is treated
  • common in long-standing poorly-controlled HTN
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10
Q

Grade 3 hypertensive retinopathy (HIGH GRADE)

A
  • preceding signs (constriction of the aterioles) now with flame-shaped hemorrhages
  • DBP is usually 110 or greater, HTN emergency
  • potential for visual change and permanent findings
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11
Q

Grade 4 hypertensive retinopathy (HIGH GRADE)

A
  • preceding signs (constriction of the aterioles, flame hemorrhages) now with papilledema
  • DBP is usually 130 or greater, HTN emergency
  • potential for visual changes (black spots in visual fields) and permanent findings
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12
Q

papilledema is a sign of….

A

increased intracranial pressure

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13
Q

JNC8 vs. AHA/ACC guidelines for blood pressure control goals

A

JNC8 = <140/<90 for nearly everyone

AHA/ACC = <130/<80 for nearly everyone

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14
Q

per ACC/AHA and JNC, what are the (4) first-line medication classes for HTN treatment

A
  • thiazide diuretic
  • calcium channel blocker
  • ACE inhibitor
  • ARB
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15
Q

per ACC/AHA and JNC, what are the (2) best choices for first-line medication class in treatment of HTN in Black adults

A
  • thiazide diuretic

- calcium channel blocker

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16
Q

Per JNC8, what is the (2) best choices for medication class in treatment of HTN in adult with CKD

A
  • ACE inhibitor

- ARB

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17
Q

Initial labs and diagnostics needed for someone with new diagnosis of HTN to facilitate CVD risk profiling, establish a baseline for medication use, and to screen for secondary causes of HTN:

A
  • fasting blood glucose
  • CBC
  • lipids
  • BMP (electrolytes, serum creatinine, eGFR)
  • TSH
  • urinalysis
  • electrocardiogram (ECG – looking for chamber enlargement)
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18
Q

optimal dietary sodium restriction in HTN

A

optimal <1500 mg/day

alternatively, can reduce from current amount by at least 1000mg/day and remove the salt shaker off the table

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19
Q

optimal potassium intake in HTN

A

aim for 3500-5000 mg/day (not supplementation, but total through diet rich in potassium)

adequate potassium can reduce BP!

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20
Q

preferred anti-hypertensive for postmenopausal females with risk for osteoporosis

A

thiazide diuretics (e.g., HCTZ, chlorthalidone)

calcium-sparing diuretics = lower observed rate of fractures in folks who are long-term thiazide diuretic users

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21
Q

HTN diuretic =______

CHF diuretic = _______

A

HTN = thiazides

CHF = loops

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22
Q

thiazide diuretics deplete vs. spare which electrolytes

A

deplete sodium (Na+), potassium (K+) and magnesium (Mg++)

spare calcium (Ca+)

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23
Q

diuretic use and eGFR: thiazides, loops

A

thiazide diuretics preferred for HTN when eGFR >30, however they become ineffective when eGFR <30

once eGFR <30, loop diuretics remain effective

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24
Q

medication class: HCTZ

A

thiazide diuretic

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25
Q

medication class: chlorthalidone

A

thiazide diuretic

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26
Q

medication class: furosemide (Lasix)

A

loop diuretic

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27
Q

medication class: torsemide (Demadex)

A

loop diuretic

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28
Q

which is more potent: HCTZ vs. chlorthalidone

A

chlorthalidone

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29
Q

medication class: lisinopril (Prinivil, Zestril)

A

ACE inhibitor

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30
Q

medication class: enalapril (Vasotec)

A

ACE inhibitor

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31
Q

medication class: losartan (Cozaar)

A

angiotensin receptor blocker (ARB)

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32
Q

medication class: telmisartan (Micardis)

A

angiotensin receptor blocker (ARB)

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33
Q

MOA: thiazide diuretics for HTN ….

  1. HR
  2. SV
  3. PVR
A

reduce peripheral vascular resistance

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34
Q

MOA: ACE inhibitors for HTN…

  1. HR
  2. SV
  3. PVR
A

reduce peripheral vascular resistance

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35
Q

MOA: ARBs for HTN….

