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Medicine > SPM > Flashcards

SPM Flashcards

1
Q

What blood test monitoring must occur when prescribing simvastatin?

A

LFTs @ baseline, 3 months, 12 months

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2
Q

How does subclavian steal syndrome present?

A

Posterior circulation symptoms e.g. dizziness, vertigo during exertion of an arm

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3
Q

How do you calculate an anion gap?

A

(sodium + potassium) - (bicarbonate + chloride

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4
Q

What are the causes of a normal anion gap or hyperchloremic metabolic acidosis?

A
  • GI bicarbonate loss: diarrhoea, fistula
  • Renal tubular necrosis
  • Drugs e.g. acetazolamide (carbonic anhydrase inhibitor)
  • Ammonium chloride injection
  • Addison’s disease
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5
Q

What are the causes of a raised anion gap metabolic acidosis?

A
  • Lactate: shock, hypoxia
  • DKA, alcohol (ketones)
  • urate: renal failure
  • Acid poisoning: salicylates, methanol
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6
Q

When can an intra-aortic balloon pump be used?

A

Cardiogenic shock

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7
Q

Which MI region is most likely to cause AV block?

A

Inferior MI

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8
Q

What time period would you expect to see pericarditis following a transmural MI?

A

In the first 48 hours

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9
Q

When does Dressler’s syndrome tend to occur?

A

2-6 weeks following MI

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10
Q

How would dressler’s syndrome present? How would you treat it?

A

fever, pleuritic chest pain, pericardial effusion, raised ESR
NSAIDs

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11
Q

When would you expect a left ventricular wall rupture to present after an MI? What is the TX?

A

1-2 weeks after

Urgent pericardiocentesis + thoracotomy

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12
Q

What type of MI is acute mitral regurgitation most common with?

A

Infero-posterior infarction

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13
Q

How can Takayasu’s arteritis present?

A

Young Asian women
Occlusion of the aorta –> absent limb pulses
Malaise, headache, unequal BP in upper limbs, carotid bruit, intermittent claudication, AR

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14
Q

Treatment of orthostatic hypotension?

A

Fludrocortisone - increases renal sodium reabsorption and increases plasma volume

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15
Q

What is Tietze’s syndrome?

A

Inflammation of costal cartilages –> chest pain with tenderness

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16
Q

When can you hear a ejection systolic murmur?

A
  • Children
  • Tachycardia
  • pregnancy
  • AS
  • Pulmonary stenosis
  • hypertrophic (obstructive) cardiomyopathy
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17
Q

When can you hear a pansystolic murmur?

A

Mitral/tricuspid regurgitation or VSD

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18
Q

when can you hear a early diastolic murmur?

A

Aortic regurgitation - high pitched

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19
Q

What is a Graham Steel murmur?

A

If pulmonary regurgitation is secondary to pulmonary HTN resulting from mitral stenosis

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20
Q

When would you hear a mid-diastolic murmur?

A

Mitral stenosis - low and rumbling

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21
Q

Describe where some murmurs radiate to

A

AS radiates to carotids, MR radiates to the axilla

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22
Q

Describe attenuation movements

A

Leaning forward attenuates aortic regurgitation

Left lateral position attenuates mitral stenosis

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23
Q

what does the S1 sound represent?

A

Closure of the mitral and tricuspid valves

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24
Q

When would S1 be loud?

A

MS, short PR interval, tachycardia

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25
Q

When is S3 loud?

A

Loud in dilated LV w/ rapid filling (MS, VSD) or poor LV function (post MI, dilated cardiomyopathy)

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26
Q

What does S4 represent?

A

Atrial contraction against a stiff ventricle e.g. AS, HTN

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27
Q

When would you see a slowly rising pulse w/ a narrow pulse pressure?

A

Aortic stenosis

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28
Q

When would you see a collapsing (water-hammer) pulse?

A

Aortic regurgitation

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29
Q

What signs are associated with mitral regurgitation?

A

Corrigan’s sign (carotid pulsation)
de Musset’s sign (head nodding w/ each heartbeat)
Quincke’s sign (capillary pulsations in nail beds)

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30
Q

Causes of systolic HF

A

IHD, MI, Cardiomyopathy

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31
Q

Causes of diastolic heart failure?

A

Ventricular hypertrophy
Constrictive pericarditis
Cardiac tamponade
Obesity

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32
Q

New York classification of heart failure

A
  1. Heart disease present but no undue dyspnoea from ordinary activity
  2. Comfortable at rest; dyspnoea during ordinary activity
  3. Less than ordinary activity causes dyspnoea, which is limiting
  4. Dyspnoea present at rest; all activity causes discomfort
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33
Q

What are the actions of BNP?

A

Increases GFR, decreases renal sodium absorption, decreases fluid load and relaxes smooth muscle thus lowering preload

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34
Q

What does CHA2DS2-VASc score stand for?

A 
C = congestive cardiac failure
H = HTN
A = Age (65-74 = 1 point; over 74 = 2 points)
D = Diabetes
S = previous stroke/TIA/Thromboembolism 
V = vascular disease 
S = sex (1 point if female)
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35
Q

What does HASBLED stand for?

A 
H = HTN 
A = Abnormal renal/liver function 
S = Stroke 
B = bleeding history/ predisposition 
L = Labile (unstable/high) INR
E = Elderly (+65 yrs)
D = drugs/alcohol
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36
Q

Give examples of ‘the pill’ used PRN in paroxysmal AF

A

Sotalol or flecainide

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37
Q

Give examples of inherited primary arrhythmias linked with sudden death

A

Congenital long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia

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38
Q

What is the most common atrial septal defect and how does it present?

A

Ostium secundum –> RBBB with right axis deviation.

Often asymptomatic until adulthood when L –> R shunt develops. –> dyspnoea/HF around 40-60 y/o

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39
Q

How does ostium primum present?

A

In childhood. RBBB w/ left axis deviation

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40
Q

What is Eisenmenger’s complex?

A

Initial L–>R shunt –> pulmonary HTN –> increased right heart pressures until they exceed left heart pressure –> shunt reversal –> cyanosis.

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41
Q

What signs will ventricular septal defect present with?

A

Harsh pansystolic murmur heard best at left sternal edge. Signs of pulmonary HTN. Ventricular hypertrophy.

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42
Q

What medications must a patient be on post PCI?

A

Aspirin and clopidogrel for at least 12 months to reduce stent thrombosis

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43
Q

What type of MI may lead to sinus bradycardia?

A

Inferior MI pts may suffer from atropine-unresponsive bradycardia due to infarction of nodal tissue.

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44
Q

What are the 1st, 2nd and 3rd lines treatments for chronic heart failure?

A

1st line: ACEi + b-blocker
2nd line: Aldosterone antagonist (spironolactone), angiotensin II receptor blocker or hydralazine (vasodilator) WITH a nitrate.
3rd line: cardiac resynchronization/ digoxin/ivabradine

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45
Q

What change occurs in Barrett’s oesophagus?

A

Squamous to columnar epithelium

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46
Q

Drugs that affect oesophageal motility and predispose to GORD

A

Nitrates, anticholinergics, calcium channel blockers

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47
Q

Drugs that damage oesophageal muscosa and predispose to GORD

A

NSAIDs, K+ salts, bisphosphonates

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48
Q

What follow up is required for patients with gastric ulcers?

