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Phase 3a Revision > GP > Flashcards

GP Flashcards

1
Q

HTN

What are the types of HTN?

A
  • Primary/essential (95%)
  • Secondary HTN (5%)
  • Malignant HTN
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2
Q

HTN

What are some causes of secondary HTN?

A

ROPE –

  • Renal disease
  • Obesity
  • Pregnancy induced or pre-eclmapsia
  • Endo (Conn’s, Cushing’s, acromegaly, pheochromocytoma)
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3
Q

HTN

What is malignant HTN?

A 
Rapid rise in BP –
- Fibrinoid necrosis
- Retinal haemorrhages
- Papilloedema
- Exudates
Severe HTN ≥180/120
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4
Q

HTN
How might malignant HTN present?
Management?

A
  • Headache ± visual loss, typically younger + black patients

- Same day specialist referral if Sx if not Ix for end-organ damage

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5
Q

HTN

What are some complications of HTN?

A
  • IHD
  • CVA
  • Hypertensive retinopathy + nephropathy
  • Heart failure
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6
Q

HTN
When would you suspect HTN?
How would you diagnose?

A
  • Clinical BP ≥140/90mmHg
  • ABPM to confirm diagnosis of ≥135/85mmHg (excludes white coat HTN >20mmHg rise)
  • 2 measurements/hour during waking hours
  • HBPM if unsuitable
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7
Q

HTN

After a diagnosis of HTN what else would you do?

A
  • QRisk 3 + check for end-organ damage:
    – Urine dipstick (proteinuria + haematuria
    – Fundoscopy for hypertensive retinopathy
    – 12 lead ECG
    – First urine albumin creatinine ratio (ACR)
  • HbA1c, U+Es, creatinine, cholesterol
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8
Q

HTN
In terms of clinical and ABPM/HBPM, how would you diagnose…

i) stage 1 HTN?
ii) stage 2 HTN?
iii) severe HTN?

A

i) ≥140/90 or ≥135/85
ii) ≥160/100 or ≥150/95
iii) ≥180 or ≥110 (clinical)

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9
Q

HTN

What is first line management of HTN?

A
  • Smoking + alcohol cessation
  • Regular exercise
  • Healthy diet, reduce dietary sodium, discourage caffeine
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10
Q

HTN
In terms of medication, what is first line treatment for…

i) 45 + T2DM?
ii) <55y/o?
iii) ≥55y/o?
iv) Afro-Caribbean?

A

i) ACEi or ARB
ii) ACEi or ARB
iii) CCB
iv) CCB

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11
Q

HTN
In terms of HTN medication, what is…

i) step 2?
ii) step 3?
iii) step 4?

A

i) The alternative
ii) Thiazide-like diuretic
iii) Beta-blocker, alpha-blocker, spironolactone if low potassium

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12
Q

HTN
What is an example and mechanism of action of…

i) ACEi?
ii) CCB?
iii) thiazide-like diuretic?
iv) ARB?

A

i) Ramipril, inhibit conversion of angiotensin I>II
ii) Amlodipine, act on L-type Ca2+ channels
iii) Indapamide, locks Na+ reabsorption at DCT by blocking Na+/Cl- symporter
iv) Candesartan, blocks effects of angiotensin II at the AT1 receptor

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13
Q

HTN
What are the side effects of…

i) ACEi?
ii) CCB?
iii) thiazide-like diuretic?
iv) beta-blocker
v) ARB?

A

i) Dry cough + rash (bradykinin), hypotension, hyperkalaemia, AKI (check renal function 1-2w after starting)
ii) Oedema, headache, flushing
iii) Hyponatremia, hypokalaemia + dehydration
iv) Headache, hypotension, erectile dysfunction
v) Hyperkalaemia

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14
Q

HTN
What are the clinical + ABPM/HBPM HTN treatment targets for…

i) <80?
ii) >80?
iii) diabetics?

A

i) <140/90 or <135/85
ii) <150/90 or <145/85
iii) <130/80

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15
Q

ANGINA
What is angina?
What is the pathophysiology?

A
  • Sx of oxygen supply/demand mismatch to the heart

- On exertion, microvascular resistance cannot reduce any more so flow can’t increase to meet metabolic demand

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16
Q

ANGINA

What are the 4 types of angina?

A
  • Stable = induced by effort, relieved by rest or GTN
  • Unstable (ACS) = crescendo, increasing frequency or severity, occurs at rest (higher risk of MI)
  • Decubitus = precipitated by lying flat
  • Prinzmetal = due to coronary artery spasm
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17
Q

ANGINA

What are some causes of angina?

A
  • Atherosclerosis
  • Increased distal resistance (LVH)
  • Reduced oxygen carrying capacity (anaemia)
  • Thrombosis
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18
Q

ANGINA

What are some risk factors for angina?

A
  • Non-modifiable = age, FHx, male

- Modifiable = smoking, obesity, high cholesterol, HTN, DM

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19
Q

ANGINA

How does angina present?

A
  • Constricting or heavy discomfort in chest, jaw, neck, shoulder or arms
  • Sx induced by exertion, relieved within 5m or GTN
  • Dyspnoea, sweating, palpitations may be present
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20
Q

ANGINA

What are some investigations for angina?

A
  • Exercise ECG, HbA1c, lipid profile, TFTs, U+Es

- CT coronary angiography = gold standard

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21
Q

ANGINA

What primary prevention may be offered in angina?

A
  • QRISK3 score >10% = start on statin (or pts with CKD or DM)
  • Lifestyle advice
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22
Q

ANGINA

What is the secondary prevention of angina?

A

4As –

  • Aspirin 75mg OD (+ second antiplatelet like clopidogrel for 12m)
  • Atorvastatin 80mg ON
  • Atenolol (or bisoprolol) titrated to max tolerated
  • ACEi (ramipril) titrated to max tolerated
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23
Q

ANGINA

What short term treatment can be given in angina?

A
  • Glyceryl trinitrate spray for vasodilation

- Take when Sx start, wait 5m, repeat spray, wait 5m > ambulance

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24
Q

ANGINA

What are some long-term symptomatic relievers of angina?

A
  • Beta-blocker (in secondary prevention)
  • CCB (amlodipine)
  • Long-acting nitrates (isosorbide mononitrate)
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25
Q

ANGINA

Ultimately, what 2 treatments may resolve angina?

A
  • Percutaneous coronary intervention (PCI) with coronary angioplasty
  • Coronary artery bypass graft (CABG)
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26
Q

ACS
What is ACS?
What occurs?

A
  • Unstable angina, NSTEMI + STEMI
  • Atheroma ruptures causing platelet aggregation leading to thrombus formation completely occluding artery.
  • Irreversible ischaemia > infarction + necrosis of cells (troponin release) > permanent myocardium damage
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27
Q

ACS

How does an MI present?

A
  • Central crushing chest pain, may radiate to jaw, neck, arm
  • Dyspnoea + palpitations
  • Sweating, N+V
  • Pallor, anxiety
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28
Q

ACS

What are the 2 most important investigations for ACS?

