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Phase 2a Medicine - Hannah's version > Top band topics > Flashcards

Top band topics Flashcards

1
Q

Most common arteries to develop atherosclerosis

A
  1. Circumflex
  2. Left anterior descending
  3. Right coronary arteries
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2
Q

7 risk factors for atherosclerosis

A
  1. Age
  2. Tobacco
  3. Cholesterol
  4. Obesity
  5. Diabetes
  6. Hypertension
  7. Family history
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3
Q

Where are atherosclerotic plaques likely to form?

A

Peripheral and coronary arteries

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4
Q

Structure of atherosclerotic plaque

A
  1. Lipid
  2. Necrotic core
  3. Connective tissue
  4. Fibrous cap
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5
Q

Outcomes of atherosclerotic plaques

A
  1. Occlusion -> ischaemia
  2. Rupture -> thrombus
  3. Embolism
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6
Q

What is the main inflammatory cytokine in atherosclerotic plaques?

A

IL-1

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7
Q

What are the stages of atherosclerosis?

A
  1. Fatty streaks
  2. Intermediate lesions
  3. Fibrous plaques
  4. Plaque rupture
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8
Q

When do fatty streaks start forming?

A

Age 10

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9
Q

What are fatty streaks made of?

A
  1. Foam cells

2. T lymphocytes

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10
Q

What are intermediate lesions made of?

A
  1. Foam cells
  2. Smooth muscle cells
  3. T lymphocytes
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11
Q

Define angina.

A

Chest pain / discomfort as a result of reversible myocardial ischaemia

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12
Q

What is stable angina?

A

Angina induced by effort and relieved by rest

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13
Q

What is unstable angina?

A
  1. Recent onset (<24hrs)
  2. Deterioration of stable angina (symptoms at rest)
  3. Increasing frequency and severity
  4. Occurs on minimum exertion / at rest
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14
Q

What can cause angina?

A
  1. Atheroma / stenosis of coronary arteries
  2. Valvular disease
  3. Aortic stenosis
  4. Arrhythmia
  5. Anaemia
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15
Q

8 risk factors for angina

A
  1. Smoking
  2. Sedentary lifestyle
  3. Obesity
  4. Hypertension
  5. Diabetes mellitus
  6. Family history
  7. Age
  8. Hypercholesterolaemia
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16
Q

Clinical presentation of angina?

A
  1. Central chest tightness
  2. Provoked by exertion, cold, anger, excitement, and large meals
  3. Relieved by rest or GTN
  4. Radiation to arms, neck, and jaw
  5. Dyspnoea
  6. Nausea
  7. Sweating
  8. Fainting
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17
Q

Diagnosis of angina?

A
  1. 12 lead ECG
  2. Treadmill test
  3. CT scan calcium scoring
  4. SPECT
  5. Cardiac catheterisation
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18
Q

What would an ECG of angina look like?

A
  1. Normal
  2. ST depression
  3. T wave inversion
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19
Q

Treatment for angina?

A
  1. Aspirin (COX inhibitor - reduced platelet aggregation)
  2. Statins (reduces cholesterol)
  3. Beta-blockers
  4. GTN
  5. CCB
  6. Revascularisation
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20
Q

How do beta-blockers help treat angina?

A
  1. Reduce force of contraction
  2. Reduce heart rate
  3. Reduce cardiac output
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21
Q

Side effects of beta-blockers?

A
  1. Tiredness
  2. Nightmares
  3. Bradycardia
  4. Erectile dysfunction
  5. Cold hands
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22
Q

How does GTN help treat angina?

A
  1. Dilates systemic veins
  2. Reduced venous return
  3. Reduces preload
  4. Reduces workload and O₂ demand
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23
Q

Side effects of GTN?

A

Profuse headache immediately after use

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24
Q

How do CCBs help treat angina?

A
  1. Dilates systemic arteries
  2. BP drop
  3. Reduces afterload
  4. Reduces workload
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25
Q

Purpose of revascularisation?

A

Restore patent coronary arteries and increase flow reserve

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26
Q

What are ACS?

A
  1. STEMI
  2. NSTEMI
  3. Unstable angina
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27
Q

What is a STEMI?

A

Complete occlusion of MAJOR artery -> full thickness damage of heart muscle

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28
Q

What is an NSTEMI?

A

Complete occlusion of MINOR / partial occlusion of MAJOR coronary artery -> partial thickness damage of heart muscle

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29
Q

What is a type 1 MI?

A

Spontaneous MI with ischaemia due to primary coronary event

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30
Q

What is a type 2 MI?

A

MI secondary to ischaemia due to increase O₂ demand or decreased supply

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31
Q

Clinical presentation of UA?

A
  1. Chest pain
  2. Breathlessness
  3. Pleuritic pain
  4. Indigestion
  5. New onset angina
  6. Recent destabilisation of pre-existing angina
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32
Q

What is the clinical presentation of ACS?

A
  1. Acute central chest pain >20mins - RADIATION
  2. Sweating
  3. Nausea and vomiting
  4. Dyspnoea
  5. Fatigue
  6. SOB
  7. Palpitations
  8. Distress / anxiety
  9. Pallor
  10. No response to GTN
  11. Hypotension
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33
Q

Diagnosis of MI?

A
  1. 12 lead ECG
  2. Bloods - cardiac enzymes
  3. CXR
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34
Q

ECG of STEMI?

A
  1. Persistent ST elevation
  2. Tall T waves
  3. New LBBB
  4. Pathological Q waves (days later)
  5. T wave inversion (days later)
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35
Q

ECG of NSTEMI or UA?