A

endoscopy @ 6-8 weeks to confirm ulcer healing

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49
Q

How many weeks off PPIs is needed before testing HP?

A

2 weeks

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50
Q

Which inflammatory bowel condition presents with hyperaemic/haemorrhagic colonic mucosa +/- pseudo-polyps

A

UC

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51
Q

Which inflammatory bowel condition is more common in non-smokers?

A

UC

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52
Q

What changes would you see on an AXR of someone with UC?

A

Mucosal thickening/islands, colonic dilatation

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53
Q

What is the treatment for mild UC?

A

Mesalazine (5-ASA), topical steroid foams PR

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54
Q

What is the treatment for moderate UC? How does one define moderate UC?

A

Moderate UC = 4-6 motions/day

Induce remission w/ oral prednisolone for 1 week then taper. Maintain on mesalazine

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55
Q

What are the side effects of mesalazine (5-ASA)?

A

Rash, haemolysis, hepatitis, pancreatitis, paradoxical worsening of colitis.

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56
Q

What monitoring is needed for mesalazine?

A

FBC + U&Es @ start then @ 3 months then annually

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57
Q

How does one define severe UC? How does one treat severe UC?

A

> 6 months + unwell
Admit: IV fluids, IV steroids
If no improvement after a few days: Ciclosporin or infliximab, then urgent colectomy.

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58
Q

What should be offered to patients with UC who flare on steroid tapering or have over 2 courses of steroids per year?

A

Immunomodulation (e.g. Azathioprine).

Monitoring: FBC, U&Es, LFTs weekly for 4 weeks, then every 4 weeks for 3 months, then at least 3 monthly.

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59
Q

Primary biliary sclerosis is linked with which inflammatory bowel disease?

A

Crohn’s

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60
Q

What are the treatments for mild/moderate Crohn’s?

A

Mild/moderate: Prednisolone for 1 week, then taper.

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61
Q

What does a positive Murphy’s sign suggest?

A

Patient had acute cholecystitis - only positive result if same test in LUQ doesn’t cause pain!

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62
Q

Antibiotic for acute cholecystitis

A

Co-amoxiclav

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63
Q

What is cholangitis? E.g. of Abx to TX it?

A

Bile duct infection. Tazocin IV.

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64
Q

What is Charcot’s triad

A
  • RUQ Pain
  • Jaundice
  • Rigors

Suggest cholangitis

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65
Q

What is gallstone ileus?

A

Gallstone erodes through GB into duodenum; may then obstruct the terminal ileum

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66
Q

What would you see on AXR in a pt with gallstone ileus?

A

Air in CBD (pneumobilia), small bowel fluid levels and a stone.

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67
Q

What is Mirizzi’s syndrome?

A

Stone in GB presses on bile duct –> jaundice.

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68
Q

Causes of pancreatitis?

A 
G: gallstones
E: ethanol 
T: trauma
S: steroids 
M: mumps
A: autoimmune hepatitis
S: Scorpion venom 
H: hyperlipidaemia, hypothermia, hypercalcaemia
E: ERCP and emboli 
D: Drugs
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69
Q

What is Cullen’s sign?
What is Grey turner’s sign?
What do they indicate?

A

Cullen’s sign = periumbilical bruising
Grey Turner’s sign = flank bruising
Suggestive of pancreatitis

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70
Q

what is a better marker for pancreatitis and why?

A

Serum lipase as it rises earlier and falls later

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71
Q

What is the modified Glasgow criteria?

A

Predicts severity of pancreatitis - over 3 factors within 48 hrs of onset means pancreatitis is severe - ITU needed!

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72
Q

What type of virus is Hep A

A

RNA virus

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73
Q

What is the incubation period of Hep A

A

2 - 6 weeks

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74
Q

Which enzyme would you see a big increase in in Hep A

A

ALT

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75
Q

What type of virus is Hep B?

A

DNA virus

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76
Q

What is the incubation period for Hep B?

A

2 - 6 months

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77
Q

What type of virus is Hep C?

A

RNA virus

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78
Q

What type of virus is Hep D?

A

Incomplete RNA virus - needs HBV for its assembly

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79
Q

What type of virus is Hep E?

A

RNA virus

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80
Q

Where can you find gluten?

A

Wheat, barley, rye, oats

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81
Q

What would happen to the following in Coeliac disease?

  • Hb
  • Red cell distribution width
  • B12
  • Ferritin
A

decreased Hb
increased red cell distribution width
decreased B12
Decreased ferritin

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82
Q

Which antibodies are associated with Coeliac disease?

A

Anti-transglutaminases Abs

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83
Q

What would you see on duodenal biopsy in someone with coeliac disease?

A

Subtotal villous atrophy, increased intra-epithelial WBCs and crypt hyperplasia.

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84
Q

Where would you see diverticula most frequently?

A

Sigmoid colon

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85
Q

How would you diagnose diverticulitis?

A

CT abdomen (colonoscopy risks perforation!)

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86
Q

What is the Rockall scoring system used for?

A

To predict prognosis in acute GI bleed. Worse prognosis if severe shock; malignancy; renal/liver failure; visible blood.

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87
Q

which laxative should you NOT prescribe in IBS

A

Lactulose as it ferments and aggravates bloating

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88
Q

What medication should you recommend to patients with IBS who are suffering from diarrhoea?

A

Loperamide (AKA Imodium) after each loose stool

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89
Q

What treatment options are available to patients with IBS who are suffering from colic/bloating?

A

Oral antispasmodics (mebeverine or hyoscine butylbromide). Combo probiotics. Low FODMAP diet.

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90
Q

When would you see micronodular liver cirrhosis?

A

Alcoholic liver disease, biliary tract disease

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91
Q

When would you see macronodular liver cirrhosis?

A

Chronic viral hepatitis

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92
Q

To diagnose portal HTN, what measure is used?

A

HVPG > 5mmHg

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93
Q

what is budd-chiari syndrome and how does it present?

A

hepatic venous outflow obstruction. –> abdo pain, ascites, liver enlargement

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94
Q

In hepatocellular injury, out of ALT/AST and Alk phos/GGT, which would be raised more?

A

ALT/AST

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95
Q

In cholestatic disease, out of ALT/AST and Alk phos/GGT, which would be raised more?

A

Alk phos/GGT

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96
Q

What is hepatic foetor?

A

It is seen in portal HTN - systemic shunting allows thiols to pass directly into lungs. Sweet, faecal smell of breath.

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97
Q

Which antibodies are associated with autoimmune hepatitis?

A

IgG, ANA, anti-smooth muscle ab

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98
Q

Which antibody is associated with primary biliary cirrhosis?

A

antimitochondrial ab

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99
Q

If Ferritin & transferrin saturations are high (> 45%) when doing a liver screen, what should you do next?

A

Perform HFE for haemochromatosis

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100
Q

Treatment for Wilson’s disease

A

Penicillamine (a copper-binding agent)

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101
Q

What screening should be done for all patients with cirrhosis?

A

Hepatocellular carcinoma screening (abdo US 6 monthly), variceal screening (gastroscopy every 1 -3 years)

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102
Q

What blood test results would you expect to see in acute alcoholic hepatitis?

A

Increased bilirubin with normal tests otherwise, impaired liver function (increased PTT, hypalbuminaemia)

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103
Q

What treatment should be offered to patients with large oesophageal varices?

