Passmed

Question 1

What is the first line management for primary axillary hyperhidrosis?

Answer 1

Topical aluminium hydrochloride

Question 2

Outline the management options for hyperhidrosis?

Answer 2

• 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

Question 3

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

Answer 3

Serum ferritin

Question 4

Causes and associations of restless leg syndrome?

Answer 4

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

Question 5

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

Answer 5

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

Question 6

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?

Answer 6

HOCM

Question 7

List some medications to be avoided in HOCM

Answer 7

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

Basically things that reduce preload / afterload

Question 8

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

Answer 8

Eosinophilic oesophagitis

Question 9

Outline management of eosinophilic oesophagitis?

Answer 9

• 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

Question 10

Outline a few complications of eosinophilic oesophagitis?

Answer 10

• Oesophageal strictures
• Impaction
• Mallory Weiss tears

Question 11

At what point do you consider fibrinolysis in STEMI?

Answer 11

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

Question 12

What are the ECG criteria for STEMI?

Answer 12

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

Question 13

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?

Answer 13

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

Question 14

Which other drugs are given during PCI?

Answer 14

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

Question 15

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

Answer 15

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

Question 16

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?

Answer 16

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

Question 17

What is the primary interleukin causing HOTN in sepsis?

Answer 17

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

Question 18

List some causes of respiratory alkalosis

Answer 18

• 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

Question 19

How to treat isolated systolic HTN?

Answer 19

Same treatment formula as standard HTN

Question 20

Most common cause of traveller’s diarrhoea?

Answer 20

E.Coli

Question 21

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

Answer 21

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

Question 22

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

Answer 22

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

Question 23

Which antibody can be tested for primary membranous glomerulonephropathy?

Answer 23

Anti-PLA2R antibodies

Question 24

What are the causes of membranous nephropathy?

Answer 24

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

Question 25

What is the triad with which TTP presents?

Answer 25

Fever Neuro signs Thrombocytopaenia Haemolytic anaemia Renal failure

Question 26

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

Answer 26

ADAMTS13 assay

Question 27

When is skin patch test vs skin prick test done?

Answer 27

* 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

Question 28

.

Answer 28

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

Question 29

What goes wrong in chronic granulomatous deficiency?

Answer 29

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

Question 30

Inheritance pattern of Wiskott-Aldrich syndrome?

Answer 30

XLR

Question 31

How does Wiskott-Aldrich syndrome present?

Answer 31

* Eczema * Thrombocytopaenia * Immune deficiency including both T and B lymphocytes

Question 32

Which anti-epileptic drug is contraindicated in absence seizures?

Answer 32

Carbamazepine

Question 33

What is a Leukaemoid reaction? Plus list some causes

Answer 33

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

Question 34

Key differentiator between leukaemoid reaction and CML?

Answer 34

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

Question 35

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

Answer 35

* More common - affects the vasopressin (ADH) receptor * Less common - affects gene encoding the AQP2 channel

Question 36

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

Answer 36

Rapidly progressive glomerulonephritis

Question 37

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

Answer 37

C5-9 deficiency

Question 38

Which complement deificiency can cause hereditary angioedema?

Answer 38

C1 inhibitor protein deficiency (C1-INH)

Question 39

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

Answer 39

Hereditary angioedema

Question 40

Give some key features of leukaemoid reaction?

Answer 40

* 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

Question 41

How does retroperitoneal fibrosis present?

Answer 41

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

Question 42

List some associations to retroperitoneal fibrosis

Answer 42

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

Question 43

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

Answer 43

Autosomal dominant mutation in FGFR-3 gene

Question 44

How do mutations causing achondroplasia usually arise?

Answer 44

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

Question 45

What is the most important association with HLA-A3?

Answer 45

Haemochromatosis

Question 46

What is the most important association with HLA-B51?

Answer 46

Behcet's disease

Question 47

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

Answer 47

Ankylosing Spondylitis Reactive arthritis Acute anterior uveitis Psoriatic arthritis

Question 48

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

Answer 48

Coeliac disease

Question 49

What are the most important associations with HLA-DR2?

Answer 49

Narcolepsy Goodpasture's

Question 50

List some of the most important associations with HLA-DR3

Answer 50

Dermatitis Herpetiformis Sjogren's syndrome PBC

Question 51

List 2 key associations with HLA-DR4

Answer 51

T1DM Rheumatoid arthritis

Question 52

How does anthrax present?

Answer 52

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

Question 53

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

Answer 53

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

Question 54

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

Answer 54

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

Question 55

True or false - memantine is indicated in mild dementia

Answer 55

False

Question 56

Which clotting factors are dependent on vitamin K?

Answer 56

Clotting factors II, VII, IX and X

Question 57

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

Answer 57

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

Question 58

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

Answer 58

Kallman's - cryptorchidism Klinefelter's - microorchidism

Question 59

Which type of allergy test is useful for irritants?

Answer 59

Skin patch testing

Question 60

Thiazides can cause which electrolyte abnormality?

Answer 60

Hypercalcaemia

Question 61

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?

Answer 61

Enhanced liver fibrosis test to aid diagnosis of liver fibrosis

Question 62

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

Answer 62

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

Question 63

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

Answer 63

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

Question 64

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?

Answer 64

Cubital tunnel syndrome

Question 65

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

Answer 65

Small bowel biopsy

Question 66

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

Answer 66

Microscopic colitis

Question 67

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

Answer 67

Glycopeptide antibiotics - teicoplanin and vancomycin

Question 68

Give some drug classes that inhibit bacterial protein synthesis

Answer 68

1. Macrolides 2. Aminoglycosides 3. Tetracyclines

Question 69

What class of antibiotics inhibit DNA synthesis?

Answer 69

Quinolones e.g. ciprofloxacin

Question 70

Give an example antibiotic that inhibits bacterial RNA synthesis

Answer 70

Rifampicin

Question 71

Name some antibiotics that inhibit bacterial folic acid formation

Answer 71

Trimethoprim Co-trimoxazole Sulphonamides

Question 72

Give an antibiotic name that damages DNA

Answer 72

Metronidazole

Question 73

Which chemotherapeutic agent can cause cardiomyopathy?

Answer 73

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

Question 74

Main side effect of Bleomycin?

Answer 74

Pulmonary fibrosis

Question 74

Main side effects of Paclitaxel and Docetaxel?

Answer 74

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

Question 75

Main side effects of Dactinomycin?

Answer 75

Myelosuppression GI toxicity

Question 76

Why can diagnosis of malaria be difficult in pregnant women?

Answer 76

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

Question 77

Which anti-malarial is contra-indicate in epilepsy?

Answer 77

Mefloquine

Question 78

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

Answer 78

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

Question 79

Which anti-malarials can be used in pregnant women?

Answer 79

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

Question 80

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

Answer 80

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

Question 81

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

Answer 81

Crescentic glomerulonephritis

Question 82

How does quinine toxicity present?

Answer 82

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

Question 83

Tinnitus is typical of overdose to which two substances?

Answer 83

1. Aspirin 2. Quinine

Question 84

Lamotrigine can cause which dermatological emergency?

Answer 84

Stevens-Johnson syndrome

Question 85

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

Answer 85

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

Question 86

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

Answer 86

Add on insulin

Question 87

Is it common for discoid lupus to progress to SLE?

Answer 87

No - only in 5-10% of cases

Question 88

How is discoid lupus managed?

Answer 88

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

Question 89

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?

Answer 89

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

Question 90

What is the most common side effect of ciclosporin?

Answer 90

Nephrotoxicity

Question 91

How is neurogenic bladder managed in MS patients?

Answer 91

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

Question 92

What is the gold standard investigation of GORD?

Answer 92

24hr oesophageal pH monitoring

Question 93

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

Answer 93

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

Question 94

What is the best marker of severity in acute pancreatitis?

Answer 94

CRP

Question 95

What investigation is diagnostic for SBOSS?

Answer 95

Hydrogen breath test

Question 96

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

Answer 96

1st line - paracetamol 1g 2nd line - NSAIDs in first and second trimester Avoid aspirin and opioids in pregnancy

Question 97

How does SIGN recommend migraines are managed in menstruation?

Answer 97

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

Question 98

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

Answer 98

360 degrees selective laser trabeculoplasty

Question 99

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?

Answer 99

First line - Latanoprost

Question 100

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

Answer 100

TRALI - HOTN TACO - HTN

Question 101

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

Answer 101

Fever, chills Rx = Slow or stop the transfusion, paracetamol, monitor

Question 102

How to manage minor allergic reaction to blood transfusion

Answer 102

Rx = temporarily stop the transfusion, antihistamine, monitor

Question 103

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

Answer 103

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

Question 104

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

Answer 104

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

Question 105

How does TRALI present and how to manage?

Answer 105

Hypoxia, pulmonary infiltrates on CXR, fever, HOTN Rx = stop the transfusion, oxygen and supportive care

Question 106

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

Answer 106

Anti-SSA / Ro antibodies Complications: congenital heart block, skin rashes and hepatosplenomegaly

Question 107

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?

Answer 107

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

Question 108

How is oscillopsia in multiple sclerosis managed first line?

Answer 108

Gabapentin

Question 109

How is fatigue in multiple sclerosis managed?

Answer 109

Trial of amantadine Other options: mindfulness training and CBT

Question 110

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

Answer 110

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'

Question 111

Summarise the duration of anticoagulant therapy in PE

Answer 111

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

Question 112

What are the management options for motion sickness?

Answer 112

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

Question 113

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

Answer 113

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

Question 114

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

Answer 114

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

Question 115

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

Answer 115

Methotrexate, Methyldopa, Amiodarone

Question 116

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

Answer 116

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

Question 117

Which clotting factors are affected by warfarin?

Answer 117

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

Question 118

What is the gold standard test for PNH?

Answer 118

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

Question 119

Outline management for PNH

Answer 119

Blood product replacement Anticoagulation Eculizumab is undergoing research SCT

Question 120

What is the half life of amiodarone?

Answer 120

Approx 20-100 days

Question 121

Outline the steps in medical management of angina pectoris

Answer 121

1.

