Wednesday [06/10/2021] Flashcards

1
Q

Features of erythema multiforme [4]

A

Target lesions

initially seen on the back of the hands/feet before spreading to the torso

upper limbs are more commonly affected than the lower limbs

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2
Q

Causes of erythema multiforme [4]

A
  • viruses: herpes simplex virus (the most common cause), Orf*
  • idiopathic
  • bacteria: Mycoplasma, Streptococcus
  • drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill, nevirapine
  • connective tissue disease e.g. Systemic lupus erythematosus
  • sarcoidosis
  • malignancy
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3
Q

What is erythema multiforme major? [1]

A

The more severe form, erythema multiforme major is associated with mucosal involvement.

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4
Q

What is vitrreous haemorrhage? [3]

A

Vitreous haemorrhage is bleeding into the vitreous humour. It is one of the most common causes of sudden painless loss of vision. It causes disruption to vision to a variable degree, ranging from floaters to complete visual loss. The source of bleeding can be from disruption of any vessel in the retina as well as the extension through the retina from other areas. Once the bleeding stops, the blood is typically cleared from the retina at an approximate rate of 1% per day1.

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5
Q

Common causes of vitreous haemorrhage in 90% cases? [3]

A
  • proliferative diabetic retinopathy (over 50%)
  • posterior vitreous detachment
  • ocular trauma: the most common cause in children and young adults
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6
Q

Presentation of vietreous haemorrhage [3]

A
  • painless visual loss or haze (commonest)
  • red hue in the vision
  • floaters or shadows/dark spots in the vision
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7
Q

Signs of vitreous haemorrhage [2]

A
  • decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
  • visual field defect if severe haemorrhage
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8
Q

Ix for vitreous haemorrhage [5]

A
  • dilated fundoscopy: may show haemorrhage in the vitreous cavity
  • slit-lamp examination: red blood cells in the anterior vitreous
  • ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
  • fluorescein angiography: to identify neovascularization
  • orbital CT: used if open globe injury
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9
Q

Common symptoms include:

  • nausea and vomiting, anorexia
  • myalgia
  • lethargy
  • right upper quadrant (RUQ) pain

Questions may point to risk factors such as foreign travel or intravenous drug use [1]

A

Viral hepatitis

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10
Q

The liver only usually causes pain if stretched. One common way this can occur is as a consequence of congestive heart failure. In severe cases cirrhosis may occur.

A

Congestive hepatomegaly

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11
Q

RUQ pain, intermittent, usually begins abruptly and subsides gradually. Attacks often occur after eating. Nausea is common.

It is sometimes taught that patients are female, forties, fat and fair although this is obviously a generalisation. [1]

A

Biliary colic

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12
Q

Pain similar to biliary colic but more severe and persistent. The pain may radiate to the back or right shoulder.

The patient may be pyrexial and Murphy’s sign positive (arrest of inspiration on palpation of the RUQ)

A

Acute cholecystitis

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13
Q

An infection of the bile ducts commonly secondary to gallstones. Classically presents with a triad of:

  • fever (rigors are common)
  • RUQ pain
  • jaundice
A

Ascending cholagnitis

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14
Q

This describes small bowel obstruction secondary to an impacted gallstone. It may develop if a fistula forms between a gangrenous gallbladder and the duodenum.

Abdominal pain, distension and vomiting are seen.

A

Gallstone ileus [2]

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15
Q

Persistent biliary colic symptoms, associated with anorexia, jaundice and weight loss. A palpable mass in the right upper quadrant (Courvoisier sign), periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen

A

Cholangiocarcinoma

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16
Q

Usually due to alcohol or gallstones
Severe epigastric pain
Vomiting is common
Examination may reveal tenderness, ileus and low-grade fever
Periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare

A

Acute pancreatitis

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17
Q

Painless jaundice is the classical presentation of pancreatic cancer. However pain is actually a relatively common presenting symptom of pancreatic cancer. Anorexia and weight loss are common

A

Pancreatic cancer

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18
Q

Typical symptoms are malaise, anorexia and weight loss. The associated RUQ pain tends to be mild and jaundice is uncommon.

A

Amoebic liver disease

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19
Q

Whom is G6PD deficiency common in? [1]

A

People from Mediterranean and Africa

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20
Q

How is G6PD inherited? [1]

A

X-linked inheritance pattern

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21
Q

signs of haemolytic anaemia [3]

A

Dark urine, reduced exercise tolerance, yellow sclerae, sinus tachycardia, raised Heinz bodies [as seen in G6PD deficiency]

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22
Q

Examples of quinolones [2]

A

Quinolones are a group of antibiotics which work by inhibiting DNA synthesis and are bactericidal in nature. Examples include:

  • ciprofloxacin
  • levofloxacin
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23
Q

MoA and mechanism of resistance of quinolones [2]

A

Mechanism of action

  • inhibit topoisomerase II (DNA gyrase) and topoisomerase IV

Mechanism of resistance

  • mutations to DNA gyrase, efflux pumps which reduce intracellular quinolone concentration
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24
Q

Adverse effects of quinolones [4]

A
  • lower seizure threshold in patients with epilepsy
  • tendon damage (including rupture) - the risk is increased in patients also taking steroids
  • cartilage damage has been demonstrated in animal models and for this reason quinolones are generally avoided (but not necessarily contraindicated) in children
  • lengthens QT interval
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25
Q

CI of quinolones [2]

A
  • Quinolones should generally be avoided in women who are pregnant or breastfeeding
  • avoid in G6PD
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26
Q

What EECG sign is in cardiac tamponade? [1]

A

Electric alternanas

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27
Q

What is Beck’s triad? [2]

A

Cardiac tamponade signs:

  • hypotension
  • raised JVP
  • soft heart sounds
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28
Q

What is electric alternans? [2]

A

Electrical alternans is a relatively specific but non-sensitive ECG sign of cardiac tamponade. Electrical alternans is characterised by beat to beat variation in QRS amplitude and morphology. This variability is due to the heart ‘swinging’ in the pericardial fluid.

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29
Q

What is a short PR interval indicative of? [1]

A

WPW

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30
Q

What is QT prolongation seen in? [2]

A

QT prolongation is usually caused by electrolyte abnormalities (hypokalemia, hypocalcemia) or medications (antipsychotics). QT prolongation is not associated with cardiac tamponade.

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31
Q

T wave inversion in leads II, III, AVF [1]

A

T wave inversion in leads II, III and AVF is highly suggestive of inferior myocardial ischaemia. It is important to remember that cardiac tamponade is a potential complication of a myocardial infarction

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32
Q

Other features of cardiac tamponade? [6]

A
  • dyspnoea
  • tachycardia
  • an absent Y descent on the JVP - this is due to the limited right ventricular filling
  • pulsus paradoxus - an abnormally large drop in BP during inspiration
  • Kussmaul’s sign - much debate about this
  • ECG: electrical alternans
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33
Q

Compare constrictive pericarditis and cardaic tamponade [4]

A

Cardiac tamponadeConstrictive pericarditisJVPAbsent Y descentPulsus paradoxusPresentKussmaul’s signRareCharacteristic features

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34
Q

Mx of cardiac tamponade? [1]

A

Urgent pericardiocentesis

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35
Q

What can phenytoin cause? [1]

A

Folic acid defiency and macroscytic anaemia

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36
Q

What is a good source of folic acid? [1]

A

Folic acid is converted to tetrahydrofolate (THF). Green, leafy vegetables are a good source of folic acid.

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37
Q

Fucntions of folic acid? [1]

A
  • THF plays a key role in the transfer of 1-carbon units (e.g. methyl, methylene, and formyl groups) to the essential substrates involved in the synthesis of DNA & RNA
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38
Q

Causes of folic acid defieincy [4]

A
  • phenytoin
  • methotrexate
  • pregnancy
  • alcohol excess
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39
Q

Consequences of folic acid defiency

A

Macrocytic, megaloblastic anaemia

Neural tube defects

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40
Q

Prevention of neural tube defects during pregnancy [3]

A
  • all women should take 400mcg of folic acid until the 12th week of pregnancy
  • women at higher risk of conceiving a child with a NTD should take 5mg of folic acid from before conception until the 12th week of pregnancy
  • women are considered higher risk if any of the following apply:
    • either partner has a NTD, they have had a previous pregnancy affected by a NTD, or they have a family history of a NTD
    • the woman is taking antiepileptic drugs or has coeliac disease, diabetes, or thalassaemia trait.
    • the woman is obese (defined as a body mass index [BMI] of 30 kg/m2 or more).
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41
Q

Which heart sound does pulmonary hypertension cause? [1]

A

Pulmonary hypertension is a cause of a loud S2 (due to a loud P2)

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42
Q

Dx of firbomyaglia [2]

A

Diagnosis is clinical and sometimes refers to the American College of Rheumatology
classification criteria which lists 9 pairs of tender points on the body. If a patient is tender in at least 11 of these 18 points it makes a diagnosis of fibromyalgia more likely

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43
Q

Mx of firbomyalgia [4]

A
  • explanation
  • aerobic exercise: has the strongest evidence base
  • cognitive behavioural therapy
  • medication: pregabalin, duloxetine, amitriptyline
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44
Q

NSTEMI [managed with PCI] antiplatelet choice [2]

A
  • if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor
  • if taking an oral anticoagulant: clopidogrel
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45
Q

Features of pernicious anaemia [3]

A
  • anaemia features
    • lethargy
    • pallor
    • dyspnoea
  • neurological features
    • peripheral neuropathy: ‘pins and needles’, numbness. Typically symmetrical and affects the legs more than the arms
    • subacute combined degeneration of the spinal cord: progressive weakness, ataxia and paresthesias that may progress to spasticity and paraplegia
    • neuropsychiatric features: memory loss, poor concentration, confusion, depression, irritabiltiy
  • other features
    • mild jaundice: combined with pallor results in a ‘lemon tinge’
    • glossitis → sore tongue
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46
Q

Ix of pernicious anaemia [4]

A
  • full blood count
    • macrocytic anaemia: macrocytosis may be absent in around of 30% of patients
    • hypersegmented polymorphs on blood film
    • low WCC and platelets may also be seen
  • vitamin B12 and folate levels
    • a vitamin B12 level of >= 200 nh/L is generally considered to be normal
  • antibodies
    • anti intrinsic factor antibodies: sensivity is only 50% but highly specific for pernicious anaemia (95-100%)
    • anti gastric parietal cell antibodies in 90% but low specificity so often not useful clinically
  • Schilling test is no longer routinely done
    • radiolabelled B12 given on two occasions, firstly on its own, secondly with oral IF. Urine B12 levels are then measured
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47
Q

Mx of pernicious anaemia [2]

A
  • vitamin B12 replacement
    • usually given intramuscularly
    • no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections
    • more frequent doses are given for patients with neurological features
    • there is some evidence that oral vitamin B12 may be effective for providing maintenance levels of vitamin B12 but it is not yet common practice
  • folic acid supplementation may also be required
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48
Q

Why is amtriptyline CI in a patient with T2DM and diabetic neuropathy that has bening prostatic hyperplasia? [1]

A

Risk of urinary retention

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49
Q

Mx of diabetic neuroapthy [5]

A
  • first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin
  • if the first-line drug treatment does not work try one of the other 3 drugs
  • tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
  • topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
  • pain management clinics may be useful in patients with resistant problems
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50
Q

Steroid dose children with asthma attack? [2]

A
  • Use a dose of 10 mg prednisolone for children under 2 years of age, 20 mg for children aged 2-5 years and 30-40 mg for children >5 years. Those already receiving maintenance steroid tablets
  • should receive 2 mg/kg prednisolone up to a maximum dose of 60 mg.*
  • Repeat the dose of prednisolone in children who vomit and consider intravenous steroids in those who are unable to retain orally ingested medication.
  • Treatment for up to three days is usually sufficient, but the length of course should be tailored to the number of days necessary to bring about recovery. Tapering is unnecessary unless the course of steroids exceeds 14 days.
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51
Q

Mx of children with mild to moderate acute asthma [2]

A

Bronchodilator therapy

  • give a beta-2 agonist via a spacer (for a child < 3 years use a close-fitting mask)
  • give 1 puff every 30-60 seconds up to a maximum of 10 puffs
  • if symptoms are not controlled repeat beta-2 agonist and refer to hospital

Steroid therapy

  • should be given to all children with an asthma exacerbation
  • treatment should be given for 3-5 days
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52
Q

Which antidaiebtic drug has had an increase risk of bladder cancer? [2]

A

Recent studies have identified that thiazolidinediones, in particular, pioglitazone, are associated with an increased risk of bladder cancer. This is a rare, but important, adverse effect to consider in a patient on thiazolidinediones.

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53
Q

Adverse effects of SLGT-2 inhibitors, biguinines like metoformin, GLP-1 mimetics and insulin [4]

A

1 - SGLT-2 inhibitors - genital infections, diabetic ketoacidosis
2 - Biguanides e.g. metformin - GI upset, lactic acidosis
4 - GLP-1 mimetics - nausea, vomiting, pancreatitis
5 - Insulin - weight gain, hypoglycaemia, lipodystrophy

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54
Q

How do thiazlidinediones work? [2]

A

Thiazolidinediones are a class of agents used in the treatment of type 2 diabetes mellitus. They are agonists to the PPAR-gamma receptor and reduce peripheral insulin resistance. Rosiglitazone was withdrawn in 2010 following concerns about the cardiovascular side-effect profile.

