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Medicine Term 2 > Cardiovascular Diseases > Flashcards

Cardiovascular Diseases Flashcards

1
Q

what is hypertension

A

high blood pressure

140/90mmHg

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2
Q

what does the framingham study show about bp

A

bp -> risk of stroke + cvd
risk rises exponentially
age plays role

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3
Q

whats stage 1 hypertension

A

140/90mmHg

ABPM daytime average - 135/85

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4
Q

whats stage 2 hypertension

A

160/100 mmHg or higher

ABPM daytime average 150/95 mmHg

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5
Q

whats stage 3 hypertension

A

Clinic systolic blood pressure is 180/120 mmHg

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6
Q

whats primary hypertension

A

no cause can be found

80-90% cases

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7
Q

whats secondary hypertension

A

cause can be found
10-20% cases
may be curable
incidence highest in younger patients

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8
Q

what risk factors are for hypertension

A 
Cigarette smoking		 
- adds 20/10 mmHg
Diabetes mellitus		increase MI
Renal disease
Male				
Hyperlipidaemia		
Previous MI or stroke
Left ventricular hypertrophy
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9
Q

what controls BP

A

Cardiac output, SV + HR

Peripheral vascular resistance

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10
Q

what is the Renin-Angiotensin-Aldosterone System responsible for

A

maintenance of sodium balance
control of blood volume
control of blood pressure

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11
Q

what is the renin angiotensin system stimulated by

A

fall in BP
fall in circulating volume
sodium depletion

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12
Q

what does Angiotensin II do

A

vasoconstrictor
anti-natriuretic peptide
stimulator of aldosterone - anti-diuretic, release from the adrenal glands

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13
Q

how does the symp NS control BP

A
  • vasoconstriction - inc peripheral resistance

- reflex tachycardia, increased stroke volume = inc cardiac output

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14
Q

whats the aetiology of hypertension

A

polygenic

  • major genes (angiotensin, diabetes)
  • poly genes (obesity, race, BP)

polyfactorial

  • environment (diet)
  • individual and shared (stress, PA)

age, genetics, environment, weight, alcohol, race

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15
Q

BP tends to rise with age, possibly as a result of decreased arterial compliance.

A

buh

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16
Q

Mental and physical stress both increase blood pressure

A

jk

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17
Q

Caucasians have a lower BP than African populations living in the same environment

A

hhj

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18
Q

what investigations would you carry out for secondary hypertension

A 
Renal function and urinalysis
Renal imaging
	– Ultrasound
	– MRA renal arteries
Aldosterone to renin rati
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19
Q

what are causes of secondary hypertension

A
  • renal disease (renal stenosis)
  • drug induced (NSAIDs, oral contraceptive)
  • pregnancy
  • endocrine
  • vascular (aortic coarctation)
  • sleep apnoea
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20
Q

how do you identify true hypertension

A

20-30 clinic readings
must use ambulatory blood pressure monitoring
or home blood pressure monitoring

sometimes if no nocturnal dip in pressure

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21
Q

what is white coat hypertension

A

normal bp apart from one reading

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22
Q

what is masked hypertension

A

bp looks normal but then shoots up

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23
Q

to diagnose hypertension must first assess risks, what might these be

A 
Previous MI, stroke, IHD
Smoking
Diabetes mellitus
Hypercholesterolaemia
Family history
Physical Examination
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24
Q

how can you assess end organ damage

A

ECG
echocardiogram
proteinuria
renal US

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25
Q

what can you use to assess/quantify risk

A

the assign risk calculator/ Q-risk

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26
Q

what drugs should you use to treat hypertension in a young patient

A

ACE inhibitor

ramipril

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27
Q

what drugs should you use to treat hypertension in an elderly patient

A

Calcium Channel Blocker

Thiazide –Type Diuretic

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28
Q

In Stage 1:
offer antihypertensive drug treatment to people aged under 80 years with ABPM >135/85 with target organ damage, renal disease, diabetes etc

A

ggg

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29
Q

in Stage 2

Offer antihypertensive drug treatment to people of any age with ABPM> 150/95

A

erf

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30
Q

in step 1 treatment, what drug would you give to patients aged >55 and black people

A

calcium channel blocker

thiazide like diuretic (black)

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31
Q

in step 1 treatment, what drug would you give to patients aged <55 for hypertension

A

ACEI/ARB

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32
Q

what drug would you add on in step 2 treatment of hypertension

A

add Thiazide-type diuretic such as indapamide to CCB or ACEI/ARB

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33
Q

what drug would you add on in step 3 treatment of hypertension

A

Add CCB, ACEI, Diuretic together

beta-blocker if stil incomplete effect

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34
Q

what drugs are angiotensin converting enzyme inhibitors (ACEI)

A

RAMIPRIL, PERINDOPRIL

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35
Q

what are some contraindications to ACE Inhibitors

A

Renal artery stenosis
Impaired renal function
Hyperkalaemia
Fertile female - teratogenic

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36
Q

what drug-drug interactions are there with ACEI

A

NSAIDs
Potassium supplements
Potassium Sparing diuretics

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37
Q

what Angiotensin II Antagonists drugs are there, what do they do

A

LOSARTAN, VALSARTAN, CANDESARTAN, IRBESARTAN

competitively block the actions of angiotensin II at the angiotensin AT1 receptor

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38
Q

what is a side effect of ACEI

A

dry cough

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39
Q

what drugs are calcium channel blockers that vasodilate

A

Amlodipine/Felodipine

reduce peripheral resistance

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40
Q

what drugs are calcium channel blockers that reduce the HR

A

Verapamil/Diltiazem

Block the L-type calcium channel in the myocytes

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41
Q

what are adverse drug reactions to CCB

A

Flushing
Headache
Ankle oedema
Indigestion and reflux oesophagitis

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42
Q

what drugs are Thiazide Type Diuretics and what do they do

A

Indapamide, Clortalidone

Urinary excretion of sodium
Resistance vessel dilatation

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43
Q

what drug is an Alpha-adrenoceptor antagonists and what do they do

A

DOXAZOSIN

Selectively block post synaptic a1-adrenoceptors
Oppose vascular smooth muscle contraction in arteries

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44
Q

what drug would you use for hypertension in pregnancy

A

METHYLDOPA
Nifedipine MR

-centrally acting agent

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45
Q

what anti-hypertensive drug would you not give to a pregnant patient

A

ACE or ARB

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46
Q

what does preeclampsia increase the risk of in women

A

Stroke
Heart failure
Atrial fibrillation

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47
Q

what is a hypertensive emergency

A

Severely elevated BP (BP>180/120 mmHg) with evidence of acute target organ damage
need admission

no ACE or ARB

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48
Q

what is a hypertensive urgency

A

Severely elevated BP with NO evidence of acute target organ damage
dont need admission, start on dual oral therapy

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49
Q

whats orthostatic hypotension

A

sudden drop in blood pressure when you stand from a seated/lying position

a blood pressure decrease of 20 mmHg systolic and/or a diastolic pressure of 10 mmHg within three minutes of standing.

prevalence in older hypertensive patients

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50
Q

what are the causes of orthostatic hypotension

A 
Ageing
Diabetes
Antihypertensive drugs
Auto-immune systemic diseases
Neurological syndromes: pure autonomic failure, Parkinson’s disease
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51
Q

how can you treat orthostatic hypotension

A

Teach manoeuvres either mobilising volume from the lower parts of the body or stimulating pressure receptors leading to vasoconstriction

at night, tilt bed in head up position

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52
Q

what is ATHEROMA /ATHEROSCLEROSIS

A

Formation of focal elevated lesions (plaques) in intima of large and medium-sized arteries

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53
Q

what can the consequences of atheroma be

A

ischaemia
angina due to myocardial ischaemia
complicated by thtomboembolism

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54
Q

whats atheriosclerosis

A 
Not atheromatous
age related change in muscular arteries
smooth muscle hypertrophy, reduplication of internal elastic laminae
intimal fibrosis 
= dec vessel diameter
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55
Q

what is the earliest lesion of atheroma

A

fatty streak
yellow linear elevation of intimal lining
lipid laden macrophages
children

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56
Q

whats early atheromatous plaque

A

Young adults onwards
Smooth yellow patches in intima
Lipid-laden macrophages

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57
Q

describe a fully developed atheromatous plaque

A

central lipid core (rich in cellular lipids/debris from macrophages)
with fibrous tissue cap, covered by arterial endothelium

collagen provide structural strength
inflammatory cells in fibrous cap, recruited from endothelium

highly thombogenic rim of foamy macrophages

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58
Q

what cells reside in the fibrous cap of atheromas

A

Inflammatory cells (macrophages, T-lymphocytes, mast cells

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59
Q

what occurs late in plaque development

A

Dystrophic calcification extensive

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60
Q

where do atheromas usually form

A

Form at arterial branching points/bifurcations (turbulent flow)

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61
Q

what are the features of a complicated atheromatous plaque

A 
established atheromatous plaque
\+
haemorrhage into plaque
plaque rupture/fissuring 
Thrombosis
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62
Q

what is the biggest risk factor for atheroma

A

Hypercholesterolaemia

lack of functional receptors for LDL cholesterol = elevate cholesterol

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63
Q

what are signs of HYPERLIPIDAEMIA

A

Biochemical evidence: LDL, HDL, total cholesterol, triglycerides

Corneal arcus (premature) (lipid in iris)
Tendon xanthomata (knuckles, Achilles)
Xanthelasmata (lipid in eyelid, yellow)
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64
Q

what are risk factors FOR ATHEROMA

A 
Smoking
Hypertension
Diabetes mellitus
Male
Elderly
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65
Q

what is the process of developing ATHEROMATOUS PLAQUES

A
  1. injury to endothelial lining of artery
  2. chronic inflammatory and healing response of vascular wall to agent causing injury
  • endothelial injury
  • LDL accumulation in wall
  • monocyte adhesion, migration to intima, foamy macrophages
  • platelet adhesion
  • smooth muscle recruitment
  • smooth muscle proliferation , T cell recruitment
  • lipid accumulation (extracellular and in foamy macrophages)
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66
Q

what can be the injury cause of developing atheroma

A

haemodynamic disturbances (turbulent flow)

hypercholesterolaemia

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67
Q

how are injured endothelial cells functionally altered

A

Enhanced expression of cell adhesion molecules (ICAM-1, E-selectin)
High permeability for LDL
Increased thrombogenicity

