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Knowledge Test > Cardiology > Flashcards

Cardiology Flashcards

1
Q

cardiac cycle

A
  1. flow into atria, continuous except when they contract. inflow leads to pressure rise
  2. opening of av valves, flow to ventricles
  3. atrial systole, completes filling of ventricles
  4. ventricular systole and atrial diastole, pressure rise closes a-v valves, opens aortic and pulmonary valves
  5. ventricular diastole - causes closure of aortic and pulmonary valves
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2
Q

heart sounds

A 
1st = closing of AV valves
2nd = closing of semilunar valves 
3rd = early diastole of young and trained athletes 
4th = turbulent blood flow, due to stiffening of walls of left ventricle`
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3
Q

do heart chambers empty fully

A

no

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4
Q

stroke volume

A

volume of blood pumped out ~75ml can double during excercise

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5
Q

ejection fraction

A

% volume pumped out, ejection fraction = 55-60% , 80 in excercise, 20 in heart failure

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6
Q

cardiac output

A

volume of blood pumped per minute by each ventricle. CO=HR x SV ~5l/min
co = bp/peripheral resistance

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7
Q

contractility

A

force of contraction, adrenaline increases this

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8
Q

end diastolic volume

A

volume of blood in ventricle at the end of diastole

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9
Q

preload

A

volume of blood in ventricles at the end of diastole

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10
Q

afterload

A

peripheral resistance

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11
Q

increased peripheral resistance

A

decreased stroke volume, increased end systolic volume, increased end diastolic volume, increased stroke volume. so overall stroke volume doesnt change much`

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12
Q

cardiac excitation pathway

A

sinus rhythm = heart rate controlled by SA node approx 72 bpm, action potential then activates atria, atrial a.p activates a-v node. av node, small cells, slow conduction velocity introduces delay of 0.1 sec. av node activates bundle of his and purkinje fibres which activate ventricles

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13
Q

myogenic

A

cardiac muscle as it generates its own action potential

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14
Q

Action potential conduction

A

aps develop spontaneously at the SAN, aps are conducted from cell to cell via intercalated discs which have gap junctions

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15
Q

Action potential diagram described

A

dovna
nvr ok
ok

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16
Q

neurogenic

A

skeletal muscle, requires nerve impulse to activate

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17
Q

cardiac action potential describes

A

OVN
Q OK
LOCA V
ICA OK

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18
Q

Cardiac cell contraction

A

ca is normally released from sarcoplasmic reticulum but needs ca from outside (ca induced ca release)

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19
Q

where are 4 ecg limb leads placed

A

red - right arm, yellow- left arm, green- left leg, black - right leg (dummy)

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20
Q

where are 6 ecg chest leads placed

A

v1 - 4th intercostal space right of sternal angle
v2 - 4th intercostal space left of sternal angle
v4 - over heart apex (5th ics mid clavicular line)
v3- halfway between v2 and v4
v 5 - at the same level as v4 but on anterior axillary line
v6- same level as v4 and v5 but on the mid axillary line

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21
Q

Leads I, II, III

A

normal = I,ll +ve III -/+ve
left axis deviation = I +ve, II,III = -ve
right axis deviation= 1 -ve, II +/-ve, III +ve

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22
Q

calibration of ecg

A

10mm tall

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23
Q

large box vs small box ecg

A 
large = 5mm / o.2 s
small = 1 mm / o.o4 s
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24
Q

what causes waves on ecg

A 
p= atrial depolarisation 
qrs = ventricular depolarisation 
t = ventricular repolarisation
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25
Q

normal waveform intervals

A 
PR = o,12 - o,2 secs
QRS = < o,12 secs
QT = < o,44 (m), o,46 (f)
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26
Q

What is the pr interval

A

time to conduct through AVN/ His

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27
Q

what is QRS duration

A

time for ventricular depolarisation

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28
Q

what us ST segment

A

start of ventricular repolarisation. ST elevation due to acute infarction, pericarditis
ST depression due to ishaemia, LV strain (LVH)

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29
Q

lack of q dip

A

wolf- parkinson whits syndrome

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30
Q

ventricular hypertrophy

A

left or right same as william marrow but super deep troughs

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31
Q

RBBB and LBBB

A

v1 - v6 MaRRoW

v1-v6 WiLLiaM

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32
Q

anatomic groups of ecg leads

A 
lateral = I, aVL, V5, V6
inferior = II,III, aVF
septal = v1, v2
anterior = V3,4 
Avr = none
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33
Q

how to calculate hr of regular rhythm

A

300 / count large squares between r waves and

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34
Q

how to calculate hr of irregular rhythm

A

6 x rhythm strip

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35
Q

brady

A

HR < 60 bpm

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36
Q

tachy

A

HR> 100 bpm

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37
Q

bradyarrhythmias
heart block
1st degree

A

regular rhythm, pr interval > 0,2 seconds constant. Causes: IHD, conduction system disease, healthy kids and athletes
no treatment req

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38
Q

bradyarrhythmias
heart block
2nd degree
aka mobitz 1 / wenckebach.

A

irregular rhythm, Pr interval continues to lengthen until a QRS is misssing
usually benign unless assoc with MI

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39
Q

bradyarrhythmias
heart block
2nd degree
aka mobitz 2

A

irregular rhythm, QRS complexes may be wide >0,12 seconds, non conducted sinus impulses appear at irregular intervals. can cause syncope or deteriotate into 3rd degree, if in conjuction with acute MI = high risk patient

causes: IHD, fibrosis of the conduction system
treatment: pacemaker

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40
Q

bradyarrhythmias
heart block
3rd degree
aka complete

A

atria and ventricles beat independant of one an other, QRS look different each time. May be caused by MI, cause angina or syncope.
treatment - pacemaker, isoprenaline

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41
Q

tachyarrhythmias

Narrow complex tachycardia

A

QRS duration <0.12s, uncontrolled fast atrial fib (almost straight line between complexes) or flutter ( n’s between complexes) , atrial tachycardia

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42
Q

Tachycardias

Broad complex tachycardia

A

a (QRS duration >0.12 s)
Ventricular tachycardia
Ventricular fibrillation

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43
Q

Sinus arrhythmia

A

Sinus node fires at a variable rate
• Speeds up during inspiration
• S l o w s d o w n during expiration
• Effect caused by variations in vagus nerve
activity (parasympathetic nervous system)

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44
Q

Sinus tachycardia

A 
Sinus node fires > 100 per minute
• Physiological causes:
– anxiety, exercise
• Pathological causes:
– fever, anemia, hyperthyroidism, heart failure
– shock (sepsis, bleeding, anaphylaxis)
– almost any acute medical emergency
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45
Q

Sinus bradycardia

A 
• Sinus node fires < 60 per minute
• Physiological causes:
– Sleep, athletic training
• Pathological causes:
– hypothyroidism
– hypothermia
– sinus node disease
– raised intracranial pressure, many others
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46
Q

Sino-atrial disease

A

A degenerative condition affecting the atria,
including the sinoatrial (SA) and
atrioventricular (AV) nodes. Characterised by patchy atrial fibrosis,
atrial dilatation and altered conduction
• Common in individuals age > 70 years. Can lead to sinus tachycardia, sinus
bradycardia, atrial ‘ectopic’ beats, and atrial
fibrillation
treatment
• permanent pacemaker to prevent slow rhythms
• antiarrhythmic drugs to prevent or moderate
rapid rhythms
– beta blocker
– digoxin
– amiodarone

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47
Q

heart block

A 
dizziness, fainting, tiredness and shortness of breath. Causes of AV nodal block
• sino-atrial disease
• coronary heart disease
• aortic valve disease
• damage during heart surgery
• drugs
– beta-blockers
– digoxin
– calcium channel blockers
Treatment
• Remove any triggering cause (e.g. drugs)
• IV atropine or isoprenaline (acute
treatment)
• permanent pacemaker
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48
Q