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55
Q

Adverse effects of thiazolidinediones [5]

A
  • weight gain
  • liver impairment: monitor LFTs
  • fluid retention - therefore contraindicated in heart failure. The risk of fluid retention is increased if the patient also takes insulin
  • recent studies have indicated an increased risk of fractures
  • bladder cancer: recent studies have shown an increased risk of bladder cancer in patients taking pioglitazone (hazard ratio 2.64)
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56
Q

Features of intraheptaic cholestasis of pregnancy [3]

A
  • pruritus - may be intense - typical worse palms, soles and abdomen
  • clinically detectable jaundice occurs in around 20% of patients
  • raised bilirubin is seen in > 90% of cases
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57
Q

What is first-line Tx for pregnant women with UTI? [1]

A

Nitrofurantoin 7 days course [though should be avoided near term]

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58
Q

Tx of UTI for non-pregnancy women [1]

A
  • NICE Clinical Knowledge Summaries recommend trimethoprim or nitrofurantoin for 3 days
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59
Q

When to send for a urine culture in non-pregnant women with LUTI [2]

A

Aged over 65, visible or non-visible haematuria

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60
Q

Summarise Mx for lower UTI in non-pregnnat women

A
  • local antibiotic guidelines should be followed if available
  • NICE Clinical Knowledge Summaries recommend trimethoprim or nitrofurantoin for 3 days
  • send a urine culture if:
    • aged > 65 years
    • visible or non-visible haematuria
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61
Q

Mx of prengnact women if symptomatic [5]

A
  • a urine culture should be sent in all cases
  • should be treated with an antibiotic for
  • first-line: nitrofurantoin (should be avoided near term)
  • second-line: amoxicillin or cefalexin
  • trimethoprim is teratogenic in the first trimester and should be avoided during pregnancy
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62
Q

Which Abx for UTI is teratogenic during the firs ttrimester? [1]

A

Trimethoprim

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63
Q

Asymptomatic bacteriuria in pregnant women Mx [4]

A
  • a urine culture should be performed routinely at the first antenatal visit
  • Clinical Knowledge Summaries recommend an immediate antibiotic prescription of either nitrofurantoin (should be avoided near term), amoxicillin or cefalexin. This should be a 7-day course
  • the rationale of treating asymptomatic bacteriuria is the significant risk of progression to acute pyelonephritis
  • a further urine culture should be sent following completion of treatment as a test of cure
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64
Q

Mx of men with lower UTI [3]

A
  • an immediate antibiotic prescription should be offered for 7 days
  • as with non-pregnant women, trimethoprim or nitrofurantoin should be offered first-line unless prostatitis is suspected
  • NICE Clinical Knowledge Summaries state: ‘Referral to urology is not routinely required for men who have had one uncomplicated lower urinary tract infection (UTI).’
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65
Q

How to Tx catheterised pts with lower UTI [2]

A
  • do not treat asymptomatic bacteria in catheterised patients
  • if the patient is symptomatic they should be treated with an antibiotic
    • a 7-day, rather than a 3-day course should be given
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66
Q

How to manage acute pyelonephritis [2]

A

For patients with sign of acute pyelonephritis hospital admission should be considered

  • local antibiotic guidelines should be followed if available
  • the BNF currently recommends a broad-spectrum cephalosporin or a quinolone (for non-pregnant women) for 10-14 days
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67
Q

What are early signs of haemochromatosis? [3]

A

Featifue, erectile dysfunction and arthralgia

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68
Q

Addison;s disease acute presentation [3]

A

Abdominal pain, weight loss, N and V

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69
Q

Wilson’s disease presentation [2]

A

Wilson’s disease normally presents in children and adolescents as neuropsychiatric symptoms as well as the symptoms of liver failure. As said above the fact it typically presents in much younger patients helps to rule this out.

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70
Q

Presentation of SLE in men [3]

A

Systemic lupus erythematosus can present with a variety of symptoms such as fatigue, arthralgia and weight loss. While these symptoms could account for his arthralgia and fatigue, erectile dysfunction is not typical. Even if it was, the fact that both his dad and grandfather died of liver conditions points towards another diagnosis.

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71
Q

How would Budd-Chiari syndrome present? [2]

A

Budd-Chiari syndrome is due to obstruction of the hepatic vein. It typically presents with right upper quadrant pain and painful ascites. You could also note hepatomegaly, jaundice and it may be associated with an acute kidney injury and so this does not fit his presentation.

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72
Q

INheritance pattern of haemachromatosis [1]

A

Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation

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73
Q

What is haemoachromatosis caused by? [2]

A

It is caused by inheritance of mutations in the HFE gene on both copies of chromosome 6*. It is often asymptomatic in early disease and initial symptoms often non-specific e.g. lethargy and arthralgia

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74
Q

Epidemiology of haemachromatosis [2]

A
  • 1 in 10 people of European descent carry a mutation in the genes affecting iron metabolism, mainly HFE
  • prevalence in people of European descent = 1 in 200, making it more common than cystic fibrosis
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75
Q

Presenting feratures of haemachromatosis [7]

A
  • early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
  • ‘bronze’ skin pigmentation
  • diabetes mellitus
  • liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
  • cardiac failure (2nd to dilated cardiomyopathy)
  • hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
  • arthritis (especially of the hands)
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76
Q

Which complications of haemachromatosis are reverisble, and whoch are irreversible? [6]

A
  • Reversible complications*Irreversible complications
  • Cardiomyopathy
  • Skin pigmentation
  • Liver cirrhosis**
  • Diabetes mellitus
  • Hypogonadotrophic hypogonadism
  • Arthropathy
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77
Q

A 64-year-old Bangladeshi man presents to the GP with blood-stained sputum and breathlessness. On further questioning, he notes fatigue, weight loss and some sweating in the night. The GP takes sputum samples and sends the man for a chest X-ray. Possible Dx likely? [1]

A

TB

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78
Q

What is primary tuberculosis? [2]

A

A non-immune host who is exposed to M. tuberculosis may develop a primary infection of the lungs. A small lung lesion known as a Ghon focus develops. The Ghon focus is composed of tubercle-laden macrophages. The combination of a Ghon focus and hilar lymph nodes is known as a Ghon complex

In immunocompetent people, the initial lesion usually heals by fibrosis. Those who are immunocompromised may develop disseminated disease (miliary tuberculosis).

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79
Q

When can secondary [post-primary] TB occur? [3]

A

If the host becomes immunocompromised the initial infection may become reactivated. Reactivation generally occurs in the apex of the lungs and may spread locally or to more distant sites. Possible causes of immunocompromise include:

  • immunosuppressive drugs including steroids
  • HIV
  • malnutrition
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80
Q

Where may extra-pulmonary inefction occur in TB? [5]

A

The lungs remain the most common site for secondary tuberculosis. Extra-pulmonary infection may occur in the following areas:

  • central nervous system (tuberculous meningitis - the most serious complication)
  • vertebral bodies (Pott’s disease)
  • cervical lymph nodes (scrofuloderma)
  • renal
  • gastrointestinal tract
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81
Q

Which test is important to do for TB? [1]

A

HIV test

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82
Q

What does head and neck cancer refer to? [3]

A
  • Oral cavity cancers
  • Cancers of the pharynx (including the oropharynx, hypopharynx and nasopharynx)
  • Cancers of the larynx
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83
Q

Features of head and neck cancers [4]

A
  • neck lump
  • hoarseness
  • persistent sore throat
  • persistent mouth ulcer
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84
Q

2w wait layrngeal cancer suspected [2]

A
  • Consider a suspected cancer pathway referral (for an appointment within 2 weeks) for laryngeal cancer in people aged 45 and over with:
    • persistent unexplained hoarseness or
    • an unexplained lump in the neck
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85
Q

2w wait oral cancer suspected [4]

A
  • Consider a suspected cancer pathway referral (for an appointment within 2 weeks) for oral cancer in people with either:
    • unexplained ulceration in the oral cavity lasting for more than 3 weeks or
    • a persistent and unexplained lump in the neck.
  • Consider an urgent referral (for an appointment within 2 weeks) for assessment for possible oral cancer by a dentist in people who have either:
    • a lump on the lip or in the oral cavity or
    • a red or red and white patch in the oral cavity consistent with erythroplakia or erythroleukoplakia.
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86
Q

2w wait thyroid cancer suspected

A

Thyroid cancer

  • Consider a suspected cancer pathway referral (for an appointment within 2 weeks) for thyroid cancer in people with an unexplained thyroid lump.
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87
Q

A 54-year-old man of Asian heritage presents with a slowly enlarging neck lump in the posterior triangle. A biopsy is performed and the histological report is ‘metastatic SCC in a lymph node.’ On inspection, there are no obvious skin lesions present. Primary site Ca and why? [1]

A

Nasopharyngeal carcinoma may present as a painless lymphadenopathy because of its tendency for early spread. Nasopharyngeal carcinoma is more common in people of Asian origin, and typically presents with epistaxis, headaches, lymph node metastasis or unilateral hearing loss.

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88
Q

Where would larynx, buccal and tonsillar fossa cancers spread into? [1]

A

The other remaining options (larynx, buccal mucosa, and tonsillar fossa) would drain to the anterior triangle.

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89
Q

Epistaxis where bleeding site difficult to manage and pinching soft area nose for 20m doesn;t work [1]

A

Anterior packing

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90
Q

When should epistaxis be referred to ENT? [1]

A

If anterior packing doesn;t work, then refer for posterior packing

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91
Q

What is epistaxis split up into? []

A

Anterior and posterior bleeds

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92
Q

Most common cause of epistaxis [1]

A

Trauma

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93
Q

Uncommon causes of epistaxis [5]

A

Bleeding can also indicate platelet function disorders such as thrombocytopenia, splenomegaly, leukaemia, Waldenstrom’s macroglobulinaemia and ITP. In adolescent males, juvenile angiofibroma is a benign tumour that may bleed as it is highly vascularised. If the nasal septum looks abraded or atrophied, inquire about drug use. This is because inhaled cocaine is a powerful vasoconstrictor and repeated use may result in obliteration of the septum. In the elderly, hereditary haemorrhagic telangiectasia may cause prolonged nasal bleeding. Granulomatosis with polyangiitis and pyogenic granuloma may also present with nosebleeds.

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94
Q

First aid measures of haemodynamically stable patients with epistaxis [2]

A
  • Asking the patient to sit with their torso forward and their mouth open- avoid lying down unless they feel faint. This decreases blood flow to the nasopharynx and allows the patient to spit out any blood in their mouth. It also reduces the risk of aspirating blood.
  • Pinch the cartilaginous (soft) area of the nose firmly and consistently for at least 20 minutes and ask the patient to breathe through their mouth.
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95
Q

What to do next if first-aid meaures are successful? [1]

A

If first aid measures are successful, consider using a topical antiseptic such as Naseptin (chlorhexidine and neomycin) to reduce crusting and the risk of vestibulitis. Cautions to this include patients that have peanut, soy or neomycin allergies, and Mupirocin is a viable alternative.

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96
Q

What should be used initially if first aid measures are unsuccessful for visible bleed epistaxis? [1]

A

If bleeding does not stop after 10-15 minutes of continuous pressure on the nose, consider cautery or packing. Cautery should be used initially if the source of the bleed is visible and cautery is tolerated- it is not so well-tolerated in younger children! Packing may be used if cautery is not viable or the bleeding point cannot be visualised. If the nose is packed in primary care, the patient should be admitted to hospital for review.