Question 122

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

Answer 122

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

Question 123

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

Answer 123

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

Question 124

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

Answer 124

1) Oral fidaxomicin 2) Oral vancomycin OR fidaxomycin

Question 125

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

Answer 125

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

Question 126

What cardiac abnormalities are associated with carcinoid syndrome?

Answer 126

Carcinoid TIPS Tricuspid insufficiency and pulmonary stenosis Affects the right side of the heart

Question 127

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

Answer 127

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

Question 128

What is the most useful marker to screen for haemochromatosis?

Answer 128

Transferrin saturation

Question 129

What are the management options for haemochromatosis?

Answer 129

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

Question 130

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

Answer 130

1. Ascites 2. Abdominal pain 3. Hepatomegaly

Question 131

What is the initial investigation in Budd-Chiari syndrome?

Answer 131

Ultrasound with doppler flow studies

Question 132

List some causes of Budd-Chiari syndrome

Answer 132

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

Question 133

What type of cells do gastrinomas originate from?

Answer 133

G cells

Question 134

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

Answer 134

Faecal elastase

Question 135

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

Answer 135

Co-danthramer

Question 136

What is the management for life threatening c.diff?

Answer 136

Oral vancomycin and IV metronidazole

Question 137

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

Answer 137

Urea breath test

Question 138

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

Answer 138

Propanolol

Question 139

How does propanolol help prevent oesophageal bleeding?

Answer 139

Reduces cardiac output and sphlanchnic blood flow

Question 139

How is terlipressin good in controlling variceal bleeding?

Answer 139

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

Question 140

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

Answer 140

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

Question 141

What is the management of autoimmune hepatitis?

Answer 141

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

Question 142

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

Answer 142

Inflammation extending beyond limiting plate 'piecemeal necrosis', bridging necrosis

Question 143

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

Answer 143

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

Question 144

What is the management of Whipple's disease?

Answer 144

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

Question 145

Whipple's disease is caused by which organism infection?

Answer 145

Tropheryma Whippeli

Question 146

Features of Whipple's disease?

Answer 146

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

Question 147

What is the management of small bowel overgrowth syndrome?

Answer 147

Rifaximin is first line, correct underlying disorder

Question 148

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

Answer 148

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

Question 149

What is the management of Gilbert's syndrome?

Answer 149

Nothing really - education and avoidance of triggers only

Question 150

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

Answer 150

Rise in bilirubin following prolonged fasting or IV nicotinic acid

Question 151

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

Answer 151

Splenic flexure - watershed area Hepatic flexure also well supplied by SMA so less likely affected

Question 152

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

Answer 152

Duodenal tumours

Question 153

FAP is what inheritance pattern and which gene on which chromosome

Answer 153

Autosomal dominant APC gene on chromosome 5

Question 154

What is the key management in FAP?

Answer 154

Proctocolectomy with ileal pouch anal anastamosis

Question 155

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

Answer 155

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

Question 156

First line investigation in ascending cholangitis?

Answer 156

Ultrasound

Question 157

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

Answer 157

Maddrey's discriminant function Score > 32 usually

Question 158

List some causes of hepatosplenomegaly?

Answer 158

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

Question 159

What is first line management for chronic anal fissure?

Answer 159

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

Question 160

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

Answer 160

Malabsorption of bile salts Managed with oral colestyramine

Question 161

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?

Answer 161

Oral colestyramine

Question 162

Features of Whipple's disease?

Answer 162

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

Question 163

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?

Answer 163

Signet ring cells

Question 164

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?

Answer 164

Laxative abuse - especially anthroquine compounds such as senna

Question 165

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

Answer 165

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

Question 166

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?

Answer 166

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

Question 167

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?

Answer 167

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

Question 168

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

Answer 168

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

Question 169

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

Answer 169

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

Question 170

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

Answer 170

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

Question 171

What is the inheritance pattern of Peutz-Jegher syndrome?

Answer 171

Autosomal dominant

Question 172

What score is used to assess malnutrition?

Answer 172

MUST score

Question 173

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

Answer 173

Ferritin and transferrin saturation

Question 174

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

Answer 174

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

Question 175

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

Answer 175

Hydrogen breath testing

Question 176

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?

Answer 176

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

Question 177

What is the inheritance pattern of Dubin Johnson syndrome?

Answer 177

Autosomal recessive

Question 178

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

Answer 178

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.

Question 179

What is the prognosis of Dubin Johnson syndrome?

Answer 179

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

Question 180

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?

Answer 180

Angiodysplasia - angiodysplasia is associated with aortic stenosis

Question 181

What heart thing is angiodysplasia associated with?

Answer 181

Aortic stenosis

Question 182

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

Answer 182

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

Question 183

What does the MELD score test?

Answer 183

MELD score assesses the severity of end-stage liver disease

Question 184

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

Answer 184

Secretin stimulation test

Question 185

What are the 2 types of hepatorenal syndrome?

Answer 185

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

Question 186

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

Answer 186

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

Question 187

What are the management options in hepatorenal syndrome?

Answer 187

Terlipressin Volume expansion with 20% HAS TIPSS Liver transplantation

Question 188

True or false, lactulose is contraindicated in IBS?

Answer 188

True - lactulose can exacerbate IBS

Question 189

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

Answer 189

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

Question 190

What is the management of autoimmune hepatitis?

Answer 190

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

Question 191

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

Answer 191

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

Question 192

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

Answer 192

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

Question 193

What is the management of gastric MALT lymphoma?

Answer 193

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

Question 194

What is the management of Barret's oesophagus?

Answer 194

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

Question 195

List some causes of villous atrophy on jejunal biopsy

Answer 195

Coeliac's disease Tropical sprue Hypogammaglobulinaemia Whipple's disease

Question 196

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

Answer 196

True - granulomas more suggestive of Crohn's than UC

Question 197

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

Answer 197

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

Question 198

Skip lesions in UC or Crohn's?

Answer 198

Crohn's

Question 199

Goblet cell depletion in UC or Crohn's?

Answer 199

UC

Question 200

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

Answer 200

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

Question 201

Hyperchylomicronaemia or hypercholesterolaemia associated with acute pancreatitis?

Answer 201

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

Question 202

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

Answer 202

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

Question 203

List the causes of LBBB

Answer 203

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

Question 204

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

Answer 204

1 week

Question 205

Outline the KCH criteria for liver transplant in paracetamol overdose

Answer 205

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

Question 206

What is the gold standard investigation for potential CLL?

Answer 206

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

Question 207

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

Answer 207

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

Question 208

What are the features of visceral leishmaniasis?

Answer 208

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

Question 209

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

Answer 209

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

Question 210

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

Answer 210

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

Question 211

Management of transfusion associated graft vs host disease?

Answer 211

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

Question 212

Which chronic electrolyte disturbance can cause cataracts?

Answer 212

Chronic hypocalcaemia

Question 213

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

Answer 213

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

Question 215

List some causes of respiratory acidosis

Answer 215

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

Question 216

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

Answer 216

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

Question 217

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?

Answer 217

Do a chest drain

Question 218

What is the management considered in patients with recurrent pneumothoraces?

Answer 218

VATS for mechanical / chemical pleurodesis +/- bullectomy

Question 219

What are the landmarks for chest drain insertion?

Answer 219

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

Question 220

How does alpha 1 antotrypsin deficiency cause emphysema?

Answer 220

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

Question 221

What is the rough percentage mortality of ARDs?

Answer 221

40%

Question 222

Outline the criteria for ARDs

Answer 222

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)

Question 223

Outline the severity classifications for ARDs

Answer 223

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

Question 224

List 4 causes of lower zone lung fibrosis

Answer 224

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

Question 225

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

Answer 225

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

Question 226

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

Answer 226

Upper / middle

Question 227

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

Answer 227

No eosinophils in peripheral blood film

Question 228

What are the causes of extrinsic allergic alveolitis?

Answer 228

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

Question 229

List some investigations for extrinsic allergic alveolitis

Answer 229

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

Question 230

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

Answer 230

Cryptogrenic organising pneumonia

Question 231

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

Answer 231

Postural drainage and inspiration muscle training

Question 232

Silicosis causes upper or lower zone fibrosis?

Answer 232

Upper zone fibrosis

Question 233

What are the x-ray features of silicosis?

Answer 233

Egg shell calcification of hilar lymph nodes Upper zone fibrosis

Question 234

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

Answer 234

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

Question 235

Bronchiectasis and raised IgE, likely diagnosis?

Answer 235

ABPA

Question 236

Management options for ABPA?

Answer 236

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

Question 237

Key investigation findings in ABPA?

Answer 237

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

Question 238

What might a gas show in obstructive sleep apnoea?

Answer 238

Compensated respiratory acidosis

Question 239

What is the equation for transfer factor?

Answer 239

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

Question 240

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

Answer 240

Concave

Question 241

List some causes of raised TLCO

Answer 241

- Exercise - Male - Hyperkinetic states - Polycythemia - Asthma - Pulmonary haemorrhage (e.g. GPA, Goodpasture's) - Left-to-right cardiac shunts

Question 242

List some causes of reduced TLCO

Answer 242

Pulmonary fibrosis Pneumonia PE Pulmonary oedema Emphysema Anaemia Low cardiac output

Question 243

List some causes of drug induced gynaecomastia

Answer 243

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

Question 244

How does Bartter's syndrome present?

Answer 244

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

Question 245

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

Answer 245

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

Question 246

Inheritance pattern of MODY?

Answer 246

Autosomal dominant

Question 247

Patients with MODY are sensitive to .... therapy

Answer 247

Patients with MODY are sensitive to sulfonylurea therapy

Question 248

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

Answer 248

Smoking

Question 249

Management of thyroid eye disease?

Answer 249

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

Question 250

How do statins work?

Answer 250

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

Question 251

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

Answer 251

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

Question 252

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

Answer 252

Macrolides e.g. erythromycin, clarithromycin

Question 253

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

Answer 253

Pregnancy and macrolide antibiotics History of intracerebral haemorrhage

Question 254

Who should take statins?

Answer 254

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

Question 255

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

Answer 255

1) 20mg NOCTE 2) 80mg NOCTE

Question 256

Mode of action of dabigatran?

Answer 256

Direct thrombin inhibitor

Question 257

What is the reversal agent for dabigatran?

