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CLIN MED II- CARDIOLOGY > HYPERLIPIDEMIA, ACUTE CORONARY SYNDROME, ANGINA > Flashcards

HYPERLIPIDEMIA, ACUTE CORONARY SYNDROME, ANGINA Flashcards

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1
Q

types of hyperlipidemia

A
  • mixed hyperlipidemia (combo of elevated HDL, LDL, or triglycerides)
  • hypercholesterolemia (high LDL)
  • hypertriglyceridemia (high TG)
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2
Q

Hyperlipidemia- definition

A

inc levels of lipids/fats in the blood

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3
Q

risk factors of HLD

A
  • diet (alcohol, saturated fats)
  • age
  • sedentary lifestyle
  • fam Hx
  • gender (men>women)
  • genetic mutations (familial hypercholesterolemia)
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4
Q

HLD clinical features

A
  • asymp
  • xanthoma in SEVERE HLD (hard yellow plaque/nodules of tendons and skin)
  • pancreatitis w/hypertriglyceridemia
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5
Q

fasting lipid panel goals for pt with HLD

A
  • cholesterol <200
  • LDL <100, <70 for DM, CAD
  • HDL >40 men, >50 women
  • triglycerides <150

LDL is most important for CAD!!!

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6
Q

HLD Tx names

A

statins, PSK9 inhibitors, niaotinic acid, fenofibrates, bile acid binding resins

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7
Q

HLD- statins

HMG-CoA reductase inhibitor

A
  • Rosuvastatin, atorvastatin, simvastatin, pravastatin
  • inhibiting cholesterol synth by inhibiting HMG-CoA reducates in the liver
  • this INC LDL receptors–>promotes LDL clearance
  • reduces progressions of plaque, reduce mortality

MOST POTENT

crestor, lipitor, zocor, pravachol

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8
Q

HLD- statins side effects

A

rhabdomyolysis, myalgia, arthralgia, elevated ALT/AST

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9
Q

HLD- PSK9 Inhibitors

A
  • Alirocumab (praluent), avolocumab (repatha)
  • inhibit degradation of LDL receptors–> inc LDL clearance

indications
- familial hypercholesterolemia
- CAD

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10
Q

HLD- PSK9 Inhibitors side effects

A

headaches, diarrhea, URI symptoms

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11
Q

HLD- Niaotinic acid

& side effects

A
  • niacin
  • lowers triglycerides
  • CAN inc HDL

side effects: facial flushing, pruritis, n/v

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12
Q

HLD- Fenofibrates

& side effects

A
  • gemfibrozil
  • lower triglycerides

side effects: n/d, abdominal pain

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13
Q

HLD- bile acid binding resins

A
  • cholestyramine colestipol, colesevelam
  • lowers LDL
  • Does not change triglycerides
    GI side effects
    RARELY USED
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14
Q

which HLD medication is the most potent?

A

statins

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15
Q

Angina Pectoris- definition and types

A

inadequate tissue perfusion of the myocardium
- imbalance in cardiac demand and tissue perfusion
- CP originates from heart
- typical or atypical
MC is CAD

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16
Q

typical Angina Pectoris- clin features

A
  • men
  • mid sternal or L sided
  • squeezing, tightness, pressure
  • “sitting on chest”
  • levine sign–> CLENCHES FIST OVER STERNUM
    - radiation to LEFT ARM
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17
Q

Atypical Angina Pectoris- clin features

A
  • females, elderly, DM, immuncomp
  • Jaw, right shoulder pain
  • radiation to RIGHT or BIL arms, back
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18
Q

Angina Pectoris- causes

what is the MC?

Study These Flashcards
A

CAD IS MC
- embolus
- arteritis
- dissection
- congenital abnormality
- vasospasm (cocaine or prinzmetals)

19
Q

Stable Angina

characteristics and tx

Study These Flashcards
A

exacerbated with activity/emotion, relieved with REST
- predictable and last less than 3 mins
- relieved with sublingual nitroglycerin

reproducible

20
Q

unstable angina

characteristics and tx

Study These Flashcards
A

grouped with acute coronary syndrome
- angina that WORSENS
1 of the following: angina at rest, new onset of angina symptoms, inc pain in stable pts

  • less responsive to sublingual nitro
  • indicates stenosis that ENLARGED
21
Q

prinzmetal angina

characteristic, when does it occur, caused by

Study These Flashcards
A

vasospasm at REST
- MC in FEMALES
- 75% with atherosclerotic lesion
- occurs early morning
- exercise capacity preserved
- from cocaine use

22
Q

what kind of angina can happen from cocaine use?