A
  1. ST depression
  2. Tall T waves
  3. T wave inversion (days later)
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36
Q

What are the biochemical markers relevant to an MI?

A
  1. Troponin I / T
  2. CK-MB
  3. Myoglobin
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37
Q

Describe the levels of troponin following an MI

A
  1. Rise within 3-12 hours
  2. Peak at 24-48 hours
  3. Return to normal over 5-14 days
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38
Q

Why is CK-MB useful in MI treatment?

A

Determines re-infarction as levels drop back within 36-72 hours

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39
Q

Immediate treatment for an MI

A

MONA

  1. Morphine IV
  2. Oxygen
  3. Nitrates (GTN)
  4. Anti-emetic
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40
Q

What anti-platelets are used following an MI?

A
  1. Aspirin (COX inhibitor)

2. Clopidigrel (P2Y12 inhibitor)

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41
Q

Treatment for an MI?

A
  1. Anti-platelets
  2. Beta-blockers (atenolol)
  3. Statins (simvastatin)
  4. ACEi (ramipril)
  5. Coronary revascularisation
  6. Risk factor modification
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42
Q

When should you do a PCI for STEMIs and what if you can’t do it?

A
  1. PCI within 120 minutes

2. If not possible, fibrinolysis with alteplase

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43
Q

Complications of MIs

A
  1. Sudden death
  2. Arrhythmias
  3. Persistent pain (due to necrosis)
  4. Heart failure
  5. Mitral incompetence
  6. Cardiac rupture
  7. Pericarditis
  8. Ventricular aneurysm
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44
Q

Define cardiac failure

A

Inability of the heart to deliver blood, thus O₂, at a rate that is commensurate with the requirement of metabolising tissue

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45
Q

Main causes of cardiac failure?

A
  1. IHD
  2. Cardiomyopathy
  3. Valvular heart disease
  4. Cor pulmonate
  5. Hypertension
  6. Alcohol excess
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46
Q

Name the compensatory mechanisms in cardiac failure

A
  1. Venous return (preload)
  2. Outflow resistance (afterload)
  3. Sympathetic system activation
  4. RAAS
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47
Q

Describe the venous return compensatory mechanism in CF

A
  1. Reduced SV
  2. Increased blood after systole
  3. Stretched myocardial fibres
  4. Increased force of contraction (STARLING’S LAW)
  5. DECOMPENSATION - increased CO cannot be maintained
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48
Q

Describe the outflow resistance compensatory mechanism in CF

A
  1. Increased after load
  2. Increased EDV & decreased SV
  3. Decreased CO
  4. COMPENSATORY CHANGE - dilatation of LV
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49
Q

Describe the sympathetic system activation compensatory mechanism in CF

A
  1. Baroreceptors detect BP drop
  2. Increased FoC
  3. Increased SV & HR
  4. Increased CO
  5. COMPENSATORY CHANGE - chronic sympathetic activation
  6. Sympathetic system acts on baroreceptors to make them less receptive to BP drop
  7. CO stops increasing in response to sympathetic activation
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50
Q

Describe the RAAS compensatory mechanism in CF

A
  1. Reduced CO
  2. Reduced renal perfusion
  3. Activation of RAAS
  4. Increased Na+ absorption & ADH secretion
  5. Increased water retention
  6. Increased BP
  7. Increased preload
  8. Stretched myocardial fibres (STARLING’S LAW)
  9. Increased CO
  10. DECOMPENSATORY CHANGE - not enough O₂ to keep up this increased workload
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51
Q

What is systolic heart failure?

A

Inability of the ventricle to contract normally -> decreased CO

  • IHD, cardiomyopathy
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52
Q

What is diastolic heart failure?

A

Inability of the ventricles to relax and fill fully -> decreased SV and CO

  • Ventricular hypertrophy, aortic stenosis
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53
Q

What are the cardinal symptoms of heart failure?

A
  1. SOB
  2. Fatigue
  3. Peripheral oedema
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54
Q

Clinical presentation of HF

A
  1. CARDINAL SYMPTOMS
  2. Dyspnoea
  3. Orthopnoea
  4. Cold peripheries
  5. Raised JVP
  6. Murmurs
  7. Displaced apex beat
  8. Cyanosis
  9. Hypotension
  10. Peripheral and pulmonary oedema (back flow from decreased CO)
  11. Tachycardia
  12. 3rd and 4th heart soudns
  13. Ascites
  14. Bi-basal crackles
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55
Q

Describe the NYHA classification of HF

A

Class I - no limitation
Class II - slight limitation (comfortable at rest, normal activity causes fatigue, dyspnoea, and palpitations - FDP)
Class III - marked limitation (gentle activity = FDP)
Class IV - inability to carry out any physical activity (FDP at rest)

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56
Q

Diagnosis of HF?

A
  1. Blood tests (increased BNP)
  2. CXR
  3. ECG
  4. Echo
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57
Q

What would you see on a CXR of someone with HF?

A
  1. Alveolar oedema
  2. Cardiomegaly
  3. Dilated upper lobe vessels of lung
  4. Pleural effusions
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58
Q

What is the treatment for HF?