A

Long-term B blocker

Variceal banding if intolerant of b-blocker

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104
Q

Define hyperacute liver failure

A

Encephalopathy within 7 days of onset of jaundice

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105
Q

Define acute liver failure

A

Jaundice to encephalopathy from 8 to 28 days

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106
Q

Define sub-acute liver failure

A

Jaundice to encephalopathy from 4 to 12 weeks

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107
Q

Aetiology of ALF/SALF:ALT >2000

A

Paracetamol OD, ischaemic hepatitis, acute Hep B

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108
Q

Main medication used in TX of paracetamol OD? How long after a POD is it still effective?

A

Acetylcysteine: 100mg/kg NAC in 100ml normal saline over 16 hours. NAC effective up to 72 hrs after POD - it decreases cerebral oedema and mortality

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109
Q

What are the stages of encephalopathy?

A

1) Slow mentation (number connection) - mild asterixis
2) Drowsy and inappropriate - asterixis present
3) Agitation and aggression –> increasing somnolence, asterixis present
4) Coma - asterixis may or may not be present

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110
Q

Name 2 RFs for bacterial overgrowth

A

DM + PPIs

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111
Q

What treatment should you try for bacterial overgrowth

A

Metronidazole

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112
Q

How do you diagnose bacterial overgrowth?

A

Breath hydrogen analysis - take samples of end-expired air; give glucose; take more samples every 30 mins; early increase in exhaled hydrogen = overgrowth

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113
Q

How low would you expect the viral load to be for oral candidiasis to be present in a patient with HIV

A

CD4 500 - 200 cells/mm3

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114
Q

How low would you expect the viral load to be for oesophageal candidiasis to be present in a patient with HIV

A

CD4 100-50 cells/mm3

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115
Q

How low would you expect the viral load to be for HHV-8 Kaposi sarcoma to be present in a patient with HIV

A

CD4 500 - 200 cells/mm3

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116
Q

How low would you expect the viral load to be for S. Pneumonia to be present in a patient with HIV

A

CD4 500 -200 cells/mm3

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117
Q

How low would you expect the viral load to be for Mycobacterium tuberculosis to be present in a patient with HIV

A

CD4 500 - 200 cells/mm3

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118
Q

How low would you expect the viral load to be for Non-Hodgkin’s Lymphoma to be present in a patient with HIV

A

CD4 500 - 200 cells/mm3

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119
Q

How low would you expect the viral load to be for Pneumocystis Jiroveci Pneumonia to be present in a patient with HIV

A

CD4 200 - 100 cells/mm3

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120
Q

How low would you expect the viral load to be for Cryptosporiadiosis/ Microsporidosis to be present in a patient with HIV

A

CD4 200 - 100 cells/mm3

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121
Q

How low would you expect the viral load to be for JC virus to be present in a patient with HIV

A

CD4 100 - 50 cells/mm3

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122
Q

How low would you expect the viral load to be for histoplasmosis to be present in a patient with HIV

A

CD4 100 - 50 cells/mm3

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123
Q

How low would you expect the viral load to be for toxoplasmosis to be present in a patient with HIV

A

CD4 100 - 50 cells/mm3

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124
Q

How low would you expect the viral load to be for Cryptococcal Neoformans Meningitis to be present in a patient with HIV

A

CD4 <50 cells/mm3

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125
Q

How low would you expect the viral load to be for Mycobacterium avium complex to be present in a patient with HIV

A

CD4 <50 cells/mm3

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126
Q

How low would you expect the viral load to be for CMV retinitis to be present in a patient with HIV

A

CD4 <50 cells/mm3

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127
Q

How would you manage a pregnant woman who has a detectable viral load at the time of delivery?

A

Caesarean section
AZT infusion running prior to and throughout delivery
Baby will require 4 weeks of treatment with 3 antiretroviral drugs

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128
Q

If a pregnant woman’s viral load is suppressed at time of delivery, how should you manage her baby?

A

Give the baby 4 weeks of single drug anti-retroviral treatment (zidovudine)

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129
Q

When should you test baby whose mother has HIV?

A

Look for HIV DNA in baby’s blood at day 1, 6 weeks and 3 months of age.
Maternal HIV Abs will be detectable in baby’s blood for 18 months - loss of these abs after confirms that the patient is HIV negative

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130
Q

How can an acute/primary HIV infection present?

A

Fevers, fatigue, rash. Glandular-fever-like.

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131
Q

How does Kaposi’s sarcoma look like?

A

Purple lesions on skin or mucus membranes

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132
Q

What is a regimen of HAART like?

A

Usually a combo of at least 3 antiretroviral drugs E.g. (non)/ nucleoside/tide reverse transcriptase inhibitors/analogues, protease inhibitors, integrase inhibitors, fusion + CCR5 inhibitors

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133
Q

Which medications do PEPSE entail?

A

Truvada (1 a day) + Raltegravir (2 a day) for 28 days

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134
Q

What is the treatment for Bacterial Vaginosis

A

Metronidazole 400mg twice daily for 5 days or 2g stat.

TX only symptomatic patients. Avoid single doses in pregnancy.

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135
Q

What is the treatment for Trichomonas Vaginalis

A

Metronidazole 400mg twice daily for 5 days.

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136
Q

What is the treatment for Candida (thrush)

A

Women: Antifungal pessary +/- cream

Men: Emollient +/- azole cream

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137
Q

What is the treatment for Chlamydia

A

Doxycycline 100mg bd for 7 days OR Azithromycin 1g stat

A test of cure should be done at least 4 weeks after completion of TX (essential in pregnant women!)

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138
Q

What is the treatment for Epididymo-orchitis

A

Doxycycline 100mg bd for 14 days + Ceftriaxone 500 mg IM

Review in 2 weeks and continue therapy for 1 month if not fully recovered.

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139
Q

What is the treatment for Gonorrhoea

A

Ceftriaxone 500mg IM as a stat dose + Azithromycin 1g PO as a stat dose

Return for test of cure in 2-4 weeks

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140
Q

What is the treatment for Herpes Simplex Virus (HSV 1/2): Primary/ 1st episode

A

Aciclovir, Valaciclovir, Famciclovir for 5 days. Analgesia. Laxatives. Bathing in dilute saline solution.

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141
Q

What is the treatment for Herpes Simplex Virus (HSV 1/2): Recurrent episode

A

Saline washes + analgesics

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142
Q

What is the treatment for Herpes Simplex Virus (HSV 1/2): Persistent recurrent episodes

A

Aciclovir for 6 months

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143
Q

What is the treatment for a Non-immune contact after potential Hep B infection

A

Specific Hep B Immunoglobulin – Works best within 48 hours, of no use after 7 days. An accelerated course of recombinant vaccine should be offered to all those given HBIG and all sexual + household contacts.

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144
Q

What is the treatment for Pelvic inflammatory disease

A

Doxycycline 100mg bd for 14 days + Metronidazole 400mg bd for 14 days + Ceftriaxone 500mg IM

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145
Q

What is the treatment for Syphilis

A

Long-acting Penicillin. Follow up for a minimum of 1 year with repeat serology.

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146
Q

What is the treatment for urethritis

A

Doxycycline 100mg bd for 7 days OR azithromycin 1g stat. All sexual contacts in last 3 months should be treated. Avoid sex (even w/ condoms) until both have completed treatment.

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147
Q

What is the treatment for

Simple external warts

A

Podophyllotoxin cream (avoid in pregnancy + nut allergy), weekly cryotherapy, Imiquimod.

