cardiology and haematology Flashcards
1
Q
what are the risk factors of atherosclerosis
A
family history age tobacco smoking high serum cholesterol - oxidised LDL obesity hypertension diabetes - pericardial fat contains lots of GF's and inflammation factors
2
Q
what are the components of a plaque
A
- lipid
- necrotic core
- connective tissue
- fibrous cap
3
Q
what is the pathogenesis of inflammation in a vessel wall
A
- LDL accumulation in wall of artery, undergoes oxidation and glycation
- endothelial dysfunction in response to injury causes leukocyte accumulation in vessel wall - inflammation
- neutrophils produce inflammatory cytokines such as IL1 which causes an inflammation cascade
4
Q
which medical test is used to measure inflammation levels
A
C reactive protein
5
Q
what are the stages of atherosclerosis
A
- fatty streaks
-aggregations of foam cells (lipid laden macrophages) and t lymphocytes within the intimal layer of the vessel wall - intermediate lesions
- foam cells
-VSM cells
-T lymphocytes
-adhesion and aggregation of platelets to vessel wall - fibrous plaques or advanced lesions
-impedes blood flow
-prone to rupture
-covered by dense fibrous cap made from ECM proteins - collagen and elastin
- Laid down by SM cells that overly lipid core and necrotic debris - plaque rupture
-fibrous cap resorbed and redeposited in order to be maintained
- if balance shift in favour of inflammatory conditions (inc enzyme activity) the cap becomes wake and plaque ruptures
4b. or plaque erosion
lesion smaller
-fibrous cap doesn’t disrupt
-sm cell rich luminal surface under clot
- non ST elevation MI
6
Q
what is the treatment of CA disease
A
- PCI - percutaneous coronary intervention
- drug elution - using drugs on stents e.g taxol to stop cell proliferation
- CABG - coronary artery bypass graft - diverts blood around the clot
7
Q
what are the intrinsic rates of the SAN, AVN and ventricular pacemaker cells
A
SAN - 60-100bpm
AVN - 40 -60bpm
ventricular cells - 20-45bpm
8
Q
what does the PR interval show and how long should it be
A
atrial depolarisation + AV node delay (allows time for atria to contract completely)
120-200ms
9
Q
how long should the QRS complex be
A
110ms
10
Q
what does a large and small ECG box depict horizontally
A
0.2s and 0.04s
11
Q
what can hyperkalaemia and hypokalaemia do to an ECG
A
hyperkalaemia - tall T, flat p, broad QRS
Hypokalaemia - flat T, QT prolongation
12
Q
what can hypercalcaemia and hypocalcaemia do to an ECG
A
hyper - short QT
hypo - QT prolongation
13
Q
which leads form einthovens triangle and where are they placed
A
Lead I - RA–LA
Lead II - RA -LL
Lead III - LL - LA
14
Q
Which are the unipolar leads and where do they view from
A
aVR, aVF, aVL - one point on the body and one virtual reference point with zero electrical potential 60% view from each other aVR right shoulder aVL left shoulder aVF symphysis pubic
15
Q
what are the 10 rules of a normal ECG ( don’t cry if u can’t remember them all)
A
- PR 120-200ms
- QRS 110ms or less
- QRS upright in I and II
- QRS + T same general direction in limb leads
- aVR - all waves negative
- R waves grow from V1-V4, S grows from V1-v3 (more muscle mass)
- ST segment should be isoelectric
- p upright in I,II, V2-V6
- Q wave not less than 0.04s in I,II,V2-V6
- T wave upright in I, II, V2-V6
16
Q
what will the appearance be of the p wave in RA and LA enlargement
A
RA - tall pointed p
LA - bifid p
17
Q
what do a long and short p wave show
A
short - WPW wolf parkinson white syndrome - accessory pathway allows early activation of ventricle
long - first degree heart block
18
Q
what is the j point
A
between QRS + ST
19
Q
what would left ventricular hypertrophy show on an ECG
A
taller S than 35mm
20
Q
what is a U wave and what can it show
A
small wave after T - depolarisation after repolarisation
can show bradycardia
21
Q
how do you determine the HR using an ECG
A
count large squares between QRD complexes
divide into 300
22
Q
what is a RBBB and what can it be caused by
A
right bundle branch block
- block in right conduction system
- caused by atrial septal defect, RVH, PE, IHD, hypertension, corpulmonale
23
Q
What can cause a LBBB
A
- IHP
- hypertension
- cardiomyopathy
- idopathic fibrosis
24
Q
what is WPW syndrome and what does it show on an ECG
A
- Congenital accessory conduction pathway between atria and ventricles
- short PR interval
- wide QRS
- type of arrhythmia
- Kent bundle
25
what are LQT's
long QT syndromes
- prolonged repolarisation phases
- patient then predisposed to ventricular arrhythmia
26
what is the pathophysiology of angina pectoris
mismatch between oxygen supply and demand
- impaired blood flow by proximal artery stenosis
- increased distal resistance e.g LVH
- reduced oxygen carrying capacity of blood e.g anaemia
during exercise microvascular resistance decreases to try and increase flow, when resistance can fall no more flow cannot meet metabolic demand - the myocardium becomes ischaemic and pain is typically experienced
27
what is a reperfusion injury
damage to a tissue caused when flow is restored due to reactive oxygen species being released when O2 restored
28
what are the modifiable and non modifiable risk factors for angina
```
non
-gender
-age
-family history
-personal history
modifiable
- smoking
-hypertension
-sedentary lifestyle
-diabetes
-stress
```
29
what are the precipitants for angina (decreased supply/increased demand)
```
dcr supply
-hypoxaemia
-anaemia
-hypothermia
-hypovolaemia
-hypervolaemia
-polycythaemia
inc demand
- hypertension
-tachycardia
-valvular heart disease
-hyperthyroidism
-hypertrophic cardiomyopathy
-cold weather
-heavy meals
-emotional stress
```
30
what is the presentation of angina
chest pain
1. heavy, central, tight, radiation to arms, jaw, neck
2. precipitated by exertion
3. relieved by rest/GTN
31
describe the different investigations for angina
1. treadmill test (NI P)
- look for ST depression
- late stage ischaemia
- many patients unsuitable
2. CT angiogram (NI A)
- high NPV low PPV
- ideal for excusing CAD in younger low risk individuals
3. invasive angiogram (I A)
- inject dye into CA
- X-ray taken
- functional flow reserve - FFR - pressure gradient against stenosis
4. stress echo
- Ultrasound
- regional wall motion abnormalities
5. SPECT myoview
- radio labelled tracer
- taken up by metabolising
- under stress and not under stress
32
what is the primary and secondary management of angina
