Passmedicine Flashcards

1
Q

What are the contraindications to percutaneous liver biopsy?

A

Deranged clotting (e.g. INR >1.4)
Low platelets (e.g. <60)
Anaemia
Extrahepatic biliary obstruction
Hydatid cysts
Haemangioma
Uncooperative patient
Ascites

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2
Q

What common drugs act on the NMDA receptor?

A

Methadone
Ketamine
Memantine

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3
Q

What analgesics are safe to use in renal impairment?

A

Oxycodone (down to eGFR 10)
Methadone
Fentanyl
Alfentanyl
Buprenorphine
Hydromorphone

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4
Q

HIV associated nephropathy (HIVAN) causes what on renal biopsy?

A

Collapsing FSGS (presents as nephrotic syndrome)

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5
Q

What are the poor prognostic factors in CLL?

A

Male sex
Age >70 years
Lymphocyte count > 50
Prolymphocytes comprising more than 10% of blood lymphocytes
Lymphocyte doubling time <12 months
Raised LDH
CD38 expression positive
TP53 mutation
Del 17p

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6
Q

What study demonstrated reduced risk of AIDS and mortality if ART is started no matter the CD4 count?

A

SMART study

Reduced chance of AIDS, a serious non-AIDS event or death by 57% with similar results in high, middle and low-income countries.

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7
Q

What is the antibiotic therapy for peritoneal dialysis peritonitis?

A

Intraperitoneal vancomycin and ceftazidime

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8
Q

What are the complications of gastrectomy?

A

Dumping syndrome:
-Early: food of high osmotic potential moves into small intestine causing fluid shift
-Late (rebound hypoglycaemia): surge of insulin following food of high glucose value in small intestine -2-3 hours later the insulin overshoots causing hypoglycaemia

Weight loss, early satiety

Iron-deficiency anaemia
-Hydrochloric acid important for reducing Fe3+ (largely insoluble) to ferrous (Fe2+) iron. Iron supplementation may be required lifelong

Osteoporosis/ osteomalacia

Vitamin B12 deficiency

Other:
-Increased risk of gallstones
-Increased risk of gastric cancer

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9
Q

When do you use venesection in erythrocytosis secondary to obstructive sleep apnoea?

A

Should be treated with venesection in the presence of hyperviscosity symptoms or a PCV (HCT) > 0.56.

A target PCV of 0.50 - 0.52 has been shown to increase exercise tolerance.

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10
Q

What antibody is present in miller-fisher syndrome?

A

Anti-GQ1b present in 85-90% of patients with Miller-Fisher syndrome.

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11
Q

What is the mechanism of action of ranolazine?
When is it contraindicated?

A

Late inward Na channel antagonist

Second line anti-anginal

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12
Q

What is the mechanism of action of ivabradine?

A

If channel antagonist to reduce heart rate.

Should not be used in patients with moderate to severe angina as it has been shown to increase the incidence of cardiovascular events in these patients.

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13
Q

What is the role of revascularisation techniques such as PCI in stable angina?

A

Has not been shown to reduce mortality or rate of MI in stable coronary artery disease. Therefore, medical therapy options should be exhausted before consideration of invasive treatment.

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14
Q

Summarise the treatment of angina

A

1st line: PRN GTN

2nd line: BB or CCB
-BB preferred as mortality benefit

3rd line (if no hypotension): ISMN or nicorandil

3rd line (if hypotension):
-Ranolazine (HR <70) - contraindicated in renal dx
-Ivabradine (HR >70)

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15
Q

What is the incidence of WPW?

A

0.1-0.3%

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16
Q

What is the abnormal pathway in WPW called?

A

Bundle of Kent

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17
Q

What drugs should be avoided in WPW?

A

Digoxin
Adenosine
Diltiazem
Verapamil
Other CCBs or B-blockers
————————

These all enhance conduction down accessory pathway by increasing refractory period in AV node.

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18
Q

What are the hypertension stage cut offs?

A

Stage 1: clinic (140/90), HBPM (135/85)

Stage 2: clinic (160/100), HBPM (150/95)

Severe Hypertension: systolic >180 or diastolic >110

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19
Q

What is the mechanism of action of disulfram?

A

This is an acetaldehyde dehydrogenase inhibitor. By inhibiting this enzyme, consumption of alcohol leads to a build-up of acetaldehyde, which can cause unpleasant symptoms such as flushing of the skin, nausea, vomiting, and arrhythmias. However, a problem with the use of disulfiram is poor compliance, as it does not reduce cravings for alcohol.

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20
Q

What is the mechanism of action of acamprostate?

A

Rather than causing unpleasant symptoms, it reduces the craving for alcohol. It is a weak antagonist of NMDA receptors.

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21
Q

Why should flumazenil only be used in reversal of anasthesia?

A

Flumazenil is the reversal agent for benzodiazepines and is a GABA receptor antagonist. It is known as a ‘dirty drug’ due to its many known complications and side effects, including arrhythmias, agitation and seizures. It is advised that flumazenil should not be given in unknown drug overdoses, even if the causative drug is presumed, due to the side effect profile and risks. It is now advised that flumazenil should only be used to reverse benzodiazepines in anaesthesia.

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22
Q

What do you monitor when starting aminocalicylates (mesalazine)?

A

Renal function should be monitored before starting an oral aminosalicylate, at 3 months and then annually thereafter. This should be done more often in the presence of renal impairment. Blood disorders can also occur with mesalazine, and patients should be asked to look out for bruising, bleeding, purpura, fever and sore throat.

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23
Q

When can corticosteroids be used in shingles?

A

Corticosteroids can be used in refractory pain in shingles if simple analgesia and neuropathic analgesia do not help, but only for acute shingles

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24
Q

What are the ECG findings in Wellen’s syndrome?

A

Wellen’s syndrome is the critical ischaemia of the left anterior descending artery. Patients typically have a history of chest pain and ECG findings include biphasic T waves in the anterior leads or deep symmetrical T wave inversion in leads I and aVL associated with 1mm ST elevation in the chest leads. These can be seen in this patient’s ECG.

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25
Q

What are the ECG findings in Brugada syndrome?

A

Brugada syndrome is an autosomal dominant inherited cardiovascular disease. It can be asymptomatic and lead to sudden cardiac death. ECG changes consistent with Brugada syndrome include convex ST-segment elevation > 2mm in at least 1 of V1-V3 that is followed by T wave inversion. A partial right bundle branch block may also be seen. Sometimes, a patient may have an appearance of a normal electrocardiogram (ECG). However, following the administration of flecainide, these ST-segment changes may appear.

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26
Q

When do you anticoagulate patients with new AF post stroke?

A

After 14 days

Recent meta-analysis collated the results of seven trials studying early anticoagulation in acute ischaemic strokes. Although the risk of further ischaemic strokes between days 7 and 14 is significantly reduced from 4.9 to 3%, the risk of symptomatic intracerebral haemorrhage was also significantly increased from 0.7% to 2.5%. As a result, early anticoagulation before 14 days is not indicated by NICE or the American Heart and Stroke Associations.

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27
Q

What auto-antibodies are found in myasthenia gravis?

A

Most (but not all) patients with MG are seropositive for the acetylcholine receptor (AChR) antibody.

Antibodies to muscle-specific receptor tyrosine kinase (MuSK), a surface membrane component essential in the development of the neuromuscular junction, have recently been identified and are found in up to 50% of MG patients who are seronegative for AChR antibodies. Emerging data suggests that the patterns of weakness and response to certain treatments may be different from those with AChR positive MG.

Anti-striated muscle antibody usually positive in MG patients that have a thymoma.

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28
Q

Meningitis as a complication of ear infection is almost always caused by which organism?

A

Streptococcus pneumoniae

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29
Q

What is the treatment for NRG-1 overdose?

A

NRG-1, a synthetic cathinone, can cause agitation, hyponatraemia and serotonin syndrome.

Treatment is with benzodiazepines, cooling and hypertonic saline if hyponatraemic. Patients may require intubation and paralysis to control hyperpyrexia

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30
Q

How does sodium thiosulphate work in cyanide poisoning?

A

In normal human physiology, detoxification of cyanide occurs via rhodanese, an enzyme found in many tissues but particularly in the liver and muscle. Rhodanese converts cyanide to thiocyanate, a water-soluble molecule excreted in the urine.

In poisoning, rhodanese is saturated and unable to remove the surplus cyanide molecules. Sodium thiosulfate serves as a sulfur donor in the reaction catalyzed by rhodanese. Hence administration of sodium thiosulfate increases cyanide to thiocyanate conversion. Hydroxocobalamin (vitamin B12) has also been approved for the treatment of cyanide poisoning.

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31
Q

What imaging should be performed in multiple myeloma?

A

NICE advises that all patients suspected to have a diagnosis of myeloma should be offered whole body MRI as first-line imaging, and only consider whole body CT if the patient declines MRI or is unable to have it. Skeletal survey should only be considered if CT and MRI are both not possible. Fluorodeoxyglucose positron emission tomography CT (FDG PET CT) can be considered once a diagnosis is confirmed.

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32
Q

What is the treatment for histioplasmosis?

A

Amphotericin or itraconazole are the pharmacological agents of choice for histoplasmosis

Histoplasmosis is due to the fungus Histoplasma capsulatum. It is most commonly encountered in the Mississippi and Ohio River valleys.

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33
Q

What is the management for xanthelasma?

A

Xanthelasma - high lipid levels leading to soft yellow/orange plaques, periorbitally.

They are not of clinical concern - except for the underlying lipid profile which should be investigated and treated accordingly.

They can be left alone, but if patients are keen for treatment, a commonly used option is topical trichloroacetic acid.

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34
Q

Peripheral neuropathy occurs in what percentage of those taking susceptible chemotherapies?

A

This is a condition that can occur in up to 40% of patients being given chemotherapy with agents such as platinum based drugs (cisplatin and oxaliplatin), vinca alakloids (vincristine and vinblastine), thalidomide and taxanes (paclitaxel and docetaxel).

In most cases it is irreversible. The best medication for treatment is gabapentin or pregabalin which should be titrated up to therapeutic levels and used in conjunction with another analgesic agents.

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35
Q

What are the surveillance timings for adenoma found on colonoscopy?

A

Low risk:
one or two adenomas smaller than 10 mm.

Intermediate risk:
three or four adenomas smaller than 10 mm or
one or two adenomas if one is 10 mm or larger.

High risk:
five or more adenomas smaller than 10 mm or
three or more adenomas if one is 10 mm or larger.

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36
Q

How do you differentiate Superior Orbital Fissure, Cavernous sinus syndrome and orbital apex syndrome?

A

Superior Orbital Fissure- Affects CN III, CN IV, CN V(1), CN VI

Carvenous sinus syndrome- Affects CN III, CN IV, CN V(1 &2), CNVI

Orbital apex syndrome- Affects CN II, CN III, CN IV, CN V(1), CN VI
i.e. Orbital apex syndrome is SOF plus visual loss

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37
Q

An aortic dissection causes ST elevation in which leads?

A

Inferior leads: II, III and aVF

The origin for the right coronary artery is the right coronary sinus which is at the bases of the aorta.

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38
Q

What is the treatment for chemotherapy induced vomiting refractory to maximum dose ondansetron?

A

Dexamethasone with ondansetron is effective in refractory chemotherapy-induced vomiting

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39
Q

What is the treatment for H. Pylori?

A

Amoxcillin, a PPI, and either metronidazole or clarithromycin (decision re: metronidazole or clarithro is taken on the basis of recent exposure to these antibiotics)

If patients are Penicillin allergic they get a PPI + Metronidazole and Clarithromycin as this question states.

IF they are penicillin allergic and have had previous exposure to clarithromycin then they get PPI + Bismuth + Metronidazole + Tetracycline.

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40
Q

How is frequency of colonoscopy determined in ulcerative colitis?

A

Lower risk

5 year follow up colonoscopy
Extensive colitis with no active endoscopic/histological inflammation
OR left sided colitis
OR Crohn’s colitis of <50% colon

3 year colonoscopy
Extensive colitis with mild active endoscopy/histological inflammation
OR post-inflammatory polyps
OR family history of colorectal cancer in a first degree relative aged 50 or over

1 year follow up colonoscopy
Extensive colitis with moderate/severe active endoscopic/histological inflammation
OR stricture in past 5 years
OR dysplasia in past 5 years declining surgery
OR primary sclerosing cholangitis / transplant for primary sclerosing cholangitis
OR family history of colorectal cancer in first degree relatives aged <50 years

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41
Q

What is the treatment escalation in Crohn’s disease?

A

The initial monotherapy of prednisolone is effective at high dose but symptoms return on tapering its dose. An add-on treatment is therefore needed. The next agent to think about is azathioprine or mercaptopurine, in accordance with NICE guidance. Before either is commenced, a TPMT level must be done. If it is deficient, very low or absent, neither azathioprine or mercaptopurine should be offered.

Methotrexate is the next most suitable agent to add if the patient cannot tolerate mercaptopurine or azathioprine.

Infliximab is used only when patients have failed conventional therapy, including immunosuppressives and corticosteroids.

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42
Q

Primary Biliary Cirrhosis is associated with which conditions?

A

Sjogren’s syndrome (seen in up to 80% of patients)
rheumatoid arthritis
systemic sclerosis
thyroid disease

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43
Q

Why do you give human albumin solution in patients with SBP?

A

Intravenous albumin treatment has been shown to reduce in-hospital mortality of patients with uncomplicated SBP. Patients with associated renal dysfunction appear to derive the most benefit. Albumin decreases renal insufficiency, probably by increasing the circulatory volume and by binding pro-inflammatory molecules.

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44
Q

How do you differentiate a sigmoid and caecal volvulus?

A

Note that a sigmoid volvulus will not retain haustra and typically originate in the left lower quadrant and extend to the right upper quadrant as is the case here.

A caecal volvulus will typically originate in the right lower quadrant and extend to the left upper quadrant. Additionally, caecal volvuli retain haustra. As both of these features are not present here, a sigmoid volvulus is a more likely diagnosis.

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45
Q

Why should you be cautious about a positive Hep C antibody test?

A

However, it must be noted that Hep C Antibody testing can throw up false positives (up to 10%).

Where Hep C antibodies are positive and RNA viral load is undetected it may be appropriate to repeat the antibody test using a different antibody assay.

The false positive rate is thought to be secondary to other similar antibodies in the circulation.

If the patient has Hep C antibodies and is Hep C RNA positive for more than 2 months they should be considered for treatment.

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46
Q

What is the histological diagnosis of Whipple’s disease?

A

Diagnosis is made with small intestinal biopsy showing macrophages containing Periodic acid-Schiff (PAS) granules infiltrating into the lamina propria.

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47
Q

How must you correct coagulation profile prior to paracentesis?

A

Paracentesis is not contraindicated in patients with an abnormal coagulation profile. The majority of patients with ascites due to cirrhosis have prolongation of the prothrombin time and some degree of thrombocytopenia. There are no data to support the use of fresh frozen plasma before paracentesis although if thrombocytopenia is severe (<40 * 109/l) most clinicians would give pooled platelets to reduce the risk of bleeding.

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48
Q

What medications inhibit oral iron replacement?

A

Antacid solutions, such as peptac, act by coating the stomach with an alkaline solution containing magnesium and calcium, thus improving heartburn symptoms. Unfortunately, this can lead to failed absorption of oral iron replacement. Alternate routes should be considered.

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49
Q

Post op transaminitis may be secondary to what?

A

Although the incidence of anaesthetic related hepatitis has decreased over recent years with the introduction of modern agents such as desflurane and sevoflurane, cases are still reported. The rapid rise in transaminases, gamma GT and alkaline phosphatase so soon after surgery fits well with the diagnosis. Supportive therapy is the only option, no therapeutic interventions, (including corticosteroids), have proved effective.

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50
Q

What examinations findings particularly relate to alcoholic hepatitis?

A

Alcoholic hepatitis almost always presents with clinical jaundice and the presence of a hepatic bruit is particularly suggestive.

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51
Q

What is the mortality benefit of using prednisolone in alcoholic hepatitis?

A

Prednisolone has been shown in meta-analyses to confer a significant reduction in 28-day mortality in patients with an MDS >32 or hepatic encephalopathy, however, there was no demonstrable benefit at 90 days or at one year.

Combination therapy with prednisolone and pentoxifylline confers no additional benefit over treatment with prednisolone alone, whilst the use of N-acetylcysteine as monotherapy in alcoholic hepatitis is not recommended. In one randomised controlled trial, combination therapy with prednisolone and N-acetylcysteine was shown to be superior to prednisolone monotherapy in reducing mortality at 28 days; largely due to a reduction in the incidence of HRS and superimposed infection.

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52
Q

What is the first, second and third line treatment for first episode C. Diff infection according to 2021 NICE guidelines?

A

First episode of Clostridium difficile infection
first-line therapy is oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
third-line therapy: oral vancomycin +/- IV metronidazole

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53
Q

What is the treatment for recurrent C diff infection?

A

Recurrent episode
recurrent infection occurs in around 20% of patients, increasing to 50% after their second episode
within 12 weeks of symptom resolution: oral fidaxomicin
after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin

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54
Q

What is the treatment for life threatening C diff infection?

A

Life-threatening Clostridium difficile infection
oral vancomycin AND IV metronidazole
specialist advice - surgery may be considered

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55
Q

What is the mechanism of action of bezlotoxumab?

A

bezlotoxumab is a monoclonal antibody which targets Clostridium difficile toxin B
NICE do not currently support its use to prevent recurrences as it is not cost-effective

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56
Q

When may faecal transplant be considered in C diff?

