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
ANGINA | Ultimately, what 2 treatments may resolve angina?
- Percutaneous coronary intervention (PCI) with coronary angioplasty - Coronary artery bypass graft (CABG)
26
ACS What is ACS? What occurs?
- 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
27
ACS | How does an MI present?
- Central crushing chest pain, may radiate to jaw, neck, arm - Dyspnoea + palpitations - Sweating, N+V - Pallor, anxiety
28
ACS | What are the 2 most important investigations for ACS?
- ECG | - Serial troponins (baseline, 6h, 12h) showing acute rise
29
ACS On an ECG, how would the following appear... i) STEMI? ii) NSTEMI?
i) New LBBB or ST-elevation, hyperacute T waves (T-wave inversion + pathological Q waves occur later) ii) ST depression + T-wave inversion
30
ACS Where on the ECG would indicate the following arteries occlusion... i) circumflex (lateral)? ii) right coronary artery (inferior)? iii) left anterior descending (anterior)?
i) I, V5, V6 ii) II, III, aVF iii) V1–V4
31
ACS | What other investigations may you consider in ACS?
- ECHO after event to assess functional damage | - CT coronary angiogram to assess for IHD
32
ACS | What are the complications following ACS?
DREAD – - Death - RUpture of heart septum or papillary muscles - oEdema - Arrhythmia or Aneurysm - Dressler's syndrome
33
``` ACS What is Dressler's syndrome? How does it present? Investigations? Management? ```
- 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
34
ACS What is the pre-hospital management of ACS? What is the management of STEMI?
- Morphine, Oxygen, Nitrates + Aspirin (300mg) | - Call for primary PCI (≤2h) or thrombolysis (>2h) with streptokinase or alteplase
35
ACS | What is the management of NSTEMI?
``` BATMAN – Beta-blocker – Aspirin 300mg – Ticagrelor 180mg – Morphine – Anticoagulant (LMWH) – Nitrates (GTN) ```
36
ACS | What is the secondary prevention of ACS?
``` 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) ```
37
HEART FAILURE | What is heart failure?
- CO insufficient to meet metabolic demands of body + suggests the efficiency of heart as pump is impaired
38
HEART FAILURE | What compensatory mechanisms are seen in heart failure and what is seen when they decompensate?
- 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)
39
HEART FAILURE | What are the two broad categories of heart failure and what do they mean?
- 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
40
HEART FAILURE | What are the 2 main types of systolic heart failure and what causes them?
- 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)
41
HEART FAILURE What is diastolic failure also referred as and why? What can cause it?
- Heart failure with preserved ejection fraction = less volume fills + low volume output so ejection fraction higher - Cardiac tamponade, cardiomyopathies, pericardial effusion
42
HEART FAILURE | What is the New york Heart Association classification of heart failure?
- 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)
43
HEART FAILURE | What are the 3 cardinal symptoms of heart failure?
- Dyspnoea (+ orthopnoea due to pulmonary oedema, lots of pillows) - Fatigue - Peripheral oedema
44
HEART FAILURE | What are some classic features of left heart failure?
- Nocturnal cough ± white or pink frothy sputum - Paroxysmal nocturnal dyspnoea - Cold peripheries - Signs = S3 + tachy (gallop), bibasal crackles from pulmonary oedema
45
HEART FAILURE | What are some classic features of right heart failure?
- Peripheral oedema, ascites, nausea | - Signs = raised JVP, hepatomegaly
46
HEART FAILURE | What are some investigations for heart failure?
- 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)
47
HEART FAILURE What NT-proBNP values are suspicious for heart failure? What can falsely raise and decrease NT-proBNP levels?
- >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
48
HEART FAILURE | Why is an ECHO diagnostic?
- Assess function of LV + any structural function | - Can measure ejection fraction (% of blood squeezed out with each ventricular contraction)
49
HEART FAILURE | What might you see on a CXR in heart failure?
- Alveolar oedema (Bat's wings) - kerley B lines (interstitial oedema) - Cardiomegaly - Dilated prominent upper lobe vessels - pleural Effusion
50
HEART FAILURE | What is the acute management of heart failure and likely cause?
