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Block 3 - Cardio > Clin Med: Cardio II > Flashcards

Clin Med: Cardio II Flashcards

1
Q

Takotsubo cardiomyopathy mimics…

A

MI, but w/o ischemia

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2
Q

Stress cardiomyopathy: Background

A

Temp heart condition w/ rapid heart muscle weakening following extreme stress

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3
Q

Stress cardiomyopathy: pathophys

A

Catecholamines released during stress affect the myocardium of the heart

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4
Q

Examples of severe emotional stress

A
  • death of loved one
  • divorce
  • breakup
  • losing job, home, money
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5
Q

Examples of severe physical stress (5)

A
  • severe pain
  • running marathon
  • asthma attack
  • stroke
  • surgery
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6
Q

Stress cardiomyopathy is more prevalent in which gender?

A

female

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7
Q

Stress cardiomyopathy: S/S

A
  • angina
  • diaphoresis
  • nausea
  • vomiting
  • dyspnea
  • palpitations
  • decr BP
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8
Q

Stress cardiomyopathy: Dx

A
  • Hx of stressful, emotional, or physical event
  • EKG (ST elevation or T wave inversion)
  • Blood test (Troponin & cardiac enzymes typically normal vs MI)
  • Coronary angiogram (no obstruction)
  • Ventriculography (LV Gram) & Echo (ballooning of LV w/ unusual muscle wall movement)
  • Cardiac MRI
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9
Q

Stress cardiomyopathy: Tx

A
  • usually resolves w/ med management
  • ACE inhibitors (control BP)
  • Beta blockers (regulate HR)
  • Diuretics (maintain fluid balance)
  • Anti-anxiety meds & stress management techniques
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10
Q

Cardiac muscle contraction is dependent on…

A
  • Na+
  • K+
  • Ca++
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11
Q

3 general categories of dysrhythmias

A
  • Slow
  • Fast
  • Other
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12
Q

Sinus bradycardia: Hx

A
  • Syncope
  • Dizziness
  • Lightheadedness
  • Chest pain
  • Shortness of breath
  • Exercise intolerance
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13
Q

Sinus bradycardia can be normal in which people?

A

athletes

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14
Q

Rate for Sinus bradycardia

A

< 60bpm

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15
Q

What can causes Sinus bradycardia?

A
  • hypothermia
  • hypothyroidism
  • drugs (beta blockers, Ca++ channel blockers)
  • myocarditis,
  • hypoglycemia
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16
Q

Sinus bradycardia: Hx

A
  • Syncope
  • Dizziness
  • Lightheadedness
  • Chest pain
  • SOB
  • Exercise intolerance
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17
Q

In pts w/ sinus bradycardia what should you ask about?

A
  • Cardiac history (MI, CHF, valve dz)
  • Meds, Toxic exposures
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18
Q

Sinus bradycardia: PE

A
  • Will depend on underlying cause & severity
  • Decr LOC
  • Cyanosis
  • Peripheral edema
  • Dyspnea
  • Syncope
  • Mottled skin
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19
Q

Which pts do we usually see heart blocks in ?

A

elderly patients

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20
Q

Sinus bradycardia: Dx Labs/imaging

A
  • EKG
  • Electrolytes (Na+, K+, Ca++, Mg++)
  • Glucose
  • Thyroid Function Test
  • Toxicology screens
  • Troponin
  • Others based on probable underlying cause
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21
Q

What is troponin?

A

cardiac enzyme that is elevated when heart muscle has died due to lack of O2 (MI)

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22
Q

Sinus Bradycardia: Tx

A
  • Treat underlying cause, but do not delay care
  • Atropine
  • Transcutaneous pacing
  • Transvenous pacing
    **Expert consult
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23
Q

What is the main med used for Sinus bradycardia?

A

Atropine

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24
Q

How does atropine work?

A

binds to & inhibitors muscarinic receptors–> producing wide range of anticholinergic effects–> increases HR

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25
Q

Define a heart block

A

term for arrhythmia where there is a delay or “block” somewhere along the conduction system

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26
Q

Why do heart blocks occur?

