Cardio Part 2

Front 1

2 features of chylomicrons:

Back 1

1. huge

2. least dense

Front 2

lipoproteins =

(3 parts)

Back 2

polar coat + apoproteins on surface + lipid core

Front 3

why do we need lipoproteins?

(2)

Back 3

they carry insoluble lipids through blood

- also zip codes for cellular receptors

Front 4

3 benefits of lowering LDL:

Back 4

1. may slow progression of, stabilize, or reverse athero

2. improves endo cell function and reduces inflammation of vessel walls

3. reduces MI and death

Front 5

dyslipidemia =

Back 5

abnormal amount of lipids

Front 6

2 approaches to lowering lipids:

Back 6

1. diet + exercise

2. drugs

Front 7

effect of diet and exercise on lipid levels:

Back 7

not great

10-20% at best

Front 8

3 kinds of w3's:

Back 8

ALA, EPA, DHA

Front 9

**there is no evidence that w3's have:**

Back 9

cardioprotective effects

- in fact, they *raise LDL*

Front 10

if w3's don't have cardioprotective effects, why are they recommended?

Back 10

they increase LDL size from small, atherogenic particles to large, non-athero ones

Front 11

w3's also have other beneficial effects:

(2)

Back 11

1. reduce HTN

2. reduce TG's

Front 12

Lovaza and other OTC w3's lower:

Back 12

TG's,

NOT LDL

- do NOT prescribe them

Front 13

4 classes of lipid-lowering drugs:

Back 13

1. statins

2. Bile Acid Sequestrants

3. Nicotinic acid/Vit B3

4. Fibric acid derivatives

Front 14

what are statins?

Back 14

HMG-CoA reductase inhibitors

Front 15

what does HMG-CoA reductase do?

Back 15

the rate-limiting enzyme that converts acetyl CoA to cholesterol

Front 16

inhibiting HMG =>

Back 16

dec. chol synth => Inc. LDL receptors on liver => dec. LDL in blood by 20-50%

Front 17

statins are contraindicated in:

Back 17

liver disease/prob's

Front 18

statins DON'T affect:

Back 18

TG's or HDL

Front 19

most potent statin =

Back 19

Rosuvastatin

Front 20

SE's of statins:

(2)

Back 20

1. inc. transaminases

2. rhabdomyolysis

Front 21

the transaminases are:

Back 21

ALT, AST

Front 22

discontinue statin therapy if:

Back 22

transaminases inc. by >3x normal

Front 23

rhabdomyolysis =

Back 23

muscle pain/weakness with inc. CPK

- use CoQ

Front 24

rhabdomyolysis occurs more frequently if:

Back 24

combos of different lipid drug classes are used

Front 25

2 targets of Simvastatin (Zocor):

Back 25

1. CYP3A4

2. liver


**same targets for Atorvastatin (Lipitor)

Front 26

2 targets of Pravastatin (Pravachol) =

Back 26

1. non-CYP

2. 50/50 liver/renal

Front 27

2 targets of Rosuvastatin (Crestor) =

Back 27

1. CYP2C9/19

2. liver

Front 28

bile acids are composed of:

Back 28

cholesterol

- normally, 40-70% of bile acids are reabsorbed back to liver

Front 29

bile acid sequestrants =

Back 29

2nd-line therapy that inhibit BA reabsorption

=> excreted

(also cause inc. in liver LDL r's)

Front 30

result of BA's being excreted due to BAS's:

Back 30

LDL taken out of blood to make more cholesterol to make more BA's

Front 31

BAS's are given when:

Back 31

1. you can't give statins (teratogen - not for preg)

2. statins are ineffective

Front 32

BAS's are frequently given in combo with ___________, to _________________________________________

Back 32

statins, to pts with familial hypercholesteremia

Front 33

BSA's lower LDL by:

Back 33

10-20%

- however, it's partially countered by a compensatory inc. in HMG-CoA reductase activity

Front 34

3 types of BAS's:

Back 34

1. cholestyramine

2. colestipol

3. colesevelam

Front 35

SE's of BAS's:

(4)

Back 35

1. similar to cholestectomy

2. GI prob's

3. interference with absorption of ADEk

4. may interfere with absorption of meds (heparin, digitalis, aspirin)

Front 36

nicotinic acid/niacin/B3 is a:

Back 36

2nd or 3rd-line therapy for LDL, but

a 1st-line therapy for inc. HDL and dec. TG

Front 37

how does Vit B3 lower LDL?