  1. HR
  2. SV
  3. PVR
A

reduce peripheral vascular resistance

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36
Q

ACE inhibitors and ARBs increase risk for which electrolyte abnormality

A

hyperkalemia (spare potassium)

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37
Q

priority medication in someone with HTN and comorbid T2DM

A

ACE inhibitors or ARB

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38
Q

angioedema risk in folks using ACE inhibitors

A

<1% of general population

risk factors = Black, Latinx, history of NSAID allergy

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39
Q

risk factors for angioedema with ACE inhibitor use (3)

A
  • NSAID allergy (most potent risk factor)
  • Black
  • Latinx
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40
Q

risk factors for hyperkalemia for someone on an ACE or ARB (4)

A
  • inadequate fluid intake (dehydrated)
  • over-diuresis (dehydrated)
  • renal impairment
  • concurrent use of aldosterone antagonist (aka potassium-sparing diuretic)
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41
Q

medication class: amlodipine (Norvasc)

A

dihydropyridine calcium channel blocker

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42
Q

medication class: diltiazem (Cardiazem)

A

non-dihydropyridine calcium channel blocker

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43
Q

MOA: CCBs for HTN….

  1. HR
  2. SV
  3. PVR
A

reduce peripheral vascular resistance

peripheral vasodilators

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44
Q

edema is more common in [DHP vs. non DHP] calcium channel blockers, avoid use in heart failure or CKD

A

dihydropyridines (e.g., amlodipine)

d/t potent peripheral vasodilators

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45
Q

most potent class of antihypertensives, per Fitzgerald

A

calcium channel blockers

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46
Q

edema in CCBs is dependent on…..

A

dose (use lower doses)

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47
Q

which antihypertensive medications are not a good choice for someone with CHF, CKD, or liver impairment

A

DHP CCBs because they cause edema s/t potent peripheral vasodilation

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48
Q

medication class: atenolol (Tenoretic)

A

beta blocker

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49
Q

medication class: metoprolol (Lopressor)

A

beta blocker

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50
Q

MOA: beta blockers for HTN….

  1. HR
  2. SV
  3. PVR
A

lowers HR and SV

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51
Q

medication class: propanolol (Inderal)

A

beta blocker

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52
Q

medication class: spironolactone (Aldactone)

A

aldosterone antagonist / potassium-sparing diuretic

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53
Q

medication class: eplerenone (Inspra)

A

aldosterone antagonist / potassium-sparing diuretic

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54
Q

(1) cardio-selective beta blocker

A

metoprolol

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55
Q

(2) non-cardioselevtive beta blockers

A

propanolol

nadolol

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56
Q

avoid ______ [cardiac med] in folks with lower airway disease

A

non-cardioselective beta blockers (e.g., propanolol, nadolol)

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57
Q

beta blockers and lower airway disease?

A

avoid beta blockers that are non-cardioselective

cardioselective beta blockers are usually ok in COPD or asthma

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58
Q

priority electrolyte abnormality risk with aldosterone antagonists

A

hyperkalemia

particularly if used with an ACE or ARB

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59
Q

which cardiac medication class can cause gynecomastia with long-term use

A

aldosterone antagonists / potassium-sparing diuretics (e.g., spironolactone)

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60
Q

why are beta blockers not first line for HTN?

A

not that effective

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61
Q

why are aldosterone antagonists not first line for HTN?

A

very effective, but lots of side effects:

  • hyperkalemia
  • volume depletion/excessive diuresis
  • gynecomastia
62
Q

after starting someone on a new HTN medication, when should they come back for fup?

A

1 month

takes 1 mo to see full benefit of that dose of therapy

63
Q

which common cold medication should be avoided in someone with HTN?

A

pseudoephedrine (Sudafed)

s/t vasoconstrictive effects

64
Q

true or false: friends don’t let friends lower BP in clinic with short-acting meds like clonidine

A

TRUE!

don’t want to drop the BP too quickly and risk poor perfusion to the brain

in hypertensive urgency, no indication for immediate in-office BP reduction with short-acting antihypertensive agents such as clonidine, hydralazine, nitroglycerin, etc.

65
Q

hypertensive urgency, aka….

A

asymptomatic elevated blood pressure

66
Q

hypertensive urgency and emergency are both defined by blood pressure higher than….

