CAD Flashcards

1
Q

CAD There are multiple causes (Bill has spasms)

A

Atherosclerosis
Thrombosis
Spasm of coronary arteries

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2
Q

The most prevalent cause is

A

ATHEROSCLEROSIS

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3
Q

Atherosclerosis is

A

insidious, progressive disease that results in coronary arterial narrowing or complete occlusion.

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4
Q

CAD: INCIDENCE / PREVALENCE - is it common?

A

LEADING CAUSE OF DEATH WORLDWIDE

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5
Q

CAD ETIOLOGY - fatty

A

CAD has a long latent period. Fatty streaks can appear within the aorta during childhood.
Symptoms don’t occur until plaque occludes 75% of the vessel’s lumen.
This usually happens in late middle age.

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6
Q

Risk factors for developing CAD include (Bill is a crepe homo)

A

AGE GENDER
FAMILY HISTORY RACE
HYPERLIPIDEMIA HIGH-FAT DIET
HOMOCYSTINE HTN
SMOKING DM
OC’s (Oral Contraceptives) OBESITY
PHYSICAL ACTIVITY STRESS/ANXIETY
ELEVATED hs-CRP

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7
Q

AGE:

A

AGE: In general CAD is seen in middle and old age

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8
Q

GENDER:

A

Women get CAD 10 years later than men.
42% of Women vs 23% of men die within one year after MI
Ten years after menopause, CAD rates are the same for both sexes.

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9
Q

family hx - before what age? (think of mom)

A

Positive family history of a close relative with an MI or STROKE before age 60

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10
Q

race

A

Nonwhite populations of both genders

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11
Q

HYPERLIPIDEMIA (Elevated Cholesterol) - leading cause of what diseases?

A

Leading cause of atherosclerosis and CAD.

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12
Q

HOMOCYSTINE (homo is an error)

A

Hyper-Homocystine is a genetic error of metabolism.
High levels are associated with ↑ atherosclerotic CAD.

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13
Q

HYPERTENSION - what area does it damage?

A

HTN causes damage to the endothelium of the arterial bld vessels where plaque can adhere

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14
Q

Cessation of smoking drops the coronary risk by

A

± 50% within 1 year. (more cigarettes the higher the risk)

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15
Q

DIABETES MELLITUS - how much does it raise chance of CAD?

A

Diabetes triples or quadruples the risk of developing CAD.

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16
Q

ANGINA: what happens? (my angie)

A

Chest Pain
Caused by diminished blood supply to myocardium.
Transient
Pain usually lasts 3 to 5 minutes
Relieved by rest or Nitroglycerin.

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17
Q

Angina: progression

A

Risk factors contribute to plaque formation
Atherosclerosis develops
At 75% occlusion myocardium is deprived of blood flow when there is a increase demand on the heart (5 E’s)

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18
Q

ANGINA
PRECIPITATING FACTORS- The 5 E’s (Angie E’s)

A

The 5 E’s
Exertion (painting, lifting, sexual activity…)
Emotion (Stimulates the sympathetic nervous system – Anger, fear)
Eating (Large heavy meal – ↑ workload to heart)
Extremes (hot/cold) (warn pts if they’re traveling to cold or hot places)
Excitation (overly excited)
Cigarette smoking (Vasoconstriction & ↑ HR)

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19
Q

There are a range of clinical presentations of CAD (4 - stable…)

A

Stable Angina
Unstable Angina
Myocardial Infarction
Sudden Cardiac Death

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20
Q

STABLE ANGINA

A

Predictable
Caused by similar precipitating factors
May describe it as “my usual chest pain”.
Pain better with rest, or nitroglycerin

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21
Q

UNSTABLE ANGINA

A

Previously stable angina changes pattern
Unpredictable
Can occur with increasing frequency
Can be provoked by minimal or no exercise
Unstable angina may require immediate hospitalization and eval for MI

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22
Q

UNSTABLE ANGINA - outcome?

A

May result from a deterioration of a once stable plaque

Pt is at risk for of complete thrombus formation

Lesion can become stable again or it can progress to MI (it can go either way)

23
Q

VARIENT (PRINZMETAL) ANGINA - (The prince is a spaz)

A

Rare.
coronary spasm

24
Q

SILENT ISCHEMIA

A

ECG monitoring and stress testing demonstrates myocardial ischemia but patient doesn’t have pain. (zero symptoms)

