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FINALS > El Panico > Flashcards

El Panico Flashcards

1
Q

No exclusion

A

Conjunctivitis
Fifth disease (slapped cheek)
Roseola
Infectious mononucleosis
Head lice
Threadworms
Hand, foot and mouth

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2
Q

What is the school exclusion time for scarlet fever?

A

24 hours after commencing antibiotics

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3
Q

What is the school exclusion for whooping cough?

A

2 days after commencing antibiotics

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4
Q

What is the school exclusion criteria for measles?

A

4 days from onset of rash

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5
Q

What is the school exclusion criteria for rubella?

A

5 days from the onset of rash?

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6
Q

What is the school exclusion criteria for chicken pox?

A

All lesions crusted over

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7
Q

What is the school exclusion criteria for mumps?

A

5 days from onset of swollen glands

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8
Q

What is the school exclusion criteria for impetigo?

A

Lesions crusted and healed

or

48 hours after commencing antibiotics

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9
Q

What is the school exclusion criteria for scabies?

A

Until treated

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10
Q

What is the school exclusion criteria for influenza?

A

Until recovered

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11
Q

What are the vaccinations that you receive at 2 months?

A

‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)
Oral rotavirus vaccine
Men B

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12
Q

Vaccinations at three months?

A

‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)
Oral rotavirus vaccine
PCV

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13
Q

Vaccination schedule at 4 months?

A

‘6-1 vaccine’ (diphtheria, tetanus, whooping cough, polio, Hib and hepatitis B)
Men B

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14
Q

Vaccination schedule

12 - 13 months

A

Hib/Men C
MMR
PCV
Men B

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15
Q

2-8 years vaccination schedule?

A

Flu vaccine

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16
Q

3-4 years

A

‘4-in-1 pre-school booster’ (diphtheria, tetanus, whooping cough and polio)
MMR

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17
Q

Vaccination schedule 12-13 years?

A

HPV vaccination

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18
Q

Vaccination schedule 13-18 years?

A

‘3-in-1 teenage booster’ (tetanus, diphtheria and polio)
Men ACWY

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19
Q

RR, SBP and HR for less than 1 year of age?

A

RR = 30-40

SBP = 70-90

HR = 110 - 160

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20
Q

RR, SBP and HR for 2-5 years of age?

A

RR = 25-30

SBP = 80-100

HR = 95-140

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21
Q

RR, SBP and HR for 5-12 years of age

A

RR = 20-25

SBP = 90-110

HR = 80-120

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22
Q

RR, SBP and HR forover 12 years?

A

RR= 15-20

SBP = 100-120

Pulse = 60-100

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23
Q

What is the weight of a macrosomic baby?

A

over 4000g

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24
Q

What is normal birth weight?

A

2500-4000

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25
Q

What is low birth weight?

A

Less than 2500 g

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26
Q

What is very low borth weight?

A

Less than 1500 g

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27
Q

What is extremely low birth weight?

A

Less than 1000g

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28
Q

What is impossibly low birth weight?

A

less than 750g

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29
Q

What is avergae weekly weight gain of baby from 0-3 months?

A

200g

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30
Q

What is average weekly weight gain from 3-6 months?

A

150g

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31
Q

What is avergae weight gain from 6-9 months?

A

100g

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32
Q

What is average weekly weight gain from 9-12 months?

A

75-50g

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33
Q

How do you calculate weight of a baby that is less than 1 year old?

A

0.5 x age in months plus 4

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34
Q

How do you calculate the weight of a child that is 1-5 years old?

A

2 x age + 8

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35
Q

How do you calculate the weight of a child that is 6-10 years olf?

A

3 x age plus 7

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36
Q

What is blood volume in a baby>

A

80 mls/kg

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37
Q

What is urine output for a child?

A

0.5-1ml/kg/hour

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38
Q

What is the insensible fluid loss for a child per day?

A

20ml/kg/day

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39
Q

What is the golden rule for fluid managmement in children (maintenance fluids)?

A

4ml/kg for the first 10 kg

2ml/kg for the next 10 kg

1ml/kilo for the next 10kg

(0.9% NaCl / 5% dextrose +/- 0.15%KCL)

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40
Q

Blood pressure flow chart

A
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41
Q

How do thiazide diuretics work?

A

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

Since more sodium reaches the collecting duct then more potassium lost

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42
Q

What are the side effects of thiazide diuretics (10)?

A
  • dehydration
  • postural hypotension
  • hyponatraemia, hypokalaemia, hypercalcaemia*
  • gout
  • impaired glucose tolerance
  • impotence

Rare adverse effects

  • thrombocytopaenia
  • agranulocytosis
  • photosensitivity rash
  • pancreatitis
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43
Q

What is stage 1 hypertension?

A

Clinic BP = 140/90

ABPM = 135/85

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44
Q

What is stage 2 hypertension?

A

160/100

150/95

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45
Q

What is severe hypertension?

A

Clinic values over

180

110

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46
Q

Whan do we start treating hypertension?

A
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47
Q

What is the choice of hypertensive in afrocarribean patient already on CCB?

A

ARB

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48
Q

What are the blood pressure targets for people under 80?

A

140/90

135/85

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49
Q

What are the blood pressure targets for people over 80?

A

150/90

145/85

(these are just 10 values more than the targets for people less than 80)

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50
Q

What can a GP do if meningococcal meningitis is suspected?

A

IM benzylpenicillin

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51
Q

What is baseline meningitis treatment?

A

IV cefotaxime

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52
Q

Under what circumstances do we not give IV cefotaxime?

A

Under 3 months or over 50 years we give IV cefotaxime plus amoxicillin

If meningococcal we give IV benzylpenicillin or IV cefotaxime

If listeria we give IV amoxicillin + gent

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53
Q

What are the components of a qSOFA?

A

Resp rate over 22

Altered mentition

Systolic BP less than 100

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54
Q

What does a sofa score of 2 indicate?

A

overall mortality risk of approximately 10% in a general hospital population with suspected infection

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55
Q

What are the likely causative organisms for neonatal sepsis?

A

Group B strep (strep agalacticae)

E.Coli

Late-onset sepsis usually occurs via the transmission of pathogens from the environment post-delivery,

coagulase-negative staphylococcal species such as Staphylococcus epidermidis, Gram-negative bacteria such as Pseudomonas aeruginosa, Klebsiella and Enterobacter, and fungal species

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56
Q

What is typical antibiotic therapy for neonatal sepsis?

A

Benzylpenicillin and gent are first line

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57
Q

What is antibiotic therapy for neutropenic sepsis?

