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ICSM Finals > Medicine > Flashcards

Medicine Flashcards

1
Q

Pellagra is caused by deficiency of…

A

Niacin/ vitamin B3

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2
Q

Features of pellagra

A

Dermatitis, diarrhoea, and mental disturbance

Niacin/ vitamin B3 deficiency

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3
Q

Commonest cause of nephrotic syndrome in children

A

Minimal change disease

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4
Q

Minimal change disease biopsy findings

A

Abnormal fused podocytes on EM

Normal light microscopy

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5
Q

Signs/symptoms of minimal change disease

A

Associated with URTI

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6
Q

Components of the blatchford score

A

Blood urea
Hb
Systolic BP

Others: 
Malaena
Syncope 
Pulse  
Hepatic disease
Cardiac failure

0 identifies low-risk patients who might be suitable for outpatient management

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7
Q

Scores used in assessment of GI bleeding

A

Rockall score

Glasgow-Blatchford score

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8
Q

Components of full Rockall score

A

Age
Shock
Comorbidities: e.g. CHF, IHD, major morbidity, renal failure
Diagnosis: e.g. mallory weiss or malignancy
Evidence of bleeding: e.g. spurting or visible vessel

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9
Q

3 key features of nephrotic syndrome

A

Proteinuria: >3g/24h
Hypoalbuminaemia: <35g/L
Oedema: periorbital, ascites, genital, peripheral

Also hyperlipidaemia

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10
Q

Key features of post-streptococcal acute glomerulonephritis

A

Young child
Smoky urine
Develops 1-2 weeks after sore throat/skin infection
Increased ASOT
Reduced C3
IgG and C3 deposition on biopsy
Most resolve, minority develop rapidly progressing glomerulonephritis

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11
Q

3 types of rapid progressing glomerulonephritis

A

Type 1: Anti-GBM/ good pastures (only 5%)
Type 2: Immune complex deposition
Type 3: Pauci immune (50%) e.g. Wegener’s

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12
Q

Examples of type 3 rapid progressing glomerulonephritis

A

Wegener’s (cANCA)
Microscopic polyangiitis (pANCA)
Churg-Strauss (pANCA)

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13
Q

Treatment for Torsades de Pointes

A

IV MgSO4

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14
Q

TSH and T4 levels in primary hypothyroidism

A

TSH High
T4 low

(if both low it is secondary)

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15
Q

What is Corrigan’s sign?

A

Carotid pulsation seen in patients with aortic regurgitation

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16
Q

Factors that increase BNP levels

A

Left ventricular hypertrophy

Ischaemia
Tachycardia
Right ventricular overload
Hypoxaemia (including pulmonary embolism)
GFR < 60 ml/min
Sepsis
COPD
Diabetes
Age > 70
Liver cirrhosis
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17
Q

Factors that reduce BNP levels

A 
Obesity
Diuretics
ACE inhibitors
Beta-blockers
Angiotensin 2 receptor blockers
Aldosterone antagonists
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18
Q

Cardiac features of Marfan’s syndrome

A

Dilation of the aortic sinuses (seen in 90%) which may lead to aortic aneurysm
Aortic dissection (leading cause of death)
Aortic regurgitation
Mitral valve prolapse (75%)

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19
Q

Normal ECG variants in athletes

A

sinus bradycardia
junctional rhythm
first degree heart block
Wenckebach phenomenon

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20
Q

Features of SIRS

A

at least 2 of the following:
body temperature less than 36°C or greater than 38.3°C
heart rate greater than 90/min
respiratory rate greater than 20 breaths per minute
blood glucose > 7.7mmol/L in the absence of known diabetes
white cell count less than 4 or greater than 12

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21
Q

Key features of HHS

A
  1. ) Severe hyperglycaemia
  2. ) Dehydration and renal failure
  3. ) Mild/absent ketonuria

Confirmation of HHS:
Dehydration
Osmolality >320mosmol/kg
Hyperglycaemia >30 mmol/L with pH >7.3, bicarbonate >15mmolL and no significant ketonenaemia <3mmol/L

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22
Q

Precipitants of HHS

A 
New diagnosis of type 2 diabetes
Infection
High dose steroids
Myocardial infarction
Vomiting
Stroke
Thromboembolism
Poor treatment compliance
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23
Q

Presentation of PBC (key features)

A

Usually Middle aged females (>50)
Jaundice occurs late (survival <2 yrs after jaundice)
Pruritus
Pigmentation of face
Bones: osteomalacia, osteoporosis (reduced vit D)
Big organs: Hepatosplenomegaly
Cirrhosis and coagulopathy (reduced Vit K)
Cholesterol raised: xanthelasma, xanthomata
Steatorrhhoea

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24
Q

Treatment of PBC

A

Symptoms
Pruritus: colestyramine, naltrexone
Diarrhoea: codeine
Osteoporosis: Bisphosphonates

Specific
ADEK vitamins
Ursodeoxycholic acid (improves LFTs but no effect on mortality or transplant need).

Transplant

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25
Q

Treatment of PSC

A

Symptoms
Pruritus: colestyramine, naltrexone
Diarrhoea: codeine

Specific
ADEK vitamins
Ursodeoxycholic acid (improves cholestasis only)
Abx for cholangitis
Endoscopic stenting for dominant strictures

Transplant

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26
Q

Key differences in pathology of PSC and PBC

A

PSC involves intra- and extra-hepatic ducts, PBC only involves intrahepatic ducts

PSC: Bile duct destroyed by chronic granulomatous inflammation leading to cirrhosis
PBC: chronic biliary obstruction leads to secondary biliary cirrhosis

Biopsy:
PBC: non-caseating granulomas
PSC: fibrous, obliterative cholangitis

Antibodies:
PBC: Anti-mitochondrial antibodies
PSC: p-ANCA

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27
Q

Presentation of PSC. Key features

A

Jaundice
Pruritus
Fatigue
Abdo pain

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28
Q

Charcot’s triad refers to presenting features of…

Features are…

A

Ascending cholangitis
RUQ pain
Fever
Jaundice

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29
Q

Dyspepsia

When to make an urgent referral for an endoscopy

A

All patients who have dysphagia

All patients who have an upper abdominal mass consistent with stomach cancer

Patients aged >= 55 years who’ve got weight loss, AND any of the following:
upper abdominal pain
reflux
dyspepsia

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30
Q

Dyspepsia

When to make a non-urgent referral for endoscopy

A

Patients with haematemesis

Patients aged >= 55 years who’ve got:
treatment-resistant dyspepsia or
upper abdominal pain with low haemoglobin levels or
raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain

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31
Q

Typical presentation of Giardiasis

A

Prolonged, non-bloody diarrhoea

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32
Q

MDRD formula for eGFR uses which variables?

A

serum creatinine
age
gender
ethnicity

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33
Q

Key test to differentiate pre-renal uraemia and ATN

A

Urine sodium
< 20 mmol/L in pre-renal uraemia (as tubules able to reabsorb sodium leading to low urine sodium
> 30 mmol/L in ATN (a necrosed tubule cant reabsorb sodium)

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34
Q

ECG Changes in pericarditis

A

Widespread concave ST elevation and PR depression throughout most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6).

Reciprocal ST depression and PR elevation in lead aVR (± V1).

Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion.

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35
Q

What is a cannon ‘A’ wave caused by?

A

It is caused by the ventricles contracting against a closed atrio-ventricular valve and sending a pressure wave up the jugular vein. This is seen in complete heart block and sometimes pulmonary embolism.

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36
Q

What is Kussmaul’s sign?

A

JVP increasing with inspiration (it should fall). It is a feature of constrictive pericarditis. It is caused by impaired filling of the right ventricle due to a poorly compliant myocardium or pericardium.

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37
Q

Hep B post exposure prophylaxis

A

HBsAg positive source: if the person exposed is a known responder to HBV vaccine then a booster dose should be given. If they are in the process of being vaccinated or are a non-responder they need to have hepatitis B immune globulin (HBIG) and the vaccine (accelerated course)

unknown source: for known responders the green book advises considering a booster dose of HBV vaccine. For known non-responders HBIG + vaccine should be given whilst those in the process of being vaccinated should have an accelerated course of HBV vaccine

Normal HBV vaccine is 3 doses. 2nd after 1 month, 3rd after an additional 5 months.