Answer 257

Idarucizumab

Question 258

Contraindications for dabigatran?

Answer 258

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

Question 259

Mechanism of action of thiamine diuretics?

Answer 259

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

Question 260

How can methadone cause sudden cardiac death?

Answer 260

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

Question 261

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

Answer 261

Males = 430ms Females = 450ms

Question 262

Management of long QT?

Answer 262

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

Question 263

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?

Answer 263

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

Question 264

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

Answer 264

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

Question 265

Give some signs / symptoms of Eisenmenger's syndrome

Answer 265

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

Question 266

Management of Eisenmenger's syndrome?

Answer 266

Heart-lung transplantation

Question 267

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

Answer 267

1) 3 2) 3.5

Question 268

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

Answer 268

Warfarin LMWH

Question 269

Most common form of thyroid cancer?

Answer 269

Papillary

Question 270

Best prognosis subtype of thyroid cancer?

Answer 270

Papillary

Question 271

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

Answer 271

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

Question 272

What is the management of papillary and follicular thyroid cancer?

Answer 272

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

Question 273

Management in anaplastic carcinoma of the thyroid gland?

Answer 273

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

Question 274

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

Answer 274

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

Question 275

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

Answer 275

Aortic stenosis

Question 276

Give 3 conditions which can cause a collapsing pulse

Answer 276

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

Question 277

Give a condition in which you might see pulses alternans

Answer 277

Severe LVF

Question 278

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

Answer 278

Double pulse - two systolic pulses Mixed aortic valve disease mainly Sometimes HOCM

Question 279

Give a condition in which there may be a jerky pulse

Answer 279

HOCM

Question 280

Outline the guidelines for management of subclinical hypothyroidism

Answer 280

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

Question 281

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

Answer 281

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

Question 282

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

Answer 282

Verapamil

Question 283

List some causes of hypophosphataemia

Answer 283

Alcohol excess Acute liver failure DKA Refeeding syndrome Primary hyperPTH Osteomalacia

Question 284

Give some consequences of hypophosphataemia

Answer 284

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

Question 285

What is the investigation of choice for upper airway compression?

Answer 285

Flow volume loop

Question 286

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

Answer 286

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

Question 287

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

Answer 287

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

Question 288

When should PCI be considered?

Answer 288

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

Question 289

When should fibrinolysis be considered?

Answer 289

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

Question 290

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

Answer 290

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)

Question 291

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

Answer 291

Aldosterone antagonists e.g. spironolactone and eplerenone

Question 292

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

Answer 292

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

Question 293

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

Answer 293

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

Question 294

In which patients are hydralazine particularly useful in heart failure?

Answer 294

In afro-caribbean patients

Question 295

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

Answer 295

Failure of the aorticopulmonary septum to spiral during septation

Question 296

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

Answer 296

Children of diabetic mothers are at an increased risk of TGA

Question 297

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

Answer 297

Aorta leaves the right ventricle Pulmonary trunk leaves the left ventricle

Question 298

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

Answer 298

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

Question 299

What is the management of transposition of the great arteries?

Answer 299

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

Question 300

Clinical features of transposition of the great arteries?

Answer 300

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

Question 301

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

Answer 301

Type A (ascending aorta)

Question 302

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

Answer 302

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

Question 303

Outline the DeBakey classification for aortic dissection

Answer 303

- 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

Question 304

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

Answer 304

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

Question 305

What is the classic finding on CXR in aortic dissection?

Answer 305

Widened mediastinum

Question 306

What is the investigation of choice in aortic dissection?

Answer 306

CT angiography - demonstrating a false lumen

Question 307

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

Answer 307

TOE (transoesophageal echo)

Question 308

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

Answer 308

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

Question 309

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

Answer 309

Conservative management - IV labetalol to prevent progression Bed rest

Question 310

What are some complications of backward tears in aortic regurgitation?

Answer 310

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

Question 311

What are some complications of forward tear in aortic dissection?

Answer 311

Unequal arm pulses and BP Stroke Renal failure

Question 312

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

Answer 312

Spirometry with bronchodilator reversibility testing + FeNO test

Question 313

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

Answer 313

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

Question 314

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

Answer 314

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

Question 315

Give two causes of regular cannon a waves

Answer 315

VT with 1:1 ventricular-atrial conduction AVNRT

Question 316

Give a cause of irregular cannon waves

Answer 316

Complete heart block

Question 317

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?

Answer 317

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

Question 318

Mechanism of action of heparin?

Answer 318

Activates anti-thrombin III

Question 319

Mechanism of action of clopidogrel?

Answer 319

P2Y12 inhibitor

Question 320

Mechanism of action of abciximab?

Answer 320

Glycoprotein IIb/IIIa inhibitor

Question 321

Mechanism of action of dabigatran?

Answer 321

Direct thrombin inhibitor

Question 322

Mechanism of action of rivaroxaban?

Answer 322

Direct factor X inhibitor

Question 323

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

Answer 323

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

Question 324

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

Answer 324

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

Question 325

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

Answer 325

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

Question 326

What are the different types of incontinence?

Answer 326

- 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

Question 327

Outline the management options for incontinence where urge incontinence is predominant

Answer 327

- 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

Question 328

Outline the management options in predominant stress incontinence

Answer 328

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)

Question 329

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?

Answer 329

> 40% reduction in non-HDL cholesterol

Question 330

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

Answer 330

Monomorphic papiar rash without comedones or cysts Taper the steroids gradually

Question 331

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

Answer 331

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

Question 332

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

Answer 332

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

Question 333

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

Answer 333

Amoxicillin first line - If penicillin allergic then use macrolide or tetracycline 5 day course of antibiotics

Question 334

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

Answer 334

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

Question 335

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

Answer 335

- 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

Question 336

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

Answer 336

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

Question 337

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

Answer 337

- Haemophilus influenzae - Streptococcus pneumoniae - Moraxella catarrhalis

Question 338

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

Answer 338

Rhinovirus

Question 339

What are the criteria for admission in exacerbation of COPD?

Answer 339

- 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)

Question 340

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

Answer 340

- 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

Question 341

Outline the management for exacerbations of COPD

Answer 341

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

Question 342

What are the 2 main complications of subclinical hyperthyroidism?

Answer 342

Supraventricular arrythmias (AF mainly) and Osteoporosis Due to increased cardiac output and heart rate and then due to increased bone turnover respectively in hyperthyroidism

Question 343

2 causes of subclinical hyperthyroidism?

Answer 343

Multinodular goitre Excessive thyroxine

Question 344

How to manage subclinical hyperthyroidism?

Answer 344

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

Question 345

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?

Answer 345

20 weeks

Question 346

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

Answer 346

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)

Question 347

List causes of peripheral neuropathy that cause predominantly motor symptoms

Answer 347

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

Question 348

List causes of peripheral neuropathy that cause predominantly sensory symptoms

Answer 348

- 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

Question 349

Is eczema herpeticum a slowly or rapidly progressing rash?

Answer 349

Rapidly progressing

Question 350

Is eczema herpeticum painful rash or not painful?

Answer 350

Painful

Question 351

What is the management for eczema herpeticum?

Answer 351

Admit IV antibiotics

Question 352

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

Answer 352

True

Question 353

Patient with eczema, develops this rash - cause?

Answer 353

Eczema herpeticum - HSV 1/2

Question 354

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

Answer 354

Negri bodies - cytoplasmic inclusion bodies found in infected neurones

Question 355

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

Answer 355

'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

Question 356

How to manage animal bites (dog) in UK?

Answer 356

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

Question 357

What type of virus is rabies?

Answer 357

RNA rhabdovirus (specifically a lyssavirus)

Question 358

Above what level is the threshold for definition of thrombocytosis?

Answer 358

> 400 x 10^9/l

Question 359

List some causes of thrombocytosis

Answer 359

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

Question 360

What is a characteristic symptom in essential thrombocytosis?

Answer 360

Burning sensation in the hands

Question 361

What mutation is most common in essential thrombocystosis?

Answer 361

JAK2

Question 362

Features of essential thrombocytosis?

Answer 362

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

Question 363

Outline management of essential thrombocytosis

Answer 363

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

Question 364

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

Answer 364

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

Question 365

List some risk factors for osteoporosis

Answer 365

- History of glucocorticoid use - Rheumatoid arthritis - Alcohol exvess - History of parental hip fracture - Low BMI - Current smoking

Question 366

List some medications that can worsen osteoporosis

Answer 366

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

Question 367

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?

Answer 367

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

Question 368

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

Answer 368

Second decade Turkish, Armenian, Arabic

Question 369

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

Answer 369

Colchicine

Question 370

Features of familial mediterranean fever?

Answer 370

- Pyrexia - Abdominal pain (due to peritonitis) - Pleurisy - Pericarditis - Arthritis - Erysipeloid rash on lower limbs

Question 371

What are the 3 opioids preferred in patients with CKD?

Answer 371

- Alfentanil - Buprenorphine - Fentanyl

Question 372

Why is pulse oximetry not useful in CO poisoning?

Answer 372

Due to similarities between oxyhaemoglobin and carboxyhaemoglobin

Question 373

Pathophysiology of CO poisoning?

Answer 373

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

Question 374

What investigations to do in suspected CO poisoning?

Answer 374

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

Question 375

What is the management of CO poisoning?

Answer 375

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

Question 376

When are 3 successive shocks given in ALS algorithm?

Answer 376

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

Question 377

How does strongyloides stercoralis infect people?

Answer 377

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

Question 378

Features of strongyloides stercoralis?

Answer 378

- 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

Question 379

What is the management of strongyloides stercoralis?

Answer 379

Ivermectin and albendazole

Question 380

Do we screen for NAFLD?

Answer 380

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

Question 381

What testing is done in NAFLD?

Answer 381

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

Question 382

Features of systemic macrocytosis?

Answer 382

- Urticaria pigmentosa - produces a wheal no rubbing (Darier's sign) - Flushing - Abdominal pain - Monocytosis on the blood film

Question 383

2 investigations in systemic macrocytosis?

Answer 383

- Raised serum tryptase levels - Urinary histamine

Question 384

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

Answer 384

Serologic testing for Aspergillus Precipitins

Question 385

What is the classic feature on CXR in aspergilloma?