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68
Q

what happens in acute atherothrombotic occlusion

A

rupture of plaque → acute event

Rupture exposes highly thrombogenic plaque contents (collagen, lipid, debris) to blood stream → activation of coagulation cascade and thrombotic occlusion

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69
Q

what happens if there is total occlusion of a vessel

A

otal occlusion → irreversible ischaemia → necrosis (infarction) of tissues

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70
Q

what happens if there is embolisation from atheromatous plaque

A

Detachment of small thrombus fragments from thrombosed atheromatous arteries → embolise distal to ruptured plaque

Embolic occlusion of small vessels → small infarcts in organs

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71
Q

what are the features of vulnerable plaques

A

Typically thin fibrous cap, large lipid core, prominent inflammation

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72
Q

what are preventative and therapeutic approaches to atheroma

A 
Stop smoking
Control blood pressure
Weight loss
Regular exercise
Dietary modifications
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73
Q

what are secondary preventions to atheroma

A

Cholesterol lowering drugs,
aspirin
(inhibits platelet aggregation to decrease risk of thrombosis on established atheromatous plaques)

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74
Q

Normal Blood Flow is LAMINAR

smooth, ordered

A

ggg

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75
Q

what is stasis

A

stagnation of flow

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76
Q

what is turbulence

A

forceful, unpredictable flow

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77
Q

what are the 2 types of abnormal blood flow

A

stasis

turbulence

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78
Q

what are the component of Virchow’s Triad

A

Changes in the blood vessel wall

Changes in the blood constituents

Changes in the pattern of blood flow

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79
Q

what is thrombosis

A

Formation of a solid mass from the constituents of blood within the vascular system

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80
Q

what are the causes of thrombosis

A

Endothelial injury, atheromatous plaque

Stasis or turbulent blood flow

Hypercoagulability of the blood

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81
Q

what are the component of thrombus

A

lines of Zhan
platelets
fibrin meshwork
RBCs trapped

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82
Q

what do the consequences of thrombosis depend on

A

Site
Extent
Collateral circulation

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83
Q

what is an embolism

A

Movement of abnormal material in the bloodstream and its impaction in a vessel, blocking its lumen

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84
Q

whats an embolus

A

detached intravascular solid, liquid or gaseous mass

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85
Q

describe thrombus embolus

A

Systemic/Arterial Thromboembolus

Travel to wide variety of sites: lower limbs most common, brain, other organs

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86
Q

what are venous thromboembolus

A

Originate from deep venous thromboses (lower limbs)

travel to pulmonary circulation may occlude pulmonary artery

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87
Q

what is the consquence of multiple pulmonary embolism over time

A

pulmonary hypertension and right ventricular failure

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88
Q

what are risk factors for DVT and pulmonary thromboembolism

A 
Cardiac failure, 
severe trauma/burns
oral contraceptive 
age
bes rest
obesity
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89
Q

can get fat embolus

A

ff

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90
Q

can get gas embolus, N2 form as bubbles which lodge in capillaries

A

yy

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91
Q

what is Rheumatic Fever

A

Disease of disordered immunity
Inflammatory changes in the heart and joints
“flitting” (painful) polyarthritis of large joints + skin rashes and fever

had recent streptococcal infection, string antibody reaction
Damage to heart tissue may be caused by combination of antibody-mediated and T cell-mediated reactions

causes mitral stenosis

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92
Q

whats pancarditis

A

inflammation affecting endocardium, myocardium, pericardium) in the acute phase; heart murmurs common

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93
Q

what are aschoff bodies

A

inflammatory cells, Seen in the heart in acute rheumatic fever

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94
Q

what can valvular heart disease be a result of

A

Valvular stenosis: valve thickened/calcified and obstructs normal blood flow into chamber/vessel

Valvular incompetence/regurgitation, loses normal function and fails to prevent reflux of blood after contraction of cardiac chamber

Vegetations: infective or thrombotic nodules develop on valve leaflets impairing normal valve mobility; may embolise

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95
Q

in chronic rheumatic heart disease what valvular abnormalities are there

A

fibrinoid necrosis of the valve cusps/chordae tendineae, form vegetations

thickening of mitral valve

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96
Q

what is ischaemia

A

Relative lack of blood supply to tissue/organ leading to inadequate O2 supply to meet needs of tissue/organ: hypoxia

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97
Q

what are the two types of hypoxic hypoxia

A

(a) Low inspired O2 level

(b) Normal inspired O2 but low PaO2

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98
Q

what is stagnant hypoxia

A

Normal inspired O2 but abnormal delivery

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99
Q

what is cytotoxic hypoxia

A

Normal inspired O2 but abnormal at tissue level

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100
Q

what are factors affecting oxygen supply

A
  1. Inspired O2
  2. Pulmonary function
  3. Blood constituents
  4. Blood flow
  5. Integrity of vasculature
  6. Tissue mechanisms
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101
Q

what is ischaemic heart diease

A

supply issues - CA atheroma, pulmonary function

demand issues - heart has high intrinsic demands

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102
Q

what type of angina is it with established atheroma in CA

A

stable angina

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103
Q

what type of angina is it with complicated atheroma in CA

A

unstable angina

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104
Q

what can happen if theres an atheroma in aorta

A

aneurysm

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105
Q

what are the consequences of atheroma

A

MI
Cerebral infarction
abdominal aortic aneurysm

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106
Q

what are the effects of ischeamia

A

functional - O2 supply fails to meet demand due to dec supply; inc demand; or both

biochemical - anaerobic metabolism, cell death

cellular - dif tissues have variable susceptibility to ischaemia

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107
Q

whats the outcome of ischeamia

A

No clinical effect

Resolution vs therapeutic intervention

Infarction

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108
Q

what is infarction

A

Ischaemic necrosis within a tissue/organ in living body produced by occlusion of either the arterial supply or venous drainage

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109
Q

what is the aetiolgoy of infarction

A

cessation of blood flow

e.g. thrombosis, embolism

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110
Q

what are the stages of MI

A

Anaerobic metabolism, onset of ATP depletion
Loss of myocardial contractility (->heart failure)
Ultrastructural changes

in 20-30mins irreversible damage

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111
Q

what appearance change would see you due to infarcts in 12 hours

A

see swollen mitochondria on Electron Microscopy

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112
Q

what appearance change would see you due to infarcts in 24-48hrs

A

Pale infarct: e.g. myocardium, spleen, kidney. Solid tissues

Red infarct: e.g. in lung, liver Loose tissues, previously congested tissue

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113
Q

what appearance change would see you due to infarcts 72hrs onwards

A

Pale infarct - yellow/white and red periphery
Red infarct - little change

Microscopically: chronic inflammation; macrophages remove debris; granulation tissue; fibrosis

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114
Q

what will infarcts look like at the end

A

Scar replaces area of tissue damage

Shape depends on territory of occluded vessel

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115
Q

what are transmural MI

A

ischaemic necrosis affects full thickness of the myocardium

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116
Q

what are Subendocardial infarction

A

ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart

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117
Q

what are acute infarcts classified by

A

whether there is elevation of the ST segment on the ECG

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118
Q

whats a non-STEMI

A

no ST segment elevation but a significantly elevated serum troponin level

correlate with a subendocardial infarct

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119
Q

what is angina

A

a discomfort in the chest and/or adjacent areas associated with myocardial ischaemia but without myocardial necrosis”

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120
Q

what causes MI and results in anginal symptoms

A

Mismatch between supply of O2 and metabolites to myocardium and the myocardial demand for them

due to reduction in CA blood flow to mycardium
- coronary atheroma

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121
Q

what is an obstructive plaque

A

obstructs > 70% lumen

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122
Q

what are acute coronary syndromes

A

Spontaneous plaquerupture & localthrombosis, with degrees of occlusion

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123
Q

how do you diagnose angina

A

history:

  • site of pain
  • character of pain (tight band, pressure)
  • radiation sites
  • aggravating (w exertion, stress)
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124
Q

what features in the history make angina less likely

A

Sharp/‘stabbing’ pain; pleuritic or pericardial.
Associated with body movements or respiration.
Very localised; pinpoint site.
lasting for hours

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125
Q

differential diagnosis for chest pain instead of angina?

A 
Aortic dissection 
pericarditis 
pneumonia
pleurisy 
cervical disease
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126
Q

when do you get symptoms of stable angina

A

breathlessness on exertion

excessive fatigue on exertion

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127
Q

what classifies severity of angina

A

Canadian classification of angina severity

1-4

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128
Q

what does class 1 mean for severity of angina

A

physical activity does not cause angina, symptoms only on significant exertion.

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129
Q

what does 2 mean for severity of angina

A

Slight limitation of ordinary activity, symptoms on walking 2 blocks or > 1 flight of stairs.

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130
Q

what does 3 mean for severity of angina

A

Marked limitation, symptoms on walking only 1-2 blocks or 1 flight of stairs.

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131
Q

what does 4 mean for severity of angina

A

Symptoms on any activity, getting washed/dressed causes symptoms.

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132
Q

what are modifiable risk factors for angina

A 
Smoking
Lifestyle- exercise & diet
Diabetes mellitus   
Hypertension 	       
Hyperlipidaemia
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133
Q

on examination for angina what is seen

A

Tar stains on fingers.
Obesity
Xanthalasma and corneal arcus (hypercholesterolaemia).
Hypertension

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134
Q

what investigations would you do for angina

A

Full blood count, lipid profile and fasting glucose; Electrolytes, liver & thyroid tests would be routine.

