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MRCP Part 1 > Passmed > Flashcards

Passmed Flashcards

1
Q

What is the first line management for primary axillary hyperhidrosis?

A

Topical aluminium hydrochloride

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2
Q

Outline the management options for hyperhidrosis?

A
  • Topical aluminium hydrochloride
  • Iontophoresis - for palmar, plantar and axillary hyperhidrosis
  • Botulimun toxin - for axillary symptoms
  • Surgery - e.g. endoscopic transthoracic sympathectomy - beware risk of compensatory sweating
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3
Q

What is the single most important blood test in restless leg syndrome?

A

Serum ferritin

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4
Q

Causes and associations of restless leg syndrome?

A
  • Family history in 50%
  • Iron deficiency anaemia
  • Uraemia
  • Diabetes mellitus
  • Pregnancy
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5
Q

Aside from conservative management e.g. with walking stretching and massaging the limb, what medical management is there for restless leg syndrome?

A
  • First lie is dopamine agonists e.g. Pramipexole and Ropinirole
  • Treat any iron deficiency
  • Others include benzodiazepines, gabapentin
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6
Q

A 27-year-old man presents to the Emergency Department after a syncopal episode. On inspection of the neck veins he has a prominent ‘a’ wave. On auscultation of the heart, there is a harsh crescendo-decrescendo systolic murmur that is heard best at the apex and lower left sternal border.

What is the diagnosis?

A

HOCM

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7
Q

List some medications to be avoided in HOCM

A
  • Nitrates
  • ACE inhibitors
  • Nifedipine type calcium antagonists / inotropes (note non-dihydropyridines are ok)

Basically things that reduce preload / afterload

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8
Q

Intermittent dysphagia to solids and food impaction in association with asthma and peripheral blood eosinophilia. Did not respond to PPI trial - diagnosis?

A

Eosinophilic oesophagitis

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9
Q

Outline management of eosinophilic oesophagitis?

A
  • Dietary modification - elemental diet, exclude six food groups (common allergy groups like nuts, seafood etc) and targeted exclusion – involve dieticians for advice
  • Topical steroids - if dietary modification fails - e.g. fluticasone and budesonide - 8 week trial
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10
Q

Outline a few complications of eosinophilic oesophagitis?

A
  • Oesophageal strictures
  • Impaction
  • Mallory Weiss tears
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11
Q

At what point do you consider fibrinolysis in STEMI?

A

Within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120 minutes

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12
Q

What are the ECG criteria for STEMI?

A

Elevation of 2.5mm in leads V2-V3 in men under 40 or > 2.0mm in men over 40
1.5mm in V2-V3 in women
1mm ST elevation in other leads
New LBBB

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13
Q

In dual antiplatelet therapy prior to PCI in STEMI, which platelet can be added alongside aspirin if there is no other oral anticoagulant that the patient is on or what if they are on one?

A

No oral anticoag - asprin + prasugrel
On oral anticoag - aspirin + clopidogrel

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14
Q

Which other drugs are given during PCI?

A

If there is radial access: unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)
If there is femoral access: bivaluridin with bailout GPI

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15
Q

What other procedures can be done during PCI excluding the medications you can give?

A
  • Thrombus aspiration
  • Complete revascularisation - considered for patients with multivessel coronary artery disease without cardiogenic shock
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16
Q

Patients undergoing fibrinolysis for STEMI management should also be given what other kind of drug?

What other monitoring should you do when you use a fibrinolytic drug plus this drug?

A

Antithrombin drugs
Repeat ECG after 60-90 minutes to see if ECG changes have resolved - if there is persistent myocardial ischaemia, then PCI should be considered

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17
Q

What is the primary interleukin causing HOTN in sepsis?

A

IL-1 0 stimulates endothelial release of PAF, NO and prostacyclin - causing vasodilation and vacular permeability

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18
Q

List some causes of respiratory alkalosis

A
  • Anxiety leading to hyperventilation
  • PE
  • Salicylate poisoning (N.B causes initial resp alk then later leads to acidosis)
  • CNS disorders: Stroke, subarachnoid haemorrhage, encephalitis
  • Altitude
  • Pregnancy
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19
Q

How to treat isolated systolic HTN?

A

Same treatment formula as standard HTN

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20
Q

Most common cause of traveller’s diarrhoea?

A

E.Coli

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21
Q

In Zolinger Ellison syndrome, what blood marker will be raised, and what secretion test can be used to further investigate Zollinger-Ellison Syndrome?

A

Serum Gastrin
Secretin stimulation test - this will increase secretion of bicarb rich fluid from pancreas and hepatic duct cells - and a positivce test will show markedly raised serum gastrin

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22
Q

What is primary and secondary prevention for hyperlidaemia management and what doses of medication do you give in each?

A

Primary prevention: 10yr cardiovascular risk >/- 10% OR most type 1 diabetics OR CKD if eGFR < 60ml/min/m2 - Atorvastatin 20mg OD

Secondary prevention: known ischaemic heart disease OR cerebrovascular disease or peripheral arterial disease - Arotvastatin 80mg OD

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23
Q

Which antibody can be tested for primary membranous glomerulonephropathy?

A

Anti-PLA2R antibodies

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24
Q

What are the causes of membranous nephropathy?

A

PRIMARY: Primary membranous nephropathy - most commonly associated with PLA2R antibodies
SECONDARY:
* Malignancy e.g. solid tumours (lung, colon, breast, kidney)
* Infections: hep B, C, HIB, malaraia, syphilis, schistosomiasis
* Autoimmune diseases - SLE, sarcoidosis, IBD
* Drugs - NSAIDs, captopril, gold, penicillamine, lithium, clopidogrel

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25
Q

What is the triad with which TTP presents?

A

Fever
Neuro signs
Thrombocytopaenia
Haemolytic anaemia
Renal failure

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26
Q

What investigation can be done to help diagnose TTP? (And therefore also helps differentiate it from HUS)

A

ADAMTS13 assay

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27
Q

When is skin patch test vs skin prick test done?

A
  • Skin patch test - contact hypersensitivity (not IgE mediated - it is a type IV hypersensitivity reaction)
  • Skin prick test - IgE mediated allergies e..g food or pollen allergies
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28
Q

.

A

Ergot derived dopamine agonists including Pergolide, Cabergoline, Bromocroptine for example can cause pulmonary and cardiac fibrosis

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29
Q

What goes wrong in chronic granulomatous deficiency?

A

Primary immunodeficiency caused by a defect in the NADPH oxidase complex, which is integral to function of phagocytic cells e.g. neutrophils. Impairs ability to generate reactive oxygen species necessary to kill certain types of bacteria and fungi

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30
Q

Inheritance pattern of Wiskott-Aldrich syndrome?

A

XLR

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31
Q

How does Wiskott-Aldrich syndrome present?

A
  • Eczema
  • Thrombocytopaenia
  • Immune deficiency including both T and B lymphocytes
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32
Q

Which anti-epileptic drug is contraindicated in absence seizures?

A

Carbamazepine

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33
Q

What is a Leukaemoid reaction? Plus list some causes

A

Presence of immature cells such as myeloblasts, promyelocytes and nucleated red cells in the peripheral blood. This may be due to infiltration of the bone marrow causing the immature cells to be pushed out or sudden demand for new cells

Causes:
* Severe infection
* Severe haemolysis
* Massive haemorrhage
* Metastatic cancer with bone marrow infiltration

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34
Q

Key differentiator between leukaemoid reaction and CML?

A

Leukaemoid reaction - high leucocyte alkaline phosphatase VS CML - low leucocyte alkaline phosphatase score

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35
Q

Genetic mutations causing nephrogenic diabetes insipidus - more and less common ones - what are they?

A
  • More common - affects the vasopressin (ADH) receptor
  • Less common - affects gene encoding the AQP2 channel
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36
Q

What type of glomerulonephritis is most characteristically associated with Wegener’s granulomatosis (Granulomatosis with Polyangiitis)?

A

Rapidly progressive glomerulonephritis

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37
Q

Deficiencies in which complement increases risk of infection with encapsulated organisms?

A

C5-9 deficiency

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38
Q

Which complement deificiency can cause hereditary angioedema?

A

C1 inhibitor protein deficiency (C1-INH)

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39
Q

C1 inhibitor protein deficiency (C1-INH) is linked to which condition?

A

Hereditary angioedema

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40
Q

Give some key features of leukaemoid reaction?

A
  • High leucocyte alkaline phosphatase score
  • Toxic granulation (Dohle bodies) in the white cells
  • ‘Left shift’ of neutrophils i.e. three or fewer segments of the nucleus
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41
Q

How does retroperitoneal fibrosis present?

A

Lower back / flank pain. Fever and lower limb oedema in some patients

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42
Q

List some associations to retroperitoneal fibrosis

A

Riedel’s thyroiditis
Previous radiotherapy
Sarcoidosis
Inflammatory abdominal aortic aneurysm
Drugs: Methysergide

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43
Q

What is the inheritance pattern of achondroplasia? And which gene is mutated?

A

Autosomal dominant mutation in FGFR-3 gene

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44
Q

How do mutations causing achondroplasia usually arise?

A

70% are sporadic mutations. Once present the mutations are inherited in autosomal dominant fashion in the remaining 30% of cases

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45
Q

What is the most important association with HLA-A3?

A

Haemochromatosis

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46
Q

What is the most important association with HLA-B51?

A

Behcet’s disease

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47
Q

List some of the most important associations with HLA-B27?

A

Ankylosing Spondylitis
Reactive arthritis
Acute anterior uveitis
Psoriatic arthritis

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48
Q

What is the most important association with HLA-DQ2/DQ8?

A

Coeliac disease

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49
Q

What are the most important associations with HLA-DR2?

A

Narcolepsy
Goodpasture’s

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50
Q

List some of the most important associations with HLA-DR3

A

Dermatitis Herpetiformis
Sjogren’s syndrome
PBC

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51
Q

List 2 key associations with HLA-DR4

A

T1DM
Rheumatoid arthritis

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52
Q

How does anthrax present?

A

Painless black eschar, may cause oedema
Can cause axillary lympadenopathy
Can cause GI bleeding

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53
Q

In terms of nephrogenic diabetes insipidus, what are the 2 ones that can occur and which is more common?

A

More common - affects the vasopressin (ADH) receptor
Less common - affects AQP2

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54
Q

What is the management of nephrogenic and then of central diabetes insipidus?

A

Nephrogenic - thiazides, low salt / protein diet
Central - desmopressin

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55
Q

True or false - memantine is indicated in mild dementia

A

False

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56
Q

Which clotting factors are dependent on vitamin K?

A

Clotting factors II, VII, IX and X

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57
Q

What is the pattern of neuro symptoms in Brown-Sequard syndrome?

A

Ipsilateral weakness, loss of proprioception and vibration sensation with contralateral loss of pain and temperature sensation

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58
Q

Between Klinefelter’s and Kallmans which typically causes cryptorchidism and which microorchidism?

A

Kallman’s - cryptorchidism
Klinefelter’s - microorchidism

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59
Q

Which type of allergy test is useful for irritants?

A

Skin patch testing

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60
Q

Thiazides can cause which electrolyte abnormality?

A

Hypercalcaemia

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61
Q

A patient with clear NAFLD based on obesity and prediabetes and a comprehensive liver screen is subsequently performed and found to be normal. A liver ultrasound shows fatty infiltration with no focal lesions, biliary duct dilatation or gallstones. What is the next step investigation?

A

Enhanced liver fibrosis test to aid diagnosis of liver fibrosis

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62
Q

Between cervical and ovarian cancer which presents in younger (<45) more commonly and which is more common in nulliparity and which in parity > 3?

A

Cervical more common in < 45 and in people with para > 3, vs ovarian more likely in nullips

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63
Q

Which strains of HPV cause cervical cancer and by what mechanism?

A

HPV 16+18
HPV 16 - E6 gene inhibits the p53 tumour suppressor gene
HPV 18 - E7 gene inhibits the RB suppressor gene

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64
Q

Initially intermittent tingling in the 4th and 5th finger
may be worse when the elbow is resting on a firm surface or flexed for extended periods
later numbness in the 4th and 5th finger with associated weakness

This is all describing which condition?

A

Cubital tunnel syndrome

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65
Q

What is the gold standard method of diagnosing coeliac’s disease?

A

Small bowel biopsy

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66
Q

Chronic diarrhoea with negative anti-TTG and no blood or abdo pain and no extra intestinal manifestations. Takes PPIs long term - likely diagnosis?

A

Microscopic colitis

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67
Q

Give a class of drugs that inhibits bacterial cell wall formation and 2 drug names

A

Glycopeptide antibiotics - teicoplanin and vancomycin

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68
Q

Give some drug classes that inhibit bacterial protein synthesis

A
  1. Macrolides
  2. Aminoglycosides
  3. Tetracyclines
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69
Q

What class of antibiotics inhibit DNA synthesis?

A

Quinolones e.g. ciprofloxacin

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70
Q

Give an example antibiotic that inhibits bacterial RNA synthesis

A

Rifampicin

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71
Q

Name some antibiotics that inhibit bacterial folic acid formation

A

Trimethoprim
Co-trimoxazole
Sulphonamides

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72
Q

Give an antibiotic name that damages DNA

A

Metronidazole

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73
Q

Which chemotherapeutic agent can cause cardiomyopathy?

A

Doxorubicin can cause dose-dependent cardiotoxicitty - can manifest as CHF

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74
Q

Main side effect of Bleomycin?

A

Pulmonary fibrosis

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74
Q

Main side effects of Paclitaxel and Docetaxel?

A

Peripheral neuropathy, Myelosuppression (and neutropaenia), and Hypersensitivity reactions

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75
Q

Main side effects of Dactinomycin?

A

Myelosuppression
GI toxicity

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76
Q

Why can diagnosis of malaria be difficult in pregnant women?

A

Due to placental sequestration of parasites - so may not be as visible on the blood film

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77
Q

Which anti-malarial is contra-indicate in epilepsy?

A

Mefloquine

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78
Q

What is the most appropriate anti-malarial prophylaxis in South East Asia?

A

Atovaquone + Proguanil (Malarone)
N.B there is high cholroquine resistance in S.E Asia therefore malarone preferable

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79
Q

Which anti-malarials can be used in pregnant women?

A

Chloroquine
Proguanil (but should be alongside folate 5mg OD)

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80
Q

Outline the early and late x-ray changes in rheumatoid arthritis

A

Early - loss of joint space, juxta-articular osteopaenia / osteoporosis and soft tissue swelling
Late - joint subluxation and periarticular erosions

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81
Q

What is likely to be found on renal biopsy in granulomatosis with polyangiitis (Wegener’s)

A

Crescentic glomerulonephritis

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82
Q

How does quinine toxicity present?

A

ECG changes e.g. prolonged QR interval
HOTN
Metabolic acidosis
Hypoglycaemia
Tinnitus
Flushing
Visual disturbance
(Sometimes flash pulmonary oedema)

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83
Q

Tinnitus is typical of overdose to which two substances?

A
  1. Aspirin
  2. Quinine
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84
Q

Lamotrigine can cause which dermatological emergency?

A

Stevens-Johnson syndrome

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85
Q

Blood glucose targets in pregnancy
1) Fasting? (mmol/L)
2) After oral glucose tolerance test?(mmol/L)

A

1) < 5.3 mmol/L
2) < 6.4 mmol/L

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86
Q

In gestational diabetes, if blood glucose targets are not met with diet / metformin - what is the next step?

A

Add on insulin

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87
Q

Is it common for discoid lupus to progress to SLE?

A

No - only in 5-10% of cases

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88
Q

How is discoid lupus managed?

A

Topical steroid cream
Oral antimalarials second line e.g. hydroxychloroquine
Avoid sun exposure

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89
Q

In management of medication overuse headaches we basically withdraw the medication, in which circumstances do we do so abruptly and in which circumstances do we do so gradually?

A

Simple analgaesia + triptans - stop abruptly
Opioid analgaesia - withdraw gradually

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90
Q

What is the most common side effect of ciclosporin?

A

Nephrotoxicity

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91
Q

How is neurogenic bladder managed in MS patients?

A

First do an ultrasound to assess post void residual volume
1. If significant residual volume: intermittent self catheterisation
2. If non-significant residual volume: anticholinergics

Note we do this because anticholinergics can actually worsen neurogenic bladder in those with high residual volume

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92
Q

What is the gold standard investigation of GORD?

A

24hr oesophageal pH monitoring

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93
Q

What is alpha-1 antitrypsin and why does deficiency cause emphysema and cirrhosis?

A

Protease inhibitor of neutrophil elastase

Alpha-1 antitrypsin is produced by the liver and by inhibiting neutrophil elastase it helps protect the lungs and liver against these

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94
Q

What is the best marker of severity in acute pancreatitis?

A

CRP

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95
Q

What investigation is diagnostic for SBOSS?

A

Hydrogen breath test

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96
Q

What is first and second line management of migraines in pregnancy?

A

1st line - paracetamol 1g
2nd line - NSAIDs in first and second trimester

Avoid aspirin and opioids in pregnancy

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97
Q

How does SIGN recommend migraines are managed in menstruation?

A

Mefenamic acid or combination of aspirin, paracetamol and caffeine
Triptans in the acute situation

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98
Q

What is first line management in open angle glaucoma with a raised IOP > 24mmHg?

A

360 degrees selective laser trabeculoplasty

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99
Q

Aside from surgical management with selective laser trabeculoplasty in those with > 24mmHg IOP, what is medical management options for open angle glaucoma - 1st line then some other second line options?

A

First line - Latanoprost

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100
Q

What is a key differentiator in clinical presentation of TRALI vs TACO?

A

TRALI - HOTN
TACO - HTN

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101
Q

How does non-haemolytic febrile reaction to blood transfusion present and what is the management of this?

A

Fever, chills

Rx = Slow or stop the transfusion, paracetamol, monitor

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102
Q

How to manage minor allergic reaction to blood transfusion

A

Rx = temporarily stop the transfusion, antihistamine, monitor

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103
Q

How does acute haemolytic reaction to blood transfusion present and how to manage this?

A

Fever, abdominal pain, HOTN

Rx = stop transfusion, fluid resuscitation
Check the identity of the patient and name on the blood product, send the blood for direct Coomb’s test, repeat typing and cross-matching

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104
Q

How does transfusion-associated circulatory overload (TACO) present and how to manage this?

A

Pulmonary oedema, HTN
Rx = slow or stop transfusion, consider IV diuretic e.g. furosemide and O2

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105
Q

How does TRALI present and how to manage?

A

Hypoxia, pulmonary infiltrates on CXR, fever, HOTN

Rx = stop the transfusion, oxygen and supportive care

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106
Q

Neonatal lupus erythematous is associated with which antibodies? and complications of this include?

A

Anti-SSA / Ro antibodies

Complications: congenital heart block, skin rashes and hepatosplenomegaly

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107
Q

A 27-year-old farmer has been brought to the emergency department after being found unconscious in a barn.

On initial examination he is agitated and combative with hypersalivation with excessive production of respiratory secretions. There is evidence of diaphoresis, urinary and faecal incontinence and miosis along with muscle fasciculations.

What is the likely diagnosis, what happens to the heart rate in this condition and what is the management of this condition?

A

Organophosphate poisoning
Bradycardia

Rx = atropine
? pralidoxime is undergoing research into viability as rx option

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108
Q

How is oscillopsia in multiple sclerosis managed first line?

A

Gabapentin

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109
Q

How is fatigue in multiple sclerosis managed?

A

Trial of amantadine
Other options: mindfulness training and CBT

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110
Q

Patient with pre-diabetes has lost weight on follow up appt but his HbA1C is still keeping creeping up - what to do?

A) Start metformin
B) Start pioglitazone
C) Review again in 12 months
D) Start orlistat
E) Do an OGTT

A

A) Start metformin

NICE recommend metformin for adults at high risk ‘whose blood glucose measure (fasting plasma glucose or HbA1C) shows they are still progressing towards type 2 diabetes, despite their participation in an intensive lifestyle-change programme’

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111
Q

Summarise the duration of anticoagulant therapy in PE

A

Provoked = 3 months
Provoked but also active cancer with confirmed proximal DVT or PE = up to 6 months
Unprovoked = 6 months
Unprovoked PE or persistent risk factors e.g. antiphospholipid syndrome, active cancer or thrombophilia

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112
Q

What are the management options for motion sickness?

A
  1. Hyoscine - transdermal patches
  2. Cyclizine or cinnarizine (non-sedating anti-histamines)
  3. Promethazine (sedating anti-histamine)
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113
Q

Drug induced liver disease - list some drugs that can cause a hepatocellular picture

A

Paracetamol
Sodium valproate, phenytoin
MAOIs
Halothane
Anti-TB meds - rifampicin, isoniazid, pyrazinamide
Statins
Alcohol
Amiodarone
Methyldopa
Nitrofurantoin

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114
Q

Drug induced liver disease - list some drugs that can cause a cholestatic picture

A

COCP
Abx: flucloxacillin, co-amoxiclav, erythromycin
Anabolic steroids, testosterones
Phenothiazines: chlorpromazine, prochlorperazine
Sulphonylureas
Fibrates
Rare reported causes: Nifedipines

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115
Q

List 3 cause of drug induced liver disease that can cause liver cirrhosis

A

Methotrexate, Methyldopa, Amiodarone

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116
Q

List the antibiotics that inhibit protein synthesis by acting on
1) 30S ribosomal subunit
2) 50S ribosomal subunit

A

1) Buy AT 30 = aminoglycosides, tetracyclines
2) CCELS at 50 = chloramphenicol, clindamycin, erythromycin / macrolides, linezolid, streptogrammins

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117
Q

Which clotting factors are affected by warfarin?