Atrial fib and flutter

A 
Sensations of a fast, fluttering or pounding heartbeat (palpitations)
Chest pain.
Dizziness.
Fatigue.
Lightheadedness.
Reduced ability to exercise.
Shortness of breath.
Weakness.
Causes of atrial flutter / fibrillation
• sino-atrial disease
• coronary heart disease
• valve disease (esp. mitral valve)
• hypertension
• cardiomyopathy
• hyperthyroidism
• pneumonia, lung pathology
Treatment
• drugs to block AV node and therefore limit
heart rate
– digoxin
– beta blocker
– calcium channel blocker
• electrical cardioversion
• catheter ablation
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49
Q

ventricular fibrilation (squiggle line)

A 
shockable ryhtmn so is ventricular tachycardiaTreatment
ACUTE
• defibrillation
• IV antiarrhythmic drugs
• remove any triggering cause
LONG TERM
• oral antiarrhythmic drugs
• treat underlying heart conditions
• implantable defibrillator for some
patients
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50
Q

oedema

A

causes: low plasma oncotic pressure (malnutrition, liver disease, nephrosis), high interstitial oncotic pressure (inflammation), high venular hiydrostatic pressure (dvt), high arteriolar hydrostatic pressure (vasodilator drugs)

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51
Q

blood pressure

A

affferent: arterial baroreceptors
efferent: ANS - sympathetic and parasympathetic
hormones: angiotensin II (i), adrenaline (I), vasopressin (i)
local factors: nitric oxide (d), endothelin (I), kninins (d), prostaglandins (D)
effector organs - heart and arterioles
response time - seconds- minutes

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52
Q

blood volume

A

afferent: volume stretch receptors, juxtaglomerular cells (secrete renin)
ANS: sympathetic nervous system
hormones: aldoesterone (causes an increase in salt and water reabsorption, and increases blood volume) vasopressin (increases blood volume),
effector organs; kidneys
response time - minutes to hours

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53
Q

how is cardiovascular system mediated

A

by receptors responding to the influence of the autonomic nervous system

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54
Q

heart rate what receptors increase and decrease it?

A

increased by noradrenaline, adrenaline, beta-1 adrenoreceptors

decreased by acetylcholine, and muscarininc receptors

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55
Q

myocardial contractility

A

increased by noradrenaline, adrenaline, beta -1 adrenoreceptors

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56
Q

blood pressure nervous regulation

A

baroreceptor regulation providing second to second control of bp.
Afferent info: arterial baroreceptors carotid sinus - glossopharyngeal nerve
aortic arch - vagus nerve
CNS - vasomotor center in medulla
efferent signals : sympathetic nerves and parasympathetic

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57
Q

BP increase and decrease (vasoconstricor and vasodilator)

A

increase: vasoconstrictor, phenylephrine
decrease: vasodilator, glyceryl trinitrate

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58
Q

treatment of atrial fibrillation/ flutter

A

beta blockers (bisoprolol, atenolol @lol) calcium channel blocker (verapamil, diltiazem), cardiac glycosides (digoxin)

reduce the risk of thromboembolic stroke (Anticoagulants) vitamin k antagonists - warfarin, DOACs - apixaban

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59
Q

Beta- blockers

A

lol, b1 selective ant, indications: atrial fib, hypertension, angina , heart failure. oral administration
adverse effects: lethargy, bronchospasm, heart block

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60
Q

calcium channel blockers

A

verapamil, diltiazem. indications: atrial fib, supraventricular tachycardia, hypertension, angina. orally.
adverse: hypotension, headache, flushing, constipation, heart block

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61
Q

supraventricular tachycardia treatment

A

vagal stimulation manouevers, valsalva maneouvre, carotid massage. immediate treatment: adensoine (IV) adverse, dizzines, flushing, headache, chest pain, dyspnoae. verapamil

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62
Q

blood volume

A

intravascular - 4 L extracellular - 12l intracellular - 24;

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63
Q

how is blood volume sensed

A

the delivery of sodium and chloride in tubular fluid to the macula dense in every renal tubule and also low pressure stretch receptors in the atria of the heart

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64
Q

low blood volume

A

increases the activity of the renin-angiotensin system and sympathetic nervous system, r

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65
Q

renin

A

promotes release of angiotensin II which causes vasoconstriction and aldosterone release from the adrenal cortex

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66
Q

action of beta1-adrenoreceptors antagonists

A

beta blockers, inhibit actions of catecholamines on the SAN and AVN, reduce generation of secondary messenger cyclic amp

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67
Q

action of calcium channel blockers

A

inhibit the entry of calcium ions through L-type calcium channels

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68
Q

action of digoxin

A

cardiac glyceride that inhibits na/k atpase and increases vagal tone on avn

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69
Q

adenosine action

A

naturally occuring purine that is an agonist to A1 receptors which open potassium channels temporary block of impulse transmission

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70
Q

anti-arrhythmic drug class 1

A

block na, mainly active on myocardial cells

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71
Q

anti-arrhythmic drug class 2

A

beta 1 adrenoreceptor antagonists, active on pacemaker cells

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72
Q

anti-arrhythmic drug class 3

A

block k+ channels to lengthen action potential mainly active on myocardial cells

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73
Q

anti-arrhythmic drug class 4

A

block ca2+ channels mainly active on pacemaker cells

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74
Q

acute haemorrhage

A

reduces intravascular volume, venous retuen to the heart, cardiac output, atrial blood pressure - these changes are sensed by arterial baroreceptors, atrial stretch receptors and juxtaglomerular kidney

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75
Q

cardiovascular disease

A

diuretics, beta-blockers, ace inhibitors, calcium channel blockers, nitrates, anti-platlets, anti-coagulants, lipid lowering drugs

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76
Q

renin- angiotensin system

A

decrease in NaCl - liver releases angiotensinogen, kidney releases renin which makes angiotensin become angiotensin 1. lungs release ACE which then converts angiotensin 1 to 2, which causes vasoconstriction, NaCl reabsorption, ADH secretion, aldosterone secretion from adrenal cortex also causing NaCl reabsorption.
Blood volume increases

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77
Q

diuretic drugs

A

reduce the reabsorption of sodium and water by the renal tubules and increase urinary flow (loop, thiazide (hypertension), potassium sparing)

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78
Q

adverse effects of thiazide diuretics

A

adverse: hypokalaemia, hyponatremia, hypomagnesaemia, alkalosis, hyperuricemia, hyperglycaemia, fluid depletion, incontinence, erectile dysfuntion

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79
Q

calcium channel blockers

A 
peripherally acting (amlodipine, nifedipine) and centrally acting drugs (verapamil, diltiazem). used for angina pectoris, svt, hypertension (oral) 
peripheral oedema,headache, flushing, constipation,
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80
Q

ACE inhibitors

A

ramipril, lisinopril reduce arterial bp, and water retetnion, first line treatment of hypertension, chronic heart failure
can cause dry cough

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81
Q

resistant hypertension

A

potassium sparing diuretics - hyperkaelemia, dizzy

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82
Q

Pulse pressure

A

SBP-DBP

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83
Q

Mean Arterial BP

A

PP/ 3 + DBP (<60 risk of ischaemia)

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84
Q

Total peripheral resistance

A

MAP/CO

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85
Q

When does BP change

A

drops at night
White coat hypertension
therefore must be meausred on at least two separate occasions to obtain BP clinic AND home/ambulatory

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86
Q

How many yearly deaths due to hypertension

A

9.4 million

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87
Q

10mmHg SBP reduction

A

32% CVA (stroke)
1 4% CHD (coronary heart disease)
20% MI
50% HF

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88
Q

Risk factors for CVD

A

Age, high BP (hypertension), high LDL cholestero (hypercholerterolaemia), High bmi (obesity/overweight), impaired glucose tolerance (diabetes mellitus) , decreased renal function (chronic kidney disease)