(CXR

electrocardiogram)

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135
Q

what specialist investigations are there for angina

A

exercise tolerance test
myocardial perfusion imaging
- comparison between stress and rest images
CT coronary angiography

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136
Q

when would you do an invasive angiography

A

Early or strongly positive ETT
Angina refractory to medical therapy.
Diagnosis not clear after non-invasive tests.
Young cardiac patients due to work/life effects.
Occupation or lifestyle with risk

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137
Q

what happens in a coronary angiography

A

under local anaesthetic
arterial cannula inserted into femoral/radial artery
into ostium of CA
radio opaque contrast injected, visualised on X-ray

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138
Q

what treatment strategies are there for angina

A

general - address risk factors, bp, cholesterol, PA
medical - druhs to reduce disease progression & symptoms
revascularisation - Percutaneous coronary intervention (PCI) & coronary artery bypass grafting

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139
Q

what medical treatment is there for angina for progression

A

Statins, if total cholesterol >3.5 mmol/l
ACE inhibitor, if inc CV risk and atheroma
Aspirin, 75mg or Clopidogrel if intolerant of aspirin

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140
Q

what medical treatment is there for angina for relief of symptoms

A 
ß-blockers; achieve resting hr <60 bpm
Ca2+ channel blockers; achieve resting hr <60 bpm, produce vasodilation- amlodipine
Ik channel blockers, ^^
nitrates - vasodilation 
K+ channel blockers - nicorandil
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141
Q

what is Percutaneous coronary intervention

A

coronary angioplasty and stenting
squash atheroma
effective for symotims

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142
Q

what patients get benefit from Coronary artery bypass surgery (CABG)

A

> 70% stenosis of left main stem artery

proximal three-vessel coronary artery disease

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143
Q

what vein is usually used for coronary artery bypass grafting

A

long saphenous vein

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144
Q

what is acute coronary syndrome

A

New onset of a collection of symptoms related to a problem with the coronary arteries
can lead to MI

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145
Q

what is the aetiology for acute coronary syndrome

A

smoking
alcohol
unhealthy food

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146
Q

what is stable angina

A

Caused by “stable” coronary lesion
Predictable symptoms due to narrowing
Symptoms relieved by rest

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147
Q

what is unstable angina

A

Caused by “unstable” coronary lesion
Unpredictable
May occur at rest

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148
Q

how do you diagnose myocardial infarction

A

Detection of cardiac cell death:
+ve cardiac biomarkers - troponin

AND one of
symptoms of ischaemia
new ECG changes
evidence of coronary problem on coronary angiogram or autopsy

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149
Q

what is a cardiac biomarker

A

troponin

myoglobin

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150
Q

what are the types of myocardial ischaemia/infarction you get

A

plaque rupture w thrombus
endotherlial dysfunction
athersclerosis
supply-demand imbalance

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151
Q

what is the history for patients with acute coronary syndrome

A

Ischaemic-sounding chest pain
may radiate to neck/arm
“discomfort” or a “weight” or “tightening”
May be nausea, sweating, breathlessness

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152
Q

what are acute coronary syndrome risk factors

A

male, age, known heart disease, hypertension, diabetes, High cholesterol
Smoker

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153
Q

what would you see on examination for patients with acute coronary syndrome

A

May look very unwell if having a STEMI
May look completely fine

check HR, BP
listen for murmurs, crackles in chest

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154
Q

what investigations would you do for coronary syndrome

A

ECG

blood test - troponin levels

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155
Q

what does ST segment depression mean

A

Partial coronary occlusion

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156
Q

what does ST segment elevation mean

A

Complete coronary occlusion

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157
Q

what is the issue with using ECG for patients with posterior myocardial ischeamia

A

may not see any ST elevation anywhere, even if the LCircumflex is completely blocked

BUT will see opposite changes in the leads opposite those looking at that area (V1-V2)

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158
Q

how can reperfusion therapy be carried out, what does it do

A

opens the blocked artery
mechanical - in cath lab w balloons and stents

pharmacological - strong blood thinner

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159
Q

when would you use thrombolysis for myocardial ischeamia

A

given in ambulance when going to hospitak

v strong blood thinner

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160
Q

what are the risks of thrombolysis

A

Bleeding

Don’t give if recent stroke, or ever had a previous intracranial bleed

Caution if had recent surgery, on warfarin, severe hypertension

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161
Q

how do you manage acute coronar syndroe

A 
Admit to hospital
ECG
Attach to a cardiac monitor
Gain iv access
Give O2 only if levels low
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162
Q

what treatment would you give for acute coronary s

A

Glycerol trinitrate (GTN) - vasodilator

Opiates - for pain

others - B blockers

  • statins, lower cholesterol
  • ACE inhibitor
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163
Q

what are some dual anti-platelet therapies

A

aspirin
clopidogrel
ticagrelor

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164
Q

what are some dual anti-coagulant therapies

A

heparin

fondaparinux

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165
Q

what would you do for ACS in hospital

A

attach to cardiac monitor 24-48hrs
listen for murmurs
organise echocardiogram

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166
Q

whats cardiac tamponade what causes it

A

blood or fluids fill the pericardium - myocardial rupture and bleeds in

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167
Q

what mechanical complications can you get post MI

A

Myocardial rupture
Acute Ventricular Septal Defect
Mitral valve dysfunction due to papillary muscle rupture

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168
Q

what is target BP in over 80 yr olds

A

< 145/85

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169
Q

at what risk of cardiovascular disease should a patient be treated for hypertension

A

if risk exceeds 10% in 10 years

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170
Q

what is colliquitive necrosis

A

breakdown of tissue to liquid

occurs in brain after infarction

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171
Q

what is coagulative necrosis

A

architecture of dead tissue is largely maintained

e.g. heart

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172
Q

what is the definition of stable angina

A

A clinical syndrome of predictable chest pain or pressure precipitated by activities such as exercise or emotional stress, which increase myocardial oxygen demand.

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173
Q

what are the risk factors fir angina

A 
Hypertension
Smoking
Hyperlipidaemia
Hyperglycaemia
male
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174
Q

why does an angina attack begin

A

result of mismatch between myocardial blood/ oxygen supply and demand

anything that increases HR, SV, BP

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175
Q

how can drugs help with angina

A

Decrease myocardial oxygen demand by reducing cardiac workload
Reduce heart rate
Reduce myocardial contractility
Reduce afterload

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176
Q

what drugs are rate limiting for angina

A

Beta-adrenoceptor antagonists
Calcium channel blockers
Ivabradine

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177
Q

what drugs are vasodilators

A

Calcium channel blockers

Nitrates oral, sublingual

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178
Q

what drug is a K channel activator

A

nicorandil

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179
Q

What drug is a Na current inhibitor

A

Ranolazine

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180
Q

what do B blockers do?

A

block the sympathetic system
reversible antagonists of the B1 and B2 receptors
- dec determinant of myocardial O2 demand
- improved perfusion of the subendocardium by increasing diastolic perfusion time

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181
Q

what are adverse drug reaction of B blockers

A

Tiredness /fatigue
Lethargy
Impotence
Bradycardia

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182
Q

examples of beta blocker drugs

A

Bisoprolol, Atenolol

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183
Q

example fo CCB drugs

A

DILTIAZEM, VERAPAMIL - rate limiting, reduce HR and force of contraction
AMLODIPINE - reduce BP and afterload, vasodilator

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184
Q

what do CCBs do

A

Prevent calcium influx into myocytes and smooth muscle lining arteries and atrerioles by blocking the L-Type calcium channel

  • rate limitng
  • vasodilating
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185
Q

NEVER USE NIFEDIPINE IMMEDIATE RELEASE may precipitate acute MI or stroke
with CCB

A

ttg

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186
Q

what are some nitrovasodilators

A

GLYCERYL TRINITRATE (GTN)
ISOSORBIDE MONONITRATE
ISOSORBIDE DINITRATE

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187
Q

what do nitro-vasodilators do

A

relax almost all smooth muscle by releasing NO which then stimulates the production of cGMP which produces smooth muscle relaxation.

Reduce preload (peripheral venodilation) and afterload (arteriolar dilation)

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188
Q

what are some second line therapies for angina after B blockers/CCB

A

Nicorandil-Potassium channel activation

Ivabradine-Sinus node inhibition

Ranolazine-Late Na+ current inhibition

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189
Q

what are some anti-platelet therapies

A

aspirin

P2Y12 inhibitors - clopidogrel, ticagrelor, prasugrel

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190
Q

what adverse effect can low dose aspirin cause

A

GI bleed

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191
Q

what are some cholesterol lowering drugs

A

statins

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192
Q

what is heart failure

A

impairment of the heart as a pump. It is caused by structural or functional abnormalities of the heart.

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193
Q

what are signs of heart failure

A

congestion in the lungs, shortness of breath, oedema in the lower extremities, and enlargement of the liver,
caused by the inability of the heart to pump blood at an adequate rate to the peripheral tissues and the lungs.

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194
Q

what is Left Ventricular Systolic Dysfunction

A

Decreased pumping function of the heart, which results in fluid back up in the lungs and heart failure

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195
Q

what is Left Ventricular Diastolic heart failure

A

Involves a thickened and stiff heart muscle
As a result, the heart does not fill with blood properly
This results in fluid backup in the lungs and heart failure

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196
Q

what are major risk factors for heart failure

A

hypertension

MI

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197
Q

in heart failure

As circulatory volume increases the heart dilates, the force of contraction weakens and cardiac output drops further

leads to vasoconstriction, RAAS

A

hbj

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198
Q

what are loop diuretics

A

furosemide
diuretics induce profound diuresis by inhibiting the NA-K-Cl transporter in the Loop of Henle
prevent reabsorption of filtered Na and water

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199
Q

what drug drug interactions does frusemide have

A

vancomycin, lithium, NSAIDs - renal toxicity

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200
Q

what are Mineralocorticoid receptor antagonists

A

block receptors that bind aldosterone and other steroid hormone

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201
Q

what does ivabradine do

A

slows the heart rate through inhibition of the If channel in the sinus node

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202
Q

what is digoxin

A

Increases availability of calcium in the myocyte

stronger contraction

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203
Q

how can you increase myocardial oxygen supply in. ACS

A

Thrombolysis

Coronary vasodilation.