A
  1. Lifestyle changes
  2. Diuretics (furosemide, bendroflumethiazide)
  3. ACEi (ramipril)
  4. Beta-blockers (bisoprolol)
  5. Digoxin
  6. Inotropes
  7. Revascularisation
  8. Surgery (to repair valve defects)
  9. Cardiac resynchronisation
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59
Q

Define stage 1 hypertension

A

Clinic BP > 140/90mmHg

24hr ABPM / HBPM > 135/85mmHg

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60
Q

Define stage 2 hypertension

A

Clinic BP > 160/100mmHg

24hr ABPM / HBPM > 150/95mmHg

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61
Q

Define severe hypertension

A

Clinic systolic BP > 180mmHg
Clinic diastolic BP > 110mmHg
IMMEDIATE ANTI-HYPERTENSIVE DRUGS

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62
Q

What is essential hypertension?

A

Primary cause is unknown

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63
Q

What can cause secondary hypertension?

A
  1. Renal (CKD)
  2. Endocrine (Cushing’s, Conn’s, Pheochromocytoma)
  3. Coarctation of aorta
  4. Drugs (corticosteroids, cyclosporin)
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64
Q

What is malignant hypertension?

A

Raised diastolic blood pressure over 120mmHg

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65
Q

What is involved in the diagnosis of hypertension?

A

Looking for end-organ damage

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66
Q

What is the treatment for hypertension?

A

GOAL - 140/90mmHg

  1. Lifestyle changes
  2. ACEi (ramipril) or ARB (candesartan)
  3. CCB (amlodipine)
  4. Diuretics (furosemide)
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67
Q

What is the hypertension treatment for <55yos?

A
  1. Ramipril / candesartan
  2. Nifedipine
  3. Bendroflumethiazide
  4. Furosemide
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68
Q

What is the treatment for hypertension in >55yos / black people?

A
  1. Ramipril / candesartan
  2. Nifedipine
  3. Bendroflumethiazide
  4. Furosemide
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69
Q

Causes of mitral stenosis?

A
  1. Rheumatic fever
  2. Group A beta-haem strep
  3. IE
  4. Calcification
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70
Q

Pathophysiology of mitral stenosis

A

LA pressure increase -> LA hypertrophy / dilatation -> pulmonary venous / pulmonary arterial / right heart pressure increase -> pulmonary capillary pressure increase -> pulmonary oedema -> reactive pulmonary hypertension -> RV hypertrophy / dilatation -> RV failure

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71
Q

Clinical presentation of mitral stenosis?

A
  1. Progressive dyspnoea
  2. Haemoptysis
  3. RHF
  4. AF
  5. Systemic emboli
  6. Prominent ‘a’ wave in JV pulsations
  7. Mitral facies (bilateral, cyanotic, or dusky pink discolouration on upper cheeks due to vasoconstriction)
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72
Q

What are the heart sounds in mitral stenosis?

A
  1. Diastolic murmur

2. Loud opening S1 snap

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73
Q

Diagnosis of valve disease?

A
  1. CXR
  2. ECG
  3. Echo
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74
Q

Treatment for mitral stenosis?

A
  1. Beta-blockers for rate control to improve diastolic filling
  2. Diuretics for fluid overload
  3. Percutaneous mitral balloon valvotomy
  4. Valve replacement
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75
Q

Clinical presentation of mitral regurgitation?

A
  1. Exertional dyspnoea
  2. Pulmonary venous hypertension
  3. Fatigue
  4. Lethargy
  5. Palpitations (increased SV)
  6. RHF symptoms
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76
Q

Heart sounds for mitral regurgitation?

A
  1. Soft S1
  2. Pansystolic murmur
  3. Prominent S3
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77
Q

Treatment for mitral regurgitation?

A
  1. ACEi (vasodilator)
  2. Beta-blockers (rate control)
  3. Anti-coagulation (AF)
  4. Diuretics (fluid overload)
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78
Q

Causes of aortic stenosis

A
  1. Calcific aortic valvular disease
  2. Congenital bicuspid valve
  3. Rheumatic heart disease
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79
Q

Clinical presentation of aortic stenosis?

A
  1. TRIAD = syncope, angina, heart failure, dyspnoea on exertion
  2. Sudden death
  3. Slow rising carotid pulse
  4. Decreased pulse amplitude
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80
Q

Heart sounds in aortic stenosis?

A
  1. Soft S2
  2. Prominent S4
  3. Ejection systolic murmur
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81
Q

Treatment for aortic stenosis?

A
  1. Dental hygiene
  2. IE prophylaxis
  3. Valve replacement
  4. TAVI
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82
Q

Clinical presentation of aortic regurgitation?

A
  1. Exertional dyspnoea
  2. Palpitations
  3. Angina
  4. Syncope
  5. Wide pulse pressure
  6. Quincke’s sign
  7. de Musset’s sign
  8. Pistol shot femoral
  9. Collapsing water hammer pulse
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83
Q

Heart sounds in aortic regurgitation?

A
  1. Diastolic blowing murmur

2. Systolic ejection murmur

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84
Q

Treatment for aortic regurgitation?

A
  1. IE prophylaxis
  2. ACEi (vasodilator)
  3. Serial echos
  4. Valve replacement
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85
Q

Clinical symptoms of anaemia?

A
  1. Fatigue
  2. Headaches
  3. Faintness
  4. Dyspnoea / SOB
  5. Angina
  6. Anorexia
  7. Intermittent claudication
  8. Palpitatinos
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86
Q

Signs of anaemia?

A
  1. Pallor
  2. Tachycardia
  3. Systolic flow murmur
  4. CF
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87
Q

Causes of microcytic anaemia?

A
  1. Iron deficiency
  2. Anaemia of chronic disease
  3. Thalassaemia
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88
Q

Clinical presentation specific to iron deficiency anaemia?

A
  1. Brittle hair and nails
  2. Koilonychia
  3. Atrophic glossitis
  4. Angular stomatitis
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89
Q

Diagnosis of iron deficiency anaemia?