A

Tazocin

if patients are still febrile and unwell after 48 hours an alternative antibiotic such as meropenem is often prescribed +/- vancomycin

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58
Q

CURB 65

A

Patients with a CURB-65 score of 0 should be managed in the community.

Patients with a CURB-65 score of 1 should have their Sa02 assessed which should be >92% to be safely managed in the community and a CXR performed. If the CXR shows bilateral/multilobar shadowing hospital admission is advised.

Patients with a CURB-65 score of 2 or more should be managed in hospital as this represents a severe community acquired pneumonia.

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59
Q

Management of pneumonia?

A

Management of low-severity community acquired pneumonia

amoxicillin is first-line

if penicillin allergic then use a macrolide or tetracycline

NICE now recommend a 5 day course of antibiotics for patients with low severity community acquired pneumonia

Management of moderate and high-severity community acquired pneumonia

dual antibiotic therapy is recommended with amoxicillin and a macrolide

a 7-10 day course is recommended

NICE recommend considering a beta-lactamase stable penicillin such as co-amoxiclav, ceftriaxone or piperacillin with tazobactam and a macrolide in high-severity community acquired pneumonia

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60
Q

What are the causative bacteria for pneumonia?

A

Community acquired pneumonia (CAP) may be caused by the following infectious agents:

Streptococcus pneumoniae (accounts for around 80% of cases)

Haemophilus influenzae = COPD patients

Staphylococcus aureus: commonly after influenza infection

atypical pneumonias (e.g. Due to Mycoplasma pneumoniae)

viruses

Klebsiella pneumoniae is classically in alcoholics

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61
Q

Treatment for LUTI

A

Trimethoprim or nitrofurantoin. Alternative: amoxicillin or cephalosporin

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62
Q

Treatment for acute pyelonephritis

A

Broad-spectrum cephalosporin or quinolone

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63
Q

Treatment for acute prostatitis?

A

Quinolone or trimethoprim

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64
Q

Treatment for impetigo?

A

Topical hydrogen peroxide, topical fusidic acid oral flucloxacillin or erythromycin if widespread

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65
Q

Treatment for cellulitis and erysipelas

A

Flucloxacillin (clarithromycin, erythromycin or doxycycline if penicillin-allergic)

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66
Q

Treatment for cellulitis near the eyes or nose / animal bite?

A

Co-amoxiclav (doxycycline + metronidazole if penicillin-allergic)

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67
Q

Mastitis treatment (antibiotic)

A

Flucloxacillin

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68
Q

Throat infections / sinusitis antibiotic?

A

Phenoxymethylpenicillin

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69
Q

Otitis media anti-biotic?

A

Amoxicillin

Erythromycin if allergic

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70
Q

Otitis externa antibiotic

A

Flucloxicillin

(plus steroid)

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71
Q

Peri-apical or peridontal abscess?

A

Amoxicillin

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72
Q

Gingivitis antibiotic

A

Metronidazole

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73
Q

Gonorrhoea antibiotic

A

IM ceftriaxone

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74
Q

Antibiotic for chlamydia

A

doxycycline (7 days) or azithromycin (1g od for one day, then 500mg od for two days)

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75
Q

Antibiotic therapy for PID

A

Oral ofloxacin + oral metronidazole

OR

intramuscular ceftriaxone + oral doxycycline + oral metronidazole

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76
Q

What is the antibiotic management for bacterial vaginosis?

A

Oral or topical metro

or topical clindamycin

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77
Q

ABX for c.diff

A

First episode: metronidazole
Second or subsequent episode of infection: vancomycin

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78
Q

Life threatening c.diff

A

for life-threatening infections a combination of oral vancomycin and intravenous metronidazole should be used

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79
Q

Campylobacter enteritis

A

Clari

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80
Q

Salmonella and shigellosis abx

A

Cipro

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81
Q

ECG changes for anteroseptal MI

Coronary artery for anteroseptal

A

V1-V4

Left-anterior descending

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82
Q

ECG changes for inferior MI

Coronary artery for inferior MI

A

2,3, aVF

Right coronary artery

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83
Q

ECG changes for anterolaterl MI

Coronary artery for anterolateral MI

A

1, AVL V4-6

LAD

Left circumflex

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84
Q

Lateral MI ECG changes and artery

A

1, AVL, +/- V5-V6

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85
Q

Posterior MI ECG changes and coronary artery

A

Tall R waves V1-V2

Usually left circumflex, also right coronary artery

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86
Q

What are the ejection systolic murmurs?

A

louder on expiration

  • aortic stenosis
  • hypertrophic obstructive cardiomyopathy

louder on inspiration

  • pulmonary stenosis
  • atrial septal defect

also: tetralogy of Fallot

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87
Q

Holosystolic murmurs

A

Holosystolic (pansystolic)

mitral/tricuspid regurgitation (high-pitched and ‘blowing’ in character)

  • tricuspid regurgitation becomes louder during inspiration, unlike mitral stenosis
  • during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole

ventricular septal defect (‘harsh’ in character)

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88
Q

Late systolic murmurs

A

Late systolic

mitral valve prolapse

coarctation of aorta

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89
Q

Early diastolic murmurs

A

Aortic regurgitation

Graham steel murmur (pulmonary regurgitation)

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90
Q

Mid-late diastolic murmur

A

Mitral stenosis

Austin flint murmur (severe aortic regurgitation ‘rumbling in character’

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91
Q

Contunous machine like murmur

A

PDA

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92
Q

Describe venous hum

A

Continous hum below clavicles

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93
Q

Describe stills murmur

A

Low-pitched sound heard at lower left sternal edge

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94
Q

Describe heart sounds of TOGA

A

No murmur

Loud S2

Prominent right ventricular impulse

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95
Q

describe murmur of tetralogy

A

Ejection systolic

Upper left sternal edge (above stills murmur)

Radiates to axilla

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96
Q

Describe tricuspid atresia murmur

A

Left upper sternal edge (same place as tetralogy, above stills)

Prominent apical pulse

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97
Q

What does S1 correlate with?

A

Closure of mitral and tricuspid valves

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98
Q

What causes a soft S1?

A

Long PR or mitral regurgitation

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99
Q

What causes a loud S1?

A

Mitral stenosis

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100
Q

What does S2 correlate with?

A

Closure of the aortic and pulmonary valves

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101
Q

What causes a soft S2?

A

Aortic stenosis

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102
Q

What is a physiological cause of splitting of S2?

A

Inspiration

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103
Q

What correlates with S3?

A

Diastolic filling of the ventricle

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104
Q

When is a third heart sound considered normal

A

If under 30

May persist in women up to 50 years old

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105
Q

What are causes of S3?