A

Usually occur as a result of damage to the conduction system (fibrosis, ischemia), but often idiopathic

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27
Q

Where is the signal delayed in a 1st degree AV block?

A

AV node

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28
Q

What is the PR interval in a 1st degree AV block?

A

> 200ms

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29
Q

How does the pt usually present w/ 1st degree AV block

A

asymptomatic & found incidentally

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30
Q

Does a 1st degree AV block require tx?

A

not usually unless underlying cause (i.e. electrolyte imbalance or due to meds)

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31
Q

Other names for 2nd degree Type I heart block

A
  • Mobitz Type I
  • Wenckebach
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32
Q

NOTE

A

2nd degree: Type I has a consistent P:QRS ratio

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33
Q

2nd degree Type I is often transient, but may occur due to…

A
  • myocardial ischemia
  • myocarditis
  • cardiac surg
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34
Q

Describe a 2nd degree Type I

A

Progressive lengthening of the PR interval until a QRS is dropped

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35
Q

When does 2nd degree Type I need tx?

A

doesn’t need treatment unless symptomatic

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36
Q

2nd degree Mobitz Type I: Tx

A

Atropine

only if symptomatic

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37
Q

Describe PR interval & QRS complex for 2nd degree Type II heart block.

A
  • PR interval consistent
  • Intermittent dropped QRS complexes (may be fixed)
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38
Q

2nd degree Type II heart block usually due to…

A
  • ischemia–> damage to the conducting system
  • Lyme Dz
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39
Q

3rd degree heart block aka…

A

complete heart block

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40
Q

3 degree heart block: Tx

A
  • required transcutaneous pacing STAT
  • transvenous cardiac pacing
  • some will req permanent cardiac pacing
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41
Q

A 3rd degree heart block is…

A

total block b/t atria & ventricles

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42
Q

3rd degree heart block: S/S

A
  • fatigue
  • chest pain
  • SOB
  • dyspnea
  • may be hemodynamically unstable
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43
Q

Describe sinus tachycardia.

A

regular narrow-complex tachycardia

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44
Q

Describe P wave and QRS complex for Sinus Tachycardia.

A
  • P wave is before every QRS

may be hard to see if fast

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45
Q

Sinus tachycardia: HR

A

> 100 in adults (peds depends on age)

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46
Q

Sinus Tachycardia: almost always due to…

A

some underlying issue

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47
Q

Sinus Tach: other common cause (10)

A
  • exercise
  • pain
  • fever
  • hyperthyroidism
  • HF
  • anemia
  • alcohol withdrawal
  • drug use
  • caffeine
  • dehydration
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48
Q

Sinus Tach: Tx

A

treat underlying issue

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49
Q

AVNRT is a type of…

A

supraventricular tachycardia

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50
Q

Describe AVNRT

A

regular, narrow tachycardia

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51
Q

AVNRT Rate

A

170 - 180
can be as high as 300

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52
Q

AVNRT: S/S

A
  • palpitations**
  • lightheadedness
  • dyspnea
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53
Q

AVNRT is most common in which gender?

A

females

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54
Q

AVNRT: Stepwise tx

A

vagal maneuvers–> adenosine–> BB–> cardioversion

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55
Q

Which “A” drug is used for AVNRT?

A

adenosine

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56
Q

Atrial flutter: Rate

A

300 -400

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57
Q

Atrial flutter pattern?

A

saw tooth pattern w/ narrow QRS

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58
Q

Atrial flutter: S/S

A

asymptomatic or have palpitations/lightheadedness

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59
Q

Atrial flutter: Tx if stable

A

rate control w/ diltiazem or verapamil

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60
Q

Atrial flutter: Tx if unstable

A

anticoagulation & cardioversion

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61
Q

What is Afib & cause?