A

Use the mnemonic warfarin 1972
10, 9, 7, 2

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118
Q

What is the gold standard test for PNH?

A

Flow cytometry of blood to detect low levels of CD59 and CD55

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119
Q

Outline management for PNH

A

Blood product replacement
Anticoagulation
Eculizumab is undergoing research
SCT

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120
Q

What is the half life of amiodarone?

A

Approx 20-100 days

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121
Q

Outline the steps in medical management of angina pectoris

A

1.

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122
Q

Between adenocarcinoma and squamous cell carcinoma which portions of the oesophagus are affected in each?

A

Squamous cell carcinoma - upper and middle portions
Adenocarcinoma - lower portion

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123
Q

What is first line then second line then third line management for c.diff infection?

A
  1. First line = oral vancomycin
  2. Second line = oral fidaxomycin
  3. Third line = oral vancomycin +/- IV metronidazole
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124
Q

What is the management in the case of recurrent c.diff infection
1) Within 12 weeks of symptom resolution
2) After 12 weeks of symptom resolution

A

1) Oral fidaxomicin
2) Oral vancomycin OR fidaxomycin

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125
Q

How is c.diff spread prevented - what are the isolation procedures?

A

Patient should be isolated in side room until no diarrhoea (type 5-7 on bristol stool chart) for at least 48 hours

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126
Q

What cardiac abnormalities are associated with carcinoid syndrome?

A

Carcinoid TIPS

Tricuspid insufficiency and pulmonary stenosis

Affects the right side of the heart

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127
Q

What is the main management of carcinoid syndrome?
What other drug can be used for management of diarrhoea in carcinoid tumours?

A

Somatostatin analogues e.g. octreotide
Diarrhoea - cyproheptadine may help

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128
Q

What is the most useful marker to screen for haemochromatosis?

A

Transferrin saturation

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129
Q

What are the management options for haemochromatosis?

A

Venesection is first line - monitoring - transferrin saturation should be kept < 50% and the serum ferritin concentration below 50 ug/L

Desferrioxamine may be used second line

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130
Q

What are the triad of symptoms / signs in Budd-Chiari syndrome?

A
  1. Ascites
  2. Abdominal pain
  3. Hepatomegaly
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131
Q

What is the initial investigation in Budd-Chiari syndrome?

A

Ultrasound with doppler flow studies

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132
Q

List some causes of Budd-Chiari syndrome

A

Polycythaemia rubra vera
Thrombophilia - activated protein C resistance, antithrombin III deficiency, protein C and S deficiencies
Pregnancy
COCP for 20% of cases

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133
Q

What type of cells do gastrinomas originate from?

A

G cells

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134
Q

What investigation is a test of exocrine function in chronic pancreatitis?

A

Faecal elastase

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135
Q

Name the laxative that is only considered in palliative patients due to its carcinogenic potential

A

Co-danthramer

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136
Q

What is the management for life threatening c.diff?

A

Oral vancomycin and IV metronidazole

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137
Q

What investigation is the most appropriate to assess the effectiveness of treatment in post-eradication therapy?

A

Urea breath test

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138
Q

What is first line management of variceal bleeding in patients with medium or large oesophageal varices that have not bled?

A

Propanolol

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139
Q

How does propanolol help prevent oesophageal bleeding?

A

Reduces cardiac output and sphlanchnic blood flow

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139
Q

How is terlipressin good in controlling variceal bleeding?

A

It is a VP analogue and causes sphlanchnic vasoconstriction thus reducing portal venous inflow

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140
Q

Which antibodies are associated with autoimmune hepatitis…?
1) Type 1?
2) Type 2?
3) Type 3?

A

1) Type 1 - anti-ANA and or anti-SMA
2) Type 2 - Anti-LKM1
3) Type 3 Soluble liver kidney antigen

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141
Q

What is the management of autoimmune hepatitis?

A

1) Steroids
2) Other immunosuppressants e.g. azathioprine
3) Liver transplant

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142
Q

What are two characteristic findings on liver biopsy of autoimmune hepatitis?

A

Inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis

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143
Q

What is the gold standard investigation in Whipple’s disease and what is the key finding?

A

Jejunal biopsy and shows deposition of macrophages containing Periodic acid-Schiff (PAS) granules

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144
Q

What is the management of Whipple’s disease?

A

Oral co-trimoxazole for 1 year sometimes preceded by course of IV penicillin

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145
Q

Whipple’s disease is caused by which organism infection?

A

Tropheryma Whippeli

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146
Q

Features of Whipple’s disease?

A

Malabsorption - diarrhoea, weight loss
Large joint arthralgia
Lymphadenopathy
Skin - hyperpigmentation and photosensitivity
Pleurisy, pericarditis
Neuro symptoms (rarely) - ophthalmoplegia, dementia, seizures, ataxia, myoclonus

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147
Q

What is the management of small bowel overgrowth syndrome?

A

Rifaximin is first line, correct underlying disorder

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148
Q

What is the most common cause of HCC
1) Worldwide?
2) In the UK?

A

1) Worldwide - Hep B
2) UK - Hep C

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149
Q

What is the management of Gilbert’s syndrome?

A

Nothing really - education and avoidance of triggers only

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150
Q

How is Gilbert’s further investigated once suspected (i.e. already know there is isolated unconjugated hyperbilirubinaemia in context of stressors)?

A

Rise in bilirubin following prolonged fasting or IV nicotinic acid

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151
Q

Which part of the colon most affected by ischaemic colitis?
Also why not the hepatic flexure as commonly?

A

Splenic flexure - watershed area

Hepatic flexure also well supplied by SMA so less likely affected

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152
Q

People with FAP are also at risk of what other type of tumours?

A

Duodenal tumours

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153
Q

FAP is what inheritance pattern and which gene on which chromosome

A

Autosomal dominant
APC gene on chromosome 5

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154
Q

What is the key management in FAP?

A

Proctocolectomy with ileal pouch anal anastamosis

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155
Q

What testing is done in NAFLD to test for enhanced liver fibrosis?

A

ELF blood test - hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase 1 - combines to create a score - score > 10/5 - enhanced liver fibrosis - refer to liver specialist and likely biopsy

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156
Q

First line investigation in ascending cholangitis?

A

Ultrasound

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157
Q

What scoring system is used to determine alcoholic hepatitis severity? And at what score do we consider corticosteroids?

A

Maddrey’s discriminant function

Score > 32 usually

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158
Q

List some causes of hepatosplenomegaly?

A

Chronic liver disease with portal HTN
Infections - glandular fever, malaria, hepatitis
Lymphoproliferative disorders
Myeloproliferative disorders e.g. CML
Amyloidosis

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159
Q

What is first line management for chronic anal fissure?

A

Topical GTN

Note if this is not effective after 8 weeks then secondary care referral should be considered for surgery (sphinchterotomy) or botulinum toxin

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160
Q

What is a common cause of diarrhoea following ileal resection in Crohn’s disease?

A

Malabsorption of bile salts

Managed with oral colestyramine

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161
Q

Patient with ileal resectio for management of Crohn’s has chronic diarrhoea and you think it is because of malabsorption of bile salts - how is this managed?

A

Oral colestyramine

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162
Q

Features of Whipple’s disease?

A

Weight loss, worn out joints (arthralgia)
Hyperpigmentation, hyperactive bowel (diarrhoea)
Inadequate absorption of vitamins, minerals
Pleurisy
Pericarditis
Lymphadenopapthy
Elevated macrophages on biopsy

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163
Q

A 67-year-old man is investigated for dyspepsia. A gastroscopy reveals a suspicious lesion which is biopsied. What is the characteristic finding on biopsy would be most consistent with a diagnosis of gastric adenocarcinoma?

A

Signet ring cells

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164
Q

Colonoscopy findings of dark brown discolouration in the proximal colon and biopsy findings of pigment laden macrophages in the lamina propria (melanosis coli) in a young woman with diarrhoea and weight loss - diagnosis?

A

Laxative abuse - especially anthroquine compounds such as senna

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165
Q

True or false, pellagra (dermatitis, dementia and diarrhoea) can be seen in carcinoid syndrome? Why / why not?

A

True - because tryptophan (which would normally be converted into niacin - vitamin B3) gets diverted into producing excess serotonin. Resulting niacin deficiency leads to pellagra

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166
Q

A 28-year-old man undergoes an ileocaecal resection to treat terminal ileal Crohns disease. Post operatively he attends the clinic and complains of diarrhoea. His CRP is within normal limits and small bowel enteroclysis shows no focal changes. What medication would be helpful?

A

Oral cholestyramine - malabsorption of bile salts is common cause of diarrhoea following ileal resection.

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167
Q

A 34-year-old female with a history of alcoholic liver disease is admitted with frank haematemesis. She was discharged three months ago following treatment for bleeding oesophageal varices. Following resuscitation, what is the most appropriate treatment whilst awaiting endoscopy?

A

Terlipressin - according to British Society of Gastroenterology guidelines, terlipressin should be administered as soon as variceal bleeding is suspected and continued until an endoscopy can be performed

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168
Q

In oesophageal cancer what investigation is used for:
1) Initial staging?
2) Locoregional staging?

A

1) Initial staging - CT
2) Locoregional staging - EUS (endoscopic u/s) - this is helpful in assessing mural invasion

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169
Q

What is the most common cause of biliary disease in patients with HIV?

A

Sclerosing cholangitis due to infections e.g. CMV, Cryptospordium and Microsporidia

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170
Q

True or false PPIs can increase risk of c.diff - why or why not?

A

True - because less gastric acid production - more facilitative to survival of c.diff

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171
Q

What is the inheritance pattern of Peutz-Jegher syndrome?

A

Autosomal dominant

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172
Q

What score is used to assess malnutrition?

A

MUST score

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173
Q

What investigation is done to monitor response to treatment (venesection) in haemochromatosis?

A

Ferritin and transferrin saturation

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174
Q

What vaccination should be given to people with Coeliac’s and how often, and why?

A

Pneumococcal vaccination every 5 years as people with Coeliac’s can have functional hyposplenism increasing susceptibility to encapsulated organisms

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175
Q

What investigation is first line for diagnosis of small bowel overgrowth syndrome?

A

Hydrogen breath testing

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176
Q

A 45-year-old man is admitted to the Emergency Department with severe abdominal pain. He smokes 20 cigarettes a day and drinks approximately 50 units of alcohol per week. He also complains of sudden deterioration in vision. Fundoscopy reveals shows multiple micro infarcts (cotton wool spots). Your consultant requests amylase as they are considering ?pancreatitis. What is likely going on with the eyes?

A

Purtscher Retinopathy - can be seen following head trauma and in conditions such as acute pancreatitis, fat embolisation, amniotic fluid embolisation and vasculitic diseases

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177
Q

What is the inheritance pattern of Dubin Johnson syndrome?

A

Autosomal recessive

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178
Q

Does Dubin Johnson syndrome cause unconjugated or conjugated hyperbilirubinaemia? Why?

A

Conjugated hyperbilirubinaemia - there is a defect in the canalicular multispecific organic anion transporter (MRP2), which hinders the excretion of conjugated bilirubin into bile. This leads to a buildup of conjugated bilirubin in the liver cells and its subsequent leakage into blood, causing a conjugated hyperbilirubinaemia.

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179
Q

What is the prognosis of Dubin Johnson syndrome?

A

Typically has a benign course with patients usually living a normal life span without clinical impairment. Main manifestation is intermittent jaundice which does not cause significant morbidity

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180
Q

A 72-year-old woman presents to the emergency department with three months of black stools and shortness of breath. She has a past medical history of knee osteoarthritis. She drinks 10 units of alcohol per week.

On examination, there is an ejection systolic murmur in the aortic area radiating to the carotids. The blood pressure is 110/90 mmHg. The abdominal examination is unremarkable. She has conjunctival pallor.

What is a unifying explanation for the presentation?

A

Angiodysplasia - angiodysplasia is associated with aortic stenosis

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181
Q

What heart thing is angiodysplasia associated with?

A

Aortic stenosis

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182
Q

Where are most gastrinomas found? And second most common place?

A

Most often in the first part of the duodenum
Second most common - pancreas

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183
Q

What does the MELD score test?

A

MELD score assesses the severity of end-stage liver disease

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184
Q

What stimulation test can be useful to investigate the cause of pancreatic malabsorption?

A

Secretin stimulation test

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185
Q

What are the 2 types of hepatorenal syndrome?

A

Type 1 - rapid onset hepatorenal syndrome
Type 2 - gradual decline in renal function often associated with refractory ascites

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186
Q

What has a better prognosis type 1 or type 2 hepatorenal syndrome?

A

Type 2 has a better prognosis but the prognosis is pretty poor in both

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187
Q

What are the management options in hepatorenal syndrome?

A

Terlipressin
Volume expansion with 20% HAS
TIPSS
Liver transplantation

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188
Q

True or false, lactulose is contraindicated in IBS?

A

True - lactulose can exacerbate IBS

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189
Q

Liver pathologies and associated raised immunoglobulin subtypes - which subtype is raised in the following liver pathologies?
1) Alcoholic liver disease
2) Primary biliary cirrhosis
3) Autoimmune hepatitis

A

1) Alcoholic liver disease - IgA
2) Primary biliary cirrhosis - IgM
3) Autoimmune hepatitis - IgG

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190
Q

What is the management of autoimmune hepatitis?

A

Steroids, other immunosuppressant drugs e.g. azathioprine
Liver transplantation

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191
Q

Which antibodies are associated with the following types of autoimmune hepatitis?
1) Type 1?
2) Type 2?
3) Type 3?

A

1) Type 1 - Anti ANA, Anti-SMA
2) Type 2 - Anti-LKM1
3) Type 3 - Anti-SLKA

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192
Q

What percentage of normal energy and protein requirements should you give via enteral feeding to avoid refeeding syndrome in starved patients?

A

50% of normal energy intake in starved patients (< 5 days) to avoid refeeding syndrome

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193
Q

What is the management of gastric MALT lymphoma?

A

H.Pylori eradication, regardless of H.Pylori status can lead to regression of the tumuor in a significant proportion of patients

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194
Q

What is the management of Barret’s oesophagus?

A

High dose PPIs then endoscopic surveillance with biopsies every 3-5 years - then if any dysplasia is found can then consider things like first line radiofrequency ablation and then endoscopic mucosal resection

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195
Q

List some causes of villous atrophy on jejunal biopsy

A

Coeliac’s disease
Tropical sprue
Hypogammaglobulinaemia
Whipple’s disease

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196
Q

True or false histologically you would find multiple granulomas in Crohn’s not UC?

A

True - granulomas more suggestive of Crohn’s than UC

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197
Q

Inflammation goes to which layer of the gut wall in UC vs in Crohn’s?

A

UC - limited to mucosal layer
Crohn’s - can affect all layers of the bowel wall including the serosa

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198
Q

Skip lesions in UC or Crohn’s?

A

Crohn’s

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199
Q

Goblet cell depletion in UC or Crohn’s?

A

UC

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200
Q

Which of the following features of haemochromatosis are reversible with treament and which are not….

1) Cardiomyopathy
2) Hypogonadotrophic hypogonadism
3) Diabetes mellitus
4) Arthropathy
5) Liver cirrhosis

A

1) Cardiomyopathy - reversible
2) Hypogonadotrophic hypogonadism - irreversible
3) Diabetes mellitus - irreversible
4) Arthropathy - irreversible
5) Liver cirrhosis - irreversible

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201
Q

Hyperchylomicronaemia or hypercholesterolaemia associated with acute pancreatitis?

A

Hyperchylomicronaemia (can be caused by hereditary lipoprotein lipase deficiency and apolipoprotein CII deficiency)

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202
Q

Which coagulation factor does low molecular weight heparin inhibit the most and how does it do this?

A

Inhibits factor Xa by activating antithrombin III (therefore prevents downstream conversion of prothrombin to thrombin, thereby reducing clotting)

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203
Q

List the causes of LBBB

A

MI
HTN
AS
Cardiomyopathy
Rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia

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204
Q

How long should a patient stop driving for following and elective cardiac angioplasty?

A

1 week

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205
Q

Outline the KCH criteria for liver transplant in paracetamol overdose

A
  1. Arterial pH < 7.3, 24 hrs after ingestion
  2. PT > 100s
  3. Creatinine > 300 umol/L
  4. Grade III or IV encephalopathy
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206
Q

What is the gold standard investigation for potential CLL?

A

Immunophenotyping (flow cytometry)
Most cases can be identified using a panel of antibodies specific for CD5, CD19, CD20 and CD23

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207
Q

Acute angle closure glaucoma vs primary open angle which is associated with hypermetropia and which is associated with myopia?

A

Acute angle closure glaucoma associated with hypermetropia (farsightedness) vs primary open-angle glaucoma is associated with myopia (short-sightedness)

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208
Q

What are the features of visceral leishmaniasis?

A
  1. Pyrexia
  2. Splenomegaly
  3. Pancytopaenia due to hypersplenism
  4. Weight loss
  5. Night sweats
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209
Q

What are the feature of transfusion associated graft vs host disease?

A

Diarrhoea, liver damage and rash, 2-6 weeks after transfusion

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210
Q

3 major risk factors for transfusion associated graft vs host disease?

A
  1. Volume and age of transfused blood
  2. Depressed immune function especially involving T-cells and cell-mediated immunity e.g. Hodgkin’s disease
  3. Similar HLA haplotype sharing
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211
Q

Management of transfusion associated graft vs host disease?

A

There is no management :( , just prevention with using gamma irradiated blood products (leucocyte depleted)

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212
Q

Which chronic electrolyte disturbance can cause cataracts?

A

Chronic hypocalcaemia

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213
Q

Which is more sensitive Chvostek’s or Trousseau’s for hypocalcaemia?

A

Trousseau’s sign (carpopedal spasm) more sensitive than Chvostek’s sign (facial twitch )

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214
Q
A
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215
Q

List some causes of respiratory acidosis

A

COPD
Decomposition in other resp conditions e.g. Life threatening asthma / pulmonary oedema
Neuromuscular disease
Obesity hyperventilation syndrome
Sedatives e.g. benzodiazepines, opiate overdose

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216
Q

In what scenarios can you consider doing chest drain for pneumothorax management?

A

When there are high risk features present and it is safe to intervene

High risk =
- Haemodynamic compromise
- Significant hypoxia
- Bilateral pneumothorax
- Underlying lung disease
- >/= 50yrs with significant smoking history
- Haemothorax

Safe to intervene = 2cm apically or laterally or any side on ct which can be safely accessed with radiological support

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217
Q

In management of pneumothorax, a needle aspiration was done in a patient without high risk features. However this was unsuccessful. What is the next step?

A

Do a chest drain

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218
Q

What is the management considered in patients with recurrent pneumothoraces?

A

VATS for mechanical / chemical pleurodesis +/- bullectomy

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219
Q

What are the landmarks for chest drain insertion?

A

Base of axilla, lateral pectoralis major, 5th ICS, anterior latissimus dorsi

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220
Q

How does alpha 1 antotrypsin deficiency cause emphysema?

A

Alpha 1 antitrypsin is a protease inhibitor which inhibits neutrophil elastase which would otherwise break down elastin in the lung parenchyma. Therefore deficiency of this causes more breakdown leading to emphysema

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221
Q

What is the rough percentage mortality of ARDs?

A

40%

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222
Q

Outline the criteria for ARDs

A

Berlin criteria:
Acute onset (within 1 week of risk factors)
Hypoxia with pO2 / FiO2 < 300mmHg (40kPa)
Pulmonary oedema - bilateral infiltrates on CXR not fully explained by effusions, lobar / lung collapse or nodules
Non cardiogenic (pulmonary artery wedge pressures needed if in doubt)

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223
Q

Outline the severity classifications for ARDs

A

Based on pO2 / FiO2 ratios:
Mild - 300- 200mmHg
Moderate - 100- 200mmHg
Severe - < 100mmHg

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224
Q

List 4 causes of lower zone lung fibrosis

A

R - Rheumatological conditions
A - Asbestos exposure
I - Idiopathic
D - Drug induced

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225
Q

What type of hypersensitivity reaction(s) are involved in extrinsic allergic alveolitis?

A

Mainly type III (immune complex mediated)
Partly type IV (delayed hypersensitivity) especially during the chronic phase

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226
Q

Does extrinsic allergic alveolitis cause an upper or lower zone fibrosis?

A

Upper / middle

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227
Q

What will eosinophils look like in the peripheral blood in extrinsic allergic alveolitis?

A

No eosinophils in peripheral blood film

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228
Q

What are the causes of extrinsic allergic alveolitis?

A

Bird fancier’s lung
Farmer’s lung - saccaroohyla rectivirgula
Malt worker’s lung - aspergillus clavatus
Mushroom worker’s lung - thermophiliv actinomycetes

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229
Q

List some investigations for extrinsic allergic alveolitis

A

Imaging showing upper / mid zone fibrosis
Bronchoalveolar lavage - lynphocytosis
Serologic assays for specific IgG antibodies
Blood - no eosinophilia

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230
Q

Main differential similar to extrinsic allergic alveolitis but with no exposure risk factors that you can consider?

A

Cryptogrenic organising pneumonia

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231
Q

What is the most important intervention for long term management of symptoms in non CF bronchiectasis?

A

Postural drainage and inspiration muscle training

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232
Q

Silicosis causes upper or lower zone fibrosis?

A

Upper zone fibrosis

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233
Q

What are the x-ray features of silicosis?

A

Egg shell calcification of hilar lymph nodes
Upper zone fibrosis

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234
Q

Silicosis is a risk factor for development of …. as silica is toxic to ….