A

faecal microbiota transplant
may be considered for patients who’ve had 2 or more previous episodes

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57
Q

What lifestyle factor significantly increases risk of relapses in crohn’s disease?

A

A prospective study suggests that continued smoking raises the risk of Crohn’s exacerbation by approximately 50%.The study examined 573 Crohn’s disease patients for a follow up period of 4 years. In comparison with nonsmokers, continuing smokers relapsed more frequently with an incidence rate ratio of 1.53 (95% confidence interval : 1.102.17). Former smokers and quitters had similar relapse incidences compared with nonsmokers.

http://www.nature.com/ajg/journal/v111/n3/full/ajg2015401a.html

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58
Q

What is the evidence for mesalazine in Crohn’s disease?

A

Mesalazine in Crohn’s disease has debatable efficacy. A meta-analysis conducted in 2004 revealed a statistically significant but probably clinically insignificant effect on disease progression.

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59
Q

Plummer-vinson syndrome is also called by what other name?

A

Paterson–Brown–Kelly syndrome

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60
Q

What is the diagnostic criteria for toxic megacolon?

A

Radiographic evidence of colonic distension

plus at least three of the following:
1) Fever >38.6°C
2) Heart rate >120 beats per minute (The most reliable sign is the pulse rate)
3) Neutrophilic leucocytosis >10.5 × 109/L, or
4) Anaemia.

Plus, at least one of the following:
1- Dehydration
2- Altered mental status
3- Electrolyte disturbances, or
4- Hypotension.

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61
Q

Why is chromogranin A no longer used for carcinoid syndrome diagnosis?

A

Although well-differentiated carcinoid tumours secrete elevated levels of plasma chromogranin A, it is increasingly recognised that falsely positive elevated levels can be produced by other neuroendocrine tumours, hyperthyroidism, hyperparathyroidism, pituitary tumours, colon carcinoma, IBD, hypertension, COPD, ACS amongst many others. The low specificity of the test means that it is recommended that it is not used on its own as a screening test.

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62
Q

What are the clinical features of Fabry’s disease?

A

Acroparaesthesia: tingling, burning pain in the hands and feet triggered by stress such as emotion, extreme temperatures, or exercise

Angiokeratoma corporis diffusum: lightly verrucous, deep-red to blue-black papules on the trunk (in the bathing trunk distribution)

Cardiac: mitral valve prolapse or regurgitation usually, but any valvular heart defect can occur

Strokes: including young strokes/TIAs

Chronic Kidney Disease: proteinuria usually, can present late in fulminant renal failure

Classically death occurred in the 4th decade but this has improved since the availability of dialysis. It would be important to organise urgent renal investigations in this young man amongst your workup.

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63
Q

What is the pathophysiology of Fabry’s disease?

A

This is an X-linked recessive lipid storage disorder in which there a deficiency in the fat enzyme alpha-galactosidase. This results in the accumulation of alpha-galactosyl-lactosyl-ceramide in various tissues, including kidney, liver, blood vessels and nerve ganglion cells.

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64
Q

How does the enhanced liver fibrosis test influence management?

A

recent guidelines suggest that individuals with an incidental finding of NAFLD should be offered an enhanced liver fibrosis (ELF) blood test. If the ELF result indicates advanced liver fibrosis ( 10.51) then the individual should receive specialist monitoring and intervention. If the ELF result is negative (< 10.51) then the individual is likely to have a benign prognosis from their NAFLD and can be monitored in primary care. For these individuals, a repeat ELF blood test is recommended every 3 years.

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65
Q

What is involved in the enhanced liver fibrosis test?

A

The Enhanced Liver Fibrosis (ELF) test is a commercially
available algorithm that combines 3 direct serum markers of extracellular matrix remodeling and fibrogenesis: hyal-
uronic acid, the N-terminal pro-peptide of collagen type III,
and tissue inhibitor of metalloproteinase-1.

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66
Q

Which drugs cause an intrahepatic liver derangement?

A

LFTs1

Drug induced

Peter - paracetamol
Had - halothane
Epilepsy - sodium valproate/phenytoin
And - amiodarone
Alcoholic - etoh
Tb - anti tb meds
He met - methyldopa
Norman in - nitro
Shadwell - statins

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67
Q

How is autoimmune hepatitis divided?

A

It is sub-divided into type I and type II depending upon the antibodies present:
-Type I Anti-smooth muscle antibodies or anti-nuclear antibodies; this constitutes 75% of patients
-Type II Anti-LKM-1 or anti-liver cytosolic-1 antibodies

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68
Q

Primary biliary cholangitis puts you at what level of increased risk of HCC?

A

20x

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69
Q

How common is vitamin A deficiency following bariatric surgery?

A

The incidence of vitamin A deficiency has been reported between 5 and 10% after bariatric surgery.

Vitamin A deficiency is associated with night blindness, xerophthalmia, and occasionally complete blindness. Night blindness usually manifests as an inability in adjustment to dimmed light and is an early feature of vitamin A deficiency.

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70
Q

What is the mechanism of action of metoclopramide?

A

whilst metoclopramide is primarily a D2 receptor antagonist, the mechanism of action is quite complicated:
it is also a mixed 5-HT3 receptor antagonist/5-HT4 receptor agonist
the antiemetic action is due to its antagonist activity at D2 receptors in the chemoreceptor trigger zone. At higher doses the 5-HT3 receptor antagonist also has an effect
the gastroprokinetic activity is mediated by D2 receptor antagonist activity and 5-HT4 receptor agonist activity

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71
Q

In UGIB what pre-endoscopy target haemoglobin level gives the best outcomes?

A

70-80

Recent evidence has shown that conservative blood transfusion in the setting of acute upper gastrointestinal bleeding produces better outcomes compared to liberal blood transfusion.

An important observation was that there was an improvement in survival rates with the restrictive transfusion strategy. There was a reduction in the risk of further bleeding, the need for rescue therapy, and the rate of complications.

In Villanueva et al patients who were transfused when the haemoglobin was below 70g/dL had better outcomes compared to those who received blood transfusion below 100g/dL.

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72
Q

What is involved with a SeHCAT scan?

A

SeHCAT is bile acid analogue which can be detected by a nuclear medicine scan. The SeHCAT test involves a baseline scan, and then a 7 day scan. A 7-day SeHCAT retention value of less than 15% is generally considered indicative of bile salt malabsorption

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73
Q

What is first second and third line management for an acute dystonic reaction?

A

First line treatment in the UK is procyclidine, a rapid acting anticholinergic, with benzodiazepines and anticholinergic antihistamines 2nd and 3rd line respectively

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74
Q

What is the target HbA1c following pancreatic resection?

A

It’s important to remember in diabetes related to pancreatic resection, both alpha cells producing glucagon, and beta cells producing insulin, are removed in the pancreatectomy. This reduces the intensity of any counter regulatory response to hypoglycaemia and thus impacts on prospects of recovery and increases the severity of individual events. For this reason a more lax HbA1c target is instigated for patients who have a history of pancreatectomy, of 53.

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75
Q

How do you manage hyponatraemia in liver cirrhosis? When do you alter diuretics?

A

Sodium 126-135 mmol/L with normal creatinine - Continue normal diuretic regimen and observe, do not fluid restrict the patient.

Sodium 121-125 mmol/L with normal creatinine - International opinion is to continue diuretics, however, the British Society of Gastroenterology recommend a more cautious approach, and suggest either stopping diuretics or reducing the dose.

Sodium 121-125 mmol/L with raised creatinine (>150 mmol/L or >120 mmol/L and rising) - Stop diuretics and volume expand with human albumin solution 4.5%, gelofusine, or haemaccel

Sodium <121 mmol/L - Incredibly controversial, but the British society of gastroenterology suggest stopping diuretics and volume expanding with human albumin solution 4.5%, gelofusine, or haemaccel (which all contain sodium concentrations similar to that of normal saline).

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76
Q

How do some drugs cause oxidative haemolytic anaemia?

A

Drugs such as sulphasalazine, dapsone, ribavirin and poisoning with paraquat ingestion leads to the oxidation of Fe2+ (ferrous) components of haem to Fe3+ (ferric), forming methaemoglobin. When the intrinsic antioxidation mechanism of NADPH and glutathione is overwhelmed, red cell components undergo oxidative damage and cell death, leading to haemolysis, explaining the significantly raised LDH. Methaemoglobin is converted to hemichromes and eventually precipitated to Heinz bodies.

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77
Q

When are platelets indicated in resus for an UGIB?

A

<50

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78
Q

When is FFP and cryoprecipitate indicated in resus for an UGIB?

A

FFP is indicated due to raised INR/APTT > 1.5 x normal.

Cryoprecipitate is only required if fibrinogen remains below 1.5 after FFP.

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79
Q

Hydatid cysts are caused by which organism?

A

They are caused by the tapeworm parasite Echinococcus granulosus

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80
Q

What are the causes of “very” high ALT = >1000

A

The 4 main causes for hepatitis with very high ALTs (>1000) = mnemonic ‘DIVA’
1. Drug-induced hepatitis
2. Ischaemic hepatitis
3. Viral hepatitis
4. Autoimmune hepatitis

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81
Q

What are the pathological findings in carcinoid heart disease?

A

The characteristic pathological findings of carcinoid heart disease are endocardial plaques of fibrous tissue that may involve the tricuspid valve, pulmonary valve, cardiac chambers, venae cavae, pulmonary artery, and coronary sinus.

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82
Q

How do you differentiate hydatid cyst and amoebic liver abcess on CT?

A

Hydatid cyst is usually loculated.

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83
Q

What is the stepwise approach to investigating occult GI bleeding?

A

The SIGN guidelines for occult bleeding recommend OGD and colonoscopy. If they are both normal they recommend either repeat OGD or capsule endoscopy. If the capsule is negative then either a second capsule or enteroscopy is indicated. CT angiography would be used for acute occult bleeding where the patient is compromised and embolisation of the bleeding vessel is needed

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84
Q

What are the absolute and relative contraindications to TIPPS procedure?

A

ABSOLUTE
Severe and progressive liver failure (Child-Pugh score >12 is associated with a high risk of early death)
Uncontrolled hepatic encephalopathy
Right-sided heart failure
Uncontrolled sepsis
Unrelieved biliary obstruction

RELATIVE
Severe uncorrectable coagulopathy (INR >5)
Thrombocytopenia <20 * 109/l
Portal and hepatic vein thrombosis
Pulmonary hypertension
Central hepatoma

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85
Q

What is the first line investigation for small bowel overgrowth syndrome?

A

Hydrogen breath testing is an appropriate first line test for diagnosis of small bowel overgrowth syndrome

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86
Q

What is the “M rule” for primary biliary cholangitis?

A

IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females

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87
Q

What are the features of Wellen’s Syndrome and what does it signify?

A

Deeply inverted T waves in V2-V3 are very suggestive of Wellens’ syndrome which is highly specific for critical stenosis of the left anterior descending artery (LAD). It should be treated as a STEMI with urgent angiography and revascularisation.

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88
Q

When are B blockers and CCBs used in angina?

A

First line therapy in the treatment of angina is beta-blockade. Beta-blockers reduce myocardial oxygen consumption by acting as a negative inotrope and also by reducing heart rate. Some patients are unable to take beta-blockers such as asthmatics, or find that side effects such as tiredness, eczema or sexual dysfunction mean they are not tolerable. In these instances, use of calcium channel blockers such as diltiazem are recommended as first-line treatment. Since both of these classes of drug cause a reduction in heart rate and blood pressure their use must be monitored carefully, especially in the elderly. Concomitant use of beta-blockers and calcium channel blockers should be avoided where possible due to the risk of high degree conduction block and cardiac arrest.

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89
Q

When are nitrates and nicorandil used in angina?

A

Long-acting nitrates, such as isosorbide mononitrate or dinitrate are considered second-line therapy in stable angina. They can be used as monotherapy or as an adjunct to beta-blocker or calcium channel blocker therapy. They work by causing vasodilatation; both drugs possess a nitric oxide moiety which causes endothelial relaxation in blood vessels. This causes coronary vasodilation and improved blood flow to the myocardium with improved symptoms. A consequence of vasodilatation is hypotension and this should be considered when prescribing this drug to patients.

Another second-line option drug for stable angina in those patients who cannot tolerate nitrates or they are ineffective is nicorandil. This drug has a similar ultimate effect in that it causes dilatation of peripheral and coronary vessels to reduce symptoms of angina. It works by activating potassium channels on endovascular smooth muscle cells reducing intracellular calcium and hence relaxing the blood vessel. It too can cause profound hypotension and severe headaches.

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90
Q

When can ivabradine be used?

A

Ivabradine is a drug which can be used for both angina and heart failure. It works by reducing heart rate to reduce myocardial oxygen demand and improve diastolic function. In this case, the heart rate is adequately controlled so reduction is not necessary. Ivabradine also works by inhibiting the hearts natural pacemaker potential in the sinoatrial node, hence it only works when the patient is in sinus rhythm.

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91
Q

How does ranolazine work?

A

Ranolazine is a viable option in the management of angina where other avenues have been exhausted. It works by inhibiting the delayed sodium influx channel in the myocardium, reducing the intracellular calcium concentrations in the heart muscle. This, in turn, leads to a negative inotropic effect and reduction in symptoms of angina. Ranolazine does not cause a profound hypotensive effect and is the best choice in this scenario.

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92
Q

What is the stepwise approach to angina management?

A

1st line: PRN GTN
2nd line: BB or CCB (dont mix BB with Diltiazem or Verapamil -> risk of CHB).
3rd line: Add on CCB/BB (whatever was missed in 2nd line)
4th line (if no hypotension after 3rd line) ISMN/nicorandil
5th line (if no hypotension after 4th line) Add on ISMN or nicorandil (wtv was missed)
6th line (if hypotension after 5th line):
HR<70: RANOLAZINE (contraindicated in severe renal/liver disease)
HR>70: IVABRADINE (contraindicated in Sick sinus syndrome)

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93
Q

What can cause a raised ALP?

A

liver: cholestasis, hepatitis, fatty liver, neoplasia
Paget’s
osteomalacia
bone metastases
hyperparathyroidism
renal failure
physiological: pregnancy, growing children, healing fractures

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94
Q

What should you do if you need to transfuse patients awaiting transplant?

A

Transfusions in patients awaiting renal transplants are usually avoided where possible, due to the potential risk of circulating antibodies and thus organ rejection.

The transplant team would need to be informed and the patient advised that a transplant will be postponed for at least 3 months, following repeat antibody screening.

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95
Q

Which diabetes medication is associated with pancreatitis?

A

GLP-1 antagonists - “glutides”

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96
Q

What is first, second and third line for bone metastasis pain?

A

NSAIDS/ Bisphosphonates
Radiotherapy
Denosumab (unlicenced)

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97
Q

What are the main adverse events of overtreatment with levothyroxine?

A

Osteoporosis and atrial fibrillation

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98
Q

How can some testicular tumours lead to hyperthyroidism?

A

hCG is homologous to TSH in structure and therefore can lead to hyperthyroidism

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99
Q

What is the treatment for sodium valproate toxicity?

A

Valproate-induced hyperammonaemic encephalopathy (VHE) is an unusual complication characterised by a decreasing level of consciousness, focal neurological deficits, cognitive slowing, vomiting, drowsiness, and lethargy. Asymptomatic hyperammonaemia occurs in 15–50% of patients on valproate.

Treatment with L-carnitine may be beneficial in reducing ammonia levels.

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100
Q

Widespread T-wave inversion in chest leads can be a normal variant in who?

A

Widespread T wave inversion in the chest leads can be a normal variant in patients with Afro-Caribbean ethnicity

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101
Q

What do you do if alendronate is not tolerated due to GI side effects?

A

NICE guidance recommends that if patients suffer significant upper gastrointestinal side effects from the use of alendronate, then this should first be changed to risedronate or etidronate

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102
Q

What heart failure patients qualify for Ivabradine therapy?

A

Ejection fraction <35%
Heart rate >75/min
Sinus rhythm
NYHA class 2-4
Maximally titrated beta blocker therapy.

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103
Q

What class of antibiotics are most effective against ESBL producing organisms?

A

Extended spectrum B-lactamase (ESBL) producing organisms are typically resistant to penicillins and cephalosporins and as such the carbapenem class of antibiotics are typically first-line although nitrofurantoin or fosfomycin are also frequently effective. ESBL producers are most commonly Escherichia coli (E. coli) and Klebsiella species.

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104
Q

How important is HLA-B27 in ankylosing spondylitis?

A

HLA-B27, although associated with the disease in textbooks, is not particularly useful in making the diagnosis. It is not particularly specific, nor sensitive. 10% of patients with ankylosing spondylitis are HLA-B27 negative, and 10% of the healthy population are HLA-B27 positive.

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105
Q

How do you manage superficial vein thrombosis?

A

Superficial vein thrombosis (also referred to as thrombophlebitis) is a common condition and in the majority of cases is self-limiting. Patients presenting with a superficial vein thrombosis are at increased risk of a venous thromboembolic event and up to 20% of patients will already have a deep vein thrombosis (DVT) on presentation. Patients are more likely to have thrombus extension into the deep venous system if they have more than 5cm of thrombus within 10cm of the saphenofemoral junction (i.e. within the proximal long saphenous vein).

The evidence for how superficial vein thrombosis should be managed comes from a Cochrane review and is used to support the Scottish intercollegiate guidelines network (SIGN) guidelines on the prevention and management of venous thromboembolism (guide 122). The guidelines recommend that all patients with clinical signs of a superficial vein thrombosis should have an ultrasound scan to exclude a DVT.