A

a common supraventricular tachyarrhythmia caused by uncoordinated atrial activation & associated w/ an irregularly irregular ventricular response

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62
Q

Most common arrhythmia that is considered as irregularly irregular?

A

Afib

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63
Q

NOTE

A

Afib is a MAJOR preventable cause of stroke

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64
Q

Define persistent AF

A

AF that fails to self-terminate w/n 7 days.
- Often req pharmacologic or electrical cardioversion to restore sinus rhythm.

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65
Q

Categories of Afib

A
  • Paroxysmal AF
  • Persistent AF
  • Long-standing persistent AF
  • Permanent AF
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66
Q

Define paroxysmal AF

A

AF that terminates spontaneously or w/ intervention w/n 7 days of onset. Episodes may recur w/ variable frequency.

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67
Q

Define long-standing persistent AF

A

AF that has lasted >12mo

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68
Q

NOTE

A

While a pt who has had persistent AF can have later episodes of paroxysmal AF, AF is generally considered a progressive disease.

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69
Q

Define permanent AF

A

used to identify ppl w/ persistent Afib where a joint decision by the pt & clinician has been made to no longer pursue a rhythm control strategy.

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70
Q

Describe prevalence of Afib

A
  • 1-2% of gen pop
  • 9% is > 65yo
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71
Q

Most common 2ndary causes for AFib

A
  • HTN
  • CAD
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72
Q

Afib: pathophys

A

several reentrant circles in the atria that causes random signals to get through to the ventricles which usually have a normal rate

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73
Q

Afib: Hx-S/S

A
  • usually firstly asymptomatic

S/S
- palpitations
- SOB
- lightheadedness/dizziness
- focal neurological deficit (embolic stroke)**

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74
Q

Afib: PE

A
  • Irregularly irregular HR
  • may have evidence of HF
  • Evidence of underlying issues (hyperthyroidism, etc)
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75
Q

Afib: Dx labs/imaging

A
  • EKG
  • TTE or TEE
  • TSH
  • Check for suspected underlying conditions
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76
Q

What fraction of pts w/ new onset Afib will spontaneously revert to NSR w/o need for cardioversion?

A

2/3

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77
Q

New Onset Unstable Afib: Tx

A
  • IV BB (esmolol, propranolol, metoprolol) or CCB (diltiazem or verapamil)
  • Heparin
  • Electrical cardioversion if severe HTN, pulmonary edema, ischemia*
  • Admit
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78
Q

If patient has new onset AFib, what is the first line tx?

A

electrical cardioversion

79
Q

New Onset stable Afib: Tx

A
  • Rate control (BB or CCB) IV or PO
  • Anticoagulation
  • Cardioversion (only after TTE shows no thrombus. If thrombus, anticoagulated for 4 weeks prior to cardioversion)
80
Q

Chronic Afib: Rate control Tx

A
  • BB or CCB
  • Goal- resting heart rate of <80 in symptomatic patients
81
Q

Chronic Afib: Anticoagulation Tx

A
  • Depends on CHAD score (if >2, anticoag recommended)
  • DOAC’s for most pts
82
Q

When should Warfarin be used in those w/ chronic Afib?

A

if mechanical heart valve, rheumatic heart disease, can’t tolerate DOAC b/c severe chronic kidney disease

83
Q

Chronic Afib: Rhythm Tx

A

If symptoms and/or Afib persist despite rate control: cardioversion and/or ablation

84
Q

What is happening during PVCs?

A

ventricular “irritability” causes a beat (or several beats) that originate in the ventricle (ectopic foci)

85
Q

PVCs are caused by:

A
  • Epi released by the adrenal glands
  • Caffeine, amphetamines, cocaine, beta 1 receptor agonists
  • Alcohol
  • Hyperthyroidism
  • Low O2
  • Hypokalemia
86
Q

Do PVCs req tx?

A

usually SL

87
Q

PVCs are usually followed by a….

A

compensatory pause

88
Q

What is ventricular tachycardia?