A

Left ventricular failure (dilated cardiomyopathy)

Constrictive pericarditis

Mitral regurgitation

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106
Q

When might you hear S4

A

Aortic stenosis

HOCM

Hypertension

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107
Q

What causes the sound of S4

A

Atrial contraction against stiff ventrical

(P wave)

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108
Q

What might you feel on the chest wall if they have a S4 heart sound?

A

Double apical impulse

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109
Q

What is the management of angina?

A

= beta blocker or calcium channel blocker first line. If CCB monotherapy, use verapamil or diltiazem. If using beta blocker and want to add ccb, add nifedipine/amlodipine/felodipine. If you can’t tolerate these two drugs and want to better control add an adjunct.

So prescribe 1

Then add another to make combination of beta blocker and nifedipine. If this combo isn’t tolerated, try adding; long-acting nitrate, ivabradine, nicorandil or ranolazine

Nicorandil is associated with ulcers that can occur anywhere along the gastrointestinal tract

Nitrates require a nitrate-free interval each day to prevent tolerance

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110
Q

Post MI medications

A

Satan playing double bass

Statin

Dual antiplatelet therapy

Beta blocker

Ace inhibitor

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111
Q

Read over STEMI/NSTEMI

A
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112
Q

What is rate control for AF?

A

Beta blockers

CCBs

Digoxin (useful if coexistant heart failure)

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113
Q

Rhythm control in AF drug therapy

A

Sotalol

Amiodarone

Flecainide

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114
Q

Factors favouring rate control

A

Over 65

History of IHD

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115
Q

Factors favouring rhythm control

A

Under 65

Symptomatic

First presentation

Lone AF or AF secondary to corrected precipitant (e.g alcohol)

Congestive heart failure

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116
Q

If CHA2DS2-VASc score suggests no need for anticoagulation what investigation is necessary?

A

echo to exclude valvular heart disease

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117
Q

Heart failure drug management

A

Ace inhibitor and Beta blocker

Spironolactone

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

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118
Q

When is cardioversion indicated in VT?

A

If systolic BP is less than 90

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119
Q

What is drug therapy for VT?

A

Amiodarone

Lidocaine

Procainamide

VERAPAMIL SHOULD NOT BE USED

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120
Q

Ventricular tachycardia with broad QRS. What is the formulation of amiodarone?

A

300mg IV over 20-60minutes

900mg over 24 hours

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121
Q

What are differentials for irregular broad QRS tachycardia?

A

AF with bundle branch block

Pre-excited AF

Polymorphic VT (torsades de pointes)

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122
Q

What is the treatment for narrow complex tachycardia with regular rhythm?

A

Vagal manouvres

Adenosine 6mg, 12mg, 12mg

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123
Q

What is management of irregular narrow complex tachycardia?

A

Probably AF

Control rate with beta blocker or diltiazem

Consider digoxin or amiodarone

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124
Q

What is the most common cause of death after MI?

A

Ventricular fibrillation

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125
Q

What type of MI might cause AV block

(causes bradycardia)

A

Inferior

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126
Q

WHen does pericarditis occur after an MI?

A

Within the first 48 hours

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127
Q

When does dresslers syndrome occur after MI?

A

2-6 weeks after

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128
Q

What are the features of dresslers syndrome?

A

Fever

Pleuritic pain

Pericardial effusion

Raised ESR

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129
Q

What is the cause of persistent ST elevation after MI?

A

Left verntricular aneurysm

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130
Q

What are the features of left ventricular free wall rupture?

A

Occurs 1-2 weeks after MI

Acute heart failure

Cardiac tamponade

Raised JVP

Pulsus paridoxus

Diminished heart sounds

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131
Q

Pansystolic murmur post-MI

A

VSD

Also has features of acute heart failure

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132
Q

Acute hypotension and pulmonary oedema after MI

A

Acute mitral regurgitation

More common in infero=posterior infarction. May be due to ischaemia or rupture of papillary muscle

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133
Q

Blind therapy for IE

A

Native valve

amoxicillin, consider adding low-dose gentamicin

If penicillin allergic, MRSA or severe sepsis

vancomycin + low-dose gentamicin

If prosthetic valve

vancomycin + rifampicin + low-dose gentamicin

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134
Q

What are the indications for surgery in IE?

A
  • severe valvular incompetence
  • aortic abscess (often indicated by a lengthening PR interval)
  • infections resistant to antibiotics/fungal infections
  • cardiac failure refractory to standard medical treatment
  • recurrent emboli after antibiotic therapy
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135
Q

General rules for IE ABX therapy

A

If staph use flucloxacillin

If strep use benzylpenicillin

If prosthetic valve use rifampicin

Back up always involves vancomycin and usually low-dose gent

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136
Q

Major bleeding with warfarin

A

Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate - if not available then FFP*

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137
Q

INR > 8.0
Minor bleeding

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0

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138
Q

INR > 8.0
No bleeding

A

Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0

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139
Q

INR 5.0-8.0
Minor bleeding

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0

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140
Q

INR 5.0-8.0
No bleeding

A

Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose

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141
Q

General rules for warfarin managment with high INR

A

Prothrombin complex concentrate only used when there is major bleeding

If bleeding the vitamin K will be IV

You always stop warfarin unless INR is 5-8 and no bleeding (in this case you withold 1-2 doses)

Restart warfarin when INR less less than 5

Standard dose of vit K is 1-3mg (major bleeding dose is 5mg, oral dose is 1-5mg)

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142
Q

p450

A
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143
Q

Pneumothorax guidelines

A
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144
Q

COPD management

A

Essentially the patient will be on SABA and LABA

if no steroid responsive features then add LAMA

If steroid responsive then give inhjaled corticosteroids

Then all of these medications as last line therapy

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145
Q

What are the features of severe asthma?

A

PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm

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146
Q

What are the features of life threatening asthma?

A
  • PEFR < 33% best or predicted
  • Oxygen sats < 92%
  • Silent chest, cyanosis or feeble respiratory effort
  • Bradycardia, dysrhythmia or hypotension
  • Exhaustion, confusion or coma

Normal PCO2

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147
Q

Asthma management

A

In child under 5

SABA

Then 8 week trial of moderate dose ICS

Then final line therapy is SABA low dose ICS and LTRA - after that you refer to specialist

In child 5-12

SABA

Plus low dose ICS

Plus LTRA

Plus LABA (stop LTRA)

Then increase steroids

Then add theophyline

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148
Q

What is a classic history of bronchopulmonary aspergillosis?

A

bronchiectasis and eosinophilia

bronchoconstriction: wheeze, cough, dyspnoea. Patients may have a previous label of asthma

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149
Q

What are investigations for allergic bronchopulmonary aspergillosis?