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97
Q

How is cautery done for epistaxis? [3]

A
  • Ask the patient to blow their nose in order to remove any clots. Be wary that bleeding may resume.
  • Use a topical local anaesthetic spray (e.g. Co-phenylcaine) and wait 3-4 minutes for it to take effect
  • Identify the bleeding point and apply the silver nitrate stick for 3-10 seconds until it becomes grey-white. Avoid touching areas which do not require treatment, and only cauterise one side of the septum as there is a risk of perforation.
  • Dab the area clean with a cotton bud and apply Naseptin or Muciprocin
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98
Q

How is packing done for epistaxis? [4]

A
  • Anaesthetise with topical local anaesthetic spray (e.g. Co-phenylcaine) and wait for 3-4 minutes
  • Pack the patient’s nose while they are sitting with their head forward, following the manufacturer’s instructions
  • Pressure on the cartilage around the nostril can cause cosmetic changes and this should be reviewed after inserting the pack.
  • Examine the patient’s mouth and throat for any continuing bleeding, and consider packing the other nostril as this increases pressure on the septum and offending vessel.
  • Patients should be admitted to hospital for observation and review, and to ENT if available
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99
Q

Epistaxis that has failed all emergency maanged should be amanged how? [1]

A

Epistaxis that has failed all emergency management may require sphenopalatine ligation in theatre

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100
Q

Features of LB dementia [3]

A
  • progressive cognitive impairment
    • in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
    • cognition may be fluctuating, in contrast to other forms of dementia
    • usually develops before parkinsonism
  • parkinsonism
  • visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
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101
Q

Dx of LB dementia [2]

A
  • usually clinical
  • single-photon emission computed tomography (SPECT) is increasingly used. It is currently commercially known as a DaTscan. Dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) is used as the radioisotope. The sensitivity of SPECT in diagnosing Lewy body dementia is around 90% with a specificity of 100%
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102
Q

Mx of LB dementia [2]

A
  • both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s. NICE have made detailed recommendations about what drugs to use at what stages. Please see the link for more details
  • neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism. Questions may give a history of a patient who has deteriorated following the introduction of an antipsychotic agent
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103
Q

What is Argyll-Robertson pupil? [2]

A

Argyll-Robertson pupil is one of the classic pupillary syndrome. It is sometimes seen in neurosyphilis. A mnemonic used for the Argyll-Robertson Pupil (ARP) is Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)

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104
Q

Features of ARP [2]

A
  • small, irregular pupils
  • no response to light but there is a response to accommodate
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105
Q

Causes of ARP [2]

A
  • diabetes mellitus
  • syphilis
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106
Q

RFs for endometrial Ca [9]

A
  • obesity
  • nulliparity
  • early menarche
  • late menopause
  • unopposed oestrogen. The addition of a progestogen to oestrogen reduces this risk (e.g. In HRT). The BNF states that the additional risk is eliminated if a progestogen is given continuously
  • diabetes mellitus
  • tamoxifen
  • polycystic ovarian syndrome
  • hereditary non-polyposis colorectal carcinoma
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107
Q

How often does endometrial Ca happen before menopause? [1]

A

Endometrial cancer is classically seen in post-menopausal women but around 25% of cases occur before the menopause. It usually carries a good prognosis due to early detection

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108
Q

Features of endometrial Ca [3]

A
  • postmenopausal bleeding is the classic symptom
  • premenopausal women may have a change intermenstrual bleeding
  • pain and discharge are unusual features
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109
Q

Ix for endometrial Ca [3]

A
  • women >= 55 years who present with postmenopausal bleeding should be referred using the suspected cancer pathway
  • first-line investigation is trans-vaginal ultrasound - a normal endometrial thickness (< 4 mm) has a high negative predictive value
  • hysteroscopy with endometrial biopsy
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110
Q

When do febrile seizures commonly occur? [1]

A

Febrile convulsions are seizures provoked by fever in otherwise normal children. They typically occur between the ages of 6 months and 5 years and are seen in 3% of children.

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111
Q

Clinical features of febrile convulsions [3]

A
  • usually occur early in a viral infection as the temperature rises rapidly
  • seizures are usually brief, lasting less than 5 minutes
  • are most commonly tonic-clonic
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112
Q

What does a sandpaper rash and strawberry tongue indicate in a child? [1]

A

Scarlet fever

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113
Q

WHen should you call an ambulance for febrile convulsions? [1]

A

If the febrile convulsion lasts longer than 5m

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114
Q

COmpare simple, to complex to febrile status elipticus [3]

A

SimpleComplexFebrile status epilepticus< 15 minutes15 - 30 minutes> 30 minutesGeneralised seizureFocal seizure Typically no recurrence within 24 hoursMay have repeat seizures within 24 hours Should be complete recovery within an hour

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115
Q

Mx following a seizure [1]

A
  • children who have had a first seizure OR any features of a complex seizure should be admitted to paediatrics
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116
Q

Prognosis of febrile seizures [3]

A
  • the overall risk of further febrile convulsion = 1 in 3. However, this varies widely depending on risk factors for further seizure. These include: age of onset < 18 months, fever < 39ºC, shorter duration of fever before seizure and a family history of febrile convulsions
  • if recurrences, try teaching parents how to use rectal diazepam or buccal midazolam. Parents should be advised to phone for an ambulance if the seizure lasts > 5 minutes
  • regular antipyretics have not been shown to reduce the chance of a febrile seizure occurring
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117
Q

Link to elilepsy for febrile seizures [3]

A
  • risk factors for developing epilepsy include a family history of epilepsy, having complex febrile seizures and a background of neurodevelopmental disorder
  • children with no risk factors have 2.5% risk of developing epilepsy
  • if children have all 3 features the risk of developing epilepsy is much higher (e.g. 50%)
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118
Q

inheritance of tuberous sclerosis [1]

A

Tuberous sclerosis (TS) is a genetic condition of autosomal dominant inheritance. Like neurofibromatosis, the majority of features seen in TS are neurocutaneous.

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119
Q

Cutaneous , nuerological and other features of tuberous sclerosis [3]

A
  • depigmented ‘ash-leaf’ spots which fluoresce under UV light
  • roughened patches of skin over lumbar spine (Shagreen patches)
  • adenoma sebaceum (angiofibromas): butterfly distribution over nose
  • fibromata beneath nails (subungual fibromata)
  • café-au-lait spots* may be seen
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119
Q

Cutaneous , nuerological and other features of tuberous sclerosis [3]

A

Cutaneous features

  • depigmented ‘ash-leaf’ spots which fluoresce under UV light
  • roughened patches of skin over lumbar spine (Shagreen patches)
  • adenoma sebaceum (angiofibromas): butterfly distribution over nose
  • fibromata beneath nails (subungual fibromata)
  • café-au-lait spots* may be seen

Neurological features

  • developmental delay
  • epilepsy (infantile spasms or partial)
  • intellectual impairment

Also

  • retinal hamartomas: dense white areas on retina (phakomata)
  • rhabdomyomas of the heart
  • gliomatous changes can occur in the brain lesions
  • polycystic kidneys, renal angiomyolipomata
  • lymphangioleiomyomatosis: multiple lung cysts
    *
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120
Q

Where is the most common site for epistaxis? [1]

A

Little’s area in the anterior nasal septum is the site of Kiesselbach’s plexus, supplied by 4 arteries. Epistaxis therefore most commonly originates from the anterior of the nose

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121
Q

Second-line Tx for neuropathic pain [1]

A

First-line treatment for neuropathic pain is amitriptyline, duloxetine, gabapentin or pregabalin. If one of these agents don’t work next line is to try one of the other remaining three drugs

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122
Q

Examples of neuropathic pain [4]

A
  • diabetic neuropathy
  • post-herpetic neuralgia
  • trigeminal neuralgia
  • prolapsed intervertebral disc
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123
Q

Summary of Mx of neuropathic pain [4]

A
  • first-line treatment*: amitriptyline, duloxetine, gabapentin or pregabalin
    • if the first-line drug treatment does not work try one of the other 3 drugs
    • in contrast to standard analgesics, drugs for neuropathic pain are typically used as monotherapy, i.e. if not working then drugs should be switched, not added
  • tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
  • topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
  • pain management clinics may be useful in patients with resistant problems
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124
Q

Patient presenting wioth flu-like Sx, RUQ pain, tender hepatomegaly and cholestatic LFTs [1]

A

Hepatitis A

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125
Q

What are cholestatic LFTs [3]

A
  • Raised bilirubin
  • Raised ALT/ AST
  • Normal or slightly raised ALP
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126
Q

Overveiw and features of hepatitis A [2]

A

Overview

  • incubation period: 2-4 weeks
  • RNA picornavirus
  • transmission is by faecal-oral spread, often in institutions
  • doesn’t cause chronic disease

Features

  • flu-like prodrome
  • abdominal pain: typically right upper quadrant
  • tender hepatomegaly
  • jaundice
  • cholestatic liver function tests
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127
Q

Cx of hepatitis A [1]

A
  • complications are rare and there is no increased risk of hepatocellular cancer
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128
Q

Immunisation of hepatitis A [5]

A

Immunisation

  • an effective vaccine is available
  • after the initial dose a booster dose should be given 6-12 months later

Who should be vaccinated? (Based on the Green book guidelines)

  • people travelling to or going to reside in areas of high or intermediate prevalence, if aged > 1 year old
  • people with chronic liver disease
  • patients with haemophilia
  • men who have sex with men
  • injecting drug users
  • individuals at occupational risk: laboratory worker; staff of large residential institutions; sewage workers; people who work with primates
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129
Q

Heart failure Mx for all patients [1]

A

IV loop diuretics e.g. furosemide or bumetanide

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130
Q

What to give patient with heart failure if not improving on oxygen and diuretifs in acute setting? [1]

A

CPAP

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131
Q

When is Ropinirole used? [1]

A

Mx of restless leg syndrome

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132
Q

What are varicose veins? [2]

A

Varicose veins are dilated, tortuous, superficial veins that occur secondary to incompetent venous valves, allowing blood to flow back, away from the heart. They most commonly occur in the legs due to reflux in the great saphenous vein and small saphenous vein. Whilst extremely common, the vast majority of patients do not require any intervention.

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133
Q

RF for varicose veins [4]

A
  • increasing age
  • female gender
  • pregnancy
    • the uterus causes compression of the pelvic veins
  • obesity
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134
Q

Sx of varicose veins [3]

A

For many patients, the cosmetic appearance may prompt presentation. However other patients may complain of symptoms:

  • aching, throbbing
  • itching
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135
Q

Cx of varicose veins [4]

A
  • a variety of skin changes may be seen:
    • varicose eczema (also known as venous stasis)
    • haemosiderin deposition → hyperpigmentation
    • lipodermatosclerosis → hard/tight skin
    • atrophie blanche → hypopigmentation
  • bleeding
  • superficial thrombophlebitis
  • venous ulceration
  • deep vein thrombosis
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136
Q

Mx of varicose veins [3]

A
  • the majority of patients with varicose veins do not require surgery. Conservative treatments include:
    • leg elevation
    • weight loss
    • regular exercise
    • graduated compression stockings
  • reasons for referral to secondary care include:
    • significant/troublesome lower limb symptoms e.g. pain, discomfort or swelling
    • previous bleeding from varicose veins
    • skin changes secondary to chronic venous insufficiency (e.g. pigmentation and eczema)
    • superficial thrombophlebitis
    • an active or healed venous leg ulcer
  • possible treatments:
    • endothermal ablation: using either radiofrequency ablation or endovenous laser treatment
    • foam sclerotherapy: irritant foam → inflammatory response → closure of the vein
    • surgery: either ligation or stripping
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137
Q

RFs for development of N and V [4]

A
  • anxiety
  • age less than 50 years old
  • concurrent use of opioids
  • the type of chemotherapy used
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138
Q

Low-risk Sx whihc drugs can be used 1st line, whihc drugs 2nd line for N and V with chemotherapy [2]

A

For patients at low-risk of symptoms then drugs such as metoclopramide may be used first-line. For high-risk patients then 5HT3 receptor antagonists such as ondansetron are often effective, especially if combined with dexamethasone

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139
Q

What do nearly all atypical antopsychotics cause? [2]

A

Nearly all typical and some atypical antipsychotics like risperidone & amisulpride cause hyperprolactinaemia. Effects of hyperprolactinemia can involve breast tenderness, breast enlargement and lactation.

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140
Q

Which antipsychotic has a tolerable SE profile in terms of hyperprolacitnoaa? [1]

A

Aripiprazole is known for its having fewer side effects especially with respect to prolactin elevation.

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141
Q

Which type of drugs are now used 1st line in schizophrenia and why? [2]

A

Atypical antipsychotics should now be used first-line in patients with schizophrenia, according to 2005 NICE guidelines. The main advantage of the atypical agents is a significant reduction in extrapyramidal side-effects.

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142
Q

Adverse effects of atypical antipsychotics [3]

A
  • weight gain
  • clozapine is associated with agranulocytosis (see below)
  • hyperprolactinaemia
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143
Q

Increased risk of antispychotics in the elderly? [2]

A
  • increased risk of stroke
  • increased risk of venous thromboembolism
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144
Q

Examples of atpyical antipsychotics [3]

A
  • clozapine
  • olanzapine: higher risk of dyslipidemia and obesity
  • risperidone
  • quetiapine
  • amisulpride
  • aripiprazole: generally good side-effect profile, particularly for prolactin elevation
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145
Q

Why does Clozapine require FBC monitoring? [1]

A

Clozapine, one of the first atypical agents to be developed, carries a significant risk of agranulocytosis and full blood count monitoring is therefore essential during treatment. For this reason, clozapine should only be used in patients resistant to other antipsychotic medication. The BNF states:

Clozapine should be introduced if schizophrenia is not controlled despite the sequential use of two or more antipsychotic drugs (one of which should be a second-generation antipsychotic drug), each for at least 6–8 weeks.

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146
Q

Adverse effects of clozapine [5]

A
  • agranulocytosis (1%), neutropaenia (3%)
  • reduced seizure threshold - can induce seizures in up to 3% of patients
  • constipation
  • myocarditis: a baseline ECG should be taken before starting treatment
  • hypersalivation
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147
Q

When might dose adjustment be neccessary for clozapine? [1]

A

Dose adjustment of clozapine might be necessary if smoking is started or stopped during treatment.