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204
Q

what are the 2 types of fibrinolytic drugs

A 
Fibrin-specific agents such as 
alteplase, 	
reteplase, 
tenecteplase 
All catalyse conversion of plasminogen to plasmin in the absence of fibrin.

Non–fibrin-specific agents such as streptokinase catalyse systemic fibrinolysis.

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205
Q

ticagrelor is more effective than clopidogrel as anti-platelt therapy

P2Y12 ADP receptor antagonist

use in combination with aspirin

A

gh

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206
Q

what are the main risk factors for CVD

A

diet, obesity, hypertension, diabetes, genetic, alcohol, smoking, PA

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207
Q

what are pro-atherogenics in diet

A 
Cholesterol
Saturated FA
Trans FA
Sodium
Alcohol
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208
Q

what are anti-atherogenics in diet

A 
poly unsaturated fatty acids PUFA
CHO-rich diet, carbohydrates
NSP, non-starch polysacharides 
MUFA
Antioxidant?
Phytochemicals?
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209
Q

how much saturated FA’s can women and men have each day

A

men - 30g

women - 20g

210
Q

what is the recommendation for salt intake

A

6g NaCl/day (2.3g
sodium)
P

211
Q

what is oleic acid

A

Monounsaturated FA
reduces both total
and LDL cholesterol in the plasma

212
Q

what is N-3 PUFA

A

fish oil

reducing sudden death and non-fatal MI

213
Q

what do whole grain foods do

A

oats lower serum cholesterol by 5-
8%
dec CVD risk

214
Q

what is stroke

A

Neurological deficit (‘loss of function’)
of sudden onset,
lasting more than 24 hours,
of vascular origin

blocked or ruptured blood vessel in the brain causing a failure of neuronal function leading to some deficit in brain function

215
Q

what is it called when you have stroke symptoms but lasts for less than 24 hrs

A

Transient Ischaemic Attack

216
Q

what causes stroke

A 
Blockage with thrombus or clot
Disease of vessel wall
Disturbance of normal properties of blood
Rupture of vessel wall
(haemorrhage)
217
Q

what is a large artery disease how does it cause stroke

A

Carotid stenosis

plaque in area of bifurcation, get a clot, can break off and travel to vessel in brain

218
Q

what is Cardioembolic stroke how does it cause stroke

A

Atrial fibrillation commonest cause

clot break off in left atrium and travel to cerebral vessels

219
Q

what is small vessel (lacunar) stroke

A

stroke in small arteries in the brain

220
Q

what are risk factors for stroke

A 
hypertension
smoking
age
fam history 
waist - hip ratio
PA 
diabetes 
cholesterol
221
Q

what is haemorrhage

A

rupture of bv in brain, causes pressure

222
Q

what is the result of ischaemia

A

hypoxia
-> anoxia (no O2)
-> infarction -> necrosis
can also get oedema (swelling)

223
Q

what is the penumbra

A

area around ischeamic core in brain

224
Q

what vessels supply the brain

A

2 common carotid arteries

  • external carotid
  • internal carotid - anterior, middle, posterior

2 vertebral arteries
-> bascillar -> posterior cerebral artery

225
Q

what does temporal lobe do

A

hearing

intellectual and emotional functions

226
Q

what does parietal lobe do

A

comprehend language

227
Q

what does occipital lobe do

A

vision

228
Q

what does frontal lobe do

A

smell
judgement
voluntary movement

229
Q

what are the symptoms of stroke

A 
Motor (clumsy or weak limb)
Sensory (loss of feeling)
Speech: Dysarthria/Dysphasia
Neglect / visuospatial problems
Vision: loss in one eye, or hemianopia
Gaze palsy
230
Q

how do stroke units save more lives than a general ward

A

nursed appropriately
therapists involved early
CT scanning and medication

231
Q

what should acute stroke therapies do

A

Restore blood supply.

Prevent extension of ischaemic damage.

Protect vulnerable brain tissue.
Avoid reperfusion injury
Be non-toxic

232
Q

what drug may be given for stroke

A

thrombolysis
alteplase
restores blood flow
use within 90mins of stroke for best benefit

233
Q

what investigations would you do for stroke

A

CT - first choice in emergency
- causes damage to hair
MRI - takes long
fast field cycling MRI

234
Q

how can the clot be removed in stroke

A

catheter up to brain, pull out clot

- thromboectomies

235
Q

what other treatments can you give for stroke apart from thrombolysis

A

antiplatlets
statins
BP management
anticoagulation

236
Q

what is the histology of the aorta

A

Tunica intima
Layer of endothelial cells
Subendothelial layer – collagen and elastic fibres
Separated from tunica media internal elastic membrane.
Tunica media
smooth muscle cells
secrete elastin in the form of sheets, or lamellae
Tunica adventitia
Thin connective tissue layer
Collagen fibres and elastic fibres

collagen in the adventitia prevents elastic arteries from stretching beyond their physiological limits during systole

237
Q

what is an aneurysm

A

A localised enlargement of an artery caused by a weakening of the vessel wall

238
Q

what are the types of aneurysm

A

true - saccular (one side), fusiform (both sides)

false

dissecting aneurysm

239
Q

what is a false aneurysm

A

Rupture of wall of aorta with the haematoma either contained by the thin adventitial layer or by the surrounding soft tissue

240
Q

what causes false aneurysm

A

Trauma
Iatrogenic
Inflammation ( eg endocarditis with septic emboli)

241
Q

what is a true aneurysm

A

Weakness & dilation of wall

Involves all 3 layers

242
Q

what is presentation of aneurysms

A

Asymptomatic
Based on the location of the aneurysm.
Shortness of breath (associated aortic regurgitation)
Dysphagia and hoarseness
Back pain
Symptoms of dissection - sharp chest pain radiating to back (between shoulder blades), hypotension
Pulsatile mass

243
Q

what investigations are done for thoracic aneurysms

A 
CXR - widened mediastinum 
CXR – widened mediastinum
Echocardiogram – assess aortic root size and aortic valve 
CT angiogram aorta – diagnostic
MRI aorta - diagnostic
244
Q

what is aortic dissection

A

Tear in the inner wall of aorta
Blood forces walls apart
Acute –medical/surgical emergency
Chronic

May occlude branches
Rupture - back into the lumen or externally in to pericardium (tamponade) or mediastinum

245
Q

what are the Aetiological factors of aortic dissection

A 
Hypertension
Atherosclerosis
Marfan's syndrome 
Bicuspid aortic valve
Trauma
246
Q

what symptoms are there for aortic dissection

A

Chest pain – severe, sharp, radiating to back (inter-scapular)
Collapse (tamponade, acute AR, external rupture)
Stroke (involvement of carotid arteries)

247
Q

what is seen in examination for aortic dissection

A 
Reduced or absent peripheral pulses 
Hypertension or hypotension
BP mismatch between sides
Soft early diastolic murmur (aortic regurgitation)
Pulmonary oedema
248
Q

what investigations are done for aortic dissection

A

ECG
CXR - widened mediastinum
Transthoracic echocardiogram (TTE)
CT angiogram aorta - confirms diagnosis

249
Q

what treatment is there for aortic dissection

A

Type A
Blood Pressure control
beta blocker, IVI nitrate, calcium channel blocker, IVI Sodium nitroprusside
Emergency Surgery

Type B
bp control
Percuraneous (endo-vascular) intervention

250
Q

what are infections that affect aortic dissection

A

Takayasu’s Arteritis

Syphilis

251
Q

what are some congenital aortic aneurysm diseases

A

Bicuspid Aortic Valve

Coarctation

Marfan’s Syndrome

252
Q

what is bicuspid aortic valve

A

usually 3 valves in aorta, only 2
reduces tensile strength
prone to aortic valve stenosis/regurg

253
Q

what is aortic coarctation

A

Aortic narrowing close to where

Ductus arteriosus inserts

254
Q

what r the 3 types of aortic coarctation

A

Pre-ductal can be life-threatening if severe narrowing
Ductal
Post-ductal, most common in adults – hypertension in upper extremities, weak pulses in lower limbs

255
Q

what are signs of coarctation

A 
Cold legs
Poor leg pulses
If before left subclavian artery:
Radial – radial and RIGHT radial-femoral delay
If after left subclavian artery:
No radial- radial delay
Right and left radio-femoral delay
256
Q

how does the pulse change if coarctation is before left subclavian artery

A

radial and RIGHT radial-femoral delay

257
Q

how does the pulse change if coarctation is after left subclavian artery

A

No radial- radial delay

Right and left radio-femoral delay

258
Q

what is treatment of coarctation

A

Percutaneous or surgical correction

259
Q

what is Marfan’s Syndrome

A

Fibrillin 1 gene
Connective tissue weakness
Aortic/ Mitral valve prolapse – regurgitation

260
Q

what is an aneurysm

A

abnormal focal dilation of an arterial wall involving all 3 layers

most common type - infra renal aortic abdominal aneurysm

261
Q

how do you screen and diagnose aneurysm

A

ultrasound

262
Q

how do you do endovascular repair for abdominal aortic aneurysm

A

Femoral access

Aortic Neck; fixation and seal with stent

263
Q

what types of stents are there

A 
Bare metal
-self expanding
-balloon expandable
Covered
-Hostile disease
-Aneurysm treatment
Drug eluting
264
Q

what is open AAA repair

A

very invasive
Requires laparotomy
Requires aortic cross clamping and usually ICU care
Blood loss

265
Q

what anatomical vascular imaging is there

A

Plain radiographs
catheter angiography
Ultrasound
Ct/mri

266
Q

what functional vascular imaging is there

A

Radionuclide imaging
Mri functional imaging
ultrasound

267
Q

what is a catheter angiography

A

VESSEL PUNCTURED AND CATHETERISED.
STERILE PROCEDURE
CONTRAST INJECTED USING PUMP INJECTOR
RAPID SERIES OF IMAGE ACQUISITION

268
Q

what do you look for in circualtory imaging

A

Is there a blockage?
Is the occlusion/stenosis clinically significant?
Is there a leak?
aneurysm rupture

269
Q

what are the limitations of CT

A

Leaks
Won’t identify small volume leaks
Snapshot images, cannot exclude intermittent bleeding
Blockages
Can’t always differentiate between acute and chronic thrombosis

270
Q

what are the different phases of a CT scan

A 
non-contrast
arterial phase
venous phase - see liver
nephrogenic phase - see renal system
delayed phase - wash out of contrast in abdominal structures
271
Q

what are the ideal properties of contrast agents

A

HAS AN ATTENUATION COMPARABLE TO SURROUNDING SOFT TISSUES.
INEXPENSIVE
INERT
EQUAL DISTRIBUTION IN AND OUT OF SELECTED BODY COMPARTMENTS
PAINLESS
EASE OF USE

272
Q

what intravenous contrast is used

A

IODINE

high density

273
Q

how does Ultrasound work

A

electricity

  • > Ultrasound waves (via piezoelectric effect)
  • > reflects back, off boundaries in tissues
  • > turned back into electricity
  • > converted into pictorial form
274
Q

what is US B-mode

A

Scans an anatomical plane
Gives anatomical representation of structures
brightness 2D image

275
Q

what is US M-mode

A

Fixed plane over time axis
To assess heart valve movement as well as heart chamber dimension and function
2D image

276
Q

what is US doppler scanning

A

Flow alters frequency of ultrasound waves returning to the probe.
To show direction/velocity of flow.
Common clinical use include the detection of deep vein thrombosis (DVT).