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89
Q

diagnosis of hypertension

A

BOTH conventional BP 140/90 AND ABPM/home 135/80`

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90
Q

white coat hypertension

A

> 20/10 higher that at home/ abpm

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91
Q

hypertension target organ damage

A

heart (left ventricular hypertrophy), kidneys (reduced eGFR, increased albumin/creatine ration), eyes (hypertensive retinopathy)

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92
Q

general advice on reducing hypertension

A

weight in ideal range, limit salt, regular excercise

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93
Q

Hypertension initial investigation

A

past BP levels, CVD and risk factors ,
blood tests (U+E/eGFR (low is bad) , lipids, HbA1c/glucose, LFTs, gamma GT (high in liver damage), urate
urinalysis : protein, glucose, blood
ECG

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94
Q

Hypertension treatments in patient with type 2 diabetes or aged under 55 and NOT of black African or African-Caribbean family origin

A
  1. ACE Inhibitor / ARB
  2. ACE Inhibitor / ARB + CCB / tl D
  3. ACE Inhibitor / ARB + CCB + thiazide like Diuretic
  4. Confirm resistant hypertension

Add low dose spironolactone if blood potassium level is 4.5 mmol/l
Add alpha-blocker or beta-blocker if blood potassium level is >4.5mmol/l

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95
Q

Hypertension in patient without type 2 diabetes AND aged 55 or over OR of Black African or African-Caribbean family origin (any age)

A
  1. CCB
  2. CCB + ACEi/ARB or tlD
  3. ACEi or ARB + CCB + tlD
  4. Confirm resistant hypertension

Add low dose spironolactone if blood potassium level is 4.5 mmol/l
Add alpha-blocker or beta-blocker if blood potassium level is >4.5mmol/l

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96
Q

Common anti-hypertensive drugs

A

ACE inhibitors - enalapril, lisinopril, ramipril
ANG-II receptor blockers - losartan, candesartan
Calcium channel blockers - nifedipine, amlodipine
[+ rate limiting: verapamil, diltiazem]
Diuretics* - bendroflumethiazide, [chlortalidone/
indapamide]
Beta-blockers - atenolol, metoprolol, bisoprolol
Mineralocorticoid-Blockers** – spironolactone, eplerenone
Alpha-Blockers - doxazosin

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97
Q

Mechanisms of action of common anti-hypertensives

A

• ACE inhibitors - inhibit ACE, block RAAS, increase BK*, dilate
arteries (and veins), AngII receptor blockers-similar (no BK effect)
• Calcium channel blockers - block voltage-operated calcium
channels, dilate arteries (± heart rate reduction)
• Thiazides - inhibit Na+
-Clsymport, distal tubular natriuresis,
dilate arteries and veins
• Beta-blockers - block beta-adrenoceptors, reduce cardiac rate
and output, block RAAS, initial vasoconstriction (ultimately
vasodilate)
• Mineralocorticoid blockers – block mineralocorticoid
receptors, distal nephron natriuresis/limit potassium loss
• Alpha-blockers – block alpha1-adrenoceptors, dilate arteries
and veins.
*BK = bradykinin a vasodilator

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98
Q

side effects of common antihypertensive drugs

A

ACE inhibitors - cough, rise in/high K+
,renal dysfunction
• Angiotensin receptor blockers – few, rise in/high K+
, renal
dysfunction
• Calcium channel blockers - headaches, flushing, ankle swelling,
tachycardia;
• [different for rate limiting CCBs eg verapamil- bradycardia,
constipation, other gastrointestinal symptoms]
• Diuretics - impotence, rashes, biochemical – low Na+, low K+,
raised glucose (risk of diabetes), high urate (risk of gout)
• Beta-blockers – wheeze [caution with asthma/COPD], cold
peripheries, lassitude, exercise intolerance, impotence,
bradycardia, heart block, raised glucose
• Mineralocorticoid blockers - rise in/high K+
, gynaecomastia
(just spironolactone)
• Alpha-blockers – dizziness (especially on standing), urinary
symptoms, tachycardia, oedema [caution with heart failure]

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99
Q

Indications and cautions of ACEi/ARB

A 
i: Heart failure
Diabetic Nephropathy
c: Severe renal artery
stenosis, High K+
Contraindicated in
Pregnancy
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100
Q

Indications and cautions of CCB (Amlodipine, Verapamil)

A

i:Older patients,
high pulse pressure
Angina
c:Heart block, Heart failure

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101
Q

Indications and cautions of Thiazides

A 
i: Older patients,
High pulse pressure
Heart Failure
c: Contraindicated in Gout
Low K
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102
Q

Indications and cautions of Beta-Blockers

A

i: Coronary Artery Disease
Stable heart failure
c: Heart block, Asthma/COPD

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103
Q

Indications and cautions of MC Blocker

A

i: Heart failure
Diabetic nephropathy
c: High K+
, MC deficiency

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104
Q

Indications and cautions of Alpha-Blocker

A

i: Benign prostatic hypertrophy
c: Impaired urine continence
Postural hypotension
Heart failure

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105
Q

Primary vs Secondary hypertension

A

primary: lifestyle ‘you’ caused it 95%
secondary: caused by disease

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106
Q

Causes of secondary hypertension

A

Primary aldosteronism, oestrogen oral contraceptives. NSAIDs, Alcohol, renal artery stenosis, vasculitis, liquorice, glucocorticoids

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107
Q

Renal artery stenosis presentation

A

May see:-
Severe, seems sudden, resistant Hypertension
recent decline in eGFR
eGFR dip on ACEI/ARB treatment (can be major dip)
1 kidney smaller, size difference >1.5cm (imaging). Severe hypertension with sudden attacks of “flash”
pulmonary oedema and no cardiac basis found
Severe hypertension in patient with evidence of
widespread atherosclerosis, (>50 yrs old)

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108
Q

Causes and management of renal artery stenosis

A

causes: – atherosclerotic stenosis (older, commonest))
- -Fibromuscular dysplasia (often <40, more women)
management: ACE-I/ARB treatment with eGFR monitoring
- +/- diuretic (eg Thiazide)
- Consider intervention eg renal stent(across stenosis)

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109
Q

Diagnosis and management of Phaeochromocytoma / Paraganglioma

A

very rare. features of excess noradrenaline/adrenaline: Headache
sweating,
palpitations,
high blood pressure
+/- in fearful/panicky “attacks”
+/- paroxysms of such symptoms
Management- special medical treatment, surgery, consider genetics
Dangerous tumour,
Initiate α-blockade – doxazosin (or a long acting α -blocker–phenoxybenzamine)
Then β-blockade – atenolol
At surgery – experienced anaesthetic/surgical team

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110
Q

primary aldosteronism

A 
Potentially consider if
Hypertension, + suspect 2O Hypertension
- with relatively low K+
(+/- relatively alkalotic)
investigate : if A/RR is above 40
causes: conn's tumour,
bilateral adrenal hyperplasia
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111
Q

What are lipids and examples

A

poorly soluble in water but miscible in organic solvents
triglycerides
steroids - cholesterol and hormones like testosterone
fat soluble vitamins - A,D,E,K
phospholipids
sphingolipids

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112
Q

lipoproteins

A

transport cholesterol and triglycerides around the body in circulation. Dietary ones are created in the small intestine, whilst endogenous ones are created in the liver
types:
chylomicrons
VLDL, LDL,IDL,HDL

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113
Q

exogenous lipid pathway

A

chylomicrons synthesised in gut deliver triglycerides to muscle and adipose tissue where converted to NEFA (post-prandial)

