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Med School > MI > Flashcards

MI Flashcards

1
Q

Risks for Atherosclerosis

A
  • Age, sex (male), total cholesterol, HDL cholesterol, smoking, DM, HTN, family history of premature CVD (Framingham heart study)
  • inter heart study then added: abdominal obesity, psychosocial index, Apo A/B ratio, exercise, alcohol (which actually seen to be protective)
  • newer risks: CRP, lipoprotein A (inherited risk factor, elevated in 20% of the population), chronic loud noise exposure, sedentarism
  • inflammation is a risk! SLE, RA, psoriasis, IBD, COPD, HIV, etc.
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2
Q

CVD in developing countries

A
  • low education has greater impact on CVD risk in low income countries
  • majority of CVD deaths are in lower income countries
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3
Q

Framingham risk score

A

Low - <10% 10 year risk
Intermediate - 10-20% 10 year risk
High - >20%10 year risk

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4
Q

Who can benefit from statins?

A
  • LDL over 5, DM, CKD, ASCVD
  • people with increased systemic inflammation but normal cholesterol
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5
Q

How does stress affect CVD?

A
  • increases SNS/ HPA axis/ HTN/ insulin resistance
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6
Q

Cholesterol

A
  • made by all cells except mature RBCs
  • major constituent of plaque
  • component of cell membranes, steroid and bile acid synthesis

input: diet and synthesis
output: bile acids and biliary cholesterol

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7
Q

Triglycerides

A
  • main dietary and endogenous fat
  • main source of immediate and stored energy
  • carried by chylomicrons and VLDLs
  • water insoluble lipid that must be solubilized and transported by lipoproteins (along with cholesterol)
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8
Q

Size of lipoproteins and their respective compositions

A
  • chylomicrons < VLDLs < LDLs < HDLs
  • smaller are more triglycerides, larger are more cholesterol/ phospholipids/ proteins
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9
Q

Journey of fat through the body
Different methods of entry into SI?

A
  • Emulsified fats are digested by lipase/ co-lipase
  • Cholesterol esters are digested by pancreatic lipase/ co-lipase into cholesterol and FFAs
  • monoglycerides and FFAs diffuse into SI
  • cholesterol enters via NPC1L1 transporter
  • these products are re-combined to form chylomicrons, which travel through the body via lymph
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10
Q

Role of lipoprotein lipase (LPL)

A
  • sits on capillaries to digest TGs and deliver FAs to issues for energy (similar role in VLDL catabolism)
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11
Q

Role of VLDL

A
  • body’s means of delivering FAs to tissues for energy, even when fasting
  • synthesized by the liver using MTP
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12
Q

How is LDL broken down?

A
  • binds to LDL receptors and internalized
  • hydrolyzed in a lysosome into cholesterol and amino acids
  • results in decreased HMG CoA reductase, decreased LDL receptors, and increased ACAT (produces cholesterol oleate with excess cholesterol)
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13
Q

Definition of dyslipidemia
Primary vs secondary

A
  • increased cholesterol and/or triglycerides and/or low HDL-C
  • Primary - genetic, often severe lipid elevations (cholesterol over 6.5 and LDL-C over 4.5 and TG over 3)
  • Secondary - diet/ obesity/ DM/ etc, often minor elevations
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14
Q

Signs of genetic hyperlipidemia?

A
  • tendon/ palmar/ eruptive xanthomas
  • xanthelasma
  • corneal arcus
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15
Q

Examples of genetic dyslipidemia

A
  • Familial hypercholesterolemia - mutations in LDL receptor/apoB, increased function of PCSK9
  • Dysbetalipoprotenemia - apoE2:E2 and overproduction of VLDL
  • Lipoprotein lipase deficiency - no LPL activity
  • Tangier disease - no ABCA1 activity (responsible for HDL formation)
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16
Q

Fat targets if low/ med/ high risk?

A

Low risk - LDL under 2.5, ApoB under 0.85, non HDL under 3.2

Med risk - LDL under 2, ApoB under 0.8, non HDL under 2.6

High risk - LDL under 1.8, ApoB under 0.7, non HDL under 2.4

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17
Q

Preferred fuel of heart when fasting?
What does the myocardium depend on?

A
  • FFAs
  • totally relies on aerobic metabolism (need enough ATP for cross bridge cycling in sarcomeres, can only be achieved if O2 is present)
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18
Q

What does the LMCA supply?
(originates from L sinus of valsalva)

A
  • L anterior descending supplies anterior wall of the L ventricle and most of the inter ventricular septum
  • Circumflex supplies the lateral wall of the L ventricle
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19
Q

What does the RCA supply?
(originates from the R sinus of valsalva)

A
  • SA and AV nodes
  • RV and posterior inter ventricular septum
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20
Q

What are the conductance vs resistance vessels of the heart?