A

a “run” of PVC’s
- wide, monomorphic tachycardia

89
Q

Variable presentations of VTach

A
  • non-sustained (3-30 in a row) or sustained
  • pulse or pulseless
  • pts may be stable or cardiac arrest
90
Q

Which type of VTach can be shocked via defibrillation?

A

Pulseless VTach

91
Q

Non sustained VTach: S/S

A

~ May have w/ lightheadedness or palpitations

  • May be asymptomatic & discovered incidentally
92
Q

How do you evaluate for non sustained VTach?

A

Look for underlying heart dz
- Hx/Physical
- EKG
- TTE
- Exercise stress testing
- Holter monitor

93
Q

Non sustained VTach: Tx

A

asymptomatic & no heart dz: no Tx

symptomatic & no heart dz: rate control (BB) or ablation

asymptomatic or symptomatic WITH heart dz: evaluate & treat underlying dz

94
Q

Sustained VTach: RFs

A
  • CAD (most common)
  • Cardiomyopathies
  • Cardiac sarcoidosis
95
Q

Sustained VTach usually causes…

A
  • cardiac arrest if untreated

may have
- SOB
- chest pain
- palpitations
-syncope

96
Q

Stable sustained VTach: Tx

A

Procainamide

not common

97
Q

Stable, but compromised (hypotension, AMS, chest) sustained VTach: Tx

A

cardioversion w/ sedation if possible

98
Q

Sustained VTach leading to cardiac arrest: Tx

A
  • chest compressions
  • Defibrillation
    –> Epinephrine or Amiodarone
99
Q

Chronic/recurring sustained VTach: Tx

A
  • treat underlying heart dz
  • catheter ablation
  • implantable cardioverter defibrillator
100
Q

Polymorphic ventricular VTach aka…

A

Torsades de Pointe

101
Q

Describe Torsades de Pointe.

A

Shape of contractions from each beat changes as signal begins in different areas of ventricles

Usually a sequalae of Long QT Syndrome

102
Q

Torsades de Pointe: Tx

A
  • Stop any causative agents
  • Fix underlying electrolyte abnormalities
  • IV magnesium sulfate***
  • Temporary pacing
103
Q

What is long QT syndrome?

A

having a QT interval longer than normal

104
Q

What causes acquired long QT syndrome?

A
  • Drugs (some anti infectives, anti psychotics, anti emetics)
  • Electrolyte abnormalities (hypoCa++, hypoMg++, hypoK+)
  • Starvation states (anorexia nervosa)
105
Q

What causes congenital long QT syndrome?

A
  • Genetics
  • > in females
  • First manifestations is 14 years old
  • Should avoid any QT prolonging drugs
  • High risk pts may get ICD, & tx chronically w/ BB
106
Q

Describe VFib.

A

“bag of worms”

  • can lead to sudden cardiac death in mins
  • uncoordinated ventricular contraction
  • each wave on EKG goes w/ a different part of ventricle contracting
107
Q

What are the two shockable rhythms?

A

VFib
Pulseless VTach

108
Q

VFib usually occurs during a…

A

MI

109
Q

What should you do if VFib leads to no pulse?

A

start CPR immediately

110
Q

VFib: Tx

A
  • defibrillation
  • epi
  • amiodarone or lidocaine
111
Q

CAD refers to

A

a spectrum of conditions that causes decreased blood flow to the myocardium

112
Q

What is the spectrum (S/S) of CAD

A

asymptomatic–> stable angina–> unstable angina–> NSTEMI–> STEMI

113
Q

Why do symptoms range so widely for CAD?

A

varying degrees of atherosclerosis (plaque buildup)

114
Q

NOTE

A

CAD is most common heart dz
In the US, someone has a MI every 40secs

115
Q

About how many adults (>/= 20) have CAD?

A

18.2 million

116
Q

Every year, how many Americans have a MI?