A

> 180/>120

67
Q

difference between hypertensive urgency and emergency

A

BP >180/>120 in both

however, urgency is asymptomatic

emergency includes symptoms or evidence of impending end organ damage such as visual changes, shortness of breath, grade 3 or 4 retinopathy, S3, tachycardia, distended neck veins (signs of CHF), pulmonary edema

68
Q

intervention for outpatient generalist NP in hypertensive urgency

A

restart or intensify standard antihypertensive therapy

NO indication for referral to ED

NO indication for immediate in-office BP reduction with short-acting antihypertensives

69
Q

intervention for outpatient generalist NP in hypertensive emergency

A

immediate transfer to the ED or ICU admission for careful BP reduction via parenteral medications

70
Q

risks of hypertensive emergency

A
  • intracerebral hemorrhage
  • hypertensive encephalopathy
  • acute ischemic stroke
  • acute MI
  • unstable angina pectoris
  • dissecting aortic aneurysm
  • acute renal failure
  • eclampsia
71
Q

lipid profile can be drawn fasting or non-fasting. however, if triglycerides are >_______, repeat in fasting state

A

TG >400 mg/dL

72
Q

which antihypertensive medication should you prioritize in someone with evidence of LVH

A

ACE or ARB

73
Q

why does she love carvedilol specifically

A
  • beta blocker
  • also has alpha blockade
  • insulin sensitizing
74
Q

components of a lipid panel for screening

A
  • total cholesterol
  • LDL cholesterol
  • HDL cholesterol
  • triglycerides
75
Q

which part of the lipid profile is most affected by fasting vs. non-fasting

A

triglycerides

76
Q

dietary change to reduce lipids

A
  • increase fiber (10-25 g/day) and plant sterols/stanols (2g/day)
  • decrease saturated fats (<7% of total calories)
  • avoid trans fats entirely
  • increase intake of omega-3 fatty acids (e.g., oily fish 2x weekly, flaxseeds, supplement)
77
Q

High vs. Mod vs. Low intensity statin therapy reduces LDL by…..

A
High = 1/2 (50%)
Mod = 1/3 (30-50%)
Low = 1/4 (<30%)
78
Q

there is no clinical indication for ____ intensity statin therapy as first line for anything

A

low

79
Q

who should you be cautious in using a high intensity statin therapy (6)

A
  • adverse effects
  • age >75yo
  • CKD
  • frailty
  • multiple comorbidities
  • concurrent use of a fibrate

THESE ARE THE FOLKS MOST LIKLEY TO DEVELOP RHABDO

80
Q

(2) high intensity statin therapy regimens

A
  • atorvastatin 40-80mg

- rosuvastatin 20-40mg

81
Q

(5) moderate intensity statin therapy regimens

A
  • atorvastatin 10-20mg
  • rosuvastatin 5-10mg
  • simvastatin 20-40mg
  • pravastatin 40-80mg
  • lovastatin 40mg
82
Q

(2) medications no longer recommended for dyslipidemia

A
  • niacin

- resins (e.g., cholestyramine)

83
Q

medication class: simvastatin (Zocor)

A

HMG-CoA reductase inhibitor

84
Q

medication class: atorvastatin (Lipitor)

A

HMG-CoA reductase inhibitor

85
Q

medication class: rosuvastatin (Crestor)

A

HMG-CoA reductase inhibitor

86
Q

medication class: pravastatin (Pravachol)

A

HMG-CoA reductase inhibitor

87
Q

expected effect of HMG-CoA reductase inhibitors on cholesterol

A
  • significant reduction in LDL, as much as 50% or more
  • minor increase in HDL
  • minor decrease in TG
88
Q

check this lab prior to starting a statin for HLD to establish a baseline (don’t need to routinely follow)

A

liver enzymes (AST/ALT)

89
Q

only (3) statins that are CYP 450 3A4 substrates

A

simvastatin, atorvastatin, lovastatin

90
Q

priority side effects of HMG-CoA reductase inhibitors

A

rhabdomyolosis, myositis

rare, but most often noted with higher statin doses and risk factors (e.g., frail elderly)

91
Q

medication class: ezetimibe (Zetia)

A

selective cholesterol absorption inhibitor

only drug in its class!

oral tablet

92
Q

effect of ezetimibe (Zetia) on cholesterol

A
  • modest reduction in LDL up to 20%

- minor increase in HDL

93
Q

side effects of ezetimibe (Zetia)

A

very well-tolerated! few side effects

works at the level of intestinal lumen alone, not really systemic-acting

94
Q

medication class: alirocumab (Praulent)