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114
Q

endogenous lipid pathways

A

VLDL synthesised in liver also deliver triglycerides to muscle, adipose again converted to NEFA
LDL: cholesterol - peripheral tissues

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115
Q

Reverse cholesterol transport

A

HDL returns cholesterol to the liver but CETP can disrupt this

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116
Q

Lipoprotein types described

A

chylomicrons: biggest, mostly triglycerides
VLDL: quite big, mainly triglycerides
IDL: medium, very short lived
LDL: small, cholesterol rich, long lived
HDL: smallest cholesterol rich, long lived

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117
Q

apolipoproteins

A

determine lipoprotein behaviour

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118
Q

Triglycerides

A

energy

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119
Q

Cholesterol

A

essential building block precursor to steroid hormones and vit D and membrane. Liver is site of synthesis, secretion,uptake.
delivered to peripheral tissues by LDL
uptaken from circulation by IDL,LDL,HDL
returned to liver from peripheral tissues by HDL

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120
Q

formation of fatty streaks

A

LDLs oxidised by O-free radicals are consumed by macrophages, now known as foam cells, this is a fatty streak

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121
Q

formation of atheromatous plaque

A

LDLs oxidised by O-free radicals are consumed by macrophages, now known as foam cells, this is a fatty streak Smooth muscle cells (SMCs) are
stimulated by macrophages to
migrate, proliferate, differentiate, SMCs differentiate into fibroblasts
which produce a fibrous collagen cap , Foam cells undergo necrosis or
apoptosis to leave a pool of
extracellular cholesterol. cholesterol pool
beneath a fibrous cap
within the arterial wall = atheroma

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122
Q

familial hypercholesterolemia

A
  • tendon xanthoma (nondules)
  • corneal arcus (white ring)
  • xanthelasma whitish lumps on eyelids
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123
Q

treatment of high cholesterol

A

smoking cessation, reduce sat fat and salt, bmi

ACEi, Beta-blocker = reduce post MI mortality
Aspirin + Clopidigrel = reduce CVD recurrence and mortality
Statins - reduce CVD recurrence and mortality. (headache, dizzy, muscle pain, increased risk of developing diabetes)

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124
Q

Statins

A

10 year CV risk , calculate using ASSIGN or QRISK3

125
Q

mechanisms of lipid lowering drugs

A

statins: reduce LDL, lower risk of coronary heart disease (1st choice. HMG-CoA reductase inhibitors, inhibit rate limiting step of cholesterol synthesis.

Ezetimibe: reduce LDL, lower risk of coronary heart disease. Inhibits cholesterol absorption at small intestine, binds to NPC1L1 protein which is a critical mediator of cholesterol absorption in GI epithelial cells

Fibrates: reduce LDL and triglycerides, increase HDL. stimulate PPAR a which is a nuclear transcription factor, causes increased LPL activity and LDL uptake, reduced VLDL synthesis

PCSK9-inhibitors
monoclonal antibodies, delivered fortnightly by s/c injection. Alirocumab, evolocumab. expensive

126
Q

sites of haematopoiesis

A

fetus: yolk sac (0-2m), liver and spleen (2-7m), bone marrow (5-9m)
infant: all bone marrow
adult: central skeleton, proximal ends of femur

127
Q

stromal cells of bone marrow

A

fibroblasts, adipocytes, macrophages, endothelial cells, osteoblasts/clasts

128
Q

control of adult haematopoiesis

A

extrinsic: growth factors , adhesion molecules
intrinsic: transcription factors

129
Q

lineage of erythropoiesis

A

regulated by renal erythropoietin whihc is stimulated by tissue oxygen

130
Q

myelopoiesis (he process in which innate immune cells, such as neutrophils, dendritic cells and monocytes, develop from a myeloid progenitor cell)

A

G-CSF – granulocytes
M-CSF – macrophages
IL-5 – eosinophils

131
Q

types of WBC

A

neutrophils, lymphocytes, monocytyes, eosinophils, basophils

132
Q

cytosis

A

too much

133
Q

penia

A

too little

134
Q

anemia symptoms

A

lethargy, breathlessness, chest pain, headache, dizzy, pallor

135
Q

anemia causes

A 
Blood loss
 Reduced RBC production
• Deficiency - Iron, B12/folate
• Malignancy
• Chronic disease, kidney disease
• Thalassaemia
• Bone marrow failure
 Increase RBC destruction
• Haemolysis e.g. autoimmune
• Sickle cell disease
136
Q

causes of iron deficiency

A 
Chronic blood loss
• Menstruation
• Gastrointestinal bleeding
•Dietary
• Vegetarian, vegan, toddlers
•Malabsorption
• Coeliac disease, gastric surgery
 Increased requirements
• Pregnancy, growth
137
Q

megaloblastic anaemia

A

Defective DNA synthesis during RBC production causing

cell growth without division

138
Q

macrocytic anaemia

A

increased MCV, usually due to B12/folate deficiency

139
Q

folate

A 
Dietary sources
• Green vegetables
• Folate free diet causes deficiency in weeks
• Deficiency
• Inadequate intake
• Malabsorption – coeliac disease
• Excess consumption – pregnancy
Drugs eg anticonvulsants
140
Q

Vitamin B12

A 
Dietary
• Meat, dairy, fish
Deficiency
• Vegan diet
• Autoimmune –pernicious anaemia
• Malabsorption
• gastric or ileal surger
141
Q

Haemolytic anaemia

A 
excessive /premature RBC breakdown 
raised bilirubin and LDH
causes :Inherited
(Hereditary spherocytosis), Acquired
 (Autoimmune haemolytic anaemia)
142
Q

Polycythaemia/ Erythrocytosis

A

absolute increased red cell mass
primary - assoc with thrombosis risk of malignancy
secondary - increased erythropoieten , COPD, renal tumours
relative (reduced plasma volume) acute dehydration, alcohol, diuretics

143
Q

Leucocytosis

A

too many wBcs leukemia, lymphoma,

144
Q

neutrophilia

A

infection, inflammation, pregnancy, steroids

145
Q

monocytosis

A

acute or chronic infection, connective tissue damage

146
Q

eosinophilia

A

allergy, parasites, skin diseases, drugs

147
Q

leucopaenia

A

mainly neutropenia NR 2-7.5)
infections :
recurrent bacterial skin infections, mouth ulcers, sepsis
causes: chemotherapy, B12/folate deficiency

148
Q

thrombocytosis

A

platelets >450
primary: essential thrombocytosis
secondary : infection, surgery, iron deficiency, malignancy

149
Q

thrombocytopenia

A

platelets <150

symptoms: bruising, gum bleeding, nose bleeds, petechiae, prolonged bleeding time

150
Q

pancytopenia

A 
red flag 
everything low 
severe infection 
hypersplenism 
bone marrow failure
TB
151
Q

formation of a thrombus

A

PLATELET ADHESION

  • PLATELET ACTIVATION / SECRETION
  • PLATELET AGGREGATION
152
Q

PLATELET/VESSEL WALL DEFECTS

A

All give rise to a “prolonged bleeding time
reduced number of platelets: thrombocytopenia
abnormal platelet function: aspirin, clopidogrel, renal failure
abnormal vessel wall: scurvy, ehlers danlos syndroms, Henoch Schӧnlein purpura, Hereditary Haemorrhagic Telangiectasia
Abnormal interactions between platelets and vessel wall : Von Willebrands disease

153
Q

Scurvy

A

feel very tired and weak all the time.
feel irritable and sad all the time.
have severe joint or leg pain.
have swollen, bleeding gums (sometimes teeth can fall out)
develop red or blue spots on the skin, usually on your shins.
have skin that bruises easily.

