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3A REVISION > GP > Flashcards

GP Flashcards

1
Q

What is angina pectoris?

A

Central chest tightness or heaviness, brought on by exertion and relieved by rest

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2
Q

Cause of angina? (6)

A

Myocardial ischaemia - mostly atheroma (atherosclerosis)
Anaemia
Aortic stenosis
Tachyarrhythmias
Hypertrophic cardiomyopathy
Small vessel disease - microvascular angina

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3
Q

Symptoms of angina? (7)

A 
Chest pain - tight/heavy
Worse on exertion
Radiation to arms, neck, jaw, teeth
Dyspnoea
Nausea
Sweatiness
Syncope
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4
Q

What can trigger angina?

A

Exercise
Emotion
Cold weather
Heavy meal

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5
Q

Types of angina?

A

Stable angina - relieved by rest
Unstable - increasing frequency/severity, on minimal exertion or at rest, high risk of MI
Decubitus - precipitated by lying flat
Variant (Prinzmetals) angina - caused by coronary artery spasm, no usual CAD RFs

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6
Q

Risk factors for angina? (6)

A 
Smoking
Lack of exercise
Obesity
Hypertension
Diabetes
Hypercholesterolaemia
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7
Q

Tests for angina?

A

ECG - may show signs of past MI, ST depression, flat/inverted T waves
Stratify likelihood of CAD:
If >90% likelihood of CAD treat as known CAD
60-90 angiography
30-60 functional imaging
10-39 artery calcification score with CT

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8
Q

Management of modifiable risk factors of angina?

A

Modify risk factors - stop smoking, exercise, lose weight
Control hypertension, diabetes
Statin!

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9
Q

Secondary prevention of angina?

A

ASPIRIN 75mg or clopidogrel
Statin
ACEi

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10
Q

Medical management of angina?

A 
Sublingual glyceryl trinitrate (GTN) spray
Beta blocker (atenolol) OR calcium channel blocker (amlodipine)
2nd line - long acting nitrate (isosorbide mononitrate), or nicorandil, or ivabradine, or ranolazine
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11
Q

Contraindications to beta blockers?

A

Asthma, COPD
2nd/3rd degree heart block
Worsening unstable heart failure

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12
Q

Mechanism of beta blockers? 3 side effects

A

Reduce heart rate and force of ventricular contraction by blocking beta-adrenoreceptors
Bronchospasm, cold peripheries, sleep disturbance

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13
Q

Mechanism of nitrates? 3 side effects

A

Dilates arteries - relaxes vascular smooth muscle

headache, postural hypotension, tachycardia

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14
Q

Mechanism of calcium channel blockers? 3 side effects

A

Reduce calcium influx to reduce force of contraction of heart
Flushing, ankle oedema, headache

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15
Q

What type of beta adrenergic receptors are in the heart? Where are the other type?

A

Type 1

Type 2 are in the lung bronchioles

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16
Q

When is surgery indicated in angina?

A

Poor response or intolerance to medical therapy

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17
Q

What surgery is indicated in angina?

A

Percutaneous transluminal coronary angioplasty PTCA - balloon dilation of stenotic vessels

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18
Q

What is ACS?

A

Acute coronary syndrome, comprising of unstable angina and MI (STEMI/NSTEMI)

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19
Q

What is the pathology of ACS?

A

Atherosclerotic plaque in coronary artery
Forms a thrombus
Breaks off and occludes artery
Leads to ischaemia of heart, eventual infarction

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20
Q

Types of ACS?

A

ACS with ST elevation

ACS without ST elevation (ST depression, T wave inversion)

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21
Q

Risk factors for ACS?

A

Non-mod: age, male, family history

Mod: smoking, hypertension, diabetes, hyperlipidaemia, obesity, lack of exercise

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22
Q

Diagnosis of ACS?

A 
Increase then decrease in cardiac markers i.e. troponin
Symptoms of ischaemia
ECG changes of ischaemia
Pathological Q waves
Loss of myocardium on imaging
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23
Q

Symptoms of MI?

A 
Central chest pain lasting >20min, radiating to arm
Nausea
Sweatiness
Dyspnoea
Palpitations
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24
Q

When may a silent infarct be more likely and what are the symptoms?

A 
The elderly, diabetics
No pain
Syncope
Pulmonary oedema
Abdo pain, vomiting
Confusion
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25
Q

Signs of MI?

A 
Distress
Anxiety
Pallor
Sweatiness 
Fast/slow pulse
Hyper/hypotension
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26
Q

Heart sounds in MI?

A

3rd/4th heart sounds

Pansystolic murmur

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27
Q

Tests for suspected MI?

A

ECG
Bloods
Cardiac enzymes
CXR

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28
Q

What is seen on ECG in STEMI initially?

A

ST elevation

Tall T waves

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29
Q

What is seen on ECG in STEMI after hours/days?