A
  • ECG

- Serial troponins (baseline, 6h, 12h) showing acute rise

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29
Q

ACS
On an ECG, how would the following appear…

i) STEMI?
ii) NSTEMI?

A

i) New LBBB or ST-elevation, hyperacute T waves (T-wave inversion + pathological Q waves occur later)
ii) ST depression + T-wave inversion

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30
Q

ACS
Where on the ECG would indicate the following arteries occlusion…

i) circumflex (lateral)?
ii) right coronary artery (inferior)?
iii) left anterior descending (anterior)?

A

i) I, V5, V6
ii) II, III, aVF
iii) V1–V4

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31
Q

ACS

What other investigations may you consider in ACS?

A
  • ECHO after event to assess functional damage

- CT coronary angiogram to assess for IHD

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32
Q

ACS

What are the complications following ACS?

A

DREAD –

  • Death
  • RUpture of heart septum or papillary muscles
  • oEdema
  • Arrhythmia or Aneurysm
  • Dressler’s syndrome
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33
Q 
ACS
What is Dressler's syndrome?
How does it present?
Investigations?
Management?
A
  • 2-3w post MI autoantibody formation against heart > pericarditis
  • Pleuritic CP, low grade fever, pericardial rub ± effusion
  • ECG = global ST (saddle shaped) elevation + T-wave inversion, raised CRP/ESR
  • NSAIDs or steroids if severe
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34
Q

ACS
What is the pre-hospital management of ACS?
What is the management of STEMI?

A
  • Morphine, Oxygen, Nitrates + Aspirin (300mg)

- Call for primary PCI (≤2h) or thrombolysis (>2h) with streptokinase or alteplase

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35
Q

ACS

What is the management of NSTEMI?

A 
BATMAN
– Beta-blocker
– Aspirin 300mg
– Ticagrelor 180mg
– Morphine
– Anticoagulant (LMWH)
– Nitrates (GTN)
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36
Q

ACS

What is the secondary prevention of ACS?

A 
5As:
– Aspirin 75mg OD
– Another antiplatelet (clopidogrel or ticagrelor for 12m post PCI to prevent thrombus on stent)
– Atorvastatin 80mg ON
– ACEi
– Atenolol (or bisoprolol)
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37
Q

HEART FAILURE

What is heart failure?

A
  • CO insufficient to meet metabolic demands of body + suggests the efficiency of heart as pump is impaired
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38
Q

HEART FAILURE

What compensatory mechanisms are seen in heart failure and what is seen when they decompensate?

A
  • Dilatation > impaired contractility + valve regurg
  • Hypertrophy > myocardial ischaemia
  • RAAS > Na+ + fluid retention > increased venous pressure > oedema
  • Sympathetic activation > increased afterload > decreased CO
  • Natriuretic peptide release (diuretic, hypotensive + vasodilating properties)
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39
Q

HEART FAILURE

What are the two broad categories of heart failure and what do they mean?

A
  • Systolic failure (EF < 40%) = inability of ventricles to contract normally > reduced CO (normal filling volume, less output)
  • Diastolic failure (EF > 50%) = inability of ventricles to relax + fill normally > increased filling pressures
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40
Q

HEART FAILURE

What are the 2 main types of systolic heart failure and what causes them?

A
  • Left ventricular systolic dysfunction (IHD, HTN, structural)
  • Right ventricular systolic dysfunction (secondary to LVSD, cor pulmonale = RHF due to lung disease leading to pulmonary HTN)
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41
Q

HEART FAILURE
What is diastolic failure also referred as and why?
What can cause it?

A
  • Heart failure with preserved ejection fraction = less volume fills + low volume output so ejection fraction higher
  • Cardiac tamponade, cardiomyopathies, pericardial effusion
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42
Q

HEART FAILURE

What is the New york Heart Association classification of heart failure?

A
  • I = no limitation (asymptomatic)
  • II = slight limitation (mild cardiac failure)
  • III = marked limitation (moderate)
  • IV = inability to carry out any physical activity without discomfort (severe)
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43
Q

HEART FAILURE

What are the 3 cardinal symptoms of heart failure?

A
  • Dyspnoea (+ orthopnoea due to pulmonary oedema, lots of pillows)
  • Fatigue
  • Peripheral oedema
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44
Q

HEART FAILURE

What are some classic features of left heart failure?

A
  • Nocturnal cough ± white or pink frothy sputum
  • Paroxysmal nocturnal dyspnoea
  • Cold peripheries
  • Signs = S3 + tachy (gallop), bibasal crackles from pulmonary oedema
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45
Q

HEART FAILURE

What are some classic features of right heart failure?

A
  • Peripheral oedema, ascites, nausea

- Signs = raised JVP, hepatomegaly

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46
Q

HEART FAILURE

What are some investigations for heart failure?

A
  • ABG ?T1 resp failure (hypoxia w/out hypercapnia)
  • N-terminal pro-B-type natriuretic peptide (NT-proBNP)
  • ECG (?arrhythmias which can cause HF like AF)
  • ECHO = diagnostic
  • CXR (ABCDE)
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47
Q

HEART FAILURE
What NT-proBNP values are suspicious for heart failure?
What can falsely raise and decrease NT-proBNP levels?

A
  • > 2000ng/L = urgent referral
  • 400-2000ng/L = raised
  • <400ng/L = unlikely HF
  • Raise = LVH, ischaemia, DM, COPD, sepsis, PE
  • Decrease = obesity, diuretics, ACEi/ARBs, beta-blockers
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48
Q

HEART FAILURE

Why is an ECHO diagnostic?

A
  • Assess function of LV + any structural function

- Can measure ejection fraction (% of blood squeezed out with each ventricular contraction)

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49
Q

HEART FAILURE

What might you see on a CXR in heart failure?

A
  • Alveolar oedema (Bat’s wings)
  • kerley B lines (interstitial oedema)
  • Cardiomegaly
  • Dilated prominent upper lobe vessels
  • pleural Effusion
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50
Q

HEART FAILURE

What is the acute management of heart failure and likely cause?

A
  • Pour SOD (#1 = MI)
    –Pour (stop) any IV fluids (monitor fluid balance)
    – Sit pt upright
    – Oxygen if desaturating
    – Diuretics (IV furosemide 40mg stat to reduce circulating volume
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51
Q

HEART FAILURE

What is the mechanism of action of furosemide?

A
  • Loop diuretic

- Inhibits Na-K-Cl co-transporter in thick ascending limb of loop of Henle to reduce absorption of NaCl

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52
Q

HEART FAILURE

What is the general management of heart failure?

A
  • Yearly flu + PCV
  • HF specialist nurse input
  • Lifestyle changes
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53
Q

HEART FAILURE

What is the first line medical treatment for heart failure?

A
  • ACEi = #1 in those with LVSD to improve prognosis/survival after MI
  • Beta-blockers
  • Loop diuretics (furosemide 40mg PO) for Sx relief or aldosterone antagonist (spironolactone) if Sx not tolerated)
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54
Q

HEART FAILURE

What other methods of management may be considered in heart failure?

