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Clin med II Eye and Cardio > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Goals of primary prevention in CAD

A

Maintain or achieve ideal weight

Physical activity

Eat healthy diet

Fruits, vegetables, fiber, low glycemic index, unsaturated fats, omega-3 fatty acids (Mediterranean diet)

Refrain from cigarette smoking (and vaping)

Maintain blood pressure at goal

<140/90 if low risk

<130/80 if risk factors of known CAD

Maintain normal ‘bad’ cholesterol levels (LDL)

Glycemic control in diabetes

High risk patients <70 y/o without bleeding risk, should take aspirin daily (*new guidelines)

Small amount of alcohol consumption (less than 2 drinks/day)

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2
Q

Risk Factors for CAD

A
  • Age >65yrs
  • Gender (male > female until menopause)
  • Cigarette smoking
  • Dyslipidemia (abnormal cholesterol levels)
  • Hypertension (HTN)
  • Abdominal obesity (central obesity)
  • Family history of 1st degree relative with premature MI (men age <55 women <65)
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3
Q

risk factor that is considered a “coronary artery disease equivalent”

A

Diabetes

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4
Q

Define Metabolic Syndrome

A

•Constellation of metabolic abnormalities that confer increased risk of CAD

Three or more of the following

  • Abdominal obesity
  • Triglycerides >150mg/dL
  • HDL <40mg/dl for men and <50mg/dl for women
  • Fasting glucose ≥ 110mg/dL (hyperglycemia/insulin resistance)
  • Hypertension
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5
Q

what artery supplies blood to left ventricle and atrium

A

Left main coronary a.

The left anterior descending artery branches off the left coronary artery and supplies blood to the front of the left

The circumflex artery branches off the left coronary artery and encircles the heart muscle. This artery supplies blood to the outer side and back of the heart.

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6
Q

Which coronary artery supplies blood to the right ventricle, the right atrium, and the SA (sinoatrial) and AV (atrioventricular) nodes

A

Right coronary artery (RCA).

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7
Q

symptoms of chronic stable angina

A
  • Chest discomfort or dyspnea with exertion lasting ~5-15 minutes, predictable & reproducible (due to flow limiting lesion)
  • Relieved by rest and/or nitroglycerin
  • Description of discomfort varies
  • Tightness, squeezing, burning, gas, indigestion or ill characterized
  • Typically located central or slightly left side of chest
  • Pre-syncope (lightheadedness)
  • Fatigue
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8
Q

exclusion criteria for ETT

A
  • ST abnormalities
  • LVH
  • LBBB
  • Vent-paced
  • WPW
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9
Q

when would we include imaging stress tests

A

include imaging if patient has known CAD or multiple risk factors 2

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10
Q

Name types of imaging and nonimaging stress tests

A
  • Non-Imaging Test
    1. Exercise tolerance testing (ETT) (uses treadmill & EKG)

Imaging Tests – include imaging if patient has known CAD or multiple risk factors 2.

  • Echocardiography (exercise or pharmacologic)
  • Radionuclide myocardial perfusion imaging (exercise or pharmacologic)
  • Positron emission tomography (PET) (almost always pharmacologic)
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11
Q

first line stress test for most pts

A

ETT

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12
Q

describe Radionuclide myocardial perfusion imaging

A

Exercise or pharmacologic

Imaging before and after stress

Inject radioactive nucleotide

Poorly perfused areas of the heart do not take up color, localize lesion to coronary artery

Highly sensitive

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13
Q

what test would we use to look for stress induced regional wall motion abnormalities (RWMAs

A

stress echo

to localize lesion to particular coronary artery

Wont contract normally with the rest of the heart

**operator dependent

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14
Q

when would we use Nuclear Medicine PET CT stress test

A

Very sensitive

Very expensive

Best test for obese patients

Not readily available

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15
Q

classif presentation of ACS

A
  • Early morning
  • Substernal chest pressure, “like and elephant sitting on my chest.”
  • Severe
  • Sense of impending doom
  • Radiates to L arm, both arms or jaw
  • Associated shortness of breath, nausea, diaphoresis, lightheadedness
  • Lasts >20min but <1 hr
  • Risk factors
  • Poor exercise tolerance at baseline
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16
Q

3 types of ACS

A
    1. Unstable Angina
    1. Non-ST Elevation Myocardial Infarction (NSTEMI)
    1. ST Elevation Myocardial Infarction (STEMI)
  • **(most serious of the three)
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17
Q

Unstable plaque without plaque rupture is what type of ACS?