A

805,000

117
Q

CAD: Modifiable RFs

A
  • Tobacco exposure
  • Physical inactivity
  • Overweight/obesity
  • HTN
  • Dyslipidemia
  • DM
  • Metabolic Syndrome
118
Q

Metabolic Syndrome includes…

A

HTN + Obesity + DM + dyslipidemia

119
Q

CAD: Non-modifiable RFs

A
  • FHx (under 55yo) of CAD or HLD
  • Sex (M>F)
120
Q

Atherosclerosis: pathophys

A
  • chronic inflammation disorder of medium & large arteries
  • buildup of plaques w/n artery lumen
  • inflammatory response to endothelial cell injury
121
Q

Describe Inflammatory response to endothelial cell injury for atherosclerosis

A
  • Injury due to endothelial stress (HTN, smoking, DM)
  • LDL particles leak into the intimal layer, are oxidized
  • Immune response (macrophages) leads to inflammation
  • Leads to a “fatty streak” in the lumen
  • Platelets adhere to the fatty streak & release growth factors
  • Leads to development a plaque that can enlarge & rupture
  • If rupture, more platelets adhere, forming a thrombus, which can occlude the vessel
122
Q

Conditions that can accelerate progression of atherosclerosis

A
  • male gender (women after meno)
  • FHx
  • Primary & 2ndary HLD
  • Smoking
  • HTN
  • DM
  • Obesity
  • Nephrotic syndrome
  • Hypothyroidism
  • High Lipoprotein
  • Elevated plasma homocysteine
123
Q

Who has an atypical presentation of Stable angina?

A

DM pts & women

124
Q

Stable angina: Hx

A
  • chest pain w/ activity & relieved by rest
  • tightness, squeezing, burning, “gas,” indigestion
  • Pain behind or slightly to left of midsternum w/ poss. radiation to the left shoulder, upper arm, jaw, back
  • > 30 minutes duration
  • Pain relieved w/ nitroglycerin and/or rest
125
Q

Stable angina: Physical

A
  • elevated BP
  • signs of underlying dz/RFs for cardiac ischemia
  • Diaphoresis
126
Q

Stable Angina Pectoris

A

Primarily a clinical diagnosis

127
Q

What should the workup include for stable angina?

A
  • Labs: look for underlying issues (lipids, kidney disease)
  • EKG will be normal at rest
  • EKG may show ST segment changes during activity
  • Pts w/ low probability of CAD -> noninvasive stress test
  • For pts w/ high probability CAD -> cardiac cath
128
Q

Stable angina: Anti anginal therapy

A
  • Acute: short acting nitrates (nitroglycerin)
  • Prevent: Beta blockers
  • If >70% stenosis in 1 vessel, coronary artery revascularization
129
Q

How to prevent dz progression of stable angina?

A
  • Anti platelet therapy (ASA–> aspirin or clopidogrel if allergic)
  • Lipid lowering therapy
  • ACEI/ARB if diabetic or CKD (chronic kidney dz)
130
Q

When should you follow up w/ stable angina?

A

6-12 months, sooner if symptoms change

131
Q

What is unstable angina?

A

pain during activity & at rest

132
Q

Unstable angina is usually due to…

A

a ruptured plaque meaning less room for blood flow leading to areas of myocardium ischemia

133
Q

Unstable angina has a high risk of progressing to a

A

MI

134
Q

NOTE

A

Unstable angina is not distinguishable from NSTEMI until cardiac enzymes are obtained

135
Q

Unstable Angina: Hx

A
  • Chest pain at rest or does not improve w/ rest
  • Pain described similarly to stable angina
136
Q

Unstable Angina: Physical

A
  • Levine sign
  • VS variable
137
Q

Workup for Unstable Angina

A
  • EKG (poss ST segment changes)
  • Cardiac enzymes (NEGATIVE) x2
  • If stable, may be observed for 24-48 hours, then stress test
  • If unstable (or high risk), may have immediate cardiac cath w/ PCI
138
Q