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148
Q

Name 2 skin changes you may see in inflammatory bowel disease and say how they would present

A 
Pyoderma gangrenosum (deep ulcers, usually on legs)
Erythema nodosum (tender red nodules usually seen on both shins - inflammation of fat cells)
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149
Q

What changes would you see in mild acne

A

Mainly comedones

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150
Q

How would you treat mild acne?

How long until the treatment becomes effective?

A

Topical benzoyl peroxide or topical retinoid or topical antibiotic alone.
Takes up to 8 weeks to be effective

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151
Q

What would you see with moderate acne?

A

Inflammatory lesions

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152
Q

What treatment options are available for moderate acne?

A

Topical antibiotic w/ benzoyl peroxide or topical retinoid
Oral antibiotic e.g. tetracycline
COCP

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153
Q

What would you see in severe acne?

A

Nodules, cysts, scars, inflammatory papules and pustules.

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154
Q

How would you treat severe acne?

A

Isoretinoin (teratogenic!)

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155
Q

What topical treatment options are available for plaque psoriasis?

A

Topical corticosteroids + topical vitamin D. Tar is widespread disease. Dithranol in TX resistance

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156
Q

What conditions are narrowband UVB phototherapy typically used for?

A

guttate or plaque psoriasis

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157
Q

What conditions are PUVA typically used for?

What is the extra component in PUVA

A

Extensive large plaque psoriasis or localised pustular psoriasis
P in PUVA stands for Psoralen

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158
Q

What oral drugs can be used in severe psoriasis?

A

Methotrexate, ciclosporin, acitretin

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159
Q

Common causes of cellulitis

A

B haemolytic streps + staphs

160
Q

Treatment for cellulitis

A

Elevate affected part

Benzylpenicillin IV + Flucloxacillin PO

161
Q

Treatment for scabies

A

Permethrin dermal cream. Oral ivermectin if severe.

Treat all close contacts!

162
Q

Cause of impetigo

A

Staph aureus

163
Q

Tx for impetigo

A

Topical fusidic acid

Oral flucloxazillin if severe

164
Q

Treatment options for eosinophilic folliculitis

A

Tacrolimus, topical steroids. UVB therapy, PUVA therapy

165
Q

Treatment for common warts and plantar warts if they are painful, unsightly or persisting

A

Topical salicylic acid (keratolytic), cryotherapy, duct-tape occlusion

166
Q

Treatment options for genital warts

A

Podophyllin or imiquimod cream

Cryotherapy

167
Q

What is herpes zoster?

A

The varicella-zoster virus lies dormant in dorsal root ganglia after chickenpox. It presents as being dermatomal. Polymorphic red papules, vesicles, pustules.

168
Q

Treatment for herpes zoster

A

If mild, no TX. Aciclovir PO 1 wk.

169
Q

How do you treat candida on the skin?

A

Imidazole cream

170
Q

How do you treat candida in the mouth?

A

Nystatin or miconazole oral gel

171
Q

How do you treat candida in the vagina?

A

Imidazole cream +/- pessary

172
Q

How does squamous cell carcinoma look like?

A

Persistently ulcerated/crusted firm irregular lesion

173
Q

2 differential diagnoses of malignant melanoma

A

Seborrheic keratosis; benign melanocytic lesions

174
Q

Is melanoma responsive to radiotherapy?

A

NO. Melanoma is not responsive to radiotherapy!

175
Q

What treatment options are available for actinic keratosis?

A 
Emollient for mild AK 
Diclofenic gel 
Fluoracil cream 
Imiquimod
Cryotherapy 
Photodynamic therapy 
Excise if atypical, unresponsive to TX or invasive SCC suspected
176
Q

What is Bowen’s disease?

A

SCC in situ

177
Q

How does Bowen’s disease look like?

A

Well-defined slowly enlarging red scaly plaque w/ flat edge (Asymptomatic). Full thickness dysplasia.

178
Q

What are the 3 stages of naevi?

A

1) Junctional: flat evenly pigmented
2) Compound: raised, evenly pigmented dome-shaped naevi
3) Intradermal: pale brown papules

179
Q

How does lentigo maligna look like and what is the treatment of it?

A

Brown macules/patches. Irregular, variably pigmented. Excise.

180
Q

How does seborrheic keratosis look like and what is the treatment of it?

A

Small, rough then thick, wart-like surface. Usually round. Harmless - most need no TX.

181
Q

How do pyogenic granuloma arise and what do they look like?

A

Vascular, due to minor trauma, usually on fingers. Fleshy moist red lesion, grows rapidly, bleeds easily.

182
Q

Which condition is pretibial myxoedema associated with?

A

Exophthalmic thyroid eye disease

183
Q

How does necrobiosis lipoidica look like? What condition is it associated with?

A

Waxy, shiny yellowish areas on shins

Linked with diabetes

184
Q

How does acanthosis nigricans look like?

What condition is it associated with?

A

Pigmented, rough thickening of axillary, neck or groin skin.
Diabetes

185
Q

What condition is localised granuloma annulare linked to?

What condition is extensive granuloma annulare linked to?

A

Localised: Autoimmune thyroiditis
Extensive: Diabetes

186
Q

How does pyoderma gangrenosum look like?

Which condition is it associated with?

A

Rapidly growing, recurring nodulo-pustular ulcers with tender necrotic edge.
IBD

187
Q

Give a few examples of drugs that can lead to pruritis

A

Statins, ACEi, opiates, antidepressants

188
Q

How and in who does bullous pemphigoid present in?

How common is oral involvement?

A

Over 65y/o, tense blisters on urticated base

Oral involvement is RARE

189
Q

What is the pathophysiology behind bullous pemphigoid?

A

IgG autoantibodies to the basement membrane

190
Q

What is the treatment for bullous pemphigoid?

A

V potent topical steroids; Prednisolone PO

191
Q

How and in who does pemphigus present in?

How common is oral involvement?

A

Affects younger people. Flaccid, superficial blisters on normal looking skin - rupture easily, leading to widespread erosions.
Oral ulceration is common.

192
Q

What is the pathophysiology of pemphigus?

A

Due to IgG autoantibodies against desmosomal components –> acantholysis (keratinocytes separate from each other)

193
Q

What is the treatment of pemphigus?

A

PO prednisolone with tapering. Rituximab and IV Igs in resistant cases.

194
Q

How can you diagnose both bullous pemphigoid and pemphigus?

A

Positive immunofluorescence

195
Q

What condition is dermatitis herpetiformis linked to?

A

Coeliac disease

196
Q

What area is 1 FTP equivalent to?

A

Palmar surface of 2 adult hands

197
Q

Where does a trichileminal (pilar) cyst derive from?
Who does it occur more commonly in?
Which area does it commonly affect?

A

Derived from cells @ bottom of hair foliicle
Most common in middle aged women
Scalp most commonly affected

198
Q

Where does an epidermoid cyst derive from?
What size are they typically?
Who does it commonly affect?

A

Epidermal cells that line the top of the hair follicle (infundibulum)
Pea-sized with a punctum
Young and middle-aged adults

199
Q

What is another name for cherry angioma? What actually are they?

A

Campbell de Morgan spots.

Acquired overgrowth of predominantly dilated capillaries

200
Q

What is another name for strawberry naevus?

How long do they last for?

A

Capillary haemangioma

Nearly all resolve over several years.