Answer 385

Crescent sign

Question 386

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

Answer 386

Gram +ve rod

Question 387

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

Answer 387

PPIs

Question 388

Outline the severity classification of c.diff

Answer 388

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

Question 389

Diagnostic for c.diff?

Answer 389

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

Question 390

What is the isolation precaution procedure for c.diff?

Answer 390

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

Question 391

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?

Answer 391

Pseudodementia in depression

Question 392

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

Answer 392

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)

Question 393

2 drugs that can cause eosinophilia?

Answer 393

Sulfasalazine, nitrofurantoin

Question 394

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

Answer 394

Gram positive

Question 395

What is the main investigation for diphtheria?

Answer 395

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

Question 396

What is the management of diphtheria?

Answer 396

- IM Penicilin - Diphtheria antitoxin

Question 397

What can be found on ENT examinatin in diphtheria?

Answer 397

- 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'

Question 398

What are the presentations of diphtheria?

Answer 398

- 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

Question 399

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

Answer 399

Eflornithine

Question 400

Outline 3 actions that ANP have?

Answer 400

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

Question 401

Where is ANP secreted from?

Answer 401

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

Question 402

Which chromosome is affected in Von-Hippel Lindau syndrome?

Answer 402

Chromosome 3

Question 403

Which chromosome is affected in tuberous sclerosis?

Answer 403

Chromosome 16

Question 404

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

Answer 404

1) Chromosome 17 2) Chromosome 22

Question 405

Outline the causes of methaemoglobinaemia

Answer 405

CONGENITAL - NADH methaemoglobin reductase deficiency ACQUIRED - Drugs: Sulphonamides, nitrates, dapsone, sodium nitroprusside, primaquine - Chemicals: Aniline dyes

Question 406

What is the classic finding in the ABG in methaemoglobinaemia?

Answer 406

Normal pO2 but decreased oxygen saturation

Question 407

What are the management options for methaemoglobinaemia?

Answer 407

- NADH methaemoglobinaemia reductase deficiency: ascorbic acid - IV methylthionium chloride (methylene blue) if acquired

Question 408

What is methaemoglobinaemia?

Answer 408

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

Question 409

Features in pityriasis versicolor?

Answer 409

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

Question 410

List some predisposing factors in Pityriasis Versicolor

Answer 410

- Immunosuppression - Malnutrition - Cushing's

Question 411

Outline first line then second line management of pityriasis versicolor

Answer 411

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

Question 412

What is the organism causing pityriasis versicolor?

Answer 412

Malassezia furfur

Question 413

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

Answer 413

Pulmonary artery pressure > / = 20mmHg

Question 414

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

Answer 414

F > M 30-50 yrs

Question 415

Risk factors for pulmonary arterial HTN?

Answer 415

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

Question 416

Features of pulmonary arterial hypertension?

Answer 416

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

Question 417

Outline management in pulmonary arterial hypertension

Answer 417

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

Question 418

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

Answer 418

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

Question 419

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

Answer 419

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

Question 420

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

Answer 420

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

Question 421

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

Answer 421

- Increasing age - Male sex - Northern latitude - Family history

Question 422

What percentage of people with Paget's are symptomatic?

Answer 422

Only 5%

Question 423

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

Answer 423

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

Question 424

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

Answer 424

- Bone pain - Skull or long bone deformity - Fracture - Periatricular Paget's

Question 425

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

Answer 425

Bisphosphonates (either oral risedronate or IV zoledronate)

Question 426

List some complications of Paget's disease of the bone

Answer 426

- Deafness - Bone sarcoma - Fractures - Skull thickening - High-output cardiac failure

Question 427

What are the definitional criteria for neutropaenic sepsis?

Answer 427

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

Question 428

Which organisms most commonly cause infection in neutropaenic sepsis?

Answer 428

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

Question 429

What is done for prophylaxis for neutropaenic sepsis?

Answer 429

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

Question 430

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

Answer 430

Most commonly 7-14 days after chemotherapy

Question 431

Outline the management of neutropaenic sepsis

Answer 431

- 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

Question 432

List some causes of lichenoid drug eruptions (lichen planus)

Answer 432

- Gold - Quinine - Thiazides

Question 433

1) Outline the management of lichen planus (exclude oral lichen planus) 2) Outline the management for oral lichen planus

Answer 433

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

Question 434

Outline some features of lichen planus

Answer 434

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

Question 435

What are two common complications of seborrheic dermatitis?

Answer 435

Otitis externa Blepharitis

Question 436

Where are the eczematous lesions typically in seborrheic dermatitits?

Answer 436

- Scalp - dandruff - Periorbital - Auricular - Nasolabial folds

Question 437

What organism involved in seborrheic dermatitis?

Answer 437

Malassezia furfur

Question 438

Name 2 conditions associated with seborrheic dermatitis

Answer 438

- HIV - Parkinson's disease

Question 439

What is first line treatment for dandruff in seborrheic dermatitis? What other treatment options are available?

Answer 439

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

Question 440

How is seborrheic dermatitis affecting the face and body managed?

Answer 440

- Topical antifungals e.g. ketoconazole - Topical steroids - for short periods

Question 441

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

Answer 441

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

Question 442

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

Answer 442

VF

Question 443

What happens in wolff-parkinson white?

Answer 443

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

Question 444

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

Answer 444

- 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

Question 445

Give some associations with wolff-parkinson-white

Answer 445

- HOCM - Mitral valve prolapse - Ebstein's anomaly - Thyrotoxicosis - Secundum ASD

Question 446

Outline the ECG features in wollf-parkinson-white

Answer 446

- 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

Question 447

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

Answer 447

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

Question 448

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

Answer 448

Aldosterone antagonist - acts in the cortical collecting duct

Question 449

2 main side effects of spironolactone?

Answer 449

- 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

Question 450

2 main features of creutzfeld-jakob disease?

Answer 450

- Dementia (rapid onset) - Myoclonus

Question 451

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

Answer 451

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')

Question 452

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

Answer 452

Sporadic CJD - 85% of cases - Mean age of onset 65 years New variant CJD - Younger patients (average age of onset = 25 years)

Question 453

What are the main features of new variant CJD?

Answer 453

Psychological symptoms e.g. anxiety, withdrawal and dysphonia

Question 454

Name 4 prion diseases

Answer 454

- CJD - Kuru - Fatal familial insomnia - Gerstmann Straussler-Scheinker disease

Question 455

What is the median survival in new variant CJD?

Answer 455

13 months

Question 456

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

Answer 456

- Cardiac arrythmia - Flash pulmonary oedema - Renal failure - more long term

Question 457

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

Answer 457

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

Question 458

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

Answer 458

- Tinnitus - Visual blurring - Flushing - Dry skin - Abdominal pain

Question 459

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

Answer 459

Serum salicylate levels

Question 460

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?

Answer 460

Aspirin - temporary, usually reversible Quinine - permanent

Question 461

What is the management of quinine poisoning?

Answer 461

- Fluids, inotropes, bicarbonate - Positive pressure ventilation for pulmonary oedema

Question 462

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

Answer 462

B-cell proliferation more common

Question 463

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

Answer 463

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

Question 464

Characteristic blood film finding in chronic lymphocytic anaemia?

Answer 464

Smudge cells

Question 465

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

Answer 465

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

Question 466

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

Answer 466

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

Question 467

What is the usual source of infection in orbital cellulitis?

Answer 467

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

Question 468

Does orbital cellulitis have high or low mortality rate

Answer 468

High

Question 469

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

Answer 469

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

Question 470

What is the usual nodus of infection in periorbital cellulitis?

Answer 470

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

Question 471

What can periorbital cellulitis progress to?

Answer 471

Orbital cellulitis

Question 472

What are the risk factors for orbital cellullitis?

Answer 472

- 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

Question 473

Features of orbital cellulitis?

Answer 473

- 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)

Question 473

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

Answer 473

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

Question 474

Investigations in suspected orbital cellulilitis?

Answer 474

- 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

Question 475

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

Answer 475

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

Question 476

Features of Waldenstrom's macroglobulinaemia?

Answer 476

- 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

Question 477

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

Answer 477

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

Question 478

What is the management of Waldenstrom's macroglobulinaemia?

Answer 478

Rituximab based combination chemotherapy

Question 479

How is Leishmaniasis spread?

Answer 479

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

Question 480

What are the three forms of Leishmaniasis?

Answer 480

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

Question 481

How is cutaneous Leishmaniasis investigated - key diagnostic?

Answer 481

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

Question 482

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

Answer 482

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

Question 483

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

Answer 483

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

Question 484

Features of visceral leishmaniasis (kala-azar)?

Answer 484

- 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

Question 485

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

Answer 485

Bone marrow or splenic aspirate

Question 486

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

Answer 486

- 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

Question 487

Give some differentials for causes of cavitating chest x ray

Answer 487

- Abscess (Staph aureus, Klebsiella and Pseudomonas) - Squamous cell lung cancer - Tuberculosis - Wegener's granulomatosis - Pulmonary embolism - Rheumatoid arthritis - Aspergillosis, histoplasmosis, coccidioidomycosis

Question 488

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

Answer 488

Varicella Zoster Virus

Question 489

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

Answer 489

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

Question 490

What is the key managment of Ramsay Hunt syndrome?

Answer 490

Oral aciclovir and corticosteroids

Question 491

Features of Ramsay Hunt syndrome?

Answer 491

- Auricular pain - Facial nerve palsy - Vesicular rash around the ear - Vertigo, tinnitus

Question 492

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

Answer 492

True

Question 493

What is the HLA association in ankylosing spondylitis?

Answer 493

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

Question 494

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

Answer 494

- M: F 3:1 (M>F) - Young - 20-30yr olds mostly

Question 495

Features of Ankylosing Spondylitis - the A's?

Answer 495

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

Question 496

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

Answer 496

Squamous cell skin cancer

Question 497

Describe the rash in erythema ab igne

Answer 497

Reticulated, erythematous patches with hyperpigmentation and telangiectasia

Question 498

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

Answer 498

True

Question 499

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

Answer 499

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

Question 500

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

Answer 500

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

Question 501

Turner's syndrome what is the karyotype?