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38
Q

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

A

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

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39
Q

Treatment of amoebiasis

A

Metronidazole

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40
Q

Advice to be given regarding safe consuption of alcohol

A

Men and women should drink no more than 14 units of alcohol per week
‘if you do drink as much as 14 units per week, it is best to spread this evenly over 3 days or more’

Pregnant women should not drink.

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41
Q

First line treatment of hereditary haemochromatosis

A

Venesection

Desferrioxamine is second line

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42
Q

Causes of chronic pancreatitis

A

Alcohol
Genetic: CF, Hereditary pancreatitis
Immune: Lymphoplasmocytic sclerosing pancreatitis (raised IgG4)
Raised Triglycerides
Structural: obstruction by tumour, pancreas divisum

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43
Q

One unit of alcohol is equivalent to…

A

One unit of alcohol is equal to 10 ml of alcohol. The ‘strength’ of an alcoholic drink is determined by the ‘alcohol by volume’ (ABV).

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44
Q

List some gluten containing foods

A

wheat: bread, pasta, pastry
barley*: beer
rye
oats

Some notable foods which are gluten-free include:
rice
potatoes
corn (maize)

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45
Q

Ovarian cancer tumour marker

A

CA125

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46
Q

What are lacunar infarcts?

A

Small infarcts around the basal ganglia, internal capsule, thalamus and pons

May result in pure motor, pure sensory, mixed motor and sensory signs or ataxia.

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47
Q

Features of a total anterior circulation stroke

A

Involves middle and anterior cerebral arteries
All 3 of following should be present:
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia

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48
Q

Features of partial anterior circulation infarcts

A

Involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery

Two of the following are present

  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia
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49
Q

Features of lacunar infarcts

A

Involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesi

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50
Q

Features of posterior circulation infarcts

A 
Involves vertebrobasilar arteries
presents with 1 of the following:
1. cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia
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51
Q

Features of normal pressure hydrocephalus

A

Caused by reduced CSF absorption at the arachnoid villi.

Triad of dementia and bradyphrenia, urinary incontinence, and gait abnormality (similar to PD)

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52
Q

Window for thrombolysis in stroke

A

Thrombolysis should only be given if it is administered within 4.5 hours of onset of stroke symptoms (unless as part of a clinical trial)

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53
Q

What constitutes a high protein level in CSF

A

> 1g

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54
Q

What constitutes a low glucose level in CSF

A

<1/2 the plasma glucose

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55
Q

Key features of multiple system atrophy

A

parkinsonism (rigidity>tremor)
autonomic disturbance (atonic bladder, postural hypotension)
cerebellar signs

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56
Q

Antiepileptic drug safest in pregnany

A

Lamotrigine

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57
Q

First line antiepileptic in generalized epilepsy

A

Sodium valproate

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58
Q

Second line antiepileptic in generalized epilepsy

A

Lamotrigine (also safest in pregnancy)

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59
Q

Migraine prophylaxis in asthmatics

A

Topiramate

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60
Q

First line antiepileptic for partial seizures

A

Carbamazepine

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61
Q

4 Types of Motor Neuron Disease (and key features)

A

Amyotrophic lateral sclerosis (50% of patients)
typically LMN signs in arms and UMN signs in legs
in familial cases the gene responsible lies on chromosome 21 and codes for superoxide dismutase

Primary lateral sclerosis
UMN signs only

Progressive muscular atrophy
LMN signs only
affects distal muscles before proximal
carries best prognosis

Progressive bulbar palsy
palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
carries worst prognosis

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62
Q

Key features of Wilson’s disease

A

Liver: hepatitis, cirrhosis

Neurological: basal ganglia degeneration, speech and behavioural problems are often the first manifestations. Also: asterixis, chorea, dementia

Kayser-Fleischer rings

Renal tubular acidosis (esp. Fanconi syndrome)

Haemolysis

Blue nails

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63
Q

Interpretation of ABCD score post TIA

A

People who have had a suspected TIA who are at a higher risk of stroke (that is, with an ABCD2 score of 4 or above) should have:
aspirin (300 mg daily) started immediately
specialist assessment and investigation within 24 hours of onset of symptoms
measures for secondary prevention introduced as soon as the diagnosis is confirmed, including discussion of individual risk factors

If the ABCD2 risk score is 3 or below:
specialist assessment within 1 week of symptom onset, including decision on brain imaging
if vascular territory or pathology is uncertain, refer for brain imaging

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64
Q

Biologicals used in MS

A

Natalizumab (anti-VLA4)

Alemtuzumab (Anti CD52)

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65
Q

Treatment of venous sinus thrombosis

A

Heparin or LMWH 1st line
If poor prognosis or lack of response endovascular treatment is another option
Lack of evidence for antiplatelets

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66
Q

Weakness in myasthenia gravis is worsened by…

A

Pregnancy
Infection
Emotion
Drugs e.g. b-blockers, gent, tetracyclines, opiates)

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67
Q

Features of cluster headache

A

pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours
clusters typically last 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
nasal stuffiness
miosis and ptosis in a minority

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68
Q

Trochlear (CNIV) nerve supplies

A

Superior oblique muscle.

Controls downward gaze

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69
Q

Features of Subacute combined degeneration of the spinal cord
Mention clinical features and tracts affected

A

Clinical features:

  1. Bilateral spastic paresis
  2. Bilateral loss of proprioception and vibration sensation
  3. Bilateral limb ataxia

Affects the:

  1. Lateral corticospinal tracts
  2. Dorsal columns
  3. Spinocerebellar tracts
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70
Q

Cranial nerve responsible for:

a) gag reflex
b) Corneal reflex

A

a) CNIX

b) CNV

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71
Q

Subacute degeneration of the spinal cord is caused by…

A

vitamin B12 & E deficiency

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72
Q

Reflexes absent in bulbar palsy

A

Jaw jerk

Gag reflex

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73
Q

Plaques involved in Alzheimer’s disease

A

Cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein

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74
Q

HIV complication leading to widespread demyelination

A

Progessive multifocal leukoencephalopathy

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75
Q

Features of Progressive multifocal leukoencephalopathy (PML)

A

widespread demyelination
due to infection of oligodendrocytes by JC virus (a polyoma DNA virus)
symptoms, subacute onset : behavioural changes, speech, motor, visual impairment
CT: single or multiple lesions, no mass effect, don’t usually enhance. MRI is better - high-signal demyelinating white matter lesions are seen

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76
Q

What is Uhthoff’s phenomenon

A

Seen in MS.

Worsening of vision with rise in body temperature.

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77
Q

Key features of neurofibromatosis type 2

A

Bilateral acoustic neuromas

Multiple intracranial schwannomas, mengiomas and ependymomas

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78
Q

Key features of neurofibromatosis type 1

A 
Café-au-lait spots (>= 6, 15 mm in diameter)
Axillary/groin freckles
Peripheral neurofibromas
Iris hamatomas (Lisch nodules) in > 90%
Scoliosis
Pheochromocytomas
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79
Q

Features of LGL (Lown-Ganong-Levine syndrome)

A

very short PR interval
normal P waves and QRS complexes
absent delta waves

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80
Q

Signs/symptoms of lateral medullary syndrome

A

DANVAH

Dysphagia
Ataxia
Nystagmus
Vertigo 
Anaesthasia: ipsilateral, absent corneal reflex, contralateral pain loss, Horners syndrome (ipsilateral) 
Horner's syndrome
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81
Q

Features of Millard-Gubler syndrome

A

Pontine infarct
6th and 7th CN nuclei and corticospinal tracts
LMN facial palsy and loss of corneal reflex
Contralateral hemiplegia

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82
Q

Causes of locked in syndrome

A 
Pontine stroke (ventral pontine infarct)
Central pontine myelinolysis
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83
Q

5 As of Complex partial seizures

A

Aura
Automatisms
Awareness lost: motor arrest, motionless stare
Autonomic: change in skin colour, temp, palps
Amnesia

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84
Q

Presentation of encephalitis

A 
Infectious prodrome: fever, rash, LNs, cold sores, congunctivitis, mengingeal signs. 
Bizarre behaviour or personality change
Confusion 
Fever
Focal neurological signs 
Seizures 
Reduced GCS can lead to coma 
Hx of travel or animal bite
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85
Q

Key investigation and finding for cerbral absecess

A

CT/MRI showing ring-enhancing lesion

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86
Q

Organisms causing cerebral absecess

A

Frontal sinus/teeth: Strep milleri, orpharyngeal anaerobes

Ear: Bacteroides, other anaerobes

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87
Q

Signs of cerebral abscesses

A 
Seizures
Fever 
Localising signs 
Signs of raised ICP
Signs of infection elsewhere
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88
Q

Features of absence seizures

A

ABrupt
Short (<10s)
Eyes (glazed, blank stare)
Normal: intelligence, examination, brain scan
Clonus or automatisms may occur
EEG: 3Hz spike and wave
Stimulated by hyperventilation and photics (light)

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89
Q

Seizure involving sensory disturbance suggests localisation in which lobe?