A
  • eosinophilia
  • flitting CXR changes
  • positive radioallergosorbent (RAST) test to Aspergillus
  • positive IgG precipitins (not as positive as in aspergilloma)
  • raised IgE
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150
Q

What organism causes allergic bronchopulmonary aspergillosis?

A

Aspergillus spores

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151
Q

What is the management of allergic bronchopulmonary aspergillosis?

A

oral glucocorticoids

itraconazole is sometimes introduced as a second-line agent

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152
Q

What is the new name for hypersensitivity pheumonitis?

A

Extrinsic allergic alveolitis

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153
Q

What type of hypersensitivity reaction is EAA?

A

Type 3 and type 4

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154
Q

What are examples of allergens that provoke EAA

A
  • bird fanciers’ lung: avian proteins from bird droppings
  • farmers lung: spores of Saccharopolyspora rectivirgula from wet hay (formerly Micropolyspora faeni)
  • malt workers’ lung: Aspergillus clavatus
  • mushroom workers’ lung: thermophilic actinomycetes*
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155
Q

What is the presentation of EAA?

A

acute (occurs 4-8 hrs after exposure)

  • dyspnoea
  • dry cough
  • fever

chronic (occurs weeks-months after exposure)

  • lethargy
  • dyspnoea
  • productive cough
  • anorexia and weight loss
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156
Q

What is the investigation for EAA?

A

Investigation

imaging: upper/mid-zone fibrosis

bronchoalveolar lavage: lymphocytosis

serologic assays for specific IgG antibodies

blood: NO eosinophilia (this is in contrast to allergic bronchopulmonary aspergillosis) (additionally, imaging shows bronchiectasis on bronchopulmonary aspergillosis)

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157
Q

Management of EAA

A

avoid precipitating factors

oral glucocorticoids

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158
Q

What causes fibrosis of upper lobes?

A

Fibrosis of upper lobes:

C- Coal worker’s pneumoconiosis

H - Histiocytosis/ hypersensitivity pneumonitis

A - Ankylosing spondylitis

R - Radiation

T - Tuberculosis

S - Silicosis/sarcoidosis

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159
Q

Which COPD patients are offered long-term oxygen therpay?

A

Assess patients if any of the following:

  • very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be ‘considered’ for patients with severe airflow obstruction (FEV1 30-49% predicted)
  • cyanosis
  • polycythaemia
  • peripheral oedema
  • raised jugular venous pressure
  • oxygen saturations less than or equal to 92% on room air

Assessment is done by measuring arterial blood gases on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management.

Offer LTOT to patients with a pO2 of < 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following:

  • secondary polycythaemia
  • peripheral oedema
  • pulmonary hypertension

Cannot be given to people who smoke

Risk assessment should include falls assessment and risk of burns/fires

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160
Q

Features of 21-hydroxylase deficiency

A

virilisation of female genitalia

precocious puberty in males

60-70% of patients have a salt-losing crisis at 1-3 wks of age

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161
Q

Features of 11-beta hydroxylase deficiency

A

virilisation of female genitalia

precocious puberty in males

hypertension

hypokalaemia

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162
Q

Features of 17 hydroxylase deficiency

A

non-virilising in females

inter-sex in boys

hypertension

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163
Q

Features of androgen insensitivity?

A

Androgen insensitivity syndrome is an X-linked recessive condition due to end-organ resistance to testosterone causing genotypically male children (46XY) to have a female phenotype. Complete androgen insensitivity syndrome is the new term for testicular feminisation syndrome

Features

‘primary amennorhoea’

undescended testes causing groin swellings

breast development may occur as a result of conversion of testosterone to oestradiol

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164
Q

Management of androgen insensitivity?

A

Management

counselling - raise child as female

bilateral orchidectomy (increased risk of testicular cancer due to undescended testes)

oestrogen therapy

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165
Q

What is the pathophysiology of kallmans?

A

X-linked

Hypogonadotrophic hypogonadism

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166
Q

What are the features of kallmans?

A
  • ‘delayed puberty’
  • hypogonadism, cryptorchidism
    • anosmia
  • sex hormone levels are low
  • LH, FSH levels are inappropriately low/normal
  • patients are typically of normal or above average height
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167
Q

What are the features of kartagener’s syndrome?

A

Primary ciliary dyskinesia

Features

  • dextrocardia or complete situs inversus
  • bronchiectasis
  • recurrent sinusitis
  • subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
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168
Q

What are the levels of sex hormones in klinefelters?

A

elevated gonadotrophin levels but low testosterone

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169
Q

What are the features of klinefelters?

A
  • often taller than average
  • lack of secondary sexual characteristics
  • small, firm testes
  • infertile
  • gynaecomastia - increased incidence of breast cancer
  • elevated gonadotrophin levels but low testosterone
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170
Q

What is the value of impaired fasting glucose?

A

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

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171
Q

How to differentiate between secondary and tertiary hyperparathyroidism?

A

Secondary hyperthyroidism = high phosphate, Calcium is porportionatel MUCH lower than PTH

Tertiary hyperthyroidism = high ALP

Remember that secondary hyperparathyroidism is due to CKD. In response to PTH kidney should REABSORB calcium, EXCRETE phosphate and Start making vitamin D. However in CKD the kidneys suck, so it can’t do these things. Hence, low calcium, high phosphate and low vit D.

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172
Q

Causes og hypoglycaemia in non-diabetic patients

A
  • Exogenous drugs such alcohol, aspirin poisoning, pentamidine, quinine sulfate, ACE-inhibitor
  • Pituitary insufficiency
  • Liver failure
  • Addison’s disease
  • Islet cell tumours eg insulinoma
    • Non-pancreatic neoplasms
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173
Q

Side effects of SGLT-2 inhibitors

A

genital infections, diabetic ketoacidosis, fourniers gangrene

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174
Q

Side effects of metformin

A

GI upset

Lactic acidosis

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175
Q

What are the side effects of GLP-1 mimetics?

A

Nause

Vomitting

Pancreatitis

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176
Q

What are the side effects of insulin

A

weight gain, hypoglycaemia, lipodystrophy

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177
Q

Side effects of thiazolidinones

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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178
Q

How to pick your T2 diabetes medication?

