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Medical Studies 1 > CVS Week 2 > Flashcards

CVS Week 2 Flashcards

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USMLE® Step 1 flashcards
1
Q

describe the impact of fixed vessel narrowing in the setting of stable coronary artery disease

A

in the presence of mild to moderate atherosclerosis, there is still preservation of coronary blood flow

however, in extensive narrowing, there is a pressure drop across the stenosis, leading to limited vessel flow

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2
Q

what are 3 factors that determines the hemodynamic significance of stenotic lesions

A

length of lesion and extent of narrowing

degree of compensatory vasodilation

myocardial O2 demand

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3
Q

how does endothelial dysfunction contribute to, and exacerbate, myocardial ischemia

A

impaired release of vasodilators, leading to a net vasoconstrictive effect

decline in antithrombotic properties of vasodilators such as NO and prostacyclins

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4
Q

describe the impact of metabolic disruption during ischemia

A

normally, the healthy myocardium uses fatty acids as the predominant substrate

however, when there is restricted O2 supply during ischemia, there is limited oxidative phosphorylation, resulting in increased rate of glycolysis and a shift from net lactate uptake to lactate production

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5
Q

what are 4 non-atherosclerotic factors that can result in ischemia

A

rapid elevation of myocardial O2 demand e.g rapid tachycardia

decreased blood O2 carrying capacity (anemia)

coronary vasospasm

congenital abnormalities or trauma to coronary arteries

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6
Q

what is coronary artery disease (CAD)

A

pathological process characterised by atherosclerotic plaque accumulation in the epicardial arteries, whether obstructive or non-obstructive

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7
Q

what are two types of stable CAD/chronic coronary syndrome (CSS)

A

fixed obstructive CAD

ischemia w non-obstructive coronary arteries (INOCA)

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8
Q

what are 3 types of angina

A

chronic stable

unstable

prinzmetal’s variant

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9
Q

describe chronic stable angina

A

demand ischemia

coronary flow impaired under conditions of high O2 demand leading to ischemia

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10
Q

describe unstable angina / prinzmetal angina

A

supply ischemia

coronary flow impaired under resting conditions leading to ischemia

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11
Q

what are the 3 characteristics/criteria of angina

A

constricting discomfort in the front of the chest or in the neck, jaw, shoulder, arm

precipitated by physical exertion

relieved by rest or nitrates within 5 min

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12
Q

typical angina meets how many things in the angina criteria

A

all 3

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13
Q

atypical angina meets how many things in the angina criteria

A

2 of the 3

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14
Q

non-anginal chest pain meets how many things in the angina criteria

A

one or none

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15
Q

describe grade 1 angina

A

angina only with strenuous exertion

presence of angina during strenuous, rapid, or prolonged ordinary activity (walking or climbing the stairs)

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16
Q

describe grade 2 angina

A

angina w moderate exertion

slight limitation of ordinary activities when performed rapidly, after meals, in cold, in wind, walking uphill etc.

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17
Q

describe grade 3 angina

A

angina w mild exertion

having difficulties walking one or two blocks, or climbing one flight of stairs at normal pace and conditions

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18
Q

describe grade 4 angina

A

angina at rest

no exertion needed to trigger angina

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19
Q

what are the 2 contemporary types of acute coronary syndrome (ACS)

A

non-ST elevatin myocardial infarction (NSTEMI)

ST-elevation myocardial infarction (STEMI)

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20
Q

traditionally, unstable angina also used to be considered as a type of ACS. why is this not the case anymore?

A

traditionally, UA was defined by absence of an elevated biomarker (troponin) level.

however, now that we have moved from sensitive tests to highly sensitive tests, the biomarker troponin can be seen to be present more often than before, meaning the diagnosis of UA under these conditions has now changed to NSTEMI

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21
Q

what is cardiac troponin

A

specific and sensitive biomarker of cardiac injury

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22
Q

what is the most common reason of ACS

A

obstruction of coronary artery blood flow by thrombus that develops as a result of underlying atherosclerotic plaque complication

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23
Q

what are 4 less common causes of ACS

A

spontaneous coronary artery dissection (SCAD)

coronary artery spasm

coronary microvascular dysfunction

MI w non obstructed coronary arteries (MINOCA)

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24
Q

describe plaque rupture

A

most frequent

develops in a lesion w a necrotic core and thin overlying fibrous cap

following disruption of fibrous cap, a luminal thrombus develops due to physical contact b/w platelets and thrombogenic necrotic core