Patients with a confirmed diagnosis of a superficial vein thrombosis should be considered for treatment with anti-embolism stockings and prophylactic doses of low molecular weight heparin (LMWH) for 30 days or fondaparinux for 45 days. In cases where LMWH is contraindicated, 8-12 days of oral non-steroidal anti-inflammatory drugs should be offered as this has been shown to reduce the risk of thrombus extension.

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106
Q

How do you differentiate CMV colitis and cryptosporidiosis?

A

Cytomegalovirus (CMV) colitis is usually seen in patients who are immunocompromised. It is a member of the herpes virus, for which around 50-80% of the general population are seropositive. The virus lays dormant until the patient is sufficiently immunocompromised.

Approximately 30% of all patients with AIDS will develop a gastrointestinal CMV infection. This usually occurs when the CD4+ counts drop to below 100 mm3.

CMV can affect the gastrointestinal tract from the oesophagus to the rectum, and symptoms depend on the site of infection. CMV oesophagitis causes odynophagia and retrosternal chest pain. CMV enterocolitis commonly presents with diarrhoea, fever, weight loss and per rectal bleeding. Tenesmus can occur if there is rectal involvement.

Cryptosporidiosis is a protozoal infection caused by cryptosporidium parvum. Immunocompromised individuals are particularly susceptible. The incubation period is between 2-10 days (average 7) and symptoms usually last about 1 to 2 weeks, although can occur for longer. The most common symptom is watery diarrhoea. Other symptoms include stomach cramps, dehydration, nausea and vomiting and fever.

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107
Q

How do you manage hiccups in palliative care?

A

chlorpromazine is licensed for the treatment of intractable hiccups

haloperidol, gabapentin are also used

dexamethasone is also used, particularly if there are hepatic lesions

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108
Q

What is the treatment for scleroderma renal crisis?

A

The optimal drug of choice is an ACE inhibitor, preferably captopril, which has been trialed with the greatest experience, but other ACEi are also likely to be beneficial. In a 15 year prospective cohort, one year survival increased from 15% to 76% with the use of ACEi against other anti-hypertensives1. Steroids should be strictly avoided in SRC, they increase the risk of SRC prior to the event and may exacerbate SRC in the acute setting. Renal dialysis may be required in patients who progress to end-stage renal failure despite ACEi treatments.

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109
Q

What are the good prognostic features in MS?

A

female sex
age: young age of onset (i.e. 20s or 30s)
relapsing-remitting disease
sensory symptoms only
long interval between first two relapses
complete recovery between relapses

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110
Q

Why do you give oxygen in pneumothorax?

A

Patients who are diagnosed with a pneumothorax should be given high-flow oxygen as it allows the exchange of nitrogen from the air trapped forming the pneumothorax with the additionally inspired oxygen from given to the patient. This exchange increases the oxygen content of the pneumothorax whilst decreasing the nitrogen concentration. Oxygen is more readily absorbed, and therefore the pneumothorax resolves more quickly.

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111
Q

When do you investigate anaemia in CKD?

A

As per NICE guidelines, for patients with chronic kidney disease, investigations for anaemia should be considered if their haemoglobin falls below 110g/L OR they develop symptoms suggestive of anaemia. This should begin with testing for iron deficiency using percentage of hypochromic red cells or reticulocyte haemoglobin content. In patients with anaemia of CKD, do not request transferrin saturation or serum ferritin measurement alone to assess iron deficiency status.

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112
Q

What antiretroviral therapy causes mitochondrial toxicity?

A

NRTIs - in particular stavudine, didanosine and zidovudine - classically cause mitochondrial toxicity as an unwanted side effect. This can result in nausea, pancreatitis, lactic acidosis and lipoatrophy as demonstrated above.

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113
Q

When do you start biologic therapy in rheumatoid arthritis?

A

Current NICE guidelines recommend the starting of biologic therapy when the patient has been on at least two DMARDs, including methotrexate, reporting two DAS 28 scores of greater than 5.1 at least one month apart

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114
Q

How do you use renin and aldosterone values in hypertension?

A

Helps divide primary and secondary hyperaldosteronism.

Primary
Renin is low due to something directly making or stimulating aldosterone meaning kidneys well filled so no renin needed
Cushing’s
Conns
CAH all examples

Secondary think kidney being underfilled despite euvolemia/hypervolemia , leading to high renin >high aldosteronism
RAS
Heart failure (bp less likely todav htn)
Excess diuretics

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115
Q

What is the most common electrolyte abnormality in alcohol withdrawal?

A

Hypophosphataemia is the most common electrolyte abnormality during alcohol withdrawal and is a recognised cause of seizures. It is often present at baseline in alcoholic patients and can further decrease in withdrawal. It is thought that this is due to effects on the proximal renal tubule. It can cause muscle pain and disorientation at very low levels (< 0.3 mmol/l).

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116
Q

When do you use tolvaptan in ADPKD?

A

Tolvaptan is a selective vasopressin receptor 2 antagonist and has been shown to reduce the annual rate of kidney growth and reduce the rate of decline of renal function over a three year period. In England and Wales, tolvaptan is recommended for patients with rapidly progressive disease at CKD stages 2-3. There is no current definition of rapidly progressive disease although an increase in total kidney volume of > 5 % per year is a predictor of rapid disease progression.

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117
Q

When is pravistatin used in ADPKD?

A

Pravastatin was shown to slow disease progression in children with ADPKD, but there is no evidence of benefit in adult patients.

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118
Q

What is the treatment for methotrexate toxicity?

A

Folinic Acid

methotrexate inhibits the enzyme which converts folic acid to folinic acid. So if you have methotrexate toxicity you’re unlikely to respond to folic acid as the enzyme is already inhibited, thus you have to give folinic acid.

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119
Q

Why should you avoid digoxin in cardiac amyloidosis?

A

Digoxin administration is not recommended in cardiac amyloidosis owing to a higher risk of digoxin toxicitiy, as the drug binds avidly to amyloid fibrils.

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120
Q

How do you manage amiodarone induced hypothyroidism?

A

Continue amiodarone and start levothyroxine.

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121
Q

How do you treat amiodarone induced thyrotoxicosis type 1

A

Continue amiodarone and start carbimazole.

This is excess iodine- induced thyroid hormone synthesis. A goitre will be present

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122
Q

How do you treat amiodarone induced thyrotoxicosis type 2?

A

Stop amiodarone and start prednisolone

This is amiodarone related destructive thyroiditis with an absent goitre.

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123
Q

What test do you carry out in normal T4 and suppressed TSH?

A

T3

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124
Q

How does combination nicotine replacement compare with non-combination

A

Combination = long acting patch and short acting formulation (either oral or nasal spray) to help manage acute cravings

Combination absolute abstinence rate 32% compared to 25% for non-combination nicotine replacement.

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125
Q

When is the arginine-GHRH stimulation test employed to assess GH secretion?

A

In patients with ischaemic heart disease or seizure where insulin tolerence test will be inappropriate. (risks of hypoglycaemia)

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126
Q

What percentage of growth hormone deficiency patients will have normal IGF-1 level?

A

30-40%

low IGF-1 may point to diagnosis of GHD but needs to be confirmed with dynamic tests for GH secretion. IGF-1 levels are influenced by age, time of onset of GHD, and degree of hypopituitarism. Insulin tolerance test is considered the gold standard.

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127
Q

What medications increase lithium toxicity risk without increasing serum lithium levels?

A

Carbamazepine increases risk of toxicity without affecting levels

Amiodarone increases risk of VT without increasing lithium levels.

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128
Q

JAK2 V617F mutation is present in >95% PRV. However when do you need to test for the rarer JAK2 exon 12 mutation?

A

Low serum erythropoietin is suggestive of primary bone marrow disease even in the absence of JAK2 mutation and should prompt testing for the rarer exon 12 mutation of JAK2. This test should be performed before the more invasive bone marrow biopsy.

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129
Q

How do you differentiate thiazide use from familial hypocalciuric hypercalcaemia?

A

Both present with hypercalcaemia and low urinary calcium (other causes of hypercalcaemia cause high urinary calcium)

FHH has an inappropriately NORMAL PTH due to loss of function mutations in the CASR calcium sensing receptor. This decreases sensitivity to calcium, meaning PTH remains unsuppressed at higher than normal serum calcium levels.

Hypocalciuria results from a loss of CASR-mediated negative feedback of tubular reabsorption/excretion of calcium.

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130
Q

When do you consider haemodialysis in lithium toxicity?

A

Dialysis should be considered in symptomatic lithium toxicity and:
-A lithium concentration greater than 5.0 mmol/L in patients with acute lithium overdose and who are not prescribed lithium
-A lithium concentration greater than 2.5 mmol/L in patients with chronic poisoning

Haemodialysis should be continued until:
-All new neurological features have resolved, and
-Lithium concentration remains stable at less than 1mmol/L

Acute on chronic overdose of lithium can lead to serious toxicity even after a modest overdose, as the extracellular tissues are already saturated with lithium.

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131
Q

What liver enzyme metabolises theophylline?

A

CYP1A2

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132
Q

Why do patients with end stage renal failure require IV rather than oral iron replacement?

A

Elevated serum levels of hepcidin preventing intestinal absorption of iron.

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133
Q

What is the treatment for iron overdose?

A

< 40mg/kg elemental iron and are asymptomatic can be observed at home.

> 40mg/kg elemental iron or who are symptomatic need medical assessment with serum iron levels measured 2-4 hours post-ingestion and abdominal x-ray.

> 60mg/kg elemental iron or have undissolved tablets on abdominal x-ray within 4 hours who have ingested = Whole bowel irrigation

If tablet still present after irrigation give Desferrioxamine.

> 90mg/kg elemental iron or in SHOCK= Desferrioxamine.

No role for activated charcoal

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134
Q

Captecitabine is broken down by which enzyme? What side effect may people suffer if they are deficient?

A

Capecitabine is the oral analog of 5-flourouraxil, a chemotherapeutic agent which is broken down predominantly, by dihydropyramidine dehydrogenase (DPD). Deficiency is autosomal recessive and can lead to a toxin buildup which in homozygous patients is usually fatal

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135
Q

What blood sugar levels should people with type 1 diabetes aim for: on waking, before meals and after eating?

A

5-7 mmol/litre on waking
4-7 mmol/litre before meals
5-9 mmol/litre 90 mins after eating.

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136
Q

How do you manage HIV in pregnancy?

A

It is recommended that women conceiving on an effective antiretroviral (ART) regimen should continue this even if it contains efavirenz or does not contain zidovudine.

Exceptions are: (1) Protease inhibitor (PI) monotherapy should be intensified to include (depending on tolerability, resistance and prior antiretroviral history) one or more agents that cross the placenta. (2) The combination of stavudine and didanosine should not be prescribed in pregnancy

Although there is most evidence and experience in pregnancy with zidovudine plus lamivudine, tenofovir plus emtricitabine or abacavir plus lamivudine are acceptable nucleoside backbones. In the absence of specific contraindications, it is recommended that the third agent in ART should be efavirenz or nevirapine (if the CD4 cell count is less than 250 cells/L) or a boosted PI.

No routine dose alterations are recommended for ARVs during pregnancy if used at adult licensed doses.

With a viral load <50 at 36 weeks a vaginal delivery is recommended in the absence of any obstetric complications.

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137
Q

What is the treatment for lymphatic filariasis?

A

Diethylcarbamazine

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138
Q

How do you achieve formal diagnosis of idiopathic intracranial hypertension?

A

Formal diagnosis (by Modified Dandy criteria), requires CSF opening pressure greater than 25 cmH2O and normal brain imaging. Imaging is required to exclude venous sinus thrombosis, which could result in the same signs and symptoms and is also more common in women on the oral contraceptive pill. The gold standard imaging for this would be MRI with contrast of the head and orbits and MR venogram.

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139
Q

At what level of PTH do you begin supplementation with calcium and vitamin D in secondary hyperparathyroidism?

A

Supplementing calcium and vitamin D in secondary hyperparathyroidism runs the risk of adynamic bone disease if this is begun at less than twice the upper limit of the normal range for PTH. For this reason levels are usually tracked until they cross this threshold, where upon supplementation is commenced.

In the event that patients with PTH levels greater than twice the upper limit of normal are left untreated, there is significant risk of progression to tertiary disease, and increased propensity to complications associated with hyperparathyroidism including bone resorption, fracture and ectopic calcification.

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140
Q

What is the difference between autoimmune polyendocrinopathy syndrome type 1 and 2?

A

APS type 2 has a polygenic inheritance and is linked to HLA DR3/DR4. Patients have Addison’s disease plus either:
type 1 diabetes mellitus
autoimmune thyroid disease

APS type 1 is occasionally referred to as Multiple Endocrine Deficiency Autoimmune Candidiasis (MEDAC). It is a very rare autosomal recessive disorder caused by mutation of AIRE1 gene on chromosome 21

Features of APS type 1 (2 out of 3 needed)
chronic mucocutaneous candidiasis (typically first feature as young child)
Addison’s disease
primary hypoparathyroidism

Vitiligo can occur in both types

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141
Q

How can you differentiate Conn’s adenoma and adrenal hyperplasia in hypokalaemia alkalosis and low renin?

A

Aldosterone on standing

Aldosterone is increased on prolonged standing in adrenal hyperplasia.

In Conn’s adenoma, the aldosterone would stay the same or drop on standing.

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142
Q

What is a normal short synACTHen test?

A

30 minute serum cortisol concetration greater than 420 nmol/L

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143
Q

What is the long synACTHen test?

A

Once adrenal insufficiency is confirmed with the short synACTHen test the location of the lesion can be achieved by measurement of ACTH or by performing the long Synacthen test.

Interpretation of this test is governed by the following:
1. In primary adrenal failure: we would not expect there to be a significant rise in cortisol during the long Synacthen rest since the adrenal glands are intrinsically dysfunctional
2. In secondary adrenal failure: chronically low levels of ACTH due to pituitary failure result in atrophy of the adrenal glands. Prolonged stimulation of the adrenal glands by ACTH in the long Synacthen test results in a degree of recovery by the adrenal glands resulting in a significant rise in cortisol. A response that rises gradually to a peak at 24 hours occurs in secondary adrenal failure. This pattern of results also occurs due to prolonged corticosteroid therapy use.

An important point is to remember that in some cases of long-standing adrenal atrophy due to secondary adrenal insufficiency, the adrenal glands will not respond even after 24 hours and will require several daily doses of depot Synacthen before an adrenal response is seen. The majority of these cases should be identifiable by measurement of plasma ACTH, which would be expected to be very low (in contrast to primary adrenal insufficiency where ACTH levels are very high).

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144
Q

What are the contraindications to commencing testosterone replacement in individuals who have panhypoputiutarism?

A

Elevated PSA >4ng/ml
Male breast Ca
Severe sleep apnoea
Severe LUTS due to BPH

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145
Q

What are the steroid sparing agents in GCA?

A

1st line MTX
2nd line MMF, Azathioprine, cyclophosphamide

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146
Q

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

A

Azetozolamide
Topiramate
RTA Type 1 and Type 2
Diarrhoea
Ureterosigmoidostomy
Post hypocapnic state

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147
Q

What further diagnostic testing should you carry out in Type 1 RTA?

A

Type 1 RTA can be the first presentation of Sjogren’s so these patients should have autoimmune screening (anti-Ro, anti-La, RF and ANA)

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148
Q

What urine test can you do to differentiate RTA type 1 and 2?

A

Urine pH
High in RTA type 1 due to a failure to acidify the urine.

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149
Q

What are the features of listeria meningitis?

A

Low glucose
Raised protein
lymphocytic predominant WCC

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150
Q

What are the features of tuberculous meningitis?

A

Normal or slightly reduced glucose
Low protein
Monocyte predominant WCC (count usually <500)

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151
Q

How often do you retinal screen diabetic patients during pregnancy?

A

All patients with type 1 or type 2 diabetes should have retinal screening during pregnancy as there is an increased risk of developing retinopathy. Patients should be advised to have retinal screening before 13 weeks unless their yearly screening has been done very recently. If any signs of retinopathy are picked up, repeat testing between 16-20 weeks is recommended, otherwise further testing at 28 weeks would suffice.

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152
Q

What is the management of lupus nephritis?

A

Initially managed with high dose steroids alongside either mycophenolate or cyclophosphamide.

Maintanence 1st line: Mycophenolate
Other maintanence options: azathioprine, tacrolimus

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153
Q

What is the first and second line treatment in alzheimer’s disease?

A

Donepezil first line

Memantine second line

(donepezil is generally avoided in patients with bradycardia and is used with caution in other cardiac abnormalities)

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154
Q

Why do you delay radio-iodine therapy post contrast CT for 8 weeks?

A

Iodine in IV contrast stays in body for 2 months and limits therapeutic uptake of radio-iodine by the thyroid gland.

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155
Q

What is the Leser-Trelat sign?

A

The abrupt appearance of multiple seborrhoeic keratoses.

Suggests underlying cancer and most associated with gastrointestinal adenocarcinomas and hepatic cancers.

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156
Q

Why do you stop aspirin in acute thyrotoxicosis?

A

It can worsen the storm by displacing T4 from thyroid binding globulin.

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157
Q

When can degludec (Tresiba) be used in T1DM over detemir (Levemir)?

A

Degludex has a much higher half life than levemore and therefore maintains a basal insulin level when the patient omits or forgets doses. This can prevent DKA.

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158
Q

What are the cut offs and management of vitamin D deficiency?

A

> 50 nmol/L = dietary recommendations
30-50 nmol/L = maintenance dose vitamin D
<30 nmol/L = loading dose vitamin D

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159
Q

What is the treatment of Cryptosporidiosis?

A

First line: Nitazoxanide
Second line: Rifaximin

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160
Q

What drugs alter the effect of adenosine?