A

PCSK9
(proprotein convertase subtilisin/kexin type 9)

SC injection only, VERY expensive

95
Q

medication class: evolocumab (Repatha)

A

PCSK9

proprotein convertase subtilisin/kexin type 9

96
Q

effect of PCSK9s on cholesterol

A
  • significant reduction in LDL of 60% or more in folks already on a statin therapy
97
Q

who is a possible candidate for PCSK9s? (2)

A
  • add on to statin therapy in someone with familial hypercholesterolemia
  • clinical ASCVD when goal LDL cannot be met on other therapies
98
Q

effect of omega-3 fatty acids on cholesterol

A
  • up to 30% reduction in TG
  • minor increase in HDL
  • no significant effect on LDL

this is only at the 4g dose

99
Q

prescription strength omega-3 fatty acids

A

4g/day supplement

100
Q

side effects of omega-3 fatty acid supplements

A
  • increased risk of bleeding s/t modest antiplatelet effects
  • GI upset
  • “fishy” taste (this can be minimized by freezing the capsules, taking with food, and avoiding hot beverages after taking)
101
Q

modest increased risk of bleeding with this dyslipidemia medication

A

omega-3 fatty acid supplements

102
Q

medication class: fenofibrate (Tricor)

A

fibric acid derivatives (fibrates)

103
Q

medication class: fenofibric acid (Triplipix)

A

fibric acid derivatives (fibrates)

104
Q

effect of fibrates on cholesterol

A
  • significant increase in HDL by 20%
  • significant reduction in TG by up to 50%
  • minor reduction in LDL
105
Q

side effects of fibrates

A

myopathy, including rhabdomyolysis, particularly if taken with a statin

106
Q

which two cholesterol medications should not be taken together d/t risk for rhabdo

A

statins + fibrates

107
Q

(5) priority medication classes in the treatment of dyslipidemia

A
  • HMG-CoA reductase inhibitors (statins)
  • selective cholesterol absorption inhibitor (ezetimibe)
  • PCSK9s (-mab)
  • omega-3 fatty acids
  • fibrates
108
Q

best cholesterol medications for LDL (3)

A
  • PCSK9s (60% or more reduction if already on statin)
  • statins (up to 50% or more reduction)
  • ezetimibe (up to 20% reduction)
109
Q

best cholesterol medications for HDL (1)

A
  • fibrates (up to 20% increase)
110
Q

best cholesterol medications for triglycerides (2)

A
  • omega-3 fatty acids (up to 30% reduction)

- fibrates (up to 50% reduction)

111
Q

anyone with an LDL of _____, recommend high intensity statin therapy regardless of ASCVD score or presence of other risk factors

A

LDL >190 mg/dL

112
Q

anyone with _______ comorbidity, recommend at least moderate intensity statin therapy regardless of presence of cholesterol levels, ASCVD score, or presence of other risk factors

A

T2DM and ages 40-75yo

113
Q

low risk on ASCVD calculator %

A

<5%

114
Q

borderline risk on ASCVD calculator %

A

5% - 7.5%

115
Q

intermediate risk on ASCVD calculator %

A

7.5% - <20%

116
Q

high risk on ASCVD calculator %

A

20% or higher

117
Q

low risk on ASCVD calculator, recommend….

A

healthy lifestyle

118
Q

borderline risk on ASCVD calculator, recommend….

A

healthy lifestyle

consider moderate intensity statin

119
Q

intermediate risk on ASCVD calculator, recommend….

A

healthy lifestyle

moderate intensity statin

120
Q

high risk on ASCVD calculator, recommend….

A

healthy lifestyle

high intensity statin

121
Q

if risk-decision-making is ever uncertain in dyslipidemia, can consider measuring….

A

coronary artery calcium (CAC) scoring

122
Q

interpretation of CAC scoring results

A

0 = low risk, don’t need to consider a statin unless they also have diabetes, family history of premature CHD, or smoke cigarettes

1 or higher = favors statin therapy, especially after age 55

100+ or 75% percentile = definitively recommends statin therapy

123
Q

normal range triglycerides

A

<150 mg/dL

124
Q

mildly elevated triglycerides range

A

150-199 mg/dL

125
Q

moderately elevated triglycerides range

A

200-999 mg/dL

126
Q

severely elevated triglycerides range

A

1000-1999 mg/dL

127
Q

very severely elevated triglycerides range

A

2000 or higher mg/dL

risk for acute pancreatitis!