A

T wave inversion

Pathological Q wave

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30
Q

What is seen on ECG in other ACS?

A

ST depression
T wave inversion
May be non specific/normal

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31
Q

What is seen on CXR in ACS?

A

Cardiomegaly
Pulmonary oedema
Widened mediastinum

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32
Q

What bloods do you do in ACS?

A

FBC
U+E
Glucose
Lipids

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33
Q

What cardiac enzymes would you test for in ACS?

A

Cardiac troponin T and I - increased within 3-12 hours peak at 24-48 then fall
Creatine kinase - increased within 3-12 hour, peak within 24 then fall
Myoglobin - rise within 1-4

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34
Q

Changes in which ECG leads suggest anterior MI?

A

V1-V4

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35
Q

What is an anterior MI?

A

Blockage of left anterior descending LAD artery

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36
Q

Changes in what ECG leads suggest inferior MI?

A

II, III, aVF

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37
Q

What is an inferior MI?

A

Blockage of the right coronary artery

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38
Q

Changes in which ECG leads would suggest a lateral MI?

A

I, V5-V6

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39
Q

What is a lateral MI?

A

Blockage of the left circumflex artery

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40
Q

Initial management of STEMI?

A

Morphine
Oxygen if <95%
Nitrates
Aspirin 300mg

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41
Q

How is reperfusion done in STEMI?

A

Percutaneous coronary intervention if within 2hrs

If not, fibrinolysis

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42
Q

Other medications given in STEMI?

A

Clopidogrel
Beta blockers/CCB
ACEi
LMWH

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43
Q

What is the difference between NSTEMI and unstable angina?

A

NSTEMI has a rise in cardiac enzymes

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44
Q

Initial management for NSTEMI?

A 
Morphine
Oxygen
Nitrates
Aspirin
Clopidogrel
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45
Q

Other medications given in NSTEMI?

A 
Beta blocker/CCB
LMWH
IV nitrate
Glycoprotein IIb/IIIa inhibitors
ACEi
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46
Q

Long term management (secondary prevention) of ACS?

A

Aspirin and clopidogrel
Beta blocker or CCB
ACEi
Statin

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47
Q

What is PCI?

A

Balloon dilatation of stenotic vessels and stent insertion usually

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48
Q

What is CABG?

A

Coronary artery bypass graft

Internal mammary artery or saphenous vein grafted on the bypass stenosed coronary artery

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49
Q

Indications for CABG?

A

Left main stem disease
Triple vessel disease
Unresponsive to PCI or medical management

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50
Q

Complications after MI?

A 
Bradycardias/heart block
Tachyarrhythmias
Right ventricular failure
Pericarditis
VTE
Cardiac tamponade
Mitral regurg
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51
Q

How does a statin work? 3 side effects

A

HMG-CoA reductase inhibitor - stops the enzyme that is needed to produce cholesterol, so reduces cholesterol
Muscle pain, hyperglycaemia/increased diabetes risk, memory loss

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52
Q

Contraindications for statins?

A

Liver disease
High alcohol intake
Previous history of muscle toxicity

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53
Q

Contraindications for beta blockers?

A

Asthma
2nd/3rd degree heart block
Worsening unstable heart failure

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54
Q

Contraindications of nitrates?

A

Aortic stenosis
Cardiac tamponade/constrictive pericarditis
Hypotension

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55
Q

Types of calcium channel blockers? Examples

A

Dihydropyridines (amlodipine, nifedipine)

Non-dihydropyridines (dilitiazem, verapamil)

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56
Q

How do the two classes of calcium channel blockers differ?

A

Both relax/widen arteries

Dilitiazem/verapamil also affect heart conduction i.e. for arrhythmias

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57
Q

Contraindications of calcium channel blockers?

A

Dilitiazem/verapamil avoid in heart failure, avoid concurrent use with beta blockers!

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58
Q

How does clopidogrel work? 3 side effects

A

Irreversibly inhibits platelet aggregation
Haemorrhage, GI upset, dizziness
ANTIPLATELET

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59
Q

Contraindications of clopidogrel?

A

Active bleeding

Caution with increased risk of bleeding i.e. surgery, conditions

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60
Q

Mechanism of ace inhibitors? 3 side effects

A

Inhibit conversion of angiotensin I to angiotensin II by ace to relax blood vessels, lower blood pressure
Cough (accumulation of bradykinin), chest pain, dizziness

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61
Q

Contraindications of ace inhibitors?

A

Use with aliskiren - direct renin inhibitor

Concomitant diuretics

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62
Q

Examples of and mechanism of glycoprotein IIb/IIIa inhibitors?