Acute Unstable Angina: Tx

A
  • ASA (aspirin)
  • Antiplatelet therapy (P2Y12 Inhibitor) (Plavix)
  • Anticoagulation
    –>heparin (if invasive therapy)
    –> LMWH (if noninvasive therapy)
  • Cardiology consult
  • Likely cardiac cath w or w/o PCI
    (percutaneous coronary intervention)
139
Q

Ongoing Unstable Angina: Tx

A
  • ASA
  • Antiplatelet therapy
  • Nitroglycerin
  • BB & ACEI
  • Lipid reduction
  • Glucose control
140
Q

NSTEMI stands for

A

Non-ST Elevation Myocardial Infarction

141
Q

Describe a NSTEMI

A

Unstable Angina w/ elevated cardiac enzymes
NO ST elevations on EKG (will likely have ST segment depression)

142
Q

NSTEMI: Tx

A

Consult cardiology
- Treated like STEMI (not quite the same urgency)
- PCI is preferred tx

143
Q

What is a STEMI?

A

ST elevation MI

144
Q

STEMI: median age

A

68 years

145
Q

STEMI: gender prevelance

A

male>female

146
Q

STEMI: RFs

A
  • prior MI
  • CAD
  • Cocaine uses
147
Q

STEMI: Pathophys

A
148
Q

STEMI: Hx Typical

A
  • pain starts in retrosternal area & may radiate to 1 or both arms, neck, or jaw
  • occurs at rest or w/ minimal exertion
  • ≥ 10 mins in duration
  • may be new-onset angina or angina w/ incr intensity
  • unrelieved w/n < 5 minutes of rest or nitroglycerin
149
Q

STEMI: Hx Atypical

A
  • arm
  • shoulder
  • back
  • neck
  • jaw
  • epigastric

seen in women, DM & every elderly pts

150
Q

STEMI: Hx anginal equivalents

A
  • new-onset or incr exertional dyspnea (most common)
  • nausea
  • vomiting
  • diaphoresis
  • abdominal pain
  • syncope
  • unexplained fatigue
151
Q

STEMI: Physical

A

~ bradycardia or tachycardia
- JVD indicates right atrial HTN
- Soft heart sounds indicate left ventricular dysfunction
- S4 common
- Mitral regurg due to papillary muscle dysfunction
- Cyanosis
- Decr peripheral pulses

152
Q

STEMI: Dx labs/imaging

A
  • EKG (w/n 10 mins of pt arrival)
    –>Repeat @ 15min intervals if non-dx
  • Cardiac biomarkers
    –>Troponin (preferably high sensitivity)
  • Other tests (to aid in evaluation and treatment)
    –> CXR
    –> Echo
    –> PT/PTT/INR
    –> BNP
153
Q

STEMI: Tx

A
  • PCI w/n 90 mins of arrival if available
  • PCI w/n 120 mins of arrival if transfer needed
  • If PCI unavailable w/n 120 mins, pharmacologic reperfusion (fibrinolysis) w/ plans for PCI ASAP
154
Q

What should be given to any patent presenting w/ chest chain & could be having a heart attack?

A

MONA

  • morphine
  • O2 (some pts)
  • Nitroglycerin
  • Aspirin (chewable 325mg)
155
Q

Ongoing treatment after STEMI

A
  • ASA (aspirin)
  • Antiplatelet therapy (Plavix)
  • Nitroglycerin
  • BB & ACEI
  • Lipid reduction
  • Glucose control
  • Evaluate EF w/ echo
  • Stress test–> look for residual ischemia
156
Q

Prinzmetal angina aka

A

Vasospastic angina

157
Q

What is Prinzmetal Angina?

A

Chest pain that occurs at rest & is associated w/ transient ST segment elevation

158
Q

Prinzmetal Angina is caused by…

A
  • focal spasm of the coronary artery
  • Unclear pathophysiology
159
Q

Prinzmetal Angina is usually seen in…

A

younger pts w/ fewer RFs

160
Q

Prinzmetal Angina: Dx

A

Coronary angiography
(acetylcholine given to provoke spasm)

161
Q

Prinzmetal Angina: Tx

A

nitrates & CCB

162
Q

How long does Prinzmetal Angina usually last before it resolves?