128
Q

how high are triglycerides before risk factor for acute pancreatitis

A

> 1000-2000 mg/dL

129
Q

common causes of high trigylcerides

A
  • lifestyles = high carb diet, excess alcohol, sedentary, obesity
  • T2DM, especially with poor glycemic control
  • untreated hypothyroidism
  • some medications (2nd gen antipsychotics, systemic corticosteroids, systemic estrogen, systemic retinoids)
130
Q

recommended treatment for Triglycerides 199-499 mg/dL

A

statin therapy, lifestyle

131
Q

recommended treatment for Triglycerides 500 mg/dL or higher

A

lifestyle, statins, consider omega-3 fatty acids or fibrates

132
Q

at what level do you start to consider adding omega-3 fatty acids or fibrates to statin therapy for someone with elevated TG

A

TG 500 mg/dL or higher

133
Q

lab test that can be used evaluate myositis in someone on statin therapy

A

serum creatinine kinase (CK)

134
Q

INR goal in someone on warfarin therapy for a fib

A

2.0 - 3.0

135
Q

why do almost all antibiotics increase risk of bleeding in someone on warfarin?

A

because warfarin is antagonized by vitamin K

vitamin K is produced by the gut microflora

all antibiotics disrupt the gut microflora

136
Q

for any patient on warfarin, be concerned for increased risk of bleeding if on these other meds:

A
  • all antibiotics (altered gut microflora reduces vitamin K)
  • all NSAIDs (antiplatelet effect)
  • gingko biloba (antiplatelet effect)
137
Q

warfarin + St. Johns Wort

A

St Johns Wort is a CYP450 inducer

will increase metabolism of warfarin

decrease efficacy of warfarin

lowers INR, risk for clots

138
Q

warfarin + antibiotics

A

increased risk for bleeding

altered gut microflora > decreased vitamin K synthesis > increased warfarin effect

139
Q

warfarin + NSAIDs

A

increased risk for bleeding (NSAID antiplatelet effect)

140
Q

warfarin + gingko biloba

A

increased risk for bleeding (antiplatelet effect)

141
Q

(3) triad of symptoms in heart failure

A
  • dyspnea
  • fatigue
  • edema
142
Q

possible physical exam findings suggestive of CHF

A
  • tachycardia
  • increased JVP
  • displaced apex
  • S3 heart sound
  • heart murmur
  • pulmonary crackles
  • dependent edema
143
Q

PMH history suggestive of possible CHF

A
  • previous MI or ACE inhibitor use
  • HTN
  • angina
  • valvular disease or rheumatic heart disease
  • palpitations
144
Q

possible etiologies of CHF (6)

A
  • LV dysfunction (systolic or diastolic)
  • valvular disease
  • congenital heart disease
  • pericardial disease
  • endocardial disease
  • rhythm/conduction disturbance
145
Q

ACC/AHA Stage A heart failure in primary care

A

Stage A = high risk for HF, but without structural heart disease or symptoms of HF

e.g., someone with HTN, DM, obesity, metabolic syndrome, family history

goals of therapy are to prevent ASCVD and LV abnormalities via heart healthy lifestyle, ACEI/ARB, statins prn

can be managed in outpatient primary care NP generalist

146
Q

ACC/AHA Stage B heart failure in primary care

A

Stage B = evidence of structural heart disease but without signs or symptoms of CHF

e.g., patients with a previous MI, LVH, low EF, asymptomatic valvular disease

goals of therapy include preventing HF symptoms and preventing further cardiac remodeling

treatment includes ACI/ARB, beta blockers, statins

ICD, revascularization surgery, or valvular surgery as appropriate

thus, should be co-managed with a specialist (cardiologist)

147
Q

LVH and reduced EF are both examples of….

A

cardiac remodeling (problematic)

148
Q

(3) primary care medications for Stage A and B heart failure

A
  • ACE/ARBs
  • statins
  • beta blockers (minimize risk of sudden cardiac death)
149
Q

role of beta blockers in Stage B heart failure

A

minimize risk of sudden cardiac death (a risk in LVH)

150
Q

ICD in heart failure is used to prevent….

A

sudden cardiac death