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AY Cardiovascular > Disease summary > Flashcards

Disease summary Flashcards

1
Q

What diseases can cause secondary hypertension?

A

Cushing’s syndrome
Conn’s syndrome
Phaeochromocytoma
Renal disease

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2
Q

What investigations are used to diagnose hypertension?

A 
ABPM/HBPM
Urine test (protein, blood)
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3
Q

First line treatment for hypertension in Caucasian under the age of 55?

A

ACE inhibitor (ramipril)

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4
Q

First line hypertension treatment in possibly pregnant women

A

Beta blocker (e.g. propranolol)

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5
Q

First line hypertensive treatment in caucasians over the age of 55 or black people

A

Calcium channel blocker

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6
Q

Second line treatment of hypertension

A

ACE inhibitor + Calcium channel blocker
OR
ACE inhibitor + diuretic

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7
Q

Side effect of calcium channel blockers

A

ankle oedema

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8
Q

Side effect of thiazide diuretics

A

gout

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9
Q

Risk factors for coronary heat disease

A 
Rage
Smoking
Alcohol
Obesity
Hypertension
Diabetes
Hyperlipidaemia
Family History
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10
Q

How to estimate someones risk of a cardiovascular event

A

ASSIGN score

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11
Q

Investigations for angina

A

If > 90% risk of cardio event just treat
If >61% risk of cardio event - catheter angiography
If > 30% risk should have functional testing
If > 10% risk should have CT angiography

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12
Q

First line management of stable angina

A

GTN spray

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13
Q

Second line treatment of angina

A

Beta blocker or Calcium channel blocker (if not adequately controlled both)

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14
Q

Next step angina treament if no adequately controlled on BB and CCB

A 
Long acting nitrate
OR
Ivabradine
OR
Nicorandil 
OR
Rranolazine
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15
Q

3 Types of acute coronary syndrome

A

Unstable angina
NSTEMI
STEMI

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16
Q

First line investigations for acute coronary syndrome

A

ECG

Cardiac Troponins, CK enzyme

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17
Q

Does unstable angina give elevated troponin?

A

not typically

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18
Q

ECG changes in NSTEMI

A

ST depression

T wave inversion

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19
Q

Managment of low risk unstable angina or NSTEMI

A

aspirin
clopidogrel
nitrates

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20
Q

Management of NSTEMI

A

MONA+C

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21
Q

Where is the MI if there is ST elevation in II, III and avF?

A

Inferior MI

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22
Q

What artery is typically involved in inferior MI’s?

A

right coronary artery

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23
Q

Where is the MI if there is ST elevation in V1-V4?

A

Anterior MI

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24
Q

What artery is typically involved in anterior MI’s?

A

LAD

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25
Q

Where is the MI if there is ST elevation in I, aVL and V5-V6?

A

Lateral MI

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26
Q

Where is the MI if there is ST elevation in I, aVL and V1-V6?

A

Anterolateral MI

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27
Q

Where is the MI if there is ST elevation in V1-V4?

A

anteroseptal

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28
Q

What is the immediate treatment of a STEMI?

A

MONA+C

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29
Q

If able to be seen within 90 minutes what is the best choice of treatment for STEMI?

A

PCI (angioplasty)

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30
Q

If not able to be seen within 90 minutes what is the best treatment for STEMI?

A

Thrombolysis

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31
Q

What drugs are used in thrombolysis after an MI?

A

streptokinase + aspirin

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32
Q

When is thrombolysis contraindicated?

A 
trauma
haemorrhage
Stroke
Recent surgery
Severe hypertension
Ulcers
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33
Q

Why does heart failure happen?

A

Heart fails to function as a pump to support the circulation, usually due to low cardiac coutput. Because of low CO the body tinks fluid is low so it retains fluid

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34
Q

Colour of sputum in pulmonary oedema?

A

Pink frothy sputum

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35
Q

Treatment of heart failure

A

Diuertics for fluid
ACE inhibitors
Beta blocker (START LOW GO SLOW)

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36
Q

What drugs are involved in late stage heart failure?

A

Spironolactone

Digoxin

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37
Q

When are ACE inhibitors and ARBs contraindicated in heart failure?

A

renal artery stenosis

pregnancy

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38
Q

What is it important to monitor when prescribing diuretics?

A

K+ concentration (watch for hypokaelemia)

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39
Q

Which diuretic is K+ sparing?

A

spironolactone

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40
Q

Investigation for arrhythmia’s

A

ECG

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41
Q

What is the mechanism of action of class I anti-arrhthmic drugs?

A

Na+ channel blockers (prolong repolarisation) (phase O)

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42
Q

Example of class I anti-arrhythmic drugs?