277
Q

what is the US contrast

A

Contrast made from microbubbles

Inert gas, surrounded by a shell

278
Q

what are the indications for US contrast

A

Characterising lesions (dynamic uptake pattern)
Assessment of organ perfusion
Delineating organ edge (eg. For irregularity of heart valves)
Alternative to CT/MRI if unable to tolerate/allergic to other forms of contrast.

279
Q

what is windowing

A

changes shading of pixels to make easier for human eye to appreciate particular structures

280
Q

what are varicose veins

A

A varicose vein is a dilated and tortuous, often superficial vein
n lower limbs
due to valvular failure

281
Q

what veins are there anteriorly in lower limb

A

Dorsal venous arch drains into the LSV, which passes anterior to the medial malleolus - > femoral vein

282
Q

what veins are there posteriorly in lower limb

A

The plantar venous arch drains into the SSV which travels posterior to the lateral malleolus, up the posterior aspect of the leg and drains into the popliteal vein

283
Q

what assists flow against gravity in veins in lower limbs

A

Valves
Calf muscle pump
Perforating veins to drain blood into the deep system

284
Q

what are causes of valvular failure

A

DVT
Hormonal changes
large pelvi tumour
surgery/trauma

285
Q

what occurs if one valve fails

A

venous pressure increases, there is dilatation of the distal vein and further valvular incompetence.

286
Q

what are the risk factors for varicose veins

A 
Age
Females
Pregnancies
DVT
Standing for long periods (occupation)
Family history
287
Q

how do you diagnose varicose veins

A 
Burning
Itching
Heaviness
Tightness
Swelling
Discolouration
288
Q

what are special tests you can do to diagnose varicose veins

A

Tap test
Trendelenburg test
Doppler

289
Q

what investigations do you do for varicose veins

A

US

290
Q

how do you treat varicose veins

A

First line: Endovenous treatment
Second line: Ultrasound guided foam sclerotherapy
Third line: Open surgery

if intervention unsuitable - compression hosiery

291
Q

what is endovenous treatment

A

The LSV or SSV is cannulated under ultrasound guidance
catheter passed up
causes injury to vein, cause fibrosis and occlusion of vessel = disappearance of vein

292
Q

what is chronic venous insufficiency

A

Failure of calf muscle pump
Superficial venous reflux
Deep venous reflux
Venous obstruction

cam lead to impaired tissue perfusion

293
Q

what are signs of chronic venous insufficiency

A 
Oedema
Telangiectasia
Eczema
Haemosiderin pigmentation
Hypopigmentation
ulcers
294
Q

what are venous ulcers

A 
Breach in the skin between the knee and ankle joint, present for >4 weeks
Granulomatous (red) base
Shallow
Exudative, oedematous
Painless, pulses present
295
Q

what investigations do you do for venous ulcers

A

History
Examination
ABPI
ankle brachial pressure index

296
Q

what treatment is there for venous ulcers

A

Exclude arterial disease (ABPI)

Wound care – little role for systemic antibiotics
Elevation
Compression bandaging
Shockwave therapy

297
Q

what is lymphoedema

A

primary - congenital, puberty, or >35

secondary - malignancy, surgery

298
Q

what is the treatment of lymphoedema

A

Elevation

Drainage

299
Q

what is chronic limb ischaemia

A

Atherosclerotic disease of the arteries supplying the lower limb

300
Q

what are the risk factors for limb ischeamia

A 
Male
Age
Smoking
Hypercholesterolemia
Hypertension
Diabetes
301
Q

what is in the history of chronic limb ischaemia

A

Claudication: Exercise tolerance, effect of incline, change over time, relieved by rest? Where in the leg, type of pain.
Rest pain: Type of pain, relieving factors
Tissue loss: Duration, history of trauma, peripheral sensation

302
Q

what would you see/do on examination for chronic limb ischaemia

A

Ulceration
Pallor
Hair loss

feel - temp, capillary refill, sensation, pulse

auscultate - w doppler

303
Q

what are special examination tests for chronic limb ischaemia

A

Ankle Brachial Pressure Index

Buerger’s test

304
Q

what investigations would you do for chronic limb ischaemia

A

Duplex
CT/MRI
Digital subtraction angiography

305
Q

how do you treat chronic limb ischaemia

A 
combo of antiplatelet + statins
control BP
smoking cessation
diabetic control
PA
306
Q

how can you revascularize chronic limb ischaemia

A

Open Surgery

Endovascular intervention

307
Q

what is acute limb ischaemia

A

Arterial embolus: MI, AF, proximal atherosclerosis (NOT DVT/PE)
Thrombosis: Usually thrombosis of a previously diseased artery.
Trauma
Dissection
Acute aneurysm thrombosis

308
Q

what is the presentation of acute limb ischaemia

A 
Pain
Pallor
Pulse Deficit
Paraesthesia
Paresis/Paralysis
Poikilothermia (cold)
309
Q

history of acute limb ischaemia

A 
Cardiac history
Onset/duration of symptoms 
History of chronic limb ischaemia
Risk factors for CLI
Functional status
310
Q

how do you manage acute limb ischaemia if limb is salvageable

A

embolectomy

thrombectomy/thrombolysis

311
Q

how do you manage acute limb ischaemia if limb is not salvageable

A

palliate

amputate

312
Q

what is diabetic foot disease

A

foot ulcer

313
Q

how do you manage diabetic foot disease

A

Prevention
Diligent wound care
Infection – consider systemic antibiotics

revascularization - by angioplasty/stent
amputate

314
Q

what is the interstitium of the lung

A

connective tissue space
around the airways and vessels
and the space between the basement membranes of the alveolar walls

315
Q

what is restrictive lung disease

A

restrict lung expansion on inspiration

Reduced Lung Compliance
low FEV1 & Low FVC but FEV1/FVC normal ratio

Reduced Gas Transfer
- Diffusion abnormality
Ventilation/Perfusion Imbalance

316
Q

how does restrictive lung disease present

A

DYSPNOEA
Shortness of Breath on exertion
Shortness of Breath at rest

Respiratory Failure – Type 1
Heart Failure

317
Q

what is the outcome of interstitial lung injury in chronic response

A

Fibrosis or End-Stage Honeycomb Lung

318
Q

what is diffuse alveolar damage

A 
acute response to interstitial lung disease
Protein rich oedema
Fibrin
Hyaline membranes
Denuded basement membranes
Epithelial proliferation
Fibroblast proliferation
Scarring - interstitium and airspaces
319
Q

what can cause DADs

A

Major trauma
Chemical injury / toxic inhalation
Circulatory shock
Drugs

320
Q

what is sarcoidosis

A 
A multisystem granulomatous disorder 
of unknown aetiology
histological - non-caseating granuloma
F>M
multisystem - lymph nodes, lungs etc involved
upper zone disease
321
Q

how does sarcoidosis present

A 
1      Young adult
joint pain
Erythema nodosum - red spotty painful legs
Bilateral hilar lymphadenopathy
red eyes
2	Incidental abnormal CXR or CT 
3	SOB, cough and abnormal CXR
322
Q

how do you diagnose sarcoidosis

A 
Clinical findings
CXR - spotty lungs, lymph gland swelling at hilum bilaterally
pulomary function tests
bloods, urine, eye exam
(bronchoscopy)
biopsy
323
Q

what is Hypersensitivity Pneumonitis

A

granulomatous response to interstitial lung disease

antigens - Thermophilic actinomycetes, bird proteins, fungi

324
Q

how does Hypersensitivity Pneumonitis present acutely

A

Fever, dry cough, myalgia,
Chills 4-9 hours after Ag exposure
Crackles, tachyopnoea, wheeze
Precipitating antibody

325
Q

how does Hypersensitivity Pneumonitis present chronically

A

Insidious
Malaise, SOB, cough
Low grade illness
Crackles and some wheeze

326
Q

what is usual interstitial pneumonitis

A 
scarring of lung tissue
seen in 
Connective tissue diseases
Drug reaction
Post infection
Industrial exposure
327
Q

what is the histopathology of interstitial pneumonitis

A

Patchy interstitial chronic inflammation
Type II pneumocyte hyperplasia
Smooth muscle and vascular proliferation

328
Q

what is idiopathic pulmonary fibrosis

A

usual interstitial pneumonitis
eldery
m>f
reduces gas transfer

329
Q

how does idiopathic pulmonary fibrosis present

A

Dyspnoea, Cough,
Basal Crackles, Cyanosis, Clubbing
restrictive pulmonary function test

330
Q

how do you treat mild sarcoidosis

A

no treatment

331
Q

how do you treat erythema nodosum (red spots on leg)