- 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
51
HEART FAILURE | What is the mechanism of action of furosemide?
- Loop diuretic | - Inhibits Na-K-Cl co-transporter in thick ascending limb of loop of Henle to reduce absorption of NaCl
52
HEART FAILURE | What is the general management of heart failure?
- Yearly flu + PCV - HF specialist nurse input - Lifestyle changes
53
HEART FAILURE | What is the first line medical treatment for heart failure?
- 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)
54
HEART FAILURE | What other methods of management may be considered in heart failure?
- ?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
55
ATRIAL FIBRILLATION | What is the pathophysiology of AF?
- 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
56
ATRIAL FIBRILLATION | What are some causes of AF?
- Sepsis - Mitral valve (stenosis/regurg) - IHD - Thyrotoxicosis - HTN
57
ATRIAL FIBRILLATION | What is the clinical presentation of AF?
- Palpitations, dyspnoea, syncope, CP | - Irregularly irregular pulse
58
ATRIAL FIBRILLATION What is paroxysmal AF? Management?
- 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
59
ATRIAL FIBRILLATION | What does the ECG in atrial fibrillation look like?
- Absent P waves - Irregularly irregular ventricular rhythm - Narrow QRS complex tachycardia
60
ATRIAL FIBRILLATION What is the main complication of AF? Management?
- Embolic stroke due to stagnation of blood in atria due to ineffective mechanical action of atria - Calculate CHADSVASC score + ≥2 = anticoagulate
61
ATRIAL FIBRILLATION | How can you control the rate in AF?
- Beta-blocker first line - Rate-limiting CCB - Digoxin only if they fail
62
ATRIAL FIBRILLATION How would you control the rhythm acutely? What can be used?
- 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
63
ATRIAL FIBRILLATION | What other treatment can be used in AF?
- Catheter ablation if not responded or wish to avoid antiarrhythmic meds, must be anticoagulated 4w before
64
ATRIAL FIBRILLATION What should you use for anticoagulation in AF? Which is better?
- 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
65
OTITIS EXTERNA What is otitis externa? What is it associated with?
- Inflammation of external ear canal | - Swimmer's ear as associated with frequent swimming
66
OTITIS EXTERNA | What is malignant otitis externa?
- Immunocompromised, DM or elderly where it can spread to the surrounding bones (mastoid + temporal)
67
OTITIS EXTERNA | What are some causes of otitis externa?
- Infection (staph. aureus, pseudomonas aeruginosa or fungal) - Seborrhoeic dermatitis - Contact dermatitis (allergic + irritant)
68
OTITIS EXTERNA | What is the clinical presentation of otitis externa?
- Ear pain (mild), itchy + discharge common, ?hearing loss | - Otoscopy = red, swollen or eczematous canal
69
OTITIS EXTERNA | What is the management of otitis externa?
- 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
70
COPD What are the two diseases that make up COPD? What is the main cause of COPD?
- Pink puffers = emphysema - Blue bloaters = chronic bronchitis - Smoking (alpha-1-antitrypsin is a major protease inhibitor that can be inactivated by smoke)
71
COPD | What causes emphysema?
- Alveoli lose elastic recoil > air trapping after exhalation - Unable to oxygenate so hyperventilate (puffing), no cyanosis
72
COPD | What causes chronic bronchitis?
- 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
73
COPD What are the 3 typical signs of COPD? What are some other signs?
- Chronic cough, sputum (often clear white), dyspnoea | - Pursed lip breathing, tachypnoea, hyperinflated barrel chest, cachexic
74
COPD | How is COPD classified into stages?
- 1 = mild (FEV1 ≥80% predicted) - 2 = mod (FEV1 50–79% predicted) - 3 = severe (FEV1 30–49% predicted) - 4 = very severe (FEV1 <30% predicted)
75
COPD | What are some investigations for COPD?
- 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
76
COPD | What is the conservative management of COPD?
- Smoking cessation - Annual flu vaccine - One off PCV - Pulmonary rehab (exercise, nutrition, breathing exercises)
77
COPD | What are steps 1 and 2 of the COPD management?
