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phase 2a mine > cv top tier > Flashcards

cv top tier Flashcards

1
Q

which gender is IHD more common in

A

men

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2
Q

non modifiable risk factors for IHD

A 
family history
age
smoking
ethnicity- SE asia
man
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3
Q

what ethnicity is associated with IHD

A

se asia

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4
Q

what lifestyle factors are associated with IHD

A

smoking
diet/obesity
excercise/activity

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5
Q

what clinical factors are associated with IHD

A 
Diabetes
Hypertension
High lipids, high cholesterol
Previous history of CHD
Kidney disease
Premature menopause (i think oestrogen is protective somehow)
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6
Q

psychosocial factors are associated with IHD

A

Behaviour pattern - type A (modifiable)
–Hostile, impatient, anger, anxiety, determined, competitive

Depression/ Anxiety

  • -These cause CHD and CHD causes these :/
  • -Could have common antecedents eg deprivation

Work

  • -High demand, low control
  • -Stress
  • -Many hours

Social support

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7
Q

IHD cause (general)

A

atherosclerosis

  • more resistnace, so flow rate slows
  • pressure increased with reduced radius
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8
Q

angina causes

A

mismatch of supply and demand

SUPPLY OF HEART
Anaemia
Hypoxia
Atherosclerosis stenosis = main eg aortic stenosis

DEMAND OF HEART
Hypertension
Tachycardia, arrythmia
Vascular heart disease

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9
Q

causes of MI

A 
IHD/CHD (plague stenosis)
Thrombus 
Embolus
Muscle spasm
Drug use eg cocaine
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10
Q

excarberating factors of angina

A 
Cold
Activity
Stress
Post prandial
(anger/excitement)mi
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11
Q

types of angina

A

PRINZMETAL (CORONARY SPASM)

MICROVASCULAR

UNSTABLE / CRESCENDO

CUBITIS

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12
Q

prinzmetal’s angina=

-triggers

A

coronary spasm

  • at rest, cold, smoking, cocaine, stress, vasoconstriction, atheroscl
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13
Q

microvascular angina

A

microartery stenosis

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14
Q

unstable angina

aka crescendo angina

A

= acute coronary syndrome

stenosis is not constant, the atherosclerosis is changing and so thrombus is more likely. Pain changes/worsens. Pain at rest/minimal exertion, more serious

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15
Q

cubitis angina

A

when lying down (=recumbent)

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16
Q

MI pathophysiology

A

ischaemia of heart muscle –> cardiac tissue necrosis/infarction

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17
Q

STEMI vs NSTEMI

A

STEMI- damage to full thickness of wall due to full coronary occlusion

NSTEMI- damage to partial thickness of wall due to partial coronary occusion of ful occlusion of minor coronary artery

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18
Q

which area of heart does LAD occlusion infarct

A

anterior

septal

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19
Q

what area of heart does L circymflex occlusion infarct

A

posterior

lateral

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20
Q

what area of heart does right coronary artery occlusion infarct

A

inferior

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21
Q

what blood test reveals MI

why

A

raised troponin I and T (measure ev 3h)

enzyme that regulates actin/myosin contraction and is a sensitive marker of cardiac muscle injury

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22
Q

unstable agina/MI heart murmur

A

pansystolic heart murmur

also mitral regurg

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23
Q

is blood pressure high or low with MI/angina

A

can be either

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24
Q

describe pain of stable angina

A

weight /tight band
middle of chest
worse when cold/postprandial/ stress/ excercise
may radiate to arm/jaw/neck/teeth/shoulder
relieved with rest/GTN

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25
Q

what other symptoms come with IHD (other than chest pain)

A 
sob, dysponea
nausea
sweaty,
 fainty
fatigue
palpitations
distress/anxiety
(syncope
oedema)
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26
Q

stable angina ECG?

A

stress ECG = excercise test

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27
Q

imaging for IHD

A

transthoracic MRI
perfusion MRI
invasive /CT coronary angiography **
CXR

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28
Q

MI management

A

pain releif
oxygen (if hypoxic)
antiplatelet/anti-coag (clopidogrel, aspirin)
maybe b blocker

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29
Q

what type of drug is clopidogrel

A

P2Y12 inhibitor

antiplatelet/anticoag (not sure which)

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30
Q

angina medication

A 
nitrates 
opioid
oxygen
antiplatelet
antihypertensives
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31
Q

how do nitrates work

A

venodilators
reduce pre load
dilate coronary arteries
pain killer

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32
Q

dual therapy

A

aspirin + P2Y12i/glycoprotein IIb/IIa/ B block/ACEi/statin

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33
Q

angina criteria for stenting

A

1 - if STEMI elevation is significant

    • > 1mm in 2 contingous limb leads
    • > 2mm in 2 contiguous precordial (chest) leads

2- new onset LBBB

3 -posterior MI

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34
Q

stenting technical word

A

PCI (percutaneous coronary intervention)
or
angioplasty

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35
Q

where does bypass (CABG) connect

A

artery off aorta to coronary artery
+
vein graft

36
Q

what is the medical treatment for prinzmetal’s angina

A

amlopidine (CCB)

coronary spasm

37
Q

what is tamponade

A

compression of heart from fluid in pericardial sac

complication of pericarditis

38
Q

which B block is best for preventing arrythmias post-MI? and why?