A

Parietal

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90
Q

Features of seizures localised in temporal lobe

A 
Automatisms 
Delusional behaviour
Emotional disturbance Deja/Jamais vu
Abdominal (rising n/v) 
Tastes 
Smells
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91
Q

Reflex to test C5
Muscle to test for C5
Area to test C5 sensation

A

Supinator jerk
Supraspinatus
Patch area

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92
Q

Reflex to test C6
Muscle to test C6
Area to test C6 sensation

A

Biceps jerk
Biceps and barchioradialis
Thumb

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93
Q

Reflex to test C7
Muscle to test C7
Area to test C7 sensation

A

Triceps jerk
Triceps
Middle finger

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94
Q

Muscles to test C8

Area to test C8 sensation

A

(No reflex for C8)
Finger flexors and intrinsic hand muscles
Little finger

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95
Q

What is Lhermitte’s sign

A

Neck flexion causes tingling down spine. Seen in cervical spondylosis.

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96
Q

Features of NF type 1

A

Cafe au lait
Axillary freckling
Fibromas: subcutneous and plexus
Eye: lisch nodules, brown translucent iris hamartomas

Neoplasia: meningioma, ependyoma, astrocytoma, phaeochromocytoma, chronic or acute myeloid leukaemia
Orthopaedic: kyphoscoliosis, sphenoid dysplasia
IQ reduced and epilepsy
Renal: RAS leading to high BP

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97
Q

Features of corticobasilar degeneration

A

EPS+ 4As

Aphasia, dysArthria, Apraxia
Akinetic rigidity in one limb
Atereognosis (don’t recognise something by feeling)
Alien limb phenomenon

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98
Q

Features of multiple systems atrophy

A

EPS+

Autonomic dysfunction (post hypotention, bladder dysfunction)
Cerebellar and pyramidal signs (plantar extension and hyperreflexia)
Rigidity>tremor

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99
Q

Features of progressive supranuclear palsy

A

EPS+

Postural instability causing falls
Speech disturbance (and dementia)
Palsy of vertical gaze

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100
Q

Features of lewy body dementia

A

EPS+
Fluctuating cognition
Visual hallucinations

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101
Q

Causes of Parkinsonism. List the categories and give examples

A 
Degenerative e.g. PD or corticobasilar degeneration  
Infection: CJD, syphilis, HIV
Vascular: multiple infarcts in the SN 
Drugs: Antipsychotics, metoclopramide 
Trauma: CTE (dementia pugilistica) 
Genetic: Wilson's disease
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102
Q

What is cataplexy?

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.

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103
Q

Key side effects of methotrexate

A

Hepatotoxic
Pulmonary fibrosis
Myelosuppression

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104
Q

Key side effects of sulfasalazine

A

Myelosupression
Hepatotoxic
SJS
Reduced sperm count

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105
Q

Key side effect of hydroxychloroquine

A

Myelosupression
Retinopathy
Seizures

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106
Q

Key side effect of penicillamine

A

Drug induced lupus
Taste change
Myelosupression

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107
Q

Biologicals used in RA

A

Infliximab (chimeric anti-TNF)
Etanercept (TNF receptor)
Adalimumab (human anti-TNF)
Ritiximab (anti-CD20) only used if not responding to anti-TNF

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108
Q

Score used to monitor RA

A

DAS 28

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109
Q

Features of RA in hands

A 
Swan neck
Boutonnière 
Z-thumb 
Ulnar deviation of the fingers 
Dorsal subluxation of ulnar styloid
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110
Q

Features of RA

A 
Arthritis: symmetrical polyarthritis MCPs and PIPs of hands and feet. Pain swelling and deformity
Nodules 
Tenosynovitis
I
C
C
P
O
R
F
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111
Q

Cranial nerves affected by bulbar palsy

A

9-12

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112
Q

Signs of bulbar palsy

A

LMN lesions of tongue, talking and swallowing:

Flaccid fasciculating tongue
Speech: quiet or nasal
Normal/abscent jaw jerk
Loss of gag reflex

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113
Q

Features of pseudobulbar palsy

A

Bilateral lesions above the mid-pons leading to UMN lesions of swallowing and talking (not CN nuclei except lower part of 7 have bilateral cortical representation)

Signs: 
Spastic tongue
Slow tongue movements with slow and deliberate speech 
Brisk jaw jerk 
Emotional incontinence
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114
Q

Causes of pseudobulbar palsy

A

MS
MND
Stroke

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115
Q

MND Classification

A

ALS: 50% of cases. Loss of motor neurons in cortex and anterior horn. Leads to UMN signs (legs), LMN signs (arms)

Progressive bulbar palsy: 10% of cases. Only affects CN9-12 and causes LMN signs

Progressive muscular atrophy: Anterior horn cell lesion leading to LMN signs only. Distal to proximal. Better prognosis than ALS.

Primary lateral sclerosis: loss of Betz cells (giant pyramidal cells in primary motor cortex). UMN signs mainly.

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116
Q

Drug used in MND

A

Riluzole.

Prolongs life by 3 months

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117
Q

Differences between myasthenia gravis and LEMS

A

In LEMS:
Ab against Voltage gated calcium channels and:

Leg weakness early
Extra: autonomic and areflexia
Movement improves symptoms temporarily
Small response to edrophomium (tensilon)

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118
Q 
List nerve roots that form:
Median nerve 
Ulnar nerve 
Radial nerve
Phrenic nerve 
Sciatic
Common peroneal 
Tibial nerve
A 
Median: C6-T1 
Ulnar nerve: C7-T1 
Radial Nerve: C5-T1 
Phrenic nerve: C3-C5
Sciatic nerve: L4-S3 
Common peroneal: L4-S1 
Tibial: L4-S3
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119
Q

Signs of sciatic nerve damage

A

Motor: weakness and wasting of hamstrings and all muscles below knee
Sensory loss below knee laterally and foot

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120
Q

Signs of damage to common peroneal nerve

A

Sensory loss below knee laterally
Foot drop, can’t walk on heels (or do impetus turn!)
Weak ankle dorsiflexion and eversion but inversion intact.

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121
Q

Common location and cause of damage to common peroneal nerve

A

Fibular head.
Cross legged sitting
Trauma

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122
Q

Common cause of sciatic nerve damage

A

Pelvic tumour

Pelvic or femoral fracture

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123
Q

Signs of damage to tibial nerve

A

Can’t plantarflex (so can’t go en point, messy jive kicks)
Can’t flex toes or invert foot.
Loss of sensation sole of foot (stomping gait)

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124
Q

Nerves affected in Erb’s palsy

A

C5-6

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125
Q

Nerves affected in Klumpke’s palsy

A

C8-T1

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126
Q

Muscles supplied by median nerve

A

lateral two lumbricals
opponens pollicis
abductor pollicis brevis
flexor pollicis brevis

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127
Q

DIfference between a medical and surgical 3rd nerve palsy

A

“Medical”: pupil sparing (and painless)
“Surgical”: pupil fixed and dilated

Parasympathetic fibres are situated on the periphery of the 3rd nerve trunk and so are the first to be affected by compression resulting in a fixed and dilated pupil.

The classic cause of a “surgical” 3rd nerve palsy is a posterior communicating artery aneurysm. The vaso vasorum which supplies the 3rd nerve starts from the centre and supplies out radially.

In “medical” 3rd nerve palsies the centre of the 3rd nerve is affected first leaving the parasympathetic fibres and therefore pupillary constriction intact until the end.

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128
Q

Features of Webers syndrome

A

Webers syndrome: ipsilateral third nerve palsy with contralateral hemiplegia –> signifies a midbrain stroke.

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129
Q

Sites of radial nerve damage

A

Axilla
Humerus
Wrist

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130
Q

Motor signs of radial nerve damage:
Low
High
V. high

A

Low: finger drop
High: Wrist drop
V. High: Triceps paralysis and wrist drop

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131
Q

Location of sensory loss in radial nerve injury

A

Anatomical snuff box

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132
Q

Condition causing hypercoagulable state with paradoxical prolonged APTT

A

Antiphospholipid syndrome, SLE

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133
Q

Cardinal signs of syringomyelia

A

Dissociated sensory loss: absent pain and temp, but preserved proprioception, soft touch and vibration.