What would we see on EKG

A

unstable angina

Ischemic symptoms suggestive of ACS and no elevation of cardiac biomarkers (Troponin).

May or may not have ST depressions or non-specific changes (i.e. T wave inversion).

EKG can be normal

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18
Q

Potentially same manifestations as UA but do have elevated cardiac biomarkers (Troponin) suggestive of myocardial tissue death

sx?

A

NSTEMI

Unstable plaque +/- rupture (incomplete or complete occlusion)

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19
Q

Plaque rupture with complete occlusion

A

STEMI

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20
Q

what are the anterior leads and corresponding artery

A

V2, V3, V4

LAD

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21
Q

what are the left lateral leads

A

I, aVL, V5, V6

Left circumflex a

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22
Q

Name inferior leads and corresponding a.

A

II, III, aVF

Right coronary a.

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23
Q

name right ventricular leads and corresponding a.

A

aVR, V1

Right coronary a

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24
Q

name osterior leads and corresponding a

A

ST depressions in V2-V4

RCA

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25
Q

New LBBB in setting of acute CP is ____ until proven otherwise

A

MI

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26
Q

Recall which patients need urgent coronary artery reperfusion (catheterization and percutaneous intervention)

A
  • Hemodynamic instability or cardiogenic shock
  • Severe left ventricular dysfunction or heart failure
  • Recurrent or persistent rest angina despite intensive medical therapy
  • New or worsening mitral regurgitation
  • Sustained ventricular arrhythmias
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27
Q

Immediate tx of ST elevation in MI

A
  • cute Triage
  • Responsiveness, airway, breathing, and circulation
  • Evidence of systemic hypoperfusion/cardiogenic shock (hypotension, tachycardia, impaired cognition, cool/clammy)
  • Congestive heart failure
  • Ventricular arrhythmias
  • Activate cardiac catheterization lab (cath lab)
  • IV heparin bolus then continuous infusion
  • MONA (morphine, oxygen (if needed), nitrates, aspirin)
  • Oxygen if arterial O2 saturation ≤90% or respiratory distress
  • Consider Glycoprotein IIb/IIIa inhibitors (Eptifibatide- (Integrilin))
  • Percutaneous coronary intervention (PCI) – if available yields highest rates of survival if reperfusion is done within 90min (Door to balloon time). (consider transfer – ?allow 120min)
  • Fibrinolytic therapy if PCI not available
  • Beta-blocker
  • Optimize potassium & magnesium
  • * If patient is found to have severe 3 vessel disease during PCI à will need coronary artery bypass graft surgery (CABG)
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28
Q

All patients with known CAD should be on

A

•Asa, BB, and statin if no contraindications

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29
Q

recognize demand ischemia

A
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30
Q

Describe the pathophysiology of Prinzmetal angina

A

Vascular smooth muscle hyper-reactivity

  • Generally caused by focal spasm of a major coronary artery
  • Results in high grade obstruction
  • Transient myocardial ischemia
  • Occasionally myocardial infarction

Spasm occurs in the absence of oxygen supply/demand mismatch

• Can happen in normal or diseased vessels

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31
Q

clinical features of Prinzmetal angina

A

Angina symptoms at rest

Often between midnight and early morning

Associated with transient (15min) ST segment elevation

Triggered by coronary artery vasospasm

Generally in the absence of high grade coronary artery stenosis

Few if any cardiovascular risk factors

Drug use

Repeat EKG after 15min with total resolution of ST segments

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32
Q

EKG findings in vasospastic angina

A

Repeat EKG after 15min with total resolution of ST segments

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33
Q

tx of vasospastic angina

A

Sublingual nitroglycerin as needed during episodes

Smoking cessation

Long acting nitrates

CCBs

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34
Q

Si/sx of Hypertrophic obstructive cardiomyopathy

A

fatigue, dyspnea, chest pain, palpitations, presyncope or syncope

– Diastolic dysfunction

Myocardial ischemia

Mitral regurgitation

Systolic dysfunction (end-stage)

– Heart failure

Supraventricular and ventricular arrhythmias

Sudden death - most common cause in young people

Teenagers and young adults who collapse and lose consciousness during exercise

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35
Q

PE finding of Hypertrophic obstructive cardiomyopathy

A

Harsh crescendo-decrescendo systolic murmur

– Increase intensity with Valsalva maneuver

– Decrease intensity with squatting

**preload dependent

Hypertrophy of the ventricular septum – Significant left ventricular outflow tract (LVOT) obstruction

