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Ischemic Heart Disease & Vascular Disease Flashcards

1
Q

What causes a MI?

A

Atherosclerosis = MC cause (caused by plaque rupture –> acute coronary artery thrombosis

Coronary artery vasospasm: cocaine, variant (prinzmetal) angina

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2
Q

What are s/s of a MI?

A

Anginal pain: retrosternal pressure (>30mins), not relieved by rest/nitro

Levine’s sign: clenched fist on chest

Pain at rest indicates > 90% occlusion

Sympathetic stimulation: anxiety, diaphoresis, tachy/palpitations, N/V, dizziness

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3
Q

What are s/s of a silent MI? Who are they MC in?

A

MC in women, elderly, obese, DM

Abd pain, jaw pain or dyspnea w/out CP

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4
Q

What does a MI look like on PE?

A

Usually normal +/- S4

CP + bradycardia (may suggest inferior wall MI)

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5
Q

How do you dx a MI?

A

ECG:

  • NSTEMI or unstable angina
  • STEMI: ST elevation ≥ 1mm in ≥ 2 anatomically contiguous leads +/- reciprocal changes in opposite leads.

Cardiac markers: 3 sets every 8 hrs (troponin most sensitive/specific)

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6
Q

What ECG finding is considered equivalent to a STEMI?

A

LBBB

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7
Q

What is the natural STEMI progression?

A

Peaked T waves –> ST elevations –> Q waves –> T wave inversion

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8
Q

When does troponin return to baseline?

A

7-10 days

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9
Q

How do you treat unstable angina or NSTEMI?

A

Anti-thrombotic:
- Antiplatelet tx: ASA, ADP inhibitors (Clopidogrel - good for those w/ ASA allergy), GP IIb/IIIa inhibitors

-Anticoag: unfractionated heparin, LMWH (enoxaparin), fondaparinux

Adjunctive:
- BBs (metoprolol), nitrates, morphine, CCBs

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10
Q

How do you treat a STEMI?

A
  1. Reperfusion (mainstay tx, within 12hrs of sx onset)
    - PCI: within 3h of sx onset, superior to thrombolytics
    - Thrombolytic (used if PCI is not an option): Alteplase (rTPA), streptokinase
  2. Antithrombotic:
    - Chewable ASA (lowers mortality by 20%), heparin (unfractionated/LMWH), GP IIb/IIIa inhibitors
  3. Adjunct:
    - BBs (decrease mortality), ACEI (slows progression of CHF), nitrates, morphine, statin
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11
Q

What class of meds should NOT be used in MI is cocaine induced?

A

Beta blockers!!! –> unopposed alpha vasoconstriction

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12
Q

What are the 4 classes of angina pectoris?

A

I: angina only w/ strenuous activity

II: angina w/ more prolonged or rigorous activity, slight limitation of physical activity

III: angina w/ usual daily activity, marked limitation

IV: angina @ rest. Often unable to carry out activity

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13
Q

What are the s/s of angina pectoris?

A

Clinical history = utmost importance

  1. Substernal poorly localized CP brought on by exertion, radiates to arm, teeth, lower jaw, usually short in duration (< 30 mins, typically 1-5 mins). Levine’s sign. Pain relieved w/ rest or nitro
  2. Dyspnea, nausea, diaphoresis, numbness, fatigue
  3. Epigastric or shoulder pain
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14
Q

How do you dx ischemic heart disease? What is gold standard?

A
  1. ECG: ST depression, T wave inversion, normal in 50%
  2. Stress testing (most useful noninvasive tool):
    - Stress EGG
    - Myocardial perfusion imaging stress
    - Stress echo
    - MRI
  3. Coronary angiography = definitive dx/GOLD
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15
Q

What is definitive tx for angina?

A
  1. PTCA (indicated if 1 or 2 vessel disease NOT involving left main coronary artery & in whom ventricular function is normal)
  2. CABG (indicated if left main coronary artery disease, 3 vessel disease, EF < 40%)
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16
Q

How can you medically treat angina?

A

Nitro
BBs
CCBs
ASA

17
Q

What is the classic outpatient regimen for angina?

A

Daily ASA, sublingual nitro prn, daily BB & statin

18
Q

What causes rheumatic fever? Who is it MC in?

A

GABHS (aka Strep pyogenes) - infection typically precedes onset of RF by 2-6 wks

MC in children 5-15yo

19
Q

What is the “major” Jones Criteria ?

A 
"CANCER"
Carditis
Arthritis (2 or more joints)
Nodules
Chorea 
Erythema marginatum 
Rheumatic fever
20
Q

What is the “minor” Jones Criteria?

A 
"CAFE P"
CRP increased 
Arthralgia
Fever
Elevated ESR

Prolonged PR

21
Q

How do you treat rheumatic fever?

A

ASA +/- corticosteroids

PCN G = abx of choice (or erythromycin if PCN allergic)

22
Q

Describe peripheral venous disease

A

SF: greater/lesser saphenous veins

Deep: femoral, iliac, popliteal, posterior tibial & SF femoral

Perforating veins

23
Q

What is Virchow’s triad?

A
  1. Intimal damage
  2. Stasis
  3. Hypercoagulability (Factor V Leiden mutation)
24
Q

What causes varicose veins?

A

Increased estrogen: OCPs, pregnancy

Prolonged standing, obesity

25
Q

What are s/s of varicose veins?

A

Dilated, tortuous veins

Dull ache, worsened w/ prolonged standing & relieved w/ elevation

Venous stasis ulcers

26
Q

How do you treat varicose veins?

A

Leg elevation, compression stockings

Sclerotherapy, radiofrequency or ablation, ambulatory phlebectomy

Family Med EOR (15 decks)

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