Wasting and weakness of hands with/wo claw hand

Loss of reflexes in upper limb

Charcot joints: shoulder and elbow

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134
Q

Features of syringomyelia

A

Dissociated sensory loss: absent pain and temp, but preserved proprioception, soft touch and vibration.
Wasting and weakness of hands with/wo claw hand
Loss of reflexes in upper limb
Charcot joints: shoulder and elbow

UMN weakness in lower limbs and +ve babinski
Horner’s

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135
Q

Causes of synringomyelia

A

Blocked CSF circulation with reduced flow from posterior fossa due to:
Arnold Chiari malformation
Masses

Spina bifida

Cord trauma, myelitis, cord tumours, AVM

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136
Q

ABCD2 scoring

A 
A	Age >= 60 years 1
B	Blood pressure >= 140/90 mmHg 1
C	Clinical features 
- Unilateral weakness 2
- Speech disturbance, no weakness 1	
D	Duration of symptoms
- > 60 minutes 2
- 10-59 minutes 1	
Patient has diabetes 1
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137
Q

Steps to take if ABCD2 score is 4 or more (and symptoms have resolved)

A

aspirin (300 mg daily) started immediately

specialist assessment and investigation within 24 hours of onset of symptoms

measures for secondary prevention introduced as soon as the diagnosis is confirmed, including discussion of individual risk factors

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138
Q

Chromosome affected in NF type 2

A

22

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139
Q 
Movement to test:
L2 
L3
L4 
L5
S1
A

L2: Hip flexion (and adduction)
L3: Knee extension (and adduction)
L4: Foot inversion and dorsiflexion (and knee extension)
L5: Great toe dorsiflexion (also foot inversion and dorsilfexion, knee flexion, hip extension and adduction)
S1: Foot eversion (and foot and toe plantarflexion, knee flexion)

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140
Q

Knee jerk tests which nerve root?

A

L3 and L4

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141
Q

Ankle jerk tests which nerve root?

A

S1

142
Q

Back pain red flegs

A 
Age under 20 or over 55 
Neurological disturbance 
Sphincter disturbance 
Bilateral or alternating leg pain 
Current or recent infection 
Fever, wt loss, night sweats 
Hx of malignancy 
Thoracic back pain 
Morning stiffness 
Acute onset in elderly people 
Constant or progressive pain 
Nocturnal pain
143
Q

Risk factors for OA

A

Age
Obesity
Joint abnormality

144
Q

Key signs of OA

A

Bouchards and Heberdens nodes
Thumb CMC joint squaring
Fixed flexion deformity

145
Q

Radiological signs of OA

A

Loss of joint space
Subchondral cysts
Subchondral sclerosis
Osteophytes

146
Q

Radiological signs of RA

A 
Loss of joint space
Soft tissue swelling
Peri-articular osteopenia
Deformity 
Subluxation
147
Q

Common organisms causing septic arthritis

A

Staph aureus (commonest)
Gonococcus (commonest in young sexually active)
Streps
Gm -ve bacilli

148
Q

Signs and symptoms of septic arthritis

A

Acute inflamed tender swollen joint
Systemically unwell
Reduced range of movement

149
Q

Features of RA

A

Mnemonic: ANTI CCP Or RF

Arthritis, symmetrical polyarthritis, MCPs and PIPs of hands and feet. Pain swelling and deformity.
Nodules: elbows, feet, fingers, heel. Firm, non-tender, mobile or fixed
Tenosynovitis: de quervains and atlanto-axial subluxation
Immune: AIHA, vasculitis, Amyloid, Lymphadenopathy
Cardiac: peridarditis and pericardial effusion
Carpal tunnel syndrome
Pulmonary: fibrosing alveolitis, pleural effusions
Opthalmic: episcleritis, sjogrens
Raynaud’s
Felty’s: RA+splenomegaly+neutropenia

150
Q

Features required for RA diagnosis

A 
4 out of 7:
Morning stiffness of >1h for at least 6 weeks 
Arthritis in at least 3 joints 
Arthritis of hand joints 
Symmetrical
Rheumatoid nodules 
\+RF 
Radiographic changes
151
Q

What are tophi?

A

Urate deposits in pinna and tendons. Seen in gout.

152
Q

Causes of gout

A

Drugs e.g. NSAIDS, diuretics (thiazides)

Reduced urate excretion: genetic, renal impairment

Increased cell turnover: lymphoma, leukaemia, psoriasis, haemolysis, tumour lysis syndrome

Alcohol excess

Purine rich foods: red meat and seafood, port

153
Q

Gout: findings on polarised light microscopy

A

Negatively birefringent needle-shaped crystals

154
Q

Urate levels in gout

A

Increased or normal

155
Q

X-ray findings in gout

A

Changes are late.
Punchout out erosions (erosive arthritis!!) in juxta articular bone.
Reduced joint space late in disease

156
Q

Precipitants of gout

A

Prolonged fast, thiazides, cytotoxics, surgery, infection

157
Q

Differentials in cases of gout

A

Septic arthritis
Pseudogout
Haemarthrosis

158
Q

Pseudogout: findings in polarised light microscopy

A

Positively birefringent rhomboid-shaped crystals

159
Q

Crystals in pseudogout are formed of…

A

Calcium pyrophosphate

160
Q

Radiological findings in pseudogout

A

Possible soft tissue calcium deposition (chondrocalcinosis)

161
Q

Treatment of psuedogout

A

Analgesia
NSAIDs
PO, IM or intra-articular steroids

162
Q

Presentation of acute pseudogout

A 
Acute monoarthropathy (usually knee, wrist or hip) 
Usually spontaneous and self limiting
163
Q

Presentation of chronic pseudogout

A

Destructive changes like OA

Can present as polyarthritis (pseudo-rheumatoid)

164
Q

Risk factors for pseudogout

A 
Age (older) 
OA
DM
HYPOthyroidism
HYPERparathyroidism 
Wilson's disease
Hereditary haemochromatosis
165
Q

Presentation of ankylosing spondylitis

A

Presents in late teens/early 20s. Men earlier than women.

Gradual onset back pain. Pain radiates from SI joints to hips and buttocks. Pain is worse at night with early morning stiffness and is relieved by exercise.

Progressive loss of all spinal movements.

Possible thoracic kyphosis and neck hyperextension (question mark posture)

Enthesitis (is inflammation of the entheses, the sites where tendons or ligaments insert into the bone) of Achilles tendonitis and plantar fasciitis.

Chostochondritis

166
Q

Examples of seronegative spondylarthropathies

A

Ankylosing spondylitis
Psoriatic arthritis
Enteropathic arthritis

167
Q

What is Schober’s test?

A

Schober’s test assesses the amount of lumbar flexion.

In this test a mark is made at the level of the posterior iliac spine on the vertebral column
(approximately at the level of L5.)

Place one finger 5cm below this mark and another finger at about 10cm above this mark. The patient is then instructed to touch his toes. If the increase in distance between the two fingers on the patients spine is less than 5cm then this is indicative of a limitation of lumbar flexion.

168
Q

Incompetence of the… valve can be seen in ankylosing spondylitis

A

Aortic valve

169
Q

Key radiological change in anylosising spondylitis

A

Bamboo spine: calcification of ligaments, periosteal bone formation

170
Q

Extra-articular manifestations of ankylosing spondylitis

A

Osetoporosis
Acute iritis/anterior uveitis
Aortic valve incompetence
Apical pulmonary fibrosis

171
Q

Allele found in ankylosing spondylitis

A

HLA-B27

172
Q

Management of ankylosing spondylitis

A

Conservative: exercise and physio
Medical: NSAIDs, Anti-TNF if severe, Local steroid injections, Bisphosphonates
Surgical: Hip replacement to reduce pain and increase mobility

173
Q

Features of psoriatic arthritis

A

Asymmetrical oligoarthritis (2-4 joints) is commonest
Distal arthritis of the DIP joints
Symmetrical polyarthritis (like RA but no DIP sparing)
Spinal (like ank spon)
May predate the skin disease

Psoriatic plaques
Nail pitting, subungual hyperkeratosis, onchyolysis (painless separation of the nail from the nail bed.)
Enthesitis: achilles tendonitis, plantar fasciitis
Dactlylitis

174
Q

Nail changes in psoriasis

A

Nail pitting, subungual hyperkeratosis, onchyolysis (painless separation of the nail from the nail bed.)