A

propanolol

also blocks sodium channels

39
Q

how does B blockers work

A

Slows heart (chron) + reduces force of contraction (inotropic)

  • -Less output, less demand (for coronary vessels)
  • -Lower HR means better oxygen distribution
40
Q

B blockers side effects

A

low HR so tired, cold hand/feet, erectile dysfunction

41
Q

how do CCB work

A 
Dilate arteries (ca channels needed for vasoconstriction)
--Reduce afterload so less resistance
42
Q

how do ACEi work

A

Vasodilation and less water retention

Lower BP so less resistance

43
Q

why is mitral regurgitation a complication of MI

A

myocardial scarring preventing valve closure

44
Q

what is dressler’s syndrome

A

a complication of mI

secondary form of pericarditis - injury to heart/pericardium –> fever/ pericarditis/ pain/ effusion

45
Q

what causes high baseline troponin level

A 
kidney disease
chronic heart disease
sepsis
PE
myocarditis
pulmonary dissection
46
Q

bypass pros and cons

A

PROS
revascularization longer than stenting - lower risk of recurrent angina
better for diabetics

CONS
risk atherosclerosis + restenosis
invasive- worse for old and young
longer hospitalization
scar
not repeatable - high risk of mortality/morbidity
47
Q

PCI pros and cons

A 
PROS
less invasive - better for old and young
repeatable
shorter hospitalisation
no scar

CONS
high re-stenosis rate- may need repeat
requires dual antiplatelet therapy

48
Q

heart failure age distribution

A

increases with age

49
Q

risk factors/causes of heart failure, name 5

A

heart condition

1 IHD (angina)
2 pericarditis
3 hypertension
4 cardiomyopathy
5 arrythmias
6 congenital heart problem
7 valve problems
8 pulmonary hypertension

not CV related
1 anaemia
2 excess alcohol

50
Q

heart failure pathophysiology

A

efficiency of heart as a pump is impaired, so unable to deliver blood at a rate equal to the requirements of the metabolising tissues (despite normal/increeased venous return)

51
Q

acute vs chronic heart failure. which is normally associated with venous congestion and which with pulmonary/peripheral oedema

A

acute- pulmonary/peripheral oedema

chronic- venous congestion

52
Q

two types of heart failure (other than chronic/acute)

A

systolic

diastolic

53
Q

systolic heart failure

+ ejection fraction

+ causes

A

Inability for ventricle to contract normally → decreased contractility → decreased CO

HFREF =reduced ejection fraction (fraction of end-diastolic fraction ejected in systole)

Caused by IHD, MI, cardiomyopathy

54
Q

diastolic heart failure

+ ejection fraction

+ causes

A

Inability for ventricles to fully relax and fill → decreased stroke volume → decreased CO

HFPEF= preserved ejection fraction

Caused by hypertrophy (less ventricle volume) - as a result of hypertension (more resistance needs more force) and aortic stenosis, which increases afterload and decreases CO

55
Q

signs of heart failure (general)

A

tachy (not specific)

displaced apex beat (specific but insensitive)

56
Q

signs of R heart failure

A

Raised jugular venous pressure

Enlarged liver

57
Q

signs of L heart failure

A

Wheeze/crackle
Gallop heart rhythm
Murmurs possible

58
Q

symtpoms of heart failure (general)

A
  • sob (rest/exercise)
  • reduction in activity - fatigue, get tired
  • weight increase
  • dizzy
59
Q

symptoms of L heart failyre

A 
Oedema in lungs
Cough
Tachypnoea
Sputum 
wheeze
60
Q

symptoms of R heart failure

A

Oedema in legs/ankles

Cold peripheries

61
Q

what are you looking for with ecg for heart failure

A

underlying cause

ecg is abnormal

62
Q

what are you looking for in CXR for heart failure

A

size of heart
effusioons
alveolar oedema

63
Q

what are you looking for in echo for heart failure

A

chamber dimension,
valve disease
wall motion abnormalities

64
Q

heart failure bloods

A

BNP = brain natriuretic peptide

secreted in ventricles in response to myocardial stress – levels correspond to severity

diagnositc!!