A

lignocaine
Flecainide
Disopyramide
Propafenone

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43
Q

What is the mechanim of action of class II anti-arrhythmic drugs?

A

Beta adrenoceptor blockers (Phase 4)

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44
Q

Example of class II anti-arrhythmic drug?

A

Atenolol

Propranolol

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45
Q

Mechanism of action fo class III anti-arrhythmic drug?

A

K+ channel blockers (Phase 3) Prolong repolarisation

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46
Q

Example of class III anti-arrhythmic drug

A

Amiodarone

Sotalol

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47
Q

Mechanism of action of class IV anti-arrhythmic drug?

A

Calcium channel blockers (Phase 2)

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48
Q

Example of class IV anti-arrhythmic drug?

A

Verapamil

Diltiazem

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49
Q

Which classes of anti-arrhythmic drugs control rate?

A

II and IV

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50
Q

Whcih classes of anti-arrhythmic drugs control rhythm?

A

I and III

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51
Q

Causes of sinus bradycardia

A 
Ischaemia/infarction of the SA node
Fibrosis of atrium
Hypothermia
Hypothyroidism 
Drug therapy
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52
Q

What drugs can cause sinus bradycardia?

A

Beta blockers and verapamil (VERAPAKILL)

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53
Q

What does Ist degree heart block look like on an ECG?

A

Prolonged PR interval

Husband comes home late but always at same time

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54
Q

What does Mobitz type I look like on an ECG?

A

Progressive PR elongation then dropped QRS

Husband comes home later and later then doesn’t come home at all

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55
Q

What does Mobitz type II look like on an ECG?

A

Dropped QRS but no progressive PR elongation

Husband sometimes comes home but sometimes he doesn’t

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56
Q

What does complete heart block look like on an ECG?

A

Dissociation between P waves and QRS complexes

Husband and wife now on different schedules an need counselling (pacing)

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57
Q

Characteristics of RBBB on ECG

A

Deep S waves - I and V6

Tall R wave - V1

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58
Q

Characteristics of LBBB on ECG

A

Deep S wave - V1
Tall R waves - I and V6
abnormal Q waves

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59
Q

Treatment of heart block

A

IV atropinwe

Temporary or permanent pacing

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60
Q

Appearance of AF on ECG

A

no p waves

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61
Q

Treatment of acute AF

A

cardioversion +/- warfarin

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62
Q

How is rhythm controlled in AF?

A

DC cardioversion

Class I or II anti-arrhythmics

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63
Q

How is rate controlled in AF?

A

Claa II or IV anti-arrhthymics

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64
Q

ECG feature of Atrial Flutter

A

Sawtooth baseline

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65
Q

Treatment of atrial flutter

A

Electrical cardioversion

Radiofrequency ablation

66
Q

Appearance of VT on ECG

A

Broad QRS complexes

67
Q

Treatment for pulseless VT

A

Defibrillation

68
Q

Treatment of VT with well maintained BP and CO

A

Amiodarone + claa I drug (lignocaine)

69
Q

Treatment of VT if haemodynamically compromised

A

DC cardioversion

70
Q

What should be prescribed in VT if the patient is hyperkalemia

A

Calcium chloride

71
Q

Appearance of VF on ECG

A

shapeless, unorganised QRS complexes

72
Q

Treatment of VF

A

BEC + defibrillation

Magnesium Chloride

73
Q

Management for future VF

A

ICD’s

74
Q

Which sided murmurs are louder on inspiration?

A

right sided

75
Q

Cuases of mitral regurgitation

A

Rheumatic disease
Degenerative disease
Endocarditis
Chordae rupture

76
Q

Pansystolic murmur
displaced apex
radiates to the axilla
Ankle swelling

A

Mitral regurgitation

77
Q

Treatment of Mitral regurgitation for those not elligible for surgery

A

Diuretics and ACE inhibitors

78
Q

Causes of aortic stenosis

A

Congenital bicuspid valve
Degeneration/calcification with age
rheumatic disease
Hypertrophic obstructive cardiomyopathy

79
Q

Ejection systolic radites to the carotids
slow rising pulse
heaving apex

A

aortic stenosis

80
Q

treatment of aortic stenosis

A

balloon valvotomy

TAVI (transcatheter valve implantation)

81
Q

Causes of mitral stenosis

A

Rheumatic fever

congenital

82
Q

Mid diastolic rumbling murmur

tapping apex

A

Mitral Stenosis

83
Q

Treatment of Mitral Stenosis

A

Balloon valvotomy

Diuretics, Beta blocker, digoxin

84
Q

Causes of aortic regurgitation

A

Marfan’s syndrome
UC
Connective tissue disorders (SLE)

85
Q

Early diastolic murmur
collapsing pulse
displaced apex

A

Aortic regurgitation

86
Q

Treatment of aortic regurgitation if not elligble for aurgery

A

Diuretics

ACE inhibitors

87
Q

What are the typical causing organisms of infective endocarditis

A

Stph aureua
Staph viridans
Staph epidermidis

88
Q

What are the atypical causing organism of infective endocarditis?