- 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)
78
COPD What is step 3 of COPD management? Any other management?
- FEV1>50% = LABA + ICS or same as FEV1<50% - FEV1<50% = LAMA + LABA/ICS combination (FOstair) - Consider PO theophylline or mucolytics like carbocysteine
79
COPD What is the mechanism of action of LAMA? Give an example What about SAMA?
- 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
80
COPD When would you consider long-term oxygen therapy? When is it contraindicated?
- 2 separate ABGs showing PaO2 <7.3kPa or paO2 7.3–8 with pulmonary HTN or polycythaemia or peripheral oedema - Smokers as fire hazard
81
COPD What is an acute exacerbation of COPD? What is the most common cause?
- Acute worsening of Sx such as cough, dyspnoea, wheeze + sputum (?purulent) - Haemophilus influenzae (#1), strep. pneumoniae, Moraxella catarrhalis
82
COPD | What are some investigations for acute exacerbation of COPD?
- FBC (raised WCC), CRP, ?blood cultures if septic - Sputum MC&S - CXR may show consolidation
83
COPD | What is the management of an acute exacerbation of COPD?
- 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
PNEUMONIA | What are the 3 classifications of pneumonia?
- Community-acquired = develops outside hospital - Hospital acquired = develops >48h after hospital admission - Aspiration = acute aspiration of gastric contents (stroke, MG, MS, MND)
85
PNEUMONIA | What are the most common causes of CAP?
- Strep. pneumoniae #1 - Haemophilus influenzae - Moraxella catarrhalis
86
PNEUMONIA | What are the most common causes of HAP?
- S. aureus - Klebsiella pneumoniae - Pseudomonas aeruginosa
87
PNEUMONIA | What are some atypical pneumoniaes?
- 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
PNEUMONIA What is a cause of fungal pneumonia? How does it present? Management?
- Pneumocystis jiroveci pneumonia (PCP) in immunocompromised - Dry cough, SOB on exertion, night sweats - Co-trimoxazole
89
PNEUMONIA | What are some risk factors for pneumonia?
- Elderly + infants - Comorbidities = DM, COPD, bronchiectasis - Smokers, alcoholics - Immunocompromised + nursing home residents
90
PNEUMONIA What are the... i) symptoms ii) signs iii) exam findings in pnuemonia?
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
PNEUMONIA | What are some investigations for pneumonia?
- FBC (neutrophilia, raised WCC) - CRP, U+Es, ABG - Sputum MC&S + blood cultures - Pneumococcal + legionella urinary antigen tests - CXR = consolidation
92
PNEUMONIA What score can be used to assess severity of CAP? How does this guide your management?
- 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
PNEUMONIA | What is the general management for pneumonia?
- Oxygen therapy - IV fluids - PCV vaccine in children - Flu vaccine if ≥65y, immunocompromised or medical co-morbidities - Smoking cessation
94
PNEUMONIA What typical antibiotics might you use in... i) HAP? ii) aspiration? iii) atypicals?
i) Aminoglycoside like gentamycin + cephalosporin ii) IV cephalosporin + metronidazole to cover gut anaerobes iii) Macrolides (clarithromycin), fluoroquines (levofloxacin) + tetracyclines (doxycycline)
95
LUNG CARCINOMA | What are the 2 broad categories of lung cancer?
``` - Non-small cell lung carcinoma (NSCLC) – Squamous = Smokers – Adenocarcinoma = non-smokers, asbestos – Large cell (poorly differentiated) - Small cell lung carcinoma ```
96
LUNG CARCINOMA | What can happen in SCLC?
- Arise from Kulchitsky (endocrine) cells so can cause paraneoplastic syndromes like SIADH (think low sodium), Cushing's, Lambert-Eaton myasthenic syndrome
97
LUNG CARCINOMA In terms of lung cancer, what are some... i) symptoms? ii) signs? iii) signs of mets?
i) Cough + haemoptysis, CP, dyspnoea, weight loss, night sweats, recurrent pneumonia ii) Finger clubbing, lymphadenopathy (supraclavicular) iii) Bone tenderness, hepatomegaly, neurology (seizures, headache)
98
LUNG CARCINOMA | What are some investigations for lung cancer?