primary
-risk factor modification
-10 year risk of CV event calculated with SCORE tool
secondary
1. lifestyle changes
2. pharmacological - to reduce events and symptoms
3. interventional - PCI + sometimes surgery
33
what are the pharmacological interventions for angina
1. beta blockers
- B1 specific bisoprolol and atenolol
- reduce HR and contractility by antagonising sympathetic nervous system
- increase time spent in diastole, coronaries have more time to supply heart with blood
- side effects - cold extremities, erectile dysfunction, bradycardia, tiredness
- contraindications - asthma, bronchospasm, sever heart block
2. Nitrates
- 1st line anginal
- venodilators
- reduce preload
- reduce work of heart and O2 demand
3. Calcium channel antagonists
- arterodilators
- dilate systemic arteries, decrease BP
- reduce after loads
- decrease energy for same CO
- Reduce work on heart
4. antiplatelets
- reduce events
- aspirin
- cyclooxygenase inhibitor
- reduce events
- reduce LDL cholesterol
5. statins
- HMG-coA reductase inhibitors
- reduce events
- reduce LDL cholesterol
34
what are the pros and cons of PCI and CABG
```
PCI
pros
-less invasive
-convienient
-repeatable
-acceptable
cons
-risk stent thrombosis
-risk restenosis
-cant deal with complex disease
-dual anti platelet therapy
CABG
pros
-better prognosis
-deals with complex disease
cons
-invasive
-stroke risk
-cant do if frail, comorbid
-one time treatment
- increased length of stay
-increased time of recovery
```
35
what is the definition of unstable angina
- cardiac chest pain at rest
- cardiac chest pain with crescendo pattern
- new onset angina (no ECG changes, no significant troponin rise)
36
what is the presentation of an acute MI
cardiac chest pain
- unremitting
- usually severe but may be mild absent
- occurs at rest
- sweating, breathlessness, nausea or vomiting
- give aspirin 300mg asap
37
what do P2Y12 inhibitors do
used in dual anti platelet therapy with aspirin, stop amplification of platelet activation
38
why are GPIIb/IIIa antagonists used in MI
used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS, cover delayed absorption od oral P2Y12 inhibitors (due to opiates delaying gastric emptying)
39
which pathway does aspirin block
cyclooxygenase 1 pathway
40
what are the signs of a DVT
Calf warmness
tenderness
swelling
discolouration
41
what are the main tests for a DVT
d dimer - sensitive for DVT but not specific for DVT
| Ultrasound compression test proximal veins
42
what is the treatment of a DVT
-LMWheparin
compression stockings
-oral warfarin for 6 months
-treat underlying cause - malignancy, thrombophilia
43
what are the risk factors for a DVT
```
surgery
immobility
leg fracture
HRT
OC pill
pregnancy
long haul flights
inherited thrombophilia
```
44
what is the prevention of a DVT
- hydration
- early mobilisation
- Tinzaparin (LMWH)
- compression TED stockings
- foot pumps
45
give an example of a genetic cause of DVT
-Factor Vleiden
antithrombin -deficiency
-protein c/s defieciency
46
what are the causes of secondary hypertension
- renal disease - 75% of which is intrinsic renal disease, 25% renovascular disease
- endocrine disease e.g cushings syndrome
- pregnancy
- drugs
- OC pill
47
who should be treated for hypertension
1. people aged under 80 with stage 1 hypertension with one or more of the following
- target organ damage
- established CV disease
- renal disease
- diabetes
- a 10 year cardiovascular event risk of 20% or more
2. people of any age with stage 2
48
what is stage 1 and 2 hypertension
1 - 140/90mmhg
| 2 - 160/100mmhg
49
what are the three targets for hypertension
1. CO and PVR
2. RAAS and SNS
3. local vascular vasoconstrictor and dilator mediators
50
how do ACE inhibitors work in management of hypertension
block production of angiotensin II
angiotensin II causes vascular hyperplasia and hypertrophy
and salt retention by aldosterone release and tubular sodium resorption
51
what are the adverse effects of ACE inhibitors
1. related to reduced angiotensin II production
- hypotension
- acute renal failure
- hyperkalaemia
- teratogenic effects in pregnancy
2. related to increased kinin production
- cough
- rash
- anaphylactoid reaction
52
what are the adverse effects of ARB's in hypertension management
- symptomatic hypotension
- hyperkalaemia
- renal dysfunction
- rash
- angiooedema
- contraindicated in pregnancy
53
what can calcium channel blockers be used to manage
- IHD
- arrhythmia
- hypertension
54
what are the three types of CCB's and how do they work
1. dihydropyridines e.g nifedipine
- effect VSM
- peripheral arterial vasodilators
2. phenylalkylamines e.g verapamil
- main effects on the heart
- negatively chronotrophic, negatively inotropic
3. benzothiazepines - diltaiazem
- intermediate heart/ peripheral vascular effects
55
what are the adverse effects of CCB's
1. due to peripheral vasodilation (dyhydropyridines)
- flushing
- headache
- oedema
- palpitations
2. due to negatively chronotrophic effects (verapamil)
- bradycardia
- AV block
3. due to negatively inotropic effects (verapamil)
- worsening of cardiac failure
4. constipation - verapamil
56
give examples of B1 selective, mixed and non selective beta blockers
b1 slsective - bisoprolol
atenolol
propranolol
57
what are the adverse effects of BB's
- fatigue
- headache
- sleep disturbance
- bradycardia
- hypotension
- cold peripheries
- - erectile dysfunction
58
what are the classes of diuretics, where do they act and give an example
1. thiazides - act on the distal tubule e.g bendroflumethiazine
2. loop diuretics - act on loop of henle e.g. furosemide
3. potassium sparing diuretics
- spironolactone is a aldosterone receptor antagonist
- amiloride acts on Enac channels
59
what are the adverse effects of diuretics
- hypovolaemia and hypotension (loop diuretics)
- erectile dysfunction and impaired glucose tolerance (thiazides)
- hypokalaemia/natraemia/magnesaemia/calcaemia
- hyperuricaemia (gout)
60
what are the pharmacological stages of treatment for hypertension
1. under 55 yrs - ACEI or angiotensinII receptor blocker
over 55yrs or afro caribbean CCB's
2. ACE I/ARB + CCB
3. ACEI/ARB +CCB + thiazide
4. addition of spironolactone or BB or AB
61
what are the pharmacological stages for treatment of HF
1. symptomatic - diuretics
2. disease influencing therapy - inhibition of RAAS + SNS
a. ACEI and BB
b. Aldosterone antagonists
3. ACE I intolerant -ARB