A

DEAR
Dipyridamole enhances (large ventricular standstill)
Amiphyline reduces (short vent standstill)

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161
Q

What drug is used to prevent pathological bone fractures in metastatic cancer if eGFR <30

A

Denosumab

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162
Q

What drug is imipenem usually combined with and why?

A

The carbapenem - imipenem - is usually combined with cilastatin, a renal dehydropeptidase I inhibitor to decrease the renal degradation of imipenem.

163
Q

What antibiotics are effective against carbapenemase- producing organisms?

A

Polymyxins (e.g. colistrin)
Tigecycline
Fosfomycin
Aminoglycosides (e.g. gentamicin)

164
Q

What is the mechanism of action of amiophylline?

A

Amiophylline is a methylxanthine and acts as a phosphodiesterase inhibitor and adenosine receptor antagonist.

It therefore can act oppositely to adenosine in the heart and induce tachyarrhythmias. Therefore, for loading, a cardiac monitor needs to be applied.

165
Q

What is the criteria for starting Roflumilast in COPD?

A

In patients who continue to have persistent symptoms despite a long-acting muscarinic antagonist, beta-agonist and inhaled corticosteroid, roflumilast can be tried. Roflumilast is a phosphodiesterase inhibitor recommended by NICE as an option for treating severe chronic obstructive pulmonary disease if the following criteria are met:

Severe disease is defined as a forced expiratory volume in 1 second (FEV1) after a bronchodilator of less than 50% of predicted normal.

AND

The person has had 2 or more exacerbations in the previous 12 months despite triple inhaled therapy with a long-acting muscarinic antagonist, a long-acting beta-2 agonist and an inhaled corticosteroid.

166
Q

What are the features of zinc deficiency?

A

Causes a characteristic skin rash (mainly at the intertriginous and perioral areas), alopecia, taste impairment, glucose intolerance, and diarrhoea.

167
Q

How do you investigate secondary amenorrhoea?

A

First step: pregnancy test

Second step: Serum prolactin, TSH and FSH bloods

This will help differentiate between the most common causes of secondary amenorrhoes following pregnancy: hyperprolactinaemia, thyroid dysfunction and premature ovarian failure respectively.

168
Q

What are the clinical features of onchocerciasis?

A

Disease caused by the filarial nematode Onchocerca volvulus. The parasite is transmitted by blackflies of the genus Simulium, which deposit the parasites larva onto the skin when biting to extract blood. The adult worm lives in subcutaneous nodules and produces larvae, which become deposited in the skin and eyes. Disease manifests when the parasite dies in tissues and releases Wolbachia endosymbiotic bacteria into tissues, provoking a host immune response. This above patients disease has manifested as river blindness, where the worms die in the cornea and provoke chronic inflammation, eventually leading to clouding of the cornea. Inflammation in subcutaneous tissues leads to a pruritic rash and formation of a leopard-skin appearance over time. The worms can be visualised by microscopy of skin snip biopsy. The treatment of choice is ivermectin; DEC should not be used because rapid death of the worms can exacerbate damage to surround tissues and even cause complete blindness.

169
Q

What drug types should you consider stopping in linezolid therapy?

A

SSRIs

Linezolid was originally discovered as a psychotropic agent with antidepressant effects through mild reversible nonselective inhibition of monoamine oxidase (MAO), before it was found to have antibiotic efficacy against drug-resistant gram-positive cocci. In combination with serotonin agonists there is a risk of serotonin syndrome. Therefore, when using linezolid it must be considered to discontinue SSRIs.

170
Q

How do you treat tremor in parkinson’s disease? (rather than bradykinesia)

A

Tremor-predominant Parkinson’s disease can be highly disabling and tremor may persist despite standard treatment with dopaminergic agents, which primarily improve bradykinesia. First-line treatment is such cases is the addition of an anticholinergic drug such as procyclidine, orphenadrine, or trihexyphenidyl.

The main side-effect which limits the use of anticholinergics in older patients is cognitive dysfunction, and dementia is a relative contra-indication. Other side effects include blurred vision, urinary retention, nausea, constipation, and dry mouth.

Second-line treatments for persistent tremor include amantidine, clozapine, and propranolol. Deep brain stimulation may be used in refractory cases.

171
Q

How do you determine the difference between genital ulcers?

A

treponima pallidum- syphilis: painless ulcer painless lymphnodes (painless painless)

herpis simplex and haemophilus ducury (chanchroid) cause painful ulcer painful lymphnodes (painful painful)

lymphgranuloma venerum (chlamydia) and granuloma inguinale (Klebsiella granulomatosis) cause painless ulcer painful lymphnodes (painless painful)

172
Q

How do you test for Typhoid (enteric) fever?

A

B - blood culture in 1st week
A - agglutination (widal test) in 2nd wee
S - stool culture in 3rd week
U - urine culture in 4th week

173
Q

What are the diagnostic thresholds for diabetes both normally and in pregnancy?

A

A. DIABETES (normally):
fasting: >7, random(or 2 hour after 75g loading): 11.1

B. gestational diabetes: fasting:>=5.6, 2 hour glucose:>7.8

174
Q

What are the indications for hyperbaric oxygen therapy in carbon monoxide poisoning?

A

Loss of consciousness at any point
Neurological signs other than headache,
Myocardial ischaemia
Arrhythmia
Pregnancy

175
Q

When can NAC be stopped in paracetamol overdose according to toxbase?

A

INR is 1.3 or less, AND
ALT is within the normal range
If the ALT is above the normal range (with an INR of 1.3 or less),

acetylcysteine may still be stopped if:

ALT is less than two times the upper limit of normal AND
The increase in ALT value is not more than a doubling of the admission value

176
Q

What are the indications for plasma exchange in ANCA-associated vasculitis?

A

The indications for plasma exchange in ANCA-associated vasculitis are:

-Severe active renal disease (serum creatinine above 354 micromol/L or who require dialysis),
-Pulmonary haemorrhage,
-Concurrent anti-GBM autoantibody disease.

177
Q

How do you manage close contacts of TB confirmed patients?

A

If asymptomatic and younger than 65 years then test for latent TB. If Mantoux-negative and unvaccinated then offer vaccination. If at risk of HIV then test for HIV first.
If asymptomatic and older than 65 years then assess with a chest X-ray.

178
Q

How does cryptococcal meningitis cause increased intracranial pressure?

A

Raised intracranial pressure (ICP) is thought to be caused by the yeast cells and fungal polysaccharides forming microscopic plugs and blocking CSF resorption in the subarachnoid villi.

179
Q

When do you operate in mitral stenosis?

A

Cross sectional area of <1cm^2

180
Q

When should hydrazine and nitrate be considered in heart failure?

A

From most recent ESC Heart Failure guidelines (2016):

‘A subsequent RCT conducted in self-identified black patients (defined as being of African descent) showed that addition of the combination of hy- dralazine and isosorbide dinitrate to conventional therapy (ACEI, beta-blocker and MRA) reduced mortality and HF hospitalizations in patients with HFrEF and NYHA Classes III IV’

181
Q

How do you manage IgA nephropathy?

A

IgA nephropathy management

no proteinuria, normal GFR: observe
proteinuria: ACE inhibitor
signifcant fall in GFR/not responding to ACE inhibitor: corticosteroid

182
Q

What are the differentials of a complex opthalmoplegia?

A

Any patient presenting with eye movement weaknesses that cannot be explained by isolated or multiple cranial nerve palsies is called complex ophthalmoplegia. The differentials include myasthenia gravis, mononeuritis multiplex, thyroid eye disease, Kearns-Sayre syndrome, complex progressive external ophthalmoplegia, Miller-Fisher syndrome and botulinum poisoning.

183
Q

Why do you test for tropism in HIV diagnosis?

A

HIV binds to the CD4 cell via the CD4 receptor. This interaction also depends on viral interaction with the CD4 co-receptor. There are two forms of CD4 co-receptor CCR5 and CXCR4.

The test for viral tropism determines which of these co-receptors HIV will bind to. Maraviroc blocks HIV binding to the CCR5 receptor, and therefore is an effective drug in a ‘CCR5 tropic’ virus.

184
Q

What lung nodules do not need followed up?

A

Solitary, solid and non-calcified lung nodules of less than 5mm in size.

185
Q

What is the BTS guidance for lung nodules?

A

Nodule <5mm, or clear benign features, or unsuitable for treatment: can be discharged

Nodule =>8mm and high risk*: then CT-PET, and if CT-PET shows high uptake then biopsy

Nodule 5-6mm, or =>8mm and low-risk*: then CT surveillance
-CT surveillance: if 5-6mm then at 1 year, if =>6 then in three months

186
Q

What is the treatment for non-tuberculous mycobacterium?

A

It is important to have a basic understanding of two commonly identified groups: Mycobacterium avium complex (MAC) and Mycobacterium kansasii.

  • MAC: Rifampicin, clarithromycin and ethambutol. Treatment should continue until the patients sputum has remained negative for MAC for 12 months
  • M.kansasii: Rifampicin, isoniazid and ethambutol. Treatment should continue until the patient has been sputum culture negative for 12 months.

It is important that patients with NTM infection should never receive clarithromycin monotherapy due to concerns over development of resistance.

187
Q

What does elevated prolactin along with secondary hypothyroidism or hypogonadism indicate?

A

Stalk compression -> non-functioning pituitary adenoma.

188
Q

How do you adjust the gentamicin doses for someone on multiple daily dose regimens?

A

For multiple daily dose regimens of gentamicin, if the pre-dose (‘trough’) concentration is high, the interval between doses must be increased. If the post-dose (‘peak’) concentration is high, the dose must be decreased

189
Q

When do you switch rifampicin to another rifamycin in TB treatment and why?

A

Rifamycin containing anti-tuberculosis chemotherapy regimes are superior to those which do not contain a rifamycin agent. However, in this scenario the patient is also taking taking a protease inhibitor as part of their antiretroviral therapy.

Rifampicin, the common rifamycin agent in anti-tuberculosis regimes, is a potent inducer of liver enzymes, such as cytochrome P450. Furthermore, it up-regulates the expression of P-glycoprotein in the gastrointestinal tract. This leads to reduced absorption and increased metabolism of certain medications, protease inhibitors being one of these (ritonavir booster atazanavir). Co-administration of a protease inhibitor with rifampicin therefore will often lead to subtherapeutic levels of the protease inhibitor.

In this scenario, the patient is stable on his current antiretroviral treatment and not keen to switch at present. Therefore, the British HIV Association (BHIVA) suggest the substitution of rifampicin for an alternative rifamycin agent (rifabutin or rifapentine), which has less inducing action of cytochrome P450 and therefore allows the patient to continue their current HIV treatment regime. Regimes containing rifabutin (dose 150mg three times a week) have been shown to have equivocal in outcomes of treatment in the few small observational studies performed in patients with HIV/TB co-infection.

190
Q

When do you treat stage 1 hypertension?

A

treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greater

in 2019, NICE made a further recommendation, suggesting that we should ‘consider antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with stage 1 hypertension and an estimated 10-year risk below 10%. ‘. This seems to be due to evidence that QRISK may underestimate the lifetime probability of developing cardiovascular disease

191
Q

When do you add entresto in heart failure?

A

EF <35% and still symptomatic on B-blocker and ACEi

Replace ACEi after washout period

192
Q

When do you add ivabridine in heart failure?

A

Add if EF <35% and HR >75

193
Q

What is used for monitoring in medullary thyroid cancer?

A

Calcitonin is used for screening, prognosis and monitoring in medullary thyroid cancer. CEA is often used in conjunction with calcitonin

194
Q

What typical ECG finding indicates posterior infarction?

A

Tall R waves in V1-V2

195
Q

What is the new NICE guidelines regarding antiplatelets following ACS?

A

Prescribe DAPT (dual anti-platelet therapy). This is aspirin 75 mg daily plus ticagrelor 90 mg twice a day for 12 months. Ticagrelor is the preferred choice (even in those previously treated with clopidogrel) unless the bleeding risk outweighs the benefit. For people at high risk of bleeding, continue DAPT for at least one month.
For people with MI at high ischaemic risk who have tolerated DAPT without a bleeding complication, consider treatment with DAPT (ticagrelor 60 mg twice daily) in addition to aspirin for longer than 12 months and up to 36 months. If ticagrelor is not suitable, consider clopidogrel 75 mg daily (as well as aspirin) for longer than 12 months.

Aspirin and prasugrel is only recommended for patients undergoing percutaneous intervention and stenting

196
Q

What are the contraindications to renal biopsy?

A

Before a renal biopsy is performed, patients should have a renal tract ultrasound. The presence of polycystic kidneys, obstruction of the urinary tract, or hydronephrosis are regarded as absolute contraindications to biopsy

197
Q

What is the treatment for Pseudomonas bronchiectasis?

A

Ciprofloxacin

Second line: IV Taz, ceftazidime, aztreonam or meropenem

198
Q

Why do you check thyroid stimulating hormone receptor antibodies in pregnant women even if they are euthyroid?

A

The hypothalamopituitarythyroid axis is well developed at 12 weeks gestation but remains inactive until 1820 weeks. Circulating TSH receptor antibodies (TSH-RAB) in the mother can cross the placenta, and it is these, rather than the thyroid status of the mother, that cause neonatal thyrotoxicosis. The risk of hyperthyroidism to the neonate can be assessed by measuring TSH-RAB in the maternal circulation at the beginning of the third trimester. Antithyroglobulin antibody and thyroid peroxidase antibodies have no effect on the fetus.

199
Q

What is the treatment for actinic keratoses?

A

Prevention of further risk: e.g. sun avoidance, sun cream

fluorouracil cream: typically a 2 to 3 week course. The skin will become red and inflamed - sometimes topical hydrocortisone is given following fluorouracil to help settle the inflammation

topical diclofenac: may be used for mild AKs. Moderate efficacy but much fewer side-effects

topical imiquimod: trials have shown good efficacy

cryotherapy

curettage and cautery

200
Q

How does theophylline work?

A

Theophylline is a methylxanthine derivative drug which is structurally and clinically similar to caffeine. Aminophylline is the name given to theophylline when it is ligand bound to the chemical ethylenediamine which increases water solubility and hence aminophylline tends to be the intravenous form. Methylxanthine derivatives are used clinically for the treatment of bronchoconstriction in asthma, chronic obstructive pulmonary disease and in neonatal apnoea. They work in a two-fold fashion; firstly they inhibit the family of metabolic enzymes, the phosphodiesterases which increase levels of cyclic adenosine monophosphate and dampens the inflammatory cytokine cascade, and secondly they are competitive antagonists at the endogenous adenosine receptors located in the central nervous system, heart and lungs.

Inhibition of various phosphodiesterases causes a reduction in the circulating population of inflammatory cytokines and also increases cardiovascular and peripheral blood flow. Due to increased metabolism, hypokalaemia is common and gluconeogenesis and glycogenolysis is stimulated causing a rise in the plasma glucose load.

Competitive antagonism at the adenosine receptor causes roughly the opposite effects of adenosine. Whereas this drug is used clinically to slow the heart rate and block transmission at the AV node, theophyllines cause tachycardia and an increase in AV conduction, cardiac automaticity and an increase in myocardial contractility, ultimately leading to an increased cardiac output with hypertension and flushing. Inhibition of adenosine receptors in bronchioles causes relaxation and improved airflow, and in the central nervous system leads to agitation, headache, anxiety, tremor and insomnia.

Other symptoms of methylxanthine toxicity include extreme nausea and vomiting, pancreatitis, gastroesophageal irritation, psychiatric symptoms and seizures. Tachyarrhythmias may deteriorate into ventricular rhythms quickly which may be fatal. Competing metabolic acidosis and respiratory alkalosis may cause a mixed arterial blood gas picture and many electrolyte disturbances can occur but an unexplained hyperglycaemia with a hypokalaemia is very suggestive of theophylline toxicity. Theophylline has a narrow window of therapeutic efficacy and patients may become toxic rapidly if drugs which inhibit their metabolism are given concurrently, particularly antibiotics such as macrolides or fluoroquinolones.
Management of theophylline toxicity is largely supportive with seizures controlled by benzodiazepines or intubation. Phenytoin is best avoided as it can worsen arrhythmia. Electrolyte abnormalities must be corrected, particularly hypokalaemia and hypomagnesaemia. Hypertension and tachycardia may respond to beta-blockers but beware of making the situation worse in an asthmatic patient. Verapamil is an alternative. Ventricular rhythms should be electrically cardioverted.

Theophyllines are one of the few drugs which are highly adsorbed by activated charcoal and this should be considered even beyond an hour after ingestion due to the extended release nature of most preparations and the drugs slowing of gastric emptying

201
Q

What are the causes of eosinophilia?

A

Pulmonary causes
-asthma
-allergic bronchopulmonary aspergillosis
-Churg-Strauss syndrome
-Loffler’s syndrome
-tropical pulmonary eosinophilia
-eosinophilic pneumonia
-hypereosinophilic syndrome

Infective causes
-schistosomiasis
-nematodes: Toxocara, Ascaris, Strongyloides
-cestodes: Echinococcus

Other causes
-drugs: sulfasalazine, nitrofurantoin
-psoriasis/eczema
-eosinophilic leukaemia (very rare)

202
Q

What are the contraindications to NIV you should be aware about?

A
  • Recent facial or upper airway surgery or facial injuries.
  • Recent upper gastrointestinal surgery.
  • Confusion/agitation.
  • Bowel obstruction.
  • Upper airway obstruction.
  • Excessive upper airway secretions.
  • Patient actively vomiting.
203
Q

Azathioprine is associated with what type of cancer?

A

Increased risk of non-melanoma skin cancer.

204
Q

What is Mentzer’s Index?