A
  • ?Digoxin if all else fails but monitor for toxicity
  • Avoid CCBs like verapamil + diltiazem in HF with reduced ejection fraction
  • Surgical intervention if severe aortic stenosis or mitral regurgitation
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55
Q

ATRIAL FIBRILLATION

What is the pathophysiology of AF?

A
  • Contraction of atria is uncoordinated, rapid + irregular due to disorganised electrical activity overriding SAN
  • AVN struggles to keep up so responds intermittently giving irregular ventricular rhythm
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56
Q

ATRIAL FIBRILLATION

What are some causes of AF?

A
  • Sepsis
  • Mitral valve (stenosis/regurg)
  • IHD
  • Thyrotoxicosis
  • HTN
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57
Q

ATRIAL FIBRILLATION

What is the clinical presentation of AF?

A
  • Palpitations, dyspnoea, syncope, CP

- Irregularly irregular pulse

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58
Q

ATRIAL FIBRILLATION
What is paroxysmal AF?
Management?

A
  • Comes/goes in episodes, usually <48h (up to 7d)
  • Anticoagulate based on CHADSVASC, may use “pill in the pockeT” with flecainide if infrequent episodes + no underlying structural heart disease
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59
Q

ATRIAL FIBRILLATION

What does the ECG in atrial fibrillation look like?

A
  • Absent P waves
  • Irregularly irregular ventricular rhythm
  • Narrow QRS complex tachycardia
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60
Q

ATRIAL FIBRILLATION
What is the main complication of AF?
Management?

A
  • Embolic stroke due to stagnation of blood in atria due to ineffective mechanical action of atria
  • Calculate CHADSVASC score + ≥2 = anticoagulate
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61
Q

ATRIAL FIBRILLATION

How can you control the rate in AF?

A
  • Beta-blocker first line
  • Rate-limiting CCB
  • Digoxin only if they fail
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62
Q

ATRIAL FIBRILLATION
How would you control the rhythm acutely?
What can be used?

A
  • Immediate cardioversion if AF <48h + haemodynamically unstable
  • Elective cardioversion if AF present >48h + stable
  • Pharma = flecainide or amiodarone if structural heart disease
  • Electrical = sedation or GA using cardiac defib
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63
Q

ATRIAL FIBRILLATION

What other treatment can be used in AF?

A
  • Catheter ablation if not responded or wish to avoid antiarrhythmic meds, must be anticoagulated 4w before
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64
Q

ATRIAL FIBRILLATION
What should you use for anticoagulation in AF?
Which is better?

A
  • Warfarin (vit K antagonist) or DOACs such as apixaban, rivaroxaban (factor Xa inhibitors)
  • DOACs = no INR monitoring, no major interactions, equal effect but no reversal
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65
Q

OTITIS EXTERNA
What is otitis externa?
What is it associated with?

A
  • Inflammation of external ear canal

- Swimmer’s ear as associated with frequent swimming

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66
Q

OTITIS EXTERNA

What is malignant otitis externa?

A
  • Immunocompromised, DM or elderly where it can spread to the surrounding bones (mastoid + temporal)
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67
Q

OTITIS EXTERNA

What are some causes of otitis externa?

A
  • Infection (staph. aureus, pseudomonas aeruginosa or fungal)
  • Seborrhoeic dermatitis
  • Contact dermatitis (allergic + irritant)
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68
Q

OTITIS EXTERNA

What is the clinical presentation of otitis externa?

A
  • Ear pain (mild), itchy + discharge common, ?hearing loss

- Otoscopy = red, swollen or eczematous canal

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69
Q

OTITIS EXTERNA

What is the management of otitis externa?

A
  • May need to clean ear canal first with syringing or irrigation
  • Topical Abx or a combined topical Abx with steroid = 1st line
  • PO flucloxacillin if infection spreading, swab before
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70
Q

COPD
What are the two diseases that make up COPD?
What is the main cause of COPD?

A
  • Pink puffers = emphysema
  • Blue bloaters = chronic bronchitis
  • Smoking (alpha-1-antitrypsin is a major protease inhibitor that can be inactivated by smoke)
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71
Q

COPD

What causes emphysema?

A
  • Alveoli lose elastic recoil > air trapping after exhalation
  • Unable to oxygenate so hyperventilate (puffing), no cyanosis
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72
Q

COPD

What causes chronic bronchitis?

A
  • Bronchoconstriction = less oxygen enters alveoli, less carbon dioxide leaves so V/Q mismatch + hypoxia leads to cyanosis
  • Capillaries compensate + vasoconstrict to shunt blood to better ventilated alveoli > pulmonary HTN > RHF > cor pulmonale
  • Cyanotic but not breathless
  • Resp centres insensitive to carbon dioxide so rely on hypoxic drive
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73
Q

COPD
What are the 3 typical signs of COPD?
What are some other signs?

A
  • Chronic cough, sputum (often clear white), dyspnoea

- Pursed lip breathing, tachypnoea, hyperinflated barrel chest, cachexic

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74
Q

COPD

How is COPD classified into stages?

A
  • 1 = mild (FEV1 ≥80% predicted)
  • 2 = mod (FEV1 50–79% predicted)
  • 3 = severe (FEV1 30–49% predicted)
  • 4 = very severe (FEV1 <30% predicted)
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75
Q

COPD

What are some investigations for COPD?

A
  • ECG = ?P pulmonale
  • FBC to exclude secondary polycythaemia
  • Spirometry = obstructive pattern (FEV1/FVC <0.7 with FEV1 ≤80%) and no post-bronchodilator reversibility
  • CXR = hyperinflation, flat hemidiaphragm, bullae
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76
Q

COPD

What is the conservative management of COPD?

A
  • Smoking cessation
  • Annual flu vaccine
  • One off PCV
  • Pulmonary rehab (exercise, nutrition, breathing exercises)
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77
Q

COPD

What are steps 1 and 2 of the COPD management?

A
  • 1 = SABA or SAMA
  • 2:
    – FEV1>50% = LABA and/or LAMA
    – FEV1 <50% LABA + ICS and/or LAMA (also offered in those with asthma/atopic features)
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78
Q

COPD
What is step 3 of COPD management?
Any other management?

A
  • FEV1>50% = LABA + ICS or same as FEV1<50%
  • FEV1<50% = LAMA + LABA/ICS combination (FOstair)
  • Consider PO theophylline or mucolytics like carbocysteine
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79
Q

COPD
What is the mechanism of action of LAMA?
Give an example
What about SAMA?

A
  • Block ACh receptors which are stimulated by parasympathetic nervous system causing bronchial smooth muscle contraction so overall effect is bronchodilation (Tiotropium)
  • Same but shorter action, ipratropium
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80
Q

COPD
When would you consider long-term oxygen therapy?
When is it contraindicated?

A
  • 2 separate ABGs showing PaO2 <7.3kPa or paO2 7.3–8 with pulmonary HTN or polycythaemia or peripheral oedema
  • Smokers as fire hazard
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81
Q

COPD
What is an acute exacerbation of COPD?
What is the most common cause?

