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MD3001 > MD3001 Week 4 > Flashcards

MD3001 Week 4 Flashcards

1
Q

outline narrative ethics

A

this centres ethical dilemma squarely in patient’s life; to do right requires an understanding of the person

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2
Q

care provided by a doctor (GMC) must… (4)

A
  1. act in accordance w/ relevant legislation
  2. not treat patients unfairly
  3. not deny patients access to appropriate services or care
  4. not cause patients distress
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3
Q

how do medical students differ from doctors in their right to use conscientious objection?

A

medical students have this right but must meet GMC’s outcomes for graduates

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4
Q

4 arguments against conscientious objection

A
  1. inefficiency and inequity
  2. inconsistency
  3. commitments of a doc
  4. discrimination
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5
Q

what occurs when CO drops and blood flow to kidneys drop?

A

when this happens to CO, renin is released (RAAS)

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6
Q

negative effects of increased sympathetic activity due to cardiac failure (3)

A
  1. tachycardias, vasoconstriction
  2. increased workload of heart
  3. desensitization of beta but not alpha receptors (heart works less, but vessels still constricted)
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7
Q

why is increased RAAS due to cardiac failure bad?

A

increase of this compensatory mechanism can cause oedema in cardiac failure

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8
Q

negative effect of angiotensin II/aldosterone on heart

A

these hormones deposit fibroblasts and collagen in the ventricles leading to increased stiffness thus decreased contractility

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9
Q

what causes white reaction on skin?

A

myogenic response by stretched Ca2+ channels, causing pre-capillary sphincter contraction

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10
Q

triple response (3)

A
  1. red reaction (flush): to pre-capillary sphincters opening
  2. flare: stimuli travel anti-dromically to adjacent arterioles to dilate
  3. wheal: local oedema caused by increased capillary permeability
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11
Q

affects of adrenaline on damaged skin

A

this hormone causes white reaction due to intense pre capillary constriction

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12
Q

effect of chronic obstructive pulmonary disease on CVS

A

this disease displaces capillaries in lungs, so not enough O2 and RV pumps harder – causes cor pulmonale

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13
Q

amyloidosis

A

deposits of abnormal starch protein in tissues and organs

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14
Q

effect of COPD on CVS

A

this systemic disease can cause ischaemia as heart tissues can’t contract as well

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15
Q

sarcoidosis

A

abnormal collection of inflammatory cells forming granulomas

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16
Q

effect of sarcoidosis on CVS

A

this systemic disease can cause arrhythmias

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17
Q

what valvular heart disease can cause atrial fibrillation?

A

mitral stenosis has this affect on heart rhythm

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18
Q

infective endocarditis

A

infection of valve w/ formation of thrombic vegetations (fibrin + platelets)

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19
Q

what inflammatory disease can cause any valvular heart disease?

A

rheumatic fever can cause this

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20
Q

how are fatty streaks made?

A

monocytes in blood are recruited into tunica intima, turned into macrophages which engulf fat and turn into foam cells

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21
Q

how is fibrous cap of fibro-fatty plaque made?

A

foam cells release cytokines which attract smooth muscle from media to intima

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22
Q

how does angina appear on ECG?

A

causes ST depression

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23
Q

how does myogenic control affect BP vs Flow graph?

A

this mechanisms allows flow rate to stay the same with a change in BP

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24
Q

coronary flow reserve

A

maximum increase in coronary flow above the normal resting volume

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25
Q

top 2 causes of MI

A
  1. plaque rupture 75%

2. plaque erosion 25%

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26
Q

difference b/w STEMI and NSTEMI

A

former MI is caused by fully blocked coronary artery while latter is partial

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27
Q

what type of MI implies sub-endocardial ischaemia?

A

NSTEMI implies this type of ischaemia

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28
Q

2nd degree heart block

A

partial AV block causing only some Ps leading to QRS

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29
Q

Mobitz type 2 heart block

A

heart block causing most Ps having QRS but once in a while no

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30
Q

Wenckebach (Mobitz type 1) block

A

progressive lengthening of PR until P wave fails to produce a QRS, then resets

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31
Q

2 types of blocks that can cause circus re-entry movements

A
  1. unidirectional

2. transient (allows some impulses but not all)

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32
Q

possible consequences of Wolf-Parkinson-White Syndrome (2)

A
  1. paroxysmal tachycardia

2. re-entry circuit

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33
Q

effects of Wolf-Parkinson-White Syndrome on ECG

A

this disease causes a delta wave which shortens PR and widens QRS

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34
Q

atrial fibrillation on an ECG

A

no discernible P waves and irregular QRS complexes

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35
Q

junctional (nodal) tachycardia on an ECG

A

normal QRS complexes but absent P waves

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36
Q

what condition causes long QRS?