A

Mentzer’s Index = MCV/red cell count
<13 points towards thalassaemia
>13 points towards IDA

205
Q

What is the bulging fissure sign?

A

The bulging fissure sign is an increasingly rare but classical feature of Klebsiella pneumonia. It is due to large volumes of consolidation (typically in the right upper lobe) causing displacement of the adjacent fissure.

206
Q

What are the indications for starting treatment in CLL?

A

-Progressive marrow failure: the development or worsening of anaemia and/or thrombocytopenia

Massive (>10 cm) or progressive lymphadenopathy

Massive (>6 cm) or progressive splenomegaly

Progressive lymphocytosis: > 50% increase over 2 months or lymphocyte doubling time < 6 months
-Only if initial count >30

Systemic symptoms: weight loss > 10% in previous 6 months, fever >38ºC for > 2 weeks, extreme fatigue, night sweats

Autoimmune cytopaenias e.g. ITP

207
Q

What are the diagnostic criteria for eosinophilic pneumonia?

A

acute respiratory illness of less than or equal to 1-month duration

pulmonary infiltrates on chest radiography or computed tomography (CT)

pulmonary eosinophilia as demonstrated by more than 25% eosinophils in BAL fluid (can be accompanied by variably increased percentages of lymphocytes and neutrophils) or eosinophilic pneumonia on lung biopsy (bronchoscopic or surgical), and

the absence of other specific pulmonary eosinophilic diseases e.g. eosinophilic granulomatosis with polyangiitis (previously known as Churg-Strauss syndrome)

208
Q

What findings support ABPA in patients with worsening asthma symptoms or steroid dependence?

A

Serum eosinophilia in steroid naïve patients and/or no history of recent steroid use
Elevated total serum IgE level (>1000 iU/ml), positive serum Aspergillus precipitins (IgM, IgG and IgE antibodies to Aspergillus species)
Sputum showing elevated eosinophil count and/or fungal mycelia with healthy cytoplasm (cf. dead mycelia devoid of cytoplasm seen in patients with Aspergilloma)
Immediate skin test reactivity to Aspergillus antigens
A massive homogeneous shadow without fissure displacement is the most common abnormality seen on a chest radiograph with ABPA
The bronchiectasis seen in ABPA is typically central

209
Q

What diseases recur following renal transplantation?

A

Membranoproliferative glomerulonephritis (notably type II) reoccurs in 80-100% of cases. This is lower in type I.

IgA reoccurs in up to around 60% of patients.

FSGS reoccurs in up to around 50% of patients.

Polycystic kidney disease and Alport’s syndrome do not reoccur in renal transplantation.

210
Q

What is the treatment for salicylate overdose?

A

If less than 1 hour after indigestion = gastric lavage

If over 1 hour = oral activated charcoal

If any serious features (seizure, coma, renal failure or pulmonary oedema) = dialysis

If level 300-600mg/l = rehydrate
If level 600-800mg/l = sodium bicarb
If level >800 mg/l = dialysis

211
Q

What is the target haemoglobin in CKD?

A

100-120

212
Q

In CKD you shouldn’t just go by ferritin levels for iron deficiency. Instead you should have overall understanding What other tests should be carried out in order of preference?

A

1) % hypochromic red cells (requires analysis within 6 hours) a value of >6% inidcates iron deficiency.

2) Reticulocyte Hb content where <29pg is diagnostic of iron deficiency anaemia

3) A combination of transferrin saturations (<20%) and ferritin (<100 mcg/l)

213
Q

What are the target ferritin levels for CKD patients?

A

There is a significant risk of over-replacement of iron in these patients, and NICE guidelines suggest that a patients ferritin should be kept below 800 ng/ml, and one should consider changing the patient’s iron replacement therapy in order to prevent this when their ferritin is higher than 500 ng/ml.

214
Q

When do you initiate phlebotomy in hereditary haemochromatosis and what regime do you use?

A

Phlebotomy is the mainstay of treatment in hereditary haemochromatosis and is indicated in all patients with a ferritin level greater than 1,000 microgram / L. Typical initial phlebotomy regimes are 400-500 ml every 1-2 weeks. Once ferritin level falls to the range 50-100 microgram / L, phlebotomy regime can transition to a maintenance schedule every 2-4 months.

215
Q

What is the best marker in determining the risk of developing cirrhosis in chronic hepatitis B?

A

Hepatitis B DNA level

216
Q

What is the management of subclinical hypothyroidism?

A

1.5.3 Consider levothyroxine for adults with subclinical hypothyroidism who have a TSH of 10 mlU/litre or higher on 2 separate occasions 3 months apart. Follow the recommendations in section 1.4 on follow-up and monitoring of hypothyroidism.

1.5.4 Consider a 6-month trial of levothyroxine for adults under 65 with subclinical hypothyroidism who have:

a TSH above the reference range but lower than 10 mlU/litre on 2 separate occasions 3 months apart, and symptoms of hypothyroidism.

217
Q

What are the NICE recommendations for cancer screening in metastatic disease of unknown primary?

A

NICE recommends the following investigations for all patients:
FBC, U&E, LFT, calcium, urinalysis, LDH
Chest X-ray
CT of chest, abdomen and pelvis
AFP and hCG

NICE recommends the following investigations for specific patients:
Myeloma screen (if lytic bone lesions)
Endoscopy (directed towards symptoms)
PSA (men)
CA 125 (women with peritoneal malignancy or ascites)
Testicular US (in men with germ cell tumours)
Mammography (in women with clinical or pathological features compatible with breast cancer)

218
Q

Capillary wedge pressure is equal to what?

A

Left atrial pressure

Can determine if mitral stenosis is present -> CWP - Left Ventrical pressure should be <5mmHg

219
Q

How do you monitor viral load in stable HIV?

A

HIV, once stable, should be monitored with a viral load every six months and CD4 counts annually at least once virological suppression, defined as sustained viral load less than <50 copies/ml, is established. If the viral load increases to between 50-200 copies/ml on a single sample this is defined as a viral blip and is unlikely to be significant, but a viral load should be re-tested within one month. If a viral load above >200 copies/ml is sustained this is a virological rebound and can imply failure. This can be due to new viral resistance, and, if suspected, would need resistance testing.

220
Q

What is the treatment for hypertension in CKD? How does this differ to normal guidelines?

A

ACEi are still first line.
-Decrease in eGFR up to 25% or rise in creatinine of up to 30% is acceptable.

Furosemide is useful as an anti-hypertensive in patients with CKD and has the added benefit of lowering serum potassium.

Thiazides are less useful if renal output is reduced as less urine makes it to the distal tubule.

221
Q

When can you discharge patients with dengue?

A

The plasma leak phase may occur anytime within the first 48 hours after the fever has broken and manifests with leakage into pleural and peritoneal spaces. It may be accompanied by shock and in some cases haemorrhage. Platelets and renal function may be falsely reassuring as they tend to improve after the febrile phase but rising haematocrit is a sensitive sign of plasma leak. It is therefore essential to monitor patients for a full 48 hours after the febrile phase and ensure haematocrit is stable prior to discharge. Platelets should be at least 50 * 109/l and rising prior to discharge.

222
Q

How do you determine if abacavir is safe to use in HIV?

A

Abacavir can cause a severe and sometimes fatal hypersensitivity reaction. It is a cell mediated delayed hypersensitivity reaction which occurs around 6 weeks after starting treatment. Symptoms are of fever, rash, malaise and gastrointestinal symptoms.

Patients without HLA B5701 are highly unlikely to develop hypersensitivity. Those with the HLA B5701 allele have a 50% risk and therefore in these individuals abacavir should be avoided.

It is therefore routine to test HLA B*5701 status on all newly diagnosed patients with HIV.

223
Q

What are the clinical features of Hereditary Neuropathy with Liability to Pressure Palsy (HNPP)?

A

The diagnosis is Hereditary Neuropathy with Liability to Pressure Palsy (HNPP). This is a neurological syndrome in which trivial trauma to a peripheral nerve e.g. sleeping on a limb, results in a mononeuropathy which may take weeks to resolve. It usually presents in second or third decade of life. The condition is most common in families with Dutch or German ancestry. It is caused by a deletion in the peripheral myelin protein 22 gene on chromosome 17. It is an autosomal dominant condition.

The patient’s presenting mononeuropathy is a common peroneal nerve palsy. Three years ago he had an ulnar nerve palsy and eight years ago he had a radial nerve palsy (also called Saturday night palsy).

Nerve conduction studies in HNPP are characteristic of a demyelinating neuropathy: conduction is slow and action potentials are small. Nerve biopsy may show a predominance of smaller fibres and localised thickening of the myelin sheath. These investigations are helpful in supporting the diagnosis although gene testing, if positive, is confirmatory.

Management is conservative with e.g. wrist splints, ankle-foot orthoses, and protective padding.

224
Q

What are the clinical features of pulmonary eosinophilia (Loeffler’s syndrome) over time and how does this relate to life cycle?

A

Simple pulmonary eosinophilia, aka Loeffler’s syndrome. This is caused by Ascaris lumbricoides, Strongyloides, or Ancylostoma. Infection with these worms is prevalent worldwide, especially in tropical and subtropical countries. Their eggs are passed in the stool of an infected person and then ingestion in food that has had contact with human sewage (they are surprising resilient eggs). The ingested eggs mature into larval worms in the gut and seed into the blood stream via the duodenal walls, from where they circulate around in the blood to eventually enter the lungs were they are coughed up (the pulmonary eosinophilia phase with wheeze and cough for around 2 weeks) and then swallowed back down and settle into mature worms in the small intestine, resulting in a chronic malabsorption condition. The pulmonary condition is self-limmiting although mebendazole given for 3 days can help.

225
Q

What is the pathergy test?

A

Pathergy test supports the diagnosis of Behcet’s (there is no definitive test)

This involves pricking the skin with a sterile needle, usually in the forearm. If the lesion becomes indurated within 48 hours, this is supportive of a diagnosis of Behcet’s. The test is positive in approximately 60% of patients.

226
Q

When can you monitor thyroid lumps in the community?

A

Consider monitoring the person in primary care with no need for specialist referral, depending on clinical judgement, if there is:
An adult with a history of a longstanding unchanging thyroid nodule or mass over several years, with no palpable cervical lymphadenopathy and no other red flags or risk factors for malignancy.
A non-palpable, asymptomatic thyroid nodule picked up incidentally on an ultrasound scan, CT, or MRI, which is less than 1 cm in diameter, with no associated lymphadenopathy and no other red flags or risk factors for malignancy.

227
Q

What is the classical presentation of Chlamydia psittaci infection?

A

Diarrhoea, epistaxis and high fevers.
Splenomegaly and low WCC are common

228
Q

How do you replace iron in CKD and how does it vary depending if they are on dialysis or not?

A

For people who are not receiving haemodialysis, consider a trial of oral iron before offering intravenous iron therapy. If they are intolerant of oral iron or target Hb levels are not reached within 3 months (see recommendation 1.3.11), offer intravenous iron therapy.

For people who are receiving haemodialysis, offer intravenous iron therapy. Offer oral iron therapy to people who are receiving haemodialysis only if:

intravenous iron therapy is contraindicated or

the person chooses not to have intravenous iron therapy after discussing the relative efficacy and side effects of oral and intravenous iron therapy. [new 2015]

229
Q

What is the target ferritin and transferrin saturations in CKD?

A

Ferritin >/= 200 (less then give EPO)
Transferrin saturation >/= 20%

230
Q

How do you manage measles?

A

Vitamin A
Supportive
Inform public health

Need admitted if pregnant of immunocompromised

231
Q

What is the treatment for gonorrhoea?

A

ciprofloxacin used to be the treatment of choice. However, there is increased resistance to ciprofloxacin (around 36% in the UK) and therefore cephalosporins are now more widely used
there was a change in the 2019 British Society for Sexual Health and HIV (BASHH) guidelines. Previously the first-line treatment was IM ceftriaxone + oral azithromycin. The new first-line treatment is a single dose of IM ceftriaxone 1g (i.e. no longer add azithromycin). If sensitivities are known (and the organism is sensitive to ciprofloxacin) then a single dose of oral ciprofloxacin 500mg should be given

If ceftriaxone is refused (e.g. needle-phobic) then oral cefixime 400mg (single dose) + oral azithromycin 2g (single dose) should be used

232
Q

How do you use prednisone in alcoholic hepatitis?

A

Prednisolone 40mg for 28 days has been shown to increase survival in patients with severe alcoholic hepatitis. However, response to steroid treatment should be re-evaluated at 7 days, as not all patients respond and continuing immunosuppressive treatment in patients who are unlikely to benefit may prove deleterious.

As a rule of thumb, an increase in bilirubin over the first 7-days indicates non-response. The Lille score is a more formal method of assessment that takes into account a range of demographic and laboratory values to give a more nuanced evaluation. A Lille score of > 0.45 signifies the failure of prednisolone and justifies its discontinuation. The 6-month survival rate for this group of patients is approximately 25% so supportive treatment should be continued

233
Q

What is the role for anti-TNFa therapy in alcoholic hepatitis?

A

inflammatory cytokine TNF-α is thought to be key to the pathophysiology of acute alcoholic hepatitis and several studies have investigated the efficacy of anti-TNF-α therapies in this setting. Unfortunately, a number of studies have shown that infliximab and etanercept are associated with higher mortality rates at 2 and 6 months, largely secondary to the development of acute infection. As a result, these agents are not recommended for use in alcoholic hepatitis

234
Q

What are the features of AVIR?

A

accelerated idioventricular rhythm (AIVR). It is associated with atrioventricular dissociation; P waves present but not associated with QRS complexes, wide QRS complexes (>120ms) and a rate between 50-110 beats per minute. AIVR is common post-MI following the reperfusion of an ischaemic myocardium. It is usually self-limiting and therefore treatment is not necessary, especially as the patient is asymptomatic and haemodynamically stable.

235
Q

When do you need to hold methotrexate and refer to rheum in rheumatoid arthritis?

A

1.white cell count <3.5 109/l;
2.mean cell volume >105 fL;
3.neutrophils <1.6 109/l;
4.creatinine increase >30% over 12 months and/or calculated GFR <60 ml/min;
5.unexplained eosinophilia >0.5 109/l;
6.ALT and/or AST >100 U/l;
7.platelet count <140 109/l;
8.unexplained reduction in albumin <30 g/l (GRADE 1C, 99%).
9. If mucositis/oral ulceration occurs.

Usually folic acid will be increased to 6 days a week (apart from methotrexate day)

236
Q

What are the indications for surgery in mitral regurgitation?

A
  1. EF < 60%
  2. Left ventricular end systolic diameter > 40mm
  3. New onset of AF or
  4. High likelihood of durable repair with low surgical risk and absence of risk factors
237
Q

What are the specific features of Yellow fever?

A

Travel to endemic area ( West Africa and Central America )
Fever, with initial resolution
Progression to jaundice and renal failure

Presence of councilman bodies in liver

238
Q

How do you treat rabies exposure?

A

Rabies immunoglobulin should be given to provide passive antibodies at the site of exposure prior to the development of an immune response. As far as possible, the dose (20 IU / Kg) should be administered locally around the wound. In addition, post-exposure vaccination should be provided, with the WHO currently recommending a four dose schedule (given on days 0, 3, 7 and 14).

If an individual has been previously vaccinated then immunoglobulin is not required and a two dose vaccination schedule (given on days 0 and 3) should be given.

239
Q

What is the treatment for acne and hirsuitism in PCOS?

A

a COC pill may be used help manage hirsutism. Possible options include a third generation COC which has fewer androgenic effects or co-cyprindiol which has an anti-androgen action. Both of these types of COC may carry an increased risk of venous thromboembolism

if doesn’t respond to COC then topical eflornithine may be tried

spironolactone, flutamide and finasteride may be used under specialist supervision.

240
Q

What is the treatment to induce ovulation in PCOS?

A

a 2007 trial published in the New England Journal of Medicine suggested clomifene was the most effective treatment. There is a potential risk of multiple pregnancies with anti-oestrogen* therapies such as clomifene. The RCOG published an opinion paper in 2008 and concluded that on current evidence metformin is not a first line treatment of choice in the management of PCOS

metformin is also used, either combined with clomifene or alone, particularly in patients who are obese

gonadotrophins

241
Q

What is the mechanism behind autonomic dysreflexia?

A

This clinical syndrome occurs in patients who have had a spinal cord injury at, or above T6 spinal level. Briefly, afferent signals, most commonly triggered by faecal impaction or urinary retention (but many other triggers have been reported) cause a sympathetic spinal reflex via thoracolumbar outflow. The usual, centrally mediated, parasympathetic response however is prevented by the cord lesion. The result is an unbalanced physiological response, characterised by extreme hypertension, flushing and sweating above the level of the cord lesion, agitation, and in untreated cases severe consequences of extreme hypertension have been reported, e.g. haemorrhagic stroke

242
Q

What is the treatment for cluster headaches?

A

The suggested first line treatment for cluster headaches is 100% oxygen at a flow rate of at least 12 litres per minute and a subcutaneous or nasal triptan. Evidence from one small study suggests that subcutaneous sumatriptan provides faster relief of symptoms than intranasal sumatriptan.

Indometacin is used in paroxysmal hemicrania which has similar characteristics to cluster headaches, but attacks tend to be shorter (2-45 minutes) and more frequent (up to 40/day) and more common in women.

