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Block 9 Week 1 > ACS Case study-Patterson > Flashcards

ACS Case study-Patterson Flashcards

1
Q

(blank) is luminal narrowing due to plaque fomration

A

CAD

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2
Q

What is atherosclerosis made up of?

A

lipids, macrophages, calcium, fibrin

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3
Q

What are factors that increase the risk of CAD in patients?

A

Smoking, HTN, diabetes, high cholesterol (modifiable)

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4
Q

Prevalence of CAD increases with age. (blank) for men and women 45-60 and (blank%) for those over age of 65. Average age of onset for women is (blank) and for men (blank)

A

7.5%
20%
72 and 62

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5
Q

Prevention is important because CAD is associated with significant morbidity and mortality.
18% of men and 23% of women 40 years and older will die within the (blank) year after a heart attack. 33% and 43% will die within the first (blank) years.

A

first

5

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6
Q

What is coronary artery disease due to?

A

arteriosclerosis (including atherosclerosis)

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7
Q

When you have CAD and have periods of instability, what do you have?

A

ACS (acute coronary syndrome)

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8
Q

What is the greatest risk for CAD?

A

age greater than 65

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9
Q

When is family history important for the development of CAD?

A

Has to be first degree relative with heart attack at age 55 or less in men, or 65 or less in female

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10
Q

What are the three risk equivalents to CAD?

A
  • peripheral vascular disease
  • diabetes
  • stroke
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11
Q

What does the framingham data show?

A

10 yr risk of developing heart disease

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12
Q

What is considered a low risk according to the framingham risk calculator? intermediate? high?

A
  • less than 10%
  • 10-20%
  • greater than 20%
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13
Q

What is this:
any group of clinical syndromes consistent with MI (or patients with symptoms suggesting an unstable cardiac conduction due to ischemia)

A

ACS

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14
Q

What is this:

a spectrum of conditions resulting in MI including unstable angina (UA), NSTEMI and STEMI

A

ACS

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15
Q

ACS is secondary (usually) to (blank) or (Blank) leading to thrombus formation and secondary partial or complete occlusion of the vessel.

A

ruptured plaque or erosion of a plaque

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16
Q

What is this:

  • reversible ischemia
  • sudden onset at rest or change in frequency or severity of baseline angina
A

Unstable angina

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17
Q

How does unstable angina appear on EKG? Are biomarkers elevated and why?

A

Can show T wave inversion or ST depression

-no, due to lack of necrosis to myocardium

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18
Q

What is this:
symptoms indistinguishable from UA
Usually has EKG changes- ST segment depression and T wave inversion
Biomarkers are elevated due to damage to myocardium

A

NSTEMI

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19
Q

What type of ACS has an ST segment elevation?

A

STEMI

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20
Q

T or F

2% of outpatient visits are due to chest pain but the majority are not due to cardiac conditions

A

T

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21
Q

When evaluating a patient with chest discomfort, what are your main objectives?

A
  • determine pnts risk for ACS

- determine short term risk for an adverse risk

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22
Q

What are the URGENT causes for chest pain?

A
  • Aortic dissection
  • Pulmonary embolism
  • Tension pneumothorax
  • Esophageal rupture
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23
Q

What are the 5 high yield questions for determining likelihood of ACS?

A
  1. Nature of chest pain (PPQRST)
  2. History of CAD
  3. Gender/sex
  4. Age
  5. Number of traditional risk factors for CAD
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24
Q

What does PPQRST stand for?

A

-palliative, provocative, quality, radiation, severity, and timing.

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25
Q

What is the typical presentation of chest pain in ACS?

A
  • heavy or pressure sensation in the sternum or epigastrium
  • radiates to jaw, neck, throat, back or left arm
  • lasts at least 15-20 minutes
  • not relieved by rest
26
Q

T or F

25-30% of patients with ACS do not have chest pain as a complaint!

27
Q

Women with ACS are more likely to have pain in the (blank X 3) than chest pain.

A

jaw, neck and back

28
Q

Do younger or older ACS patients complain of chest pain more often?

29
Q

What will increase the odds of having ACS 7 fold?

A

Pain to the both shoulders

30
Q

What does this mean:

Pleuritic chest pain, chest pain reproduced by palpation, sharp or stabbing chest pain, positional chest pain.

A

3 x less likely to have ACS

31
Q

What is SPPIN and SNNOUT?

A

SPPIN-> highly specific test when it is positive will help you rule in a disease
SNNOUT->Highly sensitive test when it is negative will help you rule out a disease
Likely hood ratio greater than one rules in a disease while a likely hood ratio less than one rules out a disease.

32
Q

What is skin darkening and skin tags suggestive of?

33
Q

In the majority of ACS cases, what does the physical exam look like?

34
Q

What will give clinical symptoms give you evidence of cardiomyopathy with a STEMI?