175
Q

Radiological changes in psoriatic arthritis

A

Erosions: pencil in cup deformity

176
Q

Features of reactive arthritis

A

Sterile
Appears 1-4 weeks post urethritis or dysentery
Organisms:
Urethra: chlamydia
Dysentery: Campylobacter, salmonella, shigella, yersina
Asymmetrical lower limb oligoarthritis esp knee
Iritis/conjunctivitis
Keratoderma blenorrhagica: plaques on soles/palms
Circinate balanitis: painless ulceration
Enthesitis
Mouth ulcers

177
Q

Features of Behcet’s disease

A 
Systemic vasculitis (unknown cause)
Recurrent oral and genital ulceration
Anterior and posterior uveitis 
Erythema nodosum
Vasculitis 
Non-erosive large joint oligoarthropathy 
CN palsies 
Diarrhoea and colitis
178
Q

Behcet’s disease is seen in which ethnic groups

A

Turks
Mediterraneans
Japanese

179
Q

Investigation for Behcets disease

A

Skin prick leads to papule formation

180
Q

Features of sjogren’s syndrome

A

Reduced tear production and salivation
Bilateral parotid swelling
Vaginal dryness
Systemic features e.g. polyarthritis, Raynaud’s and bibasal pulmonary fibrosis.

181
Q

Sjogren’s is associated with which autoimmune conditions

A

Secondary to: RA, SLE, Systemic sclerosis

Associated with: AIHA, PBC, thyroid disease

182
Q

Antibodies found in Sjogrens

A

ANA: Anti Ro, La and RF

183
Q

Ischaemia in Raynaud’s is triggered by…

A

Cold

Emotion

184
Q

Treatment for Raynaud’s

A

Wear gloves
CCB e.g. nifedipine
ACEi
IV prostacyclin

185
Q

Causes of secondary Raynaud’s

A

Systemic sclerorosis, limited sclerosis, RA, sjogren’s
Thrombocytosis, PV
B-blockers

186
Q

Presentation of Raynaud’s

A

Triphasic colour change: White, blue, crimson

Possible digitial ulceration and gangrene

187
Q

Features of limited cutaneous systemic sclerosis

A 
Calcinosis 
Raynaud's 
oEsophageal dysmotility 
Sclerodactyly
Telangiectasia

The skin involvement is limited to the hands, feet and face. CAN get Pulmonary HTN (15%)

Slow onset (compared to diffuse systemic sclerosis)

188
Q

Features of diffuse systemic sclerosis

A

CREST with more diffuse skin involvement.
Rapid skin thickening and Raynaud’s
Organ fibrosis leading to:
GI: reflux, aspiration, dysphagia, anal incontinence
Lung: fibrosis and pulmonary HTN
Cardiac: Arrhythmias and conduction defects
Renal: Acute HTN crisis (commonest cause of death)

189
Q

Antibodies in:
CREST syndrome
Diffuse systemic sclerosis

A

CREST: anti-centromere
Diffuse: Anti-Scl70/topoisomerase, RNA polymerase 1,2,3

190
Q

Management of systemic sclerosis (limited and diffuse)

A

Conservative:
Exercise and skin lubricants to reduce contractures
Hand warmers: Raynaud’s

Medical:
Immunosuppression: cyclosporine, cyclophosphamide
Raynaud’s: CCBs, ACEi, IV Prostacyclin
Renal: Intensive BP control: ACE is 1st line.
Oesphageal: PPI, prokinetics (metoclopramide)
PHT: Sildenafil, bosentan
Telangiectasia: Make-up. Light therapy.

191
Q

Features of polymyositis

A 
Striated muscle inflammation.
Muscle weakness:  Progressive. Symmetrical. Proximal. 
Wasting: pelvic girdle, shoulder. 
Dysphagia, dysphonia,
Respiratory weakness 
Myalgia and arthralgia 
Commoner in females 
Often paraneoplastic (lung, pancreas, breast, bowel)
192
Q

Skin features of dermatomyositis

A

Heliotrope rash
Macular rash (shawl sign +ve over back and shoulders)
Nailfold erythema
Gottron’s papules: knuckles, elbows, knees
Mechanics hands: painful, rough skin, cracking of finger tips
Subcutaneous calcifications

Also get retinopathy: haemorrhages and cotton wool spots

193
Q

Extramuscular features of polymyositis and dermatomyositis

A 
Fever
Arthritis 
Bibasal pulmonary fibrosis 
Raynaud's
Myocarditis and arrhythmias
194
Q

Antibodies in polymyositis and dermatomyositis

A

Anti-Jo1

195
Q

Investigations in polymyositis

A

Muscle enzymes: raised CK, ALT, AST, LDH
Ab: anti Jo1
EMG
Muscle biopsy: inflammaed striated muscle
Screen for malignancy: CXR, mammogram, tumour markers, pelvic US, Abdo US, CT

196
Q

Treatmement of polymyositis and dermatomyositis

A

Steroids
Cytotoxics: AZT, MTX

Don’t forget to screen for malignancy!

197
Q

Features of SLE

A

Relapsing remitting. Constitutional symptoms.
A RASH POINts MD

Arthritis: non-erosive involving peripheral joints.
Renal: proteinuria and HTN
ANA positive in 95%
Serositis: pleuritis, pericarditis.
Haematological: AIHA, low WCC, low plt
Photosensitivity
Oral ulcers
Immune phenomenon: Anti-dsDNA, sm, phospholipid
Neurological: seizures, psychosis
Malar rash (nasolabial fold sparing)
Discoid rash (mainly face and chest, initally erythema then hyperkeratotic papules )

198
Q

SLE antibodies

A

ANA: anti-dsDNA, Ro, La, Sm, RNP

199
Q

Methods of monitoring SLE disease activity

A

C3, C4 (low in active)
ESR high if active
Anti-dsDNA titres

Others
Urine: dip stick for protein, PCR
FBC, U+E, CRP (usually normal)

200
Q

Drugs that induce lupus

A

Procainamide
Phenytoin
Hydralazine
Isoniazid

201
Q

Features of drug induced lupus

A

Anti-histone Ab (100%)
Mostly skin and lung signs
Remits if drug stopped

Phenytoin, procainamide, isoniazide, hydralazine.

202
Q

Antibodies in antiphospholipid syndrome

A

Anti-cardiolipin

Lupus anticoagulant

203
Q

SLE management

A

Severe flares (pericarditis, CNS disease, AIHA, nephritis): IV cyclophosphamide, High dose prednisolone.

Cutaneous: topical steroids to treat, sun cream for prevention

Maintenance for joints and skin: NSAIDs, hydroxychloroquine, low dose steroids (option)

Lupus nephritis: ACEi for proteinuria. Immunosupression if aggressive GN

204
Q

False positive anti-cardiolipin Abs seen in…

A

Syphilis

205
Q

List 4 ANCA negative vasculitides

A

Goodpasture’s
Henloch Schonlein
Cryoglobulinaemia
Cutaneous Leukocytoclastic vasculitis

206
Q

Features of GCA

A 
Associated with polymyalgia rheumatica in 50% 
Fever, malaise, fatigue
Headache 
Jaw claudication 
Amourosis fugax 
Prominant temporal arteries (with or without plusation)
Raised ESR and CRP 
Raised Plt
207
Q

Investigations in suspected GCA

A 
High ESR and CRP
High ALP
Low Hb (Normo normo)
High Plt
Temporal artery biopsy within 3 days (skip lesions can occur)
DO NOT DELAY TREATMENT
208
Q

Treatment of GCA

A

High dose steroids (e.g. pred 40-60mg oral) and taper slowly.
PPI and alendronate cover

209
Q

GCA is rare under the age of…

A

55

210
Q

Polymyalgia rheumatic increases the risk of…

A

GCA.

15% develop it.