243
Q

What is the treatment of rosacea

A

simple measures
recommend daily application of a high-factor sunscreen
camouflage creams may help conceal redness

predominant erythema/flushing CKS
-topical brimonidine gel may be considered for patients with predominant flushing but limited telangiectasia
-brimonidine is a topical alpha-adrenergic agonist
this can be used on an ‘as required basis’ to temporarily reduce redness
it typically reduces redness within 30 minutes, reaching peak action at 3-6 hours, after which the redness returns to the baseline

mild-to-moderate papules and/or pustules CKS
-topical ivermectin is first-line
alternatives include: topical metronidazole or topical azelaic acid

moderate-to-severe papules and/or pustules CKS
-combination of topical ivermectin and oral doxycycline

244
Q

What patients are candidates for “pill in the pocket regimen” for AF?

A

It can be considered in those with paroxysmal AF who:

Have no history of left ventricular dysfunction, valvular or ischaemic heart disease

Have infrequent episodes

Systolic blood pressure >100mmHg and heart rate >70bpm

Are able to understand when to take the tablet

245
Q

What is the treatment for Pseudomonas aeruginosa eradiation in CF?

A

There is no consensus on which anti-microbial strategy is best for Pseudomonas aeruginosa eradication. Options include:

-Intravenous anti-pseudomonal antibiotic plus inhaled aminoglycoside for 14 days
-A prolonged course of oral Ciprofloxacin (e.g. 6 weeks)

246
Q

What electrolyte abnormality does lithium cause?

A

Hypercalcaemia

247
Q

How do you identify and treat dialysis disequilibriation syndrome?

A

Dialysis disequilibrium syndrome is a rare but serious complication of haemodialysis. It is more likely to occur in patients with very high levels of urea, metabolic acidosis, extremes of age, and central nervous system diseases. High levels of urea result in fluid shifts in the brain. If urea is rapidly decreased, the result is a sudden drop in serum osmolarity, and a fluid shift from interstitial to intracellular compartments. The end result is cerebral oedema.

Cerebral oedema can present with headaches, focal neurological deficits, myoclonus, papilloedema and a decreased level of consciousness.

Dialysis disequilibrium syndrome can be treated with mannitol or hypertonic saline to increase plasma osmolarity and reduce cerebral oedema.

248
Q

What are the absolute contraindications to being a kidney donor?

A

Uncontrolled hypertension
Active malignancy
Chronic infection
Overt proteinuria
Bilateral renal artery atherosclerosis
Sickle cell disease

249
Q

What is the treatment for Parkinson’s dementia?

A

Rivastigmine

250
Q

What are the findings on muscle biopsy that can differentiate myosotis causes?

A

Endomysial CD8 positive T-cell mediated lymphocytic infiltrates that invade nonnecrotic muscle fibres = polymyositis

  • Perimysial inflammation by CD4 positive T-lymphocytes and parafascicular atrophy = dermatomyositis
  • Inflammatory infiltrates and inclusions within muscle fibres = inclusion body myositis
251
Q

When is systemic therapy used in psoriasis?

A

Offer systemic non-biological therapy to people with any type of psoriasis if:
It cannot be controlled with topical therapy and
It has a significant impact on physical, psychological or social wellbeing and one or more of the following apply:
psoriasis is extensive (for example, more than 10% of body surface area affected or a PASI score of more than 10) or
psoriasis is localised and associated with significant functional impairment and/or high levels of distress (for example severe nail disease or involvement at high-impact sites) or
phototherapy has been ineffective, cannot be used or has resulted in rapid relapse (rapid relapse is defined as greater than 50% of baseline disease severity within 3 months).

Choice of drugs:
Offer methotrexate as the first choice of systemic agent for people with psoriasis who fulfil the criteria for systemic therapy (above)
Offer ciclosporin as the first choice of systemic agent for people who fulfil the criteria for systemic therapy (above) and who:
need rapid or short-term disease control (for example a psoriasis flare) or
have palmoplantar pustulosis or
are considering conception (both men and women) and systemic therapy cannot be avoided.
Consider changing from methotrexate to ciclosporin (or vice-versa) when response to the first-choice systemic treatment is inadequate.
Consider acitretin for adults, and in exceptional cases only for children and young people, in the following circumstances:
if methotrexate and ciclosporin are not appropriate or have failed or
for people with pustular forms of psoriasis.

252
Q

What drugs cause bullous pemphigoid?

A

Furosemide
Captopril
Penicillin derivatives
Penicilliamine

253
Q

What patients are at risk of refeeding syndrome?

A

Patients are considered high-risk if one or more of the following:
-BMI < 16 kg/m2
-unintentional weight loss >15% over 3-6 months
-little nutritional intake > 10 days
-hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

If two or more of the following:
-BMI < 18.5 kg/m2
-unintentional weight loss > 10% over 3-6 months
-little nutritional intake > 5 days
-history of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids

254
Q

What are the diagnostic criteria for PAN?

A

Weight loss of 4 kg or more
Livedo reticularis
Testicular pain/tenderness
Myalgia or leg weakness/tenderness
Mononeuropathy or polyneuropathy
Diastolic blood pressure greater than 90 mm/Hg
Elevated blood urea nitrogen (BUN) or creatinine level unrelated to dehydration or obstruction
Presence of hepatitis B surface antigen or antibody in serum
Arteriogram demonstrating aneurysms or occlusions of the visceral arteries
Presence of polymorphonuclear neutrophils in a biopsy specimen from a small- or medium-sized artery

Three Out of 10 needed for the Dianosis of PAN.

255
Q

When do you commence medical therapy in hypertension?

A

ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)

-treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greater

in 2019, NICE made a further recommendation, suggesting that we should ‘consider antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with stage 1 hypertension and an estimated 10-year risk below 10%. ‘. This seems to be due to evidence that QRISK may underestimate the lifetime probability of developing cardiovascular disease

256
Q

What are the parameters of severe DKA?

A

pH < 7
Blood ketone > 6 mmol/L
Bicarbonate < 5 mmol/L
Anion gap >16 mmol/l
Potassium < 3.5 mmol/L on admission
Tachycardia or bradycardia
Systolic blood pressure <90 mmHg
Oxygen saturation <92% on air
GCS < 12

257
Q

What is the treatment for lead poisoning?

A

leaD
-Dmsa
-D penicillamine
-eDta
-Dimercaprol

EDta = used in ED (acute poisoning)
Others used in chronic poisoning.

258
Q

What other conditions are oligoclonal bands also found in?

A

Lyme disease
Systemic lupus erythematosus
Neurosarcoidosis
Subacute sclerosing panencephalitis
Subarachnoid hemorrhage
Syphilis
Primary central nervous system lymphoma
Sjögren’s syndrome
Guillain-Barre syndrome
Meningeal carcinomatosis
Neuromyelitis optica

259
Q

How do you differentiate Long QT 1,2 and 3 based on presentation?

A

Long QT1: adrenergic surge due to intense physical activity such as swimming

Long QT2: adrenergic surge due to intense emotion such as excitement or fear

Long QT3: death during sleep

260
Q

How do you manage gonorrhoea contacts?

A

For those presenting after 14 days of exposure we recommend treatment only following a positive test for gonorrhoea.

For those presenting within 14 days of exposure we recommend considering epidemiological treatment based on a clinical risk assessment and following a discussion with the patient. In
asymptomatic individuals, it may be appropriate to not give epidemiological treatment, and to repeat testing 2 weeks after exposure.

261
Q

What is the approach to off periods in Parkinson’s disease?

A
  • Separate levodopa from meals or take on empty stomach
  • Increase Levodopa dose or increase frequency or switch to extended release formulation
  • Add 2nd line agent
  • Consider rescue Mx for severe/unpredictable/Debilitating Off periods : S/C Apomorphine
262
Q

How do you diagnose Glanzmann’s thrombasthenia?

A

Glanzmann’s thrombasthenia is rare autosomal recessive platelet disorder caused by qualitative or quantitative deficiencies in GpIIb/IIIa, the receptor for fibrinogen.

Note the contrast to ITP, where antibodies are formed against GpIIb/IIIa.

The PFA-100 assay shows that platelets are not aggregating and this may be due to platelet glycoproteins or their interaction with von willebrand factor. The ristocetin effectively allows aggregation of von willebrand factor to GPIb and does not require GPIIb/IIIa. Therefore Glanzmann thrombasthenia will have normal platelet aggregation once ristocetin is added.

263
Q

What is the treatment for AIVR?

A

Accelerated idioventricular rhythm does NOT require treatment. But in real life, potassium would be supplemented to 4.5 and magnesium to 1.0, whether having ectopic activity or not.

Atropine can be given if symptomatic

264
Q

What is the treatment for myelofibrosis?

A

‘Ruxolitinib’ (JAK inhibitor) as first line for:
1. Symptomatic splenomegaly. (evidence grade 1A)
2. Myelofibrosis?related symptoms that are impinging upon quality of life. (evidence grade 1B)
3. Hepatomegaly and portal hypertension due to myelofibrosis are reduced by ruxolitinib (Verstovsek et al, 2010) and it can be considered for these indications. (evidence grade 2B).

Hydroxycarbamide can also be used first line but Ruxolitinib now preferred.

Thalidomide and prednisolone (in presence of cytopenias)
consider lenalidomide (if anaemic with platelet count >100 9 109/l).

265
Q

What are the types of lupus nephritis?

A

Class I Minimal mesangial lupus nephritis

Class II Mesangial proliferative lupus nephritis

Class III Focal lupus nephritis (active and chronic; proliferative and sclerosing)

Class IV Diffuse lupus nephritis (active and chronic; proliferative and sclerosing; segmental and global)
-Worst prognosis

Class V Membranous lupus nephritis

Class VI Advanced sclerosis lupus nephritis

266
Q

How do you differentiate between MMNCB and MND?

A

Multifocal Motor Neuropathy with Conduction Block

For exam purposes, the key difference between these two conditions is the nerve conduction studies. MMNCB shows conduction block. MND does not. MMNCB is a demyelinating condition, much in the same way Guillain Barré or chronic inflammatory demyelinating polyneuropathy (CIDP) are. However, in MMNCB this demyelination is in segments of a nerve rather than affecting the whole nerve. Therefore, the action potentials (as well as being slowed because of demyelination) actually don’t get past the areas of conduction block. The importance of doing nerve conduction studies is to decide whether a motor neuropathy is axonal (i.e. the axon itself getting damaged) or demyelinating. The demyelinating ones tend to be more easily and similarly treatable. MMNCB, Guillain Barré, and CIDP are all good examples of demyelinating neuropathies, all of which therefore respond to intravenous immunoglobulin (IVIG).

267
Q

What is the management of hypertension in CKD patients?

A

1.6.1 In adults with CKD and an ACR under 70 mg/mmol, aim for a clinic systolic blood pressure below 140 mmHg (target range 120 to 139 mmHg) and a clinic diastolic blood pressure below 90 mmHg. [2021]

1.6.2 In adults with CKD and an ACR of 70 mg/mmol or more, aim for a clinic systolic blood pressure below 130 mmHg (target range 120 to 129 mmHg) and a clinic diastolic blood pressure below 80 mmHg. [2021]

1.6.3 In children and young people with CKD and an ACR of 70 mg/mol or more, aim for a clinic systolic blood pressure below the 50th percentile for height. [2021]

268
Q

What percentage of GBS patients will experience long term weakness?

A

Up to 15%

269
Q

What are the 5 classes of pulmonary hypertension?

A

I pulmonary arterial hypertension
II pulmonary hypertension secondary to left heart disease
III pulmonary hypertension secondary to lung disease
IV pulmonary hypertension secondary to chronic thromboembolic disease
V pulmonary hypertension with unclear causes

270
Q

What is involved in a full myeloma screen?

A

FBC, ESR, U&E, calcium, albumin, uric acid
Serum protein electrophoresis
Urine protein electrophoresis
Immunoglobulin levels
Plain X-ray of symptomatic areas

271
Q

What is the management of Norwegian scabies?

A

Ivermectin

272
Q

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

A

Methanol
Uraemia (renal failure)
Diabetic ketoacidosis
Paracetamol use (chronic - caused by 5-oxoproline)
Isoniazid
Lactate
Ethanol or propylene glycol
Salicylates

273
Q

What side effect of ivabradine should you warn patients about?

A

Visual distubrance including the phenomenon of phosphenes, or “flashing lights”.

Other visual symptoms described include green discolouration of visual fields, blurring of vision and scintillating scotomata. Thes visual symptoms are usually transient and mild. They arise due to inhibition of similar ionic channels in the retina to the sinoatrial If channels. Approximately 20%of patients taking the drug develop some form of visual disturbance but only 1% need to discontinue therapy because of it.

274
Q

How do you differentiate the presentation of dengue and chikungunya fever?

A

It can be difficult to differentiate early in the disease. Two significant differences may help to distinguish between them:

1) In chikungunya, rashes appear on the torso and the arms while in dengue, they appear on the arms and the face.

2) Joint pain in chikungunya is experienced in the hands, wrists, feet and legs, while in dengue it is experienced in the shoulders and the knees.

275
Q

How do you differentiate between seborrheic dermatitis and scalp psoriasis?

A

Seborrhoeic dermatitis does not cross the hair line while psoriasis will.

276
Q

What is the treatment for scalp psoriasis?

A

First line is topical potent steroids for 4 weeks

Second line is either a different formulation (e.g. shampoo or mousse) and/or a topical agent to remove adherent scale (e.g. salicylic acid) before application of the potent steroid.

277
Q

What are the P450 enzyme inhibitors?

A

SICKFACES.COM

Sodium Valproate
Isoniazid
Cimetidine
Ketoconazole (and other azoles)
Fluoxetine (and other SSRIs)
Alcohol (acute) and grapefruit juice, amiodarone, allopurinol
Chloramphenicol
Erythromycin
Sulfonamides
Ciprofloxacin
Omeprazole
Metronidazole

278
Q

What is the treatment for Cryptosporidiosis?

A

Largely supportive for immunocompetent patients

If the patient has HIV and is not on antiretroviral therapy then this should be started and often will be enough to resolve the infection

Nitazoxanide may be used for immunocompromised patients.

Rifaximin is sometimes used for immunocompromised patients/ patients with severe disease.

279
Q

What are the indications for parathyroidectomy in primary hyperparathyroidism?

A

NICE recommend parathyroidectomy for most patients with diagnosed primary hyperparathyroidism due to the high cure rates (up to 98%) and reduced risk of drug side effects.

Conservative therapies are available and effective for some patients, however.

Surgery is indicated for those with one or more of:

  1. Symptomatic disease
    1a. Symptoms of hypercalcaemia
    1b. Osteoporosis and/or fragility fractures
    1c. Renal stones or nephrocalcinosis
  2. Age <50 years
  3. Serum adjusted calcium of 2.85 mmol/L or above
  4. Estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73m
280
Q

What antibiotics do you need to be careful starting in patients taking ciclosporin?

A

Ciclosporin is metabolised by CYP3A4, and clarithromycin and erythromycin are both potent CYP3A4 inhbitors, leading to a potential elevation in ciclosporin levels, and subsequent nephrotoxicity.

281
Q

What questionaire is used for diagnosing hyperventilation syndrome?

A

Nujmegen questionnaire

282
Q

What drugs are known to induce seizures?

A

Fentanyl, mefanimic acid, tramadol, aminophylline, isotretinoin, haloperidol, amitriptyline

283
Q

What patients qualify for CRT?

A

Must have all the following:

NYHA III or IV heart failure
Ejection fraction of <35%
The heart is beating regularly with evidence of electrical conduction disease
They are medication that is most effective for them

284
Q

How do you remember potency of topical steroids stronger than hydrocortisone?

A

EBCD (rather than usual ABCD) - Eumovate, Betnovate & Cutivate, Dermovate.

285
Q

What percentage of patients will re bleed following UGIE?

A

15%

The rate increases with the severity of original bleed. These patients need repeat endoscopy as an absolute indication

286
Q

What are the graft survival rates in renal transplants?

A

1 year = 90%, 10 years = 60% for cadaveric transplants

1 year = 95%, 10 years = 70% for living-donor transplants

287
Q

How do you determine if renal acute deterioration in renal function has become chronic?

A

NICE guidance would recommend the patient underwent a further renal function test in 2 weeks (to exclude causes of acute deterioration in eGFR), and then a further renal function test at 90 days after the original test. Should the patient’s eGFR remain in the same range as the initial test (45-59 ml / min / 1.73 m2) and if there continues to be no evidence of markers of kidney damage, then NICE guidance would recommend using measuring cystatin-C levels to confirm or rule out CKD.

288
Q

What is the evidence for determining prognosis post cardiac arrest with ROSC?

A

No clinical neurological signs have been shown to correlate reliably with poor outcomes when measured less than 24 hours after cardiac arrest.

Work by Rittenberger and colleagues (2010) looked at patients who suffered ventricular tachycardia or ventricular fibrillation cardiac arrests. They found that GCS motor score did not correlate with cardiac arrest outcome when measured at 24 or 72 hours. However, lack of pupillary light or corneal reflex at 72 hours was a reliable predictor of death.

Vestibulo-ocular reflexes are also used but are less reliable. No biochemical, imaging or neurophysiological studies are currently recommended for the assessment of prognosis.

289
Q

What is the criteria for hemicranectomy post stroke?

A

clinical deficits that suggest infarction in the territory of the middle cerebral artery, with a score above 15 on the NIHSS

decreased level of consciousness, with a score of 1 or more on item 1a of the NIHSS

signs on CT of an infarct of at least 50% of the middle cerebral artery territory:

with or without additional infarction in the territory of the anterior or posterior cerebral artery on the same side or

with infarct volume greater than 145 cm3, as shown on diffusion-weighted MRI scan.

290
Q

What is the conversion rate for morphine to fentanyl patch?

A

Approx 2.4

12.5 mcg = 30 mg oramorph
50 = 120
75 = 180
100 = 240

291
Q

What is the pharmacological treatment for mixed or overactive urinary incontinence?