A
  1. Hypochromic microcytic anaemia
  2. Poikilocytosis
  3. Anisocytosis
  4. Low serum ferritin
  5. Low serum iron
  6. Raised TIBC
  7. Raised transferrin receptors
  8. Low reticulocyte count
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90
Q

Treatment of iron deficiency anaemia?

A

Ferrous sulphate

S/E: nausea, diarrhoea

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91
Q

Causes of normocytic anaemia?

A
  1. Acute blood loss
  2. Anaemia of chronic disease
  3. Hypopituitarism
  4. Renal failure
  5. Pregnancy
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92
Q

Categories of macrocytic anaemia?

A
  1. Megaloblastic (presence of erythroblasts with delayed nuclear maturation due to delayed DNA synthesis)
  2. Non-megaloblastic / normoblastic
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93
Q

Causes of macrocytic anaemia?

A
  1. Vitamin B12 / folate deficiency (megaloblastic)
  2. Alcohol
  3. Liver disease
  4. Haemolysis
  5. Aplastic anaemia
  6. Bone marrow infiltration
  7. Myeloma
94
Q

Clinical presentation of pernicious anaemia?

A
  1. Insidious onset
  2. Lemon-yellow skin colour (body tries to remove defective large blood cells)
  3. Glossitis
  4. Angular stomatitis
  5. Symmetrical paraesthesia
  6. Loss of proprioception / vibration sense
  7. Weakness and ataxia
  8. Paraplegia
  9. Dementia
95
Q

Diagnosis of pernicious anaemia?

A
  1. Megaloblastic anaemia
  2. Macrocytic
  3. Raised bilirubin
  4. Low serum B12
  5. Low Hb
  6. Low reticulocytes
  7. Intrinsic factor antibodies
96
Q

Treatment of pernicious anaemia?

A

Malabsorption = injections
Dietary = oral B12
Replenish B12 = IM hydroxycobalamin

97
Q

Treatment for arterial thrombosis?

A
  1. Aspirin (COX inhibitor) - PREVENTION
  2. Clopidogrel (P2Y12 inhibitor) - PREVENTION
  3. Streptokinase (thrombolysis)
  4. Tissue plasminogen activator (stroke / MI)
98
Q

Diagnosis of venous thrombosis?

A
  1. Plasma D-dimer

2. Compression ultrasound

99
Q

Treatment of venous thrombosis?

A
  1. LMWH (SC enoxaparin) - 5+ days
  2. Oral warfarin - 6 months
  3. DOAC
  4. Compression stockings
  5. IVC filters
100
Q

Clinical presentation of ALL?

A
  1. Marrow failure - anaemia, neutropenia, thrombocytopenia
  2. Bone pain (marrow infiltration)
  3. Hepatosplenomegaly
  4. Lymphadenopathy
  5. Headaches and cranial nerve palsy
  6. Mediastinal masses w/ SVC obstruction
101
Q

Diagnosis of ALL?

A
  1. FBC - raised WCC
  2. Blood film - blast cells
  3. CXR / CT - lymph/mediastinaladenopathy
  4. Lumbar puncture
102
Q

Treatment for ALL and AML?

A
  1. Blood and platelet transfusions
  2. Prophylactic antimicrobials
  3. Allopurinol (prevent tumour lysis syndrome)
  4. IV fluids through Hickman line
  5. Chemotherapy
  6. Marrow transplant
103
Q

Clinical presentation of CML?

A
  1. Anaemia
  2. Splenomegaly
  3. Weight loss
  4. Tiredness
  5. Pallor
  6. Fever and sweats
  7. Gout
  8. Bleeding
104
Q

80% of CML patients have what?

A

PHILADELPHIA CHROMOSOME

105
Q

Diagnosis of CML?

A
  1. High WCC
  2. Low Hb
  3. Hypercellular aspirate
106
Q

Treatment for CML?

A
  1. Oral imatinib

2. Stem cell transplant

107
Q

Clinical presentation of CLL?

A
  1. Anaemia
  2. Weight loss
  3. Sweats
  4. Anorexia
  5. Hepatosplenomegaly
  6. Lymphadenopathy
108
Q

Diagnosis of CLL?

A
  1. High WCC

2. VERY HIGH LYMPHOCYTES

109
Q

Treatment of CLL?

A
  1. Blood transfusion
  2. Human IV immunoglobulins
  3. Chemo/radiotherapy
110
Q

What is the difference between Hodgkin’s and non-Hodgkin’s lymphoma?

A

Hodgkin’s = Reed-Sternberg cells

111
Q

Causes of lymphoma?

A
  1. Primary immunodeficiency
  2. Secondary immunodeficiency (e.g. HIV)
  3. Infection (e.g. EBV)
  4. Autoimmune (e.g. SLE)
112
Q

Clinical presentation of Hodgkin’s lymphoma?

A
  1. Painless cervical lymphadenopathy
  2. Cough (mediastinal lymphadenopathy)
  3. General B symptoms (weight loss, fever, night sweats)
  4. Infections
113
Q

Diagnosis of Hodgkin’s lymphoma?

A
  1. CT/MRI for staging
  2. Lymph node excision
  3. Bone marrow biopsy
  4. Bloods
  5. Immunophenotyping
  6. Cytogenetics
114
Q

What will you see on the bloods from someone with Hodgkin’s lymphoma?

A
  1. High ESR
  2. Low Hb
  3. High serum lactate dehydrogenase
115
Q

Staging of Hodgkin’s lymphoma?