65
Q

ANP vs BNP

A

atrial / brain natruiuretic peptide

anp- released by atria when dysfunctioning

bnp-released by ventricles when dysfunctioning

66
Q

NYHAclassification =

how many classes. what are each

A

new york heart association classification

class1 : no limitation, asymptoamtic. excercise= no symptoms

2- slight limitation: comfortable at rest. Normal exercise = symptoms

3- marked limitation: comfortable at rest. Gentle exercise = symptoms

4- inability to carry out any physical activity without discomfort

67
Q

heart failure treatment

pharmacological

A

better to block RAAS and symp nervoud system on heart than to make the LV do more:

  • ACE i
  • ARB
  • B blockers
  • aldosterone antagonists (sprinoloactone)
  • Nitrates
  • digoxin – slows heart, increases force
  • loop diuretics- electrolyte sparing (blood pressure and preload decrease so congestion decreases)
68
Q

heart failure treatment – nonpharmacological

A

surgery

  • stent
  • bypass
  • valve repair
  • transplant, if young
  • pacemaker

lifestyle changes

  • diet (avoid large meals)
  • exercise
  • smoking
  • lose weight
69
Q

acute heart failure treeatment

A 
monitor ecg
oxygen 
pain killers - opiates
nitrates
loop diuretics (electrolyte sparing)
70
Q

heart failure complications

A 
arrhythmia
renal dysfunction (needs 1/4 of CO)
thromboembolism, DVT, PE
LBBB, bradycardia
hepatic dysfunction
neurological /psychological complications
71
Q

hypertension risk factors

A
  • genetic
  • race
  • gender (male)
  • family history
  • smoking
  • little exercise/ sedentary
  • too much salt
  • too much alcohol
  • stress
  • diabetes
  • overweight
72
Q

hypertension causes

A

may be due to ‘white coat’- higher BP with doctors than home

Primary

  • Genetic susceptibility
  • Excessive sympathetic nervous system activity
  • Na/K transport abnormalities
  • High salt intake
  • RAAS system abnormalities

secondary hypertension

  • kidney issues
  • Coarctation of the aorta (narrowing)
  • Endocrine (cushings, conns, hyperparathyroidism, thyroid problems, pheochromocytoma)
  • medication including depression -venlafaxine, oral contraceptive, NSAIDs aspirin, blocked nose medication
  • Alcohol , amphetamine, ecstasy, cocaine

suspect secondary when patient is young, resistant to antihypertensive medication, or symptoms of an underlying cause (kidneys, adrenals)

73
Q

pathophysiology of hypertension

A 
Higher pressure in blood vessels due to 
Increased CO (HR and stroke vol)
Increased peripheral resistance
Vasoconstriction
Stenosis
Increased fluid volume (RAAS, kidneys)
74
Q

signs and symptoms of hypertension

A 
signs -- BP
symptoms -- 
usually none
fatigue
headaches, migraines
75
Q

how can you get over white coat syndrome with Hypertension

A

Do more than one reading – 24 hour ambulatory BP measured (ABPM)- worn at home

76
Q

investigations into hypertension

A

BP in clinic
ABPM at home

bloods = ANP increase

look for end organ damage (as a result)

  • eyes are an indicator of vessel damage : fundoscopy/ ophthalmoscopy for hemorrhage / papilloedema
  • bloods : serum creatinine, eGFR, glucose
  • ECG/echo : ventricular hypertrophy
  • urinalysis: albumin:creatinine ratio, haematuria

rule out secondary hypertension (medication, kidney, endocrine, coarctation of aorta)

77
Q

coarctation

A

narrowing (aorta)

78
Q

hypertension management

A

regular BP check (3-6month)

medication
first line = ACEi/ ARB if caucasian / <55
if not that person, first line is CCB (old or A-C)

then add the other (so if A-C, now take CCB and ARB OR ACEi.. )…. then all 3 …. then ….

also :
diuretics 
statins
B blockers
A blocker (doxazosin)
lifestyle (diet - reduce alc/salt, high fruit/veg, weight loss, exercise, stop smoking)
79
Q

who to treat for hypertension

A 
Treat stage one (systolic 140-160mmHg) if ‘at risk’ 
diabetes, 
qrisk2 over 20%,
 renal disease, 
CV disease eg previous MI, 
organ damage due to BP

Treat stage two (160+) always

think this may be wrong based on prev exam q - they seem to treat stage one when those conditinos arent mentioned

80
Q

hypertension complications

A 
Accelerates atherosclerosis 
Stroke 
MI
Chronic renal disease
Cognitive decline
Thrombosis etc 
Premature death
Atrial fibrilation
81
Q

should A-C patient be put on ramipril

A

no.
ramipril is ACEi
they already have repressed RAS system due to salt sensitivity and low renin

so ACE i will be less effective as opposed to those with high RAS system

82
Q

keen adrenal/ adrenal tumour. how does this relate to heart issues

A

too much aldosterone
this causes calcium retention and K+ excretion
so low K+
hypokalemia – ST segment sagging, T wave depression, and U wave elevation.

83
Q

single atenolol tablet sees what expected drop in what

A

BP

8 or 10 mmHg in systolic pressure (top number)

84
Q

what is and indicator of immediate damage to blood vessels due to hypertension

A

eyes

85
Q

how often is a hypertensive patient’s BP checked

A

3-6months in clinic

86
Q

MI ECG changes

A

ST elevation or ST depression (both diagnostic! )
abnormal Q wave
T wave inversion

phase 2a mine (38 decks)

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