A

Try lifestyle, if above 48 add metformin. If above 58 after adding metformin then add another drug. If still above 58 with two drugs then add a third (insulin therapy can be considered instead of adding a third drug)

Target is 48 mmol with metformin

If two drugs the target is now 53

​Small tips:

  • Drugs that cause weight gain = sulphonylureas and thiazolidinones
  • Weight neutral = DPPIV
  • Weight loss = GLP-1 anologues and SGLT2 inhibitors
  • If heart failure then don’t use thiazolidenones
  • Only ones really used in pregnancy is metformin and insulin
  • Gliptin in triple therapy can only be used with sulfonylurea
  • GLP-1’s are last line if metformin tolerated
  • SGLT-1’s are not used if metformin is not tolerated
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179
Q

What are the criteria for GLP-1 anologues?

A

Criteria for glucagon-like peptide1 (GLP1) mimetic (e.g. exenatide)

if triple therapy is not effective, not tolerated or contraindicated then NICE advise that we consider combination therapy with metformin, a sulfonylurea and a glucagon-like peptide1 (GLP1) mimetic if:

BMI >= 35 kg/m² and specific psychological or other medical problems associated with obesity or

BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities

(basically people who need to lose weight and people who can’t take insulin)

only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months.

Probably because they are very expensive! - Need to make sure they are working to justify using them.

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180
Q

Multiple endocrine neoplasia

A
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181
Q

What does MODY stand for?

A

Maturity-onset diabetes of the young

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182
Q

What are the features of MODY?

A

development of type 2 diabetes mellitus in patients < 25 years old

typically develops in patients < 25 years

a family history of early onset diabetes is often present

ketosis is not a feature at presentation

patients with the most common form are very sensitive to sulfonylureas, insulin is not usually necessary

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183
Q

Side effects of thyroxine

A
  • hyperthyroidism: due to over treatment
  • reduced bone mineral density
  • worsening of angina
  • atrial fibrillation
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184
Q

What is the most common type of thyroid cancer?

A

Papillary

65%, generally young females. Metastasis to cervical lymph nodes. Thyroglobulin can be used as a tumour marker. Characteristic Orphan Annie eyes on light microscopy. Good prognosis

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185
Q

What type of thyroid tumour presents as a solitary thyroid nodule?

A

Follicular adenoma

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186
Q

How do you differentiate between follicular adenoma and follicular carcinoma

A

Capsular invasion

Follicular carcinoma = 20%, generally women >50 years old. Metastasis to lung and bones. Thyroglobulin can be used as a tumour marker. Moderate prognosis

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187
Q

What thyroid cancer is predominantly comprised of C cells derived from neural crest tissue, raised serum calcitonin and has a genetic component?

A

Medullary thyroid

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188
Q

If this thyroid cancer were to occur, it would most likely occur in elderly females

A

Anaplastic carcinoma

Not responsive to treatment, can cause pressure symptoms

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189
Q

What type of thyroid cancer is associated with hashimotot’s thyroiditis?

A

Lymphoma

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190
Q

What are the causes of primary hyperparathyroidism?

A

Solitary adenoma

Hyperplasia

Multiple adenoma

Carcinoma

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191
Q

What conditions cause lower than expected HbA1c?

A

Sickle-cell anaemia
GP6D deficiency
Hereditary spherocytosis

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192
Q

What conditions may cause higher than expected HbA1c?

A

Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy

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193
Q

What conditions will cause an increased total gas transfer (rate at which gas will diffuse from alveoli into the blood.

A
  • asthma
  • pulmonary haemorrhage (Wegener’s, Goodpasture’s)
  • left-to-right cardiac shunts
  • polycythaemia
  • hyperkinetic states
  • male gender, exercise
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194
Q

Causes of decreased TLCO?

A
  • pulmonary fibrosis
  • pneumonia
  • pulmonary emboli
  • pulmonary oedema
  • emphysema
  • anaemia
  • low cardiac output
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195
Q

KCO also tends to increase with age. Some conditions may cause an increased KCO with a normal or reduced TLCO

corrected for lung volume (transfer coefficient, KCO)

A
  • pneumonectomy/lobectomy
  • scoliosis/kyphosis
  • neuromuscular weakness
  • ankylosis of costovertebral joints e.g. ankylosing spondylitis
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196
Q

Antibodies in Graves and Hashimotos?

A

Graves = TSH receptor stimulating antibodies and anti thyroid peroxidase antibodies

Hashimotos = Anti-thyroid peroxidase and anti thyroglobulin antibodies

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197
Q

What are the features of De Quervains thyroiditis?

A

There are typically 4 phases;

phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR

phase 2 (1-3 weeks): euthyroid

phase 3 (weeks - months): hypothyroidism

phase 4: thyroid structure and function goes back to normal

Investigations

thyroid scintigraphy: globally reduced uptake of iodine-131

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198
Q

What are causes of adrenal failure?

A
  • Autoimmune
  • tuberculosis
  • metastases (e.g. bronchial carcinoma)
  • meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
  • HIV
  • antiphospholipid syndrome
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199
Q

Causes of gynaecomastia?

A
  • physiological: normal in puberty
  • syndromes with androgen deficiency: Kallman’s, Klinefelter’s
  • testicular failure: e.g. mumps
  • liver disease
  • testicular cancer e.g. seminoma secreting hCG
  • ectopic tumour secretion
  • hyperthyroidism
  • haemodialysis
  • drugs: see below
  • spironolactone (most common drug cause)
  • cimetidine
  • digoxin
  • cannabis
  • finasteride
  • GnRH agonists e.g. goserelin, buserelin
  • oestrogens, anabolic steroids
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200
Q

What type of metabolic disturbance does cushings cause?

A

Hypokalaemic metabolic alkalosis

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201
Q

What is a neuroblastoma?

A

Neuroblastoma is one of the top five causes of cancer in children, accounting for around 7-8% of childhood malignancies. The tumour arises from neural crest tissue of the adrenal medulla (the most common site) and sympathetic nervous system.

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202
Q

What are the features of a neuroblastoma?

A
  • abdominal mass
  • pallor, weight loss
  • bone pain, limp
  • hepatomegaly
  • paraplegia
  • proptosis
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203
Q

What are the investigations for a neuroblastoma?

A
  • raised urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels
  • calcification may be seen on abdominal x-ray
  • biopsy
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204
Q

What does nuclear scintigraphy show for a toxic multinodular goitre

A

Patchy uptake

Treatment is radioiodine therapy

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205
Q

What is the AKI criteria?

A

increase in serum creatinine by 26.5 mol/l within 48 hours, increase in serum creatinine to 1.5 times baseline, or urine volume < 0.5 ml/kg/h for 6 hours.

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206
Q

What is protocol for DC cardioversion in a patient with AF lasting longer than 48 hours?

A
  • anticoagulation should be given for at least 3 weeks prior to cardioversion.
  • An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and cardioverted immediately
  • If there is a high risk of cardioversion failure (e.g. Previous failure or AF recurrence) then it is recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion
  • Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence
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207
Q

What is the nephrotic syndrome triad?