- CXR first line (opacity, hilar enlargement, effusion, collapse) - CT CAP for staging or if CXR clear - Bronchoscopy with EBUS + biopsy
99
LUNG CARCINOMA | What are some complications from lung carcinoma?
- 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
LUNG CARCINOMA | Complication of squamous cell carcinoma?
- Hypercalcaemia from ectopic PTH-rP = primary hyperparathyroidism
101
LUNG CARCINOMA | What is the management of lung cancer?
- NSCLC = lobectomy if isolated, radio/chemo - SCLC = chemo ± radio - Supportive = analgesia, anti-emetics, ?tracheal stenting if bronchial obstruction
102
T2DM | What is the pathophysiology of T2DM?
- 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
T2DM What are some causes of T2DM? How does it present?
- Genetics + environment (FHx, obesity, poor diet) - Asian, men, older age - No Sx but sometimes polyuria, polydipsia, lethargy, visual blurring
104
T2DM | What values are diagnostic for T2DM?
``` - 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
T2DM What values suggest... i) impaired fasting glucose? ii) impaired glucose tolerance?
i) 6.1-6.9mmol/L | ii) 7.8-11.1mmol/L
106
T2DM | What is a main complication of uncontrolled T2DM?
- Hyperglycaemic hyperosmolar state - Decrease insulin = increase serum glucose + serum osmolality + urination but no ketosis as still some endogenous insulin
107
T2DM How does HHS present? How is it diagnosed? Management?
- 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
T2DM What is the first line management of T2DM? What are the HbA1c targets in T2DM?
- Lifestyle advice = exercise, less carbs/fat, smoking cessation - <48mmol/mol for new pts or <53 if on ≥2 Tx
109
T2DM | List 6 medications that can be used in T2DM
- Metformin (biguanide, first line) - Gliclazide (sulfonylurea) - Sitagliptin (DPP4 inhibitor) - Empagliflozin (SGLT) - Glitazone (pioglitazone) - GLP-1 mimetics
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T2DM What is the mechanism of action of... i) metformin? ii) gliclazide? iii) sitagliptin?
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
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T2DM What is the mechanism of action of... i) empagliflozin? ii) glitazone? iii) GLP-1 mimetics?
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)
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T2DM What are some side effects of... i) metformin? ii) gliclazide? iii) sitagliptin? iv) empagliflozin? v) glitazone? vi) GLP-1 mimetics?
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
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HYPERTHYROIDISM | What are the 3 mechanisms explaining the causes of hyperthyroidism?
- Overproduction of thyroid hormone - Leakage of pre-formed hormone from thyroid - Ingestion of excess thyroid hormone
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HYPERTHYROIDISM What is the most common cause of hyperthyroidism? What is the pathophysiology?
- Graves' disease - Autoimmune induced excess production of thyroid hormone, esp T3 - TSH receptor stimulating antibody (TRAb, IgG), autoimmune link to T1DM, coeliac, Addison's
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HYPERTHYROIDISM | What are some other causes of hyperthyroidism?
- 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)
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HYPERTHYROIDISM | What are the general signs and symptoms of hyperthyroidism?
- Anxiety, irritability - Sweating, palpitations (?AF), tremor, tachycardia - Heat intolerance - Weight loss, increased appetite, diarrhoea - Oligomenorrhoea - Thin hair, warm skin
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HYPERTHYROIDISM | What are the Graves' disease specific features?
- Diplopia, ophthalmoplegia, increased tears - Exophthalmos, lid lag + retraction - Thyroid acropachy (clubbing, painful digits) - Pretibial myxoedema
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HYPERTHYROIDISM | How would De Quervain's thyroiditis present?
- PAIN in de QuerVAIN = tender goitre, fever, dysphagia (viral infection) - Hyperthyroid phase > hypothyroid phase (TSH falls due to -ve feedback)
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HYPERTHYROIDISM | What are some investigations for hyperthyroidism?