A

Tirofiban, bivalirudin

Inhibition of GPIIb/IIIa receptor on platelets so prevent platelet formation

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63
Q

Side effects of GPIIb/IIIA inhibitors? Contraindications

A

SE: haemorrhage, headache, nausea
CI: abnormal bleeding in last month, aneurysm history, history of haemorrhagic stroke

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64
Q

Mechanism of aspirin?

A

Irreversibly inhibits cyclooxygenase enzyme, stopping prostaglandin and thromboxane synthesis, reducing platelet aggregation
ANTIPLATELET

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65
Q

Side effects of aspirin? Contraindications

A

SE: dyspepsia, haemorrhage, skin reactions
CI: children under 16 (Reye’s syndrome), active peptic ulcer, bleeding disorders

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66
Q

When are alternative drug treatments used in angina?

A

As monotherapy if BBs or CCBs aren’t used
In combination with 1 1st line agent if symptoms are not controlled and other 1st line agent isn’t used
As a 3rd agent if symptoms aren’t controlled with 2 drugs and unsuitable/awaiting CABG/PCI

Ivabradine - symptomatic relief of angina in patients with a heart rate >70, as an alternative to first line therapies

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67
Q

What is isosorbide mononitrate?

A

Long acting nitrate

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68
Q

What is nicorandil? SE, CI

A

Potassium channel activator
SE: headache
CI: left ventricular failure, hypotension

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69
Q

What is ivabradine? SE, CI

A

Acts on sinoatrial node to lower heart rate
SE: dizzy, vision changes
CI: bradycardia, heart block, heart failure

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70
Q

What is ranolazine? SE, CI

A

Affects sodium dependent calcium channels
SE: dizzy, headache, nausea
CI: renal/liver failure

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71
Q

What is hypertension?

A

Persistently elevated blood pressure in vessels - symptomless until causes organ damage, risk factor for other CV disease/diabetes/stroke/kidney disease/PAD

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72
Q

What are the stages of hypertension?

A

1 - 140/90, ambulatory 135/85
2 - 160/100, ambulatory 150/95
Severe - systolic >180 or diastolic >110

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73
Q

Causes of hypertension?

A

Essential (unknown) - may be alcohol, obesity
Renal disease
Endocrine disease - Cushings, Conns, acromegaly
Coarctation of aorta
Pregnancy

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74
Q

Lifestyle advice for hypertension?

A 
Stop smoking
Lose weight, exercise
Reduce alcohol
Reduce salt intake, healthy diet
Decrease caffeine intake
Encourage relaxation
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75
Q

When are statins given in hypertension?

A

STATIN if CVD or everyone over 40 and 10yr CV risk >20%

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76
Q

When to treat stage 1 hypertension?

A 
<80 yrs and 1 of:
Target organ damage
Renal disease
CVD
Diabetes
10yr CVD risk >20%
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77
Q

When to treat stage 2 hypertension?

A

All patients

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78
Q

What if <40 with stage 1 hypertension and no associated features?

A

Refer for evaluation of secondary causes of hypertension and detailed assessment of CV risk

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79
Q

Step 1 hypertension treatment?

A

If under 55 years - ACEi (ramipril) or ARB if not tolerated

If over 55, or black African/Caribbean any age - CCB (amlodipine) or thiazide like diuretic if not tolerated

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80
Q

Step 2 hypertension treatment?

A

Offer ACE inhibitor (or ARB if not tolerated or of AfroCaribbean origin) PLUS CCB (or thiazide like diuretic if not tolerated)

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81
Q

Step 3 hypertension treatment?

A 
Ensurestep 2 is at optimal doses
Offer ACEi (ARB if not tolerated) PLUS CCB PLUS thiazide like diuretic
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82
Q

Step 4 hypertension treatment? If BP still >140/90

A

4th drug:
Spironolactone
OR higher dose thiazide like diuretic
If diuretic CI, add alpha or beta blocker

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83
Q

When is a beta blocker used as step 1 treatment for hypertension?

A

Younger people if intolerant to ACEi/ARB
Women of childbearing potential
People with increased sympathetic drive
NB: add CCB if second drug required

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84
Q

What are the target BP for non diabetic patients with no CKD?

A

<140/90, ambulatory <135/85

<150/90 if over 80, ambulatory <145/85

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85
Q

What are the target BP for diabetic patients?

A

<140/80 uncomplicated type 2
<135/85 uncomplicated type 1
<130/80 if complications

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86
Q

What is the target BP for paitents with CKD?

A

<130/80

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87
Q

How is hypertension treated in patients with diabetes?

A

1 - ACEi (ARB if not tolerated), if AfroCaribbean ACEi+CCB
2 - add CCB
3 - add diuretic
4 - alpha/beta blocker, spironolactone

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88
Q

What is an ARB? Mechanism, give 2

A

Angiotensin II receptor antagonist
Block angiotensin II by preventing binding, blood vessels dilate reducing BP
Candesartan, irbesartan

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89
Q

ARB SEs, CI?