A

Triad of:

  1. Proteinuria (> 3g/24hr) causing
  2. Hypoalbuminaemia (< 30g/L) and
  3. Oedema
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208
Q

Why does nephrotic syndrome lead to predisposition to thrombosis?

A

Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis. Loss of thyroxine-binding globulin lowers the total, but not free, thyroxine levels.

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209
Q

Exampleas of nephritic vs Nephrotic syndromes

A
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210
Q

What are causes of rapidly progressive glomerulonephritis?

A

Goodpasture’s syndrome

Wegener’s granulomatosis

others: SLE, microscopic polyarteritis

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211
Q

What structure is formed in the majority of glomeruli in RPGN?

A

Crescents

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212
Q

What are features of RPGN?

A
  • nephritic syndrome: haematuria with red cell casts, proteinuria, hypertension, oliguria
  • features specific to underlying cause (e.g. haemoptysis with Goodpasture’s, vasculitic rash or sinusitis with Wegener’s)
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213
Q

What is the classic presentation of IgA nephropathy?

A

macroscopic haematuria in young people following an upper respiratory tract infection.

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214
Q

How you differentiate between IgA nephropathy and Post-strep glomerulonephritis?

A

Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis

  • 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
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215
Q

Histology findings for IgA nephropathy?

A

histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3

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216
Q

What are causes of type 1 membranoproliferative glomerulonephritis?

A

Type 1

accounts for 90% of cases

cause: cryoglobulinaemia, hepatitis C

renal biopsy

electron microscopy: subendothelial and mesangium immune deposits of electron-dense material resulting in a ‘tram-track’ appearance

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217
Q

Type 2 membranoproliferative glomerulonephritis on histology

A

electron microscopy: intramembranous immune complex deposits with ‘dense deposits’

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218
Q

What causes post-strep glomerulonephritis?

A

Post-streptococcal glomerulonephritis typically occurs 7-14 days following a group A beta-haemolytic Streptococcus infection (usually Streptococcus pyogenes). It is caused by immune complex (IgG, IgM and C3) deposition in the glomeruli. Young children are most commonly affected.

C3 deposited hence low C3

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219
Q

What are renal biopsy features of post-strep glomerulonephritis?

A
  • post-streptococcal glomerulonephritis causes acute, diffuse proliferative glomerulonephritis
  • endothelial proliferation with neutrophils
  • electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
  • immunofluorescence: granular or ‘starry sky’ appearance
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220
Q

What are the common causes of minimal change disease?

A

The majority of cases are idiopathic, but in around 10-20% a cause is found:

drugs: NSAIDs, rifampicin

Hodgkin’s lymphoma, thymoma

infectious mononucleosis

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221
Q

What does renal biopsy show for minimal change disease?

A

normal glomeruli on light microscopy

electron microscopy shows fusion of podocytes and effacement of foot processes

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222
Q

What is blood pressure in minimal change

A

normotension - hypertension is rare

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223
Q

What is the commonest cause of glomerulonephritis in adults?

A

Membranous glomerulonephritis

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224
Q

What does renal biopsy show for membranous glomerulonephritis?

A

electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance

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225
Q

What are causes of membranous glomerulonephritis?

A
  • idiopathic: due to anti-phospholipase A2 antibodies
  • infections: hepatitis B, malaria, syphilis
  • malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
  • drugs: gold, penicillamine, NSAIDs
  • autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
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226
Q

What is the management of membranous glomerulonephritis?

A

Management

  • all patients should receive an ACE inhibitor or an angiotensin II receptor blocker (ARB):
  • these have been shown to reduce proteinuria and improve prognosis
  • immunosuppression
  • as many patients spontaneously improve only patient with severe or progressive disease require immunosuppression
  • corticosteroids alone have not been shown to be effective. A combination of corticosteroid + another agent such as cyclophosphamide is often used
  • consider anticoagulation for high-risk patients
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227
Q

What are the features of FSGS on renal biopsy?

A
  • focal and segmental sclerosis and hyalinosis on light microscopy
  • effacement of foot processes on electron microscopy
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228
Q

What are indications for dialysis in AKI?

A

Indications for dialysis in acute kidney injury:

Acute renal dialysis indications- HAVEPEE

  • H- hyperkalaemia (refractory)
  • A-acidosis (refractory)
  • V- volume overload
  • E- elevated urea
  • P- pericarditis
  • E- encephalopathy
  • E- (o)Edema (pulmonary)
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229
Q

What type of reaction occurs after erythromycin and simvastatin?

A

Rhabdomyolysis

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230
Q

What drug can cause acute interstitial nephritis?

A

Penicillin

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231
Q

If kidneys can no longer concentrate urine, what is the urine osmolality and urine sodium?

A

Urine osmolality is low, urine sodium is high (because kidneys try to retain sodium)

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232
Q

Core features of churg strauss

A

Features

asthma

blood eosinophilia (e.g. > 10%)

paranasal sinusitis

mononeuritis multiplex

pANCA positive in 60%

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233
Q

What are the core features of granulomatosis with polyangitis?

A

Features

  • upper respiratory tract: epistaxis, sinusitis, nasal crusting
  • lower respiratory tract: dyspnoea, haemoptysis
  • rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)
  • saddle-shape nose deformity
  • also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions
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234
Q

What are the variables for eGFR?

A

eGFR variables - CAGE - Creatinine, Age, Gender, Ethnicity

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235
Q

Causes of cranial DI?

A
  • idiopathic
  • post head injury
  • pituitary surgery
  • craniopharyngiomas
  • histiocytosis X
  • DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
  • haemochromatosis
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236
Q

What are causes of nephrogenic DI?

A
  • genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
  • electrolytes: hypercalcaemia, hypokalaemia
  • lithium
  • lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
  • demeclocycline
  • tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
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237
Q

What are the rules for drivin gafter an MI?

A

Driving Post-MI

  • For a car/motorcycle licence, you do not need to tell the DVLA
  • Can recommence driving after 1 week if successfully treated with coronary angioplasty
  • If not successfully treated with coronary angioplasty, can commence driving after 4 weeks
  • For a bus, coach or lorry licence - must tell DVLA and stop driving for 6 weeks. Assessment with doctor after 6 weeks to see if meet medical standard to start driving again.
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238
Q

What are the rules for driving with an arrhythmia?

A
  • Must not drive if arrythmia has caused or is likely to cause incapacity
  • Drive 4 weeks after underlying cause of arrythmia has been found and the arrythmia has been controlled
  • If they drive a bus, coach or lorry, licence will be revoked and only be reinstated after an underlying cause has been identified, the arrythmia has been controlled for 3 months, and they have an LV ejection fraction of >40%.