25
Diagnostic tests for Angina - (Angie exercises)
ECG Exercise Treadmill Angiogram
26
What does CRP do? (Crp cooking)
CRP (c-reactive) is a good predictor of CV disease. CRP activates the clotting system Inflammation starts and immune cascade begins leading to: Thrombus formation Thrombus grows and occludes vessel
27
CRP C-Reactive Protein - it's just elevated
hs CRP (highly sensitive CRP) is elevated in pts with atherosclerotic inflammation at risk for MI
28
Treatment of Stable Angina - what meds? (3)
NITRATES BETA-BLOCKERS CALCIUM CHANNEL BLOCKERS ASA LIFE-STYLE CHANGES quit smoking Diet Exercise ↓ stress
29
TX of Stable ANGINA- TREAT CO-EXISTING MEDICAL CONDITIONS (that's it)
CAD DM HTN HYPERLIPIDEMIA OBESITY
30
Tx Hyperlipidemia Reduce Cholesterol - Total cholest - what number? (Cholesterol in the year 200)
Low fat diet, exercise, and lipid lowering drugs Total cholest < 200
31
To lower LDL: (lov LDL)
HMG Co-A reductace “Statins” (Lovastatin). Lo-fat, lo-cholesterol diet
32
To raise HDL: (Nya had HDL)
Exercise Niacin low-cholesterol, low-fat diet
33
To lower Triglycerides: (Tri Nya)
Exercise Niacin low-fat diet
34
NITROGLYCERIN USE
SUBLINGUAL NTG Q5min X 3 DOSES FOR CHEST PAIN KEEP NTG EASILY ACCESSIBLE (NTG NECKLACE) KEEP IN TIGHTLY CLOSED DARK GLASS DON’T CARRY IN POCKETS NEAR BODY AS HEAT WILL DEGRADE POTENCY. CAUTION REGARDING POSTURAL HYPOTENSION - don't stand up right after taking it - fall precaution IF PAIN PERSISTS AFTER 3 DOSES SEEK IMMEDIATE MEDICAL ATTENTION!
35
TREATMENT OF UNSTABLE ANGINA - just chest pain protocol
Change from stable to unstable Angina can be life threatening Patient may be having an MI INITIATE CHEST PAIN PROTOCOL
36
Treatment for Unstable Angina - MONA BET
Morphine Nitroglycerin Oxygen Nitroglycerin ASA Beta Blockers ECG PCI (Percutaneous coronary intervention) with GPll/lll inhibitor Thrombolytics
37
CHEST PAIN PROTOCOL - how often for BP?
ASSUME EVERY ADULT PT C/O CP IS HAVING AN MI UNTIL PROVEN OTHERWISE. ALSO CONSIDER DISSECTION AND PE. ASSESS PAIN: Location, onset, duration, quality, radiates, 1/10 (assess EVERY time you give pt medication) RISK FACTORS: Previous MI, CAD, DM, HTN, Hyperlipidemia VS (cycle BP every minute) O2 4L pnp, O2 Sat (ask pt if they need 02) 12 Lead EKG ALERT MD IV ACCESS MEDICATIONS, DRUGS, ETOH, TOBACCO, FH ASSOCIATED SYMPTOMS: SOB, DIAPHORESIS, PALPATATIONS PHYSICAL EXAM: VS, CV (S3, S4, bruits, murm), RESP (O2 sat, rales) CXR (CHF, pneumothorax, dissection, cardiomegaly) TROPONIN, CK-MB, CBC, COAG’s (PT, INR), CHEM (Lytes, Creat, gluc…) TX: PCI with stent and GPll/lll inhibitor (Abciximab...) or Thrombolytics
38
look at slide
about locations of pain during MI
39
(highly sensitive CRP) - better indicator of MI than
cholesterol alone
40
pts on statins - does the lumen size change?
lumen size is unchanged***but lipid core is smaller - harder to get through.
41
how does Hormone Replacement Therapy (HRT) effect CAD?
Hormone Replacement Therapy (HRT) may cause an increase in CV disease.
42
CAD causes (Bill dissects)
Coronary dissesection Aneurysm
43
homocystine (amino acid - too much damages arteries) treatment (homo needs vitamins)
Tx with folic acid and vitamin B6, normal weight, exercise, and no smoking.
44
stable angina - how much blockage?
Result of fixed lesions (blocks) of more than 75%.
45
stable angina - is it during rest?
Usually exercised induced, rarely occurs at rest.
46
stable angina - EKG
EKG → normal to ST depression
47
angina labs (Angie needs a baseline) - 3 of them (Angie reacts w/ troponin and cholesterol)
Cholesterol panel, CRP test, troponin (get a baseline troponin first)
48
hs CRP levels are a better indicator of
who will have an MI in the next few months than the Cholesterol level.
49
CRP levels - the numbers (crepes are my fav number)
Levels of > 3.1 assocated with AMI
50
LDL - what level is good? (LDL is 100%)
LDL to < 100 mg/dl in pts with CAD
51
Triglycerides - what level is good? (Tri the videogame)
Triglycerides to < 140
52
HDL - what level is good? (Hiddle is middle-aged)
HDL > 35.
53
med to lower trigylcerides (tri the gem)
Gemfibrozil
54
treatment for chest pain
PCI with stent and GPll/lll inhibitor (Abciximab...) or Thrombolytics