- TFTs (primary = low TSH, high T3/4, secondary = high TSH, high T3/4 hypothalamus or pituitary pathology) - Thyroid autoantibodies - Isotope scan
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HYPERTHYROIDISM What is a complication of hyperthyroidism? Management?
- More severe presentation with pyrexia, tachycardia + delusion - Admission, supportive (fluid resus), beta-blockers, ?anti-arrhythmic
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HYPERTHYROIDISM | What is the management of hyperthyroidism?
- Beta-blockers for rapid sympathetic control (propranolol) - Carbimazole 1st line, propylthiouracil 2nd - Radioiodine therapy - Surgical thyroidectomy - NSAIDs + beta-blockers for self-limiting DeQuervain's
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HYPERTHYROIDISM What are the 2 methods for administering anti-thyroid drugs? What are side effects of them?
- Titration - Block + replace (block all production + take levothyroxine) - Carbimazole = agranulocytosis - Propylthiouracil = severe hepatic reactions
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HYPERTHYROIDISM What are some risks with... i) radioiodine therapy? ii) surgical thyroidectomy?
i) C/I in pregnancy, breastfeeding + may leave patient hypothyroid ii) Risk to recurrent laryngeal nerve (hoarse voice) + hypoparathyroidism
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HYPOTHYROIDISM | What are some common causes of hypothyroidism?
- 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)
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HYPOTHYROIDISM What is... i) atrophic thyroiditis? ii) Hashimoto's thyroiditis?
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
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HYPOTHYROIDISM | What are some symptoms of hypothyroidism?
- Weight gain, decreased appetite + constipation - Cold intolerance - Lethargy, menorrhagia
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HYPOTHYROIDISM | What are some signs of hypothyroidism?
BRADYCARDIC - Bradycardia - Reflexes relax slowly - Ataxia - Dry, thin hair/skin - Yawning - Cold hands - Ascites - Round puffy face - Defeated demeanour - Immobile - CHF
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HYPOTHYROIDISM | What are some investigations for hypothyroidism?
- 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
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HYPOTHYROIDISM What is the management of hypothyroidism? Prescribing information?
- Lifelong levothyroxine to replace (titrate up) - 30m before breakfast as iron decreases absorption of thyroxine - Repeat TFTs monthly until stable
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CONSTIPATION What is constipation? What are some causes?
- Infrequent bowel movements (<3/w) or with straining | - Obstruction, hypothyroid, neuro (MS, cauda equina), dehydration, IBS
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CONSTIPATION | What is the management of constipation?
- Hydration + increased fibre - Bulking agents = increased faecal mass + peristalsis (ispaghula husk) - Osmotic = retain fluid in bowel (lactulose) - Stimulant = increased intestinal motility (Senna) - Phosphate enemas
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GORD What is GORD? Risk factors?
- Regurg acidic gastric contents into lower oesophagus injuring squamous epithelium - Obesity + pregnancy, smoking, alcohol, caffeine, hiatus hernia
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GORD | What are the clinical features or GORD?
- Heartburn (oesophagitis) can be retrosternal/epigastric (worse after meals or lying down) - Acid regurg - Dysphagia/odynophagia - Nocturnal cough (aspiration)
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GORD | What are some investigations for GORD and when would you do them?
- OGD if new onset ≥55y or weight loss, melaena, haematemesis etc. - 24h oesophageal pH monitoring
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GORD | What are some complications of GORD?
- Benign stricture > dysphagia - Oesophageal adenocarcinoma - Barrett's oesophagus = metaplasia squamous?columnar may lead to dysplasia to adenocarcinoma
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GORD | What is the general management of GORD?
- Reduce caffeine + alcohol, weight loss, stop smoking, smaller meals - PRN OTC antacids like Gaviscon or Rennie
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GORD | What treatments can be given for GORD?
- PPI like omeprazole - H2 antagonists like ranitidine - Laparoscopic fundoplication to narrow lower oesophageal sphincter last line
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DIVERTICULAR DISEASE What is... i) diverticulum? ii) diverticulosis? iii) diverticular disease? iv) diverticulitis?