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25
Q

describe plaque erosion

A

characterised by absence of endothelium rather than fibrous cap disruption

most eroded lesions lack a necrotic core and have a thick fibrous cap

lead to disturbance of flow resulting in toll-like receptor 2 activation, recruitment of neutrophils and subsequent promotion of de-endothelialisation. this allows blood to come in contact w plaque collagen to form neutrophil-rich thrombus

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26
Q

terms STEMI and NSTEMI correctly used in patients with…

A

clinical characteristics compatible w myocardial ischemia
AND
demonstrate elevated troponin

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27
Q

what 3 things must be taken into account to diagnose ACS

A

symptoms
ECG
serum troponin

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28
Q

describe symptoms patients with acute MI may present with

A

pain - chest (most common), abdomen, intrascapular, throat, jaw

dyspnea

diaphoresis (sweating)

nausea/vomiting

palpitations

weakness

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29
Q

the typical symptoms of an MI may not be present in…

A

women

diabetics

older individuals

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30
Q

an ECG allows initial categorisation of a suspected MI into one of three groups. what are the 3 groups

A

STEMI

NSTEMI

undifferentiated chest pain (non-diagnostic ECG)

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31
Q

describe ST elevation

A

result of transmural infarct

not often seen, but earliest change is dev of hyperacute or peaked T wave (localised hyperkalemia)

then, elevation of J point

then, ST elevation pronounced

then, ST segment may eventually become undistinguished from T wave

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32
Q

what other conditions can ST elevation be seen in

A

myocarditis

acute pericarditis

benign early repolarisation variant

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33
Q

describe STEMI

A

complete thrombotic occlusion of coronary vessel

transmural infarction (‘full thickness’)

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34
Q

describe NSTEMI

A

partial thrombotic occlusion of coronary vessel

subendocardial infarction (as blood can still be supplied to surrounding tissue in areas where the vessel isnt occluded)

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35
Q

describe non-ST elevation

A

result of subendocardial infarct

manifest by ST depression and/or T wave inversions without ST segment elevations

ST-T wave abnormalities may be diffuse in many leads or more commonly localised to leads associated w region of ischemic myocardium

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36
Q

describe non diagnostic ECG

A

initial ECG often not diagnostic in those ultimately diagnosed w acute MI

for any in whom suspicion of ACS remains high, repeat ECG in 20-30 min intervals

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37
Q

what is troponin

A

complex of 3 regulatory proteins (C, I and T) integral to skeletal and cardiac muscle contraction

cardiac troponin I and T are specific and sensitive biomarkers of cardiac injury

an elevation must be interpreted in context of history and ECG

rise and fall must be document in acute MI (change of 5 requires cardiology opinion)

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38
Q

what are 6 life threatening conditions

A

ACS

stress cardiomyopathy

aortic dissection

pulmonary embolism

tension pneumothorax

esophageal rupture

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39
Q

outline stress cardiomyopathy

A

transient regional systolic left ventricular dysfunction in setting of stress

substernal pain similar to acute MI

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40
Q

outline aortic dissection

A

acute chest and back pain

sharp pain

ripping or tearing quality

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41
Q

outline pulmonary embolism

A

dyspnoea, followed by pleuritic pain and cough

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42
Q

outline tension pneumothorax

A

sudden onset of pleuritic chest pain and dyspnea

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43
Q

outline esophageal rupture

A

associated w straining and vomiting

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44
Q

what are 3 non life threatening cardiac conditions

A

stable myocardial ischemia/angina

peri(myo)carditis

aortic stenosis

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45
Q

outline peri(myo)carditis

A

sharp pain

pleuritic

decreased by leaning forward

radiates to trapezius ridge

associated w fever

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46
Q

outline aortic stenosis

A

exertional pain

dyspnea

presyncope/syncope

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47
Q

what are 5 non life threatening pulmonary conditions

A

pneumothorax

pneumonia

malignancy

asthma/COPD exacerbation

pleuritis

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48
Q

what are 4 non life threatening GI conditions

A

GORD

peptic ulcer disease

esophageal motility disorders

esophagitis

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49
Q

when should troponin be measured to diagnose MI

A

for high sensitivity troponin-T, negative test taken after 2 hrs after symptom onset is reliable for ruling out MI

if first test is negative within 2 hrs, do another test within 3 hrs

for standard sensitive troponin test, need to get negative troponin at least 6-8 hrs after symptom onset