4. both intolerant - hydrazine/nitrate combination
5. consider digoxin or ivabiadine
62
How can nitrates be used in HF
- Arterial and venous dilators
- decreased preload and after load
- decreased BP
63
what is the treatment of chronic stable angina
1. anti platelet - aspirin/clopidogrel if intolerant
2. statins
3. short acting nitrate - GTN
4. bb or cbb
5. if intolerant switch
6. if not controlled combine
7. then consider long acting nitrate
64
what is the pharmacological treatment of acute coronary syndromes
1. pain relief - GTN and opiates
2. dual anti platelet therapy - aspirin + ticagrelor
3. antithrombin therapy - fondaparinux
4. consider glycoprotein IIb/IIIa inhibitor
5. background angina therapy: BB, long acting nitrate, CCB
6. statins
7. therapy for LVSD/HF as required - ACEI, BB, aldosterone antagonist
65
what are the classes of antiarrhymatic drugs depicted in vaughan williams classification system
Class I - sodium channel blockers e.g disopyramide
Class II - BB's e.g propanolol (non selective) and bisoprolol (B1 selective)
Class III - prolong the AP - amiodarone
Class IV - CCB's - verapamil
66
how does digoxin act as an anti arrhythmic drug
- inhibits Na/K pump
- bradycardia and slowing of conduction due to increased vagal tone
- increased contractility
67
describe hypertrophic cardiomyopathy
- sarcomeric protein gene mutations
- otherwise unexplained primary cardiac hypertrophy
- causes angina, dyspnoea, palpitations, syncope
- may cause left ventricular outflow tract obstruction
68
which genes are mutated in dilated cardiomyopathy and what does this cause
- cytoskeletal gene mutations
- impaired contractility
- heart failure symptoms
- dilation of chambers
69
which genes are mutated in arrthythmogenic cardiomyopathy and what does this cause
- desmosome gene mutation
| - RV muscle cells die off and are replaced by fat and scar tissue
70
which genes are mutated in inherited arrhythmia/channelopathy
- ion channel protein gene mutation
- structurally normal heart
- recurrent syncope
- long QT, short QT, CPVT or brugada
71
what is tamponade physiology
- small volume of pericardial fluid added or removed from the pericardial sac has drastic effects on filling
( inc fluid, inc pressure, heart can't fill, heart stops)
- however chronic accumulation allows adaptation of the parietal peritoneum
- this compliance reduced the effect on diastolic filling of the chambers
-slowly accumulating effusions rarely cause tamponade
72
what volume of pericardial fluid is usually found in the pericardial sac
50ml
73
what are the diagnostic criteria of acute pericarditis
2 of 4 from
- ECG changes
- chest pain
- friction rub
- pericardial effusion
74
what are the infectious and non infectious causes of acute pericarditis
- viral - enteroviruses, herpes virus, adeno virus, parvovirus
-bacterial - mycobacterium TB
- fungal (rare)
non infectious
-neoplastic - secondary metastatic tumours most common
- autoimmune
-metabolic
- traumatic + iatrogenic
- drug related
- other - amyloidosis, aortic dissection, chronic hf, pulmonary arterial hypertension
75
what is the presentation of acute pericarditis
chest pain
-severe
-pleuritic, sharp (not crushing like ischaemic pain)
-rapid onset
- left anterior chest or epigastrium
- radiates to arm specifically trapezium ridge (phrenic nerve co innervation)
- relieved sitting forward, exacerbated lying down
- dyspnoea, cough, hiccups (phrenic)
-fever, rash, joint pain
- history of cancer, cardiac procedure, MI, pneumonia
-
76
what may be found on a clinical examination for acute pericarditis
- pericardial rub
- sinus tachycardia
- fever
- pulsus paradoxus - abnormally low drop in BP during inspiration
77
what are the differential diagnoses of acute pericarditis
- MI
- GORD
- PE
- AD
- pneumonia
- shingles
78
what are the tests for pericarditis
- ECG - diffuse ST segment elevation, saddle shaped, PR depression
- FBC - small increase in WCC, mild lymphocytosis
- CXR often normal
- troponin - elevations suggest myopericarditis
79
what is the management of pericarditis
- sedentary activity
- NSAID or aspirin
- colchicine
80
what are the factors that indicate a worse prognosis of pericarditis
```
major
-fever
-subacute onset
- tamponade
-large effusion
-lack of response to treatment
minor
-myopericarditis
-immunosuppression
-trauma
-oral anticoagulants
```
81
what is the 5 year mortality rate of heart failure
80%
82
define heart failure
an inability of the heart to deliver blood and o2 at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures
83
what is the difference between HFREF and HFPEF
HFREF - heart failure with reduced ejection fraction ( ejection fraction less than 40%)
HFPEF - heart failure with preserved ejection fraction (ejection fraction more than 50%)
84
what are the causes of heart failure
- myocardial dysfunction
- hypertension
- alcohol excess
- cardiomyopathy
- endocardial
- pericardial
85
what are the symptoms and signs of HF
symptoms
- breathlessness - congested lung due to failure to drain (left)
- tiredness
- cold peripheries
- leg swelling - increased lung pressure (right)
- increased weight
signs
- tachycardia
- displaced apex beat - LV dilation
- added heart sound
- raised JVP(right)
- hepatomegaly
- ascites (right)
- cyanosis
- oedema
- hypotension
- paroxysmal nocturnal episodic dyspnoea only in heart failure (left)
86
describe the new york classification of heart failure
```
class I - no limitation (asymptomatic)
class II - comfortable at rest, dyspnoea during normal activity
class III - limiting less than ordinary activity causes dyspnoea
class IV - dyspnoea present at rest, all activity causes discomfort
```
87
what are the complications of heart failure
- renal dysfunction
- arrhythmia
- DVT, PE
- LBBB
88
what is the treatment of heart failure
1. diuretics
- thiazides or loop diuretics
- relieve symptoms
2. ACE - I
- for LVSD
3. B blockers
- decrease mortality in small doses
4. mineralocorticoid receptor antagonists (aldosterone antagonism)
- spironolactone decrease mortality by 30%
5. digoxin
- symptoms
6. vasodilators
- hydralazine and nitrates
- transplantation
- ECG main test
89
define cor pulmonale
right heart failure caused by chronic pulmonary arterial hypertension
90
what are the causes of cor pulmonale
- chronic lung disease
- PV disorders
- Neuromuscular and skeletal diseases
91
what are the symptoms + signs of cor pulmonale
```
symptoms
- dyspnoea
- fatigue
-syncope
signs