201
Q

Define a keloid scar

A

A fibrous tissue overgrowth beyond the site of trauma

202
Q

What is the treatment of keloid scars?

A

Dressing w/ silicone. Steroid cream/tape/injection

203
Q

In which condition would you see lots of neurofibromas?
What is its inheritance pattern?
What other feature may you see?

A

Neurofibromatosis type 1
Autosomal dominant
Café au lait macules

204
Q

How does sebaceous gland hyperplasia present?

How can they be treated?

A

Soft, yellow-domed papules.

Usually no TX required but can be gently cauterised to flatten.

205
Q

What condition are sebaceous adenomas linked to?

A

Muir Torre syndrome (a cancer-prone genetic syndrome)

206
Q

What is the significance of the lamina lucida?

A

It is the weakness spot of the dermal-epidermal junction and is where most blisters occur after trauma.

207
Q

What is the pathophysiology of bullous impetigo? Which patients does it occur in?

A

S. aureus toxins can directly cleave desmoglein 1 to form blisters.
Common in paeds.

208
Q

How is staphylococcal scalded skin syndrome diagnosed?

A

Frozen section

209
Q

What is the pathophysiology behind staphylococcal scalded skin syndrome?

A

Bacterial toxin cleaves desmoglein 1 –> superficial split in dermis.

210
Q

How does erythroderma present? How dangerous is it?

A

90% of skin is involved w/ inflammatory neoplastic process

Risk of mortality due to skin failure –> fluid loss, infection, heat loss, catabolic.

211
Q

Name some examples of causes of erythroderma

A

Eczema, psoriasis, drug reactions, skin lymphomas.

212
Q

What is the pathophysiology behind toxic epidermal necrolysis? What is the most common cause?

A

Full thickness epidermal loss due to massive keratinocyte apoptosis.
Drugs are the commonest cause

213
Q

Give examples of drugs that can cause toxic epidermal necrolysis

A

Allopurinol, Abx, anticonvulsants, NSAIDs

214
Q

What is SCORTEN?

A

A predictive mortality scale used for toxic epidermal necrolysis
Higher mortality if: epidermal detachment; older; malignancy; HR >120; increased Urea and glucose; decreased bicarbonate.

215
Q

What is the treatment for toxic epidermal necrolysis?

A

Supportive (Silicon mesh). IV Igs.

216
Q

What is the treatment for angioedema?

A

Regular antihistamines and systemic steroids

217
Q

What is the treatment for guttate psoriasis?

A

UV light (too widespread for topical TX!)

218
Q

What does guttate psoriasis typically follow?

A

A strep. infection.

219
Q

What is the treatment for erysipelas?

A

IV Penicillin

220
Q

What is another name for eczema herpeticum?

A

Kaposi’s varicelliform eruption

221
Q

What is the treatment for eczema herpeticum?

What should you never ever ever give these patients?

A

Admit. High-dose anti-viral TX.

Do NOT give steroids or calcineurin blockers

222
Q

What is the pathophysiology of eczema herpeticum?

A

Herpes simplex type 1 superinfection of atopic eczema

223
Q

How does eczema herpeticum present?

A

Widespread. Multiple monomorphic vesicles, rapid onset, systemically v unwell.

224
Q

What is miliaria?

A

Sweat retention –> tiny vesicles/papules.

225
Q

What causes porphyria cutanea tarda?
How does it present?
What is it exacerbated by?

A

Disorder of haem synthesis
Blisters & erosions. Photosensitivity
Exacerbated by XS alcohol

226
Q

What is the most common form of photosensitivity and how does it present?

A

Polymorphic light eruption

V itchy, erythematous papular eruption

227
Q

What is the pathophysiology of erythema nodosum?

A

Due to inflammation in subcut tissues.

228
Q

What are the causes of erythema nodosum?

A

Sarcoidosis, drugs (e.g. the pill), IBD

229
Q

What changes in the hands can be seen in a patient with dermatomyositis?

A

Proximal nailfolds: Swelling + erythema

Violaceous erythema over knuckles

230
Q

Pathophysiology behind senile purpura?

A

Due to loss of supporting collagen in dermis with age +/- steroid TX

231
Q

How does erythema multiforme present?

A

Symmetrical eruption of discoid inflamed plaques. Some blister in the middle. Affect peripheries.

232
Q

Prognosis of Stevens Johnson syndrome?

A

Most cases settle spontaneously with symptomatic TX in 1 - 2 weeks

233
Q

How does pyoderma gangrenosum present?

A

Acutely inflamed, breakdown + ulcerate. Blue edge to ulcer.

234
Q

What measurement is used to assess CKD severity?

235
Q

What factor does eGFR take into account?

A

Creatinine, age, gender, ethnicity.

236
Q

How would you confirm that a patient has proteinuria?

A

Measure their ACR again using an early morning sample (tell the patient not to eat meat 12 hours before)

237
Q

Define CKD

A

Abnormal kidney function OR structure for over 3 months.

238
Q

What is the GFR of someone in stage 2 of CKD?

239
Q

What is the GFR of someone in stage 3b of CKD?

240
Q

What is the result for someone with proteinuria classed at A2?

241
Q

What would you do with a young patient who has a family history of autosomal dominant polycystic kidney disease?

A

I would do US screening when they’re in their early 20s

242
Q

How can you screen for renal artery stenosis?

A

Magnetic resonance angiogram

243
Q

Name 3 investigations you would do for myeloma/MGUS

A

Serum & urine free light chains +/- protein electrophoresis

244
Q

When should you NOT do a renal biopsy?

A

If there is evidence of infection/obstruction

245
Q

What should you do in terms of testing if you find an abnormal eGFR?

A

Repeat eGFR (> 2 weeks to exclude AKI. X3 over 90 days to see rate of progression)

246
Q

Generally, what 2 meds are used to proteinuria?

A

ACEi / ARBs

247
Q

What is albuminuria a risk factor for?

A

Cardiovascular disease

248
Q

What does PTH convert?

A

25 Vit D to 1,25 Vit D

249
Q

Name 2 signs on bone that can arise due to persistent secondary hyperparathyroidism

A 
Brown tumour (Cystic degeneration of bone)
Rugger Jersey spine
250
Q

What type of laxative would you give for opiate-induced constipation?
Give an example

A

Stimulant laxatives e.g. Senna

251
Q

What is Danthron and what is its clinical relevance?

A

It is a type of stimulant laxative. It turns urine orange and burns skin so avoid using in patient’s who are urine incontinent. It is a carcinogen so only use in palliative patients.

252
Q

What is a contraindication of a stimulant laxative?

A

Complete bowel obstruction - can lead to perforation

253
Q

What type of laxative is Docusate sodium?

A

A stool softener

254
Q

On what part of the bowel do stimulant laxatives act upon?

A

The large bowel

255
Q

On what part of the bowel do osmotic laxatives act on?

A

Small bowel

256
Q

Lactulose and Movicol are examples of what type of laxatives?

A

Osmotic laxatives

257
Q

What is Bisacodyl?

A

A suppository (–> anorectal stimulation)

258
Q

How does glycerol act as a suppository?

A

It draws fluid into the rectum which softens and lubricates stool

259
Q

What effect does low blood pressure have on the arterioles in the kidney?