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
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DIVERTICULAR DISEASE | What causes a diverticulum?
- High intraluminal pressures force mucosa to herniate through muscle layers of gut at weak points (adjacent to penetrating vessels)
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DIVERTICULAR DISEASE What can cause high intraluminal pressures? How does it present?
- Low fibre, sigmoid colon as smallest diameter | - >60y, asymptomatic or LIF pain, altered bowel habit, fever, bleeding
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DIVERTICULAR DISEASE What causes diverticulitis? How does it present?
- Trapped faeces | - #1 = descending colon, LIF pain, fever, tachycardia, ?intestinal obstruction
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DIVERTICULAR DISEASE Investigations for diverticulitis? Management?
- Bloods, FBC (WCC raised), ESR/CRP, tender colon ± peritonism - Mild = bowel rest ± Abx if severe = analgesia, NBM, IV fluids + Abx, surgery if peritonitis
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DIVERTICULAR DISEASE Investigations for diverticular disease? Management?
- Erect CXR (?perf), AXR, contrast CT, incidental finding at colonoscopy - Antispasmodics like Buscopan, Hartmann's if perforation or obstruction
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COLORECTAL CANCER What are some causes of colorectal cancer? Risk factors?
- Hereditary nonpolyposis colorectal cancer #1 = AD - Familial adenomatous polyposis (FAP) = AD - Peutz-Jeghers syndrome = AD - Red + processed meat, alcohol, smoking, IBD
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COLORECTAL CANCER What are some features of... i) FAP? ii) HNPCC? iii) Peutz-Jeghers?
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
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COLORECTAL CANCER | What is the clinical presentation of colorectal cancer?
``` Majority L sided: - PR bleed/mucus, altered bowel habit, obstruction R sided + caecum: - Weight loss, Fe anaemia RectumL - Fresh blood, mass, tenesmus ```
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COLORECTAL CANCER | Investigations for colorectal cancer?
- FBC (Fe anaemia) - Faecal occult blood screening 2y 60–74 - Colonoscopy + biopsy - CT CAP for Duke's staging
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COLORECTAL CANCER In terms of colorectal cancer management... i) prevention? ii) adenoma? iii) colorectal adenocarcinoma?
i) ?NSAIDs prevent adenomas ii) Endoscopic resection ideally end-end anastomosis iii) Surgical resection if no spread, chemo + palliative care if metastatic
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COLORECTAL CANCER | What is Duke's staging in colorectal cancer?
- A = bowel mucosa - B = extends through bowel wall - C = regional LNs - D = distant mets
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GALLSTONES What causes gallstones? Risk factors?
- 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
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GALLSTONES | What is the clinical presentation of gallstones?
- Severe RUQ may radiate to tip of scapula - N+V - May be triggered by heavy, fatty meal
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GALLSTONES | Management of gallstones?
- FBC, U+Es, amylase, LFTs (ALP + bilirubin raised in attacks) - USS shows dilated ducts (MRCP if case) - Conservative (analgesia + fluids) with elective lap chole
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ACUTE CHOLECYSTITIS | What is acute cholecystitis?
- Inflammation of gallbladder following impaction of stone in cystic duct or neck of gallbladder obstruction bile emptying > damage to mucosal lining
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ACUTE CHOLECYSTITIS | What is the clinical presentation of acute cholecystitis?
- 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)
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ACUTE CHOLECYSTITIS | Investigations for acute cholecystitis?
- FBC (raised WCC), LFTs, - USS shows gallstones + distended gallbladder with thickened wall - Sonographic murphy's
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ACUTE CHOLECYSTITIS | Management of acute cholecystitis?
- Conservative = NBM, IV fluids, pain relief, IV Abx | - Lap chole
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OSTEOARTHRITIS | What is osteoarthritis?
- 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)
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OSTEOARTHRITIS What causes osteoarthritis? Risk factors?
- Secondary OA can occur in joints due to congenital disease + damage - Obesity, increasing age, trauma, female, FHx, occupation (manual labour)
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OSTEOARTHRITIS | What are the main symptoms of osteoarthritis?