A

Coxiella brunetti
Brucella
Garm negatives
Fungi

89
Q

Symptoms of infective endocarditis

A 
Breathless
fever
new/changing heart murmur
sepsis
clubbing,
splinter haemorrhages
roth spots, janeways lesions, oslers nodes
90
Q

Investigations for infective endocarditis

A

3 sets of blood cultures
CRP
FBC
Echocardiography

91
Q

Main 2 antibiotics in treatment of infective endocarditis

A

vancomycin, gentamicin

92
Q

What stagin sstem is used to asses intermittent claudication?

A

Fonataine staging system

93
Q

Investigations for intermittent claudication

A

ABPI

Duplex ultrasound

94
Q

Treatment of intermittent claudication

A

Antiplatelets (aspirin)

Surgery if high risk

95
Q

The 5 P’s of acute lower limb ischaemia

A 
Pain
Pallor
Paraesthisia (tingling)
Paralysis
Perishing cold
96
Q

Treatment of acute lower limb ischaemia

A

Heparin if improving
Warfarin if severe
Surgery

97
Q

Symptoms of AAA

A 
Severe pain -- back
Pulsatile/expansile abdominal mass
Hypotension
Tachycardia
Anaemia
Discoloured peripheries
98
Q

Treatment of AAA

A

Endovascular stenting

Open surgery

99
Q

Investigations of DVT

A

D-dimers (rule out not rule in)

Doppler ultrasound

100
Q

Treatment of DVT

A

Anticoagulation

Stockings

101
Q

What causes varicose veins?

A

Back pressure due to an incompetent valve causing blood to pool in superficial vein

102
Q

Treatment for varicose veins

A

Compression stockings

Surgery

103
Q

What is thrombophebitis?

A

Local superficial inflammation with secondary thrombosis

104
Q

Treatment of thrombophlebitis

A

Analgesics
Elevation of limb
Fondaparinux

105
Q

Symptoms & signs of congential heart disease

A

Central cyanosis due to right-to-left shunt in the heart
Pulmonary hypertension from large left-to-right shunt in the heart
clubbing

106
Q

What is the mostr common congenital cardiac malformation?

A

Ventricular septal defect

107
Q

Features of VSD

A

Increased pulmonary pressure
Loud pansystolic murmur
Heart failure syptoms

108
Q

Features of atrial septal defect

A

increase pulmonary pressure
exercise intolerance
atrial arrthymias from atrial dilation
RV heave, pulmonary mid-systolic murmur

109
Q

Signs of patent ductus arterosus

A

Machine gun murmur

Bounding pulse

110
Q

Signs of coarctation of the aorta

A

Headaches
nosebleeds
Diminished, absent lower limb pulses
Rib-notching on CXR

111
Q

Features of tetralogy of fallot

A

cyanosis in first month

112
Q

Features of transposition of the reat vessels

A

Cyanosis in the first day

113
Q

How to recognise stroke

A

Face
Arm
Speech
Time

114
Q

Treatment of stroke

A

Thrombolysis

ABCDE

115
Q

What are the 3 types of cardiomyopathy?

A

Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Arrhthymogenic Right Ventricular Cardiomyopathy
Restrictive Cardiomyopathy

116
Q

What is HCM a mutation of?

A

Genes encoding sarcomeric proteins - particular myosin light chains

117
Q

Symptoms of HCM

A

Jerky pulse
4th heart sound
Chest pain
Syncope

118
Q

Investigation for HCM

A

ECG

119
Q

Treatment of HCM

A

Amiodarone in low risk patients

Betablockers or verapamil

120
Q

What is DCM?

A

Mutation in the genes encoding cytoskeletal/mmyocyte proteins - cuase contractile/conduction diseases

121
Q

Investigations for DCM

A

CXR cardiac enlargement
Echocardioraphy
ECG

122
Q

Treatment of DCM

A

Management of heart failure
Cardiac resync therapy
ICD in high risk

123
Q

What is ARVC a mutation of?

A

genes encoding desmosomal proteins (e.g. ryanodine receptor)

124
Q

Treatment of ARVC

A

Beta blockers

Amiodarone, sotalol ( for symptomatic arrhythmias)

125
Q

What change occurs in the size of chambers in restrictive cardiomyopathy?