A

Silicosis is a risk factor for development of tuberculosis as silica is toxic to macrophages

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235
Q

Bronchiectasis and raised IgE, likely diagnosis?

A

ABPA

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236
Q

Management options for ABPA?

A

Oral glucocorticoids, antifungal, prophylactic antibiotics, supportive rx
Itraconazole second line agent
Omalizumab (anti-IgE recombinant humanised monoclonal antibody)

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237
Q

Key investigation findings in ABPA?

A

Eosinophilia
+ve RAST to aspergillus
+ve IgG precipitins
Raised IgE
Flitting CXR changes

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238
Q

What might a gas show in obstructive sleep apnoea?

A

Compensated respiratory acidosis

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239
Q

What is the equation for transfer factor?

A

TLCO = KCO x VA

TLCO - transfer factor
KCO - transfer coefficient of carbon monoxide
VA - alveolar volume

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240
Q

What will the flow volume loop look like in obstructive lung disease?

A

Concave

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241
Q

List some causes of raised TLCO

A
  • Exercise
  • Male
  • Hyperkinetic states
  • Polycythemia
  • Asthma
  • Pulmonary haemorrhage (e.g. GPA, Goodpasture’s)
  • Left-to-right cardiac shunts
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242
Q

List some causes of reduced TLCO

A

Pulmonary fibrosis
Pneumonia
PE
Pulmonary oedema
Emphysema
Anaemia
Low cardiac output

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243
Q

List some causes of drug induced gynaecomastia

A

Spironolactone
Cimetidine
Digoxin
Cannabis
Finisterre
GnRh agonist e.g. goserelin, buserelin
Oestrogen, anabolic steroids

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244
Q

How does Bartter’s syndrome present?

A

Normotensive symptomatic hypokalaemia (weakness) often presenting in childhood as failure to thrive

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245
Q

Does Bartter’s syndrome cause a hypertensive or normotensive hyperkalaemia?

A

Normotensive, unlike in Cushings, Conn’s and Liddle’s syndromes

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246
Q

Inheritance pattern of MODY?

A

Autosomal dominant

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247
Q

Patients with MODY are sensitive to …. therapy

A

Patients with MODY are sensitive to sulfonylurea therapy

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248
Q

What is the biggest modifiable risk factor for development of thyroid eye disease?

A

Smoking

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249
Q

Management of thyroid eye disease?

A

Smoking cessation
Topical lubricants to prevent corneal ulceration
Steroids
Radiotherapy
Surgery
Referral to ophthalmology see EUGOGO guidelines for referral criteria guidelines

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250
Q

How do statins work?

A

Inhibit HMG-CoA reductive - the rate limiting enzyme in hepatic cholesterol synthesis

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251
Q

When to check LFTs in patients commencing statin therapy? And at what level do you consider stopping statins?

A

At baseline, at 3 months then at 12 months
Stop if serum transaminases raised 3x the upper limit of normal

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252
Q

What is one key important drug interaction in which you should avoid statins?

A

Macrolides e.g. erythromycin, clarithromycin

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253
Q

Give 2 key absolute contraindications to statin therapy and one recommended contraindication

A

Pregnancy and macrolide antibiotics

History of intracerebral haemorrhage

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254
Q

Who should take statins?

A

Anyone who scores with ten year cardiovascular risk > 10% on QRISK2 score or
Any type 1 Diabetic who were diagnosed > 10 years ago OR age > 40 OR established nephropathy

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255
Q

What dose or atorvastatin is used in
1) Primary prevention?
2) Secondary prevention?

A

1) 20mg NOCTE
2) 80mg NOCTE

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256
Q

Mode of action of dabigatran?

A

Direct thrombin inhibitor

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257
Q

What is the reversal agent for dabigatran?

A

Idarucizumab

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258
Q

Contraindications for dabigatran?

A

Creatinine clearance <30ml/min
Recent mechanical heart valve replacement

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259
Q

Mechanism of action of thiamine diuretics?

A

Inhibits sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide sensitive Na-Cl symporter

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260
Q

How can methadone cause sudden cardiac death?

A

Methadone - prolonged QT - torsades de pointes - sudden cardiac death

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261
Q

What is a normal corrected QT interval in males? Females?

A

Males = 430ms
Females = 450ms

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262
Q

Management of long QT?

A

Avoid drugs which prolong the QT interval and other precipitants e.g. strenuous exercise
Beta blockers (but beware sotalol can exacerbate)
ICD in high risk cases

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263
Q

What is the key investigation for Addison’s disease?
What is an alternative when it is not possible to do this e.g in primary care?

A

Key investigation is short synACThen test (aka ACTH stimulation test) - give synthetic ACTH then measure cortisol at baseline, at 30 mins and 60 mins and see response- if no or v small increase in cortisol this suggests primary adrenal insufficiency aka addison’s disease

An alternative is measuring the 9am cortisol - a level > 500 nmol/L makes Addison’s unlikely
100-500 warrants investigation
< 100 is definitely abnormal

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264
Q

What is Eisenmenger’s syndrome / how does it come about?

A

Reversal of left right shunt due to pulmonary hypertension
Uncorrected left right shunt e.g. in VSD, ASD, PDA leads to remodelling of pulmonary vasculature causing obstruction to pulmonary blood and pulmonary hypertension

Presents with cyanosis, clubbing, rv failure, haemoptysis / embolism, loud s2, raised jvp large a waves

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265
Q

Give some signs / symptoms of Eisenmenger’s syndrome

A

Presents with cyanosis, clubbing, rv failure, haemoptysis / embolism, loud s2, raised jvp large a waves

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266
Q

Management of Eisenmenger’s syndrome?

A

Heart-lung transplantation

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267
Q

What is the target INR in mechanical heart valve anticoagulation?
1) Aortic
2) Mitral

A

1) 3
2) 3.5

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268
Q

What are the only two anticoagulants indicated in anticoagulation in mechanical heart valves?

A

Warfarin
LMWH

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269
Q

Most common form of thyroid cancer?

A

Papillary

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270
Q

Best prognosis subtype of thyroid cancer?

A

Papillary

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271
Q

Anaplastic thyroid cancer is associated with…. whereas lymphoma of the thyroid gland is associated with…..

A

Anaplastic thyroid cancer is associated with toxic multipolar goitre, whereas lymphoma of the thyroid gland is associated with hashimoto’s thyroiditis

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272
Q

What is the management of papillary and follicular thyroid cancer?

A

Total thyroidectomy
Followed by radioiodene to kill residual cells
Yearly thryoglobulin levels to determine early recurrent disease

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273
Q

Management in anaplastic carcinoma of the thyroid gland?

A

Resection, palliation through isthmusectomy and radiotherapy.
N.b chemotherapy is ineffective

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274
Q

Define pulsus paradoxus then give 2 conditions it may occur in?

A

Greater than normal (>10mmHg) fall in systolic blood pressure during inspiration
Severe asthma, cardiac tamponade

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275
Q

Give a condition that can cause a slow rising / plateau pulse

A

Aortic stenosis

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276
Q

Give 3 conditions which can cause a collapsing pulse

A

Aortic regurgitation
PDA
Hyperkinetic states (anaemia, thyrotoxic, fever, exercise / pregnancy)

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277
Q

Give a condition in which you might see pulses alternans

A

Severe LVF

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278
Q

What is bisferiens pulse?
Give the main condition you might see it, then name another less common

A

Double pulse - two systolic pulses

Mixed aortic valve disease mainly
Sometimes HOCM

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279
Q

Give a condition in which there may be a jerky pulse

A

HOCM

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280
Q

Outline the guidelines for management of subclinical hypothyroidism

A

TSH > 10 mU/L and free thyroxine within normal range THEN consider starting levothyroxine if TSH level is > 10 mU/L on 2 separate occasions 3 months apart

TSH 5.5-10 mU/L and free thyroxine within normal range
If < 65 years consider offering 6 month trial of levothyroxine if TSH level is 5.5-10 mU/L on 2 separate occasions 3 months apart and there are symptoms of hypothyroidism

In older people watch and wait

If asymptomatic observe and repeat TFTs in 6 months

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281
Q

Broad complex tachycardia but not VF / torsades what two other possibilities could it be and how do you differentiate?

A

VT or SVT with aberrant conduction

Brugada algorithm -
- Absence of RS complexes (I.e either monophasoc R or S waves in all precordial or an R to S interval is > 100ms in one precordial lead is suggestive of VT
- AV dissociation suggests VT

Other suggesting VT
- Fusion or capture beats
- Positive QRS concordance in chest leads
- Marked LAD
- History of IHD
- Lack of response to adenosine or carotid sinus massage
- QRS > 160ms

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282
Q

What medication should you absolutely not give to patients with VT as it can lead to VF?

A

Verapamil

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283
Q

List some causes of hypophosphataemia

A

Alcohol excess
Acute liver failure
DKA
Refeeding syndrome
Primary hyperPTH
Osteomalacia

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284
Q

Give some consequences of hypophosphataemia

A

Red blood cell haemolysis
White blood cell and platelet dysfunction
Muscle weak ess ans rhabdomyolysis
CNS dysfunction

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285
Q

What is the investigation of choice for upper airway compression?

A

Flow volume loop

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286
Q

Write out or think of the regions of MI anterior, inferior and lateral against which leads you might see ST changes and which coronary artery is affected in each

A

Anterior - V1-4 - LAD
Inferior - II,III,aVF - RCA
Lateral - 1, V5-6, - LCA

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287
Q

Outline the different medications that are required as lifelong secondary prevention in ACS

A

Aspirin
Second antiplatelet (e.g. clopidogrel)
Beta-blocker
ACE-i
Statin

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288
Q

When should PCI be considered?

A

If the presentation is within 12 hours of onset of symptoms and PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is significant delay in being able to provide PCI)
Note if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI can be considered

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289
Q

When should fibrinolysis be considered?

A

Should be offered within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120 minutes

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290
Q

What are first line management for heart failure with reduced LVEF (in terms of drugs improving mortality)?

A

Beta blocker (bisoprolol, carvedilol, nebivolol and ACEi) - start one at a time
N.B these have no effect on mortality in patients with heart failure with preserved ejection fraction (HF-PEF)

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291
Q

What are second line management of heart failure with reduced ejection fraction (that improve mortality)?

A

Aldosterone antagonists e.g. spironolactone and eplerenone

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292
Q

Outline third line management options of heart failure with reduced ejection fraction (that improve mortality)

A

Ivabradine
- Criteria: sinus rhythm > 75 / min and a LVEF < 35%
Sacubitril valsartan
- Criteria : LVEF < 35%
- Considered in heart failure with reduced ejection fraction who are symptomatic on ACEis or ARBs
- Should be initiated following ACEi or ARB wash-out period
Digoxin
- Strongly indicated if there is co-existent AF
Hydralazine + nitrate
- Particularly useful in afrocarribean patients
Cardiac resynchronisation therapy
- In widened QRS (e.g. LBBB) on ECG

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293
Q

What are the criteria for ivabradine and sacubitril-valsartan in heart failure?

A

Ivabradine - sinus rhythm > 75 bpm and LVEF < 35 %
Sacubitril-valsartan - LVEF < 35%

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294
Q

In which patients are hydralazine particularly useful in heart failure?

A

In afro-caribbean patients

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295
Q

What is the embryological mechanism that leads to transposition of the great arteries?

A

Failure of the aorticopulmonary septum to spiral during septation

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296
Q

What is a risk factor for development of transposition of the great arteries?

A

Children of diabetic mothers are at an increased risk of TGA

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297
Q

What are the basic anatomical changes in transposition of the great arteries?

A

Aorta leaves the right ventricle
Pulmonary trunk leaves the left ventricle

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298
Q

What is the characteristic x-ray finding in transposition of the great artery?

A

Egg on side / egg on string appearance on chest x ray

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299
Q

What is the management of transposition of the great arteries?

A

Maintenance of the ductus arteriosus with prostaglandins
Surgical correction is the definitive treatment

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300
Q

Clinical features of transposition of the great arteries?

A

Cyanosis
Tachypnoea
Loud single S2
Prominent RV impulse
Egg on side appearance on CXR

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301
Q

What type of aortic dissection is more evidenced by a murmur of aortic regurgitation?

A

Type A (ascending aorta)

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302
Q

Why can’t nitrate therapy used in aortic dissection (so for this reason we use labetalol instead)?

A

Because it causes vasodilation. Catecholamine release due to vasodilation can cause an increase in shear forces by increasing ventricular contraction - this can result in extension of dissection or rupture

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303
Q

Outline the DeBakey classification for aortic dissection

A
  • Type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
  • Type II - originates in and is confined to the ascending aorta
  • Type III - originates in descending aorta, rarely extends proximally but will extend distally
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304
Q

Which is more common, type A (ascending aorta), or type B (descending aorta) aortic dissection?

A

Type A is more common (2/3rd of cases)

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305
Q

What is the classic finding on CXR in aortic dissection?

A

Widened mediastinum

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306
Q

What is the investigation of choice in aortic dissection?

A

CT angiography - demonstrating a false lumen

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307
Q

What investigation is better in patients who are too unstable to take to CT for CT angiography in patients with suspected aortic dissection/

A

TOE (transoesophageal echo)

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308
Q

What is the management of Type A (ascending aorta) aortic dissection?

A

Surgical management, but BP should be controlled to target systolic 100-120mmHg whilst awaiting intervention with IV labetalol

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309
Q

What is the management of Type B aortic dissection (descending aorta)?

A

Conservative management -
IV labetalol to prevent progression
Bed rest

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310
Q

What are some complications of backward tears in aortic regurgitation?

A

Aortic incompetence / regurgitation
MI: Inferior pattern often seen due to RCA involvement

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311
Q

What are some complications of forward tear in aortic dissection?

A

Unequal arm pulses and BP
Stroke
Renal failure

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312
Q

What are the gold standard investigations for new diagnosis of asthma in adults?

A

Spirometry with bronchodilator reversibility testing + FeNO test

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313
Q

What are the gold standard investigations for new diagnosis of asthma in children 5-16yrs?
What about in children < / = 5 yrs?

A

Spirometry with bronchodilator reversibility testing
FeNO test only if there is normal spirometry or obstructive spirometry with a negative bronchodilator reversibility test

Patients < 5 yrs - diagnosis made on clinical judgement

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314
Q

In spirometry with bronchodilator reversibility testing, what indicates a positive test in adults?
What about in children?

A

Adult - improvement in FEV1 of 12% or more, and increase in volume of 200mls or more
Children - improvement in FEV1 of 12% or more

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315
Q

Give two causes of regular cannon a waves

A

VT with 1:1 ventricular-atrial conduction
AVNRT

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316
Q

Give a cause of irregular cannon waves

A

Complete heart block

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317
Q

A 45-year-old man is diagnosed with endocarditis of the aortic valve. He is treated with intravenous benzylpenicillin and gentamicin. What is the most important ECG change to monitor for?

A

Prolonged PR - this could indicate the development of an aortic abscess - an indication for surgery

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318
Q

Mechanism of action of heparin?

A

Activates anti-thrombin III

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319
Q

Mechanism of action of clopidogrel?

A

P2Y12 inhibitor

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320
Q

Mechanism of action of abciximab?

A

Glycoprotein IIb/IIIa inhibitor

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321
Q

Mechanism of action of dabigatran?

A

Direct thrombin inhibitor

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322
Q

Mechanism of action of rivaroxaban?

A

Direct factor X inhibitor

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323
Q

What is the mechanism of action of SGLT-2 inhibitors such as canagliflozin, dapagliflozin and empagliflozin?

A

Inhibit the sodium glucose co-transporter 2 in the proximal convoluted tubule - therefore decreases glucose reabsorption - more renal excretion of glucose - note this also causes the side effects of increased urine output, weight loss, and urinary infections

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324
Q

Important adverse effects of SGLT-2 inhibitors (aside from common ones of increased urination, weight loss and urinary infections)?

A

Urinary and genital infection (secondary to glycosuria)
Normoglycaemic ketoacidosis
Increased risk of lower-limb amputation: feet should be closely monitored

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325
Q

What are the treatment options for management of metastatic bone pain?

A

Metastatic bone pain may respond to analgaesia (e.g. opioid), bisphosphonates or radiotherapy

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326
Q

What are the different types of incontinence?

A
  • Stress incontinence
  • Urge incontinence
  • Mixed incontinence
  • Overflow incontinence - due to bladder outlet obstruction e.g. due to prostate enlargement
  • Functional incontinence - comorbid physical conditions impairing patient’s ability to get to bathroom in time - e.g. dementia, sedating medication and injury/illness resulting in decreased ambulation
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327
Q

Outline the management options for incontinence where urge incontinence is predominant

A
  • Bladder retraining (minimum of 6 weeks)
  • Bladder stabilising drugs (antimuscarinics) - oxybutinin (IR), tolterodine (IR), darifenacin (once daily preparation)
  • Mirabegron (beta-3 agonist) in frail elderly patients
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328
Q

Outline the management options in predominant stress incontinence

A

Pelvic floor muscle training
- at least 8 contractions performed 3 times per day for minimum 3 months
Surgical procedures: e.g. retropubic mid-urethral tape procedures
Duloxetine if they decline surgical procedures
(SNRI)

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329
Q

When following up patients in whom you have started statins due to high QRISK > 10% risk of cardiovascular events, on follow up in 3 months time, what is an appropriate target for cholestererol reduction?

A

> 40% reduction in non-HDL cholesterol

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330
Q

What does a drug-induced acne (usually steroids) look like? How do you manage steroid induced acne?

A

Monomorphic papiar rash without comedones or cysts
Taper the steroids gradually

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331
Q

What is the scoring system for pneumonia in primary care, and what do the points stratification indicate?

A

CRB 65
- Confusion ( < / = 8 on AMTS)
- RR > / = 30
- BP - systolic < / = 90mmHg and /or diastolic < / = 60mmHg

0 = low risk ( < 1% mortality risk)
- Consider at home treatment
1 or 2 = intermediate risk (1-10% mortality risk)
- Hospital assessment should be considered particularly for score of 2
3 0r 4 = high risk ( > 10% mortality risk)
- Urgent hospital admission

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332
Q

What is the scoring system for hospital acquired pneumonia in hospital?

A

CURB 65
- Confusion ( < 8 on AMTS)
- Urea ( > / = 7mmol)
- RR > 30
- BP (systolic < 90mmHg or diastolic < 60mmHg)

0-1 (< 3% mortality risk) = consider at home treatment
2 (3-15% mortality risk)= consider hospital treatment
3 + = consider intensive care assessment

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333
Q

What is the antibiotic therapy for management of low-severity community acquired pneumonia?

A

Amoxicillin first line
- If penicillin allergic then use macrolide or tetracycline

5 day course of antibiotics

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334
Q

What is the antibiotic therapy for management of moderate and high severity community acquired pneumonia?

A

Dual antibiotic therapy with amoxicillin or co-amoxiclav or ceftraixone or tazocin and a macrolide
7-10 day course

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335
Q

You can discharge patients with community acquired pneumonia unless they have 2 or more of the following findings (please list)

A
  • Temp > 37.5
  • RR 24 breaths per minute or more
  • HR > 100
  • Systolic BP > 90 mmHg or less
  • O2 saturations under 90% on room air
  • Abnormal mental status
  • Inability to eat without assisstance
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336
Q

When should repeat CXR be done after clinical resolution of pneumonia, and why is it done?

A

Repeat CXR at 6 weeks to ensure consolidation has resolved and there is no underlying secondary abnormalities (e.g. a lung tumour)

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337
Q

What are the 3 most common bacterial causes of infective exacerbation of COPD?

A
  • Haemophilus influenzae
  • Streptococcus pneumoniae
  • Moraxella catarrhalis
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338
Q

What is the most important respiratory pathogen in infective exacerbation of COPD?

A

Rhinovirus

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339
Q

What are the criteria for admission in exacerbation of COPD?

A
  • Severe breathlessness
  • Acute confusion or impaired consciousness
  • Cyanosis
  • O2 sats < 90% on pulse oximetry
  • Social reasons e.g. inability to cope at home (or living alone)
  • Significant comorbidity (e.g. cardiac diseaes or insulin dependent diabetes)
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340
Q

How do you decide target oxygenation and what oxygen therapy do you start with in exacerbation of COPD?

A
  • COPD patients are at risk of hypercapnia - initial oxygen saturation target 88-92% should be used
  • Prior to availability of blood gases use 28% venturi mask at 4L/min and aim for O2 sats 88-92% with risk factors for hypercapnia but no prior history of resp acidosis
  • Adjust target to 94-98% if the PCO2 is normal
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341
Q

Outline the management for exacerbations of COPD

A

Oxygen therapy - start with 28% venturi and adjust targets as appropriate and titrate oxygen as appropriate

Nebulised bronchodilator
- Beta-adrenergic agonist e.g. salbutamol
- Muscarinic antagonist e.g. ipratropium

Steroid therapy
- Oral prednisolone
- IV hydrocortisone

IV theophylline
- If not responding to nebulised bronchodilators

If develops type 2 respiratory failure - NIV
- If resp acidosis
- BiPap used with initial settings of EPAP of 4-5cm H20 and IPAP of 10 or 12-15 cm H20

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342
Q

What are the 2 main complications of subclinical hyperthyroidism?

A

Supraventricular arrythmias (AF mainly) and Osteoporosis

Due to increased cardiac output and heart rate and then due to increased bone turnover respectively in hyperthyroidism

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343
Q

2 causes of subclinical hyperthyroidism?

A

Multinodular goitre
Excessive thyroxine

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344
Q

How to manage subclinical hyperthyroidism?