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36
Q

how does heart look in hypertrophic obst ructive cardiomyopathy

A

– Hypertrophy of the ventricular septum – Significant left ventricular outflow tract (LVOT) obstruction

Diastolic dysfunction

systolic dys (late-stage)

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37
Q

Takotsubo cardiomyopathy si/sx

A

severe psychological stress

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38
Q

Takotsubo cardiomyopathy PE / EKG findings

A

– Left ventricular apical ballooning

– ST elevation without CAD

dilated cardiomyopathy - impaired systolic function

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39
Q

cause of Chagas dz

A

– Protozoan infection (Trypanosoma cruzi)

Leading cause of DCM in Central and S. America

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40
Q

si/sx chagas dz

A

– Nonspecific EKG abnormalities

– Left ventricular apical aneurysms

•Apex of the heart dilates

– Heart failure

– Arrhythmias & heart blocks (all types)

Thromboembolism (right or left ventricular mural thrombi)

• Pulmonary Embolism

• Cerebrovascular accident (CVA) = stroke

– Chest pain

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41
Q

dilated vs restrictive cardiomyopathy

A

dilated:

Dilatation and impaired contraction of one or both ventricles –

  • Impaired systolic function
  • (Ejection Fraction (EF) <40%

restrictive

Non-dilated ventricles with impaired ventricular filling

Hypertrophy is typically absent (normal wall thickness)

Muscle layers are stiff and reduced stretching

Rigid ventricular walls resulting in diastolic dysfunction

Systolic function usually remains normal à cardiac output is reduced bc total volume in ventricle in diastole is reduced

•EF is preserved

Biatrial enlargement

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42
Q

dilated MC is a systolic / diastolic dysfunction white restrictive CM is systolic / diastolic

A

dilated - systoluc

restrictive - diastolic

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43
Q

dilated MC EF is _____ while in restrictive CM EF is ____.

A

dilated: EF reduced

restrictive EF preserved

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44
Q

common causes of dilated CM

A

1.Idiopathic (most common – often familial/gene mutations LMNA Gene mutations (LaminA/C)

Infections (i.e. viral myocarditis, Chagas disease)

  1. Toxins (drugs, meds, alcohol)
  2. Tachycardia induced CMP 5.
  3. Stress (takotsubo) – sometimes considered “unclassified”
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45
Q

which toxic CM is most common

A

alcohol

46
Q

common causes of restrictive cardiomyopathy

A
  1. Idiopathic – build up of scar tissue, unknown reason *most common
  2. Amyloidosis – build up of abnormal proteins
  3. Radiation exposure
  4. Hemochromatosis – excess iron deposition
  5. Sarcoidosis
47
Q

physiology of hypertrophic obstructive cardiomyopathy

A

Hypertrophy of the ventricular septum – Significant left ventricular outflow tract (LVOT) obstruction

When ventricles contract during normal systole they become hyperdynamic and walls collapse on themselves

More likely to develop obstruction of outflow tract

LV volume is normal or reduced, diastolic dysfunction is usually present

48
Q

treatment plan for hypertrophic obstructive cardiomyopathy

A

Stay hydrated

Restrict intense physical exertion

Medical therapy to treat chest pain and dyspnea

Medical therapy to treat arrhythmias àat risk ventricular arrythmias

•Optimize electrolytes Mg

48
Q

when would we perform alcohol septal ablation or septal myectomy)

A

Hypertrophic obstructive cardiomyopathy (HOCM

Invasive procedures to improve LV outflow tract

  • Do not perform alcohol ablation on patients <21 y/o iscourage in patient’s <40 years à
  • (scar - ↑risk of ventricular arrhythmias)
49
Q

Implantable cardioverter-defibrillator is best therapy for patients w/ HOCM who have either

A
  • survived SCD, have known ventricular arrhythmias
  • or unexplained syncope
49
Q

features of arrhythmogenic right ventricular cardiomyopathy (ARVC/D)

A

Myocardium of right ventricle is replaced by fibrous and/or fibro-fatty tissue

Genetically determined

Sudden cardiac death in young adults (can be exercise induced but not always

Right ventricular function is abnormal with regional akinesias or dyskinesis – part of the wall of the right ventricle is not contracting with the rest of the right ventricle