Answer 501

45, X0

Question 502

List some features of Turner's syndrome

Answer 502

- 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)

Question 503

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

Answer 503

Increased risk of aortic dilatation and dissection

Question 504

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

Answer 504

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

Question 505

What happens to the level of the following electrolytes in the bloods in tumour lysis syndrome? - Urate - Potassium - Phosphate - Calcium

Answer 505

- Urate - raised - Potassium - raised - Phosphate - raised - Calcium - reduced (because phosphate is a calcium chelator)

Question 506

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

Answer 506

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

Question 507

Outline what is done for prevention of tumour lysis syndrome?

Answer 507

- 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.

Question 508

What is given in treatment for tumour lysis syndrome?

Answer 508

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

Question 509

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

Answer 509

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

Question 510

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

Answer 510

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

Question 511

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

Answer 511

Lorazepam

Question 512

What is the inheritance pattern of hereditary haemorrhagic telangiectasia?

Answer 512

Autosomal dominant

Question 513

True or false - hereditary haemorrhagic telangiectasia is always hereditary?

Answer 513

False - 20% occur spontaneously without prior family history

Question 514

Outline the diagnostic criteria for hereditary haemorrhagic telangiectasia

Answer 514

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

Question 515

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

Answer 515

Ovarian fibroma + pleural effusion + ascites

Question 516

Ovarian fibroma + pleural effusion + ascites = what syndrome?

Answer 516

Meig's syndrome

Question 517

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

Answer 517

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

Question 518

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

Answer 518

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

Question 519

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

Answer 519

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

Question 520

How does gentamicin cause nephrotoxicity?

Answer 520

Acute tubular necrosis

Question 521

2 main adverse effects with gentamicin?

Answer 521

- Ototoxicity - Nephrotoxicity

Question 522

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

Answer 522

Furosemide

Question 523

In what condition is gentamicin absolutely contraindicated?

Answer 523

Myasthenia gravis

Question 524

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

Answer 524

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

Question 525

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

Answer 525

1st: Trial of amantadine Mindfulness training CBT

Question 526

What are first line for treatment of spasticity in multiple sclerosis? What are the other options for management of this?

Answer 526

Baclofen and gabapentin Diazepam, dantrolene, tinzadine Physio

Question 527

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

Answer 527

Gabapentin

Question 528

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

Answer 528

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

Question 529

Outline the risk factors for cental retinal vein occlusion

Answer 529

- Increasing age - Hypertension - Cardiovascular disease - Glaucoma - Polycythaemia

Question 530

Features of central retinal vein occlusion symptoms?

Answer 530

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

Question 531

Features on fundoscopy of central retinal vein occlusion

Answer 531

- Widespread hyperaemia - Severe retinal haemorrhages - 'stormy sunset'

Question 532

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

Answer 532

Branch retinal vein occlusion

Question 533

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

Answer 533

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

Question 534

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

Answer 534

Branch retinal vein occlusion

Question 535

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

Answer 535

Central retinal vein occlusion Note widespread hyperaemia and 'stormy sunset' - severe retinal haemorrhages

Question 536

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

Answer 536

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

Question 537

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

Answer 537

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

Question 538

2 investigations in suspected Wernicke's encephalopathy?

Answer 538

- MRI - Decreased red cell transketolase

Question 539

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

Answer 539

Petechial haemorrhages in structures including the mamillary bodies and ventricle walls

Question 540

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

Answer 540

Korsakoff syndrome Amnesia (antero-grade) Confusion

Question 541

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

Answer 541

IgG deposits on renal biopsy

Question 542

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

Answer 542

IgA immune complexes

Question 543

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

Answer 543

Macroscopic haematuria in young people following an URTI

Question 544

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

Answer 544

Longitudinal splitting of the lamina densa

Question 545

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

Answer 545

Epithelial crescents in Bowman's capsule

Question 546

What is the finding on renal biopsy in membranous glomerulonephritis?

Answer 546

Spike and dome appearance

Question 547

Goodpasture's syndrome is caused by what?

Answer 547

Anti-glomerular basement membrane antibodies against type IV collagen

Question 548

Goodpasture's syndrome more common in men or women? In what age groups does Goodpasture syndrome present?

Answer 548

Men : Women (2:1) Bimodal age distribution (20-30 and 60-70)

Question 549

Goodpasture's syndrome is associated with which HLA?

Answer 549

HLA-DR2

Question 550

Feature of Goodpasture's syndrome?

Answer 550

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

Question 551

2 investigations in Goodpasture's syndrome?

Answer 551

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

Question 552

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

Answer 552

- ANA most common - Anti-Mi-2 most specific

Question 553

Anti-Jo-1 antibodies in dermatomyositis or polymyositis?

Answer 553

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

Question 554

What is the main management for dermatomyositis?

Answer 554

Prednisolone

Question 555

Investigations in Dermatomyositis?

Answer 555

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

Question 556

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

Answer 556

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

Question 557

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

Answer 557

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

Question 558

When are loop diuretics used in hypertension?

Answer 558

In resistant hypertension, particularly in patients with renal impairment

Question 559

List some adverse effects with loop diuretics

Answer 559

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

Question 560

What should be monitored during treatment in rheumatoid arthritis?

Answer 560

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

Question 561

Contraindications for Leflunomide - a DMARD used in Rheumatoid arthritis?

Answer 561

- 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

Question 562

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

Answer 562

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

Question 563

How is leflunomide stopped?

Answer 563

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

Question 564

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

Answer 564

Proximal renal tubules

Question 565

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

Answer 565

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

Question 566

Clinical features of Fanconi syndrome?

Answer 566

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

Question 567

List some causes of Fanconi syndrome

Answer 567

- Cystinosis (most common cause in children) - Sjogren's syndrome - Multiple myeloma - Nephrotic syndrome - Wilson's disease

Question 568

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

Answer 568

Cystinosis

Question 569

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?

Answer 569

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

Question 570

List some different sickle cell crises

Answer 570

- Thrombotic - 'vaso-occlusive' - Acute chest syndrome - Anaemia - aplastic and sequestration crises - Infectino

Question 571

Where can thrombotic crises occur in sickle cell disease?

Answer 571

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

Question 572

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

Answer 572

Acute chest syndrome

Question 573

Feature of acute chest syndrome?

Answer 573

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

Question 574

Outline management of acute chest syndrome in sickle cell disease

Answer 574

- 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

Question 575

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

Answer 575

Caused by infection with parvovirus Presents as a sudden fall in haemoglobin Bone marrow suppression causes a reduced reticulocyte count

Question 576

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

Answer 576

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

Question 577

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

Answer 577

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.

Question 578

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

Answer 578

Prescribe pantoprazole or lansoprazole instead

Question 579

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

Answer 579

Mechanism of action - antagonist of P2Y12 ADP receptor, inhibiting activation of the platelets Thienopyridines - Prasugrel - Ticagrelor - Ticlopidine

Question 580

What is the key investigation in hereditary spherocytosis?

Answer 580

Eosin-5-maleimide (EMA) binding test

Question 581

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

Answer 581

Hereditary spherocytosis

Question 582

What is the inheritance pattern of hereditary spherocytosis?

Answer 582

Autosomal dominant

Question 583

In hereditary spherocytosis, what can trigger aplastic crisis?

Answer 583

Parvovirus infection

Question 584

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

Answer 584

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

Question 585

Outline the management options for hereditary spherocytosis

Answer 585

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

Question 586

Inheritance pattern of G6PD deficiency?

Answer 586

XLR - so in males

Question 587

What is the classical blood film finding in G6PD deficiency?

Answer 587

Heinz bodies

Question 588

What is the diagnostic test in G6PD deficiency?

Answer 588

Measure enzyme activity of G6PD

Question 589

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

Answer 589

Neonatal jaundice

Question 590

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

Answer 590

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

Question 590

Give some causes of oculogyric crisis

Answer 590

- Antipsychotics - Metoclopramide - Postencephalitic Parkinson's diseaes

Question 591

Management of oculogyric crisis?

Answer 591

Cessation of causative medication IV antimuscarinic - procyclidine or benztropine

Question 592

Inheritance pattern of Alport's syndrome?

Answer 592

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

Question 593

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

Answer 593

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

Question 594

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

Answer 594

- Molecular genetic testing - Renal biopsy - longitudinal splitting of the lamina densa of the glomerular basement membrane - resulting in a 'basket-weave' appearance

Question 595

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

Answer 595

- 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

Question 596

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

Answer 596

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

Question 597

Early features of tricyclic overdose?

Answer 597

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

Question 598

Feature of severe poisoning in trycyclic overdose?

Answer 598

- Arrythmias - Seizures - Metabolic acidosis - Coma

Question 599

ECG changes in tricyclic overdose?

Answer 599

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

Question 600

What antiarrythmics are contraindicated in tricyclic overdose?

Answer 600

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

Question 601

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

Answer 601

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

Question 602

True or false, dialysis is effective in removing trycyclics?

Answer 602

False - it is ineffective

Question 603

Genital warts are typically caused by what strains of HPV?

Answer 603

6 & 11

Question 604

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

Answer 604

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

Question 605

Which strains of HPV predispose to cervical cancer?

Answer 605

16,18, 33

Question 606

Prognosis of genital warts?

Answer 606

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

Question 607

Features of third nerve palsy?

Answer 607

- Eye is deviated 'down and out' - Ptosis - Pupil may be dilated (sometimes called a 'surgical' third nerve palsy)

Question 608

List some causes of third nerve palsy

Answer 608

- 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

Question 609

Give some signs of uncal herniation

Answer 609

- Hypertension - Bradycardia - Cheyne-Stokes respiration - Loss of consciousness

Question 610

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

Answer 610

Desmopressin

Question 611

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

Answer 611

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

Question 612

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

Answer 612

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

Question 613

Thyroid lymphoma is associated with what other thyroid condition?

Answer 613

Hashimoto's thyroiditis

Question 614

Medullary thorid cancer cells secrete what?

Answer 614

Calcitonin

Question 615

Outline the management of papillary and follicular thyroid cancer

Answer 615

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

Question 616

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?