- cyanosis
- tachycardia
- CXR enlarged RA and RV, prominent pulmonary arteries
```
92
what is the treatment of cor pulmonale
- management of respiratory and cardiac failure
| - heart transplant
93
what are the four features of tetralogy of fallot
1. ventricular septal defect
2. pulmonary stenosis
3. right ventricular hypertrophy
4. aorta overrides the VSD, accepting the right heart blood
94
what is the presentation of tetralogy of fallot
- cyanotic
- restless and agitated child
- boot shaped heart
95
what is the management of tetralogy of fallot
- surgery to close VSD and correction of pulmonary stenosis
- without surgery prognosis = mortality in 95% by age 25
- with surgery 85% survive to 35 years
96
what are the symptoms/signs of a ventricular septal defect
- breathlessness
-failure to thrive
- may lead to eisenmengers syndrome - reversal of left to right shunt due to increased pulmonary pressures = cyanosis
signs
- small breathless skinny baby
- inc RR
- tachycardia
- big heart on CXR
97
what % of all congenital heart diseases are VSD's
20%
98
what % of ASD's are defects in the ostium secundum
80%
99
what do ASD's cause
- slightly higher pressure in LA
- shunt left to right
- not cyanosed
- increased flow through right heart and lungs in childhood
- right heart dilation
- SOBOE
- increased chest infections
signs
- big heart and PA on CXR
- split second heart sound
- pulmonary flow murmur
100
what are AVSD's and when are they likely to occur
- atrioventricular septal defects
- one big malformed AV valve
- often in down's syndrome
101
what is a patent ductus arteriosus and what does it cause
the ductus arteriosus fails to close after birth leading to
- continuous murmur
- breathlessness
- eisenmengers syndrome
- more common in prem babies
102
what is coarction of the aorta and what signs does this cause
- narrowing at site of exertion of ductus arteriosus
- obstruction of aortic flow
- collapse with heart failure
signs
-right arm hypertension
- bruits (buzzes) over scapulae and back
-murmur
treat with balloon dilation and stenting or surgery
103
what are the causes of aortic stenosis
- senile calcification
- bicuspid valve
- rheumatic heart disease
104
what happens to the afterload in aortic stenosis
it increases due to the pressure gradient between LV and aorta
105
what is the presentation/signs of aortic stenosis
- syncope on exertion
- angina
- dyspnoea
SAD = stenosis
- sudden death
signs
-slow rising carotid pulse (pulsus tardus) and decreased amplitude (pulsus parvus)
- soft s2
- s4 gallop due to LVH
- ejection systolic murmur
106
what is the prognosis of aortic stenosis
angina + AS 50% survive for 5 years
syncope + AS 50% survive for 3 years
HF + AS < 2yrs
107
what investigations can be carried out for aortic stenosis
- ECG
| - LVH, dilation
108
what is the management of aortic stenosis
- surgical replacement
- tavi - transcatheter aortic valve implantation in patients too sick for surgery
- in asymptomatic - medical management and surveillance
109
what is mitrial regurgitation
back flow of blood from LV to LA during systole
110
what are the causes of mistrial regurgitation
```
- mitrial valve prolapse - marfans, SLE
myxomatous degeneration
ischaemic MR
rheumatic MD
infective endocarditis
```
111
what happens to the size of LV and contractility in MR
left atrial enlargement and hypertrophy, increased contractility
112
what are the signs and symptoms of MR
signs
- soft s1
- pan systolic murmur at the apex radiating to the axilla (s1-s2 murmur)
- S3 present (LA overload)
- intensity of murmur = severity
symptoms
- exertion dyspnoea
- fatigue
- palpitations
113
what are the tests for MR
- ECG - AF, LVH, L atrial enlargement
- CXR - LA enlargement, central PA enlargement
- ECHO - estimation of LA + LV size and function
114
what is the management of MR
a. vasodilator - ACE-I, hydralazine
b. rate control for AF with BB's, CCB, digoxin
c. anticoagulants in AF
d. diuretics for symptoms
e. IE prophylaxis
115
what is aortic regurgitation
leakage of blood into LV during systole due to ineffective coaptation of aortic cusps
116
what are the causes of AR
- bicuspid aortic valve
- rheumatic
- IE
117
What are the signs and symptoms of AR
signs
- wide pulse pressure
- displaced apical pulse and hyperdyamic
- diastolic blowing murmur at left sternal border - cresendo-descendo
- austin flint murmur - fluttering of valve due to regurgitant jet
- systolic ejection murmur
symptoms
- palpitations
- dyspnoea
-angina
118
what are the tests for AR
- CXR enlarged heart and aortic root
| - echo to monitor
119
what is the management of AR
IE prophylaxis
vasodilators (ACEI improve SV + decrease regurgitation in symptomatic pt)
-surgery if symptomatic or EF <50 % or LV dilated
120
what is mitrial stenosis
obstruction of LV inflow stops proper filling during diastole, mainly caused by rheumatic fever
121
what are the symptoms and signs of mitrial stenosis
symptoms
-progressive dyspnoea - LA dilation ---> pulmonary congestion
- increased transmitrial pressure - leads to LA enlargement and AF
- RHF symptoms
- haemoptysis - increased pulmonary pressure ruptures bronchial vessels
signs
- malar flush on cheeks (pink/purple), decreased CO, vasoconstriction
- low volume pulse
- rumbling diastolic murmur
- loud opening s1 snap
122
what are the tests for mitrial stenosis
- ECG - AF and p.mitriale (bifid p)
- CXR - LA enlargement + pulmonary congestion
- echo is diagnostic - mitrial orifice area decrease
123
what is the management of mitrial stenosis
- rate control AF
- diuretics
- surgery
- IE prophylaxis
- anticoagulants
124
what is infective endocarditis
infection of the heart valves or other endocardial lined structures within the heart, most likely to effect regurgitant or prosthetic valves
125
who is IE most common in
1. the elderly
2. i.v. drug abusers
3. congenital heart disease adults
4. prosthetic valves
126
what is the pathogenesis of IE
- microbial adherence - staph aureus most common
- bacterial adherence to platelet fibrin nidus
- vegetation - lumps of infected fibrin hang off heart valves
127
what is the presentation of IE
- signs of systemic infection - fever, rigor, sweats, malaise, weight loss
- embolisation, stroke, PE, MI
- splinter haemorrhages under nails
- oslers nodes (tender pulp on fingers/toes)
- janeways lesions (non tender)
- Roth spots in eye (haemorrhages)
- valve dysfunction, HF, arrhythmia
128
how is IE diagnosed?