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50
Q

which leads of ECG correspond with the lateral region of the heart

A

l, aVL, V5, V6

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51
Q

which leads of ECG correspond with the anterior region of the heart

A

V1, V2

52
Q

which leads of ECG correspond with the inferior region of the heart

A

ll, lll, aVF

53
Q

which leads of ECG correspond with the septal region of the heart

A

V3, V4

54
Q

leads V1-V4 are correlated with which artery/s

A

LAD

55
Q

leads l, aVL, V5, V6 are correlated with which artery/s

A

LCx

diagonal branch of LAD

56
Q

leads ll, lll, aVF are correlated with which artery/s

A

RCA or dominant LCx

57
Q

what are the 3 general stages of acute STEMI management

A

pre hospital

in hospital (ED, cath lab, CCU)

post hospital discharge

58
Q

what is involved in the pre hospital stage of STEMI management

A

make diagnosis

assess risk

ensure stability

aim for early reperfusion

59
Q

what is involved in the in hospital stage of STEMI management

A

establish reperfusion

prevent re-thrombosis

avoid, recognise, and manage acute complications

educate and initiate secondary prevention

60
Q

what is involved in the post hospital stage of STEMI management

A

maintain secondary prevention

monitor compliance and risk factor targets

diagnose recurrences

61
Q

outline immediate management of STEMI

A

early ECG

insert cannula

selection of reperfusion strategy (less than 30 mins for thrombolytics and less than 90 mins for PCI)

300mg aspirin

analgesia (nitrates, morphine, and oxygen if SaO2 less than 90)

occasionally IV metoprolol

maintain patient at rest

treat bradycardia and hTN

62
Q

what is the importance of early intervention to reestablish reperfusion (through either thrombolytics or PCI)

A

time = myocardium

the longer the patient goes untreated, the more of the myocardium becomes damaged and hence the risk of death increases largely

early intervention allows for prevention of extensive damage

63
Q

what is PCI

A

percutaneous coronary intervention

method of establishing reperfusion

gold standard treatment in patients with STEMI or MI w new LBBB who present within 12 hr of symptom onset

64
Q

what is thrombolysis

A

method of establishing reperfusion

uses thrombolytics for STEMI patients if Sxs <12hr

use if patient not have access to PCI or capability to transfer for PCI in 90min

aim for needle time within 30 min

65
Q

what should you do after successful thrombolysis

A

aim for routine early coronary angiography within 3-24 hr after successful thrombolysis

initiate preparatory anticoagulant + antiplatelet regimen before and during transfer to PCI hospital

66
Q

what are some notable early complications of acute STEMI

A

LV impairment w many consequences e.g acute pulmonary oedema, cardiogenic shock, long term HF, LV thrombus

arrhythmias

mechanical: papillary muscle rupture, ventricular septal defect, free wall rupture causing tamponade

pericarditis

67
Q

outline the use of echocardiogram after an acute STEMI

A

usually performed after 24-48 hr, then repeated at 3-6 months

gives assessment of LV function and regional wall motion and can look for pre existing complications from MI e.g valve dysfunction or septal rupture

68
Q

outline the use of cardiac MRI after an acute STEMI

A

less commonly done than echo, unless there is ambiguity abt the diagnosis of MI or if need to assess myocardial viability and scar formation

69
Q

describe the management of NSTEMI/UA

A

timeline for NSTEMI angiography is described as urgent, rather than an emergency

angiography within 24hr of admission

prior to angio: IV access, aspirin, sublingual GTN, therapeutic parenteral anticoagulation, admission to cardiac monitored bed, commencement of statin and possible ACE inhibitor/beta blocker