A

Decreased volume in ventricle

Atrial enlargement

126
Q

What is restrictive cardiomyopathy associated with?

A

Amyloidosis
Sarcoidosis
Endocardial fibrosis

127
Q

What is myocarditis?

A

Acute inflammation of the myocardium. Heart becomes flabby with focal haemorrhages and inflammatory infiltrate

128
Q

Causes of myocarditis

A

Infection
Coxsackie virus
Drugs causing hypersensitivity reactions
Radiation

129
Q

Investigations for myocarditis

A

CK and troponin elevated
ECG
CXR

130
Q

Treatment of myocarditis

A

ACE inhibitors
Beta blockers
Spironolactone
Digoxin

131
Q

What effects does atropine have on the heart?

A

speeds of heart rate

revers bradycardia after an MI

132
Q

Side effects of atropine

A

Arrhthymias
Hallucinations
Confusion

133
Q

Whta is the mechanism of action of digoxin?

A

Blocks Na/K ATPase pump
Increased vaal activity
slows down SA node discharge
increases force contraction and CO

134
Q

What conditions is digoxin used to treat?

A

Heart failure

AF

135
Q

Side effects of digoxin?

A

Heart block
Dysrhthmias
Myocarditis

136
Q

Mechanism of action of nitrates

A

Produce NO
No caused Ca+ efflux producing hyperpolarization and relaxation
Arteriolar dilation
Increased coronary blood flow

137
Q

Side effects of ACE inhibitors

A

Renal dysfunction
Angioneurotic oedema
Fetal abormalities

138
Q

Exampes of calcium channel blockers

A

Amlodipine
Verapamil
Diltiazem

139
Q

How do calcium channel blockers affect HR?

A

Decrease HR

140
Q

Side effects of calcium channel blockers

A

nkle oedema

Bradycardia (VERPAKILL)

141
Q

Side effects of alpha blockers

A

postural hypotension

142
Q

Example of potassium channel openers

A

Minoxidil

Nicorandil

143
Q

Effect of potassium channel openers

A

relaxes vascular smooth muscle

144
Q

Side effects of potassium channel openers

A

Slt and water retention

Tachycardia

145
Q

Side effects of diuretics

A 
Hypokaelmia
Arrhthymias
Fatigue
Hyperglycaemia
Gout (increased uric acid deposits)
146
Q

Mechanism of action of statins

A

Blocks HMG CoA reductase which inhibits cholesterol formation

147
Q

side effects of statins

A

Use in caution with hyperthyroidism and liver failure
Myalgia
Myopathy
Myositis

148
Q

Examples of fibrates

A

Bezafibrate

Gemifibrozil

149
Q

Mechanism of action of fibrates

A

Enhances transcription of LPL whcih hydrolyses triglycerides to fatty acids & glycerol

150
Q

What are fibrates used in>

A

High triglyceride levels

151
Q

Side effects of fibrates

A

myositis

152
Q

What do bile caid binding resins do?

A

cause excretion of bile salts resulting in more cholesterol to be converted to bile salts
Bile resins bind to bile in the intstine s it is not absorbed in the duodenum
Liver metabolises cholesterol to compensate for it lost

153
Q

Example of bile acid binding resin

A

colestryamine
colestipol
aolsevelam

154
Q

What is ezetimibe used in?

A

Decrease in LDL

155
Q

Side effects of ezetimibe

A

Diarrhoea
Abdmoinal pain
Headache
Contraindicated in breasting feeding

156
Q

Whatis the mechanism of action of warfarin?

A

Block clotting factors 2, 7, 8 & 10

Acts as vitamin K antagonists whcih prevents production of mature coagulation factors.

157
Q

Mechanism of action of Heparin?

A

Binds to anti-thrombin II, increasing its affintiy for serine proteases to greatly increase their rate of inactivation

158
Q

Mechanism of action of rivaroxaban?

A

Directly inhibits Factor Xa

Factor Xa - acitvates thrombin IIa
Thrombin IIa - fibrin
Fibrin - blood clot

159
Q

Mechanism of action of anti-platelets?

A

Blocks COX inhibitng formation of TXA2 which causes crosslinking of platelets
Blocks ADP from binding to P2Y12 receptor and formation of fibrin

160
Q

Examples of fibrinolytic drugs

A

Streptokinase

Tissue plasminogen

161
Q

Mechanism of action of fibrinolytic drugs

A

Fibrinolytic cascade opposes coagulation cascad

Activate formation of plasmin from plasminogen whcih lysis fibrin into fibrin fragment causing lysis of theclot

AY Cardiovascular (28 decks)

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