A

SE: abdo pain, cough, dizzy
CI: Combo with aliskiren, caution with afrocaribbean, people with LV hypertrophy, valve stenosis

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90
Q

How do alpha blockers work? Give 2

A

Alpha adrenergic antagonists - bind to alpha receptors in arteries/smooth muscle, relaxing vessels
Doxazosin, terazosin

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91
Q

Alpha blockers SE, CI?

A

SE: arrhythmias, chest pain, dizzy
CI: postural hypotension, careful in heart failure, pulmonary oedema

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92
Q

What thiazide like diuretics are used in hypertension and how do they work?

A

Chlortalidone, indapamide

Decrease cardiac output, reduce extracellular fluid volume, reduce peripheral vascular resistance - vasodilate

93
Q

Thiazide like diuretics CI, SEs?

A

CI: addisons, hypercalcaemia, hyponatraemia, hypokalaemia, hyperuricaemia
SE: constipation, electrolyte imbalance, headache, hypotension

94
Q

What is AF?

A

Atrial fibrillation, common disturbance of cardiac rhythm that may be episodic, associated with risk of stroke

95
Q

What is seen on ECG in AF?

A

Rapid irregularly irregular narrow QRS complex tachycardia with the absence of P waves

96
Q

Causes of AF?

A 
No cause
Coronary heart disease
Hypertension
Cardiomyopathy
Valvular heart disease - esp. mitral
97
Q

Causes of acute AF?

A

Infection
High alcohol
Surgery
MI, PE

98
Q

Symptoms of AF?

A 
Often asymptomatic
Palpitations
Chest pain
Stroke/TIA
Dyspnoea
Light headedness/syncope
Fatigue
99
Q

Investigations of AF?

A 
ECG
CXR
Bloods - TFTs, FBC, U+E
Ambulatory ECG
echo if <50
100
Q

Management of recent onset AF?

A

Treat precipitating cause - infection
Direct current cardioversion or chemical cardioversion
Admit if fast rate/patient compromise

101
Q

Management of not recent onset AF?

A

Address RFs i.e. alcohol, caffeine, hypertension, thyroid disease
Refer for echo and cardio assessment

102
Q

Treatment of paroxysmal not recent onset AF?

A

No drugs if can avoid triggers
Pill in pocket - beta blocker as needed
Anticoagulate - low risk give aspirin, high risk give warfarin or NOAC

103
Q

Treatment of chronic not recent onset AF?

A

Rhythm control - DC/chemical cardioversion
Beta blocker to maintain rhythm or rate limiting CCB i.e. verapamil
If ineffective, beta blocker + digoxin
If ineffective, verapamil + digoxin
If ineffective, refer
Anticoagulate - low risk give aspirin, high risk give warfarin or NOAC

104
Q

Mechanism of atrial fibrillation?

A

Irregular atrial rhythm 300-600bpm which leads to an irregular ventricular rate due to AV node only sometimes responding

105
Q

What system is used to measure stroke risk in AF?

A

CHA2D2-VASc

106
Q

Risk assessment tool for someone starting anticoagulation?

A

HASBLED

107
Q

What is atrial flutter?

A

ECG shows regular sawtooth baseline at 300bpm, with narrow complex QRS tachycardia superimposed at 150bpm

108
Q

What is used for rate control in AF?

A

Beta blocker or rate limiting CCB

Can add digoxin

109
Q

What is used for rhythm control in AF?

A

Electrical cardioversion
Dronedarone (with beta blocker)
Amiodarone if LV impairment/heart failure

110
Q

How is acute medical cardioversion done in AF?

A

Fleicainide

Amiodarone if structural heart disease

111
Q

How does digoxin work?

A

Increases the force of contraction of the heart muscle but reduces heart rate - inhibits Na/K ATPase

112
Q

Side effects of digoxin? CIs?

A

SE: arrhythmias, dizzy, vision disorders
CI: intermittent complete heart block, myocarditis, 2nd degree AV block, V fib

113
Q

How does amiodarone work?

A

Class III antiarrhythmic - prolongs the refractory period of SA and AV nodes, slowing conduction rate

114
Q

Side effects of amiodarone? CIs?

A

SE: arrhythmias, liver damage, hyperthyroid
CI: severe conduction disturbances, sinus node disease, thyroid dysfunction

115
Q

What are guidelines on returning to normal life after MI?

A

Sedentary work 4-6 weeks, light 6-8, heavy 12
Sex after 6 weeks
Fly - after 2 weeks if can climb stairs
Driving - car angioplasty 1 week, other 1 month, lorry licence revoked assess at 6 weeks

116
Q

What is heart failure?

A

Output of the heart is inadequate to meet the needs of the body, end stage of all diseases of the heart

117
Q

Causes of chronic heart failure?