A

Afferent dilatation and efferent constriction

260
Q

How can Angiotensin receptor blockers be dangerous to the kidneys? (Bear in mind the action of angiotensin II)

A

ARBs can cause acute renal failure. Angiotensin II leads to efferent vasoconstriction which helps to maintain GFR when renal perfusion is low < ARBs block this :(

261
Q

What effect does NSAIDs have on the arterioles of the kidneys?

A

NSAIDs block vasodilation of afferent arterioles, leading to reduced GFR (unable to maintain perfusion of kidneys –> decreased urine output)

262
Q

How long does acute tubular necrosis tend to last? What may the patient need in the meantime?

A

6 weeks

Patient may need haemodialysis

263
Q

What happens to the GFR of someone with nephrotic syndrome?

A

Their eGFR is usually normal

264
Q

What happens to the GFR of someone with nephritic syndrome?

A

Their eGFR is low

265
Q

What is the mechanism behind oedema in someone with nephrotic syndrome?

A

Decreased oncotic pressure

266
Q

What is the mechanism behind oedema in someone with nephritic syndrome?

A

Low salt and H20 excretion

267
Q

Out of nephrotic and nephritic syndrome, which one would you see more prominent proteinuria?
What is the mechanism of the proteinuria here?

A

Nephrotic syndrome

Podocytes lose their foot processes

268
Q

Why do you get hypercholesterolaemia in nephrotic syndrome?

A

Due to heavy albuminuria

269
Q

What condition can minimal change disease, membranous nephropathy and FSGS all lead to?

A

Nephrotic syndrome?

270
Q

What are the treatment options for nephrotic syndrome?

A

Salt +/- water restriction
Loop diuretics
ACEi/ARBs

271
Q

How can nephrotic syndrome lead to AKI?

A

V low serum albumin could –> reduced circulating volume

272
Q

How can nephrotic syndrome predispose patients to VTEs?

A

Differential loss of pro + anti - thrombotic proteins from the blood

273
Q

How can nephrotic syndrome predispose to Infection?

A

Low circulating Igs - lost in urine

274
Q

What condition can ANCA vasculitis, Anti-GBM disease, IgA disease and IE lead to?

A

Nephritic syndrome

275
Q

What are the 3 diseases that come under the umbrella of ANCA associated vasculitis?

A

Granulomatosis w/ polyangiitis (Wegener’s granulomatosis)

Microscopic polyangiitis (part of polyarteritis nodosa)

Eosinophilic granulomatosis w/ polyangiitis (Churg-Strauss syndrome)

276
Q

Give 2 antibodies that are associated with Granulomatosis w/ polyangiitis (AKA Wegener’s granulomatosis)

A

cANCA and Antiproteinase 3 Antibodies

277
Q

Give 4 ways that microscopic polyangiitis can be differentiated from Granulomatosis w/ polyangiitis (AKA Wegener’s granulomatosis)

A

Microscopic polyangiitis:

  • PNS also affected
  • Shorter onset
  • Less likely to relapse
  • No granulomatosis inflammation
278
Q

Name 2 antibodies that are associated with Microscopic polyangiitis

A

pANCA and anti-myeloperoxidase antibodies

279
Q

How does Eosinophilic granulomatosis w/ polyangiitis (Churg-Strauss syndrome) present?

A 
Late onset progressive asthma 
Peripheral neuropathy 
Nasal polyps 
Myocarditis 
CNS vasculitis 
Pulmonary infiltrates 
Peripheral eosinophilia
280
Q

What medication should all patients with vasculitis be started on?

A

Corticosteroids

281
Q

What treatment options are available for patients with mild/moderate vasculitis?

A

Prednisolone (inhibits T cell function)

Mycophenolate mofetil, methotrexate

282
Q

What treatment options are available for patients with severe vasculitis?

A

Cyclophosphamide (decreases B cells/Abs and neutrophils)
Rituximab (eradicates all peripheral B cells and Igs)
Plasma exchange

283
Q

How can cutaneous lupus present?

A

Malar rash, skin photosensitivity, discoid lesions

284
Q

What options are available for maintenance treatment of SLE?

A

Low dose steroids, azathioprine or mycophenolate mofetil

285
Q

What treatment options are available for remission induction in someone with severe SLE?

A

High dose steroids, cyclophosphamide or rituximab

286
Q

How does myeloma lead to hypercalcaemia?

A

The overexpression of receptor activator nuclear factor in myeloma activates osteoclasts which resorb more bone –> lytic lesions.

287
Q

What does the acronym CRAB stand for in relation to the effects of myeloma?

A

Calcium
Renal failure
Anaemia
Bone

288
Q

Which light chain is more problematic out of kappa and lambda?

A

Lambda! It is heavier, less renal clearance, long-half life

289
Q

What is the pathogenesis of cast nephropathy?

A

Light chains are filtered freely @ glomerulus. Normally all light chains are absorbed in PCT, but if capacity of 10 - 30g a day is exceeded, it continues to travel throughout the tubule and binds to tamm-Horsfall protein and form casts –> micro obstruction of urine

290
Q

What vaccine should you give to patients before they start dialysis?

A

HBV vaccine (to non-immune patients)

291
Q

When should you start dialysis in a patient with CKD?

A

When their eGFR <10 ml/min/1.73 m^2

292
Q

When should you start dialysis in a patient with AKI?

A

Creatinine >500 mcmol/L or oligo/anuric for AKI patients

293
Q

What leads to encapsulating peritoneal sclerosis and what is the danger of it?

A

A progressive change over 8 - 10 years due to changes that occur in the peritoneal membrane as a result of peritoneal dialysis
Can lead to recurrent bowel obstruction

294
Q

On what cells are HLA class I antigens expressed on?

A

All nucleated cells (A, B, C)

295
Q

On what cells are HLA class II antigens expressed on?

A

Antigen presenting cells (DR, DQ, DP)

296
Q

When does warm ischaemia occur?

A

When a kidney remains in situ in the donor but is under perfused due to hypotension or circulatory death

297
Q

When does cold ischaemia occur?

A

Following organ retrieval while the kidney is being transported to the recipient centre. A lot of this occurs when the donor is living.

298
Q

What side effects can arise due to tacrolimus?

A

Tremor, increased risk of post-transplant diabetes, neurotoxic, nephrotoxic

299
Q

What side effects can arise due to ciclosporin?

A

Hirsutism, gum hypertrophy

300
Q

What drug interaction can occur with azathioprine?

A

Allopurinol interaction –> bone marrow toxicity

301
Q

Name some examples of nephrotoxic drugs?

A

NSAIDs, ciclosporin, tacrolimus, penicillamine, chemo, acyclovir, methotrexate, allopurinol, x-ray contrast agent

302
Q

Is GFR over or under estimated in elderly patients based on creatinine measurements?

A

Over-estimated as production of creatinine is proportional to muscle mass. The elderly/cachetic have decreased muscle mass –> increase in creatinine production –> overestimates GFR.

303
Q

What triad do you get in Alport’s syndrome?

A

Glomerulonephritis, end-stage kidney disease and hearing loss

304
Q

Episodic macroscopic haematuria with throat infections - what is the diagnosis?

A

IgA nephropathy

305
Q

Normal ACR in men?

Normal ACR in women?

A

<2.5 in men

<3.5 in women

306
Q

What are the 3 indications for emergency dialysis?

A
  1. Severe hyperkalaemia (>7mmol/L) which is resistant to medical TX
  2. Pulmonary oedema
  3. Worsening severe metabolic acidosis (pH <7.2 or base XS <10)
307
Q

What is the programme in the UK for cervical cancer screening?

