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CABS2: Cardiology > Cardiac ischemia > Flashcards

Cardiac ischemia Flashcards

1
Q

what is hyperlipidemia associated with

A

genetic and acquired causes

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2
Q

what is total cholesterol

A

maintains cell membranes
requires building block for some nutritional absorption and hormone synthesis

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3
Q

what is LDL

A

low density lipoprotein
increases risk of cardiovascular disease - atherosclerotic plaque formation
helps to move cholesterol within the circulation
BAD

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4
Q

what is HDL

A

high-density lipoproteins
this is the “good” cholesterol, is considered bad if it is too low
brings cholesterols back to the liver

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5
Q

what are triglycerides

A

stored energy
breaks down for cellular metabolism, stored in adipose, liver

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6
Q

what is primary hyperlipidemia

A

familial
typically polygenetic source
types I-IV
can lead to xanthomas, pancreatitis, hepatosplenomegaly, atherosclerosis

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7
Q

what is secondary hyperlipidemia

A

acquired:
dietary (M/C assoicated with meat/animal fats)
medication SE
hypothyroidism,
DM
CKD
sedentary lifestyle
inflammatory disease states (psoriasis, crohn’s, IBD, COPD, smoking…)

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8
Q

what is the tunica intima

A

inner layer of simple squamous endothelium
contains properties discussed in heme (nitric oxide, PGI, heparin sulfate, TPA)
allows for immune system activation and diapedesis

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9
Q

what is the tunica media

A

smooth muscle layer, under autonomic control

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10
Q

what is the tunica externa (adventitia)

A

connective tissue layer
contains vasa vasorum

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11
Q

what is the vasa vasorum

A

vessels that feed the layers of the thichker/larger vesssels

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12
Q

what is smooth muscle

A

non-striated (thick and thin filaments but less organized)
lack sarcomere
involuntary
uninucleated fusiform cell
more elastic
spread of depolarization allow for spiral corkscrew pattern

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13
Q

where within the artery does atherosclerosis occur

A

within the intima of the arteries
foam cells (lipid filled macrophages) will accumulate in this layer
typically form in areas where there is repetitive injury to vessel wall

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14
Q

what are the stages and development of atherosclerosis

A

initial lesion- normal
fatty streak
intermediate lesion
atheroma
fibroatheroma
complicated lesion

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15
Q

what is the fatty streak

A

first stage in development of atherosclerosis
seen on the inner layer of the vessels (may be seen in earlier parts of life (by 20))
clinically silent as there is no luminal narrowing

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16
Q

what can cause the development of the fatty streak

A

associated with stressors, increased lipid deposition in the subendothelial space

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17
Q

What are foam cells

A

accumulation of monocytes (macrophages) that are engorged with cholesterol and create atherosclerotic plaques

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18
Q

what is a fibrous plaque

A

lipid rich core that will necrose and calcify = atheroma

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19
Q

what does atheroma lead to

A

remodeling with vascular expansion
allows for lumen size to stay intact
puts the patient at increased risk for unstable plaques - unstable angina
if no remodeling, have have shrinking of the atheroma included vessel - closure of the lumen - obstructive symptoms - stable angina

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20
Q

what are risk factors of CAD

A

hypercholesterolemia- elevated LDL
diabetets
hypertensions
smoking
inflammatory disorders

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21
Q

what are non-modifiable risks for CAD

A

age, gender, FH, ethnicity, genetic evidence, previous history of CVD

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22
Q

what are modifiable risks for CAD

A

BP
total cholesterol
HDL cholesterol
smoking
blood sugar/diabetes
BMI
markers of chronic inflammation

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23
Q

what are female-specific or predominant risk factors for CAD

A

pregnancy induced HTN
preeclampsia/eclampsia
gestational diabetes
PCOS
Menopause
systemic inflammatory rheumatologic diseases
mental stress/depression