```
using modified duke criteria
- 2 major, 1 major 3 minor or all 5 minor needed
major
- positive blood culture
- typical organism in two separate cultures or persistent positive cultures, or single positive for coxiella burnetii
- endocardium involved
- +ve echo
- new valvular regurgitation
minor
- predisposition
-fever >38
- vascular or immunological phenomena
- +ve blood culture doesn't meet major
```
129
what are the typical microorganisms causing IE
- Staph aureus (IVDU or prosthetic valve)
- viridians strep
HACEK - Haemophilus, actinobacillus, cardiobacterium, eikenella kingella
130
what are the two types of ECHO
- transthoracic (TTE)
| - transoesophageal (TOE/TEE) - invasive and good pictures
131
what is the treatment of IE
```
antimicrobials
- strep viridans - 4-6 week IV benpen (benzylpenicillin) +/- 2 weeks gentamicin
- staph aureus - flucloxicillin
surgery
treat complications
```
132
what are the cardiac and non cardiac causes of arrhythmias
```
cardiac
-IHD
-structural changes
-cardiomyopathy
-pericarditis
non cardiac
- caffeine
- smoking
-alcohol
-pneumonia
-drugs
-metabolic imbalance
```
133
what is the presentation of arrhythmias
- chest pain
- palpitations
- syncope
- hypotension
- pulmonary oedema
134
how is arrhythmia managed
- conservative
- pacemakers
- tablets
135
describe the 3 main types of tachycardia
1. sinus tachycardia
- impulses carried at a higher frequency
- caused by infection, pain, exercise, anxiety, dehydration, bleed. drugs, pregnancy, PE, hyperthyroidism
2. ventricular tachycardia
- broad QRS
- from circuits or from focuses of rapidly firing cells
3. supraventricular
- improper electrical activity in upper heart
4 types
- AF
-WPW
- atrial flutter
-paraoxysmal SVT
136
What are ventricular extrasystoles
- palpitations
- thumping
- heart missing a beat
- broad QRS
137
what is atrial fibrillation
- chaotic irregular atrial rhythm at 300-600bpm
- AV node responds intermittently, hence an irregular ventricular rhythm
- decreased cardiac output by 20% as ventricles not primed ready
138
what are the causes of AF
- HF
- PE
- IHD
- hypertension
- mitrial valve disease
- caffeine
- alcohol
- cardiomyopathy
- post op
139
what are the symptoms and signs of AF
- Chest pain
- palpitations
- dyspnoea
- faintness
signs
- irregularly irregular pulse
- apical pulse higher than radial
- 1st heart sound of variable intensity
140
what are the tests for AF
- ECG - absent p waves, irregular QRS complexes
141
what i the management of AF
rate control - BB or rate limiting CCB - digoxin if this fails
anticoagulant - DOAC or warfarin
rhythm control
142
what is atrial flutter
atria beat regularly but faster and more often then ventricles
143
what is an aneurysm
when a portion of an artery swells to more than 50% of its original diameter
144
what is the difference between a pseudo and true aneurysm
pseudo - blood in adventitia only
| true - all layers of vessel wall
145
what are the causes of an aortic aneurysm
- atheroma
- connective tissue disorders e.g marfans
- trauma
- infection
146
what are the complications of an aortic aneurysm
- fistulae
- rupture
- thrombosis
- pressure on other structures
- embolism
147
what is the presentation of a ruptured aortic aneurysm
intermittent or continuous abdo pain - radiates to back, iliac fossa, groin
148
what is an aortic dissection
- blood splits the aortic media with sudden tearing chest pain with or without radiation to the back
- branches of the aorta occlude sequentially leading to hemiplegia (paralysis on one side of the body) if in carotids, unequal arm pulses and BP, acute limb ischaemia, anuria (non passage of urine) in renal arteries and paraplegia (impairment of motor/sensory function)
149
what are the symptoms and signs of peripheral vascular disease
- intermittent claudation
- cramping in calf, thigh or buttock after walking for a given distance, that is relieved by rest
- ulceration, gangrene and foot pain at rest (features of critical limb ischaemia)
signs
--absent femoral, popliteal or foot pulses, cold white legs
-atrophic skin
-punched out ulcers
150
what are the tests for PVD
- ankle brachial pressure index (ABPI)
- ECG
- U+E
- FBC
- MR/CT for extent and location of stenoses
151
what is the management of PVD
1. Risk factor modification
- quit smoking
- treat hypertension
- antiplatelet - clopidogrel
- statin
2. management of claudation
- supervised exercise programmes improve collateral blood flow and reduce symptoms
- vasoactive drugs
- percutaneous transluminal angioplasty - stent
- surgical reconstruction - bypass
- amputation
- gene therapy in future
152
what are the 6P's of acute limb ischaemia
- pale
- pulseless
- painful
- paralysed
- paraesthetic
- perishingly cold
153
what are the causes of acute limb ischaemia
- thrombosis
- emboli
- graft occlusion
- trauma
154
what is meant by shock
circulatory failure resulting in inadequate organ perfusion
155
what are the 5 types of shock
```
anaphylactic
septic
haemorrhagic
neurogenic
cardiogenic
```
156
describe anaphylactic shock and its management
- type IgE mediated hypersensitivity
- release of histamine and other agents causes: capillary leak, wheeze, cyanosis, oedema, urticaria
- secure airway, 100% O2, give adrenaline
157
what is sepsis
life threatening organ dysfunction caused by a dysregulated host response to infection
infection + systemic inflammatory response (SIRS)
158
what is septic shock
sepsis + either: lactate > 2mmol/L or patient requires vasopressors to maintain MAP > 65mmHg
159
what is haemorrhagic shock
- hypovolaemia of more than 20% of bodies blood or fluid supply
- trauma, GI bleed, ruptured aortic aneurysm
160
what is neurogenic shock
- spinal cord injury, epidural or spinal anaesthetic
| - loss of SVR
161
which cell is affected in myeloma
plasma cell - terminally differentiated T lymphocytes
162
what is the pathogenesis of myeloma
cloned malignant plasma cells all produce same immunoglobulin instead of different ones
163
what are the tests for myeloma
- serum electrophoresis - looks for immunoglobulins
- marrow biopsy shows increased umber of plasma cells
- evidence of end organ damage from myeloma - hypercalcemia, renal insufficiency, anaemia (normocytic)
- bone lesions on X-ray
164
what are the four defining features of myeloma
Calcium - increase due to increased osteoclast activation due to signalling from myeloma cells
Renal - light chain deposition (Ig), increased calcium, NSAIDS, deposition
Anaemia - marrow infiltration by plasma cells, symptoms of anaemia
Bone disease
165
what conditions can abnormal plasma cells cause
-MGUS - monoclonal gammopathy of unknown significance
not a disease as no end organ damage
1% a year risk of turning into myeloma
-smoldering myeloma - asymptomatic myeloma
-myeloma - clonal plasma cells and end organ damage
- plasmocytomas - plasma cell tumours (in or out of marrow)
166
what is the prevalence of myeloma in the uk
20000
167
what is the presentation of myeloma
- high ESR
- anaemia
- Rouleux on blood film - stick together due to a high Ig
- poor renal function
- monoclonal protein in urine (Bence Jones protein) or blood
- tiredness/fatigue - secondary to anaemia
- bone pain + pathological fractures
- confused, thirsty, constipated- high calcium
168
what are the complications of myeloma
- spinal cord compression
- hyper viscosity causes decreased cognition, bleeding, disturbed vision - treat with plasmapheresis to remove light chains
- may develop amyloidosis - extracellular deposits of protein in abnormal fibrillar form, resistant to degradation
169
what is the treatment of myeloma
- aim to reach plateau phase, controlling symptoms and supportive measures
supportive
- analgesia for bone pain (avoid NSAIDS due to renal impairment)
- bisphosphonate
-anaemia transfusion
- dialysis?