49
Q

best imaging modality for diagnosis of ARVC/D

A

Cardiac MRI – gold standard à see fibrous deposits within myocardium

50
Q

where would we see

Right ventricular function is abnormal with regional akinesias or dyskinesis – part of the wall of the right ventricle is not contracting with the rest of the right ventricle

A

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

51
Q

Recognize when a cardioverter-defibrillator is indicated for treatment of dilated cardiomyopathy

A
  • Patients with dilated CMP & EF < 35% -
  • Patients with dilated CMP & significant arrhythmia -
  • Patients with dilated CMP & FmHx of sudden death OR known LMNA gene mutation
51
Q

what is considered HTN stage

1

2

crisis

A
51
Q

what is normal BP

A

•Normal Blood Pressure: 140/>90

52
Q

“gold standard” for dx HTN

A

Ambulatory blood pressure monitoring (ABPM)

53
Q

most common cause of secondary HTN

A

rendal disease

54
Q

explain masked vs white coat HTN

A

masked

A blood pressure that is consistently elevated by out-of-office measurements but does not meet the criteria based on office readings.

assoc w/ increase risk of mortality and morbidity

white coat

A blood pressure that is consistently elevated by office readings but does not meet diagnostic criteria for hypertension based on out-of-office readings.

55
Q

dx tx for HTN in CKD

A

ACEs and ARBs have been shown to delay the progress of kidney disease and protects the kidneys

56
Q

tx of HTN in lederly

A

Treatment verse non-treatment

Benefits verse risks

Diuertics

CCBs

ACE

57
Q

tx of HTN in AAs

A

Low plasma renin activity and increased sodium/fluid loading which can make them resistant to ACEs/ ARB

Diuertics

CCBs

58
Q

tx HTN in diabetics

A

Due to renal protective nature of ACEs and ARBs, it is recommended that these should be used for reduction of renal nephropathy

Most often this patient population requires multiple agents (average 3-5) to control their hypertension

59
Q

tx HTN in HF w/ EF <40%

A

Diuretics – helps with fluid maintenance and decreasing pre-load

ACE/ARB – decreases comorbidities and hospitalizations

Beta-blockers – decreases LV remodeling

60
Q

tx of HTN in prior MI

A

Found to reduce size of infarct after an acute MI

b-blockers!!!! A MUST

61
Q

labs evaluating HTN

A

chem 10 - electrolytes and renal function

fasting glucose hemaglobinn A1C

Lipid profile

62
Q

labs evaluating HTN crisis

A

ADD

EKG (LVH)

CBC

TSH

63
Q

what HTN drugs should we NEVER combine

A

ACE + ARB + potassium sparing diuretic - hyperkalemic CRISIS

64
Q

HTN drugs you should never combine

A
  • Alpha OR beta blocker + Clonidine
  • Nifedepine + diuretic synergism
  • Hydralazine + direct acting vasodilators OR Prazosin
  • Diltiazem + Verapamil + Beta-blocker
  • ACE + ARB + Potassium sparing diuretic
65
Q

define resistant HTN

A

Blood pressure remains above goal in spite of the concurrent use of 3 antihypertensive agents of different classes

Rule out secondary causes prior to labeling someone with resistant hypertension

66
Q

clasic triad of medication in reistant htn

A
  • ACE (prils)
  • ARB (sartans)

CCB (amlodipine, Diltiazem, Nifedipine, Verapamil

67
Q

management of resistant HTN

A

Consider using different drug mechanisms and optimize the management of comorbidities

Classic triad of medication:

  • ACE (prils)
  • ARB (sartans)
  • CCB (amlodipine, Diltiazem, Nifedipine, Verapamil)

Potassium sparing diuretics

•Potential to decrease SBP 5-20 mmHg and DBP 5-10 mmHg

Addition of beta-blockers if patient has:

  • CHF
  • CAD

Alpha blockers (-zosin)

68
Q

Malignant Hypertensive is characterized by

A

encephalopathy or nephropathy with accompanying papilledema

69
Q

HTN urgency is most often seen in pts who

A

Most often patients present who are not adherent to their blood pressure regimen

70
Q

tx of HTN urgency

A

Blood pressure must be reduced within a few hours and is not a medical emergency.