A

ANN-ARBOUR CLASSIFICATION

116
Q

Treatment for Hodgkin’s?

A
  1. Combination chemo (ABVD)
  2. Stage I-A to II-A = short course + radiotherapy
  3. Stage II-A to IV-B = long course ABVD
117
Q

What is ABVD?

A

Adriamycin
Bleomycin
Vinblastine
Dacarbazine

118
Q

Clinical presentation of non-Hodgkin’s lymphoma?

A
  1. Superficial lymphadenopathy
  2. Systemic B symptoms (night sweats, fever, weight loss)
  3. Pancocytopenia
119
Q

What is low grade non-Hodgkin’s?

A
  1. Slow growing
  2. Advanced at presentatino
  3. Incurable
  4. 9-11yrs survival
120
Q

What is high grade non-Hodgkin’s lymphoma?

A
  1. Rapid growing
  2. Curable
  3. Nodal presentation
121
Q

Diagnosis of non-Hodgkin’s lymphoma?

A
  1. Raised lactose dehydrogenase
  2. Marrow biopsy
  3. Node biopsy
  4. CT/MRI for staging
  5. Immunophenotyping
  6. Cytogenetics
122
Q

Treatment for non-Hodgkin’s lymphoma?

A

R-CHOP chemo

Rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine, prednisolone

123
Q

Treatment for low grade NHL?

A
  1. None

2. Radiotherapy

124
Q

Treatment for high grade NHL?

A 
Early = 3 months R-CHOP + radiotherapy
Late = 6 months R-CHOP + radiotherapy
125
Q

What is myeloma?

A

Cancer of plasma cells which accumulate in bone marrow and lead to progressive marrow failure

126
Q

Clinical presentation of myeloma?

A

OLD CRAB

Old age
Calcium elevated
Renal failure
Anaemia
Bone pain
127
Q

Diagnosis of myeloma?

A
  1. Blood
  2. U&Es
  3. Plain X-ray - lytic lesions
  4. Serum and urine electrophoresis - B2-microglobulin present
128
Q

What will bloods and U&Es show in someone with myeloma?

A
  1. Anaemia
  2. Raised ESR
  3. Rouleaux formation
  4. High calcium
  5. High alkaline phosphatase
129
Q

Treatment for myeloma?

A
  1. Analgesia (bone pain)
  2. Bisphosphonates (fractures)
  3. RBC transfusion (anaemia)
  4. 3L/day fluid (prevent renal damage)
  5. Renal dialysis
  6. Chemo (CTD or VAD)
  7. Stem cell transplant
130
Q

How is sickle cell anaemia inherited?

A

Autosomal recessive

131
Q

What is the clinical presentation of homozygous sickle cell anaemia?

A
  1. Vaso-occlusive crises
  2. Acute chest syndrome
  3. Pulmonary hypertension
  4. Anaemia -> splenic sequestration
132
Q

Long term problems of sickle cell?

A
  1. Growth and development
  2. Avascular necrosis of bones
  3. Osteomyelitis
  4. Cardiomegaly, arrhythmias, MI
  5. TIA, fits, stroke, coma
  6. Liver dysfunction
  7. Chronic tubulointerstitial nephritis
  8. Retinopathy, vitreous haemorrhage
  9. Spontaneous abortion
133
Q

Treatment of sickle cell?

A
  1. Avoid precipitating factors
  2. Folic acid
  3. Blood transfusions (for anaemia)
  4. Oral hydroxycarbamide (increased HbF conc)
  5. Stem cell transplant
134
Q

Treatment for acute painful attacks in sickle cell?

A
  1. IV fluids
  2. Analgesia
  3. Oxygen
  4. Antibiotics
135
Q

Definition of chronic bronchitis

A

Cough with sputum for 3 months for 2 or more years

136
Q

Definition of emphysema

A

Enlarged airspaces distal to terminal bronchioles, with destruction of alveolar walls

137
Q

Describe the airflow limitation in COPD

A
  1. Progressive

2. Caused by abnormal inflammatory response to noxious particles or gases

138
Q

Pathophysiology of chronic bronchitis?

A
  1. Hypertrophy & hyperplasia of mucus secreting goblet cells
  2. Bronchial wall inflammation
  3. Mucosal oedema
139
Q

What is the metaplasia present in chronic bronchitis?

A

Columnar to squamous

140
Q

What is the pathophysiology of emphysema?

A

Dilatation and destruction of tissue distal to terminal bronchioles -> loss of elastic recoil -> airways close during expiration -> airflow limitation and air trapping

141
Q

Classifications of emphysema?

A
  1. Centri-acinar emphysema (around resp bronchioles, distal alveolar ducts and alveoli are preserved)
  2. Pan-acinar emphysema (distension and damage of whole acinus) -> collection of bullae
  3. Irregular emphysema
142
Q

What is the short term effect of COPD?

A

V/Q mismatch -> hypoxia -> increased work -> alveolar hyperventilation

Increased PaCO2 = increased respiration

143
Q

What are the long term effects of COPD?

A

Patients are desensitised to CO2 so rely on hypoxia to drive respiration

  1. Less SOB
  2. Renal hypoxia -> fluid retention and EPO release -> polycythaemia and cyanosis
144
Q

Clinical presentation of COPD?

A
  1. Productive cough
  2. Wheeze
  3. SOB at rest
  4. Prolonged respiration
  5. Poor chest expansion
  6. Barrel chest
  7. Pursed lips on expiration
  8. High pack year
  9. Frequent chest colds
  10. Symptoms worsened by damp/cold weather
  11. Hypertension
  12. Osteoporosis
  13. Depression
  14. Weight loss
  15. Later stages = type 2 resp failure
  16. Advanced disease = pulmonary hypertension
145
Q

Diagnosis of COPD?