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148
Q

What can erythema nodosum be caused by? [1]

A

Streptococcal infection

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149
Q

What is polymorphic eruption of pregnancy? [2]

A

Polymorphic eruption of pregnancy is a relatively common skin disorder that can occur in women during pregnancy. It usually presents within the first pregnancy. It appears as an itchy, bumpy rash that starts in the stretch marks of the abdomen in the last 3 months of pregnancy then clears with delivery. This is unlikely to be the case here.

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150
Q

What is erythema gyratum? [2]

A

Erythema gyratum repens is a rare paraneoplastic type of annular erythema with a distinctive figurate wood-grain appearance which has a strong association with malignancy.

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151
Q

What is erythema nodosum? [3]

A
  • inflammation of subcutaneous fat
  • typically causes tender, erythematous, nodular lesions
  • usually occurs over shins, may also occur elsewhere (e.g. forearms, thighs)
  • usually resolves within 6 weeks
  • lesions heal without scarring
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152
Q

Causes of erythema nodosum? [5]

A

Causes

  • infection
    • streptococci
    • tuberculosis
    • brucellosis
  • systemic disease
    • sarcoidosis
    • inflammatory bowel disease
    • Behcet’s
  • malignancy/lymphoma
  • drugs
    • penicillins
    • sulphonamides
    • combined oral contraceptive pill
  • pregnancy
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153
Q

Infectious causes if erythema nodosum [3]

A
  • streptococci
  • tuberculosis
  • brucellosis
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154
Q

What is the most commoncause of liver disease in the developed world? [1]

A

NAFLD

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155
Q

Types of NAFLD [3]

A
  • steatosis - fat in the liver
  • steatohepatitis - fat with inflammation, non-alcoholic steatohepatitis (NASH), see below
  • progressive disease may cause fibrosis and liver cirrhosis
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156
Q

What is the key MoA leading to steatosis in NAFLD? [1]

A

NAFLD is thought to represent the hepatic manifestation of the metabolic syndrome and hence insulin resistance is thought to be the key mechanism leading to steatosis.

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157
Q

How common is NASH? [1]

A

Non-alcoholic steatohepatitis (NASH) is a term used to describe liver changes similar to those seen in alcoholic hepatitis in the absence of a history of alcohol abuse. It is relatively common and thought to affect around 3-4% of the general population.

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158
Q

Associated factors with NAFLD? Which are the most important ones? [2]

A
  • obesity
  • type 2 diabetes mellitus
  • hyperlipidaemia
  • jejunoileal bypass
  • sudden weight loss/starvation
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159
Q

Features of NAFLD [4]

A
  • usually asymptomatic
  • hepatomegaly
  • ALT is typically greater than AST
  • increased echogenicity on ultrasound
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160
Q

Key points for the Ix and Mx of NAFLD [4]

A
  • there is no evidence to support screening for NAFLD in adults, even in at risk groups (e.g. type 2 diabetes)
  • the guidelines are therefore based on the management of the incidental finding of NAFLD - typically asymptomatic fatty changes on liver ultrasound
  • in these patients, NICE recommends the use of the enhanced liver fibrosis (ELF) blood test to check for advanced fibrosis
  • the ELF blood test is a combination of hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase 1. An algorithm based on these values results in an ELF blood test score, similar to triple testing for Down’s syndrome
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161
Q

Mx of NAFLD [2]

A
  • the mainstay of treatment is lifestyle changes (particularly weight loss) and monitoring
  • there is ongoing research into the role of gastric banding and insulin-sensitising drugs (e.g. metformin, pioglitazone)
162
Q

How does IgA nephropathy classically present? [1]

A

IgA nephropathy classically presents as visible haematuria following a recent URTI

163
Q

How to post-streptococcal glomuerulonephritis typically present? How is this different to IgA nephropathy? [2]

A

It is important to not confuse it with post-streptococcal glomerulonephritis, which is caused by immune complex (IgG, IgM, and C3) deposition in the glomeruli. This happens more slowly, typically 7-14 days following a group A beta-hemolytic Streptococcus infection and causes proteinuria.

IgA is a shorter word, fewer days, post-strep longer word so more days

164
Q

Characteristics of Alport’s syndrome [3]

A

Alport’s syndrome is an X-linked dominant disease. It presents with microscopic haematuria, bilateral sensorineural deafness, and lenticonus. This patient does not have any of these characteristics.

165
Q

Characteristics of membranoproliferastive glomerulonephritis [2]

A

Membranoproliferative glomerulonephritis can present as nephrotic syndrome, haematuria, or proteinuria. It rarely affects children and it can be caused by multiple factors such as cryoglobulinaemia, hepatitis B or C, and partial lipodystrophy. This patient does not have any of these comorbidities.

166
Q

How will minimal change disease present in children [2]

A

Minimal change disease is very common in children, but nearly always presents as nephrotic syndrome. This child’s dipstick is negative for proteins but highly positive for blood, indicating a nephritic syndrome.

167
Q

Classical presentation of IgA nephropathy [4]

A
  • young male, recurrent episodes of macroscopic haematuria
  • typically associated with a recent respiratory tract infection
  • nephrotic range proteinuria is rare
  • renal failure is unusual and seen in a minority of patients
168
Q

Associated conditions with IgA nephopathy [3]

A
  • alcoholic cirrhosis
  • coeliac disease/dermatitis herpetiformis
  • Henoch-Schonlein purpura
169
Q

PP of IgA nephropathy [3]

A
  • thought to be caused by mesangial deposition of IgA immune complexes
  • there is considerable pathological overlap with Henoch-Schonlein purpura (HSP)
  • histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3
170
Q

Differentiating between IgA nephropathy and post-strep glomerulonephritis [3]

A
  • post-streptococcal glomerulonephritis is associated with low complement levels
  • main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)
  • there is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis
171
Q

Mx of IgA nephorpathy

A
  • isolated hematuria, no or minimal proteinuria (less than 500 to 1000 mg/day), and a normal glomerular filtration rate (GFR)
    • no treatment needed, other than follow-up to check renal function
  • persistent proteinuria (above 500 to 1000 mg/day), a normal or only slightly reduced GFR
    • initial treatment is with ACE inhibitors
  • if there is active disease (e.g. falling GFR) or failure to respond to ACE inhibitors
    • immunosuppression with corticosteroids
172
Q

Prognosis of IgA nephropathy [3]

A
  • 25% of patients develop ESRF
  • markers of good prognosis: frank haematuria
  • markers of poor prognosis: male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD
173
Q

Red flags for back pain [12]

A
  • Thoracic pain
  • Age <20 or >55 years
  • Non-mechanical pain
  • Pain worse when supine
  • Night pain
  • Weight loss
  • Pain associated with systemic illness
  • Presence of neurological signs
  • Past medical history of cancer or HIV
  • Immunosuppression or steroid use
  • IV drug use
  • Structural deformity
174
Q

What Ix should pts with back pain have? [3]

A

Patients with red flags should have blood tests for FBC, ESR, Calcium, Phosphate, Alkaline phosphatase and PSA if appropriate. X-ray imaging should also be arranged.

175
Q

Sx of LBP [3]

A
  • *May be acute or chronic**
  • *Pain worse in the morning and on standing**
  • *On examination there may be pain over the facets. The pain is typically worse on extension of the back**
176
Q

Compare spinal stenosis, to AS, to peripheral arterial disease presentation for LBP [3]

A

Spinal stenosisUsually gradual onset
Unilateral or bilateral leg pain (with or without back pain), numbness, and weakness which is worse on walking. Resolves when sits down. Pain may be described as ‘aching’, ‘crawling’.
Relieved by sitting down, leaning forwards and crouching down
Clinical examination is often normal
Requires MRI to confirm diagnosisAnkylosing spondylitisTypically a young man who presents with lower back pain and stiffness
Stiffness is usually worse in morning and improves with activity
Peripheral arthritis (25%, more common if female)Peripheral arterial diseasePain on walking, relieved by rest
Absent or weak foot pulses and other signs of limb ischaemia
Past history may include smoking and other vascular diseases

177
Q

Why is suxamethonium CI in patients with eye injuries? [1]

A

Suxamethonium is contraindicated for patients with penetrating eye injuries or acute narrow angle glaucoma, as suxamethonium increases intra-ocular pressure

178
Q

Compare depolarizing to non-depolarizing neuromusuclar drugs [10]

A

Mechanism of actionBinds to nicotinic acetylcholine receptors resulting in persistent depolarization of the motor end plateCompetitive antagonist of nicotinic acetylcholine receptorsExamplesSuccinylcholine (also known as suxamethonium)Tubcurarine, atracurium, vecuronium, pancuroniumAdverse effectsMalignant hyperthermia
Hyperkalaemia (normally transient)HypotensionReversal Acetylcholinesterase inhibitors (e.g. neostigmine)NotesThe muscle relaxant of choice for rapid sequence induction for intubation

May cause fasciculationsContraindicationsSuxamethonium is contraindicated for patients with penetrating eye injuries or acute narrow angle glaucoma, as suxamethonium increases intra-ocular pressure

179
Q

Drugs to give in TB [1

A

RIPE!

180
Q

MoA and SE of Rifampicin [4]

A
  • mechanism of action: inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA into mRNA
  • potent liver enzyme inducer
  • hepatitis, orange secretions
  • flu-like symptoms
181
Q

MoA and SE of Isoniazid [4]

A
  • mechanism of action: inhibits mycolic acid synthesis
  • peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
  • hepatitis, agranulocytosis
  • liver enzyme inhibitor
182
Q

MoA and SE of Pyrazinamide [4]

A
  • mechanism of action: converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase (FAS) I
  • hyperuricaemia causing gout
  • arthralgia, myalgia
  • hepatitis
183
Q

MoA and Se of Ethambutol [3]

A
  • mechanism of action: inhibits the enzyme arabinosyl transferase which polymerizes arabinose into arabinan
  • optic neuritis: check visual acuity before and during treatment
  • dose needs adjusting in patients with renal impairment
184
Q

When should patietns recieve activated charcoal? [1]

A

The minority of patients who present within 1 hour may benefit from activated charcoal to reduce absorption of the drug.

185
Q

When should acetylcysteine be given for OD? [2]

A
  • there is a staggered overdose* or there is doubt over the time of paracetamol ingestion, regardless of the plasma paracetamol concentration; or
  • the plasma paracetamol concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity
186
Q

How is acetylcysteine given? [1]

A

Acetylcysteine is now infused over 1 hour (rather than the previous 15 minutes) to reduce the number of adverse effects

187
Q

SE of acetylcysteine and how is this generally managed? [2]

A

Acetylcysteine commonly causes an anaphylactoid reaction (non-IgE mediated mast cell release). Anaphylactoid reactions to IV acetylcysteine are generally treated by stopping the infusion, then restarting at a slower rate.

188
Q

What is the King’s College hospital critera for liver transplantation? [4]

A

King’s College Hospital criteria for liver transplantation (paracetamol liver failure)

Arterial pH < 7.3, 24 hours after ingestion

or all of the following:

  • prothrombin time > 100 seconds
  • creatinine > 300 µmol/l
  • grade III or IV encephalopathy
189
Q

What is the King’s College hospital critera for liver transplantation? [4]

A

King’s College Hospital criteria for liver transplantation (paracetamol liver failure)

Arterial pH < 7.3, 24 hours after ingestion

or all of the following:

  • prothrombin time > 100 seconds
  • creatinine > 300 µmol/l
  • grade III or IV encephalopathy
190
Q

What is considered an OD of paracetamol? [1]

A

If all the tablets are not taken within 1 hour

191
Q

Which anti-anginal medications do patients commonly develop tolerance to? [1]

A

Standard release isosorbide mononitrate

192
Q

Summarise Mx for angina pectoris [8]

A
  • all patients should receive aspirin and a statin in the absence of any contraindication
  • sublingual glyceryl trinitrate to abort angina attacks
  • NICE recommend using either a beta-blocker or a calcium channel blocker first-line based on ‘comorbidities, contraindications and the person’s preference’
  • if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used. If used in combination with a beta-blocker then use a long-acting dihydropyridine calcium-channel blocker (e.g. modified-release nifedipine). Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)
  • if there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose (e.g. for atenolol 100mg od)
  • if a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa
  • if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs: a long-acting nitrate, ivabradine, nicorandil or ranolazine
  • if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG
193
Q

How should patients who develop nitrate toleracne be amanged? [1]

A
  • many patients who take nitrates develop tolerance and experience reduced efficacy
  • NICE advises that patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance
  • this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate
194
Q

What is autoimmune hepatitis? [2]

A

Autoimmune hepatitis is condition of unknown aetiology which is most commonly seen in young females. Recognised associations include other autoimmune disorders, hypergammaglobulinaemia and HLA B8, DR3. Three types of autoimmune hepatitis have been characterised according to the types of circulating antibodies present

195
Q

Compare the three types of autoimmune hepatitis [3]

A

Type IType IIType IIIAnti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA)

Affects both adults and children
Anti-liver/kidney microsomal type 1 antibodies (LKM1)

Affects children only
Soluble liver-kidney antigen

Affects adults in middle-age

196
Q

Features of autoimmune hepatitis [5]

A
  • may present with signs of chronic liver disease
  • acute hepatitis: fever, jaundice etc (only 25% present in this way)
  • amenorrhoea (common)
  • ANA/SMA/LKM1 antibodies, raised IgG levels
  • liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis
197
Q

Mx of autoimmmune hepatitis [2]

A
  • steroids, other immunosuppressants e.g. azathioprine
  • liver transplantation
198
Q

Which medicaiton should be given in patients not responding to benzos in status elipsticus? [1]

A

Phenytoin infusion

199
Q

When is carbamazepine used for seizures? [1]

A

Carbamazepine is the drug of choice for simple and complex focal seizures and can be used for generalised tonic clinic seizures, but it is not used in the treatment of status epilepticus.