Answer 616

CML - philadelphia translocation t(9;22)

Question 617

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

Answer 617

Subdural

Question 618

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

Answer 618

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

Question 619

What eye signs can be seen in subdural haematoma?

Answer 619

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

Question 620

What is Cushing's triad?

Answer 620

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

Question 621

Management of acute subdural haematoma options?

Answer 621

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

Question 622

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

Answer 622

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

Question 623

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

Answer 623

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

Question 624

Follicular lymphoma is associated with which translocation?

Answer 624

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

Question 625

Which translocation is associated with Burkitt's lymphoma?

Answer 625

t(8;14)

Question 626

Which translocation is associated with Mantle cell lymphoma?

Answer 626

t(11;14)

Question 627

Which translocation is associated with promyelocytic leukaemia?

Answer 627

t(15;17)

Question 628

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

Answer 628

6 months

Question 629

How is the water deprivation test done?

Answer 629

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

Question 630

Water deprivation test table

Answer 630

Question 631

Investigations in suspected BPH?

Answer 631

- 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

Question 632

Outline the management options for BPH

Answer 632

- 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)

Question 633

Adverse effects of alpha-1 antagonists in BPH?

Answer 633

Dizziness, postural hypotension, dry mouth, depression

Question 634

Adverse effects of 5-alpha reductase inhibitors in BPH?

Answer 634

Erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia

Question 635

Complications of BPH?

Answer 635

- UTI - Retention - Obstructive uropathy

Question 636

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

Answer 636

- 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

Question 637

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

Answer 637

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)

Question 638

What is the inheritance pattern of Wiskott-Aldrich syndrome?

Answer 638

X-linked recessive Mutation in WASP gene

Question 639

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

Answer 639

B- and T-cell

Question 640

What is the triad in Wiskott Aldrich syndrome?

Answer 640

- Recurrent bacterial infections e.g. chest - Eczema - Thrombocytopaenia (+low IgM levels)

Question 641

Preferred method of contraception in women with PCOS?

Answer 641

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

Question 642

How is hirsutism and acne managed in PCOS?

Answer 642

- COC , co-cyprindiol - Topical eflornithine - Spironolactone, flutamide, finasteride under specialist supervision

Question 643

How is infertility managed in PCOS?

Answer 643

- Under specialist supervision - Metformin / clomifene or combination - Gonadotrophins

Question 644

How is premature ovarian insufficiency defined?

Answer 644

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

Question 645

Give some causes of premature menopause

Answer 645

- 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

Question 646

Give some features of premature ovarian failure

Answer 646

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

Question 647

What will be the biochemical findings in premature ovarian failure?

Answer 647

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

Question 648

What is the management of premature ovarian failure?

Answer 648

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

Question 649

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

Answer 649

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

Question 650

Outline the management of Herpes Zoster Ophthalmicus

Answer 650

- 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

Question 651

Give some complications of Herpes Zoster Ophthalmicus

Answer 651

- Ocular - conjunctivitis, keratitis, episcleritis, anterior uveitis - Ptosis - Post-herpetic neuralgia

Question 652

Is Linezolid bacteriocidal or bacteriostatic in nature?

Answer 652

Bacteriostatic - stops formation of the 50S initiation complex

Question 653

What is the organism activity of Linezolid?

Answer 653

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

Question 654

2 main adverse effects associated with Linezolid?

Answer 654

- Thrombocytopaenia (reversible on stopping) - MOAI- avoid tyramine containing foods

Question 655

Give some causes of avascular necrosis of the hip

Answer 655

- Long-term steroid use - Chemotherapy - Alcohol excess - Trauma

Question 656

What is the gold standard investigation in suspected avascular necrosis?

Answer 656

MRI

Question 657

What is the management of avascular necrosis of the hip?

Answer 657

Joint replacement if necessary

Question 658

X-ray findings in avascular necrosis of the hip?

Answer 658

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

Question 659

Will the APTT be reduced or increased in antiphospholipid syndrome?

Answer 659

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.

Question 660

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

Answer 660

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

Question 661

Give some features of antiphospholipid syndrome

Answer 661

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

Question 662

Investigations / lab findings in anti-phospholipid syndrome?

Answer 662

- Anticardiolipin antibodies - Anti-beta2 glycoprotein 1 (anti-beta2GPI) antibodies - Thrombocytopaenia - Prolonged APTT

Question 663

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

Answer 663

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

Question 664

What is the management for primary thromboprophylaxis in antiphospholipid syndrome?

Answer 664

Low-dose aspirin

Question 665

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

Answer 665

- 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

Question 666

Give the relative, primary and secondary causes of polycythaemia

Answer 666

RELATIVE - Dehydration - Stress: Gaisbock syndrome PRIMARY - Polycythaemia rubra vera SECONDARY - COPD - Altitude - OSA - Excessive EPO: cerebellar haemangioma, hypernephroma, hepatoma, uterine fibroids

Question 667

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

Answer 667

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

Question 668

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

Answer 668

Nicotinic acetylcholine receptors

Question 669

Causes of mitral stenosis - common and then rarer?

Answer 669

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

Question 670

Typical feature on CXR in mitral stenosis?

Answer 670

Left atrial enlargement

Question 671

Features of mitral stenosis?

Answer 671

- 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

Question 672

2 Features of severe Mital Stenosis?

Answer 672

- Length of murmur increases - Opening snap becomes closer to S2

Question 673

Feature on echo in mitral stenosis?

Answer 673

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

Question 674

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

Answer 674

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

Question 675

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

Answer 675

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.

Question 676

List 3 neutrophil disorders that are primary immunodeficiency disorders

Answer 676

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

Question 677

List 3 B-cell disorders that are primary immunodeficiency disorders

Answer 677

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

Question 678

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

Answer 678

DiGeorge Syndrome

Question 679

Explain the pathophysiology in chronic granulomatous disease?

Answer 679

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

Question 680

Explain the pathophysiology in Chediak-Highashi syndrome?

Answer 680

Microtubule polymerisation defect which leads to a decrease in phagocytosis

Question 681

Explain the pathophysiology in leukocyte adhesion deficiency

Answer 681

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

Question 682

Clinical symptoms / features in chronic granulomatous disease?

Answer 682

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

Question 683

Gold standard investigations in chronic granulomatous disease?

Answer 683

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

Question 684

Clinical symptoms / features in Chediak-Higashi syndrome?

Answer 684

'Partial albinism' and peripheral neuropathy Recurrent bacterial infections

Question 685

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

Answer 685

Giant granules in neutrophils and platelets

Question 686

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

Answer 686

- Recurrent bacterial infections - Delay in umbilical caord sloughing - Absence of neutrophils / pus at sites of infection

Question 687

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

Answer 687

IgG, IgA, IgM

Question 688

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

Answer 688

Recurrent chest infections

Question 689

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

Answer 689

CVID can also predispose to autoimmune disorders and lymphoma

Question 690

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

Answer 690

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

Question 691

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

Answer 691

X-linked recessive

Question 692

Bruton's congenital agammaglobulinaemia typically in males or females?

Answer 692

Males because it is XLR inheritance pattern

Question 693

What is the pathophysiology in selective immunoglobulin A deficiency?

Answer 693

Maturation defect in B cells

Question 694

What is the most common primary antibody deficiency?

Answer 694

Selective immunoglobulin A deficiency

Question 695

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

Answer 695

All classes

Question 696

How does selective immunoglobulin A deficiency present?

Answer 696

- 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)

Question 697

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

Answer 697

Selective immunoglobulin A deficiency

Question 698

What is the pathophysiology in DiGeorge's syndrome?

Answer 698

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

Question 699

Features of DiGeorge's syndrome?

Answer 699

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

Question 700

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

Answer 700

Stem cell transplantation

Question 701

Causes of SCID?

Answer 701

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

Question 701

How can SCID present?

Answer 701

Recurrent infectinos due to viruses, bacteria and fungi

Question 702

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

Answer 702

- SCID - Ataxic telangiectasia - Wiskott-Aldrich syndrome - HyperIgM syndromes

Question 703

Causes of SCID?

Answer 703

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

Question 704

What is the inheritance pattern of ataxic telangiectasia?

Answer 704

Autosomal recessive

Question 705

Features of ataxic telangiectasia?

Answer 705

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

Question 706

Clinical features in hyperIgM syndrome?

Answer 706

Infection / pneumocystis pneumonia, hepatitis, diarrhoea

Question 707

Management options for post-LP headache?

Answer 707

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

Question 708

Which infection can lead to gastric lymphoma (MALT)?

Answer 708

Helicobacter pylori

Question 709

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

Answer 709

EBV

Question 710

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

Answer 710

HTLV-1

Question 711

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

Answer 711

HIV-1

Question 712

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

Answer 712

Malaria

Question 713

EBV can lead to or predispose to which haematological malignancies?

Answer 713

Hodgkin's and Burkitt's lymphoma Nasopharyngeal carcinoma

Question 714

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

Answer 714

Adult T-cell leukaemia / lymphoma

Question 715

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

Answer 715

High-grade B-cell lymphoma

Question 716

Helicobacter Pylori can lead to or predispose to which malignancy?

Answer 716

Gastric lymphoma (MALT)

Question 717

Malaria can lead to or predispose to which haematological malignancy?

Answer 717

Burkitt's lymphoma

Question 718

Which post-renal transplant medication can cause tremors?

Answer 718

Tacrolimus

Question 719

Red flags associated with airway and blunt force neck trauma?

Answer 719

- 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

Question 720

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

Answer 720

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)

Question 721

Mechanism of action of calcium resonium?

Answer 721

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.

Question 722

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

Answer 722

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

Question 723

ECG features of hyperkalaemia?

Answer 723

- Peaked, or 'tall tented' T-waves - Loss of p waves - Broad QRS complexes - Sinusoidal wave pattern

Question 724

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

Answer 724

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

Question 725

2 common complications with peritoneal dialysis?

Answer 725

- Peritonitis - Sclerosing peritonitis

Question 726

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

Answer 726

Coagulase negative staphylococci e.g. Staph Epidermidis - MOST COMMON Staph aureus is another cause

Question 727

Recommended antibiotic therapy for peritoneal dialysis peritonitis?