A

Therapeutic trial of low-dose anti-thyroid agents for approx 6 months to try and induce remission
Note that TSH levels often revert to normal therefore levels must be persistently low to warrant intervention

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345
Q

Hypertension in pregnant ladies is probably not prengnancy induced hypertension if it is present before x weeks ?
I.e. by how many weeks can you expect pregnancy induced hypertension?

A

20 weeks

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346
Q

Which skin disorder is commonly associated with gastric cancer and can be a paraneoplastic syndrome?

A

Acanthosis nigricans - hyperpigmentation and velvety thickening of the skin - especially in body folds e.g. armpits and neck (note also commonly associated with type 2 diabetes)

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347
Q

List causes of peripheral neuropathy that cause predominantly motor symptoms

A
  • Guillan Barre Syndrome
  • Porphyria
  • Lead poisoning
  • Hereditary Sensorimotor neuropathy - e.g. charcot marie tooth
  • Chronic inflammatory demyelinating polyneuropathy
  • Diphtheria
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348
Q

List causes of peripheral neuropathy that cause predominantly sensory symptoms

A
  • Diabetic
  • Uraemia
  • Leprosy
  • Alcoholism - usually sensory then motor symptoms
  • Vit B12 deficiency (subacute combined degeneration of spinal cord) - dorsal column affected first (joint position, vibration) then distal paraesthesia
  • Amyloidosis
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349
Q

Is eczema herpeticum a slowly or rapidly progressing rash?

A

Rapidly progressing

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350
Q

Is eczema herpeticum painful rash or not painful?

A

Painful

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351
Q

What is the management for eczema herpeticum?

A

Admit
IV antibiotics

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352
Q

True or false, central umbilication is common in eczema herpeticum?

A

True

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353
Q

Patient with eczema, develops this rash - cause?

A

Eczema herpeticum - HSV 1/2

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354
Q

What is a histological classic findinig in rabies found in infected neurones?

A

Negri bodies - cytoplasmic inclusion bodies found in infected neurones

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355
Q

What is the risk of contracting rabies in the UK from animal bite?

A

‘No risk’ - so just advise washing the wound then if individual already immunised then further 2 doses of vaccine should be given.
If not previously immunised - rabies immunoglobulin + vaccination full course. Try to administer dose locally around the wound

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356
Q

How to manage animal bites (dog) in UK?

A

Wash wound
Rabies - if already vaccinated then 2 further doses to be given
If not vaccinated - then rabies immunoglobulin + full vaccination course - if possible administer locally around the wound

357
Q

What type of virus is rabies?

A

RNA rhabdovirus (specifically a lyssavirus)

358
Q

Above what level is the threshold for definition of thrombocytosis?

A

> 400 x 10^9/l

359
Q

List some causes of thrombocytosis

A

REACTIVE
- Severe infection, surgery etc
- Iron deficiency anaemia
MALIGNANCY
- CML
PCV
ESSENTIAL THROMBOCYSTOSIS
HYPOSPLENISM

360
Q

What is a characteristic symptom in essential thrombocytosis?

A

Burning sensation in the hands

361
Q

What mutation is most common in essential thrombocystosis?

A

JAK2

362
Q

Features of essential thrombocytosis?

A
  • Platelet count > 600 x 10^9/L
  • Thrombosis (venous or arterial)
  • Haemorrhage
  • Burning sensation in hands
363
Q

Outline management of essential thrombocytosis

A
  • Hydroxyurea (hydroxycarbamide) to reduce platelet count
  • IFN-alpha also used in younger patients
  • Low dose-aspirin to reduce thrombotic risk
364
Q

What blood test is important to do in men with osteoporosis?

A

Testostreone - hypogonadism is a common cause in men. Hypergonadotrophic or hypogonadotrophic. Andtrongens stimulate bone formation during puberty and prevent bone resorption during and after puberty

365
Q

List some risk factors for osteoporosis

A
  • History of glucocorticoid use
  • Rheumatoid arthritis
  • Alcohol exvess
  • History of parental hip fracture
  • Low BMI
  • Current smoking
366
Q

List some medications that can worsen osteoporosis

A
  • SSRIs
  • Anti-epileptics
  • PPIs
  • Glitazones
  • Long term heparin therapy
  • Aromatase inhibitors e.g. anastrazole
367
Q

What is the toxic metabolite that cause harm in paracetamol overdose? How is this normally neutralised and thus what is the mechanism by which NAC helps in paracetamol overdose?

A

NAPQI
Normally glutathoine conjugates it to form the non toxic mercapturic acid
In overdose there is exhaustion of glutathione stores
NAC replenishes glutathione stores

  • N.B have a lower threshold for starting NAC in patients who take P450 inducing medications e.g. phenytoin or rifampicin
368
Q

In what age group does familial mediterranean fever typically present?
In which ethnicities typically?

A

Second decade
Turkish, Armenian, Arabic

369
Q

What is the drug used in management of familial mediterranean fever?

A

Colchicine

370
Q

Features of familial mediterranean fever?

A
  • Pyrexia
  • Abdominal pain (due to peritonitis)
  • Pleurisy
  • Pericarditis
  • Arthritis
  • Erysipeloid rash on lower limbs
371
Q

What are the 3 opioids preferred in patients with CKD?

A
  • Alfentanil
  • Buprenorphine
  • Fentanyl
372
Q

Why is pulse oximetry not useful in CO poisoning?

A

Due to similarities between oxyhaemoglobin and carboxyhaemoglobin

373
Q

Pathophysiology of CO poisoning?

A

carbon monoxide binds readily to haemoglobin, forming carboxyhaemoglobin → reduced oxygen-carrying capacity
in carbon monoxide poisoning the oxygen saturation of haemoglobin decreases leading to an early plateau in the oxygen dissociation curve

374
Q

What investigations to do in suspected CO poisoning?

A

VBG or ABG
ECG to look for cardiac ischaemia
N.B pulse oximetry is not reliable due to similarities between oxyhaemoglobin and carboxyhaemoglobin

375
Q

What is the management of CO poisoning?

A

Assess in ED
100% High flow via non-rebreather - ASAP and for at least 6 hrs (this decreases the half-life of carboxyhaemoglobin)
Target sats 100%
Treatment continued until all symptoms resolved rather than monitoring CO levels

376
Q

When are 3 successive shocks given in ALS algorithm?

A

Only used in cardiac arres if witness and monitored (on monitor) e.g. post MI infarction in a CCU

377
Q

How does strongyloides stercoralis infect people?

A

Human parasitic nematode worm. Larvae present in soil and gain access to the body by penetrating the skin

378
Q

Features of strongyloides stercoralis?

A
  • Diarrhoea
  • Abdominal pain / vomiting
  • Papulovesicular lesions where the skin has been penetrated by infective larvae e.g. soles of feet and buttocks
  • Larva currens - pruritic, linear, urticarial rash
  • If the larvae migrate to the lungs a pneumonitis similar to Loeffler’s syndrome may be triggered
379
Q

What is the management of strongyloides stercoralis?

A

Ivermectin and albendazole

380
Q

Do we screen for NAFLD?

A

No. Mnaagment is based only on incidental finding of NAFLD - typically asymptomatic fatty changes on liver ultrasound

381
Q

What testing is done in NAFLD?

A

No screening is done. Only when you incidentally have findings suggestive of NAFLD, e.g. fatty changes on u/s
Then do ELF blood test (hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase 1)
Fibroscan

382
Q

Features of systemic macrocytosis?

A
  • Urticaria pigmentosa - produces a wheal no rubbing (Darier’s sign)
  • Flushing
  • Abdominal pain
  • Monocytosis on the blood film
383
Q

2 investigations in systemic macrocytosis?

A
  • Raised serum tryptase levels
  • Urinary histamine
384
Q

After you have done CXR, what other investigation should be done in suspected aspergilloma?

A

Serologic testing for Aspergillus Precipitins

385
Q

What is the classic feature on CXR in aspergilloma?

A

Crescent sign

386
Q

C.diff is gram +ve or -ve, and what morphology is it?

A

Gram +ve rod

387
Q

Other than antibiotics, what other type of medication is a risk factor for c.diff?

A

PPIs

388
Q

Outline the severity classification of c.diff

A

Mild - normal WCC
Moderate - Raised WCC ( < 15 x 10^9/L) , 3-5 loose stools per day
Severe - Raised WCC ( > 15 x 10^9/L) or acutely raised creatinine (> 50% above baseline) or temp > 38.5 or evidence of severe colitis (abdominal or radiological signs)
Life-threatening - Hypotension, partial or complete ileus, toxic megacolon, or CT evidence of severe disease

389
Q

Diagnostic for c.diff?

A

C.diff toxin in the stool
N.B c.diff antigen only shows exposure to the bacteria, rather than current infection

390
Q

What is the isolation precaution procedure for c.diff?

A

Side-room isolation - remain isolated until there has been no diarrhoea (types 5-7 bristol stool chart) for at least 48 hours

Gloves and aprons for staff

Staff must wash hands as spores are not killed by alcohol gel alone

391
Q

In what type of cause of memory loss is there global memory loss (i.e. both short and long term memory loss), and reluctance to engage with clinical assessment?

A

Pseudodementia in depression

392
Q

How can you divide the different causes of eosinophilia and list some causes under each category?

A

PULMONARY
- Asthma
- ABPA
- Churg-strauss (eGPA)
- Loefller’s syndrome
- Tropical pulmonary eosinophilia
- Hypereosinophilic syndrome

INFECTIVE
- Schistosomiasis
- Nematodes: Toxcara, Ascaris, Strongyloides
- Cestodes: Echinococcus

OTHER
- Drugs - sulfasalazine, nitrofurantoin
- Psoriasis, eczema
- Eosinophilic leukaemia (very rare)

393
Q

2 drugs that can cause eosinophilia?

A

Sulfasalazine, nitrofurantoin

394
Q

Is the diphtheria bacterium - Corynebacterium Diphtheriae - gram positive or negative?

A

Gram positive

395
Q

What is the main investigation for diphtheria?

A

Culture of throat swabs - uses tellurite agar or Loefller’s media

396
Q

What is the management of diphtheria?

A
  • IM Penicilin
  • Diphtheria antitoxin
397
Q

What can be found on ENT examinatin in diphtheria?

A
  • Diphtheric membrane on tonsils caused by necrotic mucosal cells - grey, pseudomembrane on the posterior pharyngeal wall
  • Enlargement of cervical lymph nodes, bulky - appearance of ‘bull neck’
398
Q

What are the presentations of diphtheria?

A
  • Sore throat
  • Fevers
  • Later progress to severe cough resembling that of Croup
  • Diphtheric membrane
  • Bulky cervical lymphadenopathy - bull neck appearance
  • Neuritis e.g. cranial nerves
  • Heart block
399
Q

What topical agent is the treatment of choice for the hirsutism in PCOS?

A

Eflornithine

400
Q

Outline 3 actions that ANP have?

A
  • Natriuretic - i.e. promotes excretion of sodium
  • Lowers BP
  • Antagonises action of angiotensin II, aldosterone
401
Q

Where is ANP secreted from?

A

Secreted by both right and left atria (right > left)
Secreted mainly by myocytes of right atrium and ventricle in response to increased blood volume

402
Q

Which chromosome is affected in Von-Hippel Lindau syndrome?

A

Chromosome 3

403
Q

Which chromosome is affected in tuberous sclerosis?

A

Chromosome 16

404
Q

1) Which chromosome is affected in NF1 (Neurofibromatosis type 1)?
2) Which chromosome is affected in NF2 (Neurofibromatosis type 2)?

A

1) Chromosome 17
2) Chromosome 22

405
Q

Outline the causes of methaemoglobinaemia

A

CONGENITAL
- NADH methaemoglobin reductase deficiency

ACQUIRED
- Drugs: Sulphonamides, nitrates, dapsone, sodium nitroprusside, primaquine
- Chemicals: Aniline dyes

406
Q

What is the classic finding in the ABG in methaemoglobinaemia?

A

Normal pO2 but decreased oxygen saturation

407
Q

What are the management options for methaemoglobinaemia?

A
  • NADH methaemoglobinaemia reductase deficiency: ascorbic acid
  • IV methylthionium chloride (methylene blue) if acquired
408
Q

What is methaemoglobinaemia?

A

Methaemoglobinaemia describes haemoglobin which has been oxidised from Fe2+ to Fe3+. This is normally regulated by NADH methaemoglobin reductase, which transfers electrons from NADH to methaemoglobin resulting in the reduction of methaemoglobin to haemoglobin. There is tissue hypoxia as Fe3+ cannot bind oxygen, and hence the oxidation dissociation curve is moved to the left

409
Q

Features in pityriasis versicolor?

A
  • Trunk predominance
  • Hypopigmented or pink or brown patches (hence versicolor). May be more noticeable folllowing a suntan
  • Scaleing common
  • Mild pruritis
410
Q

List some predisposing factors in Pityriasis Versicolor

A
  • Immunosuppression
  • Malnutrition
  • Cushing’s
411
Q

Outline first line then second line management of pityriasis versicolor

A

First line = Topical Ketoconazole Shampoo
Second line = Send skin scrapings (consider alternative diagnoses) + Oral Itraconazole

412
Q

What is the organism causing pityriasis versicolor?

A

Malassezia furfur

413
Q

Pulmonary arterial hypertension - what is the definition as defined by pressure?

A

Pulmonary artery pressure > / = 20mmHg

414
Q

Pulmonary artery hypertension more common in males or females?
More common in which age group?

A

F > M
30-50 yrs

415
Q

Risk factors for pulmonary arterial HTN?

A

HIV
Cocaine
Anorexigens e.g. fenfluramine
10% inherited in autosomal dominant manner
Female
30-50yrs

416
Q

Features of pulmonary arterial hypertension?

A

Progressive exertional dyspnoea
Exertional syncope
Exertional chest pain
Peripheral oedema
Cyanosis
RV heave, loud P2, raised JVP with prominent ‘a’ waves, tricuspid regurgitation

417
Q

Outline management in pulmonary arterial hypertension

A

First do acute vasodilator testing - e..g IV epoprostenol or inhaled NO
- If +ve response then give oral CCBs

If -ve response

Prostacyclin analogues: treprostinil, iloprost
Endothelin receptor antagonists
- Non-selective: bosentan
- Selective antagonists of endothelin receptor A: ambrisentan
Phosphodiesterase inhibitors - sildenafil

Progressive symptoms - consider heart-lung transplant

418
Q

What is the ECOG score and summarise the different scores in it

A

Scoring system mainly used to assess fitness for chemotherapy

0 - fully active, no restrictions on activity
1 - symptomatic but ambulatory, restained in ability to do strenuous activity but still can do light work
2 - Ambulatory > 50% of time (in bed / chair rest of time)
3. Ambulatory < 50% of time
4. Bedbound
5. Dead

419
Q

True or false, there will be raised serum calcium levels in Paget’s?

A

False
They are however raised in hyperPTH, multiple myeloma and vitamin D disorders

420
Q

What are the markers of increased bone turnover found in Paget’s?

A

Serum / urine hydroxyproline
Procollagen type 1 N-terminal propeptide (PINP)
C-telopeptide (CTx)
N-telopeptide (NTx)

421
Q

What are the predisposing factors for Paget’s disease of the bone?

A
  • Increasing age
  • Male sex
  • Northern latitude
  • Family history
422
Q

What percentage of people with Paget’s are symptomatic?

A

Only 5%

423
Q

X-ray findings in Paget’s disease of the bone/

A

Osteolysis in early disease - mixed lytic / sclerotic lesions later
Skull x-ray - thickened vault, osteoporosis circumscripta

424
Q

What are the indications for treatment in Paget’s disease of the bone?

A
  • Bone pain
  • Skull or long bone deformity
  • Fracture
  • Periatricular Paget’s
425
Q

What is the main management for Paget’s disease of the bone?

A

Bisphosphonates (either oral risedronate or IV zoledronate)

426
Q

List some complications of Paget’s disease of the bone

A
  • Deafness
  • Bone sarcoma
  • Fractures
  • Skull thickening
  • High-output cardiac failure
427
Q

What are the definitional criteria for neutropaenic sepsis?

A

Neutrophil count < 0.5 x 10^9 and one of:
- Temp > 38C
- Other signs or symptoms consistent with clinically significant sepsis

428
Q

Which organisms most commonly cause infection in neutropaenic sepsis?

A

Coagulase negative, gram positive bacteria - especially Staphylococcus Epidermidis - due to indwelling lines in cancer patients

429
Q

What is done for prophylaxis for neutropaenic sepsis?

A

If patients expected to have neutrophils < 0.5 x 10^9 as a consequence of their treatment - they should be offered a fluoroquinolone

430
Q

At how many days after chemotherapy does neutropaenic sepsis tend to happen?

A

Most commonly 7-14 days after chemotherapy

431
Q

Outline the management of neutropaenic sepsis

A
  • Sideroom
  • Start abx immediately, empirically - piperacilin + tazobactan (tazocin)
  • Specialist review and risk stratification - to see whether they can have outpatient treatment
  • If still unwell after 48 hrs then alternative e.g. meropenem +/- vancomycin
  • If not responding after 4-6 days then Christie guidelines suggest ordering investigations for fungal infections e.g. HRCT rather than starting antifungal therapy blindly
  • G-CSF consider in some patients
432
Q

List some causes of lichenoid drug eruptions (lichen planus)

A
  • Gold
  • Quinine
  • Thiazides
433
Q

1) Outline the management of lichen planus (exclude oral lichen planus)

2) Outline the management for oral lichen planus

A

1) Potent topical steroids, note extensive lichen planus may require oral steroids or immunosuppression
2) Benzydamine mouthwash or spray

434
Q

Outline some features of lichen planus

A

Itchy, papular rash most common on the palms, soles, genitalia and flexor surfaces of arms
rash often polygonal in shape, with a ‘white-lines’ pattern on the surface (Wickham’s striae)
Koebner phenomenon may be seen (new skin lesions appearing at the site of trauma)
oral involvement in around 50% of patients: typically a white-lace pattern on the buccal mucosa
nails: thinning of nail plate, longitudinal ridging

435
Q

What are two common complications of seborrheic dermatitis?

A

Otitis externa
Blepharitis

436
Q

Where are the eczematous lesions typically in seborrheic dermatitits?

A
  • Scalp - dandruff
  • Periorbital
  • Auricular
  • Nasolabial folds
437
Q

What organism involved in seborrheic dermatitis?

A

Malassezia furfur

438
Q

Name 2 conditions associated with seborrheic dermatitis

A
  • HIV
  • Parkinson’s disease
439
Q

What is first line treatment for dandruff in seborrheic dermatitis?

What other treatment options are available?

A

Ketoconazole 2% shampoo

Over the counter preparations containing zinc pyrithione (‘Head & Shoulders’) and tar (‘Neutrogena T/Gel’) may be used if ketoconazole is not appropriate or acceptable to the person
Selenium sulphide and topical corticosteroid may also be useful

440
Q

How is seborrheic dermatitis affecting the face and body managed?

A
  • Topical antifungals e.g. ketoconazole
  • Topical steroids - for short periods
441
Q

What is the definitive management for wolff-parkinson-white?

What are the options for medical therapy for wolff-parkinson white?

A

Radiofrequency of the accessory pathway

Sotalol, amiodarone, flecainide
(note avoid sotalol if coexistent AF - risk of VF)

442
Q

What can AF degenerate into in Wolff-Parkinson-White?

A

VF

443
Q

What happens in wolff-parkinson white?

A

Cogenital accessory conducting pathway between the atria and ventricles leading to AVRT (atrioventricular re-entry tachycardia)

444
Q

Is there right axis or left axis deviation in wolff-parkinson white?

A
  • Left axis deviation if right sided accessory pathway - will have dominant r wave in V1 - TYPE A
  • Right axis deviation if left sided accessory pathway - no dominant r wave in V1 - TYPE B
445
Q

Give some associations with wolff-parkinson-white

A
  • HOCM
  • Mitral valve prolapse
  • Ebstein’s anomaly
  • Thyrotoxicosis
  • Secundum ASD
446
Q

Outline the ECG features in wollf-parkinson-white

A
  • Short PR interval
  • Wide QRS complexes with slurred upstroke - delta wave
  • Left axis deviation if right sided accessory pathway
  • Right axis deviation if left sided accessory pathway
447
Q

What are the two types of wolff-parkinson-white?

A

Type A (left-sided pathway): dominant R wave in V1
Type B (right-sided pathway): no dominant R wave in V1

448
Q

What is the mode of action of spironolactone and where does it act?

A

Aldosterone antagonist - acts in the cortical collecting duct

449
Q

2 main side effects of spironolactone?

A
  • Hyperkalaemia
  • Gynaecomastia

Note if suffering with gynaecomastia can switch to eplerenone - and for male patients with heart failure epleronone is better to start with for this reason

450
Q

2 main features of creutzfeld-jakob disease?

A
  • Dementia (rapid onset)
  • Myoclonus
451
Q

What are the key investigations in suspected creutzfeld-jakob disease and the findings?

A

CSF - usually normal , 14-3-3 in sporadic CJD
EEG - biphasic, high amplitude sharp waves (only in sporadic CJD)
MRI - hyperintense signals in the basal ganglia (pulvinar region) and thalamus - ‘hockey stick sign’ or in pulvinar region only (‘pulvinar sign’)

452
Q

What are the two different types of CJD and which is more common? Which age group do each present in typically?

A

Sporadic CJD - 85% of cases
- Mean age of onset 65 years

New variant CJD
- Younger patients (average age of onset = 25 years)

453
Q

What are the main features of new variant CJD?

A

Psychological symptoms e.g. anxiety, withdrawal and dysphonia

454
Q

Name 4 prion diseases

A
  • CJD
  • Kuru
  • Fatal familial insomnia
  • Gerstmann Straussler-Scheinker disease
455
Q

What is the median survival in new variant CJD?