A

NSAIDS

332
Q

how do you treat skin lesions from sarocidosis

A

topical steroids

333
Q

what can sarcoidosis result in if there are extra-pulmonary complications

A

progressive resp failure
bronchiectasis
haemoptysis, pneumothorax

334
Q

how do you manage idiopathic pulmonary fibrosis

A

oral anti fibrotic, pirfenidone
palliative care
surgery - transplant

335
Q

what is atrial fibrillation

A

rapid and irregular beating of the atrial chambers
no P wave sometimes, QRS irregular
pulse irregular

do ECG

336
Q

how does atrial fibrillation present

A

Asymptomatic
Palpitations, dyspnoea, chest pain, fatigue
Embolism

337
Q

what investigations would you do for atrial fibrillation

A

Document arrhythmia on ECG – 12 lead, 24 hour recording, event recorder
Blood tests esp thyroid function
Echocardiogram

338
Q

what therapeutic approaches are there for atrial fibrillation

A

Beta blocker/ca-antagonist/digoxin versus class Ic/III drugs
Electrical approaches
Pace & ablation of AV node (ocassionally)
Substrate modification eg Pulmonary vein isolation, surgical procedures

anticoagulation

339
Q

what is supraventricular tachycardia and what are its signs

A

AV-nodal re-entrant tachycardia, very fast HR

palpitations, dyspnoea, dizziness

340
Q

what is ventricular fibrillation

A

rapid and irregular electrical activity renders the ventricles unable to contract in a synchronised manner

341
Q

what is ventricular tachycardia

A

ventricles depolarising irregularly and rapidly
Palpitations, CP, dyspnoea, dizziness, syncope
Usually structural heart disease

342
Q

what is long QT syndrome

A

congenital or acquired

343
Q

what indications are there for implantable cardioverter defibrillator

A

Cardiac arrest due to VF/VT not due to transient or reversible cause eg early phase of acute MI
Sustained VT causing syncope or significant compromise
Sustained VT with poor LV function

344
Q

indication for pacemakers

A

temporary- intermittent or sustained symptomatic bradycardia

permanent - 2nd/3rd degree AV block

345
Q

brain natriuretic peptide levels elevated in heart failure

A

fssf

346
Q

what is sinus arrest

A

sinoatrial node of the heart transiently ceases to generate the electrical impulses
AV node takes over after few seconds

347
Q

what are atrial ectopic beats

A

extra heartbeat caused by a signal to the upper chambers of the heart (the atria) from an abnormal electrical focus
atrial premature beat

348
Q

what are ventricular ectopic beats

A

premature ventricular contractions

349
Q

what is an arrhythmia

A

A deviation from the “normal” rhythm of the heart

350
Q

what us the resting membrane potential of myocardial cells

A

-90mV

351
Q

what antiarrhythmic drug classification

A

The Vaughan Williams classification

352
Q

what are class 1 antiarrhytmic drugs

A

Sodium Channel Blockers
- dec amplitude of AP
- reduce velocity of conduction
quinidine, lidocaine, flecainide

353
Q

what are class 2 antiarrthymic drugs

A

Beta Blockers
block sympathetic innervation
atenolol, bisoprolol

354
Q

what are class 3 antiarrthymic drugs

A

Potassium Channel blockers
inc AP duration
for life threatening V tachycardia
amiodarone

355
Q

what are the side effects of amiodarone

A

Pulmonary fibrosis
Slate – grey pigmentation
Corneal deposits
LFT abnormalities

356
Q

what are class 4 antiarrhythmic drugs

A

Calcium Channel Blockers
slows HR and AV node conduction
verapamil, diltiazem

357
Q

what is digoxin

A 
class 5 antiarrhythmic 
Inhibits the sodium-potassium ATPase pump
long half life
358
Q

what are the results of digoxin toxicity

A

Nausea and vomiting
Xanthopsia - yellow vision
Bradycardia
Tachycardia

359
Q

what can you use to treat digoxin toxicity

A

stop

digibind

360
Q

what is adenosine

A

Slows/ Blocks conduction through the AV node

v short half life

361
Q

what are indications for anti- coag in heart failure

A

Atrial fibrillation

Risk of stroke, peripheral emboli

362
Q

what are some oral anticoagulants

A

Vitamin K antagonist
Warfarin

Direct Thrombin Inhibitor
Dabigatran

Direct Xa inhibitors

363
Q

what are the side effects of warfarin

A

Bleeding
Interaction with multiple other drugs
Pregnancy
Teratogenic

364
Q

what is darcy’s law

A

blood flow = dif in pressure/resistance

365
Q

what is congestion

A

Relative excess of blood in vessels of tissue or organ

  • passive
  • acute or chronic
366
Q

what is congestive cardiac failure

A 
Heart unable to clear blood, right & left ventricles
dec CO
dec filtration rate 
inc Na and H2O retention
inc fluid in body
367
Q

what are the effects of congestive cardiac failure

A

RV and LV cannot clear blood from ventricles
Back pressure, blood dammed back in veins
Lungs - pulmonary oedema
Left heart failure – blood dams back into lungs
Clinically, crepitations in lungs, tachycardia
Liver - central venous congestion
Right heart failure- blood dams back to systemic circulation
inc JVP, hepatomegaly, peripheral oedema

368
Q

what is the effect of right heart failure

A

blood dams back to systemic circulation

inc JVP, hepatomegaly, peripheral oedema

369
Q

what is the effect of left heart failure

A

Back pressure, blood dammed back in veins
Lungs - pulmonary oedema
Left heart failure – blood dams back into lungs
Clinically, crepitations in lungs, tachycardia

370
Q

describe the normal microcirculation

A

Constant movement of fluid through capillary beds
hydrostatic pressure from heart
Balanced by osmotic pressures and endothelial permeability
Filtration from capillary beds to interstitium

371
Q

venous side
capillary oncotic pressure > capillary hydrostatic pressure

reabsorption

A

dda

372
Q

arterial side
capillary hydrostatic pressure> capillary oncotic pressure

filtration

A

ssf

373
Q

what 3 components affect net flux and filtration

A

Hydrostatic Pressure
Oncotic Pressure
Permeability characteristics and area of Endothelium

374
Q

what is oedema

A

Accumulation of abnormal amounts of fluid in the extravascular compartment

  • intercellular tissue compartment (extracellular fluid)
  • body cavities
375
Q

what is peripheral oedema

A

increased interstitial fluid in tissues

376
Q

what are effusions

A

fluid collections in body cavities
Pleural, pericardial, joint effusions
Abdominal cavity - ascites

377
Q

what is oedema transudate

A

Alterations in the haemodynamic forces which act across the capillary wall
Not much protein/albumin (few cells)
Lots of H2O & electrolytes
Low specific gravity

378
Q

what is oedema exudate

A 
Part of inflammatory process due to inc vascular permeability
Tumour, inflammation, allergy
Higher protein/albumin content (cells)
H2O & electrolytes
High specific gravity
379
Q

what is the pathophysiology of pulmonary oedema from left ventricular failure

A

transudate
inc left atrial pressure -> passive retrograde flow to pulmonary veins, capillaries and arteries
inc pulmonary vascular pressure
inc pulmonary blood volume
inc Pc -> inc filtration and pulmonary oedema

380
Q

what is the pathophysiology of pulmonary oedema in the lungs

A

perivascular and interstitial transudate
progressive oedematous widening of alveolar septa
accumulation of oedema fluid in alveolar spaces

381
Q

what are the different pathophysiologies of peripheral oedema

A

Right heart failure – cannot empty RV in systole
Blood retained in systemic veins -> inc P in capillaries -> inc filtration -> peripheral oedema
also portal venous congestion via liver

congestive cardiac failure

382
Q

what is the pathophysiology of lymphatic blockage

A

Lymphatic Obstruction – hydrostatic pressure upset

If lymphatic system blocked -> lymphoedema

383
Q

what is the pathophysiology of oedema in abnormal renal function

A

Salt (NaCl) and H2O retention

dec renal function 
inc salt and H2O 
inc intravascular fluid volume 
secondary inc Pc
= oedema
384
Q

what can cause abnormal renal function

A

Primary: acute tubular damage eg hypotension

Secondary in heart failure - reduced renal blood flow

385
Q

what is the Pathophysiology of low protein oedema

A

capillary oncotic pressure requires normal protein levels

Hypoalbuminaemia -> dec oncoticC -> inc filtration

386
Q

what is the Pathophysiology of permeability oedema

A

Endothelial Permeability - exudate
Damage to endothelial lining
inc “pores” in membrane -> osmotic reflection coefficient of endothelium dec towards zero
Proteins and larger molecules can leak out

387
Q

what is the definition of heart failure

A

clinical syndrome comprising of dyspnoea, fatigue or fluid retention due to cardiac dysfunction, either at rest or on exertion, with accompanying neurohormonal activation

388
Q

what is the mean age for heart failure

A

74 years

389
Q

what are increasing risk factors for chronic heart failure (CHF)

A

obesity
hypertension
diabetes
ageing population

390
Q

what are the symptoms of HF

A

breathlessness
Fatigue
Oedema
Reduced exercise capacity

391
Q

what are the signs of HF

A 
Oedema
Tachycardia
raised JVP
chest crepitations or effusions
3rd heart sound
Displaced or abnormal apex beat
392
Q

how do you diagnose HF

A

1) symptoms/signs of HF (rest/exercise)
2) objective evidence of cardiac dysfunction
3) response to therapy (diuretics)

393
Q

how do you obtain objective evidence of cardiac dysfunction

what investigations do you do

A

Echocardiography, Radionuclide ventriculography,
MRI,
left ventriculography

394
Q

what is the prognosis of heart failure

A

60% one year survival rate

395
Q

how can you screen for heart failure

A

12 lead ecg

BNP brain natriuretic peptide, elevated in HF

396
Q

what can cause heart failure, the underlying abnormality

A

almost any structural cardiac abnormality

LV systolic dysfunction
Valvular heart disease
Pericardial constriction or effusion
Cardiac arrhythmias: tachy or brady
Myocardial ischaemia/infarctio
397
Q

what can cause LV systolic dysfunction

A

Ischaemic heart disease
Dilated cardiomyopathy
Severe aortic valve disease or mitral regurgitation