200
Q

When can propofol be used in seizures? [1]

A

Propofol can be used in intensive care if phenytoin fails to control the seizure at 45minutes.

201
Q

When can sodium valproate be used in seizures? [1]

A

Sodium valproate is the first-line treatment for newly diagnosed generalised tonic-clonic seizures, but it isn’t used in the acute treatment of status epilepticus.

202
Q

When can thimaine be used in seizures? [1]

A

Thiamine should be considered if a seizure is believed to be related to underlying alcohol abuse.

203
Q

Define status elipticus [2]

A
  • a single seizure lasting >5 minutes, or
  • >= 2 seizures within a 5-minute period without the person returning to normal between them
204
Q

Why is status elepticus a medical emergency? [1]

A

Can lead to irreversible brain damage

205
Q

Mx of status eliepticus [4]

A
  • ABC
    • airway adjunct
    • oxygen
    • check blood glucose
  • First-line drugs are benzodiazepines such as diazepam or lorazepam
    • in the prehospital setting diazepam may be given rectally
    • in hospital IV lorazepam is generally used. This may be repeated once after 10-20 minutes
  • If ongoing (or ‘established’) status it is appropriate to start a second-line agent such as phenytoin or phenobarbital infusion
  • If no response (‘refractory status’) within 45 minutes from onset, then the best way to achieve rapid control of seizure activity is induction of general anaesthesia.
206
Q

What is the most common cause of traveller’s diarrhoea? [1]

A

E.coli

207
Q

Define traveller’s diarrhoea [1]

A

Travellers’ diarrhoea may be defined as at least 3 loose to watery stools in 24 hours with or without one of more of abdominal cramps, fever, nausea, vomiting or blood in the stool. The most common cause is Escherichia coli.

208
Q

Common amongst travellers
Watery stools
Abdominal cramps and nausea

A

E coli

209
Q

Prolonged, non-bloody diarrhoea

A

Giardasis

210
Q

Profuse, watery diarrhoea
Severe dehydration resulting in weight loss
Not common amongst travellers

A

Cholera

211
Q

Bloody diarrhoea
Vomiting and abdominal pain

A

Shigella

212
Q

Severe vomiting
Short incubation period

A

Staphylococcus aureus

213
Q

A flu-like prodrome is usually followed by crampy abdominal pains, fever and diarrhoea which may be bloody
May mimic appendicitis
Complications include Guillain-Barre syndrome

A

Campylobacter

214
Q

Two types of illness are seen

  • vomiting within 6 hours, stereotypically due to rice
  • diarrhoeal illness occurring after 6 hours
A

bacillus cereus

215
Q

Gradual onset bloody diarrhoea, abdominal pain and tenderness which may last for several weeks

A

Amoebiasis

216
Q

How long does SHigella take to incubate? [1]

A

Incubation period

  • 1-6 hrs: Staphylococcus aureus, Bacillus cereus*
  • 12-48 hrs: Salmonella, Escherichia coli
  • 48-72 hrs: Shigella, Campylobacter
  • > 7 days: Giardiasis, Amoebiasis
217
Q

Compare adenocarcinoma to SCC of the oesophagus [3]

A

AdenocarcinomaSquamous cell cancerEpidemiologyMost common type in the UK/USLocationLower third - near the gastroesophageal junctionRisk factors

  • GORD
  • Barrett’s oesophagus
  • smoking
  • achalasia
  • obesity
218
Q

Dx of adenocarcinoma [4]

A
  • Upper GI endoscopy is the first line test
  • Contrast swallow may be of benefit in classifying benign motility disorders but has no place in the assessment of tumours
  • Staging is initially undertaken with CT scanning of the chest, abdomen and pelvis. If overt metastatic disease is identified using this modality then further complex imaging is unnecessary
  • If CT does not show metastatic disease, then local stage may be more accurately assessed by use of endoscopic ultrasound
  • Staging laparoscopy is performed to detect occult peritoneal disease. PET CT is performed in those with negative laparoscopy. Thoracoscopy is not routinely performed.
219
Q

Tx of adenocarincoma [3]

A
  • Operable disease is best managed by surgical resection - the most common procedure is an Ivor-Lewis type oesophagectomy
  • The biggest surgical challenge is that of anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis
  • In addition to surgical resection many patients will be treated with adjuvant chemotherapy
220
Q

For each of the following procedures select the most appropriate preparation with respect to ordering blood products:

16.Cystectomy

A

Cross-match 4-6 units depending on local protocols

221
Q

Appendectomy ordering blood products [1]

A

Group and save

222
Q

Elective AAA repair [1]

A

Cross-match 4-6 units depending on local protocols

223
Q

Total replacement ordering blood products

A

Chance of transfusionExample of actionExample of operationsUnlikelyGroup and saveHysterectomy (simple), appendicectomy, thyroidectomy, elective lower segment caesarean section, laparoscopic cholecystectomyLikelyCross-match 2 unitsSalpingectomy for ruptured ectopic pregnancy, total hip replacementDefiniteCross-match 4-6 unitsTotal gastrectomy, oophorectomy, oesophagectomy
Elective AAA repair, cystectomy, hepatectomy

224
Q

thyroidectomy orering blood products [1]

A

Chance of transfusionExample of actionExample of operationsUnlikelyGroup and saveHysterectomy (simple), appendicectomy, thyroidectomy, elective lower segment caesarean section, laparoscopic cholecystectomyLikelyCross-match 2 unitsSalpingectomy for ruptured ectopic pregnancy, total hip replacementDefiniteCross-match 4-6 unitsTotal gastrectomy, oophorectomy, oesophagectomy
Elective AAA repair, cystectomy, hepatectomy

225
Q

which operation definitvely needs blood products ordered? [1]

A

Chance of transfusionExample of actionExample of operationsUnlikelyGroup and saveHysterectomy (simple), appendicectomy, thyroidectomy, elective lower segment caesarean section, laparoscopic cholecystectomyLikelyCross-match 2 unitsSalpingectomy for ruptured ectopic pregnancy, total hip replacementDefiniteCross-match 4-6 unitsTotal gastrectomy, oophorectomy, oesophagectomy
Elective AAA repair, cystectomy, hepatectomy

226
Q

A 50-year-old man presents with red-eye associated with slight watering and mild photophobia. He reports no pain or tenderness and vision is not affected

What is the most likely diagnosis? [1]

A

The correct answer here is episcleritis. All the other causes of a red eye listed present with pain and either blurring of vision or decreased visual acuity. Episcleritis is classically not painful despite diffuse inflammation although mild tenderness may sometimes be reported. It can be treated with non-steroidal anti-inflammatories or steroids in resistant cases.

227
Q

Features of episcleritis

A
  • red eye
  • classically not painful (in comparison to scleritis), but mild pain may be present
  • watering and mild photophobia may be present
  • in episcleritis, the injected vessels are mobile when gentle pressure is applied on the sclera. In scleritis, vessels are deeper, hence do not move
  • phenylephrine drops may be used to differentiate between episcleritis and scleritis. Phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels. If the eye redness improves after phenylephrine a diagnosis of episcleritis can be made
228
Q

A way of differentiating between episcleritis and scleritis? [1]

A
  • phenylephrine drops may be used to differentiate between episcleritis and scleritis. Phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels. If the eye redness improves after phenylephrine a diagnosis of episcleritis can be made
229
Q

Mx of episcleritis [1]

A
  • conservative
  • artificial tears may sometimes be used
230
Q

When should you be concerned if there are no foetal movements? [1]

A

If no foetal movements by 24w, referrral to maternal fetal unit

231
Q

what can reduced fetal movements represent? [1]

A

Reduced fetal movements can represent fetal distress, as a method of fetal compensation to reduce oxygen consumption as a response to chronic hypoxia in utero. This is concerning, as it reflects risk of stillbirth and fetal growth restriction. It is believed that there may also be a link between reduced fetal movements and placental insufficiency.

232
Q

What is the first onset of fetal movements known as? [2]

A

The first onset of recognised fetal movements is known as quickening. This usually occurs between 18-20 weeks gestation, and increase until 32 weeks gestation at which point the frequency of movement tends to plateau. Multiparous women will usually experience fetal movements sooner, from 16-18 weeks gestation. Towards the end of pregnancy, fetal movements should not reduce.

233
Q

What constitutes RFM? [1]

A

Expectant mothers will usually quickly recognise a pattern to these movements. The nature of the movements themselves can be very variable. There is no established definition for what constitutes reduced fetal movements (RFM), but the RCOG considers less than 10 movements within 2 hours (in pregnancies past 28 weeks gestation) an indication for further assessment.

234
Q

How common is RFM? [1]

A

Fetal movements should be established by 24 weeks gestation.

Reduced fetal movements is a fairly common presentation, affecting up to 15% of pregnancies. 3-5% of pregnant women will have recurrent presentations with RFM.

235
Q

RFs for RFM [7]

A
  • Posture
    • There can be positional changes in fetal movement awareness, generally being more prominent during lying down and less when sitting and standing
  • Distraction
    • Awareness of fetal movements can be distractable, and if a woman is busy or concentrating on something else, these can be less prominent
  • Placental position
    • Patient with anterior placentas prior to 28 weeks gestation may have lesser awareness of fetal movements
  • Medication
    • Both alcohol and sedative medications like opiates or benzodiazepines can temporarily cause reduced fetal movements
  • Fetal position
    • Anterior fetal position means movements are less noticeable
  • Body habitus
    • Obese patients are less likely to feel prominent fetal movements
  • Amniotic fluid volume
    • Both oligohydramnios and polyhydramnios can cause reduction in fetal movements
  • Fetal size
    • Up to 29% of women presenting with RFM have a SGA fetus
236
Q

Ix for RFM [4]

A

As per RCOG Green-top guidelines, investigations are dependent of gestation at onset of RFM.

  • If past 28 weeks gestation:
    • Initially, handheld Doppler should be used to confirm fetal heartbeat.
    • If no fetal heartbeat detectable, immediate ultrasound should be offered.
    • If fetal heartbeat present, CTG should be used for at least 20 minutes to monitor fetal heart rate which can assist in excluding fetal compromise.
    • If concern remains, despite normal CTG, urgent (within 24 hours) ultrasound can be used. Ultrasound assessment should include abdominal circumference or estimated fetal weight (to exclude SGA), and amniotic fluid volume measurement
  • If between 24 and 28 weeks gestation, a handheld Doppler should be used to confirm presence of fetal heartbeat.
  • If below 24 weeks gestation, and fetal movements have previously been felt, a handheld Doppler should be used.
  • If fetal movements have not yet been felt by 24 weeks, onward referral should be made to a maternal fetal medicine unit.
237
Q

How are RFM commonly assessed? [2]

A

Fetal movements are usually based solely on maternal perception, though it can also be objectively assessed using handheld Doppler or ultrasonography.

238
Q

Prognosis for RFM [1]

A

Concern regarding absent or reduced fetal movements stems for the potential for this presentation to represent fetal distress or impending demise. Between 40-55% of women who suffer from stillbirth experience reduced fetal movements prior to diagnosis.

However, in 70% of pregnancies with a single episode of reduced fetal movement, there is no onward complication.

239
Q

Compare lichen planus to lichen sclerosus [2]

A

Lichen

  • planus: purple, pruritic, papular, polygonal rash on flexor surfaces. Wickham’s striae over surface. Oral involvement common
  • sclerosus: itchy white spots typically seen on the vulva of elderly women
240
Q

Features of lichen planus

A
  • itchy, papular rash most common on the palms, soles, genitalia and flexor surfaces of arms
  • rash often polygonal in shape, with a ‘white-lines’ pattern on the surface (Wickham’s striae)
  • Koebner phenomenon may be seen (new skin lesions appearing at the site of trauma)
  • oral involvement in around 50% of patients: typically a white-lace pattern on the buccal mucosa
  • nails: thinning of nail plate, longitudinal ridging
241
Q

Which drugs can cause lichenoid drug eruptions? [3]

A
  • gold
  • quinine
  • thiazides
242
Q

Mx of lichen planus [3]

A
  • potent topical steroids are the mainstay of treatment
  • benzydamine mouthwash or spray is recommended for oral lichen planus
  • extensive lichen planus may require oral steroids or immunosuppression
243
Q

A 55-year-old man presents with intermittent leg pain which is exacerbated by movement and relieved by rest. He denies recent injury or illness. ABPI is 0.8. Which Tx should he be on? [2]

A

Atorvastatin 80mg OD and Clopidogrel → all patietns with PAD should take these two drugs [he’s experiencing intermittent claudication]

244
Q

Commonest cause of intermittent claudication? [1]

A

Athersclerosis

245
Q

ABPI that suggests PAD [1]

A

Below 0.9

246
Q

ABPI that suggests CLI [1]

A

below 0.5

247
Q

What type of Mx has shwons significant beenfits for PAD? [1]

A

Exercise training

248
Q

How is PAD Mx? [4]

A

Peripheral arterial disease (PAD) is strongly linked to smoking. Patients who still smoke should be given help to quit smoking.