A
  • S3
  • Pulmonary Rales
  • JVD
  • Hepatojugular reflex
  • Diminished pulses
  • Hypotension
35
Q

What will a ECG distinguish between?

A

UA/NSTEMI and STEMI

36
Q

ST segment (blank) suggests irreversible ischemia from coronary occlusion. What is needed?

A

elevation (STEMI)

-urgent reperfusion

37
Q

Practice guidelines suggest ECG for suspected ACS within (blank) of arrival to ED

38
Q

How should you give EKGs for a patient who might have ACS?

A

serial EKGs every 15-30 minutes

39
Q

Biomarkers are (blank) in NSTEMI and STEMI

A

elevated

biomarkers are normal in UA

40
Q

Troponin I an T have high (blank and blank) for myocardial damage

A

specificity, sensitivity

41
Q

Troponin I and Troponin T present in circulation within (blank) hours of ACS but not elevated until (blank) hours. WHat happens if you dont see elevation at onset?

A

2 hours
8-12 hours
recheck every 8-12 hours for 24 hours

42
Q

Troponin I and troponin T remains elevated up to (blank) days after injury

43
Q

T or F

troponins can be elevated for a variety of reason such as renal disease, GI bleed, stroke etc.

44
Q

The PPV for troponins and ACS is highest with other risk factors which are (blank X 3)

A

older patients
HTN
troponin > 1.0 ng/ml

45
Q

CKMB can be detected within (blank) hours of an event .. (undetectable at 72 hours). If initial CKMB is negative, repeat every (blank) hours

A

2 hours

6-9 hours

46
Q

Where do you find myoglobin?
When is it detected?
When is it a very sensitive marker?

A

skeletal and cardiac muscle
within 1 hr
within first 6 hrs of symptoms

47
Q

What does TIMI do?

A

uses risk data normally obtained in an ED to determine overall risk of adverse outcomes in pnts with UA/NSTEMI

48
Q

How do you use a TIMI?

A

assign 1 point for each of the following:

  • age >65
  • documented prior coronary artery stenosis > 50%
  • 3 or more conventional cardiac risk factors
  • Use of ASA within the previous 7 days
  • 2 or more anginal events in past 24 hrs
  • ST segment depression or elevation > 1mm
  • elevated cardiac biomarkers
49
Q

If you have a score of 6-7 on a TIMI scale, what is the percent risk of having a serious cardiac problem?

50
Q

What are the 8 measures that the GRACE model considers to calculate risk?

A 
Advanced age 
Killip class 
Systolic blood pressure 
ST-segment deviation 
Cardiac arrest during presentation 
Serum creatinine level 
Elevation of initial cardiac enzymes
51
Q

Killip class (blank) includes individuals with no clinical signs of heart failure.

Killip class (blank) describes individuals in cardiogenic shock or hypotension (measured as systolic blood pressure lower than 90 mmHg), and evidence of peripheral vasoconstriction (oliguria, cyanosis or sweating).

52
Q 
Killip class (blank) includes individuals with rales or crackles in the lungs, an S3, and elevated jugular venous pressure.
Killip class (Blank) describes individuals with frank acute pulmonary edema.
53
Q

How do you treat a patient with chronic stable angina who has non diagnostic biomarkers and ECG?

A
  • Consider a cardiac stress test
  • If negative discharge to home and f/u with PCP
  • modification of risk factors
54
Q

What are the principles of tx in UA/ NSTEMI?

A
  • Bed rest
  • Continuous cardiac monitoring (telemetry)
  • Relief of ischemia
  • Beta blockade
  • CCB
  • Antithrombotics
  • ACEI (if cardiomyopathy or CHF)
  • Anticoagulants
55
Q

What are the antithrombotics?

A 
ASA
Clopidegrel
Prasugrel
Ticagrelor
glycoprotein IIb/IIIa inhibitors
56
Q

What are the anticoagulants?

A

Heparins
Direct thrombin inhibitors
Factor Xa inhibitors

57
Q

What is the invasive tx for UA/NSTEMI?

Who should you do this in?

A

coronary angiography w/ potential revascularization

-patients with refractory chest pain or electrical instability or patients who are stabilized with high risk for clinical events.

58
Q

1/3 of patients with STEMI die within the first (blank) of ischemia

59
Q

What is the treatment goal of a STEMI? How do you do this?

A

restore blood flow to occluded vessel

  • Fibrinolytic therapy – Glycoprotein 2b/3a inhibitors
  • Heparins
  • Percutaneous coronary intervention (PCI)
  • Coronary artery bypass grafting (CABG)
60
Q

What is the ABCDE prevention guideline?

A 
A
Aspirin, antiplatelet agents, ACEIs/ARBs
B
Beta blockers and blood pressure control
C
Cardiac rehab (if applicable), cigarette smoking cessation and cholesterol management
D
Diet, diabetes control and depression management
E
Exercise and education

Block 9 Week 1 (7 decks)

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