398
Q

how can you diagnose LVSD

A 
detailed history 
antibodies
ECG
(CXR)
always do echo 
coronary angiography
399
Q

why is an echocardiography an essential investigation for heart dysfunction

A

can identify and quantify

LV systolic dysfunction
Valvular dysfunction
Pericardial effusion / tamponade

may not identify constriction or shunts

400
Q

what is LV ejection fraction

A

a continuous biological variable
assess how impaired LV is
disease can inc or dec it

401
Q

what is the LVEF in severe cases

A

<30%

402
Q

what rule can you use to estimate volume of LV

A

Biplane modified Simpson’s Rule

volume of each slice = area x thickness

403
Q

what is MUGA scan

A

obtain an accurate figure for the LVEF

Ionising radiation

404
Q

what can you use to grade heart failure

A

new york association classification

1 (no limitation) - 4 (severe)

405
Q

how do you grade severity of HF

A

Degree of LV impairment

NYHA class ie severity of symptoms

Degree of elevation of BNP

406
Q

what pharmacological treatment is there for HF

A 
Diuretics
ACE inhibitors
Betablockers
Aldosterone receptor blockers
Now ARNI (Angiotensin receptor and Neprolysin Inhibitor)
407
Q

what drug should not be used in acute HF

A

beta blockers

408
Q

what is mitral stenosis

A

narrowing of mitral valve

409
Q

what can cause mitral stenosis

A

rheumatic heart disease
congenital MS
systemic conditions

410
Q

what is the pathophysiology of mitral stenosis

A

MV orifice <2 cm2

atrium-vent p gradient inc
LA p increase
pulmonary venous and capillary p increase
PVR (pulm vascular resist) inc
pulm arterial p inc and pulom hypertension
right heart dilatation, tricuspid regurg and pulmonary regurg

411
Q

what does m stenosis severity depend on

A

Trans-valvular pressure gradient
Trans-valvular
flow rate

412
Q

what are the signs of m stenosis

A

Dyspnoea
Haemoptisis: rupture of thin-walled veins
Systemic embolisation: LA and LAA enlargement
Infective endocard
Chest pain
Hoarseness (compression of the L recurrent laryngeal nerve)

413
Q

what do you do in clinical examination for m stneosis

A 
Mitral facies - pink cheeck
Pulse – normal
JVP – prominent a wave
Tapping apex beat and diastolic thrill
RV heave
Auscultation
414
Q

what investigations do you do for mitral stenosis

A 
ECG
(cardiac catherisation)
CXR - LA enlargement
echocardiography - thickening and scarring of leaflets 
cardiac magnetic resonance
415
Q

how would you treat m stenosis pharmacologically

A

Diuretics and restriction of Na intake
AtriaiFib: SinusRhythm restoration or ventricular rate control
Anticoagulation: all those with AF, debatable in SR

416
Q

what intervential treatment can you do for m stenosis

A

Valvotomy (balloon vs surgical)

MV replacement

417
Q

what is the aetiology of m regurg

A 
Rheumatic Heart Disease
Mitral valve prolapse (MVP)
IE
Degenerative
Functional MR due to LV and annular dilatation
418
Q

what is the pathophysiology of mitral regurg

A 
orifice not fixed
affected by:
Preload
Afterload
LV contractility
-> annular enlargement 
-> regurg vol increases

LV compenstion
acute - end systolic pressure inc and end systol volume dec, wall tension dec

chronic - EDV inc and ESV returns to normal
eccentric LVHypertrophy develops

419
Q

what can cause acute m regurg

A

valve perforation, chordal/papillary muscle

420
Q

what are the signs of acute m regurg

A

Breathlessness: pulm oedema, cardiogenick shock

421
Q

what are the signs of chronic m regurg

A

Fatigue, exhaustion (low CO), Right heart failure

Dyspnoea or palpitations due to AFib

422
Q

what clinical examinations do u do for m regurg

A 
Pulse – normal or reduced in heart failure
JVP – prominent if RH failure present
Brisk and hyperdynamic apex beat
RV heave
Auscultation
423
Q

what investigations do u do for mitral regurg

A 
ECG - LA enlargement 
CXR
cardiac catheterisation
echocardiography
magnetic resonance
424
Q

what is the medical treatment for acute m regurg

A

preload and afterload reduction may be life-saving (sodium nitroprusside, dobutamine, IABP)

425
Q

what is the aetiology of aortic stenosis

A

Degenerative
Rheumatic
Bicuspid, usually tricuspid

426
Q

what is the patho-physiology of a stenosis due to rheumatic disease

A

fusion of the commissures and retraction and stiffening of the free cusp margins

427
Q

what is the patho-physiology of a stenosis due to degenerative disease

A

slow inflammatory process resulting in thickening and calcification of the cusps from base to free margins

428
Q

what is the patho physiology of a stenosis

A 
inc LV systolic p
Severe concentric hypertrophy and inc LVMass
inc lV end diastolic p 
inc myocardial O2 consumption
MI
LV failure
429
Q

what are the symptoms of a stenosis

A

Long asymptomatic phase

cardinal symptoms
Chest pain (angina)
Syncope/Dizziness (exertional pre-syncope)
Breathlessness on exertion
Heart failure
430
Q

what clinical examinations do you do for a stenosis

A 
Pulse – small volume and slowly rising
JVP – prominent if RH failure present, low BP
Vigurous and sustained apex beat
RV heave
Auscultation
431
Q

what investigations for a stenosis

A 
ECG
CXR
cardiac catheterisation
echocardiography
magnetic resonance
432
Q

what treatment is there for a stenosis

A

limited to those who develop heart failure

aortic valve replacement/repair

433
Q

what causes aortic regurg

A

Dilated aorta
Connective tissue disorders

Bicuspid aortic valve
Rheumatic heart disease
Endocarditis

434
Q

what is pathophysiology of m regurg

A 
inc LV end diastol vol and LV systol pressure 
LV hypertrophy and dilatation
inc myocardial O2 demand
MI 
LV failure
435
Q

symptoms of chronic a regurg

A

Long asymptomatic phase

Exertional breathlesness

436
Q

symptoms of acute a regurg

A

badly tolerated as wall tension cannot acutely adapt

437
Q

what clinical examinations do you do for a regurg

A

Pulse – large volume and collapsing (Corrigan sign)
Wide pulse pressure
Hyperdynamic, displaced apex beat
Auscultation

438
Q

what investigations do you do for a regurg

A 
ECG
CXR
cardiac catherisation
echocardiogtaphy 
magentic resonance
439
Q

treatment for a regurg

A

Vasodilator therapy shown to delay the timing for surgical intervention

440
Q

what surgery can you do for ischeamic heart disease

A 
Coronary Artery Bypass Grafting (Sternotomy)
- reversed saphenous vein
- internal mammary arteries
- radial arteries
cardiopulmonary bypass
441
Q

what are sternotomy related problems

A

Wire infection
Painful wires
Sternal dehiscence
Sternal malunion

442
Q

what are some post-op problems in cardiac surgery

A

Cardiac Tamponade
Death
Stroke

443
Q

what r causes of valvular heart disease

A 
Degenerative
Congenital
Infective
Inflammatory 
LV or RV dilatation
444
Q

what is chronic rheumatic heart disease

A

heart valves damged due to rheumatic fever (inflammation due to infection)

445
Q

what are indications for surgery in endocarditis

A

Severe valvular regurgitation - heart failure
Large vegetations
Persistent pyrexia
Progressive renal failure

446
Q

what types of prosthetic heart valves are there

A

biological - no warfarin required

mechanical - warfarin required for life but lasts >40years

447
Q

what causes endocarditis

A

Strep viridans - subacute

Staph aureus - acute

448
Q

how can you treat endocarditis

A

antibiotics or surgery

449
Q

what is infective endocarditis

A

infection involving the endocardial surface

  • Valvular structures
  • Chordae tendineae
  • Sites of septal defects

M>F

450
Q

what are risk factorsfor endocarditis

A 
Mitral valve disease
Rheumatic heart disease
Congenital heart disease
Degenerative heart disease
Asymmetrical septal hypertrophy
Intravenous Drug abusers
Alcoholic cirrhosis
Diabetic mellitus
451
Q

how does valve become infected

A

Mechanical endothelial disruption exposures extracellular matrix protein _ production of tissue factors.

Deposition of fibrin and platelets_ Non-bacterial thrombotic endocarditis (NBTE).

NBTE facilitates bacterial adherence and infection.