Answer 727

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)

Question 728

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

Answer 728

- Diuretics, caffeine and alcohol - Diabetes - Lithium - HF

Question 729

How does alcohol cause polyuria?

Answer 729

ADH suppresion in the posterior pituitary gland

Question 730

What can precipitate lithium toxicity?

Answer 730

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

Question 731

Lithium is primarily excreted by?

Answer 731

The kidneys

Question 732

Features of lithium toxicity?

Answer 732

- Coarse tremor (not fine tremor which can be seen in therapeutic levels) - Hyperreflexia - Acute confusion - Polyuria - Seizures - Coma

Question 733

Management of lithium toxicity?

Answer 733

- 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

Question 734

Inheritance pattern of hereditary spherocytosis?

Answer 734

Autosomal dominant

Question 735

Features of hereditary spherocytosis?

Answer 735

- Failure to thrive - Jaundice, gallstones - Splenomegaly - Aplastic crisis precipitated by parvovirus infection - Degree of haemolysis variable - MCHC elevated

Question 736

How is hereditary spherocytosis investigated?

Answer 736

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

Question 737

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

Answer 737

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

Question 738

Which genders get G6PD and which get hereditary spherocytosis?

Answer 738

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

Question 739

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

Answer 739

G6PD - African and mediterranean Hereditary Spherocytosis - Northern European

Question 740

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

Answer 740

Parvovirus infection

Question 741

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

Answer 741

Dengue spares palms and feet Chikungunya affects palms and feet

Question 742

Give some examples of viral haemorrhagic fever?

Answer 742

- Yellow fever - Lassa fever - Ebola - Dengue can progress to viral haemorrhagic fever

Question 743

Dengue virus is RNA or DNA virus?

Answer 743

RNA

Question 744

Dengue virus is transmitted by what carrier?

Answer 744

Aedes Aegypti mosquito

Question 745

Incubation period of Dengue?

Answer 745

7 days

Question 746

True or false, dengue is haemorrhagic?

Answer 746

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

Question 747

What happens in dengue haemorrhagic fever?

Answer 747

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)

Question 748

What investigations are done in suspected dengue?

Answer 748

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

Question 749

What is the treatment for dengue?

Answer 749

- Entirely symptomatic e.g. fluid resuscitation, blood transfusion etc - No antivirals are currently available

Question 750

Features of dengue fever?

Answer 750

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)

Question 751

Korsakoff syndrome aetiology?

Answer 751

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

Question 752

Features of Korsakoff's syndrome?

Answer 752

- Anterograde amnesia: inability to acquire new memories - Retrograde amnesia - Confabulation

Question 753

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

Answer 753

10 years - 10% 15 years - 50%

Question 754

Clinical features of MGUS?

Answer 754

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

Question 755

List some differentiating features between MGUS and myeloma

Answer 755

- 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)

Question 756

3 common adverse effects in atypical antipsychotics?

Answer 756

- Weight gain - especially olanzapine - Clozapine - agranulocytosis - Hyperprolactinaemia

Question 757

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

Answer 757

- Increased risk of stroke - Increased risk of VTE

Question 758

Which atypical antipsychoitc has a good side effect profile, particularly for prolactin elevation (i.e doesn't raise it that much unlike others)?

Answer 758

Aripiprazole

Question 759

Which factors does prothrombin complex concentrate contain?

Answer 759

2, 7, 9, 10

Question 760

Which agent is used to rapidly reverse the anticoagulant effect of warfarin?

Answer 760

PCC

Question 761

What is contained in cryoprecipitate? Therefore in which situations is it useful?

Answer 761

Fibrinogen Factor 8 Therefore good when there is bleeding with low fibrinogen levels or in patients with haemophilia A

Question 762

What is contained in fresh frozen plasma, and therefore in which conditions is it useful?

Answer 762

- Contains all coagulation factors - Corrects coagulopathy in patients with severe liver disease or DIC

Question 763

What is a benefit of the use of PCC over FFP in reversing warfarin effect?

Answer 763

More concentrated and doesn't require as much volume infusion so lowers the risk of fluid overload

Question 764

What is the mode of inheritance of essential tremor?

Answer 764

Autosomal dominant

Question 765

Which limbs typically affected in essential tremor?

Answer 765

Both upper limbs

Question 766

Doing what makes essential tremor worse?

Answer 766

- Postural tremor - worse if arms outstretched

Question 767

What improves essential tremor?

Answer 767

Alcohol and rest

Question 768

What is the most common cause of titubation (head tremor)?

Answer 768

Essential tremor

Question 769

What is the management for essential tremor?

Answer 769

Propranolol is first line Primidone is sometimes used

Question 770

Inheritance pattern of Friedrich's ataxia?

Answer 770

Autosomal recessive

Question 771

25M with persistent, asymptomatic hyperglycaemia noted incidentally, no features of insulin resistance or difference in weight, and no DKA in the past, diagnosis?

Answer 771

MODY

Question 772

Treatment for MODY?

Answer 772

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

Question 773

Inheritance pattern in MODY?

Answer 773

Autosomal dominant

Question 774

2 most common types of MODY and their genetic mutations?

Answer 774

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

Question 775

What is the triad of symptoms in Behcets disease?

Answer 775

Oral ulcers + genital ulcers + anterior uveitis = Behcet's disease

Question 776

Behcet's is associated with which HLA?

Answer 776

HLA B51

Question 777

List some features in Behcet's

Answer 777

- 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

Question 778

Investigations in Behcet's

Answer 778

- No definitive test - Diagnosis based on clinical findings - Positive pathergy test is suggestive (puncture site following needle prick becomes inflamed with small pustule forming)

Question 779

In which demographic is Behcet' more common?

Answer 779

- 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)

Question 780

When to start bone protection in pateints taking steroids?

Answer 780

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

Question 781

What is the minimum steroid intake a patient should be taking before they are offered osteoporosis prophylaxis?

Answer 781

Equivalent of prednisolone 7.5mg or more each day for 3 months

Question 782

cANCA antibodies target is .... whereas pANCA target is ....

Answer 782

cANCA antibodies target is serum proteinase 3 whereas pANCA target is myeloperoxidase

Question 783

cANCA is associated with which condition(s)?

Answer 783

GPA (granulomatosis with polyangiitis) (90%) Microscopic polyangiitis (in 40%)

Question 783

pANCA is positive in which conditions?

Answer 783

Mostly eGPA (50%) and Microscopic polyangiitis (75%) Sometimes in GPA as well (25%) Others: - UC - Anti-GBM - Crohn's

Question 784

Ankylosing spondylitis associated with which HLA?

Answer 784

HLA-B27

Question 785

Ankylosing spondylitis typically male or female and what age range?

Answer 785

Male:Female (3:1) - age 20-30 yrs old

Question 786

What is the key investigation in investigation of ankylosing spondylitis?

Answer 786

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

Question 787

List some plain x-ray findings in ankylosing spondylitis?

Answer 787

- 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

Question 788

Outline management of ankylosing spondylitis

Answer 788

- Regular exercise - NSAIDs first line - Physio - DMARDs if peripheral joint involvement - Anti-TNF e.g. infliximab if high disease activity despite conventional treatment

Question 789

What is the mechanism of action of Apremilast?

Answer 789

Phosphodiesterae type-4 inhibitor

Question 790

What are the different patterns of psoriatic arthropathy, and which is the most common?

Answer 790

- 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')

Question 791

Features of psotiatic arthropathy?

Answer 791

- 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

Question 792

X-ray features in psoriatic arthropathy?

Answer 792

often have the unusual combination of coexistence of erosive changes and new bone formation periostitis 'pencil-in-cup' appearance

Question 793

Outline management of psoriatic arthropathy

Answer 793

- 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

Question 794

Which has better prognosis - psoriatic arthropathy or RA?

Answer 794

RA

Question 795

List some poor prognostic features in rheumatoid arthritis

Answer 795

- 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

Question 796

Reactive arthritis is associated with which HLA?

Answer 796

HLA-B27

Question 797

Which organism can be recovered frmo the joint in reactive arthritis?

Answer 797

Organisms cannot be recovered from the joint in reactive arthritis

Question 798

What is the most common organism behind the post-STI form of reactive arthritis?

Answer 798

Chlamydia Trachomatis

Question 799

Which organisms associated with the post-dysenteric form of reactive arthritis?

Answer 799

Shigella flexneri Salmonella typhimurium Salmonella enteritidis Yersinia enterocolitica Campylobacter

Question 800

Outline the management of reactive arthritis

Answer 800

- Symptomatic: analgesia, NSAIDS, intra-articular steroids - Sulfasalazine and methotrexate are sometimes used for persistent disease - Symptoms rarely last more than 12 months

Question 801

Patient started on oral alendronate - cannot tolerate due to oesophagitis - what is the next step for management of osteporosis in these patients?

Answer 801

Switch to risedronate or etidronate in patients unable to tolerate alendronate

Question 802

What is the mechanism of action of MMF?

Answer 802

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

Question 803

What is the management of reactive arthritis?

Answer 803

- Symptomatic: analgesia, NSAIDS, intra-articular steroids - Sulfasalazine and methotrexate are sometimes used for persistent disease - Symptoms rarely last more than 12 months

Question 804

In which age groups does tempral arteritis occur?

Answer 804

> 50 yrs old and peak incidence in 70yrs

Question 805

What will be the results of CK and EMG in temporal arteritis?

Answer 805

Normal

Question 806

Investigations in suspected temporal arteritis?

Answer 806

- 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

Question 807

What is the management of temporal arteritis

Answer 807

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

Question 808

Mechanism of methotrexate and is it reversible or irreversible

Answer 808

Reversible inhibition of dihydrofolate reductase

Question 809

List some adverse effects of methotrexate

Answer 809

- Mucositis - Myelosuppression - Pneumonitis - Pulmonary fibrosis - Liver fibrosis

Question 810

How long after completion of methotrexate should men use contraception and women avoid pregnancy?

Answer 810

6 months for both

Question 811

What to co-prescribe with methotrexate and when?

Answer 811

Folic acid 5mg once weekly taken > 24 hrs after methotrexate dose

Question 812

What bloods to monitor before starting methotrexate and how often to repeat and then monitor thereafter?