So cars = drive after 1 month of control

Buses = drive after 3 months of control

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239
Q

What are the neurological symptoms that can present via Wilsons disease?

A

Neurological problems may manifest as dementia, tremor or dyskinesias. - Wilson’s disease

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240
Q

Features of wilsons disease?

A

Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea:

liver: hepatitis, cirrhosis

neurological:

basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus

speech, behavioural and psychiatric problems are often the first manifestations

also: asterixis, chorea, dementia, parkinsonism

Kayser-Fleischer rings

green-brown rings in the periphery of the iris

due to copper accumulation in Descemet membrane

present in around 50% of patients with isolated hepatic Wilson’s disease and 90% who have neurological involvement

renal tubular acidosis (esp. Fanconi syndrome)

haemolysis

blue nails

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241
Q

What are the levels of serum caeruloplasmin, total serum copperin and free serum copper in Wilson’s disease?

A
  • reduced serum caeruloplasmin
  • reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
  • free (non-ceruloplasmin-bound) serum copper is increased
  • increased 24hr urinary copper excretion
242
Q

What electron changes are typical of refeeding syndrome?

A

low potassium, low magnesium and low phosphate and fluid shifts

243
Q

What is the management of H.Pylori?

A

a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)

244
Q

RUQ pain- colic
RUQ pain plus fever- cholecystitis
RUQ pain plus fever plus jaundice (charcot triad)- cholangitis
epigastric pain- more likely pancreatitis
RUQ pain plus jaundice (no fever) - choledocholithiasis

A
245
Q

How do you interpret ABPI?

A
246
Q

What does a raised SAAG of over 11 g/L indicate?

A

portal hypertension that has caused the ascites

247
Q

What are causes of ascites with SAAG over 11?

A

Liver disorders are the most common cause

  • cirrhosis/alcoholic liver disease
  • acute liver failure
  • liver metastases

Cardiac

  • right heart failure
  • constrictive pericarditis

Other causes

  • Budd-Chiari syndrome
  • portal vein thrombosis
  • veno-occlusive disease
  • myxoedema
248
Q

Causes of SAAG less than 11

A

Hypoalbuminaemia

  • nephrotic syndrome
  • severe malnutrition (e.g. Kwashiorkor)

Malignancy

  • peritoneal carcinomatosis

Infections

  • tuberculous peritonitis

Other causes

  • pancreatitisis
  • bowel obstruction
  • biliary ascites
  • postoperative lymphatic leak
  • serositis in connective tissue diseases
249
Q

TACS

A

involves middle and anterior cerebral arteries

all 3 of the criteria are present

  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia
250
Q

PACs

A

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

2 of the criteria are present

  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia
251
Q

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 hemiparesis
252
Q

Posterior circulation infarct

A

involves vertebrobasilar arteries

presents with 1 of the following:

  1. cerebellar or brainstem syndromes
  2. loss of consciousness
  3. isolated homonymous hemianopia
253
Q

Stroke affecting anterior cerebral artery?

A

Contralateral hemiparesis and sensory loss, lower extremity > upper

254
Q

Middle cerebral artery

A

Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia

255
Q

Posterior cerebral artery

A

Contralateral homonymous hemianopia with macular sparing
Visual agnosia

(Notice pure visual)

256
Q

Weber’s Syndrome (branches of the posterior cerebral artery that supply the midbrain)

A

Ipsilateral CN III palsy

Contralateral weakness of upper and lower extremity

257
Q

Wallenberg syndrome?

(posterior inferior cerebellar artery)

A

Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus

258
Q

Anterior inferior cerebellar artery

A

Symptoms are similar to Wallenberg’s (see above), but:
Ipsilateral: facial paralysis and deafness

259
Q

Stroke in retinal / ophthalmic artery?

A

Amaurosis fugax

260
Q

Stroke in what location causes locked in syndrome?

A

Basilar artery

261
Q

What is another term used to describe

  1. Wallenberg syndrome (posterior inferior cerebellar artery)
  2. Anterior inferior cerebellar artery stroke?
A
  1. Lateral medullary syndrome
    1. Lateral pontine syndrome
262
Q

Surgical management of achalasia

A

Heller cardiomyotomty

263
Q

a surgical procedure used to strengthen and tighten the lower oesophageal sphincter in patients suffering from severe gastro-oesophageal reflux disease (GORD).

A

Nissen fundoplication

264
Q

What is involved in whipple procedure?

A

A Whipple procedure is a surgical procedure used for the treatment of pancreatic cancers. It removes the head of the pancreas, the duodenum, the gallbladder and the bile duct.

265
Q

What is the Sister Mary Joseph node

A

Sister Mary Joseph node is a palpable nodule in the umbilicus due to metastasis of malignant cancer within the pelvis or abdomen

266
Q

Why does thrombocytopenia occur in liver cirrhosis?

A

‘Multiple factors, including splenic sequestration, reduced activity of the hematopoietic growth factor thrombopoietin, bone marrow suppression by chronic hepatitis C virus infection and anti-cancer agents, and antiviral treatment with interferon-based therapy, can contribute to the development of thrombocytopenia in cirrhotic patients’.

267
Q

What is the investigation for pancreatic cancer?

A

High Res CT

268
Q

What is first line management for constipation in patients with IBS?

A

Isphagula husk

269
Q

Where would you find signet ring cells?

A

Gastric adenocarcinoma - signet ring cells

270
Q

What causes carcinoid syndrome?

A

usually occurs when metastases are present in the liver and release serotonin into the systemic circulation

may also occur with lung carcinoid as mediators are not ‘cleared’ by the liver

271
Q

What are the features of carcinoid syndrome?

A
  • flushing (often earliest symptom)
  • diarrhoea
  • bronchospasm
  • hypotension
  • right heart valvular stenosis (left heart can be affected in bronchial carcinoid)
  • other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome
  • pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour

Carcinoid syndrome can affect the right side of the heart. The valvular effects are tricuspid insufficiency and pulmonary stenosis

272
Q

What are the grades of hepatic encephalopathy?

A

Grade I: Irritability

Grade II: Confusion, inappropriate behaviour

Grade III: Incoherent, restless

Grade IV: Coma

273
Q

What are the electrolyte abnormalities seen in tumour lysis syndrome?

A

It leads to a high potassium and high phosphate level in the presence of a low calcium

274
Q

What are complications of tumour lysis syndrome?