A

13 months

456
Q

What are the common causes of fatality in quinine toxicity (cinchonism)?

A
  • Cardiac arrythmia
  • Flash pulmonary oedema
  • Renal failure - more long term
457
Q

What cardiac arrythmias can develop in quinine toxicity (cinchonism) and why?

A

Blockade of sodium and potassium channels - prolonging QRS and QT intervals - can degenerate into ventricular tachyarrythmias or fibrillation - leading to death

458
Q

What are the hallmark features of quinine toxicity (cinchonism)?

A
  • Tinnitus
  • Visual blurring
  • Flushing
  • Dry skin
  • Abdominal pain
459
Q

What other investigation is important to do in suspected quinine toxicity (based on another differential that presents similarly - to help distinguish it from this)?

A

Serum salicylate levels

460
Q

Neural damage - tinnitus, deafness and visual defects in aspirin overdose vs in quinine overdose - in which is it temporary and in which is it permanent?

A

Aspirin - temporary, usually reversible
Quinine - permanent

461
Q

What is the management of quinine poisoning?

A
  • Fluids, inotropes, bicarbonate
  • Positive pressure ventilation for pulmonary oedema
462
Q

B-cell or T-cell proliferation more common in CLL (chronic lymphocytic leukaemia)?

A

B-cell proliferation more common

463
Q

1) 2 reasons why anaemia can happen in chronic lymphocytic anaemia?
2) 2 reasons why thrombocytopaenia can happen in chronic lymphocytic anaemia?

A

1) Either due to bone marrow replacement or AIHA (autoimmune haemolytic anaemia)
2) Either due to bone marrow replacement or immune thrombocytopaenia (ITP)

464
Q

Characteristic blood film finding in chronic lymphocytic anaemia?

A

Smudge cells

465
Q

Aside from FBC and blood film, what is the key investigation for diagnosis in chronic lymphocytic anaemia?

A

Immunophenotyping - using panel specific for CD5, CD19, CD20 and CD23

466
Q

Orbital cellulitis is the result of an infection affecting the fat and muscles posterior to the …… ……

A

Orbital cellulitis is the result of an infection affecting the fat and muscles posterior to the posterior septum

467
Q

What is the usual source of infection in orbital cellulitis?

A

Usually caused by a spreading upper respiratory tract infection from the sinuses

468
Q

Does orbital cellulitis have high or low mortality rate

A

High

469
Q

Difference between the site of infection in orbital vs periorbital cellulitis?

A

Orbital cellulitis affecss fat and muscles posterior to the orbital septum vs periorbital cellulitis is anterior to the orbital septum

470
Q

What is the usual nodus of infection in periorbital cellulitis?

A

Superficial infection anterior to the orbital septum, resulting from a superficial tissue injury (chalazion, insect bite etc)

471
Q

What can periorbital cellulitis progress to?

A

Orbital cellulitis

472
Q

What are the risk factors for orbital cellullitis?

A
  • Childhood (mean age of hospitalisation 7-12 years)
    Previous sinus infection
    Lack of Haemophilus Influenzae type B vaccination
    Recent eyelid infection / insect
    Ear or facial infection
473
Q

Features of orbital cellulitis?

A
  • Redness and swelling around the eye
  • Severe ocular pain
  • Visual disturbance
  • Proptosis
  • Ophthalmoplegia/pain with eye movements
  • Eyelid oedema and ptosis
  • Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)
473
Q

How to clinically differentiate orbital vs preseptal cellulitis (not anatomically)?

A

NOT consistent with preseptal (preorbital) cellulitis
- Reduced visual acuity
- Proptosis
- Ophthalmoplegia / pain with eye movements

474
Q

Investigations in suspected orbital cellulilitis?

A
  • FBC - raised WCC, inflammatory markers
  • Clinical exam - decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema
  • CT with contrast - inflammation of orbital tissues deep to septum, sinusitis
  • Blood culture and microbiological swab - most common bacterial causes - strep, staph aurea, haemophilus influenzae B
475
Q

Waldenstrom’s macroglobulinaemia is an uncommon condition seen in older men. It is a lymphoplasmacytoid malignancy characterised by the secretion of a monoclonal ….. …….

A

Waldenstrom’s macroglobulinaemia is an uncommon condition seen in older men. It is a lymphoplasmacytoid malignancy characterised by the secretion of a monoclonal IgM paraprotein

476
Q

Features of Waldenstrom’s macroglobulinaemia?

A
  • Systemic upset: weight loss, lethargy
  • Hyperviscosity syndrome e.g. visual disturbance
    the pentameric configuration of IgM increases serum viscosity
  • Hepatosplenomegaly
  • Lymphadenopathy
  • Cryoglobulinaemia e.g. Raynaud’s
477
Q

2 key investigations in Waldenstrom’s Macroglobulinaemia and which one is diagnostic?

A
  • Monoclonal IgM paraproteinaemia
  • Bone marrow biopsy is diagnostic - infiltration of the bone marrow with lymphoplasmacytoid lymphoma cells
478
Q

What is the management of Waldenstrom’s macroglobulinaemia?

A

Rituximab based combination chemotherapy

479
Q

How is Leishmaniasis spread?

A

Leishmaniasis is caused by the intracellular protozoa Leishmania, spread by the bites of sandflies.

480
Q

What are the three forms of Leishmaniasis?

A
  1. Cutaneous Leishmaniasis
  2. Mucocutaneous Leishmaniasis
  3. Visceral Leishmaniasis (kala-azar)
481
Q

How is cutaneous Leishmaniasis investigated - key diagnostic?

A

Punch biopsy from the edge of the lesion - histology and culture

482
Q

Which species of Leishmania cause
1) Cutaneous Leishmaniasis
2) Mucocutaneous Leishmaniasis
3) Visceral Leishmaniasis

Note the species - will dictate whether you treat conservatively or with systemic treatment due to the form of leishmania you get

A

1) Leishmania tropica or Leishmania mexicana
2) Leishmania Braziliensis
3) Leishmania donovani

483
Q

Cutaneous leishmaniasis acquired in ….. or ….. ….. merits treatment due to the risk of mucocutaneous leishmaniasis wherease disease acquired in ….. or ….. can be managed more conservatively

A

Cutaneous leishmaniasis acquired in South or Central America merits treatment due to the risk of mucocutaneous leishmaniasis wherease disease acquired in Africa or India can be managed more conservatively

484
Q

Features of visceral leishmaniasis (kala-azar)?

A
  • Fevers, sweats, rigors
  • Massive splenomegaly, hepatomegaly
  • Poor appetite, weight loss (sometimes may have increased appetite with paradoxical weight loss)
  • Grey skin (kala-azar = black sickness)
  • Pancytopaenia secondary to hypersplenism
485
Q

What is the gold standard investigation for diagnosis of visceral leishmaniasis?

A

Bone marrow or splenic aspirate

486
Q

Outline the indications for systemic therapy in leishmaniasis (cutaneous leishmaniasis)

A
  • Acquired in South / Central America (principally L braziliensis and L guyanensis)
  • Multiple (> 4) lesions
  • Large lesions ( > 5cm)
  • Lesions involving the face, hands or genitals
  • Host immunocompromised, or if local treatment has failed
487
Q

Give some differentials for causes of cavitating chest x ray

A
  • Abscess (Staph aureus, Klebsiella and Pseudomonas)
  • Squamous cell lung cancer
  • Tuberculosis
  • Wegener’s granulomatosis
  • Pulmonary embolism
  • Rheumatoid arthritis
  • Aspergillosis, histoplasmosis, coccidioidomycosis
488
Q

Ramsay Hunt Syndrome is caused by the reactivation of which virus in the geniculate ganglion of the seventh cranial nerve?

A

Varicella Zoster Virus

489
Q

Ramsay Hunt syndrome is caused by reactivation of the varicella zoster virus in the …. …… of the ….. cranial nerve

A

Ramsay Hunt syndrome is caused by reactivation of the varicella zoster virus in the geniculate ganglion of the seventh cranial nerve

490
Q

What is the key managment of Ramsay Hunt syndrome?

A

Oral aciclovir and corticosteroids

491
Q

Features of Ramsay Hunt syndrome?

A
  • Auricular pain
  • Facial nerve palsy
  • Vesicular rash around the ear
  • Vertigo, tinnitus
492
Q

True or false, vertigo and tinnitus can occur in Ramsay Hunt syndrome?

A

True

493
Q

What is the HLA association in ankylosing spondylitis?

A

HLA-B27
Associated with 90-95% of ankylosing spondylitis cases

494
Q

Ankylosing spondylitis typically presents in men or women?
Young or old?

A
  • M: F 3:1 (M>F)
  • Young - 20-30yr olds mostly
495
Q

Features of Ankylosing Spondylitis - the A’s?

A
  • Apical fibrosis (reduced chest expansion)
  • Anterior uveitis
  • Aortic regurgitation
  • Achilles tendonitis
  • AV node block
  • Amyloidosis
  • Peripheral Arthritis
  • And Cauda Equina syndrome
496
Q

What can erythema ab igne progress to if the cause is not treated?

A

Squamous cell skin cancer

497
Q

Describe the rash in erythema ab igne

A

Reticulated, erythematous patches with hyperpigmentation and telangiectasia

498
Q

True or false, telangectasia can be evident in erythema ab igne?

A

True

499
Q

What test can be found in clinical examination in Ankylosing Spondylitis?

A

Reduced lateral flexion
Reduced forward flexion (Schober’s test)
Reduced chest expansion

500
Q

In Ankylosing Spondylitis, does the stiffness improve or get worse with exercise, and is it worse or better at night?

A

Worse at night / morning and improves with exercise (typical of inflammatory picture)

501
Q

Turner’s syndrome what is the karyotype?

A

45, X0

502
Q

List some features of Turner’s syndrome

A
  • Short stature
  • Shield chest, widely spaced nipples
  • Webbed neck
  • Bicuspid aortic valve (15%), coarctation of aorta (5-10%)
    Increased risk of aortic dilatation and dissection are the most serious long-term health problems for women with Turner’s
  • Primary amenorrhoea
  • Cystic hygroma (often diagnosed prenatally)
  • High arched palate
  • Short fourth metacarpal
  • Multiple pigmented naevi
  • Lymphoedema in neonates (especially feet)
  • Raised gonadotrophin levels
  • Hypothyroidism more common in Turner’s
  • Horsheshoe kidney - most common renal abnormality in Turner’s
  • Increased incidence of autoimmune disease (especially autoimmune thyroiditis and Crohn’s disease)
503
Q

What is the most serious long-term health concern for women with Turner’s syndrome (tip - cardiac)?

A

Increased risk of aortic dilatation and dissection

504
Q

Tumour lysis syndrome (TLS) is a potentially deadly condition related to the treatment of high-grade ….. and …..

A

Tumour lysis syndrome (TLS) is a potentially deadly condition related to the treatment of high-grade lymphomas and leukaemias

505
Q

What happens to the level of the following electrolytes in the bloods in tumour lysis syndrome?

  • Urate
  • Potassium
  • Phosphate
  • Calcium
A
  • Urate - raised
  • Potassium - raised
  • Phosphate - raised
  • Calcium - reduced (because phosphate is a calcium chelator)
506
Q

True or false, calcium is reduced in tumour lysis syndrome?

A

True - because there is high phosphate in the blood, and phosphate is a calcium chelator

507
Q

Outline what is done for prevention of tumour lysis syndrome?

A
  • IV fluids
  • Either low dose rasburicase or allopurinol (note not both as allopurinol will reduce the effect of rasburicase)
  • Low dose rasburicase - recombinant version of urate oxidase, an enyme that metabolises uric acid to allantoin - allantoin much more soluble than urate and therefore more readily excreted by the kidneys - generally preferred now over allopurinol
  • Allopurinol - generally used for patients in lower-risk groups - reduces rate of hypoxanthine — xanthine — uric acid conversion. Both are more soluble than urate so less precipitation occurs in the renal tubules. However, it does not increase the rate of breakdown of uric acid that is already present so its therapeutic effect is delayed by 24-72 hours.
508
Q

What is given in treatment for tumour lysis syndrome?

A

Treatment dose rasburicase - note this is better than allopurinol because ….

Rasburicase is recombinant version of urate oxidase, an enyme that metabolises uric acid to allantoin - allantoin much more soluble than urate and therefore more readily excreted by the kidneys. It acts on urate precipitate in the renal tubules already there, so has immediate effect vs…

Allopurinol reduces rate of hypoxanthine — xanthine — uric acid conversion. Both are more soluble than urate so less precipitation occurs in the renal tubules. However, it does not increase the rate of breakdown of uric acid that is already present so its therapeutic effect is delayed by 24-72 hours

509
Q

What are the risk factors for TLS (tumour lysis syndrome)?

A

High burden, high grade tumour with rapid turnover (e.g. Burkitt’s, ALL), pre-existing renal impairment, use of highly active cell-cycle specific chemotherapy

510
Q

What are the Cairo-Bishop criteria for TLS (tumour lysis syndrome)? - Laboratory and clinical

A

LABORATORY - 2 or more of following occuring 3 days prior or 7 days post initiation of treatment for cancer:
- Uric acid ≥ 476 µmol/L or 25% increase from baseline
- Potassium ≥ 6.0 mmol/L or 25% increase from baseline
- Phosphate ≥ 1.45 mmol/L (adults) or ≥2.1 mmol/L (children) or 25% increase
- Calcium ≤ 1.75 mmol/L or 25% decrease from baseline

CLINICAL - laboratory TLS plus at least one of the following:
- Creatinine ≥1.5 x the upper limit of normal
- Cardiac arrhythmia
- Seizure
- Sudden death

511
Q

What additional medical agent is useful in the acute ACS treatment of MI secondary to cocaine use?

A

Lorazepam

512
Q

What is the inheritance pattern of hereditary haemorrhagic telangiectasia?

A

Autosomal dominant

513
Q

True or false - hereditary haemorrhagic telangiectasia is always hereditary?

A

False - 20% occur spontaneously without prior family history

514
Q

Outline the diagnostic criteria for hereditary haemorrhagic telangiectasia

A

If the patient has 2 then they are said to have a possible diagnosis of HHT. If they meet 3 or more of the criteria they are said to have a definite diagnosis of HHT:

  • Epistaxis : spontaneous, recurrent nosebleeds
  • Telangiectases: multiple at characteristic sites (lips, oral cavity, fingers, nose)
  • Visceral lesions: for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM
  • Family history: a first-degree relative with HHT

*picture shows AVMs in lungs and liver

515
Q

What is the triad of associations in Meig’s syndrome?

A

Ovarian fibroma + pleural effusion + ascites

516
Q

Ovarian fibroma + pleural effusion + ascites = what syndrome?

A

Meig’s syndrome

517
Q

Tumour markers - link the following to the most common cancer associations

1) CA-125
2) CA 19-9
3) CA 15-3
4) PSA
5) AFP
6) CEA
7) S-100
8) Bombesin

A

1) Ca-125 - Ovarian cancer
2) CA 19-9 - Pancreatic cancer
3) CA 15-3 - Breast cancer
4) PSA - Prostate cancer
5) AFP - Hepatocellular, Teratoma
6) CEA - Colorectal cancer
7) S-100 - Melanoma, Schwannoma
8) Bombesin - Small cell lung carcinoma, Gastric cancer, Neuroblastoma

518
Q

The sciatic nerve divides into the ….. and ….. ….. nerves. Injury often occurs at the …. of the …..

A

The sciatic nerve divides into the tibial and common peroneal nerves. Injury often occurs at the neck of the fibula

519
Q

What is the most common feature of a common peroneal nerve lesion and list some other features?

A

Most common = foot drop (weakness of foot dorsiflexion)
- Weakness of foot eversion
- Weakness of extensor hallucis longus
- Sensory loss over the dorsum of the foot and the lower lateral part of the leg
- Wasting of the anterior tibial and peroneal muscles

520
Q

How does gentamicin cause nephrotoxicity?

A

Acute tubular necrosis

521
Q

2 main adverse effects with gentamicin?

A
  • Ototoxicity
  • Nephrotoxicity
522
Q

Concomitant use of what other medication in particular increases the risk of nephrotoxicity with gentamicin use?

A

Furosemide

523
Q

In what condition is gentamicin absolutely contraindicated?

A

Myasthenia gravis

524
Q

What to do with gentamicin if:
1) The trough level is high?
2) The peak level is high?

A

1) Trough high - Interval between doses should be increased
2) Peak high - Dose should be decreased

525
Q

What are some specific management options for managing fatigue in Multiple Sclerosis?

A

1st: Trial of amantadine
Mindfulness training
CBT

526
Q

What are first line for treatment of spasticity in multiple sclerosis?

What are the other options for management of this?

A

Baclofen and gabapentin

Diazepam, dantrolene, tinzadine
Physio

527
Q

What is the first lien maangement of oscillopsia in MS (where visual fields appear to oscillate)?

A

Gabapentin

528
Q

Outline the management of bladder dysfunction in multiple sclerosis and how to decide on best management

A

Get ultrasound first to assess bladder emptying - as anticholinergics may worsen symptoms in some patients

If significant residual volume - intermittent self catheterisation
If no significant residual volume - anticholinergics may improve urinary frequency

529
Q

Outline the risk factors for cental retinal vein occlusion

A
  • Increasing age
  • Hypertension
  • Cardiovascular disease
  • Glaucoma
  • Polycythaemia
530
Q

Features of central retinal vein occlusion symptoms?

A

Sudden, painless reduction or loss of visual acuity, usually unilateral

531
Q

Features on fundoscopy of central retinal vein occlusion

A
  • Widespread hyperaemia
  • Severe retinal haemorrhages - ‘stormy sunset’
532
Q

What is a key differential in central retinal vein occlusion that is similar but there is a more limited area of the fundus affected?

A

Branch retinal vein occlusion

533
Q

What are two indications for management in central retinal vein occlusion and how do you manage each of these indications?

A
  1. Macular oedema - intravitreal anti-vascular endothelial growth factor agents
  2. Retinal neovascularisation - laser photocoagulation
534
Q

This patient has sudden painless loss of vision, here is the imaging on fundoscopy, what is the diagnosis?

A

Branch retinal vein occlusion

535
Q

This patient has sudden painless loss of vision, here is the imaging on fundoscopy, what is the diagnosis?

A

Central retinal vein occlusion

Note widespread hyperaemia and ‘stormy sunset’ - severe retinal haemorrhages

536
Q

True or false, Wernicke’s encephalopathy is only seen in alcoholics?

A

False - rarer causes include persistent vomiting, stomach cancer, and dietary deficiency

537
Q

What are the triad of features in Wernicke’s encephalopathy?

A
  1. Ophthalmoplegia (lateral rectus palsy or conjugate gaze palsy) / nystagmus (the most common ocular sign)
  2. Ataxia
  3. Encephalopathy: confusion, disorientation, indifference, inattentiveness
538
Q

2 investigations in suspected Wernicke’s encephalopathy?

A
  • MRI
  • Decreased red cell transketolase
539
Q

What are the features on MRI in Wernicke’s encephalopathy?

A

Petechial haemorrhages in structures including the mamillary bodies and ventricle walls

540
Q

What condition can Wernicke’s syndrome progress to, and how does this present?

A

Korsakoff syndrome

Amnesia (antero-grade)
Confusion

541
Q

What is seen in renal biopsy in Goodpasture’s syndrome?

A

IgG deposits on renal biopsy

542
Q

What is seen in renal biopsy in IgA nephropathy (Berger’s disease)?

A

IgA immune complexes

543
Q

How does IgA nephropathy (Berger’s disease) classically present?

A

Macroscopic haematuria in young people following an URTI

544
Q

What is the finding on renal biopsy in Alport’s syndrome?

A

Longitudinal splitting of the lamina densa

545
Q

What is the finding on renal biopsy in granulomatosis with polyangiitis?

A

Epithelial crescents in Bowman’s capsule

546
Q

What is the finding on renal biopsy in membranous glomerulonephritis?

A

Spike and dome appearance

547
Q

Goodpasture’s syndrome is caused by what?

A

Anti-glomerular basement membrane antibodies against type IV collagen

548
Q

Goodpasture’s syndrome more common in men or women?

In what age groups does Goodpasture syndrome present?

A

Men : Women (2:1)

Bimodal age distribution (20-30 and 60-70)

549
Q

Goodpasture’s syndrome is associated with which HLA?

A

HLA-DR2

550
Q

Feature of Goodpasture’s syndrome?

A

Pulmonary haemorrhage
Rapidly progressive flomerulonephritis
- Rapid onset AKI
- Nephritis — proteinuria + haematuria

551
Q

2 investigations in Goodpasture’s syndrome?

A

Renal biopsy - linear IgG deposits along the basement membrane, raised transfer factor (secondary to pulmonary haemorrhages

552
Q

What are the most common antibodies in Dermatomyositis?
What is the most specific antibody in Dermatomyositis?

A
  • ANA most common
  • Anti-Mi-2 most specific
553
Q

Anti-Jo-1 antibodies in dermatomyositis or polymyositis?

A

More common in polymyositis where they are seen in a pattern of disease with lung involvement, Raynaud’s and fever

554
Q

What is the main management for dermatomyositis?

A

Prednisolone

555
Q

Investigations in Dermatomyositis?

A
  • Elevated CK
  • EMG
  • Muscle biopsy
  • Anti- ANA positive in 60%
  • Anti-Mi-2 positive in 25%, however highly specific
556
Q

What is the site of action of Bumetanide, Furosemide (loop diuretics)?

A

Inhibits the Na-K-Cl cotransporter (NKCC2) in the thick ascending limb of the loop of Henle - reducing the absorption of NaCl

557
Q

Why do patients with poor renal function need higher doses of loop diuretic?

