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Internal medicine > Cardio: MI, angina, endocarditis, ASD > Flashcards

Cardio: MI, angina, endocarditis, ASD Flashcards

1
Q

What is the pathophysiology of stable angina?

A

Fixed atherosclerotic lesion that narrow major coronary arteries. Imbalance btw blood supply and O2 demand leading to inadequate perfusion.

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2
Q

What are the risk factors for ischemic HD?

A
  • DM
  • Hyperlipidemia
  • Low levels of HDL
  • Family history
  • Smoking
  • Age, men >45 women >55
  • Obesity/lifestyle
  • Excessive alcohol use
  • Stress
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3
Q

Clinical features of stable angina

A
  • Chest/substernal pressure/pain/heaviness/tightness
  • Gradual in onset
  • Brought on by increased myocardial demand: excertion, emotion
  • Releived w/ rest og nitroglycerin
  • Does not change w/ breathing or change in body position
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4
Q

How to DX stable angina?

A

1) Physical exam usually normal
2) Resting ECG: Q waves/normal/ ST, T abnormalities during pain
3) Stress test: ECG and echo
4) Pharmacologic stress test if patient cannot exercise
5) Holter monitoring: ambulatory ECG
6) Cardiac catheterization w/ coronary angiography = definite test for CAD

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5
Q

Tx for stable angina

A

1) Risk factor modification
2) Drugs: Aspirin + B-blockers + nitrates (+ Ca-channel blockers). If CHF: ACEi’s
3) Revascularization for high-risk patients ( >70% of left main occluded)

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6
Q

What is variant (prinzmetal) angina?
Clinical?
Tx

A
  • Transient coronary vasospasm, usually accompanied by a fixed atherosclerotic lesion
  • Happen at night and at rest
  • Associated w/ ventricular dysrhythmias
  • ST elevation during pain
  • Ca-channel blockers, nitrates
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7
Q

What is unstable angina?

A

Enlarged stenosis, chronic angina w/ increse in frequency/duration/intensity, new onset angina that is severe and worsening, patients w/ angina at rest

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8
Q

Dx of unstable angina

A

1) Exclude MI
2) Stabilize medically before stress test
Like angina:
3) Stress test: ECG and echo
4) Pharmacologic stress test if patient cannot exercise
5) Holter monitoring: ambulatory ECG
6) Cardiac catheterization w/ coronary angiography = definite test for CAD

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9
Q

Tx of unstable angina

A

1) Hospital admission w/ scope: O2, Iv access, pain control w/ nitrates and morphine
2) Agressive medical treatment- as MI w/o fibrinolysis
Aspirin, clopidogrel, bblockers, LMWH, abciximab/tirofiban
3) Cardiac catheterization/revascularization
4) After acute phase: continue aspirin, bblockers, nitrates, reduce risk factors

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10
Q

What is an MI ?

A

Necrosis of myocardium as a result of an interruption of blood supply

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11
Q

What is the mortality rate for MI?

A

30%

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12
Q

What kind of patient typically gets an MI?

A

Patients w/

  • Angina
  • Risk factors of CAD
  • Arrhythmia history
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13
Q

What is the characteristic chest pain in MI?

A
  • Substernal pressure (crushing elephant on chest)
  • Similar to angina but more severe and do not respond to nitroglycerin
  • Radiation to neck/jaw/arms/back of the left side
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14
Q

What other symptoms than pain might be present during a MI?

A
  • Dyspnea
  • Diaphoresis(sweating)
  • Weakness/fatigue
  • Syncope
  • N/V
  • Sense of impending doom
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15
Q

How to Dx a MI?

A

1) ECG: peaked T waves, St- segment elevation, Q-waves, T wave inversion, ST-segment depression
2) Cardiac enzymes: troponins, CK-MB

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16
Q

Tx of MI

A

1) Hospital admission: O2, nitrates, morphine
2) Meds: aspirin, bblockers, ACEi’s, statins, heparin(?)
3) Revascularization: thrombolysis (alteplase), PCI, CABG

17
Q

What is the complications after MI?

A
  • Pump failure: HF, cardiogenic shock
  • Arrhythmias
  • Recurrent infarct: Dx often difficult
  • Mechanical injury: rupture of wall/ septum / papillary muscle, ventricular aneurysm
  • Acute pericarditis
  • Dressler syndrome
18
Q

What is endocarditis?