70
Q

what can be done for post MI care according to the australian guidelines

A

dual antiplatelet therapy for 12 months

statins

ACE inhibitors

beta blockers

71
Q

what is the LDL goal for secondary prevention of CHD

A

<1.8mmol

72
Q

what is the HDL goal for secondary prevention of CHD

A

> 1.0mmol

73
Q

what is the triglyceride goal for secondary prevention of CHD

A

<2.0mmol

74
Q

describe use of beta blockers in MI patients

A

should be prescribed for most patients after an MI unless contraindicated

75
Q

describe use of ACE inhibitors in MI patients

A

should be given early after an MI/UA event and their use reviewed later

76
Q

describe BP management in CHD patients

A

achieve and maintain <130/80

77
Q

what 7 pharmacological things can be used to prevent further ischemic events

A

antiplatelets and/or anticoagulants

lipid lowering therapy

RAAS antagonists

BP control

beta blockers

colchicine

vaccination

78
Q

describe the use of antiplatelets/anticoagulants

A

ALL patients with an atherosclerotic vascular condition should be considered for some type of AP/AC treatment unless contraindicated or inappropriate

can include aspirin, anticoagulant or combination of both (dual antiplatelets, and/or w one anticoagulant)

79
Q

what are 3 indications for deciding antiplatelet/anticoagulant therapy

A

evidence base in each vascular territory

presence of other indication e.g AF

risk of thrombosis

80
Q

what are 2 contraindications for deciding antiplatelet/anticoagulant therapy

A

risk of bleeding including falls

treatment adherence issues

81
Q

what are 4 principles of antiplatelet/anticoagulant use

A

decision based on patient circumstances then set and forget

more drugs combined = higher efficacy = higher risk of bleeding

need to use dual antiplatelet for a period of time and then single when patient has a stent

if patient has AF or thrombus, then need to combine w anticoagulant

82
Q

describe the use of lipid lowering therapy

A

ALL patients w atherosclerotic vascular condition should be considered for lipid lowering therapy unless contraindicated or inappropriate

generally start w statin, then, if unsuccessful or have adverse effect, move to another LDL lowering agent

if have other issues, such as low HDL or high TG, then consider other agents like fibrates

83
Q

why target the RAAS system (ie why use RAAS antagonists)

A

upregulation of RAAS associated w remodelling of arteries when ischemic events occcur

therefore, blocking RAAS helps prevent further remodelling such as arteriolar hypertrophy which drives further ischemia

84
Q

who should get a RAAS blocker

A

recent MI

diabetics

renal disease

HTN w vascular disease

systolic HF or LV impairment

ie pretty much everyone w atherosclerotic vascular disease

85
Q

who does not need RAAS blocker

A

no recent ischemic events

well controlled BP

no diabetes

no renal disease

no systolic HF and normal LV function

low risk groups e.g non smokers

86
Q

what causes MI type 1

A

plaque rupture/erosion w occlusive thrombus

plaque rupture/erosion w non-occlusive thrombus

87
Q

what causes MI type 2

A

atherosclerosis and O2 supply/demand imbalance

vasospasm or coronary microvascular dysfunction

non-atherosclerotic coronary dissection

O2 supply/demand imbalance alone

88
Q

what are 4 non modifiable risk factors for ASCVD

A

increasing age

sex

genetic factors

race/ethnicity

89
Q

what are 3 modifiable factors for ASCVD

A

diet

smoking

physical inactivity

90
Q

how can smoking lead to ASCVD

A

damages blood vessels and promotes inflammation, accelerating atherosclerosis progression

91
Q

how can physical inactivity lead to ASCVD

A

sedentary lifestyle promotes weight gain and reduced CV fitness

92
Q

how can diet lead to ASCVD

A

poor dietary choices high in saturated fats can contribute to plaque buildup in arteries

93
Q

how can age lead to ASCVD

A

arterial dmg accumulates overtime

94
Q

how can family history lead to ASCVD

A

increase susceptibility

95
Q

how can biological sex lead to ASCVD

A

men tend to have higher risk compared to premenopausal women

96
Q

what is hyperlipidaemia

A

high levels of lipids, including cholesterol and triglycerides, in the blood

97
Q

what is hypercholesterolaemia

A

high levels of cholesterol in the blood

98
Q

how does fibre intake reduce CHD risk in terms of GI action

A

soluble fibre binds to cholesterol in the digestive tract and helps eliminate it from the body, leading to lower LDL

99
Q

how does fibre intake reduce CHD risk in terms of sugar absorption

A

fibre slows down the absorption of sugar, promoting stable blood sugar levels and reducing the risk of diabetes