154
Q

Ehlers-Danlos Syndrome

A

joint hypermobility.
loose, unstable joints that dislocate easily.
joint pain and clicking joints.
extreme tiredness (fatigue)
skin that bruises easily.
digestive problems, such as heartburn and constipation.
dizziness and an increased heart rate after standing up.

155
Q

Henoch-Schonlein Purpura

A

rash, joint pain and swelling, abdominal pain, and/or related kidney disease, including blood in urine.

156
Q

Hereditary Haemorrhagic Telangiectasia

A

Nosebleeds, sometimes on a daily basis and often starting in childhood.
Lacy red vessels or tiny red spots, particularly on the lips, face, fingertips, tongue and inside surfaces of the mouth.
Iron deficiency anemia.
Shortness of breath.
Headaches.
Seizures.

157
Q

von willebrand

A

Excessive bleeding from an injury or after surgery or dental work.
Frequent nosebleeds that don’t stop within 10 minutes.
Heavy or long menstrual bleeding.
Heavy bleeding during labor and delivery.
Blood in your urine or stool.
Easy bruising or lumpy bruises.
Autosomal dominant
tranexamic acid

158
Q

drugs that inhibit platelet function

A

Aspirin and COX inhibitors
 Reversible COX inhibitors eg. NSAIDs
 Dipyridamole inhibits phosphodiesterase
 Thienopyridines inhibit ADP-mediated activation, eg clopidogrel
 Integrin GPIIb/IIIa receptor antagonists

159
Q

petecial rash

A

pinpoint red lesions

160
Q

Ecchymosis

A

under skin bleeding

161
Q

Purpura

A

non-blanchable

162
Q

coagulation cascade

A

intrinsic pathway first: 12 → 11 → 9 → 10.In order for factor 9 to activate factor 10, there needs to be factor 8 present.

extrinsic pathway second: 3 → 7 → 10.

Common pathway. 10 needs factor 5 and calcium to activate prothrombin, which becomes thrombin 2 which activates fibrinogen then fibrin

163
Q

what triggers the extrinsic and intrinsic pathway of the coagulation cascade

A

The extrinsic pathway: This is triggered by external trauma which causes blood to escape the circulation
The intrinsic pathway: This is triggered by internal damage to the vessel wall

164
Q

f XII deficiency

A

do not bleed

165
Q

f VII deficiency

A

bleed abnormally

166
Q

f VIII deficiency

A

severe hemorrhagic

167
Q

f IX deficiency

A

severe hemorrhagic

168
Q

f XI deficiency

A

variable and mild bleeding

169
Q

steps of coagulation

A

Initiation
 Amplification
 Propagation
 Termination

170
Q

natural coagulation inhibitors

A

tissue factor pathway inhibitor ( VIII a and f Xa)
antithrombin ( thrombin and fXa)
protein c pathway (f Va and fVIIIIa)

171
Q

prothrombin time PT

A

reflects the extrinsic and common pathway. how long it takes a clot to form. Checked when taking warfarin

172
Q

 Activated Partial
Thromboplastin Time
(APTT)

A

Reflects the ‘intrinsic pathway’
and the ‘common pathway’. blood clot to form
used if patient is recieving heparin by intermittent injection

173
Q

fibrinogen

A

reflects the functional activity of fibrinogen used in diagnosis of bleeding disorder

174
Q

haemophilia A

A 
X-linked
recessive disorder
 Typically expressed i
Deficiency of fVIII (or
dysfunction)
Patients can have chronic arthopathy (joint space narrowing)
175
Q

management of hameophlia

A

coagulation factor concentrates
desmopressin (h A)
antifibrinolytic agents (tranexamic acid)

176
Q

congenital haemophila

A

Haemarthroses (bleeding into a joint)
Muscle bleeds
Soft tissue bleeds`

177
Q

acquired haemophilia

A 
Large haematomas (blood clot) 
Gross haematuria 
 Retropharyngeal & retroperitoneal
haematomas
 Cerebral haemorrhages
Compartment syndromes
178
Q

liver disease and clotting factors

A

reduced hepatic synthesis of clotting factors due to reduced vitamin K absorption

179
Q

DIC syndrome

A

An acquired syndrome of systemic intravascular
activation of coagulation
Widespread deposition of fibrin in circulation
 Tissue ischaemia and multi-organ failure.
can be caused by sepsis, tumor, burns, pancreatitis , snake bites, recreational drugs, pre-eclampsia
Prolonged PT time, Prolonged APTT time, low fibrinogen
raised D -dimers

180
Q

virchow’s triad

A

stasis, hypercoagulability, vascular injury

181
Q

venous thromboembolism

A

many present as sudden death, some as pulmonary embolism

182
Q

DVT

A

symptoms: swelling in affected leg (unilateral), pain in leg like cramping, red skin, warmth
Causes: age, immobility, pregnancy, obesity, smoking
diagnosis : ultrasound, venogram with dye
treatment: warfarin, rivaroxaban.
likely high d dimer
Well’s score: shows risk of DVT ( Clinical signs and symptoms, current PE, heart rate > 100bpm, immobilisation >/ 3 days OR surgery in past 4 weeks, previous PE or DVT, hemoptysis, mailgnacy. score 4 = PE unlikely

183
Q

pulmonary embolism

A

symptoms: Sudden shortness of breath (most common)
Chest pain (usually worse with breathing)
A feeling of anxiety.
A feeling of dizziness, lightheadedness, or fainting.
Irregular heartbeat.
Palpitations (heart racing)
Coughing and/or coughing up blood.
Sweating.
causes : DVT
diagnosis: CTPA to se blood vessels in lungs, V/Q scan. D dimer , ECG, ABG

184
Q

rapid initial anticoagulation

A

heparin, low molecular weight
heparin, fondaparinux, OR
direct oral anticoagulant

185
Q

Extended therapy

A

orally active anticoagulant : vitamin K antagonist

OR direct oral anticoagulant

186
Q

Direct Oral Anticoagulants

DOACs

A

Dabigatran, Rivaroxaban, Edoxaban & Apixaban
licensed in UK for treatment of acute DVT
 Enables rapid initial anticoagulation orally

187
Q

Heparins

A 
Sulphated glycosaminoglycan, biological
product derived from porcine intestine
 Binds to unique pentasaccharide on
antithrombin and potentiates its inhibitory
action towards factor Xa and thrombin
188
Q

Unfractioned Heparin (UH) vs Low molecular weight heparin (LMWH)

A 
UFH: Binds to plasma proteins
so requires monitoring
Monitor using APTT
Continuous iv infusion or
twice daily sc
administration
 Risk of osteoporosis,
heparin-induced
thrombocytopenia (HIT)
Reverse by d/c (vit c( infusion;
also protamine
LMWH: e.g (enoxaparin)
Nearly 100% bioavailability
means reliable dose
dependent a’coagulant
effect
 No monitoring required
(unless renal impairment or
extremes of body weight)
Once daily dosing
 Reduced risk of
osteoporosis, and HIT
Cannot be reversed
189
Q

Coumarins e.g.warfarin

A

Inhibit vit K dependent carboxylation of factors II,
VII, IX and X in the liver
Takes around 5 days to establish maintenance dosing
 Loading regimens assist early dosing
Dietary intake of vit K also affects warfarin dose
reversal: Dietary intake of vit K also affects warfarin dose

190
Q

DOACs vs Warfarin

A

DOACs are: MORE PREDICTABLE ANTICOAGULANT PROFILE
 FEWER DRUG AND FOOD INTERACTIONS
 WIDER THERAPEUTIC WINDOW COMPARED TO WARFARIN
 ORAL ADMINISTRATION
 NO NEED FOR MONITORING
 SIMPLE DOSING

191
Q

reverse dabigatran

A

dabigatran is a DOACs reversed with
IDARUCIZAMAB (Binds to free and thrombin-bound dabigatran to
neutralise activity, iv dosing by bolus or rapid infusion, immediate onset of action)