Comorbidities should be treated, including

  • hypertension
  • diabetes mellitus
  • obesity

As with any patient who has established cardiovascular disease, all patients should be taking a statin. Atorvastatin 80 mg is currently recommended. In 2010 NICE published guidance suggesting that clopidogrel should be used first-line in patients with peripheral arterial disease in preference to aspirin.

Exercise training has been shown to have significant benefits. NICE recommend a supervised exercise programme for all patients with peripheral arterial disease prior to other interventions.

249
Q

How is severe PAD or CLI Mx? [3]

A
  • angioplasty
  • stenting
  • bypass surgery
250
Q

When should amputation be consdiered for CLI? [1]

A

Amputation should be reserved for patients with critical limb ischaemia who are not suitable for other interventions such as angioplasty of bypass surgery.

251
Q

Other drugs licensed for PAD? [2]

A
  • naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life
  • cilostazol: phosphodiesterase III inhibitor with both antiplatelet and vasodilator effects - not recommended by NICE
252
Q

What is high temperature generally considered in an adult?

A

Over 38

253
Q

Other than findings resp exam, which observations will make Dx of tension pnueothorax more likely than simple pneuothorax [1]

A

Hypotension will occur in tension pneumothoraces as a result of cardiac outflow obstruction

254
Q

When can tension pneuothorax occur? [1]

A
  • May occur following thoracic trauma when a lung parenchymal flap is created.
255
Q

What does a parenchymal flap create? [1]

A
  • This acts as a one way valve and allows pressure to rise.
256
Q

Resp examination findings of tension pneuothorax [1]

A
  • The trachea shifts and hyper-resonance is apparent on the affected side.
257
Q

How is tension pneuothorax Mx? [1]

A
  • Treatment is with needle decompression and chest tube insertion.
258
Q

What is codeine to morphine equivalent dose? [1]

A

Codeine to morphine divide by 10

259
Q

Codeine to morphine

A

divide by 10

260
Q

tramadol to morhpine

A

divide by 10 [same as codeine]

261
Q

morphine to oxycodone

A

divide by 1.5-2

262
Q

What are the conversion factors for transdermal patches? [2]

A
  • a transdermal fentanyl 12 microgram patch equates to approximately 30 mg oral morphine daily
  • a transdermal buprenorphine 10 microgram patch equates to approximately 24 mg oral morphine daily.
263
Q

Oral morphine to subcut morphine

A

divide by 2

264
Q

oral morphine to subcut diamorphine

A

FromToConversion factorOral morphineSubcutaneous morphineDivide by 2Oral morphineSubcutaneous diamorphineDivide by 3Oral oxycodoneSubcutaneous diamorphineDivide by 1.5

265
Q

orla oxycodone to subcut diamorphine

A

FromToConversion factorOral morphineSubcutaneous morphineDivide by 2Oral morphineSubcutaneous diamorphineDivide by 3Oral oxycodoneSubcutaneous diamorphineDivide by 1.5

266
Q

Migraine during pregnancy Mx [3]

A
  • paracetamol 1g is first-line
  • NSAIDs can be used second-line in the first and second trimester
  • avoid aspirin and opioids such as codeine during pregnancy
267
Q

Migraine and the COCP [1]

A
  • if patients have migraine with aura then the COC is absolutely contraindicated due to an increased risk of stroke (relative risk 8.72)
268
Q

Migraine and menstruation [2]

A
  • many women find that the frequency and severity of migraines increase around the time of menstruation
  • SIGN recommends that women are treated with mefanamic acid or a combination of aspirin, paracetamol and caffeine. Triptans are also recommended in the acute situation
269
Q

Migraine and HRT [1]

A
  • safe to prescribe HRT for patients with a history of migraine but it may make migraines worse
270
Q

Which organism is responsible for Scarlet fever? [1]

A

Scarlet fever is a reaction to erythrogenic toxins produced by Group A haemolytic streptococci (usually Streptococcus pyogenes)

271
Q

A 65-year-old man calls an ambulance as he has central crushing chest pain that radiates to his left arm and jaw. As he arrives at the emergency department his heart rate is found to be 50/min. An ECG is performed which shows ST elevation and bradycardia with a 1st-degree heart block.

Given the history, which of the following are the leads will most likely show the ST elevation? [2]

A

This question is asking about the presentation of an ST-elevated myocardial infarction. The patient has presented 1st-degree heart block following his MI and so we can work out that his MI has most likely affected the inferior leads (right coronary arteries also provide blood supply to the AV node). Therefore the question requires you to know that leads II, III and aVF represent the inferior heart and the right coronary artery.

272
Q

What ECG changes correspond to the LAD? [1]

A

ECG changesCoronary arteryAnteroseptalV1-V4InferiorII, III, aVFAnterolateralV4-6, I, aVLLateralI, aVL +/- V5-6PosteriorTall R waves V1-2

273
Q

What ECG changes correspond to the left circumflex artery? [1]

A

ECG changesCoronary arteryAnteroseptalV1-V4InferiorII, III, aVFAnterolateralV4-6, I, aVLLateralI, aVL +/- V5-6PosteriorTall R waves V1-2

274
Q

Summarise inferior, aterolateral, laterla, posterior, inferior ECG changes [5]

A

ECG changesCoronary arteryAnteroseptalV1-V4InferiorII, III, aVFAnterolateralV4-6, I, aVLLateralI, aVL +/- V5-6PosteriorTall R waves V1-2

275
Q

Why may a new LBBB point towards? [1]

A

ACS

276
Q

Which territories on an ECG does the lateral, inferior, anterior and lateral leads correspond to? [4]

A
277
Q

What are the requirements for maintenance fluids? [3]

A
  • 25-30 ml/kg/day of water and
  • approximately 1 mmol/kg/day of potassium, sodium and chloride and
  • approximately 50-100 g/day of glucose to limit starvation ketosis
278
Q

So, what would an 80kg man recieve maintenance fluids over 24h? [2]

A
  • 2 litres of water
  • 80mmol potassium
279
Q

Electrolytes in plasma [4]

A

Na+Cl-K+HCO3-GlucosePlasma135-14598-1053.5-522-280.9% saline154154–5% glucose—-0.18% saline with 4% glucose3030–Hartmann’s solution131111529

280
Q

Electrolytes in 0.9% saline

A

Na+Cl-K+HCO3-GlucosePlasma135-14598-1053.5-522-280.9% saline154154–5% glucose—-0.18% saline with 4% glucose3030–Hartmann’s solution131111529

281
Q

What does Hartmann’s solution contain? [4]

A

Na+Cl-K+HCO3-GlucosePlasma135-14598-1053.5-522-280.9% saline154154–5% glucose—-0.18% saline with 4% glucose3030–Hartmann’s solution131111529

282
Q

what is there is a risk of in patients if lrge volumes of 0.9% are used? [1]

A
  • if large volumes are used there is an increased risk of hyperchloraemic metabolic acidosis
283
Q

What type of patients should Hartmann’s solution not be used for? [1]

A
  • contains potassium and therefore should not be used in patients with hyperkalaemia
284
Q

What does seborrhoeic keratosis look like? [2]

A

This lesion is characteristic of a seborrhoeic keratosis. Seborrhoeic keratoses are benign skin lesions that are common in people over 50. Note the brown nodule with a fissured greasy surface that is well demarcated against the skin. It has the classic ‘stuck on’ appearance of seborrhoeic keratoses. Most seborrhoeic keratosis lesions are asymptomatic and therefore no treatment is required.

285
Q

What does actinic keratosis look like? [2]

A

Actinic keratosis (AK) is incorrect. AK is associated with chronic UV exposure and are typically flesh-coloured, irregularly shaped, small macules or plaques. Actinic keratoses have the potential to progress to squamous cell carcinoma. The lesions are small (typically 1-5mm) and do not have a ‘stuck on’ appearance as in this case.

286
Q

Features of Bowen’s disease [2]

A

Bowen’s disease is also known as squamous cell carcinoma (SCC) in situ. Typically these lesions are slow-growing, red, scaly patches.

287
Q

Features of malignant melanoma [2]

A

Malignant melanoma is an important differential to consider. However, a malignant melanoma typically varies more in colour, such as brown/blue/black and red. Furthermore, melanomas do not have a ‘stuck on’ and greasy appearance as in this case.

288
Q

Naevus features [2]

A

Naevus is not the correct answer in this case. Naevi typically develop within the first 20 years of life, whereas seborrhoeic keratosis is more common with advancing age

289
Q

Features seborrhoeic keratoses [3]

A

Seborrhoeic keratoses are benign epidermal skin lesions seen in older people.

Features

  • large variation in colour from flesh to light-brown to black
  • have a ‘stuck-on’ appearance
  • keratotic plugs may be seen on the surface
290
Q

Seborrhoiec keratoses Mx

A

reassurance about benign nature of the lesion is an option

options for removal include crettage, cryosurgery, shave biopsy

291
Q

What does osteomylitis describe? [1]

A

Infeciton of the bone

292
Q

Subclassificaitons of osteomyelitis [2]

A
  • haematogenous osteomyelitis
    • results from bacteraemia
    • is usually monomicrobial
    • most common form in children
    • vertebral osteomyelitis is the most common form of haematogenous osteomyelitis in adults
    • risk factors include: sickle cell anaemia, intravenous drug user, immunosuppression due to either medication or HIV, infective endocarditis
  • non-haematogenous osteomyelitis:
    • results from the contiguous spread of infection from adjacent soft tissues to the bone or from direct injury/trauma to bone
    • is often polymicrobial
    • most common form in adults
    • risk factors include: diabetic foot ulcers/pressure sores, diabetes mellitus, peripheral arterial disease
293
Q

Microbiology of OM

A
  • Staph. aureus is the most common cause except in patients with sickle-cell anaemia where Salmonella species predominate
294
Q

Ix for OM [1]

A

MRI imaging of choice mdality, sensitivty of 90-100%

295
Q

Mx of OM [2]

A
  • flucloxacillin for 6 weeks
  • clindamycin if penicillin-allergic
296
Q

Gluten containing foods

A
  • wheat: bread, pasta, pastry
  • barley: beer
    • whisky is made using malted barley. Proteins such as gluten are however removed during the distillation process making it safe to drink for patients with coeliac disease
  • rye
  • oats
    • some patients with coeliac disease appear able to tolerate oats
297
Q

Notable foods that are gluten free

A

rice, potatoes, corn

298
Q

What can be checked to check compliance to gluten free diet? [1]

A

Tissue transglutaminase

299
Q

What vaccine are all coeliac patients offered? [2]

A
  • Patients with coeliac disease often have a degree of functional hyposplenism
  • For this reason, all patients with coeliac disease are offered the pneumococcal vaccine
    • Coeliac UK recommends that everyone with coeliac disease is vaccinated against pneumococcal infection and has a booster every 5 years
  • Currrent guidelines suggest giving the influenza vaccine on an individual basis.
300
Q

Which index used to assess severity of UC in adults? [1]

A

The Truelove and Witts’ severity index is recommended by NICE when assessing the severity of ulcerative colitis in adults.

301
Q

How should patients with severe UC be Mx? [1]

A

Any patient with features of severe ulcerative colitis should be admitted to hospital as an emergency. They should be treated with intravenous corticosteroids to induce remission.

302
Q

Flare ups for UC [3]

A
  • stress
  • medications
    • NSAIDs
    • antibiotics
  • cessation of smoking
303
Q

Mild vs moderate vs severe flare ups of UC [according tot eh Truelove and Witts’ severity index]

A

MildModerateSevereFewer than four stools daily, with or without blood

No systemic disturbance

Normal erythrocyte sedimentation rate and C-reactive protein valuesFour to six stools a day, with minimal systemic disturbance

More than six stools a day, containing blood

Evidence of systemic disturbance, e.g.

  • fever
  • tachycardia
  • abdominal tenderness, distension or reduced bowel sounds
  • anaemia
  • hypoalbuminaemia
304
Q

A 65-year-old woman with COPD attends surgery with a 2-day history of worsening dyspnoea, productive cough, and fever. On examination, she has basal crackles on the right side. Organism?

A

Haemophilus influenzae75%

This is an infective exacerbation of COPD, with the fever and basal crackles indicating a bacterial cause. The most common cause in COPD is Haemophilus influenzae.

305
Q

An 8-year-old boy is brought in by his mother with a history of shortness of breath and fever over the last few hours. On examination, he has a toxic appearance, has inspiratory stridor, and is drooling.