A

NICE guidelines recommends first line pharmacological treatment for mixed incontinence or overactive bladder syndrome alone is either tolterodine, oxybutynin or darifenacin.

Duloxetine should only be used if the patient does not tolerate first line therapy and is not a candidate for surgery.

292
Q

How do you work up ?PE in pregnancy?

A

Venous thromboembolic event (VTE) is an important cause of maternal death in the UK. Pregnant women are 10x more likely to have a VTE than non-pregnant women of the same age.

Where there is suspicion of a pulmonary embolism (PE) , a chest x-ray should be performed initially. If this does not explain the patient’s symptoms, compression duplex dopplers should be performed. A diagnosis of deep vein thrombosis (DVT) can indirectly confirm a PE, reducing radiation doses for the mother.

If both tests are negative, and the clinical suspicion of PE remains high, further imaging should be organised; either CTPA or ventilation-perfusion scan (V/Q scan). British thoracic society guidelines (BTS) recommend a CTPA in non-pregnant women.

The decision as to which scan to perform should be ideally taken with the input from the patient. V/Q scanning carries a slightly increased risk of childhood cancer compared with CTPA but carries a lower risk of maternal breast cancer. The ventilation component of the V/Q scan may be able to be omited, reducing the radiation dose.

A D Dimer would not assist in the diagnosis, as it may be raised anyway in pregnancy due to disturbances in the coagulation system.

293
Q

What is the treatment for normal pressure hydrocephalus?

A

The definitive treatment for NPH is VP shunting. Symptoms of NPH including dementia are reversed with successful VP shunting in 60-90 % of the patients. 10% develop complications like postural headache, subdural effusion, shunt infection, and bacterial meningitis.

294
Q

When is the only time Alport syndrome patients can develop anti-GBM disease and why?

A

Anti-GBM is not possible since the patient’s don’t possess the antigenic target (disruption of basement membrane).

Anti-GBM can only occur in an Alport’s patient post transplant when they acquire the antigen within the normal basement membrane of the donor kidney.

295
Q

What is the treatment for latent TB?

A

Latent tuberculosis treatment options:
3 months of isoniazid (with pyridoxine) and rifampicin, or
6 months of isoniazid (with pyridoxine)

296
Q

What drugs are contraindicated in patients on Eviplera (emtricitabine/rilpivirine/tenofovir). HIV

A

PPIs

They reduce the absorption of rilpivirine which can cause viral blips, with subsequent virological failure and resistance

297
Q

What is the treatment of theophylline toxicity?

A

consider gastric lavage if <1 hour prior to ingestion
activated charcoal
whole-bowel irrigation can be performed if theophylline is sustained release form
charcoal haemoperfusion is preferable to haemodialysis

298
Q

How do you differentiate between the different types of meningococcal meningitis based on location?

A

Type A - Arabia, Africa
Type B,C - Europe, South America

299
Q

What is the treatment of polycythaemia Vera?

A

The mainstay of treatment of polycythaemia vera is aspirin and venesection. A target PCV < 0.45 has been shown to have a significantly lower rate of death from cardiovascular disease and major thrombosis than target PCV 0.45-0.50. Treatment with aspirin reduces the risk of non-fatal myocardial infarction, non-fatal stroke, pulmonary embolus, major venous thrombosis or death from cardiovascular cause compared to placebo. Aspirin does not increase the incidence of major bleeding episodes compared to placebo.

Cytoreductive treatments such as hydroxyurea are used to treat high-risk polycythaemia Vera.

300
Q

For which patients do you offer testing for gestational diabetes?

A

Any of the following risk factors:

-BMI >30
-Previous delivery of a baby over 4.5kg
-Previous gestational diabetes
-FHx of diabetes (1st degree relative)
-Minority ethnic family origin with a high prevalence of diabetes.

301
Q

When do you perform 2hour 75g oral glucose tolerance test in gestational diabetes?

A

24-28 weeks.

If the patient has had gestational diabetes in a previous pregnancy then early-self monitoring of blood glucose of OGTT as soon as possible after booking could also be used for diagnosis.

A diagnosis of gestational diabetes is made if the patient has either:
-Fasting glucose of 5.6 mmol/L or above OR a 2hr plasma glucose of 7.8 mmol/L or above

302
Q

What is the dose for treatment of PMR?

A

15 mg pred OD (taper over 2 years)

Pts should have a dramatic improvement in symptoms. If not then stop pred and consider alternative diagnosis.

303
Q

What conditions cause axonal and what cause demyelinating pathology on NCS?

A
  • demyelinating pathology (reduced conduction velocity, normal amplitude) = GBS, chronic inflammatory demyelinating polyneuropathy, amiodarone, hereditary sensorimotor neuropathies (HSMN) type I, paraprotein neuropathy, multiple myeloma
  • axonal pathology (normal conduction velocity, reduced amplitude) = alcohol, DM, vasculitis, B12 deficiency, hereditary sensorimotor neuropathies (HSMN) type II
304
Q

What are the diagnostic criteria for Neurofibromatosis type 1?

A

There are diagnostic criteria for NF1 that require at least two of seven criteria. Some of these do not appear until later childhood or adolescence, and so confirmation of the diagnosis may be delayed and children should be followed up:

At least six café-au-lait spots or hyperpigmented macules. They must be at least 5 mm wide in children younger than 10 years and 15 mm in adults.
Axillary or inguinal freckles.
Two or more typical neurofibromas or one plexiform neurofibroma.
Optic nerve glioma.
Two or more iris hamartomas. They are called Lisch nodules and are seen by slit-lamp examination.
Sphenoid dysplasia or typical long-bone abnormalities such as arthrosis.
Having a first-degree relative with NF1.

305
Q

What are the diagnostic criteria for neurofibromatosis type 2?

A

At least one of the following three is required for diagnosis of NF2:

Bilateral 8th nerve masses on MRI scan.
A first-degree relative with NF2 for a unilateral 8th nerve mass.
A first-degree relative with NF2 for an individual with at least two of the following:
Meningioma
Glioma
Schwannoma
Juvenile cataracts

306
Q

What does HBsAg mean?

A

Surface antigen - detects whether a person is currently infected with hepatitis B

307
Q

What does anti-HBs mean?

A

Indicates whether immunity to the virus is present.

Is therefore present in people with either previous immunisation or infection.

308
Q

What does anti-HBc mean?

A

Indicates previous and/or ongoing infection with hepatitis B.

It can be further subdivided into IgG and IgM which indicates a timeframe for infection.

IgM is present in infection of <6 months
IgG is present in infections of >6 months

309
Q

What is the treatment for chronic prostatisis?

A

A prolonged course of a quinolone (e.g. 4 week course of ciprofloxacin)

310
Q

What is the treatment for Brucellosis?

A

Oral treatment of brucellosis is possible with a 6-week course of doxycycline and rifampicin. An alternative treatment regime combines 6 weeks of oral doxycycline with 3 weeks of either intramuscular streptomycin or intravenous gentamicin. Treatment involving parenteral antibiotics has a lower failure rate but is less convenient for the patient.

311
Q

How do you treat membranous glomerulonephritis?

A

The main difference in the management of membranous glomerulonephritis and the other glomerulopathies is that high dose steroids and azathioprine are not associated with any significant benefits in the former. The main treatment strategy involves control of blood pressure with ACE inhibitors and immunosuppression with either cyclophosphamide, chlorambucil, ciclosporin or mycophenolate mofetil along with prednisolone. Rituximab has also been shown to have a benefit in the short term.

312
Q

What are the causes of membranous glomerulonephritis?

A

idiopathic: due to anti-phospholipase A2 antibodies

infections: hepatitis B, malaria, syphilis

malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia

drugs: gold, penicillamine, NSAIDs

autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid

313
Q

What percentage of sarcoid patients have a negative ACE?

A

25%

314
Q

What are the guidelines for following up incidental pulmonary nodules?

A

Broadly:
Nodules < 5 mm require no further surveillance.
Nodules 5-6mm require CT at 1 year
Nodules 6-8 mm require CT at 3 months
Nodules > 8 mm require malignancy risk calculation using the Brock model and should then have CT or PET according to whether this risk is > 10%.

The Brock model (see McWilliams et al) takes into account age, gender, family history and features of the nodule

315
Q

How do you manage fatigue in MS?

A

Once other problems (e.g. aneamia, thyroid or depression) have been excluded NICE recommend a trial of amantadine

Other options include mindfulness training and CBT

316
Q

How do you manage spasticity in MS?

A

Baclofen and gabapentin are first line. Other options include diazepam, dantrolene and tizanidine.

Physiotherapy is important

Cannabis and botox are undergoing evaluation

317
Q

How do you manage bladder dysfunction in MS?

A

may take the form of urgency, incontinence, overflow etc

guidelines stress the importance of getting an ultrasound first to assess bladder emptying - anticholinergics may worsen symptoms in some patients
-if significant residual volume → intermittent self-catheterisation
-if no significant residual volume → anticholinergics may improve urinary frequency

318
Q

How do you mange oscillopsia in MS? (visual fields appear to oscillate)

A

Gabapentin is first line

319
Q

What is the pathophysiology of thunderstorm asthma?

A

Thunderstorm asthma is a rare event in which the pressure changes in a thunderstorm causes the release of pollen and spores which trigger asthma exacerbation, which can occur in people not previously known to have asthma. The wet conditions at the beginning of a thunderstorm can cause pollen grains to rupture leading to increased amounts of allergen as well.

320
Q

What are the findings on muscle biopsy of polymyositis?

A

Endomysial lymphocytic infiltrates that invade nonnecrotic muscle fibres

321
Q

What are the findings on muscle biopsy of dermatomyositis?

A

Perimysial inflammation of lymphocytes and parafascicular atrophy

322
Q

What are the findings on muscle biopsy of inclusion body myositis?

A

Inflammatory infiltrates and inclusions within muscle fibres

323
Q

What are the differentials for an anterior mediastinal mass?

A

thymoma
lymphoma
thyroid and parathyroid malignancies
germ cell tumours e.g. teratomas
thoracic aortic aneurysm

324
Q

What are the features of selective IgA deficiency?

A

The most common primary antibody deficiency
Affected patients may develop recurrent chest infections, bronchitis, sinusitis or even otitis media.
Associated with atopic disorders such as asthma and atopic dermatitis.
Some patients may also be at risk of severe transfusion reactions.

325
Q

What are the features of wisckott-Aldrich syndrome

A

Characterised by a triad of recurrent chest infections/recurrent sinus infections
Atopic dermatitis
Thrombocytopenia and platelet dysfunction
Inherited as an X linked recessive condition.

326
Q

When can you stop NAC in staggered overdose?

A

In staggered overdoses, clinically significant hepatotoxicity is unlikely and the patient is not considered to be at risk if all of the following criteria are fulfilled:
at least 4 hours or more since the last paracetamol ingestion
the patient has no symptoms suggesting liver damage
the paracetamol concentration is less than 10 mg/L
the ALT is within the normal range, and their INR is 1.3 or less.
Acetylcysteine can be discontinued in patients not considered to be at risk of clinically significant liver damage e.g. if all the criteria are met

327
Q

What myositis specific antibodies are there?

A

Myositis-specific antibodies are targeted against three types of proteins:

Transfer ribonucleic acid (tRNA) synthetases: whilst a number of antibodies have been described, the main one is the Anti-Jo-1 antibody. Patients who are Anti-Jo-1 positive tend to have interstitial lung disease, arthritis (non-deforming) and fevers.

Nuclear Mi-2 protein: these are seen in approximately 20% of patients with myositis, and are more specific for dermatomyositis.

Signal recognition peptide (SRP): anti-SRP antibodies are seen in approximately 5% of patients with polymyositis, and are associated with poor response to treatment and a poor prognosis.

328
Q

What is the mechanism of omalizumab?

A

Anti-IgE

Omalizumab is an anti-IgE monoclonal antibody recommended by NICE for patients with severe allergic asthma which is refractory to other treatments including multiple courses of oral corticosteroids per year. The manufacturer recommends that the drug is only used in patients who have a positive skin test to a recognised respiratory allergen.

329
Q

What is the treatment for ADPKD?

A

In an individual of 15-39 years of age with a family history of ADPKD, a renal ultrasound with a total of three or more cysts is considered to be diagnostic of the disease.

The HALT-PKD trial demonstrated that individuals aged 15-49 years with early ADPKD (eGFR > 90), treatment with an ACE inhibitor that successfully achieved a blood pressure target of < 110 / 75 mmHg benefited from a reduction in the annual increase in total kidney volume and other outcomes compared to higher blood pressure targets.

(Younger age group because obviously low blood pressure in older group may be unrealistic)

In England and Wales, tolvaptan is recommended for patients with rapidly progressive disease at chronic kidney disease stage 2-3.

330
Q

What are the HHV 1-8?

A

1 - HSV1
2 - HSV2

3-5 are in reverse alphabetical order:
3 - VZV
4 - EBV
5 - CMV

6 - sixth disease
7 - similar to sixth disease, often asymptomatic
8 - risk for Kaposi and Castleman’s

331
Q

What is the triad of Zieve’s syndrome?

A

Zieve syndrome is a triad of symptoms: haemolytic anemia, cholestatic jaundice, and transient hyperlipidemia

332
Q

What is the management of hypercalcaemia?

A

The initial management of hypercalcaemia is rehydration with normal saline, typically 3-4 litres/day. Following rehydration bisphosphonates may be used. They typically take 2-3 days to work with maximal effect being seen at 7 days

Other options include:
Denosumab- given weekly
calcitonin - quicker effect than bisphosphonates
steroids in sarcoidosis

Loop diuretics such as furosemide are sometimes used in hypercalcaemia, particularly in patients who cannot tolerate aggressive fluid rehydration. However, they should be used with caution as they may worsen electrolyte derangement and volume depletion.

333
Q

What is the risk of vertical transmission in hepatitis c?

A

Risk of vertical transmission with hepatitis C is generally low and up to 6%. The risk of transmission appears to be high in women with HIV co-infection or high viral load.

334
Q

How do you differentiate the types of congenital adrenal hyperplasia?

A

Mnemonic : 1 in front- HTN. 1 at back- virilisation

21- hydroxylase: 1 at back only so: no HTN, only virilisation
11-hydroxylase: 1 in both front and back- so both HTN and virilisation
17- only 1 in front- so only HTN,no virilisation

335
Q

What are the deficiencies that cause CAH?
How do the features of the syndrome arise?

What role does short synACTHen test have?

A
  1. 21 hydroxylase mutation (90% of CAH).

This mediates conversion of 17OH-progesterone to 11-deoxycortisol and progesterone to deoxycorticosterone. Loss of function results in reduced cortisol and aldosterone and subsequent elevation in ACTH. This causes overstimulation of the adrenal cortex (hyperplasia). The steroid precursors are forced down the sex hormone pathway leading to androgen excess (ambiguous genitalia, salt wasting, hypovolaemia and shock i.e classic type). Presentation of 21 hydroxylase deficiency can also be asymptomatic with androgen excess become a problem in late childhood i.e. non-classic (premature pubarche, accelerated bone age, acne, hirsutism, oligomenorrhoea and this mimics polycystic ovarian syndrome).

  1. 11-beta hydroxylase mutation (5% of CAH).

Raised BP as 11-deoxycortisol has some aldosterone activity. Also raised androgens.

  1. 17-alpha hydroxylase deficiency

Raised aldosterone but low androgens.

  1. 3-beta steroid dehydrogenase

Low aldosterone and low androgens.

The short synacthen test is helpful when 17OH-progesterone is only modestly elevated (if 17OH-progesterone is very high then it is diagnostic). Measuring 17OH-progesterone at 0 and 60 mins after ACTH causes elevated responses in patients with CAH (>35 nmol/L

336
Q

Direct thrombin inhibitor choice in CKD?

A

Argatroban (hepatic excretion)

Bivaludin contraindicated eGFR <30

337
Q

What are the indications for mitral valve replacement?

A
  1. EF < 60%
  2. Left ventricular end systolic diameter > 40mm
  3. New onset of AF or
  4. High likelihood of durable repair with low surgical risk and absence of risk factors
338
Q

What common drug must azathioprine not be given with?

A

azathioprine must not be given in conjunction with allopurinol as the 2 drugs cause an increased risk in haematological toxicity, such as that seen in this patient.

339
Q

What are the common side effects of checkpoint inhibitors?

A

Immune checkpoint inhibitors are a type of immunotherapy that are increasingly being used to treat certain types of cancer, as an alternative to cytotoxic chemotherapy. They are currently only used to treat solid tumours. They work by enhancing the bodies own T-cell population to destroy the cancer cells.

Their side effect profile reflects their mechanism of action and are, therefore, inflammatory and autoimmune in nature. They include:

Dry, itchy skin and rashes (most commonly)
Nausea and vomiting
Decreased appetite
Diarrhoea
Tiredness and fatigue
Shortness of breath and a dry cough.

340
Q

Who qualifies for shingles vaccine?

A

People aged between 70-79 years old are eligible for shingles vaccine

Even if had chickenpox as immunity will have worn of

341
Q

What are the pulses found in atrial regurgitation?

A

Corrigan pulse – A ‘water hammer’ or ‘collapsing’ pulse is characterised by a rapidly rising and falling arterial pulse during late systole and diastole with wide pulse pressure. This finding is best appreciated by palpation of the radial or brachial arteries (exaggerated by raising the arm) or the carotid pulses.

De Musset’s sign – A head bob occurring with each heartbeat.

Traube’s sign – A pistol shot pulse (systolic and diastolic sounds) heard over the femoral arteries.