A
  • Acute worsening of Sx such as cough, dyspnoea, wheeze + sputum (?purulent)
  • Haemophilus influenzae (#1), strep. pneumoniae, Moraxella catarrhalis
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82
Q

COPD

What are some investigations for acute exacerbation of COPD?

A
  • FBC (raised WCC), CRP, ?blood cultures if septic
  • Sputum MC&S
  • CXR may show consolidation
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83
Q

COPD

What is the management of an acute exacerbation of COPD?

A
  • Oxygen therapy for SpO2 88–92% via venturi mask 24-28%
  • Nebulised salbutamol + ipratropium
  • PO prednisolone for 1-2w
  • Abx if infection
  • Consiver NIV (BiPAP) or intubation + ventilation with ICU admission
84
Q

PNEUMONIA

What are the 3 classifications of pneumonia?

A
  • Community-acquired = develops outside hospital
  • Hospital acquired = develops >48h after hospital admission
  • Aspiration = acute aspiration of gastric contents (stroke, MG, MS, MND)
85
Q

PNEUMONIA

What are the most common causes of CAP?

A
  • Strep. pneumoniae #1
  • Haemophilus influenzae
  • Moraxella catarrhalis
86
Q

PNEUMONIA

What are the most common causes of HAP?

A
  • S. aureus
  • Klebsiella pneumoniae
  • Pseudomonas aeruginosa
87
Q

PNEUMONIA

What are some atypical pneumoniaes?

A
  • Mycoplasma pneumoniae (erythema multiforme, neuro Sx in younger, atypical chest/XR findings)
  • Chlamydophila pneumoniae (school aged child)
  • Legionella pneumophila (infected water supplies + air con, can cause hyponatraemia > SIADH
88
Q

PNEUMONIA
What is a cause of fungal pneumonia?
How does it present?
Management?

A
  • Pneumocystis jiroveci pneumonia (PCP) in immunocompromised
  • Dry cough, SOB on exertion, night sweats
  • Co-trimoxazole
89
Q

PNEUMONIA

What are some risk factors for pneumonia?

A
  • Elderly + infants
  • Comorbidities = DM, COPD, bronchiectasis
  • Smokers, alcoholics
  • Immunocompromised + nursing home residents
90
Q

PNEUMONIA
What are the…

i) symptoms
ii) signs
iii) exam findings

in pnuemonia?

A

i) Dyspnoea, cough with purulent sputum (dry in atypicals), fever
ii) Pyrexia, tachypnoea, tachycardia
iii) Bronchial breath sounds, focal coarse crackles, dullness to percuss

91
Q

PNEUMONIA

What are some investigations for pneumonia?

A
  • FBC (neutrophilia, raised WCC)
  • CRP, U+Es, ABG
  • Sputum MC&S + blood cultures
  • Pneumococcal + legionella urinary antigen tests
  • CXR = consolidation
92
Q

PNEUMONIA
What score can be used to assess severity of CAP?
How does this guide your management?

A
  • Confusion
  • Urea >7mmol/L
  • RR ≥30/min
  • BP <90 or 60
  • 65 ≤ age
  • 0-1 = PO amoxicillin in community
  • 2 = PO amoxicillin + clarithromycin in hospital
  • ≥3 = severe IV co-amoxiclav + clarithromycin ?ICU
93
Q

PNEUMONIA

What is the general management for pneumonia?

A
  • Oxygen therapy
  • IV fluids
  • PCV vaccine in children
  • Flu vaccine if ≥65y, immunocompromised or medical co-morbidities
  • Smoking cessation
94
Q

PNEUMONIA
What typical antibiotics might you use in…

i) HAP?
ii) aspiration?
iii) atypicals?

A

i) Aminoglycoside like gentamycin + cephalosporin
ii) IV cephalosporin + metronidazole to cover gut anaerobes
iii) Macrolides (clarithromycin), fluoroquines (levofloxacin) + tetracyclines (doxycycline)

95
Q

LUNG CARCINOMA

What are the 2 broad categories of lung cancer?

A 
- Non-small cell lung carcinoma (NSCLC)
–Squamous = Smokers
– Adenocarcinoma = non-smokers, asbestos
– Large cell (poorly differentiated)
- Small cell lung carcinoma
96
Q

LUNG CARCINOMA

What can happen in SCLC?

A
  • Arise from Kulchitsky (endocrine) cells so can cause paraneoplastic syndromes like SIADH (think low sodium), Cushing’s, Lambert-Eaton myasthenic syndrome
97
Q

LUNG CARCINOMA
In terms of lung cancer, what are some…

i) symptoms?
ii) signs?
iii) signs of mets?

A

i) Cough + haemoptysis, CP, dyspnoea, weight loss, night sweats, recurrent pneumonia
ii) Finger clubbing, lymphadenopathy (supraclavicular)
iii) Bone tenderness, hepatomegaly, neurology (seizures, headache)

98
Q

LUNG CARCINOMA

What are some investigations for lung cancer?

A
  • CXR first line (opacity, hilar enlargement, effusion, collapse)
  • CT CAP for staging or if CXR clear
  • Bronchoscopy with EBUS + biopsy
99
Q

LUNG CARCINOMA

What are some complications from lung carcinoma?

A
  • L recurrent laryngeal nerve = hoarse voice
  • Phrenic nerve = diaphragm weakness + dyspnoea
  • SVC obstruction = facial swelling, distended veins in neck + upper chest
  • Brachial plexus = shoulder pain
  • Sympathetic ganglion = Horner’s (miosis, anhidrosis + ptosis often Pancoast)
100
Q

LUNG CARCINOMA

Complication of squamous cell carcinoma?

A
  • Hypercalcaemia from ectopic PTH-rP = primary hyperparathyroidism
101
Q

LUNG CARCINOMA

What is the management of lung cancer?

A
  • NSCLC = lobectomy if isolated, radio/chemo
  • SCLC = chemo ± radio
  • Supportive = analgesia, anti-emetics, ?tracheal stenting if bronchial obstruction
102
Q

T2DM

What is the pathophysiology of T2DM?

A
  • Repeated exposure to glucose + insulin = resistance to effects of insulin so more required for a response
  • Beta cells fatigued + damaged so produce less
  • Low insulin + peripheral insulin resistance = impaired glucose tolerance
103
Q

T2DM
What are some causes of T2DM?
How does it present?

A
  • Genetics + environment (FHx, obesity, poor diet)
  • Asian, men, older age
  • No Sx but sometimes polyuria, polydipsia, lethargy, visual blurring
104
Q

T2DM

What values are diagnostic for T2DM?

A 
- HbA1c ≥48mmol/mol Dx
1 result if Sx, 2 separate if none:
- Random glucose ≥11.1mmol/L
- Fasting glucose ≥7mmol/L
- OGTT 2h ≥11.1mmol/L
105
Q

T2DM
What values suggest…

i) impaired fasting glucose?
ii) impaired glucose tolerance?