211
Q

Features of polymyalgia rheumatica

A 
Sudden/subacute onset 
Fever, fatigue, weight loss 
Severe pain and stiffness in the shoulders, neck and hips
Symmetrical 
Worse in morning 
No weakness 
High ESR, CRP, ALP, plasma viscosity 
Can develop mild polyarthritis, tenosynovitis and carpal tunnel syndrome 
15% develop GCA
212
Q

Investigations in suspected polymyalgia rheumatica

A

High CRP, ESR, ALP, plasma viscosity

Normal CK

213
Q

Treatment of polymyalgia rheumatica

A

15mg/day oral prednisolone and then taper according to ESR and symptoms
PPI and alendronate cover

214
Q

Features of granulomatosis with polyangiitis

A

URT: chronic sinusitis, epistaxis, saddle-nose
LRT: Cough, haemoptysis, pleuritis
Renal: RPGN, haematuria, proteinuria

Other: palpable purpura, conjunctivitis, keratitis, uveitis
cANCA
CXR: Bilateral nodular and cavity infiltrates
Granulomatous necrotizing small vessel vasculitis

215
Q

Radiological findings in granulomatosis with polyangiitis

A

CXR: Bilateral nodular and cavity infiltrates

216
Q

Treatment of granulomatosis with polyangiitis

A

Immunosuppression:
Cyclophsphamide, Rituximab, MTX

Azathioprine, Rituximab or MTX for maintenance.

217
Q

Features of eosinophilic granulomatosis with polyangiitis (Churg-Strauss)

A 
Late onset asthma 
Eosinophilia
Granulomatous small vessel vasculitis leading to:
RPGN
Palpable purpura
GIT bleeding

pANCA

218
Q

Treatment of Features of eosinophilic granulomatosis with polyangiitis (Churg-Strauss)

A

Prednisolone
Cyclophosphamide is severe multi-organ
Azathioprine or MTX for maintenance

219
Q

Key features of microscopic polyangiitis

A

RPGN
Haemoptysis
Palpable purpura
pANCA

220
Q

What is sarcoidosis?

A

Sarcoidosis is a multi-system disease involving abnormal collections of inflammatory cells known as granulomas. Sarcoidosis can cause facial palsies, parotid enlargement, hypercalcaemia and ocular problems, as seen in this case.

221
Q

Features of Marfan’s syndrome

A

tall stature with arm span to height ratio > 1.05
high-arched palate
arachnodactyly
pectus excavatum
pes planus
scoliosis of > 20 degrees
heart: dilation of the aortic sinuses (seen in 90%) which may lead to aortic aneurysm, aortic dissection, aortic regurgitation, mitral valve prolapse (75%),
lungs: repeated pneumothoraces
eyes: upwards lens dislocation (superotemporal ectopia lentis), blue sclera, myopia
dural ectasia (ballooning of the dural sac at the lumbosacral level)

222
Q

Genetics of marfans (mode of inheritance and affected gene)

A

Marfan’s syndrome is an autosomal dominant connective tissue disorder. It is caused by a defect in the fibrillin-1 gene on chromosome 15

223
Q

Anti Ro is associated with

A

Foetal heart block
SLE
Sjogrens

224
Q

Anti La is associated with

A

SLE, Sjogren’s

225
Q

Anti-Sm antibodies are associated with…

A

SLE

226
Q

Anti-RNP antibodies are associated with…

A

SLE

MCTD (mixed connective tissue disease)

227
Q

Anti-Jo1 antibodies are associated with…

A

Polymyositis and dermatomyositis

228
Q

Anti-centromere antibodies are associated with…

A

Limited cutaneous systemic sclerosis

229
Q

Anti-Scl70 antibodies are associated with…

A

Diffuse systemic sclerosis

230
Q

Anti RNA polymerase (1,2,3) antibodies are associated with…

A

Diffuse systemic sclerosis

231
Q

Features of sarcoidosis

A

Acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia

Insidious: dyspnoea, non-productive cough, malaise, weight loss

Skin: lupus pernio

Hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)

232
Q

Signs of iron deficiency anaemia

A

Koilonychia
Angular stomatitis/cheilosis
Post-cricoid web (Plummer-Vinson)

233
Q

Causes of sideroblastic anaemia

A

Congenital

Acquired:
Myelodysplastic/myeloproliferative disease
Drugs: chemo, anti-TB, lead

234
Q

Site of B12 absorption

A

Terminal ileum

235
Q

Sources of folate

A

Green veg, nuts, liver, poultry, pork, shellfish

236
Q

Sources of B12

A

Meat, fish, dairy

237
Q

B12/folate deficiency blood film

A

Macrocytic anaemia
Hypersegmented PMN
Target cells if ETOH/liver

238
Q

Causes of folate deficiency

A

Intake: poor diet
Demand: pregnancy, malignancy, haemolysis
Malabsoprtion: coeliac, crohns
Drugs: alcohol, phenytoin, MTX

239
Q

Location of folate absorption

A

Proximal jejunum

240
Q

Causes of B12 deficiency

A 
Reduced intake (vegan)
Reduced intrinsic factor: pernicious anaemia, post-gastrectomy
Terminal ileum: Crohn's, ileal resection, bacterial overgrowth
241
Q

Features of subacute degeneration of the spinal cord

A

Pernicious anaemia
Symmetrical dorsal column and corticospinal tract loss.
Distal sensory loss esp proprioception and vibration
Ataxia with wide gait and +ve Rombergs

Mixed upper and lower motor neuron signs:
Spastic paraparesis
Brisk knee jerk, upgoing plantars
Absent ankle jerk

242
Q

Pernicious anaemia increases the risk of…

A

Gastric adenocarcinoma

243
Q

Features of warm AIHA

A

IgG mediated bind at 37 degrees
Extravascular haemolysis and spherocytes
DAT+ve
Caused by: SLE, RA, idiopathic

244
Q

Treatment of warm AIHA

A

Immunosupression

Splenectomy

245
Q

Treatment of cold AIHA

A

Avoid cold

Rituximab

246
Q

Features of cold AIHA

A 
IgM mediated bind at <4 degrees
Intravascular haemolysis 
May cause agglutination 
DAT+ve for complement alone
Causes: mycoplasma, idiopathic
247
Q

Organism that causes haemolytic uraemic syndrome

A

E.coli O157:H7

248
Q

Features of HUS

A 
MAHA 
Thrombocytopenia 
Renal failure 
Bloody diarrhoea and abdo pain
Usually resolves spontaneously
249
Q

Blood film in HUS

A

Shistocytes

Low plt

250
Q

Features of thrombotic thrombocytopenic purpura

A 
Adult females with the pentad:
Fever
CNS signs: confusion, seizures 
MAHA
Thrombocytopenia 
Renal failure

Can be genetic or acquired

251
Q

Treatment of TTP

A

Immunosupression
Plasmaphoresis
Splenectomy

252
Q

Complications of hereditary spherocytosis

A 
Aplastic crisis (parvovirus B19)
Megaloblastic crisis
253
Q

Treatment of hereditary spherocytosis

A

Folate and splenectomy (after childhood)

254
Q

Features of hereditary spherocytosis

A 
Anaemia and reticulocytosis
Splenomegaly 
Pigment gallstones 
Jaundice 
DAT -ve
(MCV of little value due to high MCV of reticulocytes and spherocytes with low MCV. Results in normal or slightly low MCV)
255
Q

Investigations in hereditary spherocytosis

A 
Osmotic fragility (high)
DAT: -ve 
Spherocytes 
Low Hb
High reticulocytes (depends on severity)
256
Q

Triggers for haemolysis in G6PD deficiency

A

Fava beans (broad beans)
Mothballs (napthalene)
Infection
Drugs: antimalarials, henna, dapsone, sulphonamides

257
Q

Mode of inheritance:
G6PD deficiency
Hereditary spherocytosis

A

G6PD deficiency: x-linked recessive

Spherocytosis: autosomal dominant

258
Q

G6PD deficiency affects which metabolic pathway

A

Pentose phosphate shunt

259
Q

G6PD deficiency blood film features

A

Irregularly contracted cells
Heinz bodies
Bite cells

260
Q

Investigations in suspected G6PD deficiency

A

Film:
Irregularly contracted cells
Heinz bodies
Bite cells

G6PD assay after 8 weeks as reticulocytes have high G6PD

261
Q

Mutation in sickle cell anaemia

A

Point mutation (glu to val) in the B globin chain

262
Q

Hb levels in sickle cell anaemia

A

60-90

263
Q

Features if HbS red cells

A 
Sickled
Dehydrated 
Rigid 
Adherant (to vessel wall)
Reduced life span (haemolysis)
264
Q

Investigations in suspected HbSS

A 
Hb 60-90 
Sickle cells 
Target cells
Hb electrophoresis (neonatal screening)
Reticulocytes 
Raised bilirubin
265
Q

Triggers for sickle cell crisis

A

Dehydration
Infection
Cold
Hypoxia

266
Q

Complications of HbSS

A

Sequestration crisis
Splenic infarction: leads to atrophy and hyposplenism
Infection e.g. osteomyelitis
Aplastic crisis: parvovirus B19 infection
Gallstones

267
Q

Clinical features of sickle cell anaemia

A

Mnemonic: SICKLED

Splenonomegaly: possible sequestration crisis
Infarction: stroke, spleen, AVN, leg ulcers
Crises: pulmonar, mesenteric, pain
Kidney disease
Liver, lung disease
Erection: priapism
Dactylitis

268
Q

Management of sickle cell anaemia (chronic)

A

Pen V 250mg BD
Folate 5mg OD
Hydroxycarbamide if frequent crises

269
Q

vWF stabilises which coagulation factor?