- Morning stiffness <30m - Stiffness after rest (gelling) - Bony swellings/joint deformities - Reduced ROM, weak grip + reduced functioning
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OSTEOARTHRITIS | What bony swellings may be seen in osteoarthritis?
- 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)
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OSTEOARTHRITIS | What joints may be affected in osteoarthritis?
- Hips, knees, sacroiliac joints, MCP joint at base of thumb (squaring), wrist, cervical spine
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OSTEOARTHRITIS | What would plain radiograph show in osteoarthritis?
LOSS – - Loss of joint space - Osteophytes - Subarticular sclerosis (increased density of bone along joint line) - Subchondral cysts (fluid filled holes in the bone)
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OSTEOARTHRITIS | What is the conservative management of osteoarthritis?
- Education - Lifestyle (weight loss) - Physio to improve strength - Orthotics to support activities + function (walking aids)
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OSTEOARTHRITIS | What medical treatment may be given for osteoarthritis?
- Regular PO + topical NSAIDs - PO NSAIDs (?+PPI) for intermittent use - ?Opiates like codeine + morphine - Intra-articular steroid injections to reduce inflammation
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OSTEOARTHRITIS | What surgery may be offered in osteoarthritis?
- Arthroscopy for loose bodies (can cause locking e.g. knee) - Osteotomy (changing bone length) - Arthroplasty (joint replacement, risk of infection) - Fusion (often ankle + foot)
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GOUT What is gout? Pathophysiology?
- Inflammatory arthritis due to hyperuricaemia + intra-articular monosodium urate crystals - Urate derived from breakdown of purines (adenine + guanine)
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GOUT What are some causes of gout? Who is it most common in?
- Increased uric acid production = chemo, pyrazinamide - Decreased uric acid excretion = diuretics, renal impairment, alcohol excess - Older men
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GOUT What are some risk factors for gout? What are some factors that may precipitate an attack?
- Alcohol, high purine diet (red meat + seafood), cell damage + Death (surgery, chemo) - Dietary excess, diuretics, dehydration, sepsis
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GOUT | How does gout present?
- Acute hot, swollen + painful joints (exclude septic) | - Wrists, base of thumb (carpometacarpal joint) + metatarsophalangeal joint of big toe
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GOUT | What are some signs of gout?
- 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
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GOUT | What investigations would you do for gout?
- 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
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GOUT What is the management for gout for... i) an acute flare? ii) long-term prophylaxis?
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)
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PSEUDOGOUT What is pseudogout? What is it associated with?
- Microcrystal synovitis due to deposits of calcium pyrophosphate crystals - Hyperparathyroid, hypothyroid, haemochromatosis, hypophosphataemia
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PSEUDOGOUT | How does pseudogout present?
- Acute hot, swollen + stiff joints | - Monoarthropathy affecting shoulders, wrists + knees
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PSEUDOGOUT | What are the investigations for pseudogout?
- 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
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PSEUDOGOUT | What is the management of pseudogout?
- NSAIDs, colchicine - Intra-articular steroids or PO - Joint aspiration of arthrocentesis if severe
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PMR What is polymyalgia rheumatica (PMR)? Associations?
- Inflammatory condition (vasculitis) causing pain + stiffness in shoulder, pelvic girdle + neck - GCA
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PMR | What is the clinical presentation of PMR
- 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
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PMR | What is the management of PMR?
- ESR/CRP raised, CK normal | - PO prednisolone shows dramatic response (diagnostic)
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B12/PERNICIOUS ANAEMIA | What is the pathophysiology of B12 deficiency?
- Absorption of B12 in terminal ileum + intrinsic factor (via gastric parietal cells) dependent for transport across intestinal mucosa
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B12/PERNICIOUS ANAEMIA | What are some causes of B12 deficiecny?
- 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)
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B12/PERNICIOUS ANAEMIA | What are the B12 specific features of the anaemia?