192
Q

reverse apixaban and rivaroxaban

A

both DOACs reversed by ANDEXANET,

193
Q

Atheroma

A 
Refers to plaques found particularly in elastic and medium-tolarge muscular arteries. 
rfs: Age
Male sex
 Genetics
 Hyperlipidaemia
 Hypertension
 Smoking
 Diabetes mellitus
194
Q

Atherosclerosis

A

The consequence of atheroma

195
Q

Arteriosclerosis

A

‘Hardening of the arteries’
• Atheroma is one cause
• Other causes include age-related sclerosis and calcification

196
Q

Pathogenesis of atheroma

A

Chronic endothelial injury / dysfunction
• Accumulation of intimal lipid and foamy
macrophages
• Smooth muscle proliferation
• Fibrosis forming a fibro-lipid plaque
• Plaque injury – thrombosis and haemorrhage

197
Q

complications of atheroma

A 
Calcification
• Ulceration
• Plaque rupture
• Haemorrhage
• Thrombosis
• Aneurysmal dilatation
vessel obstruction and downstream ischaemia
198
Q

thrombus

A

A thrombus is a solidification of blood constituents that

forms within the vascular system during life (virchow’s triad)

199
Q

haematoma

A

Solidification of blood constituents outside the vascular
system or after death is termed blood clot or
haematoma

200
Q

Endothelial Injury

A

Ulcerated atheromatous plaques, Abnormal cardiac valves
• Rheumatic fever
• Infective endocarditis
• Prosthetic valves
• Left ventricular endocardium after myocardial
infarction

201
Q

Abnormal Blood Flow

A

Disrupts laminar flow
• Prevents the dilution of clotting factors
• Retards the inflow of inhibitors of clotting factors
• Promotes endothelial cell activation
• Turbulence
• Contributes to the development of arterial and
cardiac thrombi
• Stasis
• Important in the formation of venous thromb

202
Q

Complications of Thrombosis

A

Occlusion of artery or vein (Arterial occlusion
Loss of pulses distal to the thrombus
Area becomes cold, pale, painful
Eventually tissue dies and gangrene results)
• Embolism

203
Q

Venous Thrombosis

A

Superficial (saphenous system) varicose veins
• Congestion, swelling, pain, tenderness (rarely
embolise)

Deep
• Foot and ankle oedema
• May be asymptomatic and recognised only when
they have embolised (to the lung)

204
Q

embolus

A

An embolus is a detached intravascular solid,
liquid, or gaseous mass that is carried by the
blood to a site distant from its point of origin

205
Q

Infarct

A

• Is an area of ischaemic necrosis caused by
occlusion of arterial supply or venous drainage in a
particular tissue

206
Q

Necrosis

A

• Refers to a spectrum of morphological changes that
follow cell death in living tissue, largely resulting
from the progressive action of enzymes on the
lethally injured cells

207
Q

Causes of Infarction

A 
Thrombosis and thromboembolism account
for the vast majority
• Other causes include:
• Vasospasm
• Expansion of atheroma
• Compression of a vessel
• Twisting of the vessels through torsion
• Traumatic rupture
208
Q

Factors That Influence

Development of an Infarct

A

Nature of the vascular supply
• Single (e.g. spleen) or dual (e.g. lung, small bowel)
• Rate of development of occlusion
• Rapid occlusion more likely to cause infarction
• Vulnerability of affected tissue to hypoxia
• More metabolically active tissues more vulnerable e.g.
heart
• Oxygen content of blood
• Hypoxia increases risk

209
Q

Types of Infarct

A
  • Red (haemorrhagic):
  • Venous occlusion e.g. torsion
  • Loose tissues
  • Tissues with a dual circulation e.g. lung
  • White (anaemic):
  • Arterial occlusions
  • Solid organs e.g. heart, spleen
  • Septic
  • Infected infarcts
210
Q

Systemic Hypertension

A 
Classification by cause:
• ~ 90% primary (essential) ( obesity, diabetes, high salt) 
• ~ 10% secondary
• ~ 90% due to renal disease
• ~ 10% due to other causes especially
endocrine disease
211
Q

end organ effects of systemic hypertension on heart

A
  • Left ventricular hypertrophy
  • Fibrosis
  • Arrhythmias
  • Coronary artery atheroma
  • Ischaemic heart disease
  • Cardiac failure
212
Q

end organ effects of systemic hypertension on kidney

A

Nephrosclerosis
• ‘Drop-out’ of nephrons due to vascular narrowing
• Proteinuria
• Chronic renal failure
• Malignant hypertension is associated with acute
renal failure

213
Q

end organ effects of systemic hypertension on brain

A

intracerebral haemorrhage causing stroke

214
Q

end organ effects of systemic hypertension on eye

A

hypertensive retinopathy

215
Q

Ischaemic Heart Disease

A 
Blood supply to the heart is insufficient for its
metabolic demands
• Deficient supply
• Coronary artery disease (commonest)
• Reduced coronary artery perfusion
• Shock
• Severe aortic valve stenosis
• Excessive demand
• Pressure overload: e.g. hypertension, valve disease
• Volume overload: e.g. valve disease
216
Q

Coronary Artery Disease

A

• Coronary blood flow is normally independent of
aortic pressure
• Initial response to narrowing is autoregulatory
compensation
• >75% occlusion leads to ischaema

217
Q

Myocardial Infarction

A 
• An area of necrosis of heart muscle resulting
from reduction (usually sudden) in coronary
blood supply
• Due to
• Coronary artery thrombosis
• Haemorrhage into a coronary plaque
• Increase in demand in the presence of ischaemia
Clinical features
• Central, ‘crushing’ chest pain
• Features of heart failure
• Diagnosis
• Clinical history
• ECG changes
• Blood markers
• enzymes e.g. creatine kinase
• other proteins e.g. troponin
218
Q

Chronic Ischaemic Heart Disease

A

Chronic angina
• Exercise-induced chest pain
• Heart failure
• Related to reduced myocardial function
• Usually widespread coronary artery atheroma
• Areas of fibrosis often present in the myocardium

219
Q

What is Cardiac Failure

A

Failure of the heart to pump sufficient blood to
satisfy metabolic demands
• Leads to underperfusion which causes fluid
retention and increased blood volume
• Two different, but linked, circulations
• Systemic
• Pulmonary

220
Q

Acute heart failure

A

Rapid onset of symptoms, often with definable

cause e.g. myocardial infarction

221
Q

Chronic heart failure

A

Slow onset of symptoms, associated with, for

example, ischaemic or valvular heart disease

222
Q

• Acute-on-chronic heart failure

A

Chronic failure becomes decompensated by an

acute event

223
Q

Causes of heart failure

A 
Pressure overload
• Hypertension (pulmonary or systemic)
• Valve disease e.g. aortic stenosis
• Volume overload
• Valve disease e.g. aortic incompetence
• Intrinsic cardiac disease
• Ischaemic heart disease
• Primary heart muscle disease
• Myocarditis
• Pericardial disease
• Conducting system disorders
224
Q

Left Ventricular Failure

A

Dominates hypertensive and ischaemic heart
failure
• Causes pulmonary oedema, with associated
symptoms
• Leads to pulmonary hypertension and,
eventually, right ventricular failure
• Combined left and right ventricular failure is
often called ‘congestive’ cardiac failure

225
Q

Right Ventricular Failure

A

Common causes
• Secondary to left ventricular failure
• Related to intrinsic lung disease – ‘cor’ pulmonale
e.g. chronic obstructive pulmonary disease (COPD)

226
Q

Clinical Features

• Left ventricular failure

A 
Hypotension
• Pulmonary oedema
• Paroxysmal nocturnal dyspnoea
• Orthopnoea
• Breathlessness on exertion
• Acute pulmonary oedema with production of frothy fluid
227
Q