A

F8

270
Q

Staging system for Hodgkin’s and Non-Hodgkin’a Lymphoma

A

Ann Arbor system:

1: single LN region
2: >= nodal areas on same side of the diaphragm
3: Nodes on both sides of the diaphragm
4: Spread beyond nodes e.g. liver and BM

add B if constitutional symptoms

271
Q

Features of Hodgkin’s lymphoma

A

Painless lymphadenopthy. Asymetric. Usually cervical.
Possible Alcohol induced LN pain.
Mediastinal LN may cause mass effect due to bronchial or SVC obstruction
Spreads contigiously to other LNs

Fever, night sweats, weight loss

Reed-Sternberg cells

272
Q

Treatment of Hodgkin’s Lymphoma

A

ABVD regimen

A – Doxorubicin (Adriamycin ®)
B – Bleomycin
V – Vinblastine (Velbe ®)
D – Dacarbazine (DTIC).

273
Q

Features of Non-Hodgkin’s lymphoma

A

Painless symmetric lymphadenopathy
Multiple sites
Spreads discontinuously

Fever, night sweats, weight loss

Pancytopenia and hyperviscosity

Extranodal features: 
Skin (esp is T cell) 
CNS
Oropharynx and GI tract
Splenomegaly
274
Q

Classification of non-Hodgkin’s Lymphoma

A 
Low Grade B Cell
Follicular 
Small cell lymphocytic 
Marginal zone (inc MALTomas) 
Lymphoplasmacytoid (e.g. Waldenstrom's)

High Grade B Cell
Diffuse large B cell (commonest type of NHL)
Burkitt’s

T Cell:
Adult T cell lymphoma: Caribbeans and Japanese- HTLV-1
Enteropathy associated T cell lymphoma: Chronic coeliac
Cutaneous T cell lymphoma
Anaplastic large cell

275
Q

Treatment of polycythaemia vera

A

Aspirin 75mg OD
Venesection if young
Hydroxycarbamide if older/high risk

276
Q

Complications of polycythaemia vera

A

Thrombosis and haemorrhage
30% progress to myelofibrosis
5% progress to AML

277
Q

Features of essential thrombocythaemia

A

Thrombosis: arterial and venous
Bleeding e.g. mucous membranes (abnormal plt function)
Erythromelagia: sudden, severe burning in hands and feet with redness of the skin

Plt>600 (often >1000)
Increased megakaryocytes in BM
50% JAK2+ve

278
Q

Features of primary myelofibrosis

A

Clonal proliferation of megakaryocytes leading to increased PDGF expression and myelofibrosis.

Extramedullary haematopoesis e.g. liver, spleen

Elderly
Massive HSM
Fever, night sweats, weight loss
BM failure: Anaemia, infections, bleeding

279
Q

Treatment of essential thrombocythaemia

A

Hydroxycarbamide if Plt>1000

Anagralide may be used

280
Q

Primary myelofibrosis investigations

A

FBC: Cytopenias
Film: leukoerythroblastic with teardrop poikilocytes
BM: dry tap, need trephine biopsy
50% JAK2+ve

281
Q

Treatment of primary myelofibrosis

A

Supportive: blood products
Splenectomy
Allogeneic BMT may be curative in younger patients

Ruxolitinib (anti-JAK2) for improvement of severe constitutional symptoms or severely symptomatic splenomegaly.

282
Q

Gene mutation in acute promyelocytic leukaemia

A

t(15;17)

283
Q

Features of chronic lymphocytic leukaemia

A 
Clone of mature B cells 
Often asymptomatic 
Symmetrical painless lymphadenopathy 
HSM
Anaemia 
Fever, weight loss, night sweats 
Lymphocytosis 
Smear cells 
Reduced Ig 
\+ve DAT
Can remain stable for years death commonly due to infection.
284
Q

Evan’s syndrome is…

A

AIHA + ITP

285
Q

Chemotherapy for CLL

A

Cyclophosphamide
Fludarabine
Rituximab

286
Q

Complications of CLL

A

Evan’s syndrome
Infection
Marrow failure/infiltration
Transformation to large B cell lymphoma

287
Q

Features of CML

A 
Fever, lethargy, weight loss, night sweats 
Massive HSM causing abdo discomfort 
Bruising/bleeding (platelet dysfunction) 
Gout
Hyperviscosity 
High WCC (myeloid) 
Anaemia and low plt 
High urate
Ph chromosome positive
288
Q

CML investigations

A 
Philadelphia chromosome +ve. t(9;22) formation of BCR-ABL fusion gene. Positive in 80% of CML 
WCC: raised. Myeloid cells. 
Anaemia and low plt
High urate
Blasts dependent on phase of disease.
289
Q

Treatment of CML

A

Imatinib (tyrosine kinase inhibitor)

BMT is blast crisis or TK-refractory

290
Q

3 Phases of CML

A

Chronic phase: <5% blasts
Accelerated phase: 10-19% blasts
Blast phase: usually AML >20% blasts

291
Q

Key features of multiple myeloma

A

CRAB

Calcium high
Renal insufficiency
Anaemia <100g/L (BM infiltration. Also low plt and low neutrophils)
Bone lesions: bone pain and backache, vertebral collapse, pathological fractures

Clonal plasma B cells
Urinary monoclonal light chains (Bence Jones Protein)
Recurrent bacterial infections

292
Q

Complications of multiple myeloma

A 
Hypercalcaemia 
Neuro: compression, raised Ca, amyloid 
AKI
Stroke due to hyperviscosity 
AL-amyloid
293
Q

Investigations in suspected multiple myeloma

A 
FBC: normocytic, normochromic anaemia 
Film: rouleaux, plasma cells, cytopenias 
Raised ESR, raised Cr and urea, 
High calcium but normal ALP 
Urine: bence jones proteins

X-ray: punched out lytic lesions, pepper pot skull, vertebral collapse, fractures

294
Q

For diagnosis of multiple myeloma BM plasma cells must be at least…

A

10%

295
Q

Treatment of multiple myeloma

A

Specific: chemo e.g. lenalidomide and low dose dex followed by BMT. Chemo only if unfit.

Supportive:
Bone pain: analgesia (avoid NSAIDs) and bisphosphonates
Anaemia: transfusions and EPO
Renal impairment: adequate hydration and dialysis
Infections: broad spectrum abx and IVIG if recurrent

Complications:
High Ca: aggressive hydration, furosemide, bisphosphonates
Cord compression: MRI, Dex, local radiotherapy
Hyperviscosity: plasmapheresis (remove light chains)
AKI: rehydration and dialysis

296
Q

Features of smouldering myeloma

A

Asymptomatic
Monoclonal protein
BM plasma cells of at least 10%
No CRAB

297
Q

MGUS (Monoclonal gammopathy of undetermined significance)

A

Serum monoclonal protein under 30g/L
Clonal BM plasma cells under 10%
No CRAB

298
Q

Features of Waldenstroms Macroglobulinaemia

A

Lymphoplasmacytoid lymphoma producing monoclonal IgM band
Hyperviscosity producing CNS and ocular symptoms
Lymphadenopathy and splenomegaly

299
Q

Ig type in Waldenstroms Macroglobulinaemia

A

IgM

300
Q

Investigations in suspected Waldenstroms macroglobulinaemia

A

Monoclonal IgM paraprotein in serum

High ESR

301
Q

Definition of amyloidosis

A

Group of disorders

Extracellular deposits of protein in an abnormal fibrillar form that is resistant to degradation

302
Q

Signs of hyperviscosity syndrome

A

CNS: headache, confusion, seizures, falls
Visual: retinopathy producing visual disturbance
Bleeding: mucus membranes, GI, GU
Thrombosis

303
Q

Causes of AL amyloidosis

A

Primary occult plasma cell proliferation (primary AL amyloid)

Secondary: Multiple myeloma, Waldenstroms, MGUS, lymphoma

304
Q

Causes of AA amyloidosis

A

Chronic inflammation:
RA
IBD
Chronic infection e.g. TB, bronchiecyasis

305
Q

Amyloid in AA amyloidosis is derived from…

A

SAA (serum amyloid A). An acute phase protein.

