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phase 2a mine > cv > Flashcards

cv Flashcards

1
Q

chonotropic

A

relating to Heart rate

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2
Q

ionotropic

A

relating to force of heart contraction

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3
Q

how do MI, ACS, angina, IHD, CHD and atherosclerosis , atherogenesisrelate?

A

IHD (ischeamic heart disease) is the same as CHD (coronary heart disease) and is the same as coronary atherosclerosis.

These terms refer to MI (heart attack) and ACS (acute coronary syndrome, = unstable angina) and stable angina.

atherosclerosis (formation = atherogenesis) is the cause for angina, ACS, and MI .

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4
Q

types of angina
5
what they are

A

stable angina (=pectoris) - painful periods are regular

unstable angina (=ACS, = crescendo angina) - painful periods are increasing in severity / frequency/ occurring at rest

prinzemental’s (=variant) = spasm of coronary arteries

microvascular = stenosis of small coronary vessels – increase in resistance and pressure

decubitus = when lying down/recumbent

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5
Q

excarbeating factors of angina (4)

A
  • cold
  • exercise/activity
  • post prandial
  • stress
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6
Q

opioid vs opiate

A

opiates are naturally occurring, acting on opioid receptors.

opioid is a synthetic/partially synthetic molecule - may act/ replicate opiates to get same response

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7
Q

orthopnea=

A

sob when lying down

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8
Q

paroxysmal nocturnal dyspnoea

A

sudden attacks of severe sob and coughing occurring at night

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9
Q

stage 1 hypertension

stage 2 hypertension

stage 3 hypertesnion

A

1

  • clinic : 140/90 - 160/100
  • ABPM: 135/85 - 150/95

2

  • clinic: 160/100 - 180/110
  • ABPM: 150/95 +

3
- clinic: 180/110 +

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10
Q

gangrene

A

tissue death due to ischeamia/ infarction

typically feet

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11
Q

what is amourosis fugax

A

blindness due to lack of blood flow

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12
Q

atrophic skin

- eg of disease its seen in

A

thin skin (eg PAD)

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13
Q

CRP blood test

A

c-reactive protein
detects inflammation, released after tissue injury
quite vague, non-specific but can be used to rule things out (eg claudication)

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14
Q

ESR blood test

A 
erythrocyte sedimentation rate
measure degree of inflammation such as cancer, autoimmune etc
non specific (excludes claudication)
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15
Q

haematoma vs haemorrhage

A

both refer to localised bleeding from a blood vessel. haematoma is associated with clotted bleed whereas haemorrhage implies ongoing bleed

usually large vessels i think

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16
Q

haemoptysis

A

coughing up blood

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17
Q

early diastolic murmur

A

mitral stenosis
opening snap could be considered early diastolic (valves closer together so friction sound when blood is pushed through (diastole = blood moves from a –> v)
then mid diastolic as well

aortic regurgitation

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18
Q

mitral stenosis’ murmur =

A

opening snap (early diastolic)
— valves closer together so friction sound when blood is pushed through (end of diastole)
blood moves from a –> v in disatole

then mid diastolic (rumble) to end of diastole

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19
Q

early systolic click murmu

A

mitral valve replacement (working fine)

click= metal

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20
Q

mitral valve replacement murmur

A

early systolic click

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21
Q

ejection systolic crescendo-decrescendo murmur

A

aortic stenosis

- systole as after aorta is after ventricles. de/crescendo is due to the rise/fall of pressure

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22
Q

aortic stenosis murmur

A

ejection systolic crescendo-decrescendo murmur

systole as after aorta is after ventricles. de/crescendo is due to the rise/fall of pressure

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23
Q

pansystolic murmur

A

mitral /tricuspid regurgitation
-valves flap through ventricular systole blood moving past them

  • maybe also MI/angina
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24
Q

mitral regurgitation murmur

A

pansysolic murmur

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25
Q

ANP raised

  • suggests
  • causes what
A

atrial dysfunction
high BP

causes kidney to excrete more in order to correct for high BP

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26
Q

CK MB

  • when
A

Is a marker of damaged heart muscle

raised in MI

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27
Q

troponin I elevated when

A

MI

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28
Q

sepsis =

A

systemic inflammatory response associated with an infection

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29
Q

where in the blood vessel does atherosclerosis occur

A

intima

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30
Q

pericarditis ecg

A

Saddle shaped ST and PR depression

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31
Q

Saddle shaped ST and PR depression

A

pericarditis

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32
Q

hyperkalemia ecg

A

Tall tented T waves + pathological Q waves + flattened - absent p waves

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33
Q

Tall tented T waves + pathological Q waves + flattened - absent p waves

A

hyperkalemia

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34
Q

stemi ecg

A

st elevation

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35
Q

st elevation ecg

A

stemi

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36
Q

angina ecg

A

st depression

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37
Q

st depression ecg

A

angina

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38
Q

general heart block ecg

A

increase PR interval

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39
Q

increased pr interval

A

heart block

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40
Q

more than one atria p wave to each QRS block

A

2nd degree heart block

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41
Q

no relation between p and QRS

A

3rd degree heart block

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42
Q

3 rd degree heart block ecg

A

no relation between p and QRS

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43
Q

2nd degree heart block ecg

A

more than one atria p wave to each QRS block

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44
Q

mobitz type 1

A

pr interval increases gradually until QRS dropped/missing (p wave not conducted)