- broad spectrum antibiotics for viral infections
- chemo and radiotherapy
170
what is the pathogenesis of lymphoma
- malignant proliferations of lymphocytes
- accumulate in lymph nodes causing lymphadenopathy
- caused by primary or secondary immunodeficiency, infection or autoimmune disorders
- impaired immunosurveillance of epsein-Barr virus infected cells (EBV)
- infected B cells proliferate autonomously
- however most cases unknown
171
what are the tests for lymphoma
- blood film
- bone marrow biopsy
- lymph node biopsy
- immunophenotyping
- cytogenetics - karyotyping/FISH
- molecular techniques (PCR)
- PET scans for staging
172
what are the subtypes of lymphoma
- Hodgkins - Reed sternberg cells with mirror image nuclei are found - painless lymphadenopathy and B symptoms - sweats/weight loss
- Non hodgkins:
- -low grade e.g follicular lymphoma - slow growing, incurable, usually advanced at presentation
- - high grade e,g diffuse large B cell lymphoma - usually nodal presentation, short history, short course chemo + monoclonal antibodies
- - very high grade e.g. Burkitt's
173
which age groups are affected most by Hogkins lymphoma
- teenagers and young adults
| - 70+ year olds
174
what are the stages of hogkins lymphoma
Ann Arbor staging
1. 1 lymph area
2. 2 or more - one side of diaphragm
3. both sides of diaphragm
4. widespread extra nodal
175
how do monoclonal antibodies treat lymphoma
- anti CD-20 on surface of B cells
- stops proliferation of B cells
- e.g rituximab
176
how does T engaging therapy treat lymphoma
- targets CD19 on B cells
- and CD3 on T cells
- directs own immune system
177
what are the 4 types of leukaemia and which cells are affected in each
- Acute myeloid leukaemia - myeloblasts (precursor of neutrophil)
- Chronic myeloid leukaemia - neutrophil
- Acute lymphoblastic leukaemia - lymphoblast (precursor of B lymphocyte)
- chronic lymphoblastic leukaemia - B lymphocyte
178
what are the risk factors for leukaemia
- congenital
- environmental
radio, chemotherapy, benzene
179
what is the presentation of leukaemia
- anaemia - SOB, fatigue
- thrombocytopenia - bruising, mucosal bleeding, rash
- infection - fevers/rigor
180
what are the tests for leukaemia
- FBC
- coagulation screen
- CXR + CT to look for mediastinal lymphadenopathy
- U + E
- bone marrow biopsy
- cytogenic analysis - genetic changes in the leukaemia
-bone marrow biopsy
-
181
which leukaemia is commonest in childhood
Acute lymphoblastic
182
what can cause ALL
- ionising radiation during pregnancy
| - downs syndrome
183
what are the symptoms of ALL
marrow failure: anaemia (decreased Hb), infection (decreased WCC) + bleeding (decreased platelets)
organ infiltration - CNS involvement e.g cranial nerve palsy
184
what is the genetic association of CML and ALL
philadelphia chromosome - T9,22
185
what is the treatment of ALL
- induction - remission induction
- consolidation - high-medium dose therapy chemo in blocks
- delayed intensification
- maintenance
- CNS directed therapy - intrathecal
- stem cell transplant
- prognosis 70-90% cure in children
186
describe CLL
- most common leukaemia
- gradual accumulation of b lymphocytes
- often incidental finding on FBC
- generally elderly pts
- progressive lymphadenopathy/hepatosplenomegaly
187
what are the complications of CLL
1. autoimmune haemolysis
2. infection due to hypogammaglobulinaemia (decreased Ig)
3. marrow failure due to replacement
188
what is the Binet staging for CLL
A - lymphocytosis - 10-15yr
B + nodes 5-7yrs
C + anaemia 2-3yrs
189
what is the treatment of CLL
- nothing
- chemo
- monoclonal antibodies
- targeted therapy
- transplant
190
what are the two types of stem cell transplant
```
Autologous
- own
- enables escalation of chemo with stem cell rescue
- straightforward
-mortality 2%
Allogeneic
-other peoples
-more toxic
- mortality 15-30%
- stem cells attack residual tumour and recipient
```
191
what can increase your risk of getting AML
- preceding haematological disorders
- exposure to ionising radiation
- prior chemo
192
what are the symptoms of AML
- marrow failure - anaemia, infection or bleeding
| - infiltration
193
what is the treatment of AML
- blood transfusion
- prompt infection treatment
- chemo - curative vs palliative
- transplant
- prognosis reflects ability to tolerate treatment and leukaemia related factors
194
what gene is associated with acute promyelocytic leukaemia
PML/RARA
| - t15:17
195
what are the symptoms of CML
- splenomegaly
- metabolic fractures
- weight loss
- fatigue
- fever
- sweats
- increased WBC on FBC
196
what is the treatment of CML
targeted molecular therapy
| - tyrosine kinase inhibitors e.g imakinib
197
what is anaemia
- low haemoglobin concentration due to either:
- -low red cell mass - not enough made or too much lost
- -increased plasma volume
198
what are the consequences of anaemia
- decreased o2 transport
- tissue hypoxia
- compensatory changes - increased tissue perfusion, increased O2 transfer to tissues, increased RBC production
- myocardial + liver fatty change
- aggravate angina/claudation
- skin and nail atrophy
- CNS cell death
199
what are the symptoms and signs of anaemia
- fatigue
- dyspnoea
- faintness
- palpitations
- headache
- tinnitus
- anorexia
signs
- pallor of conjunctivae (lacks vasculature)
- tachycardia
- flow murmurs
200
what are the causes of a low RBC count due to less being made
```
hypoplastic
- renal failure
- endocrine
- PRCA
defective Hb synthesis
-iron deficiency (haem group)
- thalassaemia (globin)
- defective DNA synthesis e.g folate
```
201
what are the causes of a low RBC count due to loss of RBC
- post haemorrhage
haemolytic
- intrinsic RBC abnormality - acquired or due to Hb disorders e.g sickle cell
-extrinsic abnormality - infections e.g malaria, antibody mediated, mechanical trauma
202
what are the causes of microcytic anaemia (Low MCV)