A

Conductance - epi/myocardial penetrating vessels
Resistance - arterioles and pre-capillary sphincters

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21
Q

How is coronary flow affected by diastole? With ischemia, which part of the heart suffers first?

A
  • coronary flow to the LV is almost ALL diastolic
  • in systole, aortic root pressure is equal to LV pressure, thus almost no coronary flow
  • diastolic root pressure is higher than diastolic LV pressure, and so duration of diastole is important
  • endocardial ischemia will occur earlier and more severely

*Coronary perfusion gradient = aortic root pressure - LV pressure

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22
Q

Methods of Coronary resistance?

A

1 metabolic - ischemia increases adenosine, H/K/CO2/ decreased O2 that all lead to vasodilation

  • endothelial - production of NO/ prostacyclin (dilates) and endothelin (constricts)
  • neurogenic - SNS (constricts) and PNS (dilates)
  • myogenic - pressure/ flow sensitive smooth muscle in arteriolar walls
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23
Q

What can cause an increase in O2 demand?

A
  • bigger radius (preload)
  • bigger intraventricular pressure (impedence)
  • increased HR
  • increased contractility

*interestingly, a thicker wall requires less O2

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24
Q

What is the law of LaPlace?

A

Force in ventricular wall = (pressure x radius)/ 2x wall thickness

25
Q

What is coronary reserve?

A

difference between resting coronary flow and maximum coronary flow

26
Q

What leads to the chest discomfort experienced in angina?

A

Adenosine –> vasodilation

27
Q

When is flow reduced in atherosclerosis?

A

70% - reduction of flow
75% - angina
90% - cannot increase flow to meet demands

28
Q

What is an example of an acute rise of demand vs chronic?
Acute reduction of supply vs chronic?

A

Acute demand - exercise
Chronic demand - anemia, respiratory failure, CHF, shunt, HTN

Acute supply - MI
Chronic supply - atherosclerosis

29
Q

Where does atherogenesis most commonly occur?

A
  • occurs in the arterial intima (superficial to media and adventitia)
  • bends and branches w low shear forces/ turbulence and non-laminar flow (i.e. lesser curve of aorta)
30
Q

Role of endothelial cells

A
  • tight junctions act as a barrier to protect sub endothelial space
  • make mediators that maintain a non-thrombotic lumen, maintain sm cell relaxed state
31
Q

ECM composition

A
  • fibrillar collagen (strength), proteoglycans and elastin (flexibility)
32
Q

Process of artherogenesis

A
  • loss of endothelial cell alignment results in increased permeability and increased leukocyte adhesion molecules (ICAM/ VCAM/ P-selectin)
  • sub endothelial chemokine promote diapedesis of WBCs into sub endothelial space
  • monocytes retain lipids, resulting in macrophage foam cells
  • macrophages express scavenger proteins that uptake mLDL to the point of destruction, resulting in cholesterol/ crystal spillage and inflammation
33
Q

How are smooth muscle cells affected in atherosclerosis?

A
  • increased endothelin and angiotensin II and decreased prostacyclin/NO results in constriction
  • more IL-6, TNF-A, PAI-1 and tissue factor (inflammation)
  • proliferate and migrate to sub endothelial space, produce free radicals, synthesize excess ECM, fibrous cap formation
34
Q

Vulnerable vs. Stable plaque

A

Vulnerable - large lipid/ necrotic core, few sm cells, thin fibrous cap, little ECM, many foam cells esp. in shoulder, proteases, big plaque

Stable - thick fibrous cap, less lipids, fewer inflamm cells, dense ECM
*can be achieved by decreased LDL/BP/ATII and increasing HDL

35
Q

Optimal therapy for atherosclerosis

A
  • ASA (decrease platelet activity)
  • statins/ezetimibe/PCSK9 inhibitors (reduce cholesterol)
  • no smoking (reduces oxidized LDL, platelets, sm constriction)
  • DM therapy (reduces irritating glycated products)
  • exercise (increases laminar shear)
  • anti-hypertensives (reduces barotrauma and ox radicals)
36
Q

Chest pain criteria for angina

A
  1. Substernal chest discomfort with characteristic quality and duration
  2. Provoked by exertion/ emotional distress
  3. Relieved promptly by rest or nitroglycerin

*consider other causes if males under 40 and females under 60 with few risks, but test anyway if over these ages or severe/ multiple risks

37
Q

Ischemic symptoms

A
  • chest pain, dyspnea, shoulder/arm/hand/jaw/neck pain, nausea/ vomiting, diaphoresis, presyncope, arrhythmia
38
Q

Prognostic factors for stable CAD

A
  • anatomical distribution/ burden
  • ischemic burden
  • LVEF and wall motion abnormalities
39
Q

Criteria for myocardial injury (i.e. HF, myocarditis) vs. acute MI?