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45
Q

mobitz type 2

A

pr interval does not increase, it is constant. and then a qrs beat dropped/missing (p wave not conducted)

46
Q

atrial fibrillation

A

irregularly irregular
atrium contracts rapidly irregularly, uncoordinately
av node responds intermittently - only some conducted to ventricles (irreg vents)

47
Q

atrial fibrillation ecg

A 
absent p wave
rapid heart rate
irregular QRS
jaggedy
no isoelectric baseline
48
Q 
absent p wave
rapid heart rate
irregular QRS
jaggedy
no isoelectric baseline
A

atrial fibrilation

49
Q

atrial flutter ecg

A

saw tooth
narrow tachycardia
flutter waves

50
Q

atrial flutter

A

regularly irregular

due to re-entry circuit in RA from AV back to sinus

51
Q

atrial fib/ flutter - which is reg?

A

atiral fib= irregularly irregualr

atrial flut = regularly irregular

52
Q

saw tooth
narrow tachycardia
flutter waves

A

atrial flutter

53
Q

p waves

A

atrial depolarization
SAN –> AVN
general direction is SE so + on trace

54
Q

PR inteval

- length?

A

SAN to ventricle muscle including AV node delay

should be 120-200ms (3-5 small squares)

55
Q

QRS

A

ventricular depolarization
AVN to septum and ventricles
septum is SE so big postive up to R then negative as goes opposite direction up ventricle walls
narrow is good

56
Q

T wave

A

ventricular repolarization

57
Q

time of ECG square

A

small square = 0.04s

big square = 0.2s (5 small squares)

58
Q

how long does ECG measure for

A

10s

59
Q

lead 1

A

lateral

60
Q

lead 2

A

inferior

61
Q

lead 3

A

inderior

62
Q

aVR

A

not a heart face, it is aorta

63
Q

aVL

A

lateral

64
Q

aVF

A

inferior

65
Q

v1

A

septal

66
Q

v2

A

septal

67
Q

v3

A

anterior

68
Q

v4

A

anterior

69
Q

v5

A

lateral

70
Q

v6

A

lateral

71
Q

inferior heart – vessel?

A

R coronary

R marginal branch of it

72
Q

lateral hear – vessel?

A

L circumflex

73
Q

septal heart – vessel?

A

LAD

74
Q

anterior heart – vessel?

A

LAD

75
Q

ecg rate calculation

A
  1. ) number of R peaks x 6 (ecg is 10s–> min)
    - - reg/irreg HR

2) 300 / distance between R peaks in large squares
- – reg HR only

76
Q

IHD race risk facotrs

A

SE asia

AF-CArib

77
Q

QRISK2

aim for?

A

risk of CV ecent in next 10 y

aim for <10%

78
Q

ACE i action

A

Inhibits angiotensin converting enzyme which converts angiotensin 1-2 in the RAAS system. Effect is to less aldosterone so reduce reabsorption of sodium and water in the kidneys so lowers BP,
also vasodilates

79
Q

ACE I names

A

“-pril”

ramipril

80
Q

ACE i side effects

A

Decreased angiotensin 2 formation

  • Hypotension
  • Hyperkalemia (aldosterone blocked aldosterone causes K+ excretion). this is esp bad for bilateral renal artery stenosis)
  • Acute renal failure (less kidney perfusion due to efferent arteriole constriction)

Increased (brady)kinin production (normally ACE converts kinin to inactive peptides– metabolism) - not with ARB as doesn’t stop ACE’s other action (brady(kinin) causes)–

  • Cough !
  • rash
  • allergic reaction
81
Q

contraindications for ACEi

A
  • Pregnancy (teratogenic)
  • Hyperkalemia
  • Renal dysfunction (hyperkalemic S/E esp bad for bilateral renal artery stenosis)
  • Afro-carribean patients
  • —- Have Salt sensitivity so less renin
  • —– means lower angiotensin 1 so already repressed RAAS so medication is less effective for other patients
  • asthma? cos of cough side effect?
82
Q

ARB action

A

Stops angiotensin 2 binding to peripheral AT1 receptor

does not stop ACE’s other function of bradykinin metabolism, so no high bradykinin so no cough

83
Q

ARB names

A

” -sartan”

84
Q

ARB side effects

A
  • painful breast tissue
  • Breast tissue increase in males
  • Hypotension (esp volume depleted patients)
  • Hyperkalemia (aldosterone causes K+ excretion). this is esp bad for bilateral renal artery stenosis
  • Renal dysfunction
  • Rash
  • Angio -oedema

No cough as ACE still able to do other function : convert kinin to inactive peptides so no (brad)kinin hanging about

85
Q

ARB contraindications

A

Pregnancy
Renal issue
Hyperkalemia
postural hypotension

86
Q

alpha blockers example

A

doxazosin

87
Q

alpha blockers action

A

block adrenoreceptors - which act on smooth muscle so decreases preripheral resistance (vasodilation)

88
Q

clopidogrel =

A

antiplatelet

89
Q

ticagrelor=

A

antiplatelet

90
Q

B blocker name

A

“-onol”
“-olol”
“-llol”
metoprolol bisoprolol

91
Q

B blocker action

A

Block noradrenaline attaching to B adrenoceptors by continued binding to them

Decreases cardiac output (less oxygen demand for the heart)
Decreased HR (chronotropic)
Decreased heart contractility (inotropic)
Lower HR means better oxygen distribution
(beta1 receptors)

(beta 2 receptors – vasodilation)?