Study These Flashcards
A

prinzmetal/vasospastic angina

23
Q

Acute Coronary Syndrome- definition

Study These Flashcards
A

SUDDEN dec coronary blood flow

these grouped conditions may occur when blood flow is blocked to myocardium
- unstable angina
- NSTEMI (partial thickness necrosis)
- STEMI (full thickness necrosis)

24
Q

MI- MC cause

Study These Flashcards
A
  • thrombosis (ruptured plaque–thrombus formed–occlusion)
  • MI can be silent, common w pt that has atypical symptoms
25
ACS- symptoms
- typical or atypical CP - diaphoresis - SOB/dyspnea - n/v - dizzy/lightheaded - syncope - anxiety
26
ACS- signs
- HTN - hypotension - tachycardia - bradycardia/heart block (inferior wall MI) - murmur - friction rub - bibasilar rales
27
ACS- Dx with EKG
12 lead EKG STEMI-> st elevation >1 mm in 2 leads NSTEMI and unstable angina--> ST depressions or T wave inversions - POS CARDIAC ENZYMES = NSTEMI
28
positive cardiac enzymes indicate?
NSTEMI
29
ACS- Dx labs | names
- Cardiac Enzymes - Creatine Kinase MB (CK-MB) - myoglobin
30
ACS- Dx cardiac enzymes - names - released when? - how often are samples taken
Cardiac Enzymes - released w necrosis of myocardial tissue - GOLD STANDARD DX for MI - 3 sets every 6 hrs - troponin T and I most specific ## Footnote might take up to 6 hours for it to be created
31
ACS- Dx CK-MB - when does it inc, peak, normalize
Creatine Kinase MB (CK-MB) - inc 4-6 hrs - peaks in 12-24 hrs - normalizes in 48-72 hrs
32
ACS- Dx Myoglobin - when does it inc, peak, normalize
- inc 1-4 hrs - peaks 4-6 hrs - normalizes in 24 hrs
33
ACS- Tx types
- MONAB (morphine, oxygen, nitroglycerin/NTG, aspirin, beta blocker) - statins - UFH or LMWH - Reperfusion (PCI/percutaneous transluminal coronary angioplasty OR thrombolytics)
34
what artery corresponds to this wall MI ? - inferior - posterior - septal - anterior - lateral
- inferior: R coronary - posterior: Pos descending - septal: L anterior descending - anterior: L anterior descending - lateral: L anterior descending OR circumflex
35
ACS Tx- MONAB
Morphine- pain control that isnt controlled w/NTG Oxygen NTG Aspirin- can use adenosine diphosphate receptor inhibitors if allergic (clopidogrel, ticlopidine prasugrel--> inhibit platelet aggregation) Beta Blocker ## Footnote caution if bleeding w ADP receptor inhibitors if bleeding or planned CABG within 7 days
36
ACS Tx- statins
reduce risk of further coronary events - stabilizes plaque, lowers cholesterol
37
ACS Tx- UFH or LMWH
UFH- inactivates thrombin by inhibiting fibrin formation LMWH- binds to and potentiates antithrombin IIIs ability to inactivate factor Xa
38
ACS Tx- reperfusion PCTA - door to cath time - stents require how long of DAPT
PTCA (percut. transluminal angio) - PCI is superior - door to cath time is 90 MINS - drug eluting stent (DES) and bare metal stents (BMS) - DES dual antiplatelet therapy x12 months, BMS DAPT x1 month
39
ACS Tx- reperfusion Thrombolytics - door to cath time
- door to cath 30 mins - reduce mortality and infarction - tissue plasminogen activators--> alteplase, reteplase, teneceplase * dissolve clot by activating tissue plasminogen
40
ACS DX thrombolytic therapy ABSOLUTE CONTRAINDICATIONS
- previous hemorrhagic CVA - CVA within last yr - intracranial neoplasm - active internal bleeding - suspected aortic dissection - trauma or major surgery <2 wks
41
ACS DX thrombolytic therapy RELATIVE CONTRAINDICATIONS
- trauma within past 2-4 wks - major surgery within past 3 wks - BP >180/110 - bleeding diathesis (inc tendency to bleed) - prolonged or traumatic CPR - recent internal bleeding - noncompressible vascular puncture - current anticoag use - active diabetic retinopathy - pregnancy - PUD
42
ACS- MI complications
- V tach, v fib - cardiogenic shock - ventricular aneurysm/rupture - papillary muscle rupture - HF - pericarditis - dressler syndrome (post MI type of pericarditis) - sudden death
43
ACS management strategies
Unstable angina needs management strategy - TIMI scale- thrombolysis in MI - GRACE- global registry of acute coronary events LOW score= conservative tx (antiplatelet, anticoag) HIGH SCORE= invasive tx (cardiac angiogram/plasty) ## Footnote TIMI- estimates mortality for unstable angina/NSTEMI pts (low is 0-2, high 5-7)
44
Cocaine induced MI - definition - DX - TX
coronary artery vasospasm secondary to cocaine activation of SNS and a1 receptors DX- 12 lead EKG (transient diffuse ST elevations), pos troponin, pos utox TX- CCB and nitrates, ASA and heparin/LMWH until CAD ruled out, BB CI due to inc risk of vasospasm ## Footnote cocaine causes vasoconstriction

CLIN MED II- CARDIOLOGY (16 decks)

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