A

6 months

163
Q

What two scoring methods are used for chest pain?

A

TIMI & Heart score

164
Q

What does the TIMI score do?

A

estimates mortality for pts w/ unstable angina & STEMI

165
Q

What does the heart score do?

A

6wk risk of having a major cardiac event (used on every pt)

166
Q

Two types of lipids in the blood?

A
  • cholesterol
  • triglycerides
167
Q

What does cholesterol do in the body?

A

backbone of a lot of hormones

168
Q

What does triglyceride do in the body?

A

transfer energy from food s into the cells

169
Q

Lipids are carried throughout the body on…

A

lipoproteins

170
Q

What are the density classifications of lipids?

A
  • HDL
  • LDL
  • Very low-density lipoprotein
171
Q

Higher LDL means what related to CAD

A

higher risk of CAD

172
Q

Higher HDL means what related to CAD?

A

lower risk of CAD

173
Q

Higher levels of VLDL means what related to CAD?

A

higher risk of CAD

174
Q

What are the functions of cholesterol?

A
  • Cell membrane structure
  • Precursor to steroid hormones, bile acids, & Vit D
175
Q

What do triglycerides do?

A

store fat for energy

176
Q

What are lipid disorders?

A

Disorders of lipoprotein metabolism
- clinical disorders associated w/ abnormal levels of total, HDL, & LDL cholesterol, as well as triglycerides

177
Q

What is dyslipidemia?

A

Used for lipid values that are associated w/ dz or incr risk of dz & for which lipid-altering therapy might be of value.

178
Q

What is hyperlipidemia?

A

Elevation of serum total, LDL cholesterol or triglyceride.

179
Q

High cholesterol affects what percentage of adults in the US?

A

35%

180
Q

RFs for Lipid disorders?

A
  • FHx
  • Type II DM
  • older age
  • male
  • overweight or obesity
181
Q

Lipid Disorders:
AHA/ACC screening

A
  • repeat every 5 years if no RFs
  • more often w/ RFs (1-2 yrs)
182
Q

Lipid Disorders: AAP screening

A

Age 9-11 yo
Age 2-9 if high risk
–> immediate family have had MIs or have been dx w/ blocked arteries or stroke, at age </=55yo in men, or </= 65yo in women
–> immediate family have total blood cholesterol levels of >/= 240
–> Those whose family health background is not known

183
Q

Lipid disorders: Hx

A
  • Usually asymptomatic
  • Ask about:
    –> FHx
    –> Activity levels
    –> Medication use (progestins, steroids can incr)
    –> Diet
184
Q

Lipid disorders: PE

A
  • Usually unremarkable
  • May develop xanthomas if extremely high triglycerides
185
Q

Lipid disorders: Dx/Labs

A

Lipid profile (FASTING)
- HDL
- LDL
- Triglycerides
- VLDL

186
Q

People who would benefit form statin therapy?

A
  • Pts w/ any form of clinical ASCVD
187
Q

All patients w/ elevated lipids should be counseled on…

A

lifestyle changes

188
Q

Lipid disorders: Medications

A
  • Statins (atorvastatin, etc.)
  • Ezetimibe
  • Bempedoic
189
Q

Hypertriglyceridemia: serum triglycerides above 150mg/dL would benefit from what meds?

A
  • Statins
  • Fibrates
190
Q

STUDY SLIDE 10 in Cardio III

A

10 mins

191
Q

What is familial hypercholesterolemia?

A

an inherited disorder of low-density lipoprotein cholesterol metabolism

192
Q

What things can suggest familial hypocholesteremia?

A
  • FHx
  • Early onset (<50)
  • Extreme hypocholesteremia
193
Q

What should be done in children: have measurable atherosclerosis by age 12..

A
  • begin meds around age 8
  • expert consult (pediatric Cardiologist)

Block 3 - Cardio (13 decks)

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