A

L/R bundle branch blocks cause this on ECG

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37
Q

what abnormal ST is a sign of infarction?

A

elevation > 2mm in 2 adjacent chest leads OR elevation > 1mm in 2 adjacent limb leads

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38
Q

what is depressed ST a sign of?

A

this ECG characteristic is a sign of ischaemia

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39
Q

digoxin effects on ECG (2)

A
  1. T wave inversion

2. ST segment sloping depression

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40
Q

abnormal T wave

A

abnormal if inverted in I, II, and V4-6 (ischaemia/infarct)

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41
Q

L axis deviation on ECG

A

negative QRS deflections in II and III

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42
Q

R axis deviation on ECG

A

negative QRS deflection in I

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43
Q

ECG signs of hyperkalaemia

A

tall T wave, widened QRS

44
Q

ECG signs of hypercalcaemia

A

short QT interval

45
Q

alternate treatment of hypertension (2)

A
  1. alpha blocker (doxazosin)

2. spironolactone

46
Q

treating chronic heart failure (3)

A
  1. DAB (sacubitril-valsartan instead of ACE/ARB in severe)
  2. spironolactone/epleronone
  3. cardiac resynchronization therapy to those w/ long QRS (BBB)
47
Q

sacubitril-valsartan

A

former inhibits Neprilysin preventing breakdown of b type natriuretic peptide (BNP), latter is an ARB

48
Q

four causes of acute chest pain

A
  1. non cardiac chest pain
  2. troponin negative ACP
  3. NSTEMI
  4. STEMI
49
Q

STEMI treatment

A

Emergency: Aspirin and angioplasty (if near hospital)/thrombolysis (if far). Also blood thinners: aspirin and clopidogrel/ticagrelor (blood thinners), low MW Heparin or fondaparinux

50
Q

fondaparinux

A

synthetic pentasaccharide that inhibits activated factor x

51
Q

atrial fibrillation treatment (3)

A
  1. prevent emboli w/ Warfarin/Rivaroxaban
  2. control rate w/ beta blocker or digoxin
  3. control rhythm (seldom done) w/ cardioversion
52
Q

treatment for stroke

A

(if NO haemorrhage) Thrombolysis for emergency, aspirin acutely and for 2 weeks, then clopidogrel

53
Q

side effects of diuretics (3)

A
  1. hypokalaemia (thiazide)
  2. diabetes
  3. gout
54
Q

furosemide

A

loop diuretic used in heart failure

55
Q

mechanism of Digoxin (2)

A
  1. increase vagal activity, which decreases HR and AV conduction speed
  2. increase contractility by inhibiting Na/K ATPase, which accumulates Na+ in SR so NCX reverses and stores more Ca2+
56
Q

initial drug treatment for acute heart failure (3)

A
  1. IV loop diuretics
  2. IV opiates/opioids
  3. IV buccal or sublingual nitrates
57
Q

second line drug treatment for acute heart failure (3)

A
  1. beta-agonists (dobutamine)
  2. dopamine - increases renal perfusion and BP
  3. adrenaline - increase contractility
58
Q

effects of nephrosclerosis (3)

A
  1. lose nephrons due to vascular narrowing
  2. proteinuria
  3. haematuria
59
Q

in which situations does BMA support conscientious objection? (3)

A
  1. abortion
  2. fertility treatment
  3. withdrawal of life-sustaining treatment
60
Q

what type of infarct presents pathology Q waves and ST elevation in II, III, and AVF?

A

inferior infarct has this ECG

61
Q

outline Janaway case

A

case where secretary refused to type abortion letter on conscientious objection. But you can only CO if you play a role in the actual procedure

62
Q

outline Eweida case

A

Christian working for BA that was told to conceal her cross

63
Q

human right

A

right to freedom of thought, conscious and religion. However subject to limitations in interest of public safety, protection of public order, health or morals, or protection of rights and freedoms of others

64
Q

define afterload

A

force the heart must generate to eject blood from heart

65
Q

normal ejection fraction

A

50-65% of EDV pumped out

66
Q

define systolic ventricular dysfunction

A

impaired cardiac contractility (ejection fraction <40%)

67
Q

define diastolic ventricular dysfunction

A

normal ejection fraction but impaired diastolic ventricular relaxation and decreased filling

68
Q

common causes of systolic dysfunction (3)

A
  1. contractility (cardiomyopathy)
  2. volume overload
  3. pressure overload (ex. stenosis, hypertension)
69
Q

causes of diastolic dysfunction (4)