- Peripheral neuropathy with numbness or paraesthesia - Loss of vibration sense or proprioception - Visual, mood or cognitive changes - Glossitis = beefy-red sore tongue
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B12/PERNICIOUS ANAEMIA | Investigations for B12/pernicious anaemia?
- 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)
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B12/PERNICIOUS ANAEMIA | What is the management of B12/pernicious anaemia?
- 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
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AOCD | What are some mechanisms in anaemia of chronic disease (AOCD)?
- 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)
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AOCD | What are some causes of AOCD?
- Chronic inflammatory diseases = Crohn's, RA) - Chronic infections (TB) - Malignancy - TB
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AOCD | What is the management of AOCD?
- FBC (low Hb) - Blood film = normochromic normocytic - Low serum iron, transferrin saturation + TIBC - High ferritin - Treat underlying cause, sometimes recombinant erythropoietin
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CLL | What is chronic lymphocytic leukaemia (CLL)?
- Monoclonal proliferation of well differentiated lymphocytes, 99% B cells - #1 leukaemia in adults
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CLL | What are some complications of CLL?
- Warm autoimmune haemolysis > anaemia - Infection (hypogammaglobulinaemia) - Richter's transformation = high-grade (large B cell) lymphoma
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CLL | What is the clinical presentation of CLL
- 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
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CLL | What are some investigations for CLL?
- FBC = pancytopenia - Blood film = smudge or smear cells - LDH may be raised - Bone marrow biopsy is diagnostic - CT CAP to stage
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CLL | What is the management of CLL?
- No sx = watch + wait - Chemo + radio to help lymphadenopathy + splenomegaly - Bone marrow transplant
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MYELODYSPLASTIC What is myelodysplastic syndrome? Risk?
- Immature blood cells in bone marrow do not mature properly + so do not become healthy blood cells - Transform to AML
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MYELODYSPLASTIC | How might myelodysplastic syndrome present?
- >60y + previous chemo or radiotherapy - ?Incidental finding - Signs of bone marrow failure – low Hb = anaemia, low WCC = infections, thrombocytopenia = bruising
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MYELODYSPLASTIC | Investigations for myelodysplastic syndrome?
- FBC = pancytopenia, reduced reticulocytes - Blood film = blasts (ring sideroblasts) - Bone marrow aspiration + biopsy = hypercellular bone marrow
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MYELODYSPLASTIC | What is the management of myelodysplastic syndrome?
- Watch + wait with supportive Tx = blood transfusions, EPO, G-CSF - Chemo or stem cell transplant
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BPH What is benign prostatic hypertrophy (BPH)? Complications?
- Overgrowth of prostatic tissue in transitional (inner) zone which compresses prostatic urethra - Obstruction not relieved may get infection (stasis) or hydroureter/nephrosis
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BPH | How does BPH present?
LUTS: - Storage Sx (FUN) = Frequency, Urgency, Nocturia - Voiding Sx (HIT) = Hesitancy, Intermittent flow, Terminal dribbling UTI secondary to stasis, acute or chronic retention
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BPH | What are some investigations for BPH?
- 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
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BPH | What is the conservative management of BPH?
- Avoid caffeine + alcohol - Relax when voiding + void twice in a row to aid emptying - Control urgency with distraction methods
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BPH | What 2 medications can be used in BPH and what is their mechanism of action?
- 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
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BPH What are the side effects of... i) alpha blockers? ii) 5-alpha reductase inhibitors?
i) Postural hypotension (vasodilation), dizziness, dry mouth | ii) Erectile dysfunction, reduced libido, ejaculation issues
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BPH What surgical options may be considered for BPH? Complications?
- Transurethral resection of prostate (TURP) - SEs = urethral stricture, retrograde ejaculation, prostate perforation - Retropubic prostatectomy if very large (open surgery)
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HAEMATURIA What can cause... i) transient or non-visible haematuria? ii) persistent non-visible haematuria? iii) other?
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
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HAEMATURIA | What investigations might you do for haematuria?
- Urine dipstick initially (persistent = present in 2/3 samples 2w apart) - Check renal function, ACR or PCR + BP
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HAEMATURIA | What would warrant an urgent referral regarding haematuria?
- ≥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