Clinical Feature • Right ventricular failure

A

Ankle swelling

• Hepatic congestion (may be painful)

228
Q

Clinical Features• Forward failure

A

Reduced perfusion of tissues

• Tends to be more associated with advanced failure

229
Q

Clinical Features • Backward failure

A

Due to increased venous pressures
• Dominated by fluid retention and tissue congestion
• Pulmonary oedema (left ventricular failure)
• Hepatic congestion and ankle oedema (right ventricular
failure)

230
Q

layers of artery

A

Intima, media, adventia (Strong, smooth, flexible)

231
Q

aneurysm

A

Dilated

232
Q

stenosis

A

Narrowed

233
Q

occluded

A

Blocked

234
Q

dissection

A

Split

235
Q

vasospasm

A

Over sensitive

236
Q

vasculitis

A

Inflamed

237
Q

Claudication

A 
Stenosis 
Pain on walking a fixed distance
• Worse uphill
• Eases rapidly when you stop
• ANGINA of the leg!
238
Q

Acute Blocked arteries

A 
Pain (sudden onset)
• Palor
• Perishingly cold
• Parasthesia
• Pulselessness
• Paralysis
239
Q

Chronic Blocked arteries

A 
Short distance claudication
• Nocturnal pain
• Pain at rest
• Numbness
• Tissue necrosis
• Gangrene
• Things falling off
240
Q

Acute limb ischaemia

A

(sudden event with <2 weeks ischaemia)
• 7.5% limb loss at 1 year
• 25% mortality at 30 days

241
Q

Chronic Limb Ischaemia

A

(ischaemia >2 weeks with rest pain/tissue loss = Critical)
• 5 year survival of 71%
• 43% limb loss rate at 5 years

242
Q

Amputation

A 
Median survival after
amputation is 2.25 years
• 30 day mortality of 17%
• 30% lose the other leg with 2
years
• 6000 per year in UK
243
Q

vasospasm

A 
Over active vasoconstriction
• Capillary beds shut down
• Triggers – cold, stress
• Can have underlying connective
tissue disease
244
Q

Vasculitis

A

Inflamed arteries
Large vessel – Takayasu’s disease – “the pulseless disease”
• Medium vessel – Giant Cell Arteritis / Polymyalgia
• Small vessel – lots of polyangiitis conditions usually involving the
kidneys
treated with steroids

245
Q

Diabetic foot

A

• Neuropathic
• Ischaemic
• Infected
• Calcified vessels
• Small vessel arterial disease
• Patients can’t see their feet (retinopathy)
The lifetime incidence of diabetic foot ulceration is 19-34%
• At 1 year
• 46% of patients will have a healed ulcer at 1 year with 10% recurrence thereafter
• 15% will have died
• 17% require an amputation

246
Q

Charcot Foot

A 
– end stage diabetic foot changes
Neuropathic
• Warm (>2℃ than normal)
• AV shunting
• Multiple fractures
• “Rocker bottom” sole
247
Q

Venous return

A

Muscle pumps – venous pressure at ankle 100mmHg standing, 25mmHg walking
• Thoracic pump action during respiration
• Gravity – lying down
• Right heart function
• Requires functioning competent valves

248
Q

Venous reservoir –

A

64% of the total systemic circulation is within the veins
• 18% in the large veins
• 21% in large venous networks such as liver, bone marrow
• 25% in venules and medium sized veins

249
Q

Venous insufficiency

A 
Failure of the muscle pump
(typically calf muscle)
• Immobility
• Dependency
• Fixed ankle
• Loss of muscle mass
• Failure of the valves
250
Q

Venous hypertension

A 
Haemosiderin (brown stain discolouration) staining
• Swollen legs
• Itchy, fragile skin
• “Gaiter” distribution (shinpad)
• Risk of ulceration
 can cause Right heart failure
• Liver failure
• Compression of the pelvic veins
(baby/tumour etc)
• Deep venous occlusion (ilio- femoral DVT)
• Morbid obesity
• Valve failure
• Immobility
251
Q

treatment of venous hypertension

A 
Emollient to stop skin cracks
• Compression
• Bandages
• Wraps
• Stockings
• Elevate and mobilise
252
Q

Valve failure

A 
Superficial veins = Varicose veins
• Deep veins = venous
hypertension
treatment:
Superficial veins
• Endothermal ablation
• Surgical removal
• Foam sclerotherapy
• Adhesive occlusion
• Compression
• Deep veins
• Compression
253
Q

Superficial thrombophlebitis

A 
Minor trauma
• Usually underlying varicose veins
• Symptomatic treatment
• Heparin to stop propagation
• Consider treating varicose veins
254
Q

Porto-systemic venous system

A 
Mesenteric or ‘portal venous’
drainage is via the liver before
the heart
• Systemic circulation is returns to
the heart directly
• The two circulation systems
combine a number of points
255
Q

Dilated systemic veins from portal hypertension

A

Oesophageal
Varices
Caput
Medusa

256
Q

vein layers

A

adventia, media, intima

257
Q

lymphatic vessel layers

A

adventia, media, intima

258
Q

Lymphoedema

A

If the lymphatic channels are blocked interstitial fluid accumulates

259
Q

most common cause worldwide of lymphodema

A

filariasis aka elephantitis
caused by parasitic worm infection (Wuchereria bancrofti) spread by mosquitos or black flies
treated by antihelminitic drugs

260
Q

general treatment of lymphoedema

A 
Compression
• Skin care
• Exercise
• Manual lymphatic drainage
• Specialised massage technique
• Rarely surgery to debulk, liposuction or connecting lymph channel to veins
261
Q

Reduced oncotic pressure

A 
Oncotic pressure is the colloid
osmotic pressure induced by
protein in the blood plasma
• Low protein (albumin) states
lead to limb swelling and
oedema
Liver failure
• Renal disease
• Low protein
• Too much water
• Malnutrition - kwashiorkor
262
Q

Lower limb cellulitis

A 
caused by streptococcus aureus 
ot swollen leg
• Tissue oedema
• Unfortunately chronic cellulitis
can lead to lymphatic
obstruction
263
Q

Right ventricular failure

A

Central venous pressure rises
• Peripheral venous pressure rises
• Increased interstitial fluid
• Oedema

264
Q

Preload

A 
Volume of blood in the
ventricles at the end of
diastole.Determined by
• blood volume
• venous ‘tone’,
capacity of the
venous circulation to
hold blood
Increased
• Sympathetic NS activation
• renal failure
• heart failure
265
Q

Afterload

A 
Resistance the heart
must overcome to
circulate blood
Determined by
• tone in arterial
circulation
Increased
• SNS activation
• hypertension
266
Q

Angina pectoris

A

intermittent chest pain caused by mismatch between
demand of oxygen by the heart and supply of oxygen
to the heart

treatment:
during attack = Rapid acting organic nitrate
e.g.Glyceryl Trinitrate

prophylactic = Nicorandil Targets blood vessels
longer lasting nitrate
KATP channel opener
Targets heart
β adrenoreceptor antagonist
Calcium ‘antagonist’
267
Q

Nitrates

A 
Venous
circulation: dilate
veins, decrease
venous
return and preload
on heart, reduce O2
demand

Coronary arteries: improves
supply (coronary spasm)

Arterioles: dilate
and reduce
afterload on heart,
therefore
reduce O2 demand
268
Q

Nitrates examples

A

Glyceryl trinitrate Acute (sub-lingual or spray), chronic
use leads to tolerance ie loss of responsiveness
Isosorbide dinitrite (slow release patch or oral), can be
prophylactic, nitrate free periods required