306
Q

Investigations in suspected amyloidosis

A

Biopsy affected tissue

Apple green birefringence with Congo red stain under polarised light

307
Q

Features of AL amyloidosis

A

Renal: proteinuria and nephrotic syndrome
Heart: restrictive cardiomyopathy, arrhythmias (sparkling appearance on echo)
Nerves: peripheral and autonomic neuropathy. Carpal tunnel
GIT: macroglossia, malabsorption, perforation, haemorrhage, hepatomegaly, obstruction
Vascular: periorbital purpura (characteristic)

308
Q

Features of AA amyloidosis

A

Renal:
Proteinuria and nephrotic syndrome
Hepatosplenomegaly

309
Q

Treatment of AA amyloidosis

A

May improve with underlying condition

310
Q

Treatment of AL amyloidosis

A

May respond to therapy for multiple myeloma

311
Q

Features of familial amyloidosis

A

Autosomal dominant
Mutations in transthyretin
Sensory or autonomic neuropathy
Liver transplant may be curative

312
Q

Treatment of familial amyloidosis

A

Liver transplant may be curative

313
Q

Causes of massive splenomegaly (above 20cm)

A 
CML
Myelofibrosis
Malaria
Leishmaniasis 
Gaucher's
314
Q

Blood film in hyposplenism

A

Howell Jolly bodies
Target cells
Pappenheimer bodies

315
Q

Hyposplenisms increases susceptibility to which organisms

A

Encapsulated: Haemophilus, pneumococcus, meningococcus

316
Q

Immunisations post splenectomy

A

Pneumovax (repeat every 5 years)
Hib if not done in childhood
Men C if not done in childhood
Yearly flu

317
Q

Causes of hyposplenism

A

Splenectomy
Sickle Cell Disease
Coeliac disease
IBD

318
Q

Causes of splenomegaly

A

Haematological:
Haemolysis: Hereditary spherocytosis, SCD
Myeloproliferative disease: MF, CML, PV
Leukaemia, lymphoma

Infective:
EBV, CMV, hepatitis, HIV
TB, infective endocarditis
malaria, leishmaniasis, hydatid disease

Portal HTN: budd chiari, cirrhosis

Connective tissue disease: Sjogren’s RA, SLE

Other: Sarcoid, amyloidosis, Gaucher’s, primary antibody deficiency

319
Q

PEFR % of predicted in asthma exacerbations:
Moderate
Severe
Very severe

A

PEF >50–75% best or predicted
PEF 33–50% best or predicted
PEF <33% best or predicted

320
Q

Causes of upper zone lung fibrosis

A

A PENT

Aspergillosis 
Pneumoconiosis 
Extrinsic allergic alveolitis 
Negative sero-arthropathy 
TB
321
Q

Causes of lower zone lung fibrosis

A

STAIR

Sarcoidosis (mid zone)
Toxins 
Asbestosis
Idiopathic pulmonary fibrosis 
Rheum: SLE, RA, Scleroderma, Sjogren's, PM/DM
322
Q

Drugs causing lung fibrosis

A

BANS ME

Bleomycin/busulfan
Amiodarone 
Nitrofurantoin 
Sulfasalazine 
MEthotrexate
323
Q

Patients with a CURB-65 score of… should be managed in hospital

A

2 or more

324
Q

Most common organism causing infective exacerbation of COPD

A

H. influenzae

325
Q

Features of PCP infection

A 
Caused by pneumocystis jiroveci 
Dry cough 
Exertional dyspnoea 
Fever 
HIV complication 
CXR shoes bilateral perihilar interstitial shadowing 
Diagnose by visualizing in sputum
326
Q

Features of CMV retinitis

A

Reduced acuity
Eye pain
photophobia
Pizza sign on fundoscopy

327
Q

Kaposi sarcoma caused by infection with…

A

HHV8

328
Q

Treatment of progressive multifocal leukoencephalopathy (in HIV)

A

HAART

Lack of evidence for other treatments

329
Q

Complications of chickenpox

A

Pneumonitis, haemorrhage, encephalitis

Teratogenic

330
Q

Complications of EBV

A 
Splenic rupture 
CN lesion
Ataxia
GBS
Pancytopenia with megaloblastic marrow 
Meningioencephalitis 
Chronic fatigue
Burkitt's lymphoma (jaw or abdo mass)
331
Q

Features of EBV infection

A 
Fever
Malaise 
Sore throat 
Cervical lymph nodes +++ 
Splenomegaly 
Hepatitis causing hepatomegaly and jaundice
332
Q

Investigations in suspeced EBV

A

Blood smear shows lymphocytosis

Positive monospot test (previously Paul Bunnel test) a test for Ab produced in response to EBV infection.

333
Q

EBV infects which cell type?

A

B cells

334
Q

Owl’s eye inclusions are seen in…

A

CMV

335
Q

…% of people infected with hepatitis C develop chronic infection

A

85%

336
Q

Indications for Hepatitis C treatment

A

Chronic hepatitis (detectable HCV viral level over a six-month period)
Fibrosis
Raised ALT

337
Q

Hepatitic C treatment

A

If indicated e.g. chronic infection

Interferon
Ribavarin

However choice is complex and depends on genotyping. Many new options are available.

338
Q

Infective causes of bloody diarrhoea

A 
EHEC E.coli 
Campylobacter
Shigella 
C. Diff (but usually watery)
Entamoeba histolytica
339
Q

Commonest cause of travellers’ diarrhoea

A

E. coli (ETEC)

340
Q

Features of giardiasis

A 
Bloating 
Explosive diarrhoea 
Offensive gas
1-4 incubation period 
Malabsorption leading to steatorrhoea and weight loss
341
Q

Features of amoebic dysentery

A 
Dysentery 
Wind
Tenesmus 
Bloody stools 
1-4 week incubation period 
Weight loss if chronic 
Can lead to liver abscess
342
Q

Treatment of amoebic dysentery

A

Metronidazole (800mg TDS) 5 days or 10 days if liver abscess

Tinidazole

343
Q

Features of Lyme disease

A

Early localised: erythema migrans (target lesion)

Early disseminated:
Malaise, LN, migratory arthritis, hepatitis

Late persistent: arthritis, focal neuro (Bell’s Palsy), heart block, myocarditis

Lymphocytoma: red/blue ear lobe.

344
Q

List the Centor criteria

A 
The Centor criteria* are as follows:
Presence of tonsillar exudate
Tender anterior cervical lymphadenopathy or lymphadenitis
History of fever
Absence of cough
345
Q

Formula for corrected QT interval

A

Framingham formula: QT + 0.154 (1 – RR)

Bazett’s formula: QTC = QT / √ RR

346
Q

On an ECG 1 small square=

A

0.04ms/0.1mV

347
Q

Features of polycystic kidney disease

A

MISSHAPES

Mass: abdo mass and flank pain
Infected cyst
Stones
SBP raised
Haematuria or haemorrhage into cyst
Aneurisms: berry leading to SAH
Polyuria 
Extra-renal cysts e.g. liver
Systolic murmur: mitral valve prolapse
348
Q

What is Kussmaul’s sign

A

The JVP increasing with inspiration is known as Kussmaul’s sign and can be a feature of constrictive pericarditis. It is caused by impaired filling of the right ventricle due to a poorly compliant myocardium or pericardium. The JVP should fall with inspiration due to reducing pressure in the thoracic cavity.

349
Q

Key differences between cardiac tamponade and constrictive pericarditis

A

Cardiac tamponade Constrictive pericarditis
JVP Absent Y descent X + Y present
Pulsus paradoxus Present Absent
Kussmaul’s sign* Rare Present
Characteristic features Pericardial calcification on CXR

350
Q

ECG changes tricyclic overdose

A

ECG changes include:
sinus tachycardia
widening of QRS
prolongation of QT interval

ICSM Finals (7 decks)

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