A

injury –> elevated cardiac tropnin
acute MI –> evidence of ischemia on ECG, rise and fall of troponin, pathological Q waves, loss of myocardium or wall motion abnormalities

40
Q

Unstable angina vs. non ST elevation MI vs. ST elevation MI

A

unstable angina –> transient acute ischemia not resulting in myocardial injury
- typical sx, negative biomarkers, +/- ischemia on ECG

Non-ST MI –> subendocardial ischemia resulting in myocardial injury
- typical sx, positive biomarkers, +/- ischemia on ECG

ST MI –> acute transmural ischemia (occlusive thrombus) resulting in MI and ECG changes
- typical sx, ECG changes, +/- imaging of ischemia
- do not need biomarkers for initial diagnosis

41
Q

What are ischemic biomarkers? when do they peak?

A
  • troponin I - cardiac myocytes
  • troponin T - cardiac myocytes and some skeletal muscle
  • creatine kinase - cytosol of most myocytes
  • creatine kinase-MB isoenzyme - specific to cardiac myocytes
  • myoglobin (muscle cells)
  • AST (myocytes and hepatocytes)
  • LDH (erythrocytes, muscle, kidneys, brain)

*linear peak at 1-2 days post AMI

42
Q

Type I MI vs. Type II

A

1 - plaque rupture/ erosion
2 - severe HTN/ sustained tachyarrythmis

43
Q

Stable vs unstable CAD?

A

Stable - predictable and low mortality, at least 70% lesion

Unstable - higher mortality, can be any size

44
Q

How does an MI kill you?

A
  • Mechanical VSD - short term, prevent with B-blocker and treat w surgery
  • Heart failure - long term, prevent with LV enhancers, treat with transplant

Recurrent MI - long term, prevent via risk factors, treat w revascularization

Ventricular arrythmias - prevent with B-blockers and LVEF preservation, treat with ICD

45
Q

Ways to help supply/demand/ cardioprotection?

A

Supply - antithrombotics and antiplatelets (prevent re-occlusion)

Demand - anti-ischemics

Cardioprotection - anti-arrythmics and anti-inflammatories

46
Q

Examples of antiplatelets and antithrombins used to prevent MI?

A

antiplatelet - ASA (aspirin) - inhibits TXA2 which activates platelets
- ticagrelor (collagen), voraxapar (thrombin), clopidogrel, prasugrel

antithrombin - unfractionated heparin - prevents conversion of fibrinogen to fibrin
- LMWH, fondaparinux (factor X),
* DOACs (rivaroxaban, apixaban, dabigatran are NOT used as they bleed you out!)

47
Q

Treatment if PI due to STEMI

A
  • dual antiplatelet therapy for 1 year (ASA and clopidogrel)
  • if after 1 year high risk of bleed -> SAPT or clopidorel
  • if low risk of bleed -> DAPT up to 3 years
48
Q

When should angiography be done?

A
  • only if medium risk (DM, CKD, EF <40%, PCI in last 6 months)
  • urgent only if high risk (elevated troponin, ST depression, T wave inversion, refractory angina, sx of heart failure, arrythmias)
49
Q

What should the initial anticoagulant given be?

A

IV heparin in invasive, fondaparinux if conservative (though avoid if PCI in the next 7 days)

50
Q

Medications to:
- lower afterload
- lower contractility
- lower HR
- lower preload
- increase fibrillatory threshold

A

afterload - Ca blocker, B-blocker, RAS antagonists

contractility and HR - Ca blocker, B-blocker

preload - diuretic, nitroglycerin

fibrillary threshold - B–blocker

51
Q

Sx of acute MI

A
  • chest pain radiating to both arms, 3rd heart sound, hypotension
  • women and elderly can present with R-sided chest pain, abnormal T waves, normal physical exam and troponin (always do serial troponins)
52
Q

Sx of acute thoracic aortic dissection

A
  • acute chest/ back pain and pulse differential in upper extremities, wide mediastinum, sinus tach
53
Q

Heart healthy diet

A
  • avoid saturated fats (ideally under 9%)
  • mediterranean diet, DASH diet (lowers both systolic and diastolic BP), portfolio diet
54
Q

Signs of a STEMI on ECG?

A
  • ST elevation in leads that overlie the affected tissue
  • often reciprocal ST depression in opposite leads
  • if a patient has had an MI before, they will have a pathological Q wave (inverted)
55
Q

Signs of ischemia on ECG?

A
  • ST depression or T wave flattening/ inversion
  • changes do not localize to an anatomical location
56
Q

Signs of pericarditis on ECG?

A
  • see diffuse ST elevation, diffuse PR depression, and PR elevation in aVR
57
Q

Which leads correspond to which anatomical region of the heart?

A

Inferior - II, III, aVF

Anteroseptal - V1, V2

Anterior - V3, V4

Lateral - V5, V6

58
Q

Consequences of an inferior STEMI?

A
  • hypotension, mitral regurgitation, complete heart block

Med School (21 decks)

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