1. iron deficiency - blood loss, poor diet, malabsorption e.g coeliac
2. chronic disease
3. Thalassaemia - abnormal haemoglobin
203
what are the causes of normocytic anaemia
1. acute blood loss
2. chronic disease
3. bone marrow failure
204
what are the causes of macrocytic anaemia (high MCV)
1. B12/folate deficiency
2. alcohol excess
3. hypothyroidism
4. haemolysis, chemo, congenital
205
what are the two categories of haemoglobinopathies
- disorders of quality - sickle cell
| - disorders of quantity - e.g alpha or beta thalassaemia
206
what is the pathogenesis of sickle cell disease
- amino acid substitution in the gene coding for the beta chain
- Glu ----> Val which leads to production of HbS
- HbS polymerises when deoxygenated causing RBC's to deform, producing sickle cell which are fragile and haemolyse
- sickle cell diseases arise in the homozygous state (SS)
- heterozygotes are carriers and are protected from falciparum malaria (SC or Sbeta thalassaemia)
207
what are the complications of sickle cell disease
acute
- crisis - microvascular occlusion (10/10 pain)
-sickle chest syndrome - hypoxia --> sickles ---> lung infarction
-aplastic crisis - caused by parvovirus - B12 suddenly reduces marrow production
- stroke
chronic
- renal impairment
- pulmonary hypertension
- joint damage
208
what is the treatment of sickle cell
- transfusion
- hydroxycarbamine
- stem cell transplant
209
what is the pathogenesis of Thalassaemia
- global chain disorders resulting in diminished synthesis of one or more global chains, reducing the Hb
- deletions - mainly alpha and beta thalassaemia
210
what are the main types of thalassaemia
- minor - carriers
- intermedia - moderate anaemia and can survive without regular transfusions
- B major - significant abnormalities - failure to feed, restless, crying, pale, decreased MCV and MCH (mean corpuscular haemoglobin), transfusion dependent, endocrine supplements, psychological support
- Alpha thalassaemia - mainly gene deletions, found in eastern med and far east
211
what are membranopathies and what do they cause
- autosomal dominant
- deficiency of red cell membrane proteins caused by a variety to genetic lesions
- neonatal jaundice
- mild to moderate haemolytic anaemia
- gallstones
- spherocytosis and eliptocytosis most common
212
give an example of an enzymopathy
- glucose 6 phosphate dehydrogenase deficiency
- x linked
- haemolysis
- jaundice
- precipitated by infections, drugs, broad beans
- usually self limiting
- presence of bite and blister cells
213
what is polycythaemia
- increased RBC
214
what are the causes of polycythaemia
```
primary/proliferative
- polycythaemia rubra vera
--- myeloproliferative disorder 'overactive bone marrow'
--- predominantly red cells but also white and platelets
-- JAK2 mutation in 95%
secondary/reactive
- smoking
-lung disease
-cyanotic heart disease
-altitude
-androgen excess
```
215
what is the presentation of polycythaemia rubra vera
- plethoric (redness)
- itching
- thrombosis
- splenomegaly
- abnormal FBC
216
what is the treatment of polycythaemia rubra vera
- aspirin
- venesection
- bone marrow suppressive drugs
217
what is neutrophilia
increase WBC/increased neutrophils
218
what are the causes of neutrophilia
```
proliferative
- CML
reactive
- infection - bacterial
-inflammation
-malignancy
```
219
what is lymphocytosis
increased lymphocytes
220
what are the causes of lymphocytosis
```
proliferative
-CLL
reactive
-infection - viral
- inflammation
- malignancy
```
221
what is thrombocytopenia
low platelets e.g immune thrombocytopenia (anti platelet antibodies)
222
what is thrombocytosis
increased platelets
223
what are the causes of thrombocytosis
```
proliferative
- essential thrombocythaemia (overreactive bone marrow)
reactive
-infection
-inflammation
-malignancy
```
224
what is neutropenia
decreased neutrophils
225
what are the causes of neutropenia
```
underproduction
- marrow failure
- marrow infiltration
- marrow toxicity
increased removal
-autoimmune
-feltys syndrome
-cyclical
```
226
which molecule produced in the liver regulates platelets
thrombopoietin
227
what are the main platelet surface proteins
- ABO
- HPA
- glycoproteins
228
how are platelets activated and what does this lead to
- adhesion to collagen via GPIa
- adhesion to VWF by GPIb+ IIb/IIIa
- release of alpha granules containing PDGF, fibrinogen, VWF, PF4
- dense granules - ADP, calcium, serotonin
- membrane phospholipids activate clotting factors II (prothrombin), V and X
229
what happens to platelets when they encounter exposed collagen in endothelial wall
- adhere to collagen and VWF
- this stimulates cytoskeleton shape change within the platelets and they spread out
- increased surface area and results in activation, granules released that facilitate the clotting cascade ending with production of fibrin
- cross linking by fibrin ---. aggregation
- activated platelets also provide negatively charged phospholipid surface which allows coagulation factors to bind and enhance clotting cascade
230
what tests can be used to see if platelets are working correctly
- FBC
- blood film
- PFA i.e response to aggregating agents e.g ADP, collagen (Platelet Function Assay or Platelet Function Analyser)
- surface proteins flow cytometry
231
what problems cause bleeding
1. low platelets
2. abnormal platelet function
3. vascular disorders
4. defective coagulation
5. injury
232
what are the clinical features of platelet dysfunction
- mucosal bleeding
- - epistaxis, gum bleeding, menorrhagia
- easy bleeding
- traumatic haematomas
233
what are the causes of impaired platelet function
- congenital - platelet disorders, Von willebrand disease
| - acquired - uraemia, drugs
234
what are the causes of thrombocytopenia caused by decreased production
- congenital
absent/reduced/malfunctioing megakaryocytic in BM
- infiltration of BM