A

Because loop diuretics work on the apical membrane so they must first be filtered into the tubules by the glomerulus before they can have an effect on the Na-K-Cl cotransporter in the thick ascending loop of Henle

558
Q

When are loop diuretics used in hypertension?

A

In resistant hypertension, particularly in patients with renal impairment

559
Q

List some adverse effects with loop diuretics

A
  • hypotension
  • hyponatraemia
  • hypokalaemia, hypomagnesaemia
  • hypochloraemic alkalosis
  • ototoxicity
  • hypocalcaemia
  • renal impairment (from dehydration + direct toxic effect)
  • hyperglycaemia (less common than with thiazides)
  • gout
560
Q

What should be monitored during treatment in rheumatoid arthritis?

A

Monitor FBC
Monitor LFTs
Monitor BP - check every 2 weeks for the first 6 months and then every 8 weeks thereafter

561
Q

Contraindications for Leflunomide - a DMARD used in Rheumatoid arthritis?

A
  • Pregnancy - use effective contraception during treatment and for at least 2 years after treatment in women and at least 3 months after treatment in men (plasma concentration monitoring required)
  • Pre-existing lung and liver disease
562
Q

List some adverse effects associated with leflunomide - a DMARD used in rheumatoid arthritis

A

gastrointestinal, especially diarrhoea
hypertension
weight loss/anorexia
peripheral neuropathy
myelosuppression
pneumonitis

563
Q

How is leflunomide stopped?

A

Very long wash-out period of up to one year which requires co-administration of cholestyramine

564
Q

Fanconi syndrome is characterised by a defect in which part of the kidneys?

A

Proximal renal tubules

565
Q

What are the lab findings (bloods / urine findings) in Fanconi syndrome?

A

Glycosuria, proteinuria, hypophosphataemia, hypokalaemia

This is because there is impaired reabsorption of various substances such as amino acides, glucose, bicarbonate and phosphate

566
Q

Clinical features of Fanconi syndrome?

A

The clinical manifestations include polyuria, polydipsia, generalised weakness, fatigue, bone pain and muscle weakness due to excessive urinary excretion of these substances

Osteomalacaia
Type 2 (proximal) renal tubular acidosis

567
Q

List some causes of Fanconi syndrome

A
  • Cystinosis (most common cause in children)
  • Sjogren’s syndrome
  • Multiple myeloma
  • Nephrotic syndrome
  • Wilson’s disease
568
Q

What is the most common cause of Fanconi’s syndrome in children?

A

Cystinosis

569
Q

A 4-year-old girl with sickle cell anaemia presents with abdominal pain. On examination, she is noted to have splenomegaly and is clinically anaemic. What is the most likely diagnosis?

A

Sequestration crisis - This is more common in early childhood as repeated sequestration and infarction of the spleen during childhood gradually results in an auto-splenectomy

570
Q

List some different sickle cell crises

A
  • Thrombotic - ‘vaso-occlusive’
  • Acute chest syndrome
  • Anaemia - aplastic and sequestration crises
  • Infectino
571
Q

Where can thrombotic crises occur in sickle cell disease?

A

Various organs including the bones e.g. avascular necrosis of the hip
Hand-foot syndrome in children
Lungs
Spleen
Brain

572
Q

What is the most common cause of death after childhood in sickle cell crises?

A

Acute chest syndrome

573
Q

Feature of acute chest syndrome?

A

Dyspnoea, chest pain, pulmonary infiltrates on CXR, low PO2

574
Q

Outline management of acute chest syndrome in sickle cell disease

A
  • Pain relief
  • Respiratory support e.g. oxygen therapy
  • Antibiotics - since infection can precipitate acute chest syndrome and can be difficult to distinguish from pneumonia
  • Transfusion - improves oxygenation
575
Q

What precipitates aplastic crisis in sickle cell disease?
How do aplastic crises present?

A

Caused by infection with parvovirus
Presents as a sudden fall in haemoglobin

Bone marrow suppression causes a reduced reticulocyte count

576
Q

What is a key investigation finding difference between aplastic crises and sequestration crises?

A

Aplastic crises will cause a reduced reticulocyte count vs sequestration crises are associated with an increased reticulocyte count

577
Q

A patient who is intolerant of aspirin is started on clopidogrel for the secondary prevention of ischaemic heart disease. Concurrent use of which one of the following drugs may make clopidogrel less effective?
A) Warfarin
B) Omeprazole
C) Codeine
D) Long-term tetracycline use (e.g. for acne rosacea)
E) SSRIs

A

B) Omeprazole

Clopidogrel is a prodrug which requires conversion into its active form by the liver enzyme CYP2C19. Omeprazole, a proton pump inhibitor (PPI), inhibits this enzyme and therefore can reduce the effectiveness of clopidogrel. This interaction has been associated with an increased risk of adverse cardiovascular events. UK guidelines recommend that patients requiring both clopidogrel and a PPI should be prescribed pantoprazole or lansoprazole instead, as these do not interact.

578
Q

What to do if patient requires both PPI and clopidogrel to prevent interaction?

A

Prescribe pantoprazole or lansoprazole instead

579
Q

Mechanism of action of clopidogrel?
Then give 3 other medications belonging to the same class of drugs?

A

Mechanism of action - antagonist of P2Y12 ADP receptor, inhibiting activation of the platelets

Thienopyridines
- Prasugrel
- Ticagrelor
- Ticlopidine

580
Q

What is the key investigation in hereditary spherocytosis?

A

Eosin-5-maleimide (EMA) binding test

581
Q

What is the most common hereditary haemolytic anaemia in people of northern european descent?

A

Hereditary spherocytosis

582
Q

What is the inheritance pattern of hereditary spherocytosis?

A

Autosomal dominant

583
Q

In hereditary spherocytosis, what can trigger aplastic crisis?

A

Parvovirus infection

584
Q

Aside from a positive eosin-5-maleimide binding test, what other laboratory investigation findings would be typical in hereditary spherocytosis?

A

Spherocytes on blood film
Raised MCHC
Increase in reticulocytes

Note if there is a positive family history and all of the above are present, there is usually no need to progress to doing the eosin-5-maleimide binding test

585
Q

Outline the management options for hereditary spherocytosis

A

Acute haemolytic crisis:
- Treatment is generally supportive
- Transfusion if necessary
Longer term treatment:
- Folate replacement
- Splenectomy

586
Q

Inheritance pattern of G6PD deficiency?

A

XLR - so in males

587
Q

What is the classical blood film finding in G6PD deficiency?

A

Heinz bodies

588
Q

What is the diagnostic test in G6PD deficiency?

A

Measure enzyme activity of G6PD

589
Q

How do G6PD deficiency and hereditary spherocytosis typically present in neonates?

A

Neonatal jaundice

590
Q

G6PD deficiency typically presents in people of .. and … descent, whereas hereditary spherocytosis typically presents in people of … … descent

A

G6PD deficiency typically presents in people of African and descent, whereas hereditary spherocytosis typically presents in people of Northern European descent

590
Q

Give some causes of oculogyric crisis

A
  • Antipsychotics
  • Metoclopramide
  • Postencephalitic Parkinson’s diseaes
591
Q

Management of oculogyric crisis?

A

Cessation of causative medication
IV antimuscarinic - procyclidine or benztropine

592
Q

Inheritance pattern of Alport’s syndrome?

A

X-linked dominant - defect in gene coding for type IV collagen

593
Q

Is Alport’s syndrome more severe in males or females?

A

More severe in females as it is X-linked dominant - females rarely develop renal failure whereas men do

594
Q

What are the 2 definitive investigations for suspected Alport’s syndrome?

A
  • Molecular genetic testing
  • Renal biopsy - longitudinal splitting of the lamina densa of the glomerular basement membrane - resulting in a ‘basket-weave’ appearance
595
Q

What are the triad of clinical findings in Alport’s syndrome?

A
  • Haemorrhagic nephritis - microscopic haematuria, progressive renal failure
  • Bilateral sensorineural hearing loss
  • Characteristic ocular findings - lenticonus (protrusion of the lens surface into the anterior chamber), Retinitis pigmentosa
596
Q

What is the gene defect encoding for in Alport’s syndrome?

A

Defect in the gene encoding type IV collagen - resulting in an abnormal glomerular basement membrane.
Note XLD inheritance pattern

597
Q

Early features of tricyclic overdose?

A

Early features relate to anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision

598
Q

Feature of severe poisoning in trycyclic overdose?

A
  • Arrythmias
  • Seizures
  • Metabolic acidosis
  • Coma
599
Q

ECG changes in tricyclic overdose?

A
  • Sinus tachy
  • QRS widening (NOTE: QRS > 100ms - associated increased risk of seizures, QRS > 160ms associated with ventricular arrythmias
  • Prolonged QT
600
Q

What antiarrythmics are contraindicated in tricyclic overdose?

A

Class 1a (e.g. quinidine) and class 1c antiarrythmis (e.g. Flecainide) - as they prolong depolarisation

Note class III drugs e.g. amiodarone should also be avoided as they prolong the QT interval

601
Q

What is the first-line management option for tricyclic overdose?
What else can be considered?

A

IV bicarbonate

IV lipid emulsion to bind free drug and reduce toxicity

Please note though that the priority is correction of the acidosis, so IV bicarbonate is the first line

602
Q

True or false, dialysis is effective in removing trycyclics?

A

False - it is ineffective

603
Q

Genital warts are typically caused by what strains of HPV?

A

6 & 11

604
Q

What are the two main first line treatments for genital warts and how do you choose between the two?

A

Topical podphyllum or cryotherapy
- Multiple, non-keratinised warts - best treated with topical agents
- Solitary, keratinised warts respond better to chemotherapy

605
Q

Which strains of HPV predispose to cervical cancer?

A

16,18, 33

606
Q

Prognosis of genital warts?

A

Often resistant to treatment, and recurrence is common, although the majority of infections with HPV clear without intervention within 1-2 years

607
Q

Features of third nerve palsy?

A
  • Eye is deviated ‘down and out’
  • Ptosis
  • Pupil may be dilated (sometimes called a ‘surgical’ third nerve palsy)
608
Q

List some causes of third nerve palsy

A
  • Diabetes mellitus
  • Vasculitis e.g temporal arteritis, SLE
  • False localising sign due to uncal herniation through tentorium if raised ICP
  • Posterior Communicating Artery Aneurysm - (often with dilated pupil and associated pain)
  • Cavernous sinus thrombosis
  • Weber’s syndrome: ipsilateral third nerve palsy with contralateral hemiplegia - caused by midbrain strokes
  • Other possible causes - amyloid, multiple sclerosis
609
Q

Give some signs of uncal herniation

A
  • Hypertension
  • Bradycardia
  • Cheyne-Stokes respiration
  • Loss of consciousness
610
Q

What medication is an analogue of ADH that can be used to treat cranial DI?

A

Desmopressin

611
Q

Antidiuretic hormone is secreted from the … pituitary gland. It promotes water reabsorption in the …. …. of the kidneys by the insertion of …. …. …..

A

Antidiuretic hormone is secreted from the posterior pituitary gland. It promotes water reabsorption in the collecting duct of the kidneys by the insertion of aquaporin-2 channels

612
Q

List by order of how common they are, the different thyroid cancers

A

Papillary - 70%
Follicular - 20%
Medullary - 5%
Anaplastic - 1%
Lymphoma - Rare

613
Q

Thyroid lymphoma is associated with what other thyroid condition?

A

Hashimoto’s thyroiditis

614
Q

Medullary thorid cancer cells secrete what?

A

Calcitonin

615
Q

Outline the management of papillary and follicular thyroid cancer

A
  • Total thyroidectomy
  • Followed by radioiodine (I-131) to kill residual cells
  • Yearly thyroglobulin levels to detect early recurrent disease
616
Q

A patient is investigated for leukocytosis. Cytogenetic analysis shows the presence of the following translocation: t(9;22)(q34;q11). Which haematological malignancy is most strongly associated with this translocation?

A

CML - philadelphia translocation t(9;22)

617
Q

Between extradural and subdural haemorrhage, which one causes fluctuating consciousness?

A

Subdural

618
Q

What are the different timelines of onset of symptoms in acute, subacute and chronic subdurals?

A

Acute - symptoms develop within 48hrs of injury, characterised by rapid neurological deterioration
Subacute - symptoms develop within days to weeks post-injury, with a more gradual progression
Chronic - common in elderly - develop over weeks to months

619
Q

What eye signs can be seen in subdural haematoma?

A

Papilloedema - indicating raised intracranial pressure
Pupil changes - unilateral dilated pupil, especially on the side of the haematoma, indicating compression of the third cranial nerve

620
Q

What is Cushing’s triad?

A

Triad of symptoms in raised intracranial pressure
- Bradycardia
- Hypertension
- Respiratory irregularities e.g. Cheynes-Stokes breathing

621
Q

Management of acute subdural haematoma options?

A

Small or incidental acute subdurals - observe conservatively
Surgical options - monitor intracranial pressure and decompressive craniectomy

622
Q

How do acute subdurals present on CT imaging vs chronic subdurals?

A

Acute subdurals will be bright whereas chronic will be dark (hypodense) compared to the substance of the brain

623
Q

Management options for chronic subdurals and when treatment beyond conservative management is considered?

A

If it is incidental finding or small in size with no associated neurological deficit - conservative

If patient is confused, has associated neurological deficit or has severe imaging findings - consider surgical decompression with burr holes

624
Q

Follicular lymphoma is associated with which translocation?

A

t(14;18)
Ig heavy chain on chromosome 14 and BCL2 on chromosome 18

625
Q

Which translocation is associated with Burkitt’s lymphoma?

A

t(8;14)

626
Q

Which translocation is associated with Mantle cell lymphoma?

A

t(11;14)

627
Q

Which translocation is associated with promyelocytic leukaemia?

A

t(15;17)

628
Q

How long does finasteride treatment of BPH usually take before results are seen?

A

6 months

629
Q

How is the water deprivation test done?

A

Prevent patient drinking water, ask patient to empty their bladder, hourly urine and plasma osmolalities

630
Q

Water deprivation test table

A
631
Q

Investigations in suspected BPH?

A
  • Urine dipstick
  • U&Es
  • PSA
  • Urinary frequency-volume chart - should be done for at least 3 days
  • IPSS - international prostate symptom score - to classify severity of LUTS and assessing the impact of LUTS on quality of life
    • 20-35 - Severely symptomatic
    • 8-19 - Moderately symptomatic
    • 0-7 - Mildly symptomatic
632
Q

Outline the management options for BPH

A
  • Watchful waiting
  • Alpha-1 antagonists e.g. tamsulosin, alfusozin
  • 5- alpha-reductase inhibitors e.g. finasteride
  • Combination therapy
  • NOTE: if there is combincation of storage and voiding symptoms that persist after treatment with an alpha-blocker alone, then an antimuscarinic (anticholinergic) drug e.g. tolterodine or darifenacin may be tried
  • Surgery - TURP (transurethral resection of the prostate)
633
Q

Adverse effects of alpha-1 antagonists in BPH?

A

Dizziness, postural hypotension, dry mouth, depression

634
Q

Adverse effects of 5-alpha reductase inhibitors in BPH?

A

Erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia

635
Q

Complications of BPH?

A
  • UTI
  • Retention
  • Obstructive uropathy
636
Q

Outline medical management of angina pectoris? Including medications they should all be on and then the different options for first and second line therapy, and third line

A
  • All patients should be on aspirin and statin if not contraindicated
  • First line either beta-blocker OR rate-limiting CCB e.g. verapamil or diltiazem (NEVER BOTH - risk of complete heart block)
  • If on beta-blocker first line max dose and still symptomatic, you can add on a longer-acting dihydropyridine CCB e.g. amlodipine, modified release nefidipine
  • If on CCB max dose and still symptomatic you can add on beta blocker but ensure you switch the CCB to a longer-acting dihydropyridine e.g. amlodipine or modified release nifedipine
  • If they cannot tolerate addition of CCB then consider either longer acting nitrate, ivabradine, nicorandil, ranolazine
  • Note: only add third drug whilst a patient is awaiting assessment for PCI or CABG
637
Q

How to avoid nitrate tolerance in patients taking nitrates for management of angina pectoris symptoms?

A

If taking standard release isosorbide mononitrate then use an asymmetric dosing interval to maintain a daily nitrate free time of 10-14 hours

Take once daily modified release isosorbide mononitrate 10mg BD starting (this formulation prevents nitrate tolerance)

638
Q

What is the inheritance pattern of Wiskott-Aldrich syndrome?

A

X-linked recessive

Mutation in WASP gene

639
Q

Wiskott Aldrich syndrome is due to dysfunction in which types of cells?

A

B- and T-cell

640
Q

What is the triad in Wiskott Aldrich syndrome?

A
  • Recurrent bacterial infections e.g. chest
  • Eczema
  • Thrombocytopaenia

(+low IgM levels)

641
Q

Preferred method of contraception in women with PCOS?

A

COC pill - may help regulate cycle and induce a monthly bleed, and help manage hirsutism

642
Q

How is hirsutism and acne managed in PCOS?

A
  • COC , co-cyprindiol
  • Topical eflornithine
  • Spironolactone, flutamide, finasteride under specialist supervision
643
Q

How is infertility managed in PCOS?

A
  • Under specialist supervision
  • Metformin / clomifene or combination
  • Gonadotrophins
644
Q

How is premature ovarian insufficiency defined?

A

Onset of menopausal symptoms and elevated gonadotrophin levels before the age of 40 years. Occurs in 1/100 women

645
Q

Give some causes of premature menopause

A
  • Idiopathic - most common cause, there may be a family history
  • Bilateral oophorectomy
  • Radiotherapy
  • Chemotherapy
  • Infection e.g. mumps
  • Autoimmune disorders
  • Resistant ovary syndrome: due to FSH receptor abnormalities
646
Q

Give some features of premature ovarian failure

A

climacteric symptoms: hot flushes, night sweats
infertility
secondary amenorrhoea
raised FSH, LH levels
e.g. FSH > 30 IU/L
elevated FSH levels should be demonstrated on 2 blood samples taken 4-6 weeks apart
low oestradiol
e.g. < 100 pmol/l

647
Q

What will be the biochemical findings in premature ovarian failure?

A

Raised FSH, LH levels e.g. FSH > 30 IU/L
Note elevated FSH samples should be demonstrated on 2 samples taken 4-6 weeks apart

Low oestradiol e.g. < 100 pmol/L

648
Q

What is the management of premature ovarian failure?

A

HRT or COC should be offered to women until the average age of menopause (51 years)

649
Q

What is a key sign that indiactes a strong risk factor for ocular involvement in Herpes Zoster Opthalmicus?

A

Hutchinson’s sign - rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement

650
Q

Outline the management of Herpes Zoster Ophthalmicus

A
  • Oral antiviral treatment for 7-10 days
  • Ideally started within 72 hours
  • IV antivirals may be given for very severe infection or if the patient is immunocompromised
  • Topical corticosteroids to treat any secondary inflammation of the eye
  • Ocular involvement requires urgent ophthalmology review
651
Q

Give some complications of Herpes Zoster Ophthalmicus

A
  • Ocular - conjunctivitis, keratitis, episcleritis, anterior uveitis
  • Ptosis
  • Post-herpetic neuralgia
652
Q

Is Linezolid bacteriocidal or bacteriostatic in nature?

A

Bacteriostatic - stops formation of the 50S initiation complex

653
Q

What is the organism activity of Linezolid?

A

Highly active against gram positive organisms including:
- MRSA
- VRE (vancomycin resistant enterococcus)
- GISA (glycopeptide intermediate S. Aureus)

654
Q

2 main adverse effects associated with Linezolid?

A
  • Thrombocytopaenia (reversible on stopping)
  • MOAI- avoid tyramine containing foods
655
Q

Give some causes of avascular necrosis of the hip

A
  • Long-term steroid use
  • Chemotherapy
  • Alcohol excess
  • Trauma
656
Q

What is the gold standard investigation in suspected avascular necrosis?

A

MRI

657
Q

What is the management of avascular necrosis of the hip?

A

Joint replacement if necessary

658
Q

X-ray findings in avascular necrosis of the hip?

A

Plain x-ray findings may be normal initially
- Osteopenia and microfractures may be seen early on
- Collapse of the articular surface may result in the crescent sign

659
Q

Will the APTT be reduced or increased in antiphospholipid syndrome?

A

Antiphospholipid syndrome causes a paradoxical rise in the APTT. This is due to an ex-vivo reaction of the lupus anticoagulant autoantibodies with phospholipids involved in the coagulation cascade.

660
Q

Antiphospholipid syndrome may occur as a primary disorder or secondary to other conditions, most commonly …

A

Antiphospholipid syndrome may occur as a primary disorder or secondary to other conditions, most commonly systemic lupus erythematous (SLE)

Note: Around 30% of patients with SLE have positive antiphospholipid antibodies

661
Q

Give some features of antiphospholipid syndrome

A
  • Venous / arterial thrombosis
  • Recurrent miscarriages
  • Thrombocytopaenia
  • Raised APTT
  • Livedo Reticularis
  • Other features: pre-eclampsia, pulmonary hypertension
662
Q

Investigations / lab findings in anti-phospholipid syndrome?

A
  • Anticardiolipin antibodies
  • Anti-beta2 glycoprotein 1 (anti-beta2GPI) antibodies
  • Thrombocytopaenia
  • Prolonged APTT
663
Q

A 36-year-old female presents with her second unprovoked pulmonary embolus 3 months after ceasing warfarin after her first pulmonary embolus. She has a series of tests done to evaluate for the presence of thrombophilia, in particular anti-phospholipid syndrome. What is the greatest predictor of future thrombosis in patients with anti-phospholipid syndrome?