A

i) 6.1-6.9mmol/L

ii) 7.8-11.1mmol/L

106
Q

T2DM

What is a main complication of uncontrolled T2DM?

A
  • Hyperglycaemic hyperosmolar state
  • Decrease insulin = increase serum glucose + serum osmolality + urination but no ketosis as still some endogenous insulin
107
Q

T2DM
How does HHS present?
How is it diagnosed?
Management?

A
  • Marked dehydration (polydipsia, polyuria, hypovolaemia) + impaired consciousness
  • Plasma glucose >30mmol/L, plasma osmolality >320mOsm
  • IV fluid replacement, infuse insulin, LMWH prophylaxis as hyperviscous blood
108
Q

T2DM
What is the first line management of T2DM?
What are the HbA1c targets in T2DM?

A
  • Lifestyle advice = exercise, less carbs/fat, smoking cessation
  • <48mmol/mol for new pts or <53 if on ≥2 Tx
109
Q

T2DM

List 6 medications that can be used in T2DM

A
  • Metformin (biguanide, first line)
  • Gliclazide (sulfonylurea)
  • Sitagliptin (DPP4 inhibitor)
  • Empagliflozin (SGLT)
  • Glitazone (pioglitazone)
  • GLP-1 mimetics
110
Q

T2DM
What is the mechanism of action of…

i) metformin?
ii) gliclazide?
iii) sitagliptin?

A

i) Increased insulin sensitivity, reduced gluconeogenesis in liver + helps weight
ii) Stimulates beta cells to secrete insulin
iii) Increases incretin levels which inhibit glucagon production

111
Q

T2DM
What is the mechanism of action of…

i) empagliflozin?
ii) glitazone?
iii) GLP-1 mimetics?

A

i) Blocks glucose reabsorption in PCT of kidneys + promotes excretion of excess glucose in urine
ii) Increases insulin sensitivity + decreases liver production of glucose
iii) Incretin (GLP-1) mimetic inhibits glucagon secretion (after triple therapy)

112
Q

T2DM
What are some side effects of…

i) metformin?
ii) gliclazide?
iii) sitagliptin?
iv) empagliflozin?
v) glitazone?
vi) GLP-1 mimetics?

A

i) GI upset (D+V, abdo pain), lactic acidosis
ii) Hypoglycaemia + weight gain
iii) GI upset, pancreatitis
iv) Glucosuria, weight loss + UTI risk
v) Weight gain, fluid retention, heart failure
vi) Weight loss, N+V, pancreatitis

113
Q

HYPERTHYROIDISM

What are the 3 mechanisms explaining the causes of hyperthyroidism?

A
  • Overproduction of thyroid hormone
  • Leakage of pre-formed hormone from thyroid
  • Ingestion of excess thyroid hormone
114
Q

HYPERTHYROIDISM
What is the most common cause of hyperthyroidism?
What is the pathophysiology?

A
  • Graves’ disease
  • Autoimmune induced excess production of thyroid hormone, esp T3
  • TSH receptor stimulating antibody (TRAb, IgG), autoimmune link to T1DM, coeliac, Addison’s
115
Q

HYPERTHYROIDISM

What are some other causes of hyperthyroidism?

A
  • Toxic multinodular goitre = nodules secrete excess thyroid hormones (elderly women)
  • Toxic adenoma = solitary nodule producing T3/4
  • DeQuervain’s thyroiditis = acute inflammation
  • Exogenous iodine (food, amiodarone)
116
Q

HYPERTHYROIDISM

What are the general signs and symptoms of hyperthyroidism?

A
  • Anxiety, irritability
  • Sweating, palpitations (?AF), tremor, tachycardia
  • Heat intolerance
  • Weight loss, increased appetite, diarrhoea
  • Oligomenorrhoea
  • Thin hair, warm skin
117
Q

HYPERTHYROIDISM

What are the Graves’ disease specific features?

A
  • Diplopia, ophthalmoplegia, increased tears
  • Exophthalmos, lid lag + retraction
  • Thyroid acropachy (clubbing, painful digits)
  • Pretibial myxoedema
118
Q

HYPERTHYROIDISM

How would De Quervain’s thyroiditis present?

A
  • PAIN in de QuerVAIN = tender goitre, fever, dysphagia (viral infection)
  • Hyperthyroid phase > hypothyroid phase (TSH falls due to -ve feedback)
119
Q

HYPERTHYROIDISM

What are some investigations for hyperthyroidism?

A
  • TFTs (primary = low TSH, high T3/4, secondary = high TSH, high T3/4 hypothalamus or pituitary pathology)
  • Thyroid autoantibodies
  • Isotope scan
120
Q

HYPERTHYROIDISM
What is a complication of hyperthyroidism?
Management?

A
  • More severe presentation with pyrexia, tachycardia + delusion
  • Admission, supportive (fluid resus), beta-blockers, ?anti-arrhythmic
121
Q

HYPERTHYROIDISM

What is the management of hyperthyroidism?

A
  • Beta-blockers for rapid sympathetic control (propranolol)
  • Carbimazole 1st line, propylthiouracil 2nd
  • Radioiodine therapy
  • Surgical thyroidectomy
  • NSAIDs + beta-blockers for self-limiting DeQuervain’s
122
Q

HYPERTHYROIDISM
What are the 2 methods for administering anti-thyroid drugs?
What are side effects of them?

A
  • Titration
  • Block + replace (block all production + take levothyroxine)
  • Carbimazole = agranulocytosis
  • Propylthiouracil = severe hepatic reactions
123
Q

HYPERTHYROIDISM
What are some risks with…

i) radioiodine therapy?
ii) surgical thyroidectomy?

A

i) C/I in pregnancy, breastfeeding + may leave patient hypothyroid
ii) Risk to recurrent laryngeal nerve (hoarse voice) + hypoparathyroidism

124
Q

HYPOTHYROIDISM

What are some common causes of hypothyroidism?

A
  • Primary autoimmune (atrophic thyroiditis, Hashimoto’s thyroiditis)
  • Iodine deficiency (#1 worldwide)
  • Secondary to carbimazole, radioactive iodine, thyroidectomy, lithium + amiodarone
  • Central causes like hypopituitarism (Sheehan’s, tumours, radiation)
125
Q

HYPOTHYROIDISM
What is…

i) atrophic thyroiditis?
ii) Hashimoto’s thyroiditis?

A

i) Diffuse lymphocytic infiltration of thyroid leading to atrophy + so no goitre
ii) Goitre due to lymphocytic + plasma cell infiltration, #1 cause in developed world

126
Q

HYPOTHYROIDISM

What are some symptoms of hypothyroidism?

A
  • Weight gain, decreased appetite + constipation
  • Cold intolerance
  • Lethargy, menorrhagia
127
Q

HYPOTHYROIDISM

What are some signs of hypothyroidism?