A

3 yearly 25-50

5 yearly 50-64

308
Q

How often is faecal occult blood testing done in the UK?

A

2 yearly for those between 60 and 74 years old

309
Q

What is the programme in the UK for mammography?

A

3 yearly for patients aged 50-70

310
Q

What are the diagnostic categories of breast biopsy?

From B1 to B5b

A 
B1: Normal 
B2: Benign 
B3: Atypical (probably benign)
B4: Suspicious of carcinoma 
B5: Malignant 
B5a: DCIS 
B5b: Invasive disease
311
Q

In terms of TNM staging for breast cancer, what stage would a tumour get that is 3 cm

A

T2: bigger than 2cm but smaller than 5cm

312
Q

In terms of TNM staging for breast cancer, what stage would a tumour get that is 1 cm and has directly extended into the skin

A

T4 = any size tumour with direct extension into chest wall and/or skin (ulceration or nodules)

313
Q

How many lymph nodes would have to be involved for a breast cancer to be graded as N2?

A

4 - 9 Lymph nodes

314
Q

If a breast cancer is Her-2 positive, what medication is effective in treating it?

A

Trastuzumab AKA Herceptin

315
Q

In terms of TNM staging for bowel cancer, how many nodes would have to be involved for it to be graded N2?

A

Over 4 lymph nodes

316
Q

In terms of TNM staging for bowel cancer, what grade would a tumour get if it invaded the muscularis propria?

317
Q

In terms of TNM staging for bowel cancer, what must have a tumour invaded to be considered T3

A

T3 = Tumour has invaded subserosa

318
Q

In terms of TNM staging for bowel cancer, what does a grade T4 tumour mean?

A

It has directly invaded adjacent organs/structures or through the visceral peritoneum

319
Q

In terms of TNM staging for bowel cancer, what grade would a tumour get that has invaded the submucosa?

320
Q

What mutated gene is inherited in FAP?

A

APC gene (a tumour suppressor gene)

321
Q

What mutation occurs in HNPCC?

A

Germline mutation in DNA mismatch repair system (diagnosed by loss of expression of MMR proteins on immunohistochemistry

322
Q

Which gene mutation is associated with a reduced response to EGFR targeted treatment (e.g. cetuximab)?

A

Activating KRAS mutations

323
Q

What are the WHO performance statuses from 0 to 4?

A 
0 = fully active 
1 = Cannot carry out heavy physical work, but can do anything else 
2 = Up and about more than half the day - not well enough to work
3 = In bed/ sitting more than half the day - need some help looking after yourself 
4 = In bed/ chair all the time, need a lot of looking after
324
Q

A man is still independent but has had to give us his job - what is his WHO performance status?

325
Q

A woman spends most of her day in her bed. She can cook for herself but has a carer coming in for an hour or 2 a day to clean her flat for her - what is her WHO performance status?

326
Q

What does CHART stand for and in what context may it be used?

A

CHART = Continuous Hyperfractionated Accelerated Radiotherapy
Is used as radical radiotherapy in lung cancer

327
Q

In which 3 groups are EGFR mutations in lung cancer more common? What is the clinical relevance?

A 
More common in...
1) Adenocarcinomas 
2) Never smokers 
3) Asians 
Can use antibodies that target EGFR mutations e.g. Iressa :)
328
Q

Where must a small cell carcinoma be to be classed as ‘limited’?

A

Ipsilateral hemithorax and supraclavicular lymph nodes

329
Q

Name the palliative care treatments for the following in patients with lung cancer…

a) Symptomatic pleural effusions
b) Cough
c) Hoarse voice
d) Symptomatic brain mets

A

a) Drain pleural effusions
b) Opiates
c) ENT referral
d) Dexamethasone

330
Q

What is the most common prostate cancer and where does it occur?

A

Adenocarcinoma - arising in peripheral prostate

331
Q

At what age would you consider a radical prostatectomy?

A

< 70 year olds

332
Q

Name 2 ways that radical radiotherapy for prostate cancer can be delivered?

A

As an external beam or brachytherapy

333
Q

How would you manage someone who is over than 70 years old with low-risk prostate cancer?

A

Active surveillance

334
Q

What is the role of hormone therapy in prostate cancer? In whom should you consider it?

A

Hormone treatment alone temporarily delays tumour progression but refractory disease eventually develops - consider in old unfit patients with high-risk prostate cancer
They may give benefit in metastatic disease for 1 - 2 years.

335
Q

What is an example of a hormonal drug used in prostate cancer? How does it work?

A

Goserelin - it is a LHRH agonist. It first stimulates then inhibits pituitary gonadotrophin

336
Q

Name 5 types of cancer where spinal cord compression is common?

A

Breast, prostate, lung, myeloma and lymphoma

337
Q

In which part of the spinal cord does spinal cord compression commonly affect?

A

Thoracic cord

338
Q

List symptoms/signs of spinal cord compression

A 
- Radicular pain exacerbated by coughing/ straining, not relieved by bed rest
Late signs: 
- Weakness of limbs 
- Sensory loss 
- Retention 
- Dribbling 
- Incontinence
339
Q

What symptoms would you get in anterior spinal cord compression?

A

Partial loss of pain and temperature below the lesion

340
Q

What symptoms would you get in posterior spinal cord compression?

A

Loss of vibration and position.

Band of dysesthesia (abnormal sensation) @ level of lesion.

341
Q

What is another term for lateral cord compression? How does it present?

A

Brown-Sequard syndrome.
Ipsilateral loss of vibration and position and UMN weakness
Contralateral loss of pain and temperature

342
Q

At what point in the spinal cord may lesions below cause cauda equina syndrome?

A

Lesions below L1/2

343
Q

How does cauda equina syndrome present?

A
  • Sciatic pain (often bilateral)
  • Bladder dysfunction with retention and overflow incontinence
  • Impotence
  • Sacral (saddle) anaesthesia
  • Loss of anal sphincter tone
  • Weakness and wasting of gluteal muscles
  • Band of hyperaesthesia at level of lesion
  • Motor and sensory loss at and below level of lesion
344
Q

What is a gibbus? When might you see it?

A

It is a structural kyphosis @ the site of wedged/ collapsed vertebra. Spinal cord compression/ cauda equina syndrome.

345
Q

What imaging must you do in spinal cord compression/ cauda equina compression?

A

MRI scanning of the whole spine

346
Q

What treatment must you give someone with spinal cord compression/ cauda equina syndrome?

A

Dexamethasone ASAP to decrease peritumoral oedema

Surgical decompression then radiotherapy

347
Q

At what level of free Ca2+ does hypercalcaemia become an urgent matter?

A

If free Ca2+ is 3 mmol/L or over

348
Q

What 2 things is the level of free Ca2+ dependent on?

A

Serum albumin and arterial pH.

349
Q

List 3 causes of general hypercalcaemia in the context of malignancy?

A

1) Osteolysis
2) Humoral mediators e.g. PTHrP in SCC
3) Dehydration

350
Q

What is a specific way that myeloma leads to hypercalcaemia?

A

Myeloma leads to deposition of Bence-Jones proteins which cause renal impairment and decreases calcium excretion.

351
Q

What is a specific way that some lymphomas lead to hypercalcaemia?