A
  1. Lung function test - OBSTRUCTIVE
  2. Bloods - polycythaemia
  3. PEFR - non-variable
146
Q

Treatment for COPD?

A
  1. SMOKING CESSATION
  2. Bronchodilators (tiotropium bromide (LAMA) + SABA)
    • LABA
  4. Corticosteroids (to assess reversibility)
  5. Vaccines
  6. Oxygen therapy
  7. Anti-mucolytics
  8. Diuretics (oedema)
  9. Pulmonary rehabilitation
147
Q

What should you do if you see improvement in lung function in a COPD patient following oral prednisolone for 2 weeks?

A

Move to an ICS beclometasone twice a day

148
Q

What are the three characteristics of asthma?

A
  1. Airflow limitation (reversible)
  2. Airway hyper-responsiveness
  3. Bronchial inflammation
149
Q

What are the two types of asthma?

A
  1. Allergic / eosinophilic asthma (70%)

2. Non-allergic / non-eosinophilic asthma (30%)

150
Q

What triggers non-allergic asthma?

A
  1. Cold
  2. Exercise
  3. Stress
151
Q

What are the classifications of allergic asthma?

A
  1. Extrinsic (atopic)

2. Intrinsic

152
Q

What is atopy?

A

Ready development of IgE against common environmental antigens, such as house-dust mites, grass pollen, and fungal spores

153
Q

What gene is thought to be linked to airway hyper responsiveness and tissue remodelling?

A

ADAM33

154
Q

6 risk factors for asthma?

A
  1. Personal history of atopy
  2. Family history of asthma or atopy
  3. Obesity
  4. Inner-city environment
  5. Premature birth
  6. Socio-economic deprivation
155
Q

Name some precipitating factors of asthma

A
  1. Occupational sensitisers (e.g. wood dust, bleach, dyes)
  2. Cold air
  3. Exercise
  4. Emotion
  5. Drugs (particularly NSAIDs)
  6. Allergens
156
Q

Define asthma.

A

Narrowing of the airway, due to smooth muscle contraction, thickening of the airway wall by cellular infiltrate and inflammation and the presence of secretions within the lumen

157
Q

Describe the role of mast cells in asthma

A
  1. Increased in epithelium, smooth muscle, and mucous glands
  2. Sensitised when bound to IgE
  3. Release histamine, tryptase, prostaglandin 2 Cys-LTs, and cytokines
158
Q

What do histamine and cysteine leukotrienes cause in asthma?

A

Bronchoconstriction and inflammation

159
Q

What is the role of IL-3, IL-4, and IL-5 in asthma?

A 
IL-3 = increases mast cell numbers
IL-4 = IgE synthesis 
IL-5 = essential for eosinophil survival
160
Q

What decreases numbers / activation of eosinophils?

A

CORTICOSTEROIDS!

161
Q

Describe the response 30 minutes after an allergen challenge

A

Bronchoconstriction

162
Q

Describe the response 3 hours after an allergen challenge

A
  1. Bronchoconstriction DECREASES
  2. Inflammation due to vasodilation
  3. Increased vascular permeability
  4. Adhesion molecules
163
Q

Describe the response 6 hours after an allergen challenge

A
  1. Worsening inflammation (eosinophils)

2. Second wave of bronchoconstriction

164
Q

What happens in remodelling in asthma?

A
  1. Smooth muscle hypertrophy and hyperplasia -> larger fraction of wall is muscle
  2. Deposition of repair collagens in basement membrane
  3. Expansion of submucosa due to deposition of matrix proteins, swelling, and cellular infiltrate
  4. Reduced retractile forces -> airways close more easily
  5. Metaplasia -> more goblet cells
165
Q

Describe the clinical presentation of asthma

A
  1. Intermittent dyspnoea
  2. Wheeze
  3. Cough
  4. Sputum
  5. Worse at night
  6. Episodic SOB
166
Q

What happens during an asthma attack?

A
  1. Reduced chest expansion
  2. Prolonged expiratory time
  3. Bilateral expiratory polyphonic wheezes
  4. Tachypnoea
167
Q

Describe uncontrolled asthma

A
  1. PEFR <50%
  2. Resp rate < 25
  3. Pulse < 110
  4. Normal speech
168
Q

What happens during a severe asthma attack?

A
  1. Inability to complete sentences
  2. Pulse > 110
  3. Resp rate > 25
169
Q

What happens during a life threatening asthma attack ?

A
  1. Silent chest
  2. Confusion
  3. Exhaustion
  4. Cyanosis
  5. Bradycardia
  6. PEFR <33%
170
Q

What is the immediate management of a life threatening asthma attack?

A
  1. Oxygen
  2. Nebulised 5mg salbutamol (± ipratropium)
  3. Prednisolone
  4. ABGs
  5. CXR (if doesn’t respond to treatment)
  6. PEFR every 15-30 mins
  7. Oximetry
171
Q

What are the RCP3 questions?

A
  1. Recent nocturnal waking?
  2. Usual asthma symptoms in the day?
  3. Interference with ADLs?
172
Q

What is the diagnosis for asthma?

A
  1. PEFR
  2. Spirometry
  3. CO test
  4. Exercise tests
  5. Trial of corticosteroids + SABA
  6. Exhaled nitric oxide
  7. Blood and sputum tests
  8. Skin prick tests
  9. History
173
Q

What is the result of the PEFR in asthmatics?