A

Haemophilus influenzae type B64%

The history indicates acute epiglottitis, and this child would obviously need an ambulance to transfer him to the emergency department urgently. The most common cause of acute epiglottitis in children is Haemophilus influenzae type B, and the incidence of acute epiglottitis has fallen since the introduction of the Hib vaccine.

306
Q

A 27-year-old man attends with a 2-day history of right-sided otalgia and discharge. He is a keen swimmer. On examination, the external auditory canal is swollen and erythematous, with purulent material on the walls.

A

Pseudomonas aeruginosa34%

Bacterial causes of otitis externa are most common, with Pseudomonas aeruginosa being most prevalent. Other causes include Staphylococcus aureus.

307
Q

What are the two types of bacteria? [2]

A
  • Gram-positive cocci = staphylococci + streptococci (including enterococci)
  • Gram-negative cocci = Neisseria meningitidis + Neisseria gonorrhoeae, also Moraxella catarrhalis
308
Q

Name all the gram-positive rods? [5]

A

Therefore, only a small list of Gram-positive rods (bacilli) need to be memorised to categorise all bacteria - mnemonic = ABCD L

  • Actinomyces
  • Bacillus anthracis (anthrax)
  • Clostridium
  • Diphtheria: Corynebacterium diphtheriae
  • Listeria monocytogenes
309
Q

Name gram-negative rods

A

Remaining organisms are Gram-negative rods, e.g.:

  • Escherichia coli
  • Haemophilus influenzae
  • Pseudomonas aeruginosa
  • Salmonella sp.
  • Shigella sp.
  • Campylobacter jejuni
310
Q

What is Pharyngeal pouch? [2]

A

Phayngeal pouch: During swallowing an outpouching of the posterior hypopharyngeal wall is visualised at the level C5-C6, right above the upper oesophageal sphincter.

A pharyngeal pouch is a posteromedial diverticulum through Killian’s dehiscence. Killian’s dehiscence is a triangular area in the wall of the pharynx between the thyropharyngeus and cricopharyngeus muscles. It is more common in older patients and is 5 times more common in men

311
Q

Features of pharyngeal pouch [5]

A
  • dysphagia
  • regurgitation
  • aspiration
  • neck swelling which gurgles on palpation
  • halitosis
312
Q

Mx of pharyngeal pouch

A

Surgery

313
Q

A 62-year-old woman presents with a one day history of pain around her right eye. She feels nauseated and has vomited once. On examination her right eye is red

A

Acute glaucoma

314
Q

A 42-year-old man presents with pain in the posterior and left side of his head. This came on over one minute and is now severe. The pain is worse when he bends his neck. His temperature is 37.3ºC

A

SaH

315
Q

A 22-year-old woman presents with recurrent headaches around the time of her periods. These are typically on the left-side and severe. When she gets a headache it lasts several hours and she usually goes to bed.

A

Migraine

316
Q

Pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours with clusters typically lasting 4-12 weeks
Intense pain around one eye (recurrent attacks ‘always’ affect same side)
Patient is restless during an attack
Accompanied by redness, lacrimation, lid swelling
More common in men and smokers

A

Cluster headache

317
Q

Typically patient > 60 years old
Usually rapid onset (e.g. < 1 month) of unilateral headache
Jaw claudication (65%)
Tender, palpable temporal artery
Raised ESR

A

Temporal artery

318
Q

Present for 15 days or more per month
Developed or worsened whilst taking regular symptomatic medication
Patients using opioids and triptans are at most risk
May be psychiatric co-morbidity

A

Medicaiton overuse headache

319
Q

Suggest other causes of an acute headache

A
  • meningitis
  • encephalitis
  • subarachnoid haemorrhage
  • head injury
  • sinusitis
  • glaucoma (acute closed-angle)
  • tropical illness e.g. Malaria
320
Q

Suggest causes of a chronic headache

A
  • chronically raised ICP
  • Paget’s disease
  • psychological
321
Q

A 77-year-old man presents to his GP with a painful rash around his ear. He first noticed pain in his left ear 3 days ago and is now also complaining of vertigo and tinnitus. On examination, you note a vesicular rash around his left ear.

Given the most likely diagnosis, what is the most appropriate treatment for this patient?

A

Ramsey Hunt syndreom: Oral aciclovir and oral prednisolone for 5d

322
Q

What is Ramsey Hunt syndrome? [2]

A

Ramsay Hunt syndrome (herpes zoster oticus) is caused by the reactivation of the varicella zoster virus in the geniculate ganglion of the seventh cranial nerve.

323
Q

Features of Ramsey Hunt syndrome [4]

A
  • auricular pain is often the first feature
  • facial nerve palsy
  • vesicular rash around the ear
  • other features include vertigo and tinnitus
324
Q

A 11-year-old boy with severe lower abdominal pain is rushed to the Emergency Department by his mother. On examination, you note that the left testicle is swollen, higher than the right and it is exquisitely tender to touch. He is apyrexial. The cremasteric reflex is absent. He denies any urinary symptoms. The pain started approximately 120 minutes ago. What is the most appropriate next step in his management?

A

Emergency surgical exploration as this is presentation of testicular torsion!

325
Q

When is testicular cacner most common? p[1]

A

Men aged 20-30 y/o

326
Q

Where do the testicular tumours derive from? [1]

A

Around 95% are germ-cell tumours

327
Q

Features, tumour markers and pathology of seminoma

A
  • Tumour typeKey featuresTumour markers*PathologySeminoma
  • Commonest subtype (50%)
  • Average age at diagnosis = 40
  • Even advanced disease associated with 5 year survival of 73%
  • AFP usually normal
  • HCG elevated in 10% seminomas
  • Lactate dehydrogenase; elevated in 10-20% seminomas (but also in many other conditions)
    Sheet like lobular patterns of cells with substantial fibrous component. Fibrous septa contain lymphocytic inclusions and granulomas may be seen.
328
Q

Features, tumour markers and pathology of non-seminomatous tumours [4]

A

Non seminomatous germ cell tumours (42%)

  • Teratoma
  • Yolk sac tumour
  • Choriocarcinoma
  • Mixed germ cell tumours (10%)
  • Younger age at presentation =20-30 years
  • Advanced disease carries worse prognosis (48% at 5 years)
  • Retroperitoneal lymph node dissection may be needed for residual disease after chemotherapy
  • AFP elevated in up to 70% of cases
  • HCG elevated in up to 40% of cases
  • Other markers rarely helpful
    Heterogenous texture with occasional ectopic tissue such as hair
329
Q

RFs for testicular Ca

A
  • Cryptorchidism
  • Infertility
  • Family history
  • Klinefelter’s syndrome
  • Mumps orchitis
330
Q

Features of testicular Ca

A
  • A painless lump is the most common presenting symptom
  • Pain may also be present in a minority of men
  • Other possible features include hydrocele, gynaecomastia
331
Q

Dx of testicular Ca [3]

A
  • Ultrasound is first-line
  • CT scanning of the chest/ abdomen and pelvis is used for staging
  • Tumour markers (see above) should be measured
332
Q

Mx of testicular Ca [3]

A
  • Orchidectomy (Inguinal approach)
  • Chemotherapy and radiotherapy may be given depending on staging
  • Abdominal lesions >1cm following chemotherapy may require retroperitoneal lymph node dissection.
333
Q

Prognosis of testicualr tumours [2]

A
  • 5 year survival for seminomas is around 95% if Stage I
  • 5 year survival for teratomas is around 85% if Stage I
334
Q

Feeatures of epididymo-orchitis

A

Acute epididymitis is an acute inflammation of the epididymis, often involving the testis and usually caused by bacterial infection.

  • Infection spreads from the urethra or bladder. In men <35 years, gonorrhoea or chlamydia are the usual infections.
  • Amiodarone is a recognised non infective cause of epididymitis, which resolves on stopping the drug.
  • Tenderness is usually confined to the epididymis, which may facilitate differentiating it from torsion where pain usually affects the entire testis.
335
Q

Features of testicular torsion [5]

A
  • Twist of the spermatic cord resulting in testicular ischaemia and necrosis.
  • Most common in males aged between 10 and 30 (peak incidence 13-15 years)
  • Pain is usually severe and of sudden onset.
  • Cremasteric reflex is lost and elevation of the testis does not ease the pain.
  • Treatment is with surgical exploration. If a torted testis is identified then both testis should be fixed as the condition of bell clapper testis is often bilateral.
336
Q

Features of a hydrocele [5]

A
  • Presents as a mass that transilluminates, usually possible to ‘get above’ it on examination.
  • In younger men it should be investigated with USS to exclude tumour.
  • In children it may occur as a result of a patent processus vaginalis.
  • Treatment in adults is with a Lords or Jabouley procedure.
  • Treatment in children is with trans inguinal ligation of PPV.
337
Q

A 32-year-old woman presents with a tender breast lump. She has a 2 month old child. Clinically there is a tender, fluctuant mass of the breast.

A

The correct answer is: Breast abscess70%

This lady is likely to be breast feeding and is at risk of mastitis. This may lead to an abscess if not treated. Staphylococcus aureus is usually the causative organism.

338
Q

A 53-year-old lady presents with a creamy nipple discharge. On examination she has discharge originating from multiple ducts and associated nipple inversion.

A

Duct ectasia55%

Duct ectasia is common during the period of breast involution that occurs during the menopausal period. As the ducts shorten they may contain insipiated material. The discharge will often discharge from several ducts

339
Q

A 52-year-old lady presents with an episode of nipple discharge. It is usually clear in nature. On examination the discharge is seen to originate from a single duct and although it appears clear, when the discharge is tested with a labstix it is shown to contain blood. Imaging and examination shows no obvious mass lesion.

A

Intraductal papilloma65%

Intraductal papilloma usually cause single duct discharge. The fluid is often clear, although it may be blood stained. If the fluid is tested with a labstix (little point in routine practice) then it will usually contain small amounts of blood. A microdocechtomy may be performed.

340
Q
  • Present at younger age than duct ectasia
  • May present with features of inflammation, abscess or mammary duct fistula
  • Stongly associated with smoking
  • Usually treated with antibiotics, abscess will require drainage
A

Periductal mastitis

341
Q
  • Growth of papilloma in a single duct
  • Usually presents with clear or blood stained discharge originating from a single duct
  • No increase in risk of malignancy
A

Intraductal papilloma

342
Q

Duct ectasia features [4]

A
  • Mammary duct ectasia may be seen in up to 25% of normal female breasts
  • Patients usually present with nipple discharge, which may be from single or multiple ducts (usually present age >50 years)
  • The discharge is often thick and green
  • Duct ectasia is a normal varient of breast involution and is not the same condition as periductal mastitis
343
Q

Breast abscess features [5]

A
  • Lactational mastitis is common
  • Infection is usually with Staphylococcus aureus
  • On examination there is usually a tender fluctuant mass
  • Treatment is with antibiotics and ultrasound guided aspiration
  • Overlying skin necrosis is an indication for surgical debridement, which may be complicated by the development of a subsequent mammary duct fistula.
344
Q

TB in breasts features [4]

A
  • Rare in western countries, usually secondary TB
  • Affects women later in child bearing period
  • Chronic breast or axillary sinus is present in up to 50% cases
  • Diagnosis is by biopsy culture and histology
345
Q

. Which of the following is the most likely location of the ectopic pregnancy?

A

Ampulla fallopian tube

346
Q

Chance of having a tubal ecoptic

A

tubal ectopic: 93-97%

  • ampullary ectopic: most common ~70% of tubal ectopics and ~65% of all ectopics
  • isthmal ectopic: ~12% of tubal ectopics and ~11% of all ectopics
  • fimbrial ectopic: ~11% of tubal ectopics and ~10% of all ectopics
347
Q

What is an ectopic pregnancy? [1]

A

Implantation of a fertilized ovum outside the uterus results in an ectopic pregnancy

348
Q

How common are ecotpics? [1]

A
  • incidence = c. 0.5% of all pregnancies
349
Q

RFs for ecoptics [5]

A
  • damage to tubes (pelvic inflammatory disease, surgery)
  • previous ectopic
  • endometriosis
  • IUCD
  • progesterone only pill
  • IVF (3% of pregnancies are ectopic)
350
Q

What is Kartagener’s syndrome? [2]

A

Kartagener’s syndrome (also known as primary ciliary dyskinesia) was first described in 1933 and most frequently occurs in examinations due to its association with dextrocardia (e.g. ‘quiet heart sounds’, ‘small volume complexes in lateral leads’)

351
Q

Pathogenesis and features of Kartagener’s syndrome [5]

A

Pathogenesis

  • dynein arm defect results in immotile cilia

Features

  • dextrocardia or complete situs inversus
  • bronchiectasis
  • recurrent sinusitis
  • subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
352
Q

How would minimal change disease present? [1]

A

Minimal change disease would have been the most likely differential of nephrotic syndrome were the patient a child.

353
Q

How would mesangiocapillary glomerulonephritis present? [2]

A

Mesangiocapillary glomerulonephritis causes a nephritic syndrome with at least a small amount of blood being present in the urine, which is absent in this patient.