Duroziez’s sign – A systolic and diastolic bruit heard when the femoral artery is partially compressed.

Quincke’s pulses – capillary pulsations in the fingertips or lips.

Mueller’s sign – systolic pulsations of the uvula

342
Q

How do you differentiate Romano ward and Jervell-Lange-Nielsen syndrome

A

RomaNO Ward = NO deafness

343
Q

What are the contraindications to peritoneal dialysis?

A

Absolute
Patient or carer unable to train adequately in the technique.
Inguinal, umbilical, or diaphragmatic hernias (esp.
pleuroperitoneal leak).
Ileostomy or colostomy.
Abdominal wall infections or intra-abdominal sepsis, e.g. active
diverticular disease.

Relative
Abdominal surgeries (adhesions). The more extensive the surgery, the
more likely PD will be unsuccessful.
Morbid obesity (inadequate clearance).
Huge polycystic kidneys (insufficient intraperitoneal space).
Severe gastroparesis (worsening vomiting).
Severe lung disease (diaphragmatic

344
Q

What are the choices of DMARD in psoriatic arthritis?

A

Methotrexate is very effective at improving psoriatic arthritis but in addition to this it also has a dramatic effect on skin disease to a much greater extent than the other disease modifying anti-rheumatic drugs (DMARDs) listed. Therefore it is the DMARD of choice in psoriatic arthritis. If there was a contraindication to methotrexate leflunomide would be used second line for peripheral psoriatic arthritis. You would only use infliximab or another anti-TNF drugs first line if the patient had a predominantly axial spondyloarthropathy.

345
Q

What is the treatment for anterior uveitis?

A

Cyclopentolate is a muscarinic antagonist, and cycloplegic. It relieves the pain associated with uveitis as it dilates the pupil and prevents iridospasm. Atropine is another cycloplegic medication that can be used in anterior uveitis. Used alone it is less appropriate than the combination of cyclopentolate drops and steroids

346
Q

What are the features of mitral stenosis?

A

dyspnoea
↑ left atrial pressure → pulmonary venous hypertension
haemoptysis
due to pulmonary pressures and vascular congestion
may range from pink frothy sputum to sudden haemorrhage secondary to rupture of thin-walled and dilated bronchial veins
mid-late diastolic murmur (best heard in expiration)
loud S1
opening snap
indicates mitral valve leaflets are still mobile
low volume pulse
malar flush
atrial fibrillation
secondary to ↑ left atrial pressure → left atrial enlargement

347
Q

What is the urgent treatment of botulism?

A

Trivalent antitoxin

348
Q

What is the treatment for Wilson’s disease?

A

First line pharmacological treatment aims to prevent copper absorption by using chelating agents. Penicillamine is a potential first line treatment however, in this case, there is a high risk of a hypersensitivity reaction given this patients history of penicillin allergy.

Trientine is now a popular first line treatment of neurological and hepatic disease in Wilsons as it has a better side-effect profile than penicillamine. In this patient with a penicillin allergy it would certainly be the treatment of choice.

349
Q

What is the workup for thyroid nodules?

A
  1. Check TSH
  2. TSH suppressed → Thyroid uptake scan → Cold/iso nodule → FNA cytology
  3. TSH suppressed → Thyroid uptake scan →Hot nodule → No FNA required
  4. TSH normal/elevated → Thyroid USS → Suspicious features → FNA cytology
  5. FNA cytology is then graded using the Royal College of Pathologist classification on a spectrum from benign → malignant.
350
Q

What patients should be referred for a carotid endarterectomy?

A

Patients with a TIA or small ischaemic stroke with evidence of significant carotid artery stenosis (male patients with a carotid artery stenosis of 50-99% or female patients with a carotid artery stenosis of 70-99%) that corresponds to the same side as the stroke/TIA should be considered for an urgent carotid endarterectomy (CEA) within 14 days.

351
Q

What are the contraindications to lung cancer surgery?

A

FEV1<1.5 Litres
Vocal cord paralysis
Malignant effusion
SVCO
Stage IIIb or IV (mets)

352
Q

When do you give PRC in UGIB?

A

Transfuse as per local massive bleeding protocol, recognising that over transfusion is as damaging as under transfusion and that a restrictive transfusion policy (aiming for 70-80 g/L is suggested in haemodynamically stable patients.

353
Q

When do you give platelets in UGIB?

A

Do not offer platelets to patients who are actively bleeding and are haemodynamically stable. To those still actively bleeding, offer platelets if count is <50 x 109/L. This patient does not need platelets as his platelet count is above the threshold at which it would be beneficial.

354
Q

How do you differentiate nocardosis from TB on AAFB

A

Acid-fast stain which shows partially acid fast branching rods organism in contrast to mycobacterium which does fully stain.

355
Q

What is oligosecretory myeloma?

A

In approximately 1-2% of myeloma cases, the myeloma cells produce very low amounts of paraprotein, which can only be detected using the serum free light chain test. This is called oligosecretory myeloma

356
Q

How do you confirm eradication in strongyloides?

A

Repeat serological testing is the best method of confirming Strongyloides stercoralis eradication following treatment. A post-treatment to pre-treatment titre ratio of < 0.6 is taken to represent a good indicator of treatment success

357
Q

What is the treatment escalation of HOCM?

A

Medical treatment of HOCM consists of starting either a beta blocker, typically propranolol (but contraindicated in this case due to asthma) or a non-dihydropyridine calcium channel blocker, typically verapamil. In the case of persistent symptoms despite monotherapy, American Heart Association and European Society of Cardiology recommend consideration of disopyramide, a negative inotropic 1a anti-arrhythmic that demonstrated a significant decrease of LVOT gradients and mortality when compared to placebo. However, its significant cholinergic side effects and concerns of pro-arrhythmias, restricts its use to a second line agent. Surgical myectomy, DDDR pacemakers and alcohol ablation should be considered in patients who continue to be symptomatic despite 2 agents.

358
Q

What timescale does SJS usually develop?

A

1-4 weeks

359
Q

How do you manage confirmed isoniazid resistance in TB?

A

First 2 months: Rifampicin, pyrazinamide and ethambutol

Continue: rifampicin and ethambutol for 7 months (up to 10 months for extensive disease)
In MDR TB you add a quinolone or aminoglycoside.

360
Q

What is the treatment for multibacillary leprosy?

A

Dapsone, rifampicin and clofazimine for a two year period.

361
Q

What is the treatment escalation for IBS with predominant constipation?

A

Recent changes in NICE guidelines suggested that when a patient with IBS has resistant constipation despite using multiple laxatives with proper doses, linaclotide (which is a guanylate cyclase-C receptor agonist) should be used as the next step in management. It works by increasing intestinal fluid secretion and transit and decreases visceral pain.
Lactulose is not advised by NICE to be given in patients with IBS.
Adding a TCA or SSRI is the next step after linaclotide if it is found to be of no benefit.

362
Q

What are the clinical features of POEMS syndrome?

A

POEMS
Polyneuropathy
Organomegaly
Endocrinopathy
M-protein band from a plasmocytoma
Skin pigmentation

363
Q

What is the treatment for optic neuritis?

A

The recent optic neuritis treatment trial (ONTT) compared the use of oral prednisolone and intravenous methylprednisolone in acute optic neuritis1. Intravenous methylprednisolone increased the speed of visual recovery and reduced the risk of conversion to multiple sclerosis at 2 years while oral prednisolone demonstrated neither benefits. Intravenous steroids do not improve visual function at 2 years compared to placebo however. Intravenous immunoglobulin has no proven benefit.

364
Q

How do you differentiate UIP from NSIP?

A

the HRCT findings of basal predominance fibrosis and honeycombing is consistent with a usual interstitial pneumonia (UIP) pattern. Traction bronchiectasis may or may not be present in UIP.

Non-specific interstitial pneumonia (NSIP) is radiologically characterized by symmetric bilateral areas of ground-glass opacity with superimposed fine reticular opacities but with no or only minimal

365
Q

When do you use theophylline first line in bradycardia?

A

Atropine is usually the first line treatment for bradycardia and if that fails then consider transcutaneous or transvenous pacing. However, in patients with heart transplant atropine is contraindicated. The hearts of these patients are denervated and do not respond to vagal blockade by atropine, which might precipitate paradoxical sinus arrest of high-grade block. In these cases, theophyline intravenousely is indicated.

366
Q

What is the treatment for nephrogenic diabetes insipidus?

A

Hydrochlorothiazide and indometacin are used in the management of nephrogenic DI, however, indometacin is contraindicated in patients with recurrent gastrointestinal bleeding, therefore hydrochlorothiazide is the correct

367
Q

Talk through the different medications used in C1-esterase deficiency

A

A C1-esterase inhibitor can be used for short-term prophylaxis before procedures or to terminate acute attacks of hereditary angioedema. Conestat alfa and icatibant are licensed for the treatment of acute attacks of hereditary angioedema in adults with C1-esterase inhibitor deficiency. Tranexamic acid and danazol are used for short-term and long-term prophylaxis

368
Q

When do you carry out thymectomy in myasthenia gravis?

A

Thymectomy is a well recognised treatment for myasthenia gravis and should also be considered in non-thymomatous generalised myasthenia in patients with antibodies to acetylcholine receptor who are aged under 50. Biopsy is not generally required prior to surgery.

However, thymectomy is not generally carried out in myasthenia gravis when patients have antibodies to MUSK, late onset disease or purely ocular disease

369
Q

When do you perform surgery for aortic regurgitation in Marfan’s syndrome?

A

Surgery for aortic regurgitation is indicated if there is significant enlargement of the ascending aorta, severe regurgitation with symptoms or if severe with an ejection fraction of less than 50%. ACE inhibitors can be useful when there is hypertension, when surgery is contraindicated or when ventricular dysfunction persist following surgery

370
Q

What is the treatment for flu in severe immunosuppression?

A

Whilst in most cases, oseltamivir (a neuraminidase inhibitor) is first line treatment for influenza, the BNF advises that for severely immunocompromised individuals zanamivir should be first line treatment. This can help reduce the length of symptoms and prevent complications from developing during the course of the infection.

371
Q

What post renal transplant complications are caused by EBV infection?

A

Post transplant lymphoproliferstive disorder (PTLD):

-weight loss
-anaemia
-lymphadenopathy

Immunosuppression precipitates infection with EBV and subsequent B cell proliferation. PTLD incidence is highest in the first year post transplantation, Wbu CV is the time when immunosuppression is the most intense.

Treatment involves reducing current immunosuppression therapy and giving additional chemotherapy.

372
Q

What is the post renal transplantation complications of BK virus?

A

Graft dysfunction and ureteric stenosis

373
Q

What are the features of a Holmes tremor?

A

Irregular low frequency tremor which is a combination of RESTING (unlike cerebellar), postural and action tremor.

Lesion in the red nucleus. Most commonly previous stroke but may also be structural disorders like MS, tumour etc.

Treatment includes medical therapy such as levodopa however thalamotomy or Groningen thalamus stimulation have also shown to play a role in managing this condition.

374
Q

What is the hallmark feature of iron overdose on bloods?

A

Hyperglycaemia. Not many drugs in overdose cause this at all.

375
Q

Which people exposed to a patient with bacterial meningitis require prophylaxis?

A

Close contacts within 7 days.

Ciprofloxacin is the drug of choice with rifampicin second line.

376
Q

What drug should you avoid in atrial flutter?

A

Flecainide

377
Q

What is the classic triad of neurology in B12 deficiency?

A

Brisk knee, absent ankle and extensor plantar reflexes.

378
Q

What are the features of POEMS syndrome?

A

POEMS syndrome is a rare paraneoplastic syndrome caused by a clone of abnormal plasma cells. It is associated with polyneuropathy, organomegaly, endocrinopathy, M-protein band from a plasmocytoma, and skin pigmentation

379
Q

What is the treatment for relapsed Grave’s Disease?

A

Radio-iodine therapy

380
Q

What is the treatment escalation for HOCM?

A

1st line: B-Blocker (verapamil if asthma)

2nd line: Disopyramide

3rd line: Myectomy, DDDR pacemaker, alcohol ablation

381
Q

Define Mild, Moderate and Severe ulcerative colitis.

A

Mild: <4 stools per day, only a small amount of blood

Moderate: 4-6 stools per day, varying amounts of blood, no systemic upset.

Severe: >6 bloody stools per day and features of systemic upset (pyrexia, tachy, inflammatory markers)

382
Q

What is the treatment for mild to moderate colitis flare?

A

Topical (rectal aminosalicylate)
-If extensive also add an oral aminosalicylate

If remission not achieved within 4 weeks then add oral aminosalicylate

If remission still not achieved add topical or oral corticosteroid

383
Q

What is the treatment for severe colitis?

A

IV steroids (ciclosporin may be used if steroids contraindicated)

If after 72 hours there is no improvement, consider adding IV ciclosporin to IV steroid or consider surgery

384
Q

How do you manage ulcerative colitis following severe relapse or >/=2 exacerbations in past year?

A

Oral azathioprine or oral mercaptopurine

385
Q

What are the features of thallium poisoning?

A

Triad is virtually pathognomic:
-Fluctuating mood, with or without confusion
-Painful distal parasthesia
-Alopecia

In massive exposure, death from neuromuscular respiratory failure is rapid, but in more prolonged exposure insidious symptoms of neuropathy, abdominal pain, gastrointestinal bleeding, optic neuritis, confusion and weakness occur. Skin changes such as palm and sole scaling, stomatitis, glossitis, keratitis, eczema and classical alopecia and Mee’s lines on the nails typically occur within two weeks of continual exposure. Treatment is with Prussian Blue which is administered orally at a dose of 250-300mg/kg/day (approximately 10g twice daily for an adult) and this complexes with thallium and is excreted in the faeces.

Thallium poisoning is often diagnosed late or not at all due to a low index of suspicion; indeed it is often misdiagnosed as Guillain-Barre syndrome due to the glove and stocking distribution of sensory symptoms and patients may receive intravenous steroids or immunoglobulins unnecessarily. In Guillain-Barre syndrome (GBS), classically there is ascending paralysis that is not seen in thallium poisoning and typically sensory symptoms in GBS are of numbness not hyperalgesia.

386
Q

When should you give stat insulin in inpatient setting?

A

Avoid stat insulin to correct hyperglycaemia unless symptomatic or ketones >0.6.

It is safer to increase the ‘usual’ insulin if patient is persistently hyperglycaemic.

387
Q

What are Auer rods associated with?

A

Strongly suggest acute promyelocytic leukaemia

388
Q

What level is fibrinogen in DIC?

A

Classically low

HOWEVER Fibrinogen is an acute phase marker. Therefore in DIC fibrinogen levels can be normal or elevated in over 50% of cases especially early on.

389
Q

What is the difference between AA amyloidosis and AL amyloidosis?

A

AA occurs due to chronic inflammation

AL occurs due to light chain disease (where cardiac manifestations are very common)

390
Q

How do you treat pyrazinamide resistant TB?

A

First 2 months:
-rifampicin, isoniazid (with pyridoxine) and ethambutol

Continue:
-rifampicin and isoniazid for 7 months

391
Q

How do you treat ethambutol resistant TB?

A

First 2 months:
-rifampicin, isoniazid (with pyridoxine) and pyrazinamide

Continue:
-rifampicin and isoniazid (with pyridoxine) for 4 months

392
Q

What is the treament for tics in Tourette syndrome?

A

Habit reversal therapy (HRT)

Atypical Antipsychotics (risperidone) or clonidine

393
Q

What ECG findings are associated with dextrocardia?

A

Inverted P wave in lead I
Right axis deviation
Loss of R wave progression

394
Q

What drugs can cause a myaasthenic crisis?

A

Magnesium
Penicillamine
Quinidine
Procainamide
Beta-blockers
Lithium
Phenytoin
Antibiotics: gentamicin, macrolides, quinolones, tetracyclines

395
Q

What is the treatment for lupus nephritis?

A

Lupus nephritis is initially managed with high dose steroids alongside either mycophenolate or cyclophosphamide.

The preferred treatment for maintenance is mycophenolate.

396
Q

What is the treatment for acute flares of AIP?

A

IV Haem arginate

397
Q

What is the biochemical profile seen in Kallman’s syndrome?

A

LH and FSH low-normal and testosterone is low

398
Q

What are the features of quinine toxicity (cinchonism)?

A

ECG changes
Hypotension
Metabolic acidosis
Hypoglycaemia
Tinnitus
Flushing
Visual disturbances
Flash pulmonary oedema

399
Q

How do you differentiate Vivax vs Ovale infection based on epidaemiology?

A

Vivax - India
Ovale - Africa

400
Q

How do you endoscopically manage varices depending on grade in cirrhotic patients?

A

No Varices - Repeat endoscopy 2-3 years
Grade 1 - Repeat endoscopy in 1 year
Grade 2-3 or signs of bleeding - Non-cardio selective beta blocker

401
Q

What are the classic hormonal biochemistry findings in pregnancy?

A

Elevated estradiol and progesterone
Slight rise in LH
Mild rise prolactin

402
Q

How do you identify struvite stones?

A

Struvite stones are formed in the presence of increased urinary ammonia and alkaline urine (>7.2)

403
Q

What are the features of the plague?

What is the causative organism?

A

Caused by the gram-negative bacterium Yersinia pestis.

It is transmitted by fleas and is endemic to the Democratic Republic of the Congo, Madagascar, and Peru. Symptoms typically include flu-like symptoms from 3-7 days post-exposure followed by the eruption of inflamed, tense and painful lymph nodes. The disease carries a significantly high mortality rate if not treated and prompt recognition and antibiotic administration (i.e. Streptomycin) can reduce the mortality from 60% to 15%.