A

High output - needs of the body are more than what heart can give
Low output - increased preload, pump failure, chronic excessive afterload

118
Q

Causes of high output heart failure?

A

Hyperthyroidism
Anaemia
Paget’s disease

119
Q

Causes of increased preload?

A

Mitral regurgitation

Fluid overload

120
Q

Causes of pump failure?

A

IHD
Cardiomyopathy
Restrictive cardiomyopathy, constrictive pericarditis
Inadequate rate - beta blockers, heart block
Arrhythmia - AF
Negatively inotropic drugs - verapamil

121
Q

Causes of chronic excessive afterload?

A

Hypertension

Aortic stenosis

122
Q

Classification of heart failure?

A

Left ventricular systolic dysfunction - decreased left ventricular ejection fraction (LVEF) on echo
Heart failure with preserved ejection fracture - normal LVEF but signs/symptoms of heart failure

123
Q

Tests for heart failure?

A 
Echo
Blood - FBC, U+E, TFT, eGFR, creatinine, HbA1C, glucose
ECG
CXR
PEFR/spirometry
Serum natriuretic peptides
124
Q

What is the NY heart association grading of heart failure severity?

A

I - no limitation
II - slight limitation, ordinary activity causes fatigue/palpitations/dyspnoea
III - marked limitation, less than ordinary activities causes symptoms
IV - unable to carry out any physical activity without discomfort, symptoms present at rest

125
Q

Symptoms of heart failure? (8)

A 
SoB - on exertion, orthopnoea, paroxysmal nocturnal dyspnoea
Decreased exercise tolerance
Nocturnal cough
Ankle oedema
Abdo discomfort - liver distension
Confusion, dizziness
Gain or lose weight
Wheeze
126
Q

Signs of heart failure? (11)

A 
Increased RR
Cyanosis
Increased pulse
Increased JVP
Displaced apex beat - cardiomegaly
3rd heart sound
Hepatomegaly
Right ventricular heave
Crepitations, pleural effusions
Pitting oedema ankles
Ascites
Cachexia, wasting
127
Q

Features of PMH that may indicate heart failure?

A

MI, AF, hypertension

128
Q

What serum natriuretic peptides are tested for in heart failure?

A

BNP - B-type natriuretic peptide

NTproBNP - N-terminal prohormone of BNP

129
Q

If high SNPs, or previous MI what is next management?

A

Refer in <2wks for specialist and doppler echo

130
Q

If low SNPs what is next management?

A

If medium, refer in 6wks for doppler echo

If low, heart failure unlikely

131
Q

How often is review needed in heart failure? What is checked?

A 
6 months - check functional capacity, fluid status, heart rhythm, cognition and nutrition
Depression
Co-morbidities
Medication compliance/SEs
Bloods - U+E, creatinine, eGFR
132
Q

Non medical management of heart failure? (6)

A 
Educate - discuss prognosis
Ease - benefits, mobility, blue badge
Diet - low salt, lose weight if obese, low alcohol
Lifestyle - smoking, exercise
Restrict fluid intake if severe
Vaccination - pneumococcal and influenza
133
Q

What is given in all types of heart failure?

A

Diuretics.
1st - loop i.e. furosemide
2nd - thiazide i.e. bendroflumethiazide if oedema/hypertension continue

134
Q

What is first line treatment in LV systolic dysfunction?

A

(Diuretics)
ACE inhibitor (or ARB) and beta blocker
If ACEi/ARB not tolerated, use hydralazine with a nitrate
Add mineralocorticoid receptor antagonist (spironolactone)

135
Q

What is treatment of heart failure with preserved ejection fraction?

A

(Diuretics)
No specific treatment
Treat diabetes, hypertension, IHD…

136
Q

When is anticoagulation given in heart failure?

A

If AF or history of thromboembolism, LV aneurysm, intrathoracic thrombus

137
Q

When is aspirin used in heart failure?

A

If concurrent with atherosclerotic arterial disease

138
Q

When to refer heart failure?

A

Severe failure, not controlled by first line medication, concurrent with angina/arrhythmia

139
Q

What 2nd line treatments for heart failure are given?

A 
Digoxin
Ivabradine
Amiodarone
Implantable cardioverter defibrillator
Surgery - valve replacement, coronary angioplasty
140
Q

How does spironolactone work?

A

Aldosterone antagonist - increases sodium and water excretion in DCT, spares potassium
(aldosterone normally increases resorption of sodium and water)

141
Q

CI and SE of spironolactone?

A

CI: addisons, anuria, high potassium
SE: AKI, dizzy, electrolyte imbalance

142
Q

How do loop diuretics (furosemide) work?

A

Inhibit reabsorption of sodium and water from the ascending loop of loop of Henle, increasing excretion

143
Q

CI and SE of furosemide?