24
Q

when do the coronary vessels fill

A

during diastolic relaxation

25
what determines coronary vascular resistance
hormones neural stimulation metabolic demand peripheral vascular resistance
26
what is a STEMI characterized by
complete occlusion of blood vessel lumen, resulting in trasmural injury and infarct to the myocardium, which is reflected by ECG changes and rise in troponin
27
what are ischemia symptoms
classic: chest pain, +/- radiation anginal equivalent: dyspnea, Nausea, diaphroesis and fatigue
28
what is levines sign
gripping the chest
29
what is angina
chest discomfort typically substernal or slightly to the left
30
what is myocardial ischemia
oxygen demand of the cardiac muscle outweight the oxygen being delivered when O2 demand increases, so do the symptoms: elevated HR, BP, wall tension/stress, increased contractility
31
what is chronic coronary syndrome
stable angina (reproducible)
32
what is stable angina
chronic ischemic heart disease history of reproducible angina (exercise induced myocardia ischemia) PLUS known risk factors for atherosclerotic disease symptoms last < 20 minutes once provocative activity has stopped has for atleast 2 months
33
what are the symptoms of stable angina
angina with increased cardiac demand non-anginal symptoms: dyspnea, pain away from substernal area, nausea, diaphrosesis, fatigue
34
what occurs during stable angina
acidosis, decreased ATP K+/Na+ pumps, increased lactate, release of serotonin, bradykinin, histamine, adenosine, increase thromboxane A2
35
what is stimulated with stable angia
stimulates sympathetic afferent pathways - syumpathetic ganglia discomfort can spread along corresponding dermatomes, neck, shoulder, jaw discomfort
36
What is acute coronary syndrome (ACS)
ST segment elevation - STEMI Non ST segment elevation - NSTEMI and Unstable angina
37
what are typical ACS descriptors
onset: gradual, varies based on activity provocation: exertional increase in symptoms Quality: discomfort, pressure, aching, tightness Radiation: arms and neck Site: can be diffuse Time: typically lasts < 30 minutes
38
how many types of acute myocardial infarctions are there
Type 1-type 5
39
what is type 1 MI due to
coronary atherothrombosis
40
what is the cause of type 2 MI
supply-demand mistmatch
41
how long does it take without blood supply does it take to cause tissue pallow and decreased contractility with AMI
one minute without blood supply
42
how long does it take for AMI to lose contraction
3-5 minutes ATP depletes, glycogen stores used up, lactate accumulates
43
what is unstable angina
new-onset angina or change in precipitating factors - takes less exertion/stress to induce symptoms than previous - may occur at rest - length of symptoms may last longer - increases severity or frequency increase risk of AMI no necrosis
44
what is a NSTEMI
acute coronary syndrome (ACS) m/c d/t disrupted atherosclerotic plaque - partial or intermittent blockage - ischemic disease - apoptosis/necrosis of myocytes - release of troponin
45
What is STEMI
event typically begins with atherosclerotic plaque rupture TRANSMURAL MI (complete obstruction of blood flow)
46
What is the J point
transition point into the ST portion
47
what is seen on a STEMI ECG
J point elevation > 1mm in 2+ contiguous leads
48
what is right ventricular infarction
associated with right coronary artery occlusion hypotensive - preload dependent decrease CO d/t decrease LV filling - shock DO NOT give nitroglycerine
49
What are STEMI mimics
Acute pericarditis myopericarditis (typically viral or autoimmune) left ventricular hypertrophy aortic dissection severe hypercalcemia
50
what is coronary vasospasm
presents like a STEMI diffuse or focal spasm of the coronary arteries defined as nitrate responsive angina with transient ECG findings may occur when at rest
51
what causes coronary vasospasm
hyper-reactivity of smooth muscle
52
what are the triggers of coronary vasospasm
Drugs: COCAINE smoking (major risk) vagal response PCI Botulism low magnesium Kounis syndrome
53
what is the presentation of coronary vasospasm
chronic, recurrent episodes of CP present like typical ACS from atherosclerotic disease gradual onset/offset may have radiation of discomfort Nausea, sweating, dizziness, dyspnea often younger patients GET A GOOD HISTORY
54
what are complications of ischemia
arrhythmias blocks cardiogenic shock ventricular free wall rupture ventricular septal defect decrease CO acute mitral regurgitation
55
what is papillary muscle dysfunction
rupture that may be due to ACS (STEMI or NSTEMI) may be partial or complete rupture most common at posteromedial papillary muscle - causes acute mitral regurgitation
56
what is ventricular aneurysm
complication of acute myocardial infarction infarcted areas of ventricles weakens chamber will enlarge overtime will scar- calcification increase risk for arrhythmias, HF increased risk for clot formation within ballooned areas
57
what is a mural thrombi
M/c with anterior STEMI - left anterior descending artery (LAD) associated with pts who have suffered apical aneurysm poor contractility of the apex relative blood stasis thrombus formation can lead to arterial embolic events

CABS2: Cardiology (11 decks)

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