A

> 15% improvement after bronchodilator

174
Q

What are the aims of treating asthma?

A
  1. Abolish symptoms
  2. Restore best possible lung function
  3. Reduce risk of severe attacks
  4. Enable normal growth in children
  5. Minimise absence from school / employment
  6. Lowest effective dose possible to minimise S/Es
175
Q

What is the treatment of asthma?

A
  1. SABA (salbutamol) + LABA (salmeterol)
  2. Muscarinic antagonist (ipratropium)
  3. Methylxanthines (theophylline)
  4. ICS (prednisolone)
176
Q

Name 6 risk factors of bronchial cancer

A
  1. Smoking
  2. Asbestos
  3. Radon exposure
  4. Radiation
  5. Pre-existing lung disease
  6. Genetics
  7. Iron oxide
177
Q

Describe small cell lung cancer

A
  1. STRONG ASSOCIATION WITH SMOKING
  2. Metastasis by presentation
  3. Central bronchus
  4. From neuroendocrine cells
  5. Secretes polypeptide hormones
  6. Chemotherapy
  7. Poor prognosis
178
Q

Describe squamous cell carcinoma

A
  1. MOST STRONGLY ASSOCIATED WITH SMOKING
  2. Central location
  3. Cavitation with central necrosis
  4. From epithelial cells
  5. Secrete keratin
  6. Cause obstruction
  7. Local spread
  8. Surgical ablation
179
Q

Describe adenocarcinoma

A
  1. Most common
  2. Most common in non-smokers
  3. Central or peripheral
  4. Single lesions or multifocal pattern
  5. From mucus secreting glandular cells
  6. Metastasis to pleura, lymph nodes, brain, bones, and adrenals
  7. Associated with asbestos
180
Q

Where do bronchial cancers metastasis to?

A
  1. Liver
  2. Bone
  3. Adrenals
  4. Brain
181
Q

Which tumours metastasis TO the lungs?

A
  1. Breast
  2. Bowel
  3. Kidney
  4. Bladder
182
Q

Clinical presentation of bronchial cancer

A
  1. Cough
  2. Breathlessness
  3. Haemoptysis
  4. Chest pain
  5. Wheeze
  6. Infections
  7. Clubbing
183
Q

What classification system is used for lung cancer?

A

TNM

184
Q

How do you diagnose lung cancer?

A
  1. CXR
  2. CT
  3. Bronchoscopy
  4. Cytology
  5. Bloods
185
Q

What would you see on a CXR of lung cancer?

A
  1. Round shadow
  2. Hilar enlargement
  3. Consolidation
  4. Lung collapse
  5. Pleural effusion
186
Q

Treatment for NSCLC?

A
  1. Surgical excision (if no metastasis)
  2. Curative radiotherapy
  3. Chemotherapy ± radiotherapy
187
Q

Treatment for SCLC?

A
  1. Chemo ± radio (if no metastasis)
  2. Chemotherapy (if metastasis)
  3. Palliation
  4. SVC stent + radiotherapy + dexamethasone (for SVC obstruction)
  5. Endobronchial therapy
  6. Pleural drainage
188
Q

Risk factors of PE?

A
  1. Change in blood flow (immobility, obesity, pregnancy)
  2. Change in blood vessel (smoking, hypertension)
  3. Change in blood constituents (dehydration, malignancy, COCP)
189
Q

Clinical presentation of a PE?

A
  1. May be asymptomatic (small emboli)
  2. Sudden onset dyspnoea
  3. Pleuritic chest pain / haemoptysis (infarction)
  4. Dizziness
  5. Past history of thromboembolism
  6. Pyrexia
  7. Cyanosis
  8. Tachypnoea
  9. Tachycardia
  10. Hypotension
  11. Raised JVP
  12. Pleural rub
  13. Pleural effusion
190
Q

How do you diagnose a PE?

A
  1. Plasma D-dimer
  2. Compression ultrasound
  3. CT pulmonary angiography - GOLD STANDARD
191
Q

Treatment of a PE?

A
  1. High flow oxygen
  2. LMWH (oral enoxaparin)
  3. IV fluids + inotropic agents
  4. Thrombolysis (alteplase) for massive PE
  5. Surgical embolectomy
  6. Vena cava filter
192
Q

Prevention of further PE?

A
  1. Warfarin
  2. Mobilisation
  3. Compression stockings
193
Q

Management of massive PE?

A
  1. Oxygen
  2. Morphine
  3. Anti-emetic
  4. Immediate thrombolysis
  5. IV heparin
194
Q

Name three emergency upper respiratory tract infections

A
  1. Severe acute respiratory distress (coronavirus, from China)
  2. Middle East Respiratory Syndrome novel Coronavirus
  3. Avian influenza
195
Q

Bacterial cause of pharyngitis / tonsillitis?

A

Lancefield Group A beta-haemolytic strep - S.PYOGENES

196
Q

Bacterial cause of sinusitis?

A
  1. S.pneumoniae

2. H.influenzae

197
Q

Clinical presentation of sinusitis?

A
  1. Frontal headache
  2. Purulent rhinorrhoea
  3. Unilateral pain
  4. Fever
  5. Facial pain
198
Q

Treatment for sinusitis?

A
  1. Nasal decongestant (xylometazoline)

2. Broad spectrum antibiotics (co-amoxiclav)

199
Q

Treatment for acute epiglottis?

A

IV ceftazidime

200
Q

Causes of whooping cough?

A

Bordatellla pertussis (G-ve rod)

201
Q

Treatment of whooping cough?