A

CI: anuria, renal failure, severe hypokalaemia or hyponatraemia
SE: Dehydration, dizzy, electrolyte imbalance

144
Q

How do thiazide diuretics (bendroflumethiazide) work?

A

Inhibits sodium reabsorption at beginning of the distal convoluted tubule, increasing excretion

145
Q

CI and SE of bendroflumethiazide:

A

CI: addisons, hypercalcaemia, hyponatraemia, hypokalaemia
SE: constipation, electrolyte imbalance, headache

146
Q

What causes systolic failure?

A

MI, IHD, cardiomyopathy

147
Q

What causes diastolic heart failure?

A

Inability of ventricle to relax and fill - constrictive pericarditis, tamponade, restrictive cardiomyopathy

148
Q

Compensatory mechanisms when cardiac output compromised?

A

Sinus tachycardia
Increased venous pressure
Myocardial dilation/hypertrophy

149
Q

Why does decreased CO lead to fluid retention?

A

Poor renal perfusion activates RAAS

150
Q

What is positive inotropism and chronotropism?

A

Inotrope - Increase in force of contractility

Chronotrope - Increase in rate of contractions

151
Q

3 cardinal symptoms of heart failure?

A

SOB
Ankle swelling
Fatigue

152
Q

What are 3 major and 4 minor criteria in Framingham criteria?

A

Major - nocturnal SOB, crepitations, S3 gallop third heart sound
Minor - ankle oedema, SOB, tachycardia, nocturnal cough

153
Q

Which 2 investigations if normal exclude heart failure?

A

ECG, BNP

154
Q

Features on CXR in heart failure? (5)

A 
Alveolar oedema (batwing)
Kerley B lines (interstitial oedema)
Cardiomegaly
Dilated pulmonary vessels
Pleural effusion
155
Q

Features on echo of heart failure?

A

Dilated chambers, valve incompetence, cardiomyopathy,LV dysfunction

156
Q

What is cor pulmonale?

A

Right sided heart failure due to chronic pulmonary hypertension - COPD, asthma, fibrosis

157
Q

What is preload and afterload?

A

Preload - initial stretching of cardiac myocytes prior to contraction
Afterload - load against which the heart has to contract to eject blood

158
Q

What is CKD?

A

Chronic kidney disease

Impaired renal function for >3months based on abnormal structure or function, or GFR <60mL persistently

159
Q

What are the stages of CKD?

A

1 - eGFR>90, kidney damage normal GFR
2 - eGFR 60-89, kidney damage mildly low GFR
3a - 45-49, 3b - 30-44, moderately low GFR
4 - 15-29 severely low GFR
5 - <15 renal failure

160
Q

Causes of CKD?

A 
Diabetes
Hypertension
Urinary tract obstruction
Polycystic kidneys
Glomerulonephtritis
Renovascular disease
SLE
161
Q

Who should be screened for CKD?

A 
Diabetics
Hypertension
CV disease
Chronic stones
BPH
Recurrent UTI
Multisystem i.e. SLE
FHx
162
Q

How may CKD present?

A 
Often asymptomatic until ~stage 4
Nausea
Anorexia/lethargy
Itch
Nocturia
Impotence
Oedema
Dyspnoea
163
Q

Signs of CKD?

A 
Pallor
Lemon tinge to skin - uraemic
Pulm/peripheral oedema
Pericarditis
Pleural effusions
Metabolic flap
Retinopathy
Hypertension
164
Q

Investigations of CKD?

A

Bloods - U+E, creatinine, eGFR, glucose, protein, FBC
Urinalysis - MC+S, albumin:creatinine
Renal tract USS - usually small kidneys

165
Q

What would be on bloods in CKD?

A

Anaemia
High calcium
High phosphate
Raised alkaline phosphatase

166
Q

General management of CKD?

A

Treat reversible cause i.e. nephrotoxic drugs (NSAIDs)
Manage CVD risk i.e. statin, antihypertensives, antiplatelet
Treat diabetes
Stop smoking
Treat anaemia, renal bone disease

167
Q

When to refer?

A 
Stage 4 or 5
Significant proteinuria
Sudden drop in eGFR
Persistent haematuria if under 50yo
Bone disease, anaemia
168
Q

How to treat CKD?

A 
ACEi (lisinopril) or ARB (losartan)
Statin
Loop diuretics for oedema, restrict fluid/salt
VitD/calcium supplements
Sodium bicarb supplements
Replace iron/B12/folate/EPO if anaemia
Gabapentin for restless legs
169
Q

When to start dialysis?

A

eGFR 8-10

170
Q

What are types of RRT?

A

Haemodialysis, haemofiltration (if critically ill), peritoneal dialysis (ambulatory)

171
Q

How does haemodialysis work?

A

Blood flows opposite dialysis fluid and substances cleared along a concentration gradient across semi permeable membrane

172
Q

Complications of dialysis?