A

BRADYCARDIC

  • Bradycardia
  • Reflexes relax slowly
  • Ataxia
  • Dry, thin hair/skin
  • Yawning
  • Cold hands
  • Ascites
  • Round puffy face
  • Defeated demeanour
  • Immobile
  • CHF
128
Q

HYPOTHYROIDISM

What are some investigations for hypothyroidism?

A
  • TFTs = primary (high TSH, low T3/4), secondary (low TSH, low T3/4)
  • Thyroid peroxidase antibody (TPO-Ab) + anti-thyroglobulin in Hashimoto’s
  • Anti-TSH positive + TPO in atrophic thyroiditis
129
Q

HYPOTHYROIDISM
What is the management of hypothyroidism?
Prescribing information?

A
  • Lifelong levothyroxine to replace (titrate up)
  • 30m before breakfast as iron decreases absorption of thyroxine
  • Repeat TFTs monthly until stable
130
Q

CONSTIPATION
What is constipation?
What are some causes?

A
  • Infrequent bowel movements (<3/w) or with straining

- Obstruction, hypothyroid, neuro (MS, cauda equina), dehydration, IBS

131
Q

CONSTIPATION

What is the management of constipation?

A
  • Hydration + increased fibre
  • Bulking agents = increased faecal mass + peristalsis (ispaghula husk)
  • Osmotic = retain fluid in bowel (lactulose)
  • Stimulant = increased intestinal motility (Senna)
  • Phosphate enemas
132
Q

GORD
What is GORD?
Risk factors?

A
  • Regurg acidic gastric contents into lower oesophagus injuring squamous epithelium
  • Obesity + pregnancy, smoking, alcohol, caffeine, hiatus hernia
133
Q

GORD

What are the clinical features or GORD?

A
  • Heartburn (oesophagitis) can be retrosternal/epigastric (worse after meals or lying down)
  • Acid regurg
  • Dysphagia/odynophagia
  • Nocturnal cough (aspiration)
134
Q

GORD

What are some investigations for GORD and when would you do them?

A
  • OGD if new onset ≥55y or weight loss, melaena, haematemesis etc.
  • 24h oesophageal pH monitoring
135
Q

GORD

What are some complications of GORD?

A
  • Benign stricture > dysphagia
  • Oesophageal adenocarcinoma
  • Barrett’s oesophagus = metaplasia squamous?columnar may lead to dysplasia to adenocarcinoma
136
Q

GORD

What is the general management of GORD?

A
  • Reduce caffeine + alcohol, weight loss, stop smoking, smaller meals
  • PRN OTC antacids like Gaviscon or Rennie
137
Q

GORD

What treatments can be given for GORD?

A
  • PPI like omeprazole
  • H2 antagonists like ranitidine
  • Laparoscopic fundoplication to narrow lower oesophageal sphincter last line
138
Q

DIVERTICULAR DISEASE
What is…

i) diverticulum?
ii) diverticulosis?
iii) diverticular disease?
iv) diverticulitis?

A

i) Pouch of colonic mucosa herniating through muscularis propria lying in the thin subserosa fat
ii) Presence of diverticula but asymptomatic
iii) Implies symptomatic diverticula
iv) Inflammation of a diverticulum

139
Q

DIVERTICULAR DISEASE

What causes a diverticulum?

A
  • High intraluminal pressures force mucosa to herniate through muscle layers of gut at weak points (adjacent to penetrating vessels)
140
Q

DIVERTICULAR DISEASE
What can cause high intraluminal pressures?
How does it present?

A
  • Low fibre, sigmoid colon as smallest diameter

- >60y, asymptomatic or LIF pain, altered bowel habit, fever, bleeding

141
Q

DIVERTICULAR DISEASE
What causes diverticulitis?
How does it present?

A
  • Trapped faeces

- #1 = descending colon, LIF pain, fever, tachycardia, ?intestinal obstruction

142
Q

DIVERTICULAR DISEASE
Investigations for diverticulitis?
Management?

A
  • Bloods, FBC (WCC raised), ESR/CRP, tender colon ± peritonism
  • Mild = bowel rest ± Abx if severe = analgesia, NBM, IV fluids + Abx, surgery if peritonitis
143
Q

DIVERTICULAR DISEASE
Investigations for diverticular disease?
Management?

A
  • Erect CXR (?perf), AXR, contrast CT, incidental finding at colonoscopy
  • Antispasmodics like Buscopan, Hartmann’s if perforation or obstruction
144
Q

COLORECTAL CANCER
What are some causes of colorectal cancer?
Risk factors?

A
  • Hereditary nonpolyposis colorectal cancer #1 = AD
  • Familial adenomatous polyposis (FAP) = AD
  • Peutz-Jeghers syndrome = AD
  • Red + processed meat, alcohol, smoking, IBD
145
Q

COLORECTAL CANCER
What are some features of…

i) FAP?
ii) HNPCC?
iii) Peutz-Jeghers?

A

i) >100 polyps as teenager, 100% lifetime risk
ii) Accelerated progression of adenoma > carcinoma as no DNA repair proteins
iii) Mucocutaneous hyperpigmentation (macules on palms + buccal mucosa), multiple GI hamartomatous polyps

146
Q

COLORECTAL CANCER

What is the clinical presentation of colorectal cancer?

A 
Majority L sided:
- PR bleed/mucus, altered bowel habit, obstruction
R sided + caecum:
- Weight loss, Fe anaemia
RectumL
- Fresh blood, mass, tenesmus
147
Q

COLORECTAL CANCER

Investigations for colorectal cancer?

A
  • FBC (Fe anaemia)
  • Faecal occult blood screening 2y 60–74
  • Colonoscopy + biopsy
  • CT CAP for Duke’s staging
148
Q

COLORECTAL CANCER
In terms of colorectal cancer management…

i) prevention?
ii) adenoma?
iii) colorectal adenocarcinoma?

A

i) ?NSAIDs prevent adenomas
ii) Endoscopic resection ideally end-end anastomosis
iii) Surgical resection if no spread, chemo + palliative care if metastatic

149
Q

COLORECTAL CANCER

What is Duke’s staging in colorectal cancer?

A
  • A = bowel mucosa
  • B = extends through bowel wall
  • C = regional LNs
  • D = distant mets
150
Q

GALLSTONES
What causes gallstones?
Risk factors?

A
  • Imbalance between cholesterol + bile salts (75% mixed, 20% large yellow cholesterol, 5% bilirubinate)
  • Fat, Female, Forty, Fertile
  • Crohn’s as malabsorption of bile salts from terminal ileum
  • Haemolytic anaemias as increased bilirubin > bilirubinate stones
151
Q

GALLSTONES

What is the clinical presentation of gallstones?

A
  • Severe RUQ may radiate to tip of scapula
  • N+V
  • May be triggered by heavy, fatty meal
152
Q

GALLSTONES

Management of gallstones?

A
  • FBC, U+Es, amylase, LFTs (ALP + bilirubin raised in attacks)
  • USS shows dilated ducts (MRCP if case)
  • Conservative (analgesia + fluids) with elective lap chole
153
Q

ACUTE CHOLECYSTITIS

What is acute cholecystitis?