A) Lupus anticoagulant
B) Anticardiolipin antibodies
C) Beta-2-glycoprotein-1 antibody

A

A) Lupus anticoagulant - the strongest risk factor for thrombosis out of these

664
Q

What is the management for primary thromboprophylaxis in antiphospholipid syndrome?

A

Low-dose aspirin

665
Q

What is the management for secondary thromboprophylaxis in anti-phospholipid syndrome?

A
  • Initial venous thromboembolic event: lifelong warfarin with target INR of 2-3
  • Recurrent venous thromboembolic event: lifelong warfarin; if occured whilst taking warfarin then consider adding low dose aspirin, increase target INR to 3-4
  • Arterial thrombosis should be treated with lifelong warfarin with target INR 2-3
666
Q

Give the relative, primary and secondary causes of polycythaemia

A

RELATIVE
- Dehydration
- Stress: Gaisbock syndrome

PRIMARY
- Polycythaemia rubra vera

SECONDARY
- COPD
- Altitude
- OSA
- Excessive EPO: cerebellar haemangioma, hypernephroma, hepatoma, uterine fibroids

667
Q

What investigation can be used to differentiate between true (primary or secondary) polycythaemia and relative polycythaemia?

A

Cell mass studies. In true polycythaemia, the total red cell mass in males > 35ml/kg and in women 32ml/kg

668
Q

Skeletal muscle contraction is dependent on the action of acetylcholine on which specific receptors, that are therefore also indicated in myasthenia gravis?

A

Nicotinic acetylcholine receptors

669
Q

Causes of mitral stenosis - common and then rarer?

A

Most common cause - rheumatic fever
Rarer - mucopolysaccharidoses, carcinoid and endocardial fibroelastosis

670
Q

Typical feature on CXR in mitral stenosis?

A

Left atrial enlargement

671
Q

Features of mitral stenosis?

A
  • Dyspnoea
  • Haemoptysis - ranging from pink frothy sputum to sudden haemorrhage
  • Mid-late diastolic murmur (best heard in expiration)
  • Loud S1
  • Opening snap - indicates mitral valve leaflets still mobile
  • Low volume pulse
  • Malar flush
  • AF - secondary to increased left atrial pressure - left atrial enlargement
672
Q

2 Features of severe Mital Stenosis?

A
  • Length of murmur increases
  • Opening snap becomes closer to S2
673
Q

Feature on echo in mitral stenosis?

A

Reduced cross sectional area of mitral valve - normal area is 4-6 sq cm. A ‘tight’ mitral stenosis implies cross-sectional area of < 1 sq cm

674
Q

Outline management for mitral stenosis, including general management in both asymptomatic and symptomatic patients and then respectively the management in these patients

A

In either, if they have AF - anticoagulate
- Currently warfarin still recommended for moderate / severe MS
- However emerging consensus that DOACs might be useful for patients with mild MS who develop atrial fibrillation

ASYMPTOMATIC:
- Monitor with regular echocardiograms
- Percutaneous / surgical management usually not recommended

SYMPTOMATIC:
- Percutaneous mitral balloon valvotomy
- Mitral valve surgery (commisurotomy or valve replacement) - commisurotomy is preferred for severe MS. Transcatheter Mitral Valve Repair is only for patients not suitable for percutaneous mitral commisurotomy or open surgery

675
Q

In epilepsy, you can consider stopping anti-epileptics if seizure free for > x years, with AEDs being stopped over y-z months

A

In epilepsy, you can consider stopping anti-epileptics if seizure free for > 2 years, with AEDs being stopped over 2-3 months

Note should be done under specialist guidance.
Note benzodiazepines should be withdrawn over a longer period.

676
Q

List 3 neutrophil disorders that are primary immunodeficiency disorders

A
  1. CHronic granulomatous disease
  2. Chediak-Higashi syndrome
  3. Leukocyte adhesion deficiency
677
Q

List 3 B-cell disorders that are primary immunodeficiency disorders

A
  1. CVID
  2. Bruton’s (x-linked) congenital agammaglobulinaemia
  3. Selective immunoglobulin A deficiency
678
Q

Give one T-cell disorder that is a primary immunodeficiency disorder - tip - part of a syndrome - name the syndrome

A

DiGeorge Syndrome

679
Q

Explain the pathophysiology in chronic granulomatous disease?

A

Lack of NADPH oxidase reduces ability of phagocytes to produce reactive oxygen species

680
Q

Explain the pathophysiology in Chediak-Highashi syndrome?

A

Microtubule polymerisation defect which leads to a decrease in phagocytosis

681
Q

Explain the pathophysiology in leukocyte adhesion deficiency

A

Defect of LFA-1 integrin (CD18) protein on neutrophils

682
Q

Clinical symptoms / features in chronic granulomatous disease?

A

Recurrent pneumonias and abscesses, particularly due to a catalase-positive bacteria (Staphylococcus aureus) and fungi (e.g. Aspergillus)

683
Q

Gold standard investigations in chronic granulomatous disease?

A

NBT nitroblue-tetrazolium test - NEGATIVE
Abnormal dihydrorhodamine flow cytometry test

684
Q

Clinical symptoms / features in Chediak-Higashi syndrome?

A

‘Partial albinism’ and peripheral neuropathy
Recurrent bacterial infections

685
Q

What can be seen in the blood film in Chediak-Higashi syndrome (neutrophil disorder primary immunodeficiency disorder)?

A

Giant granules in neutrophils and platelets

686
Q

Clinical symptoms / features in Leukocyte adhesion deficiency (neurophil disorder primary immunodeficiency disorder)?

A
  • Recurrent bacterial infections
  • Delay in umbilical caord sloughing
  • Absence of neutrophils / pus at sites of infection
687
Q

Which immunoglobulins are low in CVID (common variable immunodeficiency)?

A

IgG, IgA, IgM

688
Q

Apart from low antibody levels and immunoglobulin levels of IgG, A and M, what is a common clinical presentation of CVID?

A

Recurrent chest infections

689
Q

CVID can also predisoposer to ….. …… and …..

A

CVID can also predispose to autoimmune disorders and lymphoma

690
Q

Explain the pathophysiology of Bruton’s (x-linked) congenital agammaglobulinaemia

A

Defect in Bruton’s Tyrosine Kinase (BTK) gene that leads to a severe block in B -cell development. Reduced immunoglobulins of all classes. B-cell disorder primary immunodeficiency disorder

691
Q

What is the inheritance pattern of Bruton’s congenital agammaglobulinaemia?

A

X-linked recessive

692
Q

Bruton’s congenital agammaglobulinaemia typically in males or females?

A

Males because it is XLR inheritance pattern

693
Q

What is the pathophysiology in selective immunoglobulin A deficiency?

A

Maturation defect in B cells

694
Q

What is the most common primary antibody deficiency?

A

Selective immunoglobulin A deficiency

695
Q

Which classes of immunoglobulins will be reduced in Bruton’s agammaglobulinaemia?

A

All classes

696
Q

How does selective immunoglobulin A deficiency present?

A
  • Recurrent sinus and respiratory infections
  • Severe reactions to blood transfusions may occur (anti-IgA antibodies — anaphylaxis)
  • Can be associated with coeliac disease (note and may also cause false negative coeliac antibody screen)
697
Q

Which primary immunodeficiency disorder is associated with coeliac’s disease, and can cause a false negative coeliac antibody screen?

A

Selective immunoglobulin A deficiency

698
Q

What is the pathophysiology in DiGeorge’s syndrome?

A

22q11.2 deletion, failure to develop 3rd and 4th pharyngeal pouches

699
Q

Features of DiGeorge’s syndrome?

A
  • Congenital heart disease (e.g. Tetralogy of Fallot)
  • Learning difficulties
  • Hypocalcaemia
  • Recurrent viral / fungal diseases
  • Cleft palate
700
Q

What can be done for management of SCID (severe combined immunodeficiency)?

A

Stem cell transplantation

701
Q

Causes of SCID?

A

Many varying causes. Most common (X-linked) due to defect in the common gamma chain, a protein used in the receptors for IL-2 and other interleukins. Other causes include adenosine deaminase deficiency

701
Q

How can SCID present?

A

Recurrent infectinos due to viruses, bacteria and fungi

702
Q

List 4 combined B- and T-cell disorders that are primary immunodeficiency disorders

A
  • SCID
  • Ataxic telangiectasia
  • Wiskott-Aldrich syndrome
  • HyperIgM syndromes
703
Q

Causes of SCID?

A

Many varying causes. Most common (X-linked) due to defect in the common gamma chain, a protein used in the receptors for IL-2 and other interleukins. Other causes include adenosine deaminase deficiency

704
Q

What is the inheritance pattern of ataxic telangiectasia?

A

Autosomal recessive

705
Q

Features of ataxic telangiectasia?

A
  • Cerebellar ataxia
  • Telangiectasia (spider angiomas)
  • Recurrent chest infections
  • 10% risk of developing malignancy, lymphoma or leukaemia
706
Q

Clinical features in hyperIgM syndrome?

A

Infection / pneumocystis pneumonia, hepatitis, diarrhoea

707
Q

Management options for post-LP headache?

A

Supportive management initially (analgaesia, rest)
If pain continues for > 72 hrs then specific treatment indicated, to prevent subdural haematoma
- Blood patch
- Epidural saline
- IV caffeine

708
Q

Which infection can lead to gastric lymphoma (MALT)?

A

Helicobacter pylori

709
Q

Which infecvtive cause can lead to or increase risk of Hodgkin’s lymphoma or Burkitt’s lymphoma, nasopharyngeal carcinoma?

A

EBV

710
Q

Which infection can lead to or increase the risk of Adult T-cell leukaemia/lymphoma?

A

HTLV-1

711
Q

Which infection can lead to or increase the risk of high grade B-cell lymphoma?

A

HIV-1

712
Q

Which infection can lead to or predispose to Burkitt’s lymphoma?

A

Malaria

713
Q

EBV can lead to or predispose to which haematological malignancies?

A

Hodgkin’s and Burkitt’s lymphoma
Nasopharyngeal carcinoma

714
Q

HTLV-1 can lead to or predispose to which haematological malignancies?

A

Adult T-cell leukaemia / lymphoma

715
Q

HIV-1 can lead to or predispose to which haematological malignancy?

A

High-grade B-cell lymphoma

716
Q

Helicobacter Pylori can lead to or predispose to which malignancy?

A

Gastric lymphoma (MALT)

717
Q

Malaria can lead to or predispose to which haematological malignancy?

A

Burkitt’s lymphoma

718
Q

Which post-renal transplant medication can cause tremors?

A

Tacrolimus

719
Q

Red flags associated with airway and blunt force neck trauma?

A
  • Neck trauma with noisy breathing
  • Neck trauma associated with laryngeal voice change: hoarse, croaky, husky or no voice
  • Expanding swellings in the neck that could be indicative of haematoma
  • Any history or signs of head and neck burns: singed eyebrows, mucosal burns, soot in nostrils, swollen lips
720
Q

What three categories can airway and blunt force neck trauma be divided into?

A
  1. Blunt force airway trauma (fracture, transection, cord palsy etc of the airway itself)
  2. Inhalational burn injury
  3. Expanding space occupying lesion threatening the airway (usually haematoma)
721
Q

Mechanism of action of calcium resonium?

A

Increases potassium excretion by preventing enteral absorption

Calcium resonium is a polystyrene cation exchange resin, acting to increase potassium excretion from the body through cation ion exchange. It exchanges potassium for the Ca++ in the resin. The onset of action is usually 2-12 hours when given orally, and longer if given rectally.

722
Q

Outline the cut-offs for hyperkalaemia severity by mild-moderate-severe by values

A

Mild: 5.5 - 5.9 mmol/L
Moderate: 6.0 - 6.4 mmol/L
Severe > / = 6.5 mmol/L

723
Q

ECG features of hyperkalaemia?

A
  • Peaked, or ‘tall tented’ T-waves
  • Loss of p waves
  • Broad QRS complexes
  • Sinusoidal wave pattern
724
Q

2 benefits or uses of peritoneal dialysis as a form of renal replacement?

A
  • As a stop gap to haemodialysis
  • In often younger patients who do not want to have to visit hospital three times a week
725
Q

2 common complications with peritoneal dialysis?

A
  • Peritonitis
  • Sclerosing peritonitis
726
Q

What is the most common organism behind peritonitis in peritoneal dialysis?

A

Coagulase negative staphylococci e.g. Staph Epidermidis - MOST COMMON

Staph aureus is another cause

727
Q

Recommended antibiotic therapy for peritoneal dialysis peritonitis?

A

Vanc or Teico + Ceftazidime
OR
Vanc added to dialysis fluid + Cipro by mouth

(note sometimes aminoglycosides sometimes used instead of ceftazidime to cover gram negatives)

728
Q

List some common causes of polyuria ( > 1 in 10)

A
  • Diuretics, caffeine and alcohol
  • Diabetes
  • Lithium
  • HF
729
Q

How does alcohol cause polyuria?

A

ADH suppresion in the posterior pituitary gland

730
Q

What can precipitate lithium toxicity?

A
  • Dehydration
  • Renal failure
  • Drugs - diuretics (especially thiazides), ACEis / ARBs, NSAIDs and metronidazole
731
Q

Lithium is primarily excreted by?

A

The kidneys

732
Q

Features of lithium toxicity?

A
  • Coarse tremor (not fine tremor which can be seen in therapeutic levels)
  • Hyperreflexia
  • Acute confusion
  • Polyuria
  • Seizures
  • Coma
733
Q

Management of lithium toxicity?

A
  • Mild-moderate toxicity may respond to volume resuscitation with normal saline
  • Haemodialysis may be needed in severe toxicity
  • Sodium bicarbonate sometimes used - increases alkalinity of urine to promote lithium excretion - note limited evidence base
734
Q

Inheritance pattern of hereditary spherocytosis?

A

Autosomal dominant

735
Q

Features of hereditary spherocytosis?

A
  • Failure to thrive
  • Jaundice, gallstones
  • Splenomegaly
  • Aplastic crisis precipitated by parvovirus infection
  • Degree of haemolysis variable
  • MCHC elevated
736
Q

How is hereditary spherocytosis investigated?

A

No additional tests required if high clinical suspicion - with family history positive, typical clinical features, and lab investigations - spherocytes on blood film, raised MCHC, increase in reticulocytes

If diagnosis is equivocal:
- EMA binding test gold standard
- Cryohaemolysis test

For atpyical presentations:
- Electophoresis analysis of erythrocyte membranes

737
Q

Outline treatment of hereditary spherocytosis - in terms of management in acute haemolytic crisis and then in terms of longer term treatment?

A

Acute haemolytic crisis:
- Treatment is generally supportive - i.e. folic acid
- Transfusion if necessary (if symptomatic of anaemia)
Longer term treatment:
- Folate replacement
- Splenectomy

738
Q

Which genders get G6PD and which get hereditary spherocytosis?

A
  • G6PD - XLR so male
  • Hereditary spherocytosis - Male and female (as autosomal dominant no X-linked)
739
Q

Which ethnicities typically get G6PD and which typically get hereditary spherocytosis?

A

G6PD - African and mediterranean
Hereditary Spherocytosis - Northern European

740
Q

What typically triggers apalstic or acute haemolytic reactions in hereditary spherocytosis?

A

Parvovirus infection

741
Q

In dengue and chikungunya you can have rashes in both - which one spares the palms and feet and which one affects it?

A

Dengue spares palms and feet
Chikungunya affects palms and feet

742
Q

Give some examples of viral haemorrhagic fever?

A
  • Yellow fever
  • Lassa fever
  • Ebola
  • Dengue can progress to viral haemorrhagic fever
743
Q

Dengue virus is RNA or DNA virus?

A

RNA

744
Q

Dengue virus is transmitted by what carrier?

A

Aedes Aegypti mosquito

745
Q

Incubation period of Dengue?

A

7 days

746
Q

True or false, dengue is haemorrhagic?

A

Depends, severe dengue is. Dengue haemorrhagic fever in severe cases

747
Q

What happens in dengue haemorrhagic fever?

A

This is a form of disseminated intravascular coagulation (DIC) resulting in:
- Thrombocytopenia
- Spontaneous bleeding
- Around 20-30% of these patients go on to develop dengue shock syndrome (DSS)

748
Q

What investigations are done in suspected dengue?

A

Typically blood results:
- Leukopenia, thrombocytopenia, raised aminotransferases
Diagnostic tests:
- Serology
- Nucleic acid amplification tests for viral RNA
- NS1 antigen test

749
Q

What is the treatment for dengue?

A
  • Entirely symptomatic e.g. fluid resuscitation, blood transfusion etc
  • No antivirals are currently available
750
Q

Features of dengue fever?

A

fever
headache (often retro-orbital)
myalgia, bone pain and arthralgia (‘break-bone fever’)
pleuritic pain
facial flushing (dengue)
maculopapular rash
haemorrhagic manifestations e.g. positive tourniquet test, petechiae, purpura/ecchymosis, epistaxis
‘warning signs’ include:
abdominal pain
hepatomegaly
persistent vomiting
clinical fluid accumulation (ascites, pleural effusion)

751
Q

Korsakoff syndrome aetiology?

A

thiamine deficiency causes damage and haemorrhage to the mammillary bodies of the hypothalamus and the medial thalamus
in often follows on from untreated Wernicke’s encephalopathy

752
Q

Features of Korsakoff’s syndrome?

A
  • Anterograde amnesia: inability to acquire new memories
  • Retrograde amnesia
  • Confabulation
753
Q

What is the rate of progression of MGUS to myeloma at 10 years? and at 15 years?

A

10 years - 10%
15 years - 50%

754
Q

Clinical features of MGUS?

A
  • Usually asymptomatic
  • No bone pain or increased risk of infections
  • Around 10-30% have a demyelinating neuropathy
755
Q

List some differentiating features between MGUS and myeloma

A
  • Normal immune function in MGUS
  • Normal beta-2 microglobulin levels in MGUS
  • Lower level of paraprteinaemia than myeloma (e.g. < 30g/L IgG, or < 20g/L IgA)
  • Stable level of paraproteinaemia
  • No clinical features of myeloma (e.g. lytic lesions on x-rays or renal disease)
756
Q

3 common adverse effects in atypical antipsychotics?

A
  • Weight gain - especially olanzapine
  • Clozapine - agranulocytosis
  • Hyperprolactinaemia
757
Q

What are some specific risks with the use of antipsychotics in elderly patients?

A
  • Increased risk of stroke
  • Increased risk of VTE
758
Q

Which atypical antipsychoitc has a good side effect profile, particularly for prolactin elevation (i.e doesn’t raise it that much unlike others)?

A

Aripiprazole

759
Q

Which factors does prothrombin complex concentrate contain?

A

2, 7, 9, 10

760
Q

Which agent is used to rapidly reverse the anticoagulant effect of warfarin?

A

PCC

761
Q

What is contained in cryoprecipitate?

Therefore in which situations is it useful?

A

Fibrinogen
Factor 8

Therefore good when there is bleeding with low fibrinogen levels or in patients with haemophilia A

762
Q

What is contained in fresh frozen plasma, and therefore in which conditions is it useful?

A
  • Contains all coagulation factors
  • Corrects coagulopathy in patients with severe liver disease or DIC
763
Q

What is a benefit of the use of PCC over FFP in reversing warfarin effect?

A

More concentrated and doesn’t require as much volume infusion so lowers the risk of fluid overload

764
Q

What is the mode of inheritance of essential tremor?

A

Autosomal dominant

765
Q

Which limbs typically affected in essential tremor?

A

Both upper limbs

766
Q

Doing what makes essential tremor worse?

A
  • Postural tremor - worse if arms outstretched
767
Q

What improves essential tremor?

A

Alcohol and rest

768
Q

What is the most common cause of titubation (head tremor)?

A

Essential tremor

769
Q

What is the management for essential tremor?

A

Propranolol is first line
Primidone is sometimes used

770
Q

Inheritance pattern of Friedrich’s ataxia?

A

Autosomal recessive

771
Q

25M with persistent, asymptomatic hyperglycaemia noted incidentally, no features of insulin resistance or difference in weight, and no DKA in the past, diagnosis?

A

MODY

772
Q

Treatment for MODY?

A

MODY2 - does not require specific treatment - mild hyperglycaemia and does not usually lead to complications

MODY associated with HNF1A - responds to treatment with low-dose sulfonylureas
Insulin therapy may be needd if sulfonylureas are contraindicated or ineffective

773
Q

Inheritance pattern in MODY?

A

Autosomal dominant

774
Q

2 most common types of MODY and their genetic mutations?

A

MODY2 (GCK mutation) and MODY3 (HNF1A mutation)

MODY2 - typically mild, stable fasting hyperglycaemia and rarely develop severe complications

MODY3 and 1 - progressive hyperglycaemia and higher risk for complications typically associated with diabetes e.g. retinopathy, nephropathy and cardiovascular disease

775
Q

What is the triad of symptoms in Behcets disease?

A

Oral ulcers + genital ulcers + anterior uveitis = Behcet’s disease

776
Q

Behcet’s is associated with which HLA?

A

HLA B51

777
Q

List some features in Behcet’s

A
  • Classical triad:1) oral ulcers 2) genital ulcers 3) anterior uveitis
  • Thrombophlebitis and deep vein thrombosis
  • Arthritis
  • Neurological involvement (e.g. aseptic meningitis)
  • GI: abdo pain, diarrhoea, colitis
  • Erythema nodosum
778
Q

Investigations in Behcet’s

A
  • No definitive test
  • Diagnosis based on clinical findings
  • Positive pathergy test is suggestive (puncture site following needle prick becomes inflamed with small pustule forming)
779
Q

In which demographic is Behcet’ more common?