100
Q

outline the benefits of food fortification with plant sterols and stanols

A

they are structurally very similar to cholesterol and can compete w dietary cholesterol for absorption in the digestive tract via competitive inhibition

this competition leads to reduced cholesterol absorption, resulting in lower LDL

101
Q

what components does the DASH diet place an emphasis on and why

A

fruits and veg - primary source of nutrients that help lower BP

whole grains - sustained energy and additional fibre to diet

lean protein - helps reduce saturated fat intake

102
Q

what components does the mediterranean diet place and emphasis on and why

A

plant-based foods - provides essential vitamins, minerals, fibre, antioxidants

healthy fats - provides monounsaturated fats and omega-3 fatty acids

moderate dairy - sources of calcium and protein but contain less fat

103
Q

outline the australian dietary guidelines

A

encourages consumption of food from all 5 food groups

emphasises importance of maintaining healthy body weight

not directly related to dietrary, but also encourages physical activity

104
Q

describe peripheral artery disease (PAD)

A

atherosclerotic affection of the peripheral arterial tree, rather than cerebrovascular, cardiac, or abdominal vasculature

it has a tendency towards lower limbs

105
Q

what are the symptoms/signs of PAD

A

often asymptomatic

most common symptom is intermittent claudication

HTN

arcus cornealis

tar staining

106
Q

outline the pathophysiology of PAD

A

atherosclerotic plaque > arterial stenosis > collateral blood supply > further stenosis in these too > reduced peripheral perfusion > peripheral arterial ischemia > claudication and other symptoms/signs

107
Q

what is cerebrovascular atherosclerosis

A

condition characterised by the build-up of fatty deposits in the blood vessels that supply the brain

this can also cause clots which can occlude or stenose the arteries leading to ischemic stroke

108
Q

what are the symptoms/signs of cerebrovascular atherosclerosis

A

unilateral weakness

confusion

unilateral vision loss

hemi-negligence

trouble speaking

dizziness/syncope

109
Q

explain the mechanism of intermittent claudication

A

atherosclerotic plaque > arterial stenosis > reduced peripheral perfusion > increased O2 demand during exertion > insufficient perfusion > ischaemia > buildup of metabolites > intermittent claudication

110
Q

what are pharmacological options to manage PAD and cerebrovascular atherosclerosis

A

dual antiplatelet therapy

statin therapy

ACE inhibitor

111
Q

what are non pharmacological options to manage PAD and cerebrovascular atherosclerosis

A

smoking cessation

dietary modification

regular exercise

112
Q

what is chronic limb ischemia

A

range of symptoms and signs of limb ischemia that have developed over time

ranges from asymptomatic to limb-threatening

113
Q

what is chronic limb threatening ischemia

A

collection of symptoms and signs depicting a critical reduction in perfusion which is inadequate to maintain healthy tissues at their lowest metabolic demands ie at rest

114
Q

what is acute limb ischemia

A

sudden decrease in limb perfusion leading to potential threat to limb viability

115
Q

what are the 3 stages of acute limb ischemia

A

subcritical - doppler signal/no neurological deficit

critical - no doppler signal/neurological deficit

irreversible - complete neuro deficit/tense muscles/no cap. refill

116
Q

what the 6 signs (6 p’s) of acute limb ischemia

A

pain

pallor

pulseless

paraesthesia

paralysis

perishingly cold

117
Q

what are 2 conservative interventions for PAD

A

exercise

analgesia

118
Q

what are 4 pharmacological interventions for PAD

A

antiplatelets

statins

anticoagulants

thrombolytics

119
Q

what are 4 endovascular interventions for PAD

A

balloon angioplasty

stents

thrombolysis

embolisation

120
Q

what are 5 surgical interventions for PAD

A

amputation

thrombectomy

endarterectomy

patch plasty

grafts

121
Q

aside from PAD, what are 3 differential diagnoses for leg pain

A

osteoarthritis

lumbar nerve root irritation

spinal canal stenosis

122
Q

outline osteoarthritis for leg pain

A

pain w exercise

pain w sitting/lying down

not relieved by just standing still, need to sit down

123
Q

outline lumbar nerve root irritation for leg pain

A

aching in calf

pain radiation from back of leg from buttock to ankle

need to sit or lie down for relief

spinal flexion may help

straight leg raise may precipitate the pain

124
Q

outline spinal canal stenosis for leg pain

A

pain can be very similar to claudication

have to sit or lie down to relieve pain

pain can occur while just standing

often takes a long time to settle after walking

125
Q

what are 4 investigations that can be used for carotid disease

A

duplex ultrasound

CT-angiography

MR-angiography

DSA

Medical Studies 1 (16 decks)

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