Answer 812

FBC, U+Es, LFTs before starting treatment - then weekly until therapy stabilised - then monitor every 2-3 months

Question 813

What is the treatment of methotrexate toxicity?

Answer 813

Folinic acid

Question 814

How can Behcet's present neurologically?

Answer 814

Aspetic meningitis

Question 815

Key adverse effects in bisphosphonate therapy

Answer 815

- 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

Question 816

Predisposing factors for Paget's disease of the bone?

Answer 816

- Increasing age - Male sex - Northern latitude - Family history

Question 817

Bloods features in Paget's disease?

Answer 817

- 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

Question 818

X-ray features in Paget's disease of the bone?

Answer 818

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

Question 819

Feature in bone scintigraphy in Paget's disease of the bone?

Answer 819

Increased uptake is seen focally at the sites of active bone lesions

Question 820

Indications for treatment in Paget's disease of the bone?

Answer 820

- Bone pain - Skull or long bone deformity - Fracture - Periarticular Paget's

Question 821

Management for Paget's disease of the bone?

Answer 821

Bisphosphonate (either oral risedronate or IV zoledronate)

Question 822

Key complications of Paget's disease of the bone?

Answer 822

- Deafness (cranial nerve entrapment) - Bone sarcoma - Fractures - Skull thickening - High output cardiac failure

Question 823

What is the inheritance pattern of Marfan's syndrome?

Answer 823

Autosomal dominant

Question 824

Marfan's syndrome is caused by defect on which gene and on which chromosome/

Answer 824

Defect in the FBN1 gene on chromosome 15 that codes for the protein fibrillin 1

Question 825

List some features of Marfan's syndrome?

Answer 825

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)

Question 826

What is the main cardiac complication of Marfan's syndrome? Second most common?

Answer 826

Dilation of the aortic sinuses (90%) - which may lead to aortic aneurysm, aortic dissection, aortic regurgitation Mitral valve prolapse (75%)

Question 827

Eye features of Marfan's?

Answer 827

- Upwards lens dislocation (superotemporal ectopia lentis) - Blue sclera - Myopia

Question 828

TNF inhibitors improve all of the following except which of the following: - QOL - Radiological progression - Spinal mobility - Extra-articular features - Early morning stiffness

Answer 828

Improves all except radiological progression

Question 829

List causes of osteomalacia

Answer 829

- Vit D deficiency - CKD - Drug induced - e.g. anticonvulsants - Inherited: hypophosphatemic rickets - Liver disease e.g. cirrhosis - Coeliac's disease

Question 830

Features of osteomalacia?

Answer 830

- Bone pain - Bone/muscle tenderness - Fractures: especially femoral neck - Proximal myopathy - may lead to a waddling gait

Question 831

Investigations in osteomalacia?

Answer 831

- Low vit D - Low calcium, phosphate - Raised ALP X-ray - transluscent bands (Looser's zones or pseudofractures)

Question 832

Treatment of osteomalacia?

Answer 832

- Vitamin D supplementation - loading dose often needed initially - Calcium supplementation if dietary calcium is inadequate

Question 833

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)

Answer 833

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

Question 834

What is the inheritance pattern of osteogenesis imperfecta?

Answer 834

Autosomal dominant

Question 835

Osteogenesis imperfecta occurs due to an abnormality in which type of collagen?

Answer 835

Type 1 collagen

Question 836

Features of osteogenesis imperfecta?

Answer 836

- Presents in childhood - Fractures following minor trauma - Blue sclera - Deafness secondary to otosclerosis - Dental imperfections are common

Question 837

What will the bloods be like in osteogenesis imperfecta?

Answer 837

- Adjusted calcium, phosphate, parathyroid hormone and ALP results are usually normal

Question 838

What is a key adverse effect associated with the use of TNF-alpha inhibitors?

Answer 838

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)

Question 839

Outline the management of rheumatoid arthritis?

Answer 839

- 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

Question 840

What is a common complication with use of Rituximab?

Answer 840

Infusion reactions

Question 841

What is the mechanism of aciton of Rituximab?

Answer 841

- Anti-CD20 monoclonal antibody

Question 842

What is the mechanism of action of abatacept?

Answer 842

Fusion protein that that modulates a key signal required for activation of T lymphocytes - leads to decreased T-cell proliferation and cytokine production

Question 843

What are two early x-ray changes in rheumatoid arthritis?

Answer 843

- Loss of joint space - Juxta-articular osteopaenia

Question 844

Two later x-ray findings in rheumatoid arthritis?

Answer 844

- Articular erosions - Subluxation

Question 845

List some x-ray findings in rheumatoid arthritis

Answer 845

- Loss of joint space - Juxta-articular osteoporosis - Soft tissue swelling - Periarticular swelling - Subluxation

Question 846

Polyartertitis nodosa is associated with which infection?

Answer 846

Hepatitis B infection

Question 847

Polyarteritis nodosa is a vasculitis affecting what size arteries?

Answer 847

Medium-sized

Question 848

What is the pathophysiology in polyarteritis nodosa?

Answer 848

Vasculitis affecting medium-sized arteries with necrotising inflammation leading to aneurysm formation

Question 849

Polyarteritis nodosa is more common in which age group and in men or women?

Answer 849

Middle-aged men

Question 850

List some features of Polyarteritis Nodosa

Answer 850

- 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

Question 851

Anti-Ro antibodies associated with? Give 3 conditions

Answer 851

Sjogren's syndrome, SLE, congenital heart block

Question 852

Anti-La antibodies associated with which condition?

Answer 852

Sjogren's syndrome

Question 853

Anti-Jo1 antibodies associated with which condition?

Answer 853

Polymyositis

Question 854

Anti-scl-70 associated with which condition?

Answer 854

Diffuse cutaneous systemic sclerosis

Question 855

Anti-centromere antibodies associated with which condition?

Answer 855

Limited cutaneous systemic sclerosis

Question 856

What is the first line management of gout?

Answer 856

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

Question 857

When to offer prophylaxis in gout (allopurinol - urate lowering therapy)?

Answer 857

After the first attack of gout

Question 858

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?

Answer 858

1. Allopurinol 2. Febuxostat 3/4: Uricase, pegloticase

Question 859

Which diuretic can precipitate gout attacks?

Answer 859

Thiazides

Question 860

Targets for uric acid levels and what effects this?

Answer 860

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

Question 861

Pseudogout is a form of microcrystal synovitis caused by the deposition of ...... ..... ..... crystals in the synovium

Answer 861

Pseudogout is a form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium

Question 862

Risk factors for pseudogout in younger patients?

Answer 862

- Haemochromatosis - Hyperparathyroidism - Low magnesium, Low phosphate - Acromegaly, Wilson's disease

Question 863

What can be found on joint aspiration in pseudogout?

Answer 863

Weakly positively birefringent rhomboid shaped crystals

Question 864

Classic X-ray feature in pseudogout?

Answer 864

Chondrocalcinosis

Question 865

What is the management for pseudogout?

Answer 865

- Aspiration of joint fluid, to exclude septic arthritis - NSAIDs or intra-articular, intra-muscular or oral steroids as for gout

Question 866

There are many risk factors for developing pseudogout in younger patients, but otherwise what is the main risk factor?

Answer 866

Increasing age

Question 867

What is the long term drug treatment for SLE?

Answer 867

Hydroxychloroquine If there is internal organ involvement e.g. renal, neuro, eye then consider prednisolone, cyclophosphamide

Question 868

Outline management of SLE

Answer 868

Basics - NSAIDs, sun block Long-term - Hydoxychlroqione If there is internal organ involvement e.g. renal, neuro, eye then consider prednisolone, cyclophosphamide

Question 869

What is the most common organism behind septic arthritis overall? And in young, sexually active adults? Most common cause?

Answer 869

Staph Aureus Young, sexually active adults - Neisseria gonorrhoea

Question 870

Most common cause of septic arthritis in adults is due to .... spread from distal bacterial infections e.g. abscesses

Answer 870

Most common cause of septic arthritis in adults is due to haematogenous spread from distal bacterial infections e.g. abscesses

Question 871

Why is it important to take blood cultures in septic arthritis?

Answer 871

Because the most common cause is due to haematogenous spread from distal bacterial infections

Question 872

What investigations are done in septic arthritis?

Answer 872

- Synovial fluid sampling - Blood cultures - Joint imaging

Question 873

Outline management of septic arthritis

Answer 873

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

Question 874

What is the pattern of muscle weakness in dermatomyositis?

Answer 874

Symmetrical, proximal

Question 875

Dermatomyositis may be associated with .... .... .... or underlying ....

Answer 875

Dermatomyositis may be associated with connective tissue disorders or underlying malignancies

Question 876

List some skin features in dermatomyositis

Answer 876

- 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

Question 877

What are some resp manifestations of dermatomyositis that are possible?

Answer 877

- Resp muscle weakness - Interstitial lung disease e.g. fibrosing alveolitis or organising pneumonia

Question 878

Which antibodies are present in Dermatomyositis?

Answer 878

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

Question 879

True or false - atlanto-axial instability is seen in ankylosing spondylitis?

Answer 879

False - it's in rheumatoid arthritis

Question 880

Adhesive capsulitis - what is the main association?

Answer 880

Diabetes mellitus

Question 881

What are the different phases in adhesive capsulitis?

Answer 881

Painful freezing phase, adhesive phase and recovery phase

Question 882

Which movements affected in adhesive capsulitis?

Answer 882

External rotation > internal rotation or abduction Both passive and active movement is affected

Question 882

Outline the management of adhesive capsulitis

Answer 882

- NSAIDs - Physio - Oral corticosteroids - Intra-articular corticosteroids

Question 883

Define mononeuritis multiplex

Answer 883

Peripheral neuropathy affecting 2+ non-contiguous nerve trunks

Question 884

Which antibodies most specific for dermatomyositis? Which most common for it?

Answer 884

Most specific = Anti-Mi-2 Most common = ANA

Question 885

Outline the management of De Quervain's tenosynovitis

Answer 885

- Analgaesia - Steroid injection - Immobilisation with a thumb splint (spica) - Surgical treatment sometimes required

Question 886

What clinical test in De Quervain's tenosynovitis?

Answer 886

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