A

Clarithromycin

202
Q

Causes of CAP?

A
  1. S.pneumoniae - MOST COMMON
  2. S.aureus
  3. Legionella
203
Q

Definition of HAP?

A

New onset of cough with purulent sputum, along with a compatible CXR demonstrating consolidation, in patients who are beyond 48hrs of initial admission to hospital

204
Q

Who is at risk of HAP?

A
  1. Elderly
  2. Ventilator assisted
  3. Post-operative patients
205
Q

Most common causes of HAP?

A
  1. Pseudomonas Aeruginosa
  2. E.coli
  3. Klebsiella pneumoniae
  4. MRSA
206
Q

How is pneumonia spread?

A

Respiratory droplets

207
Q

Clinical presentation of pneumonia

A
  1. Fever
  2. Night sweats
  3. Raised resp rate
  4. Productive cough
  5. NO URTI SYMPTOMS
  6. Rigors
  7. Malaise
  8. Anorexia
  9. Dyspnoea
  10. SOB
  11. Dry or productive cough
  12. Purulent sputum (S.pneumoniae)
  13. Pleuritic chest pain
  14. Cyanosis
  15. Confusion
208
Q

Signs of pneumonia?

A
  1. Dull to percussion
  2. Decreased air entry
  3. Bronchial breath sounds
209
Q

Diagnosis of pneumonia?

A
  1. CXR
  2. Blood tests (FBC, ESR, biochem)
  3. Pulse oximetry / ABG
  4. Sputum culture
  5. Blood culture
  6. Serology
210
Q

Describe the CXR results for each type of causative microorganism in pneumonia

A

Multi-lobar = S.pneumoniae, S.aureus, Legionella
Multiple abscesses = S.aureus
Upper lobe cavity = Klebsiella pneumoniae

211
Q

What does CURB65 stand for?

A 
Confusion
Urea > 7mmol/L
Respiratory rate > 30/min
BP < 90mmHg sys / 60mmHg dias
Age > 65
212
Q

Describe the treatment for 0-1/mild pneumonia

A
  1. Treat at home
  2. Amoxicillin 5-7 days
  3. Oxygen
  4. Analgesia (for pleuritic pain)
213
Q

Describe the treatment for 2/moderate pneumonia

A
  1. Admit to hospital
  2. PO co-amoxiclav
  3. Oxygen
  4. Analgesia
214
Q

Describe the treatment for 3/severe pneumonia

A
  1. Hospitalisation and close monitoring

2. IV co-amoxiclav or clarithromycin

215
Q

How do you treat pneumonia caused by legionella?

A

Fluroquinolone

216
Q

How do you treat necrotising pneumonia?

A
  1. IV linezolid
  2. IV clindamycin
  3. IV rifampicin
217
Q

How do you treat pneumonia caused by pseudomonas aeruginosa?

A
  1. IV ceftazidime

2. IV gentamicin

218
Q

Name 4 complications of pneumonia

A
  1. Respiratory failure
  2. Hypotension
  3. Parapneumonic effusion and empyema
  4. Lung abscesses
219
Q

Describe mycobacterium

A
  1. Aerobic
  2. Non-motile
  3. Non-sporing
  4. Slight curved bacilli
  5. Thick waxy capsule
  6. Acid-fast bacilli
  7. Slow growing
  8. Resistant to phagolysosomal killing
  9. Can remain dormant
220
Q

Name 6 risk factors of tuberculosis

A
  1. Origination from high-incidence country
  2. HIV
  3. Immunosuppression
  4. Diabetes mellitus
  5. IVDU
  6. Ageing
  7. Malnutrition
  8. Prisons
  9. Homeless
  10. Smoking
  11. Alcohol
221
Q

Describe the pathophysiology of primary tuberculosis

A
  1. Inhalation of bacteria
  2. Ingestion by macrophages
  3. Proliferation inside macrophages
  4. Inflammatory response in lungs
  5. Macrophages present antigen to T cells
  6. Hypersensitivity reaction -> necrosis and granulomas
  7. Fibrosis
222
Q

Where can TB affect?

A
  1. GI
  2. Bone and spine
  3. Miliary (systemic)
  4. CNS
  5. Pericardium
  6. Skin
223
Q

Describe the clinical presentation of TB

A
  1. Weight loss
  2. Low grade fever
  3. Anorexia
  4. Night sweats
  5. Malaise
  6. Productive cough >3w
  7. Haemoptysis
  8. Chest pain
  9. Breathlessness
224
Q

What are the signs of TB in the lungs

A
  1. Consolidation
  2. Pleural effusion
  3. Pulmonary collapse
225
Q

How can you diagnose TB?

A
  1. CXR
  2. Sputum culture
  3. Broncoscopy
  4. Histology
  5. Culture
  6. Nucleic acid amplification
  7. Lumbar puncture
  8. Tuberculin skin test - Mantoux
226
Q

What is the treatment for TB?

A
  1. Rifampicin - 6 months
  2. Isoniazid - 6 months
  3. Pyrazinamide - 2 months
  4. Ethambutol - 2 months
227
Q

S/E of rifampicin

A
  1. Red urine
  2. Hepatitis
  3. Drug interactions
228
Q

S/E of isoniazid

A
  1. Hepatitis

2. Neuropathy

229
Q

S/E of pyrazinamide

A
  1. Hepatitis
  2. Arthralgia
  3. Rash
230
Q

S/E of ethambutol

A
  1. Optic neuropathy

Phase 2a Medicine - Hannah's version (9 decks)

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