Usually this can be treated within the office setting and does not require transfer to a higher level of care

71
Q

define HTN emergency

A

an elevated BP (usually DBP >120 mmHg) with evidence of end-organ damage

72
Q

tx of HTN emergency

A

Required substantial reduction in BP within 1 hour to avoid the risk of severe morbidities or mortality

IV MEDS

Goal is to reduce the pressure by no more the 25% within minutes to 1-2 hours and then towards a level of 160/100 mmHg within 2-6 hours

•Excessive reduction in BP may precipitate coronary, cerebral, or renal ischemia.

73
Q

examples of meds used to tx HTN emergency

A

IV

  • Nitroprusside (Nipride)
  • Nitroglycerin
  • Beta-Blockers (Labetalol or Esmolol)
  • Nicardipine
  • Diuretics
  • Hydralazine
  • Multiple other choices that are less widely used
74
Q

compare good vs bad chlesterol

A

Low-density lipoprotein (LDL) “bad cholesterol”

•Main carrier of cholesterol, deliver to cells

High-density lipoprotein (HDL) “good cholesterol”

  • Acceptor of cholesterol from various tissues
  • 50% protein
75
Q

LDL is removed from system in 2 ways:

A

Receptor- dependent

Binds to cell surface receptors → endocytosis

LDL is enzymatically degraded → chol released into cytoplasm and excreted

Non-receptor-dependent

Ingestion by phagocytic monocytes

Macrophage uptake of LDL in the arterial wall can result in accumulation of insoluble cholesterol ester → formation of foam cells →development of atherosclerosis due to large foam cell deposition next to arterial walls

76
Q

define limits of dyslipidemia in regards to

HDL

LDL

TGs

A
  • LDL >160 mg/dL
  • HDL < 40 mg/dL
  • Triglyceride > 150mg/dL

(all three are independent risk factors for CAD)

77
Q

•Total cholesterol is not a risk factor for heart disease but rather the ratio of plasma___ to plasma ____.

A

LDL to HDL

78
Q

how do we measure LDL

A

•LDL = total cholesterol – HDL – Triglycerides

Friedwald equation

79
Q

primary vs secondary causes of dyslipidemia

A
  • Primary causes
  • Disorders of lipid metabolism (overproduction and/or impaired removal of lipoproteins)
  • Secondary causes
  • Type2 DM
  • Excessive alcohol consumption
  • Cholestatic liver disease
  • Nephrotic syndrome
  • Chronic renal failure
  • Hypothyroidism
  • Cigarette smoking
  • Obesity

Drugs

80
Q

who do we screen for dyslipidemia

A
  • Age; men > 35yrs & women >45yrs (LDL levels increase with age)
  • Men >25yrs with cardiovascular risk factors (more than one RFs, including HTN, tobacco use, or +FMHx or one RF that is severe)
  • Women >35 with cardiovascular risk factors
  • Patients with diabetes
  • Patients with a first degree relative with premature CAD (before 55yrs for men and before 65yrs for women)
81
Q

how often do we screen pts for dyslipidemia

A

every 5 years in patients clearly above therapy threshold.

Every 3 years in patients near threshold.

82
Q

Explain familial dyslipidemia

A
  • Autosomal dominant
  • Strongly link to premature CAD
  • >200 LDL receptor mutations

french canadiana and lebonese

underexpression of LDL R

83
Q

clinical presentation of familial disorders of LDL R

A
  • Xanthomas
  • high LDL
  • FHx
84
Q

first line tx for dyslipidemia

A

lifestyle modifications

Unsaturated fats Decrease cholesterol by upregulating the LDL receptor - removing more LDL

85
Q

name the most commonly used lipid lowering medication anf the ONLY medication to prove positive CV outcomes

A

Statins

86
Q

•All patients with known atherosclerosis (CAD, CVD, PVD) regardless of LDL level should receive ____ therapy

A

statin

87
Q

4 statin benefit groups

A
  • Clinical Atherosclerotic cardiovascular disease (ASCVD)
  • LDL-C ≥190 mg/dL, Age ≥21 years
  • Primary prevention – Diabetes: Age 40-75 years, LDL-C 70-189 mg/dL
  • Primary prevention - No Diabetes: ≥7.5% 10-year ASCVD risk, Age 40-75 years, LDL-C 70-189 mg/dL
88
Q

High Intensity statin therapy lowers LDL on average by ___

A

about 50%

atorvastatin (40-80mg)