A

Pulmonary oedema
Infection
Hypotension

173
Q

End stage treatment of CKD?

A

Transplant

174
Q

What is COPD?

A

Chronic obstructive pulmonary disease
Progressive disorder characterised by airway obstruction with little or no reversibility
Includes emphysema and chronic bronchitis

175
Q

What is the FEV1 and FEV1/FVC needed to diagnose COPD?

A

FEV1 <80%

FEV1/FVC <0.7

176
Q

Difference between obstructive and restrictive airways disease?

A

Obstructive - conditions that hinder ability to exhale all the air from lungs
Restrictive - difficulty fully expanding lungs

177
Q

What are the obstructive lung diseases?

A

Chronic bronchitis
Emphysema
Asthma
Bronchiectasis

178
Q

What would indicate COPD instead of asthma? (6)

A 
Increasing age
History of smoking/smoke
Chronic sob
Sputum
Little diurnal FEV1 variation
Irreversible
179
Q

What is chronic bronchitis?

A

CLINICAL diagnosis

Cough, sputum production on most days for 3 months of 2 successive years

180
Q

What is emphysema?

A

HISTOLOGICAL diagnosis

Enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls

181
Q

What causes COPD?

A

Smoking

182
Q

What inherited trait can cause COPD?

A

Alpha1 antitrypsin deficiency on chromosome 14

Inhibits neutrophil elastase - enzyme that disrupts connective tissue, so develop emphysema at young age

183
Q

Pathological features seen in COPD? (4)

A 
Goblet cell hyperplasia
Inflammatory infiltration
Squamous epithelium replaced with columnar
Fibrosis
Loss of elasticity - emphysema
184
Q

What is a pink puffer?

A

Breathless NOT cyanosed
Normal Co2 from increased ventilation
Pursed lips and barrel chest
From emphysema

185
Q

What is a blue bloater?

A

Cyanosed NOT breathless
High Co2 due to insensitivity, rely on hypoxic drive
Bloat due to right heart failure
From chronic bronchitis

186
Q

Symptoms of COPD? (4)

A

Cough
Sputum
Dyspnoea
Wheeze

187
Q

Signs of COPD? (8)

A 
Tachypnoea
Use of accessory muscles
Hyperinflation
Decreased chest expansion
Hyperresonant percussion
Quiet breath sounds
Cyanosis
Cor pulmonale
188
Q

Complications of COPD? (4)

A

Acute exacerbations/infections
Polycythaemia - more RBCs
Resp failure
Cor pulmonale - oedema

189
Q

Triggers for COPD exacerbations? (3)

A

Cold weather
Pollution/smoke
Exertion

190
Q

Investigations for COPD? (6)

A 
FBC - high circulating RBCs
ABG - hypoxia, possible hypercapnia
Lung function
CXR 
ECG
Steroid trial
191
Q

What is seen on CXR in COPD? (4)

A

Bullae - air filled spaces
Hyperinflation (>6 ribs above diaphragm), flat hemidiaphragms, large pulmonary arteries, decreased peripheral vascular markings

192
Q

What is seen on ECG in COPD?

A

Right atrial and ventricular hypertrophy

193
Q

What is FEV1 and FVC?

A

Forced expiratory volume in 1 second into a spirometer

Forced vital capacity into a spirometer - until no more can be exhaled

194
Q

Steroid trial in COPD?

A

Oral prednisolone for 2 weeks
If FEV1 > by 15% COPD is steroid responsive
Not done much

195
Q

How is severity of COPD tested?

A

1 mild - FEV1 >80% predicted
2 moderate - 50-79% predicted
3 severe - 30-49% predicted
4 very severe - <30% predicted

196
Q

General management of COPD? (7)

A 
Stop smoking
Exercise
Nutrition/lose weight
Flu and pneumoccocal vaccine
Pulmonary rehabilitation
Mucolytics
Diuretics for oedema
197
Q

What is first line for COPD?

A

Short acting beta 2 agonist as needed - salbutamol

OR short acting muscarinic antagonist as needed - ipatropium bromide

198
Q

What is second line for COPD if persistent sob?

A

FEV1 >50%:
Long acting beta 2 agonist - formoterol
OR Long acting muscarinic antagonist - tiotropium (discontinue ipatropium)

FEV <50%:
Long acting beta 2 agonist - formoterol AND inhaled corticosteroid - budesonide
OR Long acting muscarinic antagonist - tiotropium (discontinue ipatropium)

199
Q

What is third line for COPD if remain symptomatic?

A

Long acting beta 2 agonist - formoterol PLUS inhaled corticosteroid - budesonide PLUS long acting muscarinic antagonist (tiotropium)

200
Q

Treatments for more advanced COPD?