leukaemia, metastatic malignancy, lymphoma, myeloma, myelofibrosis
- reduced production by BM
low B12, reduced TPO, medication, toxins, infections, aplastic anaemia
-dysfunction production of platelets
235
what are the causes of thrombocytopenia caused by increased destruction
- autoimmune -ITP, primary or secondary
- hypersplenism - splenomegaly, portal hypertension
- drugs related immune destruction - heparin induced
- consumption of platelets - haemorrhage, haemolysis, TTP, DIC
236
what is the pathogenesis of immune thrombocytopenia (ITP) and how is it caused
- anti platelet antibodies attach to platelet and megakaryocyte surface glycoproteins
- opsonised platelets removed by reticuloendothelial system
primary
-viral infection
secondary
- malignancies e.g CLL
- infections e.g HIV/HepC
237
What is the treatment of ITP
- give platelets if bleeding
- immunosuppression
- treat underlying cause
- Tranexamic acid - decreased fibrin breakdown
238
what is the pathogenesis of disseminated intravascular coagulation (DIC)
- cytokine release in response to systemic inflammatory response syndrome (SIRS)
- causes activation of clotting cascade, microvascular thrombosis and consumption of platelets and clotting factors
- leading to organ failure and bleeding
239
a reduction in which enzyme causes thrombotic thrombocytopenic purpura
- ADAMTS13 - failure to break down VWF
| - causes spontaneous platelet aggregation in microvasculature
240
what is the presentation of neutropenic sepsis
- fever > 38
- rigors
- malaise
- hypotension
- CV collapse and death
- often chemo patients
241
what should you do in neutropenic sepsis
1. see the patient
2. put in a cannula
3. antibiotics
242
what is the presentation of spinal cord compression
- back pain, leg weakness
- loss of urinary retention
- decreased anal tone
- neuropathic pain
- decreased reflexes
- give dexamethasone
- urgent MRI
243
What is tumour lysis syndrome
as cancer cells die - intracellular components released, kidneys are overwhelmed, and crystallisation happens
- prevent with I.V. throughout chemo
244
what are the tests for arrhythmia
- FBC
- U&E
- glucose
- ECG - for signs of IHD, AF, short PR (WPW) long QT (drugs, metallic imbalance, congenital0
- cardiac monitoring
- echo to look for structural heart disease
245
what is the difference between 1st, 2nd and third degree heart block
1st degree - PR interval prolonged and unchanging
2nd Mobitz I - PR interval becomes longer and longer until a QRS is missed, then resets
2nd Mobitz II - QRS regularly missed
3rd - no impulses passed from atria to ventricles so p and QRS appear independently of each other. As tissue distal to the AVM paces very slowly the patient becomes bradycardic
246
what are the causes of total heart block
```
IHD
fibrosis
congenital
trauma
aortic valve calcification
```
247
what would be seen on an examination for haemolytic anaemia
- hepatosplenomegaly
- jaundiced
- dark urine
248
Which scoring system is used for DVT
Wells scoring system
| - 2 or above is likely DVT
249
what are the associations of acute promyeloid leukaemia
- DIC
| - t15:17
250
which stain is used to differentiate between types of leukaemia
- sudan black stain
251
how is AML diagnosed by blood film
Auer rods
252
what are the side effects of chemo
```
immediate
-neutropenia
-nausea and vomiting
-anaemia
-alopecia
- thrombocytopenia
late
- infertility
-psychological
-cardiac toxicity
- increased malignancy
```
253
which type of lymphoma causes pain in lymph nodes with alcohol?
hodgkins
254
what are the criteria for diagnosis of SIRS
- temperature > 38.3 or < 36
- heart rate > 90
- white cell count < 12
- hypoxia
255
what is the sepsis 6
- Shivering, fever or very cold
- Extreme pain or general discomfort
- Pale of discoloured skin
- Sleepy, difficult to wake up, confused
- I feel like i might die
- Short of breath
256
describe BUFALO sepsis intervention tool
```
Blood cultures + septic screen, U+E
Urine output - minitor hourly
- Fluid resuscitation
- Antibiotics IV
- Lactate measurement
- Oxygen to correct hypoxia
```
257
what is the management of MI
Morphine
Oxygen
Nitrates
Aspirin
```
ST elevation
PCI within 2 hours
Beta blocker
ACE inhibitor
Clopidogrel
```
Non ST elevation
BB
antithrombotic - fondaparinux
clopidogrel and aspirin
258
what are the causes of systolic heart failure
- cardiomyopathy
- ischaemia
- hypertension
259
what are the causes of diastolic heart failure
- cardiac tamponade
- pericarditis
- hypertension
260
what is seen on a CXR for heart failure
```
Alveolar oedema
Kerley B-lines - interstitial oedema
Cardiomegaly
Dilated prominent upper lobe vessels
Effusions
```
261
what is BNP and how are its results linked to disease
BNP - brain natruetic peptide
- released from the heart when the ventricles are stretched
- higher levels indicate heart failure
262
what organism is the mean cause of rheumatic fever
- streptococcus pyogenes
263
what is the treatment of an SVT
- vagal maneuveres
- drug - adenosine
- surgery
- carotid massage
264
what can a ventricular tachycardia lead to if not treat
- Ventricular fibrillation
265
what is the treatment of a VT
- Inserted cardioversion
266
what is the bundle affected in WPW
- kent bundle
267
what is the scoring system used to calculate the risk of stroke in AF
CHA2DS2-VASc
268
which system assesses risk of bleed on anticoagulants
HAS-BLED
269
which scoring system is used to assess risk of cardiac event in net 10 years
Qrisk2
- age
- sex
- height
- weight
- cholesterol
- comorbidities
- family history
- DM
270
what troponin level is indicative of acute MI
>14ng/l
271
give one sign of coarction of the aorta that can be found on examination
- radiofemoral delay
272
what is the reversal agent of warfarin
- vitamin K
273
what are the tests for Von willebrand disease
- increased APTT
- increased bleeding time
- vWF Ag decreased