A
  • Inflammation of gallbladder following impaction of stone in cystic duct or neck of gallbladder obstruction bile emptying > damage to mucosal lining
154
Q

ACUTE CHOLECYSTITIS

What is the clinical presentation of acute cholecystitis?

A
  • RUQ pain radiating to tip of scapula
  • FEVER (differentiates from biliary colic), N+V
  • Murphy’s sign = tenderness worse on inspiration with 2 fingers on RUQ
  • NO jaundice (differentiates from ascending cholecystitis)
155
Q

ACUTE CHOLECYSTITIS

Investigations for acute cholecystitis?

A
  • FBC (raised WCC), LFTs,
  • USS shows gallstones + distended gallbladder with thickened wall
  • Sonographic murphy’s
156
Q

ACUTE CHOLECYSTITIS

Management of acute cholecystitis?

A
  • Conservative = NBM, IV fluids, pain relief, IV Abx

- Lap chole

157
Q

OSTEOARTHRITIS

What is osteoarthritis?

A
  • Non-inflammatory wear + tear arthritis
  • Destruction of articular cartilage makes exposed subchondral bone sclerotic > increases vascularity + subchondral cysts form where repair produces cartilaginous growth from chondrocytes which calify (osteophytes)
158
Q

OSTEOARTHRITIS
What causes osteoarthritis?
Risk factors?

A
  • Secondary OA can occur in joints due to congenital disease + damage
  • Obesity, increasing age, trauma, female, FHx, occupation (manual labour)
159
Q

OSTEOARTHRITIS

What are the main symptoms of osteoarthritis?

A
  • Morning stiffness <30m
  • Stiffness after rest (gelling)
  • Bony swellings/joint deformities
  • Reduced ROM, weak grip + reduced functioning
160
Q

OSTEOARTHRITIS

What bony swellings may be seen in osteoarthritis?

A
  • Distal IPJ = Heberden’s nodes
  • Proximal IPJ = Bouchard’s nodes
  • Squaring at base of thumb at carpometacarpal joint (saddle joint used in many activities so prone to wearing)
161
Q

OSTEOARTHRITIS

What joints may be affected in osteoarthritis?

A
  • Hips, knees, sacroiliac joints, MCP joint at base of thumb (squaring), wrist, cervical spine
162
Q

OSTEOARTHRITIS

What would plain radiograph show in osteoarthritis?

A

LOSS –

  • Loss of joint space
  • Osteophytes
  • Subarticular sclerosis (increased density of bone along joint line)
  • Subchondral cysts (fluid filled holes in the bone)
163
Q

OSTEOARTHRITIS

What is the conservative management of osteoarthritis?

A
  • Education
  • Lifestyle (weight loss)
  • Physio to improve strength
  • Orthotics to support activities + function (walking aids)
164
Q

OSTEOARTHRITIS

What medical treatment may be given for osteoarthritis?

A
  • Regular PO + topical NSAIDs
  • PO NSAIDs (?+PPI) for intermittent use
  • ?Opiates like codeine + morphine
  • Intra-articular steroid injections to reduce inflammation
165
Q

OSTEOARTHRITIS

What surgery may be offered in osteoarthritis?

A
  • Arthroscopy for loose bodies (can cause locking e.g. knee)
  • Osteotomy (changing bone length)
  • Arthroplasty (joint replacement, risk of infection)
  • Fusion (often ankle + foot)
166
Q

GOUT
What is gout?
Pathophysiology?

A
  • Inflammatory arthritis due to hyperuricaemia + intra-articular monosodium urate crystals
  • Urate derived from breakdown of purines (adenine + guanine)
167
Q

GOUT
What are some causes of gout?
Who is it most common in?

A
  • Increased uric acid production = chemo, pyrazinamide
  • Decreased uric acid excretion = diuretics, renal impairment, alcohol excess
  • Older men
168
Q

GOUT
What are some risk factors for gout?
What are some factors that may precipitate an attack?

A
  • Alcohol, high purine diet (red meat + seafood), cell damage + Death (surgery, chemo)
  • Dietary excess, diuretics, dehydration, sepsis
169
Q

GOUT

How does gout present?

A
  • Acute hot, swollen + painful joints (exclude septic)

- Wrists, base of thumb (carpometacarpal joint) + metatarsophalangeal joint of big toe

170
Q

GOUT

What are some signs of gout?

A
  • Chronic tophaceous gout = tophi (s/c deposits of urate crystals in skin + joints, often small joints of hands, elbows, ear)
  • Chronic polyarticular gout = painful erythematous swelling
171
Q

GOUT

What investigations would you do for gout?

A
  • Serum urate elevated
  • Joint fluid aspiration MC&S = no bacteria, Needle shaped crystals with Negative birefringent under polarised light
  • XR = joint space maintained, lytic bone lesions, punched out erosions
172
Q

GOUT
What is the management for gout for…

i) an acute flare?
ii) long-term prophylaxis?

A

i) NSAIDs like ibuprofen first line (unless C/I), colchicine second line (inhibits mitosis but SEs of diarrhoea), steroids last
ii) Allopurinol (xanthine oxidase inhibitor but start after acute attack settled in about 2w)

173
Q

PSEUDOGOUT
What is pseudogout?
What is it associated with?

A
  • Microcrystal synovitis due to deposits of calcium pyrophosphate crystals
  • Hyperparathyroid, hypothyroid, haemochromatosis, hypophosphataemia
174
Q

PSEUDOGOUT

How does pseudogout present?

A
  • Acute hot, swollen + stiff joints

- Monoarthropathy affecting shoulders, wrists + knees

175
Q

PSEUDOGOUT

What are the investigations for pseudogout?

A
  • Joint fluid aspiration MC&S = no bacteria, Rhomboid shaped crystals with Positive birefringent under polarised light
  • XR = may show soft tissue calcium deposition (chondrocalcinosis) = thin white line in middle of joint space
176
Q

PSEUDOGOUT

What is the management of pseudogout?

A
  • NSAIDs, colchicine
  • Intra-articular steroids or PO
  • Joint aspiration of arthrocentesis if severe
177
Q

PMR
What is polymyalgia rheumatica (PMR)?
Associations?

A
  • Inflammatory condition (vasculitis) causing pain + stiffness in shoulder, pelvic girdle + neck
  • GCA
178
Q

PMR

What is the clinical presentation of PMR

A
  • Bilateral shoulder pain, may radiate to elbow
  • Bilateral pelvic girdle pain
  • Worse with movement + sleep interference
  • Morning stiffness ≥45m
  • Systemic Sx = weight loss, fatigue, low grade fever
179
Q

PMR

What is the management of PMR?

A
  • ESR/CRP raised, CK normal

- PO prednisolone shows dramatic response (diagnostic)

180
Q

B12/PERNICIOUS ANAEMIA

What is the pathophysiology of B12 deficiency?

A
  • Absorption of B12 in terminal ileum + intrinsic factor (via gastric parietal cells) dependent for transport across intestinal mucosa
181
Q

B12/PERNICIOUS ANAEMIA

What are some causes of B12 deficiecny?