A

Inf. of the endocardial surface, usually involving the cusps of the valves

19
Q

Classification of endocarditis

A
  • Acute: S. aureus most common, normal heart valve, if untreated-fatal in <6w
  • Subacute: S.viridans/enterococcus, damaged heart valve, if untreated >6w to cause death
20
Q

What organisms cause endocarditis in native valve?

A
  • S. virridans most common
  • Staph spieces and enterococci
  • HACEK: haemophilus, actinobacillus, cardiobacterium, eikenella, kingella
21
Q

What organisms cause endocarditis in prosthetic valve?

A
  • Staph epidermidis (early onset)

- Strep (late onset)

22
Q

What organisms typically cause endocarditis in IV drug users?

A
  • Right sided
  • S. aureus
  • Other: enterococci, Strep, candida, gram negs (pseudomonas)
23
Q

What are the complications of endocarditis?

A
  • Cardiac failure
  • Myocardial abscess
  • Various solid organ damage from emboli
  • Glomerulonephritis
24
Q

What do you need to do to DX endocarditis?

A

Use DUKE clinical criteria

  • 2 major
  • 1 major + 3 minor
  • 5 minor
25
Q

What are the major duke clinical criteria?

A
  • Sustained bacteremia

- Endocardial involvement: new valvular regurgitation

26
Q

What are the minor duke clinical criteria?

A
  • Predisposing condition
  • Fever
  • Vascular phenomena: emboli, aneurysm, hemorrhage, Janeway lesion
  • Immune phenomena: GN, Osler nodes, Roth spots, RF
  • Positive blood culture: not meeting major criteria
  • Positive echo: not meeting major criteria
27
Q

What are the treatment of endocarditis?

A
  • Parenteral AB’s based on culture for 4-6 w

- If neg culture but high suspicion: empirical Tx w/ penicillin/vancomycin + aminoglycoside

28
Q

What are the cardiac indications for prophylaxis of endocarditis?

A
  • Prosthetic heart valves
  • History of inf. endocarditis
  • Congenital HD: unrepaired cyanotic, repaired w/ prosthetic material
  • Cardiac transplant w/ valvulopathy
29
Q

What are the qualifying procedures requiring prophylaxis for endocarditis?

A
  • Dental procedures
  • Involving biopsy/incision of resp. mucosa
  • Procedure involving inf. skin/skeletal muscle
30
Q

What is Marantic endocarditis?

A
  • Also called nonbacterial thrombotic endocarditis
  • Associated w/ metastatic cancer
  • Sterile deposits of fibrin and plot form on the closure line of valve leaflets
  • Vegetations may embolize to the brain
31
Q

What is Libman-Sacks endocarditis?

A
  • Also called nonbacterial verrucous endocarditis
  • Involves aortic valve in SLE
  • Regurg murmurs
  • May embolize
32
Q

What are the 3 types of ASD?

A
  • Ostium secundum: most common, central portion
  • Ostium primum: low in septum
  • Sinus venosus: high in septum
33
Q

What is the pathophysiology of ASD?

A
  • O2 rich blood from LA -> RA -> increase RH output and pulm. flow
  • Increase work og RH -> shunt size increase -> RA and RV dilatation w/ pulm-to-systemic flow ratio > 1,5:1
  • Pulm. HT is a serious sequela
34
Q

What is the clinical features of ASD?

A
  • Often asymptomatic until middle-aged (40y)
  • After this symptoms may start
  • Exercise intolerance, dyspnea on exertion, fatigue
  • Mild systolic ejection murmur at pulm. area
  • Fixed split S2
  • Diastolic flow “rumble” mumur over tricuspid valve
35
Q

How to Dx ASD?

A

1) TEE : “bubble study”
2) CXR: large pulm. arteries and markings
3) ECG: RBBB, right axis deviation, atrial abnormalities

36
Q

What are the complications of ASD?

A
  • Pulm. HT
  • Eisenmenger disease: fainting seplls, thromboembolism, hypovolemia, hemoptysis, preeclampsia
  • Right HF
  • Atrial arrhythmias
  • Stroke (paradoxical emboli/afib)

Internal medicine (4 decks)

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