354
Q

How would granulomatosis present? [1]

A

Granulomatosis with polyangiitis is associated with a more nephritic picture.

355
Q

How would Goodpasture’s present? [2]

A

Goodpasture’s is associated with haematuria and concurrent pulmonary disease in which haemoptysis is a feature, neither of which this patient has.

356
Q

What is FSGS a cause of? WHome does it present in? [2]

A

Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome and chronic kidney disease. It generally presents in young adults.

357
Q

Causes of FSGS [5]

A
  • idiopathic
  • secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
  • HIV
  • heroin
  • Alport’s syndrome
  • sickle-cell
358
Q

Ix for FSGC [2]

A
  • renal biopsy
    • focal and segmental sclerosis and hyalinosis on light microscopy
    • effacement of foot processes on electron microscopy
359
Q

Mx and prognosis of FSGS

A

Management

  • steroids +/- immunosuppressants

Prognosis

  • untreated FSGS has a < 10% chance of spontaneous remission
360
Q

Which drugs are known to improve long term survival for congestive HF? [3]

A

This patient has features of congestive heart failure. While loop diuretics (furosemide, bumetanide) and nitrates are important in the management of acute or decompensated cardiac failure, they have no effect on long-term survival.

The following drugs have all been shown to reduce mortality in patients with left ventricular failure:

  • ACE-inhibitors
  • Beta-blockers
  • Angiotensin receptor blockers
  • Aldosterone antagonists
  • Hydralazine and nitrates
361
Q

Does digoxin improve mortality for CHF? [1]

A

Digoxin has been shown to reduce hospital admissions but not mortality. It is generally used in patients with worsening heart failure despite first or second line treatments, or in patients with co-existant atrial fibrillation

362
Q

1st line Tx for all patients with heart failure [3]

A

The first-line treatment for all patients is both an ACE-inhibitor and a beta-blocker

  • generally, one drug should be started at a time. NICE advise that clinical judgement is used when determining which one to start first
  • beta-blockers licensed to treat heart failure in the UK include bisoprolol, carvedilol, and nebivolol.
  • ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction
363
Q

2nd line Tx for heart failure [2]

A

Second-line treatment is an aldosterone antagonist

  • these are sometimes referred to as mineralocorticoid receptor antagonists. Examples include spironolactone and eplerenone
  • it should be remembered that both ACE inhibitors (which the patient is likely to already be on) and aldosterone antagonists both cause hyperkalaemia - therefore potassium should be monitored
364
Q

Third-line Tx for heart failure [5]

A

Third-line treatment should be initiated by a specialist. Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy

  • ivabradine
    • criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%
  • sacubitril-valsartan
    • criteria: left ventricular fraction < 35%
    • is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
    • should be initiated following ACEi or ARB wash-out period
  • digoxin
    • digoxin has also not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties
    • it is strongly indicated if there is coexistent atrial fibrillation
  • hydralazine in combination with nitrate
    • this may be particularly indicated in Afro-Caribbean patients
  • cardiac resynchronisation therapy
    • indications include a widened QRS (e.g. left bundle branch block) complex on ECG
365
Q

What immunisations should CHF pts also recieve? [2]

A
  • offer annual influenza vaccine
  • offer one-off pneumococcal vaccine
    • adults usually require just one dose but those with asplenia, splenic dysfunction or chronic kidney disease need a booster every 5 years
366
Q

What is allergic bronchoplumonary aspergillosis? [2]

A

Allergic bronchopulmonary aspergillosis results from an allergy to Aspergillus spores. In the exam questions often give a history of bronchiectasis and eosinophilia.

367
Q

Features of ABA [2]

A
  • bronchoconstriction: wheeze, cough, dyspnoea. Patients may have a previous label of asthma
  • bronchiectasis (proximal)
368
Q

Ix for ABA [5]

A
  • eosinophilia
  • flitting CXR changes
  • positive radioallergosorbent (RAST) test to Aspergillus
  • positive IgG precipitins (not as positive as in aspergilloma)
  • raised IgE
369
Q

Mx of ABA [2]

A
  • oral glucocorticoids
  • itraconazole is sometimes introduced as a second-line agent
370
Q

How can a patient be diagnosed with DM? [1]

A

The diagnosis of type 2 diabetes mellitus can be made by either a plasma glucose or a HbA1c sample. Diagnostic criteria vary according to whether the patient is symptomatic (polyuria, polydipsia etc) or not.

371
Q

How to Dx DM [3]

A

If the patient is symptomatic:

  • fasting glucose greater than or equal to 7.0 mmol/l
  • random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.

372
Q

Diagnosis of DM for HbA1c [4]

A
  • a HbA1c of greater than or equal to 48 mmol/mol (6.5%) is diagnostic of diabetes mellitus
  • a HbAlc value of less than 48 mmol/mol (6.5%) does not exclude diabetes (i.e. it is not as sensitive as fasting samples for detecting diabetes)
  • in patients without symptoms, the test must be repeated to confirm the diagnosis
  • it should be remembered that misleading HbA1c results can be caused by increased red cell turnover (see below)
373
Q

Conditions where HbA1c may not be used for diagnosis [5]

A
  • haemoglobinopathies
  • haemolytic anaemia
  • untreated iron deficiency anaemia
  • suspected gestational diabetes
  • children
  • HIV
  • chronic kidney disease
  • people taking medication that may cause hyperglycaemia (for example corticosteroids)
374
Q

What is the definition of impaired fasting lgucose and impaired glucose tolerance? [3]

A

A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)

Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

Diabetes UK suggests:

  • ‘People with IFG should then be offered an oral glucose tolerance test to rule out a diagnosis of diabetes. A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person doesn’t have diabetes but does have IGT.’
375
Q

What should be offered to women who’ve had wide-local excision procedure [1]

A

Whole breast radiotherapy

376
Q

Features of chronic plaque psoriasis

A
  • erythematous plaques covered with a silvery-white scale
  • typically on the extensor surfaces such as the elbows and knees. Also common on the scalp, trunk, buttocks and periumbilical area
  • clear delineation between normal and affected skin
  • plaques typically range from 1 to 10 cm in size
  • if the scale is removed, a red membrane with pinpoint bleeding points may be seen (Auspitz’s sign)
377
Q

How common is chronic plaque psoriasis? [1]

A

Chronic plaque psoriasis is the most common form of psoriasis seen in clinical practice, accounting for around 80% of presentations.

378
Q

Which antibiotics are used in the respriatory system for excerbations of chronic bronchitis, CAP, pneuomnia, HAP [4]

A

Exacerbations of chronic bronchitisAmoxicillin or tetracycline or clarithromycinUncomplicated community-acquired pneumoniaAmoxicillin (Doxycycline or clarithromycin in penicillin allergic, add flucloxacillin if staphylococci suspected e.g. In influenza)Pneumonia possibly caused by atypical pathogensClarithromycinHospital-acquired pneumoniaWithin 5 days of admission: co-amoxiclav or cefuroxime
More than 5 days after admission: piperacillin with tazobactam OR a broad-spectrum cephalosporin (e.g. ceftazidime) OR a quinolone (e.g. ciprofloxacin)

379
Q

Abx for LUTI, pyelonephritis, acute prostitis

A

Lower urinary tract infectionTrimethoprim or nitrofurantoin. Alternative: amoxicillin or cephalosporinAcute pyelonephritisBroad-spectrum cephalosporin or quinoloneAcute prostatitisQuinolone or trimethoprim

380
Q

Abx for skin conditions: impetigo, cellulitis, erysipelas, animal bite, mastitis [6]

A

ConditionRecommended treatmentImpetigoTopical hydrogen peroxide, oral flucloxacillin or erythromycin if widespreadCellulitisFlucloxacillin (clarithromycin, erythromycin or doxycycline if penicillin-allergic)Cellulitis (near the eyes or nose)Co-amoxiclav (clarithromycin, + metronidazole if penicillin-allergic)ErysipelasFlucloxacillin* (clarithromycin, erythromycin or doxycycline if penicillin-allergic)Animal or human biteCo-amoxiclav (doxycycline + metronidazole if penicillin-allergic)Mastitis during breast-feedingFlucloxacillin

381
Q

Abx for throat infections, sinusitis, otitis media, otitis externa, periapical or periodontal abscess, ginigitivits [6]

A

Throat infectionsPhenoxymethylpenicillin (erythromycin alone if penicillin-allergic)SinusitisPhenoxymethylpenicillinOtitis mediaAmoxicillin (erythromycin if penicillin-allergic)Otitis externa**Flucloxacillin (erythromycin if penicillin-allergic)Periapical or periodontal abscessAmoxicillinGingivitis: acute necrotising ulcerativeMetronidazole

382
Q

Abx for gonorrhoea, chlamydia, PID, syphilis, bacterial vaginosis

A

ConditionRecommended treatmentGonorrhoeaIntramuscular ceftriaxoneChlamydiaDoxycycline or azithromycinPelvic inflammatory diseaseOral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline + oral metronidazoleSyphilisBenzathine benzylpenicillin or doxycycline or erythromycinBacterial vaginosisOral or topical metronidazole or topical clindamycin

383
Q

Abx for C.diff, campylobacter enteritis, salmonella [4]

A

Clostridium difficileFirst episode: metronidazole
Second or subsequent episode of infection: vancomycinCampylobacter enteritisClarithromycinSalmonella (non-typhoid)CiprofloxacinShigellosisCiprofloxacin

384
Q

A 23-year-old man presents to his GP. He describes episodes of leg weakness following bouts of laughing whilst out with friends. The following weekend his friends described a brief collapse following a similar episode. What is the most likely diagnosis?

A

Laughter → fall/collapse ? cataplexy

384
Q

A 23-year-old man presents to his GP. He describes episodes of leg weakness following bouts of laughing whilst out with friends. The following weekend his friends described a brief collapse following a similar episode. What is the most likely diagnosis?

A

Laughter → fall/collapse ? cataplexy

385
Q

What is cataplexy? What is it closely related? [2]

A

Cataplexy describes the sudden and transient loss of muscular tone caused by strong emotion (e.g. laughter, being frightened). Around two-thirds of patients with narcolepsy have cataplexy.

Features range from buckling knees to collapse.

386
Q

What is one of the biggest cuases of heptaitis E? [1]

A

Undercooked pork

387
Q

Which types of hepatitis are spread through the faecal-oral route? [1]

A

Hepatitis E and A

388
Q

What hepatitis requires co-infection with hepatitis B? [1]

A

Hepatitis D requires co-infection with hepatitis B.

389
Q

Features of hepatitis E

A
  • RNA hepevirus
  • spread by the faecal-oral route
  • incubation period: 3-8 weeks
  • common in Central and South-East Asia, North and West Africa, and in Mexico
  • causes a similar disease to hepatitis A, but carries a significant mortality (about 20%) during pregnancy
  • does not cause chronic disease or an increased risk of hepatocellular cancer
  • a vaccine is currently in development, but is not yet in widespread use
390
Q

Which hepatitis type is commonly vaccinated against when young? [1]

A

Hep B I think

391
Q

WHat can cause ground-glass opacities in the lower zones and how much generally needed to cause this? [1]

A

This patient has developed pulmonary fibrosis secondary to long term amiodarone use. It typically occurs with doses that exceed 400mg daily after two or more months of therapy. Estimates range from 1 to 5% in the patients who are on long term amiodarone. The mechanism is not entirely understood however, current hypotheses include direct toxic injury to the lung or an indirect immunological reaction.

392
Q

Fibrosis predominantly affecting the upper zones

A

Acronym for causes of upper zone fibrosis:

CHARTS

  • C - Coal worker’s pneumoconiosis
  • H - Histiocytosis/ hypersensitivity pneumonitis
  • A - Ankylosing spondylitis
  • R - Radiation
  • T - Tuberculosis
  • S - Silicosis/sarcoidosis
393
Q

Fibrosis preodminantly affecting the lower zones [4]

A
  • diopathic pulmonary fibrosis
  • most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
  • drug-induced: amiodarone, bleomycin, methotrexate
  • asbestosis
394
Q

History of alcohol excess
Stigmata of chronic liver disease: spider naevi, bruising, palmar erythema, gynaecomastia etc
Evidence of decompensation: ascites, jaundice, encephalopathy

A

Liver disease

395
Q

Pallor
Other signs: koilonychia, atrophic glossitis, post-cricoid webs, angular stomatitis, pruritis

A

iron defieincy anaemia

396
Q

Pruritus particularly after warm bath
‘Ruddy complexion’
Gout
Peptic ulcer disease

A

PCV

397
Q

Lethargy & pallor
Oedema & weight gain
Hypertension

Pruritis

A

CKD

398
Q

Night sweats
Lymphadenopathy
Splenomegaly, hepatomegaly
Fatigue

Pruritis

A

Lymhpoma

399
Q

Signs of iron defieicny anaemia in a man over 60 what should be done? [1]

A

Colonscopy to r/o colorectal Ca

400
Q

What is ringworm caused by?

A

Fungal infection

401
Q

3 types of ringworm? [3]

A
  • tinea capitis - scalp
  • tinea corporis - trunk, legs or arms
  • tinea pedis - feet