A
  • Autoimmune (pernicious) = atrophic gastritis leading to destruction of parietal cells in stomach > less intrinsic factor + B12 deficiency (associated with other autoimmune)
  • Malabsorption = Crohn’s, coelaic
  • Dietary (vegans)
182
Q

B12/PERNICIOUS ANAEMIA

What are the B12 specific features of the anaemia?

A
  • Peripheral neuropathy with numbness or paraesthesia
  • Loss of vibration sense or proprioception
  • Visual, mood or cognitive changes
  • Glossitis = beefy-red sore tongue
183
Q

B12/PERNICIOUS ANAEMIA

Investigations for B12/pernicious anaemia?

A
  • FBC (MCV>100fL, low Hb)
  • Serum B12 decreased
  • Blood film = hypersegmented neutrophil nuclei
  • Intrinsic factor Ab for pernicious (gastric parietal cell Ab can be tested by less helpful)
184
Q

B12/PERNICIOUS ANAEMIA

What is the management of B12/pernicious anaemia?

A
  • PO B12 (cyanocobalamin) if dietary origin
  • IM hydroxocobalamin if pernicious
  • Do NOT give folate as can cause subacute combined degeneration of cord = distal sensory loss, ataxia + mixed UMN/LMN signs
185
Q

AOCD

What are some mechanisms in anaemia of chronic disease (AOCD)?

A
  • Decreased release of iron from bone marrow to developing erythroblasts
  • Inadequate erythropoietin response to anaemia
  • High levels of hepcidin expression (reduces iron transport from duodenal cells to plasma)
186
Q

AOCD

What are some causes of AOCD?

A
  • Chronic inflammatory diseases = Crohn’s, RA)
  • Chronic infections (TB)
  • Malignancy
  • TB
187
Q

AOCD

What is the management of AOCD?

A
  • FBC (low Hb)
  • Blood film = normochromic normocytic
  • Low serum iron, transferrin saturation + TIBC
  • High ferritin
  • Treat underlying cause, sometimes recombinant erythropoietin
188
Q

CLL

What is chronic lymphocytic leukaemia (CLL)?

A
  • Monoclonal proliferation of well differentiated lymphocytes, 99% B cells
  • # 1 leukaemia in adults
189
Q

CLL

What are some complications of CLL?

A
  • Warm autoimmune haemolysis > anaemia
  • Infection (hypogammaglobulinaemia)
  • Richter’s transformation = high-grade (large B cell) lymphoma
190
Q

CLL

What is the clinical presentation of CLL

A
  • Incidental finding on FBC
  • Signs of bone marrow failure – low Hb = anaemia, low WCC = infections, thrombocytopenia = bruising
  • Weight loss, sweats + anorexia
  • Hepatosplenomegaly, rubbery non-tender lymphadenopathy
191
Q

CLL

What are some investigations for CLL?

A
  • FBC = pancytopenia
  • Blood film = smudge or smear cells
  • LDH may be raised
  • Bone marrow biopsy is diagnostic
  • CT CAP to stage
192
Q

CLL

What is the management of CLL?

A
  • No sx = watch + wait
  • Chemo + radio to help lymphadenopathy + splenomegaly
  • Bone marrow transplant
193
Q

MYELODYSPLASTIC
What is myelodysplastic syndrome?
Risk?

A
  • Immature blood cells in bone marrow do not mature properly + so do not become healthy blood cells
  • Transform to AML
194
Q

MYELODYSPLASTIC

How might myelodysplastic syndrome present?

A
  • > 60y + previous chemo or radiotherapy
  • ?Incidental finding
  • Signs of bone marrow failure – low Hb = anaemia, low WCC = infections, thrombocytopenia = bruising
195
Q

MYELODYSPLASTIC

Investigations for myelodysplastic syndrome?

A
  • FBC = pancytopenia, reduced reticulocytes
  • Blood film = blasts (ring sideroblasts)
  • Bone marrow aspiration + biopsy = hypercellular bone marrow
196
Q

MYELODYSPLASTIC

What is the management of myelodysplastic syndrome?

A
  • Watch + wait with supportive Tx = blood transfusions, EPO, G-CSF
  • Chemo or stem cell transplant
197
Q

BPH
What is benign prostatic hypertrophy (BPH)?
Complications?

A
  • Overgrowth of prostatic tissue in transitional (inner) zone which compresses prostatic urethra
  • Obstruction not relieved may get infection (stasis) or hydroureter/nephrosis
198
Q

BPH

How does BPH present?

A

LUTS:
- Storage Sx (FUN) = Frequency, Urgency, Nocturia
- Voiding Sx (HIT) = Hesitancy, Intermittent flow, Terminal dribbling
UTI secondary to stasis, acute or chronic retention

199
Q

BPH

What are some investigations for BPH?

A
  • DRE = smooth but enlarged prostate
  • U+Es, serum PSA (rise)
  • Urine dip + MC&S
  • International prostate symptom score (I-PSS) looks at LUTS + how much affect day-to-day life
  • Transrectal USS ± biopsy
  • Flexibly cystoscopy
200
Q

BPH

What is the conservative management of BPH?

A
  • Avoid caffeine + alcohol
  • Relax when voiding + void twice in a row to aid emptying
  • Control urgency with distraction methods
201
Q

BPH

What 2 medications can be used in BPH and what is their mechanism of action?

A
  • Alpha blockers 1st line (doxazosin, tamsulosin) to relax prostate smooth muscle
  • 5-alpha reductase inhibitor (finasteride) which decreases prostate size by less conversion of testosterone into dihydrotestosterone
202
Q

BPH
What are the side effects of…

i) alpha blockers?
ii) 5-alpha reductase inhibitors?

A

i) Postural hypotension (vasodilation), dizziness, dry mouth

ii) Erectile dysfunction, reduced libido, ejaculation issues

203
Q

BPH
What surgical options may be considered for BPH?
Complications?

A
  • Transurethral resection of prostate (TURP)
  • SEs = urethral stricture, retrograde ejaculation, prostate perforation
  • Retropubic prostatectomy if very large (open surgery)
204
Q

HAEMATURIA
What can cause…

i) transient or non-visible haematuria?
ii) persistent non-visible haematuria?
iii) other?

A

i) UTI, menstruation, vigorous exercise (normally settles after 3d), sex
ii) Cancer (TCC, RCC, prostate), stones, BPH, prostatitis, urethritis
iii) Red/orange urine but no haematuria = beetroot, rifampicin

205
Q

HAEMATURIA

What investigations might you do for haematuria?

A
  • Urine dipstick initially (persistent = present in 2/3 samples 2w apart)
  • Check renal function, ACR or PCR + BP
206
Q

HAEMATURIA

What would warrant an urgent referral regarding haematuria?

A
  • ≥45 + unexplained visible haematuria or persists after successful UTI Mx
  • ≥60 + unexplained non-visible haematuria + dysuria or raised WCC
  • Non-urgent if ≥60 + recurrent or persistent unexplained UTI

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