A
  1. constricted ventricular expansion (ex. constrictive pericarditis)
  2. increased wall thickness (ex. hypertrophy)
  3. delayed diastolic relaxation (ex. aging)
  4. increased HR
70
Q

direct result of R heart failure

A

this type of heart failure causes congestion of peripheral tissues

71
Q

direct results of L heart failure (2)

A
  1. decreased CO

2. pulmonary congestion

72
Q

4 compensatory mechanisms of decreased CO

A
  1. sympathetic activity
  2. RAAS
  3. Frank-starling
  4. fluid movement
73
Q

problem w/ increased Frank-starling in cardiac failure

A

this compensatory mechanism increases EDV -> muscle stretch -> O2 consumption

74
Q

what heart condition can COPD cause?

A

this lung disease can cause cor pulmonale - R hypertrophy caused by pulmonary hypertension

75
Q

define angina

A

mismatch of supply (coronary blood flow) and demand (myocardial O2 consumption)

76
Q

3 degrees of heart blocks

A
  1. affected AV
  2. partial block
  3. full block (separate A V innervation)
77
Q

Mobitz type 1 heart block

A

heart block causing QRS to occur occasionally after P

78
Q

Wolf-Parkinson-White Sydrome

A

condition characterized by “accessory” electrical connection b/w atria and ventricles (usually L); no delay in accessory so depo reaches ventricle early

79
Q

normal P wave

A

<0.25mV

80
Q

normal QRS complex

A

<0.12s, >5mm

81
Q

ventricular tachycardia on ECG

A

wide QRS complexes

82
Q

P-mitrale on ECG

A

bifid P wave denoting L atrial hypertrophy

83
Q

P-pulmonale on ECG

A

peaked P wave denoting R atrial hypertrophy

84
Q

ECG sign of L ventricular hypertrophy

A

R wave in V5 (isoelectric line to tip) >25mm/2.5mV

85
Q

ECG sign of R ventricular hypertrophy

A
  • dominant R wave in V1 (ie. bigger than S)
  • T wave inversion in V1-3
  • deep S wave in V6
86
Q

how to measure QT interval

A

measure from Q to end of T and use QTc = QT/√RR

87
Q

normal QTc interval

A

0.38-0.42s

88
Q

drugs to prolong survival in angina (4)

A

Statin
Aspirin
ACE inhibitor
Beta blocker

89
Q

drugs to relieve symptoms of angina

A

sequentially:

  1. BB
  2. Ca2+ or NO
  3. coronary angioplasty
  4. ivabradine/ranolazine
  5. coronary artery surgery
90
Q

side effects of ACE inhibitors (4)

A
  1. cough

2. renal dysfunction

91
Q

tirofiban

A

glycoprotein IIb/IIIa inhibitor (anti platelet) for ongoing chest pain

92
Q

causes of stroke (3)

A
  1. cerebral thrombosis
  2. cerebral embolus
  3. cerebral haemorrhage
93
Q

side effects of beta blockers (3)

A
  1. bradycardia/heart block
  2. tired
  3. asthma
94
Q

spironolactone

A

aldosterone blocker

95
Q

ARB used in chronic heart failure

A

candesartan

96
Q

define forward and backward failure

A

former is caused by reduced perfusion of tissues. backwards is due to increased venous pressures

97
Q

pulmonary hypertension

A

pulmonary BP >30mmHg

98
Q

barriers to exercise

A
  • too tired
  • not in mood
  • don’t know how
  • fear
  • no time
99
Q

define cardiac rehab

A

process by which patients w/ cardiac disease, in partnership w/ multidisciplinary team of health professionals, are encouraged and supported to achieve and maintain optimal physical and psychological health

100
Q

SMART goals in cardiac rehab

A 
Specific
Measurable
Achievable
Realistic
Time based
101
Q

steps for NHS exercise for cardiac rehab (3)

A
  1. 15m warm up
  2. 20m conditioning phase (circuit based, comfortably short of breath)
  3. 10m cool down
102
Q

FITT principle of exercise

A

Frequency
Intensity
Time
Type

103
Q

macro and microscopic changes 1-2 days after MI

A

macro: pale, oedematous
micro: oedema, neutrophil

104
Q

macro and microscopic changes 3-4 days after MI

A

macro: yellow, rubbery centre
micro: inflammation and early granulation tissue

105
Q

macro and microscopic changes 1-3 weeks after MI

A

macro: infarcted area more pale
micro: granulation tissue, some fibrosis

106
Q

macro and microscopic changes 3/6 weeks after MI

A

macro: silvery scar
micro: dense fibrosis

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