A

They produce active metabolites of vitamin D that lead to increased intestinal absorption of calcium.

352
Q

How does hypercalcaemia present?

A

Drowsiness, N&V, constipation, polydipsia, dehydration, arrhythmias

353
Q

What 3 ECG changes would you see with hypercalcaemia?

A
  • Increased PR interval
  • Decreased QT interval
  • Wide QRS
354
Q

What are the treatments for hypercalcaemia?

A
  • Rehydration (3 - 6 L/24 hours, 0.9% saline), monitor U&Es
  • Consider bisphosphonates if Ca2+ remains 3.0mmol/L or over despite rehydration
  • Loop diuretics
  • Avoid immobility (increases osteoclast activity)
355
Q

Define neutropenic sepsis

A

Temperature over 38 degrees and a neutrophil cound less than 0.5 x 10^9.

356
Q

How do you treat neutropenic sepsis? What medication would you add if you suspect a gram positive organism e.g. Hickmann line sepsis?

A

Treat empirically with piperacillin/ tazobactam AKA Tazocin.
Add vancomycin if gram positive organism is suspected

357
Q

Other than antibiotics, what is the regimen for neutropenic sepsis patients?

A
  • Barrier nursing
  • Avoid IMs
  • Do swabs
  • Do cultures
  • Candida prophylaxis
358
Q

What cultures need to be taken in a patient with neutropenic sepsis?

A

3 Blood samples peripherally +/- Hickmann line

Urine, sputum and stool samples

359
Q

What is the MASCC score?

Which score would reassure you and what would you do about it?

A

It predicts risk of serious complications in febrile neutropenia.
A score of 21 or above suggests that the risk of complications are low and so the patient should not be admitted.

360
Q

How long should you continue antibiotics for in a person with neutropenic sepsis?

A

Continue antibiotics until afebrile for 72hrs/5 days and until neutrophils are over 0.5 x 10^9/ L

361
Q

Which antibiotic can be given prophylactically to patients to prevent sepsis?

A

Give a fluroquinoline e.g. ciprofloxacin before neutropenia gets serious

362
Q

What cancers does Li-Fraumeni syndrome increase your risk of getting?

A
  • Sarcomas
  • Adrenocortical cancer in childhood
  • Early onset BC
  • Brain tumours
  • Leukaemia
363
Q

What cancers does Von Hippel Lindau syndrome increase your risk of getting?

A
  • Retinal angiomas
  • Cerebellar and spinal cord haemangiomas
  • Renal cell carcinoma
  • Phaechromocytoma
364
Q

What cancers does Lynch syndrome increase your risk of getting?
What is another name for Lynch syndrome?

A

AKA HNPCC (Hereditary nonpolyposis colorectal cancer)

  • Bowel
  • Endometrial
  • Ovarian
365
Q

What breast surveillance must take place for women found to be BRCA positive?

A

Annual MRI and mammogram 30-50 year olds

Mammograms in 50-70 years olds.

366
Q

What ovarian surveillance must take place for women found to be BRCA positive?

A

Transvaginal US + CA125 from 35 years old.

367
Q

How can BRCA positive men be affected by this gene mutation?

A

Increases their risk of prostate and breast cancer.

368
Q

What is a bilateral salpingoophorectomy and when would it decrease the risk of breast cancer in women?

A

Removal of fallopian tubes and ovaries. It decreases the risk of breast cancer if done 10 years before menopause.

369
Q

What mutation occur in Lynch syndrome?

A

Mutations in mismatch repair genes: MLH1. MSH2, MSH6, PMS2

370
Q

Which 2 criteria may be used in the diagnosis of Lynch syndrome?

A

Revised Amsterdam criteria and Bethesda criteria

371
Q

What colorectal screening should occur in someone with Lynch syndrome?

A

2 yearly colonoscopy from 25 to 75 years old.

372
Q

How does Familial Adenomatous Polyposis present?

A

Bowel cancer

>100 adenomatous polyps in the colon and rectum

373
Q

Whom should be offered mutation testing for Familial Adenomatous Polyposis and at what age?

A

Offer mutation testing age 10-12 years old for those at 50% risk and family mutation known.

374
Q

If found to have the mutation for Familial Adenomatous Polyposis, what screening must be done in those individuals and at what age?

A

Annual colonoscopy from 10 - 12 years old.

375
Q

When polyp load becomes high in someone with Familial Adenomatous Polyposis, what is the treatment?

A

Elective colectomy

376
Q

Is Multiple Endocrine Neoplasia 2 (MEN 2) dominant or recessive?

A

Autosomal dominant

377
Q

Which 3 things do Multiple Endocrine Neoplasia 2 (MEN 2) predispose to?

A

Medullary thyroid carcinoma and hyperplasia C cells and phaechromocytoma

378
Q

What gene mutation occurs in MEN2?

A

RET mutation

379
Q

Why must you refer all patients with Medullary Thyroid Carcinoma?

A

Medullary Thyroid Carcinoma has a high rate of germline RET mutations (think MEN2)

380
Q

A 29 year old patient develops thyroid cancer - which genetic condition are you worried about?

A

Multiple endocrine neoplasia 2 (MEN 2)

381
Q

In someone with a family history of Multiple Endocrine Neoplasia 2, when should you test them? What should you do if this test comes back as positive?

A

Should do a pre-symptomatic test in 5 year olds. Perform thyroidectomy if positive.

382
Q

What screening must you do in someone with Multiple Endocrine Neoplasia 2?

A

Annual urine testing for phaechromocytoma.

383
Q

Which cancer can an infection of EBV cause?

A

Burkitt lymphoma

384
Q

Which cancer can an infection of Helicobacter pylori cause?

A

Gastric cancer

385
Q

Define neutropenia

A

An absolute neutrophil count of <1.0 x 10^9/L

386
Q

Define Nadir. When does it tend to occur?

A

The lowest count that neutrophils fall to. Usually occurs 7 - 14 days post chemo and after large area radiotherapy.

387
Q

Define severe neutropenia

A

<0.5 x 10^9

388
Q

Define febrile neutropenia

A

> 38 degrees and <1.0x10^9/L

389
Q

What can candida albicans lead to in an immunocompromised patient?

A

Oropharyngeal candidiasis

390
Q

What can Aspergillus lead to in an immunocompromised patient? What is the sign seen on imaging?

A

Respiratory infection

Would see a crescent of lucency - ‘air crescent’ on CXR = typical of invasive aspergillosis.

391
Q

How does pneumocystic jirovecu (carinii) appear on CXR?

A

Ground glass appearance

392
Q

What can Listeria monocytogenes lead to? Why is it difficult to treat? What is the treatment?

A

Meningitis
Resistant to harsh conditions (can grow @ 4 degrees!)
TX = High dose amoxicillin

393
Q

What is the treatment for severe Crohn’s?

A

Severe: IV steroids, IV fluids.

394
Q

What 3 other treatment options are available for severe Crohn’s if steroids do not work?

A
  • Azathioprine if refractory to steroids (Takes 6-10 weeks to work!)
  • Anti-TNF a (decreases disease activity - screen pts for TB before starting!)
  • Anti-integrin (Monoclonal Abs targeting adhesion molecules)
395
Q

What diets can you suggest to patients experiencing a Crohn’s flare up?

A

Elemental diets can give remission

396
Q

How many people with Crohn’s will eventually need surgery?

A

Most will need surgery

Medicine (15 decks)

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