452
Q

how can endothelial valve be damaged

A 
Turbulent blood flow 
electrodes
catheters
inflammation
degenerative valve disease
453
Q

how do you diagnose IE

A

Bacteraemia with audible murmur
Atypical presentation: elderly or immunocompromised patients

Acutely :fever, embolic signs/symptoms or decompensated HF

Subacute: fever, non-specific constitutional symptoms or palpitation and immunologic/vascular phenomena

454
Q

what are common symptoms of IE

A 
fever/chills
night sweats, malaise, fatigue
weakness
headache
SoB
455
Q

clinical signs of IE

A 
Cardiac murmur 
Janeway lesions - haemorgae on palms
Cutaneous infarcts
osler nodes
splinter haemorrhages
456
Q

investigations of IE

A 
Blood culture
FBC.ESR/CRP- elevated acute inflammatory makers
renal failure
Urinalysis- +ve for blood 
ECG: PR interval prolongation >200ms
CXR: Pulmonary congestion or abscess.
echocardiography
457
Q

what IV antibiotics would you give more community acquired IE

A

ampicillin
cloxacillin
getamicin

458
Q

what IV antibiotics would you give more nosocomial IE

A

vancomyicin
getamicin
rifampin

459
Q

what should be done for high risk patients for IE

A

antibiotic prophylaxis

460
Q

how can you prevent IE

A 
Strict dental and cutaneous hygiene
Disinfection of wounds
Eradication or decrease of chronic bacterial carriage :skin, urine 
No self-medication with antibiotics
limit invasive procedures
461
Q

what is a thrombus

A

blood clot in flowing blood
fibrin
platlets
red blood cells

462
Q

what usually causes venous thrombus

A

stasis (immobility)
hypercoagulability (pregnancy, cancer, sepsis)
vessel damage

463
Q

what is a thromboembolisms

A

Movement of blood clot along a vessel

464
Q

what are risk factors for venous thromboembolisms

A 
hypertension
copd
obesity
congenital heart disease
fracture
465
Q

VTembolism
f>m in young
m>f elderly

A

hth

466
Q

how does DVT present

A 
Unilateral limb swelling
Persisting discomfort
Calf tenderness
[Warmth]
[Redness- erythema]
[Prominent collateral veins]
[Unilateral pitting oedema]

may be silent

467
Q

how can you diagnose DVT

A

Clinical assessment and pretest probability score (Wells score)
Blood test: D-dimer if low pre-test probability score

Imaging: Compression ultrasound if positive D-dimer or high pre-test probability score

468
Q

what is a D-dimer

A

Breakdown product of cross-linked fibrin
Produced during fibrinolysis

High sensitivity for VTE
Low specificity for VTE

469
Q

what are Symptoms and signs of PE

A 
Pleuritic chest pain
Breathlessness-  dyspnoea
[Blood in sputum- haemoptysis]
Rapid heart rate- tachycardia
Pleural rub on auscultation
470
Q

what are Symptoms and signs of massive PE

A 
Severe dyspnoea of sudden onset
Collapse
Blue lips and tongue - cyanosis
Tachycardia
Low blood pressure
Raised jugular venous pressure

May cause sudden death

471
Q

what imaging can you do diagnose PE

A

Isotope ventilation/perfusion scan

CT pulmonary angiogram

472
Q

how can you treat PE

A

Anticoagulation is main treatment

473
Q

for PE what treatment can you give IV

A

low molecular weight heparin

474
Q

for PE what treatment can you give through GI tract

A

Direct Oral Anticoagulants
Direct thrombin inhibitors
warfarin

475
Q

what is dilated cardiomyopathy

A

the ventricular function is impaired

heart muscle becomes weakened and enlarged, cant pump blood as well

476
Q

what is the aetiology of dilated cardiomyopathy

A

genetic and familial, SCN5A gene
inflammatory
toxic - drugs
injury

477
Q

what are symptoms of dilated cardiomyopathy

A

Progressive, slow onset, dyspnoea, fatigue, orthopnoea, PND, ankle swelling, weight gain of fluid overload, cough.

478
Q

on examination what would you see for dilated cardiomyopathy

A

Poor superficial perfusion, thready pulse, irreg if in AF, SOB at rest, narrow pulse pressure, JVP elevated+/- TR waves, displaced apex, S3 and S4, MR murmur often, pulmonary oedema, pleural effusions, ankle oedema

479
Q

what investigations for dilated cardiomyopathy

A 
Repeated ECG 
CXR
N termial pro Brain Natriuetic Peptide
 Basic bloods FBC, U+E
 Echo
 CMRI, probably best imaging modality
 Coronary angiogram
480
Q

how would u treat dilated cardiomyopathy

A

general measures

  • correct anaemia
  • remove exacerbating drugs

specific

  • ACEI
  • beta blockers
  • spironolactone
  • anticoag
481
Q

what is restrictive and infiltrative cardiomyopathy

A

physiology of filling and myocyte relaxation capacity, the systolic function may or not be impaired

inability to fill well a ventricle whose wall has reduced compliance

482
Q

what investigations for restrictive cardiomyopathy

A 
Repeated ECG 
 CXR
 N termial pro Brain Natriuetic Peptide
 Basic bloods FBC, U+E
echo
CMRI
483
Q

how would you treat restrictive cardiomyopathy

A

Limited diuretic use as low filling pressures will cause problems
Beta blockers limited ACEI use
Anticoagulants as required

cardiac transplant

484
Q

what is hypertrophic cardiomyopathy

A

impaired relaxation, affect diastole
systolic function with some functional abnormality
thickened myocaridum, less compliant

sarcomere gene defect, autosomal dominant

wall thickness >14mm or >12mm

485
Q

symptoms for hypertrophic cardiomyopathy

A

Breathless, palpitations, syncope, exertional symptoms

486
Q

on examination what can be seen for hypertrophic cardiomyopathy

A

Notched pulse pattern
Irreg pulse if in AF or ectopy
Double impulse over apex, thrills and murmurs,
LVOT murmur will increase with valsalve and decrease with squatting
JVP can be raised in very restrictive filling

487
Q

investigations for hypertrophic cardiomyopathy

A

ECG
Echo
CMRI

488
Q

treatment for hypertrophic cardiomyopathy

A

general -
Avoid heavy exercise
Avoid dehydration

specific
Drugs to try and enhance relaxation
beta blockers, verapamil, disopyrimide
If in AF anticoagulate

Obstructive form; surgical or alcohol septal ablation

489
Q

what is myocarditis

A

Acute or chronic inflammation of the myocardium, viral

Can impair myocardial function, conduction and generate arrhythmia

490
Q

what is the pathology of myocarditis

A

Infiltration of inflammatory cells into the myocardial layers, reduced function and heart failure, heart block as conduction system is involved and arrhythmias

491
Q

what are symptoms of myocarditis

A

Heart failure with fatigue, SOB,
May not have fever
Signs of HF

492
Q

investigations for myocarditis?

A 
ECG
biomarkers 
echo 
CMRI
viral dna PCR
493
Q

treatment for myocarditis

A

Supportive with treatment of heart failure and support for brady and tachy arrhythmias.
Immunotherpay if biopsy or other Ix point to a specific diagnosis
Stop possible drugs or toxic agent exposure

494
Q

what is pericarditis

A

Inflammation of the pericardial layers with or without myocardial involvement

495
Q

causes of pericarditis?

A

bacterial, post MI, perforation, dissection of proximal aorta, neoplasia

496
Q

symptoms and signs of pericarditis

A 
chest pain with pleuritic features and postual features
Fever
pyrexia
pericardial rub
JVP, raised
low BP
497
Q

investigations for pericarditis

A

ECG and echo, troponin might be raised

498
Q

how do you treat pericarditis

A

Viral is conservative
idiopathic gets colchicine and limited use of NSAIDs
Bacterial must be drained even if small effusion and antimicrobials

499
Q

what is pericardial effusion

A

buildup of extra fluid in the pericardium

tamponade or not

500
Q

what are the symptoms of pericardial effusion

A

fatige, SOB, dizzy with low BP, occasionally chest pain.

pulsus paradoxus, JVP raised, low BP, +/- rub, +/- muffled HS

501
Q

tests for pericardial effusion

A

echo, CXR can show large cardiac shadow

502
Q

treatment for pericar effusion?

A

drainage Send for MCS, neoplasic cells, protein and LDH

might need surgery if persistant

503
Q

what is constrictive pericarditis

A

pericardium becomes thickened and scarred

impaired filling although myocardium is normal

504
Q

causes of constrictive pericarditis

A

idopathic, radiation, post surgery, autoimmune, renal failure, sarcoid.

505
Q

signs and symptoms of constrictive pericarditis

A

fatigue, SOB, cough

right heart failure with oedema, ascites, high JVP, jaundice, hepatomegally, AF, TR, pleural effusion, pericardial knock

506
Q

investigations for constrictive pericarditis

A

echo and right heart cath to differentiate from restrictive cardiomyopathy

507
Q

treatment for constrictive pericarditis

A

careful and limited diuretics and pericardectomy

508
Q

what can be the cause of congenital heart disease

A

Copy number variation (CNV)
Single nucleotide variation(SNV)
Multifactorial
teratogens

509
Q

what is downs syndrome

A

trisomy 21
15% atrio ventricular septal defects
duodenal atresia

510
Q

what is turners syndromee

A 
45 chromosomes, X
coarctation of aorta
short stature
gonadal dysgenesis
puffy hands
511
Q

what syndromes can cause neck webbing and what is it

A

Excess nuchal folds

Turner syndrome
l Noonan syndrome
l CFC syndrome
l Leopard syndrome
l Costello syndrome
512
Q

what is noonan syndrome

A 
Pulmonary stenosis
l Short stature
l neck webbing
l cryptorchidism
l characteristic face
l PTPN11 gene (chr 12)
513
Q

what is 22q11 deletion syndrome

A 
C ardiac malformation
A bnormal facies
T hymic hypoplasia
C left palate
H ypoparathyroidism
22 q11 deletion

Speech delay/palatal dysfunction common

514
Q

what is Williams syndrome

A 
Deletion of Elastin on
chromosome 7
Deletion of contiguous
genes
LIM kinase
Aortic stenosis
(supravalvar)
l Hypercalcemia
l 5th finger clinodactyly
l characteristic face
l cocktail party manner
515
Q

what are some teratogens

A 
Fetal alcohol syndrome
Antiepileptic drugs
l Rubella
l Maternal Diabetes
Mellitus
516
Q

what is marfans syndrome

A 
Autosomal dominant
Multisystem
Connective tissue
Fibrillin 1 gene
chromosome 15q21

tall stature

517
Q

what can you use to diagnose marfans

A

Ghent 2010

need 2 positive findings

518
Q

how can you treat marfans syndrome

A 
echocardiogram
l b blockers
l Angiotensin II Receptor
Blockers
l Prophyllactic aortic surgery
519
Q

what is long QT syndrome

A 
Romano-Ward syndrome
Syncope,
“seizure”
sudden death
Emotion, exercise, drugs
ECG shows prolonged QTc
interval
Repolarisation anomalies
520
Q

what is brugada syndrome

A 
SCD or VF/VT and
l Type 1Brugada ECG
l Other features:
l prolonged PR interval
l enlarged LV/poor LV function
l more common in young men
especially of far Eastern origin

Medicine Term 2 (5 decks)

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