269
Q

Nicorandil

A

used in treatment of angina reduces preload and afterload on heart and
therefore O2 demand
• dilates coronary arteries and can increase O2
supply in coronary spasm

270
Q

β-adrenoreceptor

antagonists e.g. atenolol

A 
used in treatment of angina 
blocks cardiac β1
adrenoreceptor - reduce heart rate
and therefore O2
demand
blocks renal β1
adrenoreceptor - reduce blood volume by reducing
renin release &
activation of RAAS,
reduce preload, therefore O2
demand
271
Q

Ivabradine

A

Treatment of angina in patients in normal sinus rhythm
reduce heart rate
and therefore O2 demand

272
Q

Calcium antagonist

A

lower blood pressure.
nifedipine, dilthiazem
prevent opening of voltage dependent Ca2+ channels, prevents Ca2+ entry into cardiac muscle
cells from extracellular space, therefore
reduce availability to contractile apparatus,
reduce force of contraction and
therefore O2 demand,

273
Q

aspirin

A

taken prophylactically to reduce the risk of thrombus
cyclooxygenase inhibitor
rreversible inhibition of COX, prevents formation of TxA2 & platelet
activation

274
Q

clopidogrel, ticagrelor

A

taken prophylactically to reduce the risk of thrombus

P2Y12 inhibitor blocks effect of ADP and prevents platelet activation

275
Q

voripaxar

A

taken prophylactically to reduce the risk of thrombus
thrombin-receptor antagonist
• prevent activation of PAR-1 receptors on platelets

276
Q

Fondaparinux

A

Anti-coagulant not orally active
Synthetic pentasaccharide
• Also acts through anti-thrombin III but selective
for factor Xa inhibition

277
Q

Bivalirudin

A

Anti-coagulants not orally active
Directly binds thrombin and inhibits thrombin induced
conversion of fibrinogen to fibrin, synthetic congener of hirudin

278
Q

warfarin

A

orally active
Common clinical indications
atrial fibrillation, the presence of artificial heart valves, deep venous
thrombosis, pulmonary embolism and, occasionally, after myocardial
infarction.

279
Q

Dabigatran

A

Directly Acting Oral Anti-Coagulants
Direct inhibitor of thrombin (factor II) enzyme activity
• Competitive and reversible
severe bleeding can be reversed by Idarucizumab

280
Q

Fibrinolytic drugs

A

clot buster
•most effective to reduce mortality if given immediately (<3h) after MI
or stroke
• accelerates conversion of plasminogen to plasmin, which degrades
fibrin in thrombus
• can cause bleeding (reversed by tranexamic acid)

281
Q

Heart Failure

A

two types:
impaired contractility and emptying of ventricle HF with
reduced ejection fraction, HFrEF, systolic HF): most
common and drugs directed here

impaired relaxation and filling of ventricle (HF with preserved ejection
fraction, HFpEF, diastolic HF): growing recognition, more common in
women, diabetes, mechanisms less understood

282
Q

common causes of heart failure

A

Myocardial infarction: damage to heart muscle
after loss of blood supply due to ischaemic heart
disease
l Volume Overload: due to damage to heart valves or
increased plasma volume
l Pressure Overload: due to uncontrolled
hypertension & increased afterload
l Myocarditis :bacterial infection of myocardium
l Cardiomyopathy: inherited defect in muscle
structure influencing function

283
Q

Drugs for Heart failure

A

Digoxin cardiac glycoside hat
increase the force of contraction: +ve inotrope,
therefore increases kidney perfusion and fluid loss
Cardiac glycosides inhibit Na+/K+ ATPase

dobutamine (ß1 adrenoreceptor agonist iv for rapid
response), increases heart rate and contractility

284
Q

Renin inhibitor

A

aliskiren heart failure

285
Q

ACE inhibitor examples

A

enalapril, lisinopril heart failure

286
Q

AT receptor antagonists

A

AT receptor antagonists heart failure

287
Q

Loop diuretics

A

for heart failure
. frusemide, bumetamide
impair Na+/K+/Cl- readsorption in the ascending
loop of Henle

288
Q

Mineralocortoid receptor antagonists

A

heart failure
spironolactone, eplerenone
• block effects of aldosterone on Na/K
readsorption

289
Q

ß adrenoreceptor antagonists and the RAAS

A

block renin release from the kidney, therefore
decrease RAAS activation, decrease pre-load &
after-load
reduce sympathetic drive to the heart (reduced O2
demand)
few side-effects, but not useful in asthmatics
(especially non-selective)

290
Q

Nitrovasodilators

A 
heart failure 
isosorbide mononitrate (long acting
but risk of tolerance)
venous circulation: decrease venous return and preload
arterioles: reduce PVR and afterload
291
Q

Hydralazine

A

dilator that targets arteries > veins and reduces afterload
nitrates and hydralazine can be used to treat
acute heart failure or in patients with chronic
heart failure who fail to respond to other drugs

292
Q

High Sensitivity CRP

A

Acute phase protein produced by liver and
adipose tissue.
- Assists in complement binding and phagocytosis
of damaged cells

293
Q

Creatine Kinase

A

Not cardiac specific
Present in Skeletal
Muscle

294
Q

Troponin

A

The troponin complex is a component of the thin filaments in
striated muscle complexed to actin. Regulates muscle contraction
Troponin – 3 subunit complex: Predicts Future Cardiac Events
gender specific

295
Q

heart disease diagnosis

A

naturitic peptides
Naturetic peptides can be used for the rule out of
chronic heart failure and have a role in stratifying
treatment

296
Q

VȩO2

is dependent upon:

A 
Ventilatory capacity to provide oxygen
- Circulation to deliver O2
to exercising muscle
- Muscle ability to utilise O2
for energy conversion
297
Q

VȩO2 max

A

Maximal oxygen uptake

– Used as a global measure of fitness

298
Q

Ventilation adapts to meet needs for

A
  • Uptake of oxygen

- Clearance of CO2 produced

299
Q

Respiratory quotient (RQ) also known as Respiratory Exchange Ratio (RER):

A
  • CO2 produced / O2
    consumed
  • RQ increases with exercise
300
Q

Increased ventilation achieved by:

A

Increases in respiratory rate (RR) – Increased size (tidal volume - VT) of each breath
–Ventilation per minute (V̇E)= RR x VT

301
Q

Maximal exercise ventilation (V̇E max) can be estimated as

A

maximal
voluntary ventilation (MVV)
- MVV = FEV1
x 40

302
Q

increase in cardiac output during exercise

A

Five-fold.

Increases in HR
- Increases in stroke volume

303
Q

Rate-limiting factor to maximal exercise in health

A

CARDIAC PHYSIOLOGY

maximal heart rate

304
Q

Anaerobic Threshold

A

Point at which ventilation increases at a faster rate than oxygen uptake (VO2
) and reflects the point at which anaerobic
metabolism begins to predominate with exponentially increasing carbon dioxide production and accumulation of fatigue-related metabolites including lactate.

305
Q

Ventilatory threshold

A

This is actually what we are measuring if non-invasively when performingexercise tests keep incorrectly referring to it as AT

306
Q

Effects of deconditioning

A

Reduced muscular capillary numbers
(reduced O2 transfer at muscular level)
• Reduced mitochondrial density
(reduced O2 utilisation at muscular level)
• Reduced oxidative enzyme concentrations
(reduced energy transformation in muscles)
Impaired ability for exercising muscle to extract and utilise oxygen
from blood

307
Q

CPET

A

limitations of excercise capacity

Diagnostic Importance:
Exercise-induced arrhythmias
Exercise-induced asthma

308
Q

EXERCISE-INDUCED ASTHMA

A

Acute, reversible, usually self-terminating airway obstruction– During or after strenuous exercise or hyperpnoea – Especially if breathing dry and/or cold air – May occur in atypical or latent asthmatics.

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