Block reflex sympathetic responses which stress heart in HF

Propanolol best B blocker for post MI arryhtmia as also blocks sodium channels (also in class 1 = soidum channel blockers , as well as b blocker class 2 )

92
Q

B blocker contraindications

A

Asthma !!!!!! (bronchospasm)
COPD
PVD - peripheral vascular disease

93
Q

B blocker side effects

A 
Fatigue
Headache
Sleep disturbances inc nightmares
Bradycardia
Hypotension
Cold peripheries 
Erectile dysfunction
94
Q

calcium channel blockers types with examples

A

all = L type CCB

1) phenylalkyonines (verapamil, diltiazem)
2) dihydropiridines -“dipine”. (amlodipine)
3) benzothiazapines
* in maudative-
dihy. . = multi purpose - including hypertension (amlodipine)

Non-dihy.. = specific to heart, not hypertension (diltiazem)

95
Q

CCB action

A

Increase cGMO and reduces intracellular Ca2+ concentration
inhibits opening of voltage gated Ca channels (L type) in vascular smooth muscle), so lower calcium entry so less Ca available for contraction so decrease in peripheral resistance

vasodilation

prevents artery and heart hardening

1)phenylalkyonines (verapamil) cardiac:
Decreases CO- negatively chronotropic (decrease HR)
Negatively inotropic (reduce force of contraction)
Doesn’t act on calcium channel at rest (more effective)
type 4 anti arrythmia drugs

2) dihydropiridines (class 1 ?) -“dipine”. (amlodipine) - vascular:
Vasodilates peripheral arteries so decreases peripheral resistance
Acts on calcium channel at rest (less effective)
- good for coronary spasm angina (not sure why)

3) benzothiazepines - both heart and vascular effects - between 1 and 2

96
Q

corticosteroid 2 examples

A

prednisolone

hydrocortisone

97
Q

corticosteroid action

A

Dampens immune system

- Suppress prostaglandin and leukotryin mediators

98
Q

digoxin action

A

inhibit Na/K pump (blocks Na out and K in action)
So more Ca in heart
– Increased force of contraction (ionotropic)

Increased vagus (parasympathetic supply increased) stimulation ACh released (increases)

    • Bradycardia (chonotropic)
    • Slows AV node conduction

this is a cardiac glycoside (class 5 ) antiarrythmia drug

99
Q

digoxin side effects

A

More ectopic activity (extra beats)

Narrow therapeutic range

  • Vom
  • Nausea
  • Diar
  • confusion
100
Q

diuretics types and names

A

1) thiazides - distal tube “-thiazide”
2) loop diuretics- loop of Henle”-mide”
3) k (spironolactone)

101
Q

diuretics action

A

Pass more urine, more electrolytes lost

Decrease blood pressure

1) thiazides = block sodium and chloride reabsorption at the Na/Cl luminal co transporter
2) loop diuretics block Na / K/ 2Cl transporter (moving Na, K, 2 Cl into cells from urine via Na movement). This then reduces water outflow

102
Q

nitrates action

A

Arterial and venous vasodilators
Reduce preload and afterload
(it’s the reduced preload that reduces anginal pain as less heart demand)
Lowers BP for IHD/ heart failure (not hypertension)

103
Q

statins action

A

Lowers serum LDL cholesterol by reducing production in the liver

104
Q

lidocaine action

A

sodium channel blocker (decrease Na)

class1 antiarrythmia drug

105
Q

amiodarone action

A

prolong duration of action potential (by decrease K + )

type 3 antiarrythmia drug

amiodarone has long half life and is selective for long action potential

106
Q

thiazides SE

A

hypokalaemia (increased K+ secretion)

107
Q

chlorthalidone =

A

non thiazide drug (but still antihypertensive)
acts on DCT (reduce reabsorption)
for longer duration

108
Q

indapamide =

A

non thiazide drug (but still antihypertensive)
acts on DCT (Reduce reabsorption)
also vasodilator

109
Q

what effect do beta blockers have on RAAS

A

reduce plasma renin

110
Q

spironolactone effect on RAAS

A

aldosterone antagonist

111
Q

when is CCB contraindicated / cautioned

A

heart failure

as in cardiac muscle - negatively inotropic (contractility)

112
Q

hypocalceamia ECG looks like?

- other causes for same ecg?

A

long QT (QT syndrome)

hypokalemia
MI
DM
drugs - amiodarone, antidep
congenital - romano-ward, jervell-large-neilson

phase 2a mine (38 decks)

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