Rosuvstatin 20, 40 mg

89
Q

moderate intensity statins lower LDL by approx ____ to ____

A

30-<50%

atorv 10, 20

simvas 20-40

pravas 40,80n

90
Q

pts with an LDL > 190 should be started on

A

high intensity

91
Q

pts w DM and LDL 70-189 should be started on

A

mod intensity

UNLESS ASCVD risk is >7.5% = start on high intesity

92
Q

pts w/ clinical ASCVD should be started on

A

high-intensity

unless >75 moderate

93
Q

pt starting statin therapy complains of severe fatigue and muscle weakness - CK is extremely high

dx

tx

A

Rhabdomyolysis

  • Promptly discontinue the statin
  • Address possibility of rhabdomyolysis with:
  • CK
  • Creatinine –
  • acute kidney injury as myoglobin can deposit onto kidney
  • Urinalysis for myoglobinuria
  • (+) for blood
  • (-) for red cells
94
Q

what labs should we check before initiating statin therapy

A

fasting lipid

ALT

CK

95
Q

other reasons for elevated CK

A

Thyroid disease

Inflammatory myopathies

Polymyalgia Rheumatica (age greater than 50)

Injury/Trauma or excessive exercise

Alcohol misuse/DT’s

Seizures/CVA

Neuropathies/motor neuron dz (GBS,ALS,post-polio syndrome

96
Q

what would we see in UA of pt w Rhabdomyolysis

A

  • myoglobinuria
  • (+) for blood
  • (-) for red cells
97
Q

exosgenous causes of increased statin intolerance

A
  • Erythromycin
  • Cyclosporin
  • HIV retroviral inhibitors
  • Grapefruit juice
  • Combination lipid therapy
  • Fibrates
  • Niacin
98
Q

what could we use

  • In combination with statin, reduces LDL even more
  • May be good alternative to high dose statin (if pts don’t tolerate high dose statin)
A

Cholesterol Absorption Inhibitors

  • Ezetimibe (Zetia) -
  • Inhibits intestinal absorption of cholesterol

monitor LFTs

99
Q

when would we tx increased TGs

A

>500

100
Q

Severe hypertriglyceridemia (levels over 1000 mg/dL) what are we concerned for

A
  • Risk of pancreatitis
  • Fibrates & fish oils

SEE Lipemic blood sample

101
Q

Tx of elevated TGs

A
  • Weight loss in obese patients
  • May reduce TG levels by 22% and increase HDL 9%
  • Aerobic exercise
  • Avoid concentrated sugars
  • Low fat diets coupled with complex carbohydrates reduce LDL and HDL
  • Diet consisting of complex carbs and mono- and polyunsaturated fats probably a good approach.
  • Avoid medications that raise triglyceride levels
  • Strict glycemic control in diabetics
102
Q

pharmacotherapies used to tx elevated TGs

A

unclear if they make a differenc

  • Fish Oil
  • Decreases TG by 15 to 30% o 1 to 2 Grams a day
  • Niacin
  • 15 to 30 % increase in HDL and 20-30 % decrease in TG
  • Lots of side effects, flushing (15 to 50% don’t tolerate; ?Worsens diabetes
  • Titrate very slowly
  • Fibrates
  • 15% increase in HDL and 15-20% reduction in TG
  • Fenofibrate, Gemfibrozil
  • ACCORD showed no differences in primary outcomes, CVD death, all cause death with Fenofibrate
103
Q

define metabolic syndrome

A
  • Perfect “storm” of risk factors for atherogenesis
  • DM, CAD, CVA, NAFLD, CA
  • Pro-inflammatory state
104
Q

how would we Dx metabolic syndrome

A
  • Need 3/5 RF’s to be considered metabolic syndrome
  • Glucose intolerance
  • FBG 100 to 125 mg/dL
  • Hgb A1c 5.7 to 6.4%
  • Elevated Blood pressure
  • SBP > 135
  • DBP > 85
  • Dyslipidemia (Trig and HDL are separate RF’s)
  • Elevated triglyclerides > 150 mg/dL
  • Low HDL <40 mg/dl
  • Elevated apolipoprotein B
  • Central obesity
  • Waist circumference greater than 40 inches in men
  • 35 inches in women
105
Q
A
106
Q

when initiating statin therapy it is important to check

A

baseline LFTs and CK

Clin med II Eye and Cardio (2 decks)

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