A
  • More common in the eastern Mediterranean (e.g. Turkey)
  • More common in men (complicated gender distribution which varies according to country - Overall, Behcet’s is considered to be more common and more severe in men)
    tends to affect young adults (e.g. 20 - 40 years old)
780
Q

When to start bone protection in pateints taking steroids?

A

If over 65 or previously had fragility fracture - immediate

If < 65 - do bone density scan then
- if > 0 - reassure
- if 0- -1.5 - repeat bone density scan in 1-3 years
- < -1.5 - offer bone protection

781
Q

What is the minimum steroid intake a patient should be taking before they are offered osteoporosis prophylaxis?

A

Equivalent of prednisolone 7.5mg or more each day for 3 months

782
Q

cANCA antibodies target is …. whereas pANCA target is ….

A

cANCA antibodies target is serum proteinase 3 whereas pANCA target is myeloperoxidase

783
Q

cANCA is associated with which condition(s)?

A

GPA (granulomatosis with polyangiitis) (90%)
Microscopic polyangiitis (in 40%)

783
Q

pANCA is positive in which conditions?

A

Mostly eGPA (50%) and Microscopic polyangiitis (75%)
Sometimes in GPA as well (25%)

Others:
- UC
- Anti-GBM
- Crohn’s

784
Q

Ankylosing spondylitis associated with which HLA?

A

HLA-B27

785
Q

Ankylosing spondylitis typically male or female and what age range?

A

Male:Female (3:1) - age 20-30 yrs old

786
Q

What is the key investigation in investigation of ankylosing spondylitis?

A

Plain x-ray of the sacro-iliac joints

  • Sacroiliitis: subchondral erosions, sclerosis
  • Squaring of the lumbar vertebrae
  • ‘Bamboo spine’
  • Syndesmophytes: due to ossification of outer fibres of anullus fibrosus

N.B - CXR - apical fibrosis

787
Q

List some plain x-ray findings in ankylosing spondylitis?

A
  • Sacroiliitis: subchondral erosions, sclerosis
  • Squaring of the lumbar vertebrae
  • ‘Bamboo spine’
  • Syndesmophytes: due to ossification of outer fibres of anullus fibrosus

N.B - CXR - apical fibrosis

788
Q

Outline management of ankylosing spondylitis

A
  • Regular exercise
  • NSAIDs first line
  • Physio
  • DMARDs if peripheral joint involvement
  • Anti-TNF e.g. infliximab if high disease activity despite conventional treatment
789
Q

What is the mechanism of action of Apremilast?

A

Phosphodiesterae type-4 inhibitor

790
Q

What are the different patterns of psoriatic arthropathy, and which is the most common?

A
  • Symmetric polyarthritis - MOST common
  • Asymmetrical oligoarthritis (typically affects hands and feet) - second most common
  • Sacroiliitis
  • DIP joint disease
  • Arthritis mutilans (severe deformity fingers / hand, ‘telescoping fingers’)
791
Q

Features of psotiatic arthropathy?

A
  • Symmetric polyarthritis - MOST common
  • Asymmetrical oligoarthritis (typically affects hands and feet) - second most common
  • Sacroiliitis
  • DIP joint disease
  • Arthritis mutilans (severe deformity fingers / hand, ‘telescoping fingers’)

Other features:
- Psoriatic skin lesions
- Periarticular disease - tenosynovitis and soft tissue inflammation resulting in….enthesitis e.g. achilles tendonitis, plantar fasciitis
- Tenosynovitis - typically of the flexor tendons of the hands
- Dactylitis
- Nail changes - pitting, oncholysis

792
Q

X-ray features in psoriatic arthropathy?

A

often have the unusual combination of coexistence of erosive changes and new bone formation
periostitis
‘pencil-in-cup’ appearance

793
Q

Outline management of psoriatic arthropathy

A
  • Managed by rheumatologist
  • Mild peripheral arthritis / mild axial disease - treat with just NSAID
  • If more moderate / severe - methotrexate
  • Mabs e.g. ustekinumab (targets IL-12 and IL-23) and secukinumab (targets IL-17)
  • Apremilast (PDE4 inhibitor) - suppression of pro-inflammatory mediator synthesis and promotion of anti-inflammatory mediators
794
Q

Which has better prognosis - psoriatic arthropathy or RA?

A

RA

795
Q

List some poor prognostic features in rheumatoid arthritis

A
  • Rheumatoid factor positive
  • Anti-CCP antibodies
  • Poor functional status at presentation
  • X-ray: early erosions (e.g. after < 2 years)
  • Extra articular features e.g. nodules
  • HLA DR4
  • Insidious onset
796
Q

Reactive arthritis is associated with which HLA?

A

HLA-B27

797
Q

Which organism can be recovered frmo the joint in reactive arthritis?

A

Organisms cannot be recovered from the joint in reactive arthritis

798
Q

What is the most common organism behind the post-STI form of reactive arthritis?

A

Chlamydia Trachomatis

799
Q

Which organisms associated with the post-dysenteric form of reactive arthritis?

A

Shigella flexneri
Salmonella typhimurium
Salmonella enteritidis
Yersinia enterocolitica
Campylobacter

800
Q

Outline the management of reactive arthritis

A
  • Symptomatic: analgesia, NSAIDS, intra-articular steroids
  • Sulfasalazine and methotrexate are sometimes used for persistent disease
  • Symptoms rarely last more than 12 months
801
Q

Patient started on oral alendronate - cannot tolerate due to oesophagitis - what is the next step for management of osteporosis in these patients?

A

Switch to risedronate or etidronate in patients unable to tolerate alendronate

802
Q

What is the mechanism of action of MMF?

A

Inosine 5 monophosphate dehydrogenase inhibitor
Thereby inhibits purine synthesis

as T and B cells are particularly dependent on this pathway it can reduce the proliferation of immune cells

803
Q

What is the management of reactive arthritis?

A
  • Symptomatic: analgesia, NSAIDS, intra-articular steroids
  • Sulfasalazine and methotrexate are sometimes used for persistent disease
  • Symptoms rarely last more than 12 months
804
Q

In which age groups does tempral arteritis occur?

A

> 50 yrs old and peak incidence in 70yrs

805
Q

What will be the results of CK and EMG in temporal arteritis?

A

Normal

806
Q

Investigations in suspected temporal arteritis?

A
  • Raised inflammatory markers
    ESR > 50 mm/hr (note ESR < 30 in 10% of patients)
    CRP may also be elevated
  • Temporal artery biopsy
    skip lesions may be present
  • Note creatine kinase and EMG normal
807
Q

What is the management of temporal arteritis

A

Urgent high dose glucocorticoids as soon as diagnosis suspected and before biopsy
- If no visual loss then high dose pred
- If evolving visual loss IV methylpred prior to high-dose prednisolone
- N.B there should be a dramatic response otherwise reconsider the diagnosis

Urgent opthalmology review

Bone protection with bisphosphonates

Low dose aspirin

808
Q

Mechanism of methotrexate and is it reversible or irreversible

A

Reversible inhibition of dihydrofolate reductase

809
Q

List some adverse effects of methotrexate

A
  • Mucositis
  • Myelosuppression
  • Pneumonitis
  • Pulmonary fibrosis
  • Liver fibrosis
810
Q

How long after completion of methotrexate should men use contraception and women avoid pregnancy?

A

6 months for both

811
Q

What to co-prescribe with methotrexate and when?

A

Folic acid 5mg once weekly taken > 24 hrs after methotrexate dose

812
Q

What bloods to monitor before starting methotrexate and how often to repeat and then monitor thereafter?

A

FBC, U+Es, LFTs before starting treatment - then weekly until therapy stabilised - then monitor every 2-3 months

813
Q

What is the treatment of methotrexate toxicity?

A

Folinic acid

814
Q

How can Behcet’s present neurologically?

A

Aspetic meningitis

815
Q

Key adverse effects in bisphosphonate therapy

A
  • Oesophagitis
  • Oesophageal ulcers
  • Osteonecrosis of the jaw (higher risk in patients receiving IV bisphosphonates in treatment of cancer than in oral for osteoporosis or Paget’s), poor dental hygiene / prior dental procedures are a risk factor, do dental check up in these patients before starting treatment
  • Increased risk of atypical stress fractures of proximal femoral shaft
  • Acute phase response - fever, myalgia, and arthalgia
  • Hypocalcaemia - due to reduced calcium efflex from bone. Usually clinically unimportant
816
Q

Predisposing factors for Paget’s disease of the bone?

A
  • Increasing age
  • Male sex
  • Northern latitude
  • Family history
817
Q

Bloods features in Paget’s disease?

A
  • Isolated raised ALP
  • Calcium and phosphate normal typically. Hypercalcaemia can occur occasionally with prolonged immobilisation
    Other markers of bone turnover include
  • Procollagen type I N-terminal propeptide (PINP)
  • Serum C-telopeptide (CTx)
  • Urinary N-telopeptide (NTx)
  • Urinary hydroxyproline
818
Q

X-ray features in Paget’s disease of the bone?

A
  • Osteolysis in early disease - mixed lytic / sclerotic lesions
  • Skull x-ray - thickened vault, osteoporosis circumscripta
819
Q

Feature in bone scintigraphy in Paget’s disease of the bone?

A

Increased uptake is seen focally at the sites of active bone lesions

820
Q

Indications for treatment in Paget’s disease of the bone?

A
  • Bone pain
  • Skull or long bone deformity
  • Fracture
  • Periarticular Paget’s
821
Q

Management for Paget’s disease of the bone?

A

Bisphosphonate (either oral risedronate or IV zoledronate)

822
Q

Key complications of Paget’s disease of the bone?

A
  • Deafness (cranial nerve entrapment)
  • Bone sarcoma
  • Fractures
  • Skull thickening
  • High output cardiac failure
823
Q

What is the inheritance pattern of Marfan’s syndrome?

A

Autosomal dominant

824
Q

Marfan’s syndrome is caused by defect on which gene and on which chromosome/

A

Defect in the FBN1 gene on chromosome 15 that codes for the protein fibrillin 1

825
Q

List some features of Marfan’s syndrome?

A

tall stature with arm span to height ratio > 1.05
high-arched palate
arachnodactyly
pectus excavatum
pes planus
scoliosis of > 20 degrees
heart:
dilation of the aortic sinuses (seen in 90%) which may lead to aortic aneurysm, aortic dissection, aortic regurgitation
mitral valve prolapse (75%),
lungs: repeated pneumothoraces
eyes:
upwards lens dislocation (superotemporal ectopia lentis)
blue sclera
myopia
dural ectasia (ballooning of the dural sac at the lumbosacral level)

826
Q

What is the main cardiac complication of Marfan’s syndrome? Second most common?

A

Dilation of the aortic sinuses (90%) - which may lead to aortic aneurysm, aortic dissection, aortic regurgitation
Mitral valve prolapse (75%)

827
Q

Eye features of Marfan’s?

A
  • Upwards lens dislocation (superotemporal ectopia lentis)
  • Blue sclera
  • Myopia
828
Q

TNF inhibitors improve all of the following except which of the following:
- QOL
- Radiological progression
- Spinal mobility
- Extra-articular features
- Early morning stiffness

A

Improves all except radiological progression

829
Q

List causes of osteomalacia

A
  • Vit D deficiency
  • CKD
  • Drug induced - e.g. anticonvulsants
  • Inherited: hypophosphatemic rickets
  • Liver disease e.g. cirrhosis
  • Coeliac’s disease
830
Q

Features of osteomalacia?

A
  • Bone pain
  • Bone/muscle tenderness
  • Fractures: especially femoral neck
  • Proximal myopathy - may lead to a waddling gait
831
Q

Investigations in osteomalacia?

A
  • Low vit D
  • Low calcium, phosphate
  • Raised ALP

X-ray - transluscent bands (Looser’s zones or pseudofractures)

832
Q

Treatment of osteomalacia?

A
  • Vitamin D supplementation - loading dose often needed initially
  • Calcium supplementation if dietary calcium is inadequate
833
Q

How to manage uncomplicated GCA (with no visual involvement and / or tongue claudication)?
How to manage complicated GCA (with visual involvement and / or tongue claudication)

A

Uncomplicated GCA: oral prednisolone 40-60mg daily until symptoms and investigations normalise

Complicated GCA - IV methylprednisolone 500-1000mg for 3 days before starting oral prednisolone

Bisphosphonate and vit D and omeprazole
Consider aspirin

834
Q

What is the inheritance pattern of osteogenesis imperfecta?

A

Autosomal dominant

835
Q

Osteogenesis imperfecta occurs due to an abnormality in which type of collagen?

A

Type 1 collagen

836
Q

Features of osteogenesis imperfecta?

A
  • Presents in childhood
  • Fractures following minor trauma
  • Blue sclera
  • Deafness secondary to otosclerosis
  • Dental imperfections are common
837
Q

What will the bloods be like in osteogenesis imperfecta?

A
  • Adjusted calcium, phosphate, parathyroid hormone and ALP results are usually normal
838
Q

What is a key adverse effect associated with the use of TNF-alpha inhibitors?

A

Reactivation of TB
(Because plays key role in granuloma formation and containment of mycobacterium tb - therefore screening for latent TB is often recommended before starting treatment)

839
Q

Outline the management of rheumatoid arthritis?

A
  • Initially: DMARD monotherapy + / - short course bridging prednisolone
  • Methotrexate, sulfasalazine, leflunomide, hydroxychloroquine (latter should only be considered for initial therapy if mild or palindromic disease)
  • Flares: corticosteroids - oral or IM
  • TNF inhibitor if inadequate response to 2 DMARDs including methotrexate e.g. etanercept, infliximab, adalimumab
  • Rituximab - anti-CD20 antibody - results in B-cell depletion - two 1g infusions given two weeks apart - infusion reactions are common
  • Abatecept
840
Q

What is a common complication with use of Rituximab?

A

Infusion reactions

841
Q

What is the mechanism of aciton of Rituximab?

A
  • Anti-CD20 monoclonal antibody
842
Q

What is the mechanism of action of abatacept?

A

Fusion protein that that modulates a key signal required for activation of T lymphocytes - leads to decreased T-cell proliferation and cytokine production

843
Q

What are two early x-ray changes in rheumatoid arthritis?

A
  • Loss of joint space
  • Juxta-articular osteopaenia
844
Q

Two later x-ray findings in rheumatoid arthritis?

A
  • Articular erosions
  • Subluxation
845
Q

List some x-ray findings in rheumatoid arthritis

A
  • Loss of joint space
  • Juxta-articular osteoporosis
  • Soft tissue swelling
  • Periarticular swelling
  • Subluxation
846
Q

Polyartertitis nodosa is associated with which infection?

A

Hepatitis B infection

847
Q

Polyarteritis nodosa is a vasculitis affecting what size arteries?

A

Medium-sized

848
Q

What is the pathophysiology in polyarteritis nodosa?

A

Vasculitis affecting medium-sized arteries with necrotising inflammation leading to aneurysm formation

849
Q

Polyarteritis nodosa is more common in which age group and in men or women?

A

Middle-aged men

850
Q

List some features of Polyarteritis Nodosa

A
  • Fever, malaise, arthralgia
  • Weight loss
  • HTN
  • Mononeuritis multiplex, sensorimotor polyneuropathy
  • Testicular pain
  • Livedo reticularis
  • Haematuria, renal failure
  • P-ANCA in 20% of cases with ‘classic’ PAN
  • Hep B serology positive in 30% of patients
851
Q

Anti-Ro antibodies associated with? Give 3 conditions

A

Sjogren’s syndrome, SLE, congenital heart block

852
Q

Anti-La antibodies associated with which condition?

A

Sjogren’s syndrome

853
Q

Anti-Jo1 antibodies associated with which condition?

A

Polymyositis

854
Q

Anti-scl-70 associated with which condition?

A

Diffuse cutaneous systemic sclerosis

855
Q

Anti-centromere antibodies associated with which condition?

A

Limited cutaneous systemic sclerosis

856
Q

What is the first line management of gout?

A

NSAIDs or colchicine are first line - max dose of NSAID should be prescribed until 1-2 days after symptoms settled

Colchicine

If the above contraindicated, consider oral steroids - dose of prednisolone 15mg/day usually used

Intra-articular steroid injection

857
Q

When to offer prophylaxis in gout (allopurinol - urate lowering therapy)?

A

After the first attack of gout

858
Q

What is the first line prophylactic agent in gout?

What other agent is second line if this is not tolerated or ineffective?

For bonus points - other options third and fourth line?

A
  1. Allopurinol
  2. Febuxostat

3/4: Uricase, pegloticase

859
Q

Which diuretic can precipitate gout attacks?

A

Thiazides

860
Q

Targets for uric acid levels and what effects this?

A

Initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 360 µmol/l CKS
a lower target uric acid level below 300 µmol/L may be considered for patients who have tophi, chronic gouty arthritis or continue to have ongoing frequent flares despite having a uric acid below 360 µmol/L

861
Q

Pseudogout is a form of microcrystal synovitis caused by the deposition of …… ….. ….. crystals in the synovium

A

Pseudogout is a form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium

862
Q

Risk factors for pseudogout in younger patients?

A
  • Haemochromatosis
  • Hyperparathyroidism
  • Low magnesium, Low phosphate
  • Acromegaly, Wilson’s disease
863
Q

What can be found on joint aspiration in pseudogout?

A

Weakly positively birefringent rhomboid shaped crystals

864
Q

Classic X-ray feature in pseudogout?

A

Chondrocalcinosis

865
Q

What is the management for pseudogout?

A
  • Aspiration of joint fluid, to exclude septic arthritis
  • NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
866
Q

There are many risk factors for developing pseudogout in younger patients, but otherwise what is the main risk factor?

A

Increasing age

867
Q

What is the long term drug treatment for SLE?

A

Hydroxychloroquine

If there is internal organ involvement e.g. renal, neuro, eye then consider prednisolone, cyclophosphamide

868
Q

Outline management of SLE

A

Basics - NSAIDs, sun block
Long-term - Hydoxychlroqione

If there is internal organ involvement e.g. renal, neuro, eye then consider prednisolone, cyclophosphamide

869
Q

What is the most common organism behind septic arthritis overall?

And in young, sexually active adults?

Most common cause?

A

Staph Aureus

Young, sexually active adults - Neisseria gonorrhoea

870
Q

Most common cause of septic arthritis in adults is due to …. spread from distal bacterial infections e.g. abscesses

A

Most common cause of septic arthritis in adults is due to haematogenous spread from distal bacterial infections e.g. abscesses

871
Q

Why is it important to take blood cultures in septic arthritis?

A

Because the most common cause is due to haematogenous spread from distal bacterial infections

872
Q

What investigations are done in septic arthritis?

A
  • Synovial fluid sampling
  • Blood cultures
  • Joint imaging
873
Q

Outline management of septic arthritis

A

Antibiotic treatment - IV fluclox or clinda if pen allergic usually given for several weeks (4-6 weeks) - often switched to oral after 2 weeks

Needle aspiration to decompress the joint

Arthroscopic lavage may be required

874
Q

What is the pattern of muscle weakness in dermatomyositis?

A

Symmetrical, proximal

875
Q

Dermatomyositis may be associated with …. …. …. or underlying ….

A

Dermatomyositis may be associated with connective tissue disorders or underlying malignancies

876
Q

List some skin features in dermatomyositis

A
  • Photosensitivity
  • Macular rash over back and shoulders
  • Heliotrope rash in the periorbital region
  • Gottron’s papules - rougheneed red papules over extensor surfaces of fingers
  • Mechanics hands
  • Nail fold capillary dilatation
877
Q

What are some resp manifestations of dermatomyositis that are possible?

A
  • Resp muscle weakness
  • Interstitial lung disease e.g. fibrosing alveolitis or organising pneumonia
878
Q

Which antibodies are present in Dermatomyositis?

A

80% are ANA positive
30% have antibodies to aminoacyl tRNA synthetases (anti-synthetase antibodies), including:
- Antibodies against histidine-tRNA ligase (aka Jo-1)
- Antibodies to signal recognition particle (SRP)
- Anti-Mi-2 antibodies

879
Q

True or false - atlanto-axial instability is seen in ankylosing spondylitis?

A

False - it’s in rheumatoid arthritis

880
Q

Adhesive capsulitis - what is the main association?

A

Diabetes mellitus

881
Q

What are the different phases in adhesive capsulitis?

A

Painful freezing phase, adhesive phase and recovery phase

882
Q

Which movements affected in adhesive capsulitis?

A

External rotation > internal rotation or abduction

Both passive and active movement is affected

882
Q

Outline the management of adhesive capsulitis

A
  • NSAIDs
  • Physio
  • Oral corticosteroids
  • Intra-articular corticosteroids
883
Q

Define mononeuritis multiplex

A

Peripheral neuropathy affecting 2+ non-contiguous nerve trunks

884
Q

Which antibodies most specific for dermatomyositis?
Which most common for it?

A

Most specific = Anti-Mi-2
Most common = ANA

885
Q

Outline the management of De Quervain’s tenosynovitis

A
  • Analgaesia
  • Steroid injection
  • Immobilisation with a thumb splint (spica)
  • Surgical treatment sometimes required
886
Q

What clinical test in De Quervain’s tenosynovitis?

A

Finkelstein’s test - the examiner pulls the thumb of the patient in ulnar deviation and longitudinal traction. In a patient with tenosynovitis this action causes pain over the radial styloid process and along the length of extensor pollisis brevis and abductor pollicis longus

887
Q
A

MRCP Part 1 (1 decks)

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