A

Theophylline PLUS inhaled corticosteroid - budesonide PLUS long acting beta 2 agonist - formoterol
Pulmonary rehabilitation
LTOT if oxygen <7.3kPa

201
Q

What is ipatropium and tiotropium, how do they work?

A

Short and long acting antimuscarinics

Decrease bronchial secretions by antagonising M3 muscarinic receptors, cause bronchodilation

202
Q

SE/CI for antimuscarinics

A

SE: arrhythmias, cough, dizziness
CI: parodoxical bronchospasm, susceptible to angle closure glaucoma

203
Q

What is salbutamol and formoterol, how do they work?

A

Short and long acting beta 2 agonists

Activates beta 2 receptors which relax bronchial smooth muscle

204
Q

SE/CI for S/LABAs

A

SE: fine tremor, headache, hypokalaemia
CI: severe pre-eclampsia

205
Q

How does budesonide work? SE, CI

A

Glucocorticoid agonist, prevents inflammation
SE: headache, oral candidiasis, taste change
CI: acute exacerbations

206
Q

How does theophylline work? SE, CI

A

Phosphodiesterase inhibitor causing bronchodilation of airway smooth muscle
SE: anxiety, arrhytmias, dizzy
CI: arrhythmias, hypokalaemia risk

207
Q

Surgery available for COPD?

A

Bullectomy, lung transplant

208
Q

Treatment of acute COPD exacerbations? (4)

A

Nebulised salbutamol and ipratropium
Oxygen
Steroids - prednisolone
Antibiotics - amoxicillin

209
Q

What is asthma?

A

Recurrent episodes of dyspnoea, cough, wheeze caused by REVERSIBLE airways obstruction

210
Q

What factors contribute to asthma pathogenesis?

A

Bronchial muscle contraction
Mucosal inflammation - mast cell and basophil degranulation
Increased mucous production

211
Q

Symptoms of asthma?

A 
Intermittent dyspnoea
Wheeze
Cough - often nocturnal
Sputum
Disturbed sleep - indicates severe
Acid reflux
Eczema, hayfever
212
Q

Precipitants of asthma?

A 
Cold air
Exercise
emotion
Allergens - dust, pollen, fur
Infection
Smoke inhalation/pollution
Job - if better at weekends
213
Q

What drugs can precipitate asthma?

A

NSAIDs

Beta blockers

214
Q

What is diurnal variation seen in asthma?

A

In symptoms OR peak flow - worse in morning

215
Q

Signs of asthma?

A 
Tachypnoea
Audible wheeze - widespread, polyphonic
Hyperinflated chest
Hyperresonant percussion
Decreased air entry
216
Q

Signs of a severe asthma attack?

A

Inability to complete sentences
Pulse >110bpm
Resp rate >25
PEF 33-50% expected

217
Q

Signs of a life threatening asthma attack?

A 
Silent chest
Confusion
Exhaustion
Cyanosis - oxygen <8kPa (low), <92%, co2 4.6-6 (normal)
Bradycardia
PEF <33% predicted
218
Q

Sign of a near fatal asthma attack?

A

Increased PaCO2 - shows failing respiratory effort

219
Q

Tests for asthma? (4)

A

Peak expiratory flow monitoring - diurnal variation >20% for 3 days a week for 2 weeks
Spirometry - obstructive, FEV1/FVC <0.7 FEV1 <80%
Steroid/b2 agonist trial - 15% increase in FEV1
CXR - hyperinflation

220
Q

General management of asthma?

A

Stop smoking
Avoid precipitants
CHECK INHALER TECHNIQUE
Teach peak flow technique for 2x daily monitoring

221
Q

Step 1 of asthma treatment?

A

Inhaled short acting beta 2 agonist - salbutamol

222
Q

Step 2 of asthma treatment?

A

If using SABA/having symptoms more than 3 times a week or woken at night

ADD inhaled corticosteroid - beclometasone

223
Q

Step 3 of asthma treatment?

A

Offer leukotriene receptor antagonist (montelukast) in addition to SABA and ICS

224
Q

Step 4 of asthma treatment?

A

Add a long acting beta 2 agonist (formoterol) with the SABA, ICS, LTRA

225
Q

What if uncontrolled asthma on SABA, ICS, LABA, LTRA?

A

Change ICS and LABA therapy to maintenance and reliever (MART) with fast acting LABA
Then increase ICS to moderate

226
Q

What if uncontrolled with moderate ICS dose?

A

Trial of high ICS
OR theophylline
OR muscarinic receptor antagonist (ipratropium)

227
Q

What are leukotriene receptor antagonists?

A

Block the effects of cysteinyl leukotrienes in the airways which normally cause narrowing/swelling of the airways

228
Q

SE/CI of LTRAs

A

SE: diarrhoea, GI upset, headache, URTI
CI: pregnancy. none really - may be linked to depression/suicide

3A REVISION (17 decks)

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