Back 37

blocks FFA disperal from adipose to liver => dec. TG's made in liver => dec. VLDL => dec. LDL

Front 38

**Vit B3 is currently the most effective drug on the market to:**

Back 38

raise HDL (15-35%)

Front 39

most pertinent SE of Vit B3 =

Back 39

hot flushes

Front 40

Vit B3 = ___________ in animals

Back 40

*teratogen*

- DON'T give to pregnant women at high levels

Front 41

Niaspan =

Back 41

programmed-release version of niacin

=> less flushing, better tolerance

Front 42

fibric acid derivatives are are a 1st-line therapy for:

Back 42

decreasing TG's

- 2nd-line for inc. HDL, dec. LDL

Front 43

FAD's are used for pts with either:

Back 43

1. low HDL

or

2. high TG's

Front 44

only two FAD's =

Back 44

1. Gemfibrozil (Lopid)

2. Tricor

Front 45

Gemfibrozil should be avoided in people with:

Back 45

hepatic or renal dysfunction

Front 46

Tricor is only for pts with:

Back 46

severe hyperTG in pts at risk for pancreatitis

Front 47

SE's of FAD's =

(2)

Back 47

1. GI disorders

2. skin rxns

Front 48

**FAD's are NOT used used ___________, b/c together they cause _______________________

Back 48

statins;

inc. risk of rhabdomyolysis

Front 49

new classes of lipid-lowering drugs include:

(2)

Back 49

1. Ezetimibe (Zetia)

2. Mipomersen (Kynamoro)

Front 50

Ezetimibe (Zetia) localizes on ____________________ and targets _______________________________

Back 50

brush border;

NP C-1 like protein

Front 51

the NP C-1 like protein is critical for:

Back 51

cholesterol absorption into the intestine

- prevents uptake of chol from diet

Front 52

Ezetimibe is used in combo with:

Back 52

statins

- but can be used alone if statins are ineffective

Front 53

3 SE's of Ezetimibe =

Back 53

1. HA

2. diarrhea

3. rhabdomyolysis

Front 54

Mipomersen =

Back 54

injection that leaves LDL by an avg. of 44% in pts with **familial hypercholesteremia**

Front 55

acute coronary syndrome =

Back 55

ischemic disorders across a continuum, from UA to NSTEMi to STEMI

Front 56

ALL ACS's present with:

Back 56

ischemic symptoms - chest pain, SOB, diaphoresis

Front 57

UA and NSTEMI ~~

Back 57

**partially** occlusive thrombus

STEMI ~~ *completely* obstructive thrombus (diagnosed via EKG)

Front 58

6 endogenous anti-thrombics that prevent excessive thrombus:

Back 58

1. anti-thrombin

2. Prot C/S

3. TF-pathway inhibitor

4. tissue plasminogen activator (plasminogen degrades fibrin)

5. prostacyclin (dec. plat activation/aggregation)

6. NO (also dec. plat act.)

Front 59

>90% of ACS results from:

Back 59

disruption of atherosclerotic plaque

(with subsequent clot formation)

Front 60

rupture =>

Back 60

thrombogenesis => clot => inc. obstruction

Front 61

3 other triggers of ACS:

Back 61

1. strenuous physical activity

2. emotional stress

3. SNS activity

Front 62

ACS is exacerbated by:

Back 62

endo dysfunction

(~~ vasoconstriciton, dec. anti-thrombic function)

Front 63

MI occurs when ischemia is:

Back 63

*bad enough* to cause myocyte necrosis

Front 64

transmural MI ~~

(2)

Back 64

1. TOTAL occlusion of epicardial coronary artery

2. ST elevation (signifying injury)

Front 65

(**Q waves signify:**

Back 65

*infarction*

Front 66

subendothelial infarction involves only the innermost layers of:

Back 66

the **MYOcardium**

Front 67

the myocardium is most susceptible to problems from ischemia due to:

(2)

Back 67

1. poor collateral flow

2. location next to high-Pressure ventricle

Front 68

3 early MI changes:

Back 68

1. switch to anaerobic metabolism (~lactic acid)

2. **irreversible damage in 20 min if no intervention**

3. cellular edema

Front 69

3 late MI changes:

Back 69

1. scar tissue

2. structural weakness

3. scarring complete by 7 weeks post

Front 70

functional changes during AND following MI come in the form of:

(2)

Back 70

1. impaired ventricular contraction

2. impaired relaxation

Front 71

"impaired ventricular contraction" is also called:

Back 71

systolic dysfunction

Front 72

systolic dysfunction takes the form of:

(3)

Back 72

1. hypokinesis (local region with reduced contraction)

2. akinesis

3. dyskinesis (local region that bulges outward with contraction)

Front 73

impaired relaxation =

Back 73

diastolic dysfunction

Front 74

diastolic dysfunction takes the form of:

Back 74

stiffness (decreased compliance)

Front 75

3 other functional changes during and following MI:

Back 75

1. stunned myocardium

2. ischemic preconditioning

3. ventricular remodeling

Front 76

stunned myocardium ~~

Back 76

prolonged but gradually-reversible period of contractile dysfunction

- takes days to weeks to recover

Front 77

ischemic preconditioning: *brief* ischemia may render tissues:

Back 77

more R to future episodes of ischemia

=> Mi following recent anginal episodes ~~ less M/M

Front 78

ventricular remodeling =

Back 78

ventricular dilation of infarcted AND non-infarcted myocardium

Front 79

ventricular remodeling increases:

Back 79

wall stress

=> inc. dysfunction

Front 80

2 PE findings of MI:

Back 80

1. systemic hypoperfusion

2. evidence of HF

Front 81

4 features of systemic hypoperfusion ~~

Back 81

1. hypotension

2. tachycardia

3. impaired cognition

4. end-organ injury

Front 82

4 evidences of HF:

Back 82

1. inc. JVP

2. crackles

3. gallops (S3, S4)

4. new murmurs

Front 83

5 risk factors during MI that lead to a worse prognosis:

Back 83

1. AGE

2. hypotension

3. tachycardia

4. HF

5. anterior location (~greater risk to LV)

Front 84

Kilip classifications of HF, I through IV:

Back 84

I = no congestion

II = S3, rales

III = acute pumonary edema

IV = cardiogenic shock

Front 85

rales =

Back 85

abnormal rattling sound of the lungs

Front 86

STEMI =

Back 86

elevated ST via EKG

- a medical emergency

Front 87

3 ways to define STEMI ST elevation:

Back 87

1. >1 mm in *at least 2* anatomically-contiguous leads

OR

2. >2mm in 2 contiguous *precordial* leads

OR

3. *new* LBBB

Front 88

****4 examples of contiguous leads,

what location of the heart they represent,

and which artery is responsible for that location****

Back 88

II, III, and aVF => inferior heart => RCA

v1, v2 => anteroseptal => high LAD

v3, v4 => anterior => LAD

I, aVL, v5, v6 => lateral heart => LCx

Front 89

v1, v2 *depression* ~~

Back 89

posterior heart ==> RCA/PDA

Front 90

electrically silent EKG ~~

Back 90

circumflex branch problem

Front 91

time is muscle -

Back 91

don't wait for biomarkers to come in, assume MI

Front 92

**main difference between UA and NSTEMI:**

Back 92

NSTEMI is POS for Troponin biomarkers,

UA is negative

Front 93

UA may or may not have:

Back 93

ECG changes

Front 94

**2 features of NSTEMI that correlate to a really bad prognosis:**

Back 94

1. ST change at least 0.5 mm

2. elevated biomarkers

Front 95

Q waves at once indicate:

(2)

Back 95

1. complete occlusion

2. transmural MI

Front 96

*persistent* Q wave ~~

Back 96

scarring

Front 97

POS Tn is *always* prognostically worse,

Back 97

whether it's cardiac-related or not

Front 98

4 non-cardiac causes of Tn elevation:

Back 98

1. acute HF

2. PE

3. shock

4. myocarditis

Front 99

how to tell it's an MI when Tn levels are raised:

(2)

Back 99

1. Tn is in 99th percentile

2. rise and fall is observed

3. typical symptoms of MI

Front 100

CAD =

Back 100

narrowing or blockage or ANY of the coronary vessels

Front 101

CAD is manifested as:

(2)

Back 101

stable angina OR ACS

(ACS = UA/NSTEMI, STEMI)

Front 102

5 kinds of drugs to prevent cardiac events:

Back 102

1. anti-anginals

2. aspirin

3. clopidogrel

4. statins

5. ACE inhibitors

Front 103

3 kinds of anti-anginals:

Back 103

1. B-blockers

2. nitrates

3. Ca2+ chan blockers

Front 104

clopidogrel =

Back 104

P2Y12 inhibitor

= **an antiplatelet substitue for pts with aspirin allergy**

Front 105

when to revascularize in stable angina:

(3)

Back 105

1. refractory to anti-anginal meds

2. unacceptable SE's to meds

3. extensive CAD, such that CABG confers survival benefit

Front 106

PCI comes in the form of:

(2)

Back 106

balloon angioplasty / coronary stenting

=> vessel of original size

Front 107

ranking of effectiveness of PCI methods:

(3)

Back 107

DES > BMS > POBA

Front 108

DES:

(3)

Back 108

1. drug-eluting

2. drastically dec. restenosis rate

3. but inc. thrombic rates

Front 109

CABG provides better survival for:

(3)

Back 109

1. >50% stenosis in left main

2. 2- and 3-vessel CAD (esp. with concomittant LV dysfunction)

3. diabetes with multivessel disease

Front 110

3 goals of therapy for ACS:

Back 110

1. restore epicardial coronary blood flow

2. limit myocardial damage

3. minimize risk of complications

Front 111

5 general therapies for ACS:

Back 111

1. bed rest

2. supp. O2

3. analgesia (dec. chest pain and anxiety)

4. anti-ischemics

5. anti-plat/thrombics

Front 112

**key with STEMI is to:**

Back 112

open the artery ASAP

Front 113

key for UA/NSTEMI, use:

(2)

Back 113

1. anti-ischemics to restore supply-demand balance

2. anti-thrombotics to prevent further occlusion

Front 114

3 anti-ischmics:

Back 114

1. B-blockers

2. nitrates

3. non-hydro Ca2+ blockers

Front 115

non-hydro Ca2+ blockers:

Back 115

1. used if B-blockers can't be

2. NO dec. of mortality

3. INC mortality in pts with LV dysfunction

Front 116

aspirin and B-blockers reduce:

Back 116

mortality

Front 117

what's the most potent anti-platelet med:

Back 117

IV glycoprotein IIB/IIIA inhibitor

- reserved as adjunctive to PCI

- NO benefit to upfront admin, unlike aspirin

Front 118

fondaparinux is a drug that's NOT:

Back 118

used

Front 119

Bivalirudin =

Back 119

direct thrombin inhibitor

- less bleeding risk

Front 120

conservative approach to UA/NSTEMI =

Back 120

medical management, cath only with recurrent ischemia or positive stress test

Front 121

early invasive approach to UA/NSTEMI =

Back 121

coronary angiography within 24 hrs,

revascularization if indicated

Front 122

spectrum of approach to UA/NSTEMI:

(3)

Back 122

anti-ischmics => anti-plat/thrombics => early/conservative

Front 123

3 goals of STEMI therapy:

Back 123

1. restore blood flow

2. prevent further occlusion

3. restore balance b/w supply and demand

Front 124

restoration of blood blow in STEMI is achieved by:

Back 124

1. fibrinolysis

2. PCI (needs to be performed within 90 minutes)

(rescue PCI is performed if refractory to fibrinolysis)

Front 125

a pleotropic effect of statins is:

Back 125

restoration of endo function

Front 126

10 complications of MI:

Back 126

1. recurrent ischemia

2. arrthymias

3. HF

4. right ventricular infarct

5. pap. muscle rupture

6. ventricular free wall rupture

7. ventricular septal rupture

8. ventricular aneurysm

9. pericarditis

10. thrmoboembolism

Front 127

recurrent ischemia ~~

(3)

Back 127

1. post-infarct angina

2. a POOR prognosis - indicates mycardium at risk for REinfarction

3. may be a prob. with the stent

Front 128

arrhythmias are frequent:

Back 128

during AND after MI

Front 129

3 mechanisms of arrhythmias:

Back 129

1. impaired perfusion to conduction system

2. autonomic stimulation

3. drugs that WE prescribe

Front 130

ventricular tachy/fibrillation: if early (<48 hrs after MI),

Back 130

better - will go away

- if late, usually due to scarring => high Mortality risk

Front 131

superventricular arrhythmias are common after MI; 3 kinds:

Back 131

1. sinus brady

2. sinus tachy

3. atrial fib

Front 132

conduction blocks also result in:

Back 132

arrhythmias

Front 133

HF comes in two forms:

Back 133

1. left HF

2. cardiogenic shock

Front 134

left HF is due to ischemia causing:

Back 134

systolic or diastolic dysfunction

Front 135

5 signs/symptoms of left HF =

Back 135

1. dyspnea

2. rales

3. S3

4. peripheral edema

5. orthopnea

Front 136

treat left HF with:

Back 136

1. revascularization

2. ACE inhibitors

3. diuretics

4. B-blockers

(consider aldosterone if LVEF <40% of nl)

Front 137

cardiogenic shock =

Back 137

severely-decreased CO, hypotension

Front 138

cardiogenic shock results in:

Back 138

inadequate tissue perfusion (liver, brain, etc)

=> high mortality
(early revascularization reduces mortality)

Front 139

1/3 of pts with LV inferior wall infarct will have:

Back 139

right ventricle infarct,

usually due to block in RCA

Front 140

4 signs of right HF:

Back 140

1. JVD

2. hypotension

3. clear lungs

4. ST elevation in III, v4R

Front 141

treatment of right ventricular infarction =

Back 141

reperfusion

THEN: volume, volume, volume

Front 142

pap. muscle rupture =>

Back 142

severe mitral regurgitation

- usually happens to PM pap. muscle

Front 143

free wall rupture occurs in:

Back 143

torn necrotic tissue

Front 144

2 risk factors for free wall rupture:

Back 144

1. female

2. history of HTN

Front 145

free wall rupture =>

Back 145

rapidly-fatal tamponade

- occasionally, a thrombus forms a temporary plug, resulting in a pseudoaneurysm, a surgical emergency

Front 146

ventricular septal rupture =>

Back 146

left-to-right shunt => HF due to overload of pulm. circulation

- pt CAN lie flat

Front 147

ventricular aneurysm is a LATE complication; develops as:

Back 147

wall weakens with phag clearance of necrotic tissue

Front 148

a regular aneurysm has a smaller risk of rupture than a pseudoaneurysm, because:

Back 148

all three layers are still intact

Front 149

aneurysms ~~ *persistent*:

Back 149

ST elevations, weeks after STEMI

Front 150

pericarditis comes in two forms:

Back 150

acute

Dressler's

Front 151

acute pericarditis happens early, often in the hospital; ~~

Back 151

sharp, pleuritic pain, fever, and friciton rub

Front 152

treat acute pericarditis with:

Back 152

aspirin

- AVOID anticoagulants

Front 153

Dressler's syndrome (weeks later) =

Back 153

immune process against necrotic tissue

Front 154

treat Dressler's with:

(2)

Back 154

aspirin, NSAIDS

Front 155

high chance of thromboembolism requires:

Back 155

anticoagulants

Front 156

6 features of post-MI standard of care:

Back 156

1. B-blockers

2. statins

3. ACE inhibitors (if LV dysfunction)

4. aldosterone antagonists (if LV dysfunction)

5. risk factor modification

6. implantable defibrilator (if indicated)

Front 157

ICD is indicated in pts with:

Back 157

LVEF less than or equal to 30%,

at least 40 days after MI

Front 158

universal definition of acute MI includes:

Back 158

detection of rise and/or fall of cardiac biomarkers (esp. Tn) >99th percentile of range

Front 159

TnC is the same no matter which muscle dies, so ignore it; instead, use:

Back 159

TnI or TnT, which are unique to the heart and are released followed necrosis

Front 160

any increase in TnI or TnT =

Back 160

cell injury/necrosis

Front 161

**normal levels of TnI/T are:

Back 161

EXTREMELY low

Front 162

TnI and TnT do NOT tell you:

Back 162

what pathology caused the cell death

Front 163

creatine kinase =

Back 163

dimer of M and/or B subunits

Front 164

CK-MB =

Back 164

most specific CK to cardiac tissue

- assume that high CK-MB indicates death of myocytes, unless proven otherwise

Front 165

how to tell if Ck-MB is from skeletal muscle:

Back 165

CK-Mb / CK x 100% must be < or = 5%

Front 166

always collect _________ samples, to look for:

Back 166

serial;

rise and fall

Front 167

myoglobin rises and falls within the day; CKMB, within:

Back 167

two days

- TnI and TnT decrease slowly but surely - elevated for 2 weeks

Front 168

lipids are a great way to see:

Back 168

who's due for an MI

- although there's LOTS of biological variation

Front 169

if you want to get a *complete* lipid profile, the sample needs to be:

Back 169

a **fasting sample** (fast for 10-12 hrs

Front 170

if not a fasting sample, the lipid profile you'll get will only include:

(3)

Back 170

1. chol

2. HDL

3. non-HDL

Front 171

a sample for lipid profile also NEEDS to be:

Back 171

serum

- and NO heparin, which falsely lowers TG's

Front 172

lipemic serum:

(2)

Back 172

1. pink in tube

2. ~~ >250 mg/dL of TG's

3. often observed postprandially (following a meal)

Front 173

chylomicrons rise to the top of a tube as:

Back 173

foam, if refrigerated

Front 174

to calculate LDL:

Back 174

LDL = total chol - (HDL + TG/5)

**MUST be fasting**

*can't be done if TG's are >400 mg/dL*

Front 175

HDL ranges:

Back 175

<40 = bad

great than that = optimal

Front 176

optimal levels of total chol, LDL, and TG's:

Back 176

<200 (TC)

<100 (LDL)

<150 (TG's)

Front 177

screen children and adolescents between 2 and 19 y.o., esp if:

Back 177

1. family history of CHD

OR

2. one parent with cholesterol >240 mg/dL

Front 178

acceptable total chol for children =

Back 178

<170

Front 179

acceptable LDL for children =

Back 179

<110

Front 180

high total chol for children =

Back 180

> or = 200

Front 181

high LDL for children =

Back 181

> or = 130

Front 182

every 30 mg/dL rise in LDL =

Back 182

inc. of 30% in risk (adults)

Front 183

smaller, denser LDL particles are:

Back 183

more proatherogenic than bigger ones

- HDL2 is more protective than HDL3

Front 184

***secondary lipid disorders are:***

Back 184

MUCH more common than primary ones,

so rule secondary ones out before diagnosing

Front 185

lipids aren't the only part of the story, b/c:

Back 185

35% of CHD's occur in people with optimal total chol (<200)

Front 186

C-reactive protein =

Back 186

marker of inflammation

- measure hsCRP, much lower on the scale, ~ heart issue

Front 187

pts with inc. hsCRP and inc. Tn =>

Back 187

INC mortality

Front 188

hsCRP: persistent, low levels are seen in early ACS;

Back 188

inc'd in smoking, insulin R, and high BMI

Front 189

**high levels of CKMB and/or Tn in pts with UA suggest: **

Back 189

MI event in 6-9 months

Front 190

(pts with renal disease also have:

Back 190

measurable Tn)

Front 191

****early assessment of MI ~~***

(2)

Back 191

1. hsCRP

2. lipids

Front 192

MI ~~

Back 192

TnI, TnT

- correlate levels with time of onset of symptoms

Front 193

routine lipid testing measures:

(5)

Back 193

1. TC

2. TG

3. HDL

4. LDL

5. calculated non-HDL