A

Complications of tumour lysis syndrome:

  • hyperkalaemia
  • hyperphosphataemia
  • hypocalcaemia
  • hyperuricaemia
  • acute renal failure
275
Q

General rules for DVT management

A

Wells of 2 or more

  • Skip D-Dimer
  • Do doppler - if positive then start DOAC, if negative do D-dimer
  • If D-dimer comes back positive (scan negative) stop any DOACs, repeat doppler 6-8 days later
  • If doppler is going to take a 4 hours or more - do D-dimer and start DOAC

Wells of 1 or less

  • Do D-dimer
  • DOAC if D-dimer is going to take more than 4 hours
  • if D-dimer is positive then do doppler
  • If doppler is going to take more than 4 hours then DOAC should be started
276
Q

General rules for PE management

A

DOAC

LMWH followed by VKA (warfarin) for Severe renal impairment and antiphospholipid syndrome.

3 months of anticoagulation for provoked

6 months of anticoagulation for unprovoked

277
Q

What disease is this?

  • monoclonal IgM paraproteinaemia
  • systemic upset: weight loss, lethargy
  • hyperviscosity syndrome e.g. visual disturbance
  • the pentameric configuration of IgM increases serum viscosity
  • hepatosplenomegaly
  • lymphadenopathy
  • cryoglobulinaemia e.g. Raynaud’s
A

Waldenstorm’s macroglubulinaemia

278
Q

In sickle cell, what causes;

  1. Low reticulocyte count
  2. High reticulocyte count
A
  1. Parvovirus
  2. Acute sequestration and haemolysis
279
Q

What is the diagnostic criteria for myeloma?

A

one major and one minor criteria or three minor criteria in an individual who has signs or symptoms of multiple myeloma.

Major criteria

Plasmacytoma (as demonstrated on evaluation of biopsy specimen)

30% plasma cells in a bone marrow sample

Elevated levels of M protein in the blood or urine

Minor criteria

10% to 30% plasma cells in a bone marrow sample.

Minor elevations in the level of M protein in the blood or urine.

Osteolytic lesions (as demonstrated on imaging studies).

Low levels of antibodies (not produced by the cancer cells) in the blood.

280
Q

What is the definition of normocytic anaemia?

A

normocytic anaemia, leukopenia and thrombocytopenia is the definition of aplastic anaemia

281
Q

How does Rivaroxaban, Apixaban, Dabigatran and Heparin work?

A

Rivaroxaban is a direct factor Xa inhibitor. Apixaban is also a direct factor Xa inhibitor.

Dabigatran is a direct thrombin inhibitor.

Heparin activates antithrombin III.

282
Q

How does beta thalassaemia show up on lab results?

A

Mild anaemia with big reduction in MCV = beta thalassaemia

283
Q

Intravascular hemolysis occurs when erythrocytes are destroyed in the blood vessel itself, whereas extravascular hemolysis occurs in the hepatic and splenic macrophages within the reticuloendothelial system. Intravascular hemolysis is often dramatic, with free hemoglobin released into the plasma leading to hemoglobinuria (positive blood on urine dipstick but few erythrocytes on microscopic examination). Examples of intravascular hemolysis include enzyme defects such as glucose-6-phosphate dehydrogenase (G6PD) deficiency or certain immune-mediated processes. Extravascular hemolysis usually results from more subtle RBC destruction, typically with chronic splenic enlargement and jaundice. Extravascular hemolysis is more common with RBC membrane disorders such as hereditary spherocytosis.

A
284
Q

What are the features of hodgkin lymphoma?

A

Reed-sternberg cell

Bimodal age distribution (3rd and 7th decades)

  • lymphadenopathy (75%) - painless, non-tender, asymmetrical
  • systemic (25%): weight loss, pruritus, night sweats, fever (Pel-Ebstein)
  • alcohol pain in HL
  • normocytic anaemia, eosinophilia
  • LDH raised

B-symptoms with blood findings and alcohol pain

285
Q

What are the histological classifications of Hodgkin’s lymphoma?

A
286
Q

Describe a reed-sternberg cell

A

Reed-sterberg cell: either multinucleated or have a bilobed nucleus with prominent eosinophilic inclusion-like nucleoli (thus resembling an “owl’s eye” appearance).

287
Q

What are thresholds for platelet transfusion?

A

30 with clinically significant bleeding

100 for severe bleeding or bleeding at critical sites such as the CNS

Platelet transfusion for thrombocytopenia before surgery/ an invasive procedure. Aim for plt levels of:

  • > 50×109/L for most patients
  • 50-75×109/L if high risk of bleeding
  • >100×109/L if surgery at critical site

A threshold of 10 x 109 except where platelet transfusion is contradindicated or there are alternative treatments for their condition

For example, do not perform platelet transfusion for any of the following conditions:

  • Chronic bone marrow failure
  • Autoimmune thrombocytopenia
  • Heparin-induced thrombocytopenia, or
  • Thrombotic thrombocytopenic purpura.
288
Q

What are the live attenuated vaccines?

A

BCG

MMR

Influenza (intranasal)

Oral rotavirus

Oral Polio

Yellow Fever

Oral typhoid

289
Q

what are inactivated preparations of vaiccine

A

Rabies

Hepatitis A

Influenza (IM)

290
Q

Which vaccinations are toxoid?

A

Tetanus

Diptheria

Pertussis

291
Q

Which bacteria have the following incubation periods?

  1. 1-6 hours
  2. 12-48 hours
  3. 48-72 hours
  4. > 7 days
A

1-6 hrs: Staphylococcus aureus, Bacillus cereus*

12-48 hrs: Salmonella, Escherichia coli

48-72 hrs: Shigella, Campylobacter

> 7 days: Giardiasis, Amoebiasis

292
Q

What type of HPV causes genital warts?

A

Genital warts, They are caused by the many varieties of the human papillomavirus HPV, especially types 6 & 11. It is now well established that HPV (primarily types 16,18 & 33) predisposes to cervical cancer.

293
Q

Descriptions of genital ulcers

  1. Herpes
  2. Syphillis
  3. Chancroid (haemophylus ducreyi)
  4. LGV
A
  1. Herpes = painful ulcers
  2. Syphillis = Painless ulcer (chancre). Local non-tender lymphadenopathy.
  3. Chancroid = Painful ulcer, unilateral painful inguinal lymphadenopathy
  4. LGV = Painless ulcer, painful inguinal lymphadenopathy
294
Q

What are primary, secondary and tertiary features of syphillis?

A

Primary = chancre, non-tender lymphadenopathy

Secondary = Fever, rash, buccal snail track ulcers, condylomata lata (painless warty lesions on the genitalia)

Tertiary = Gummas, ascending aortic aneurysms, generaly paralysis of the insane, tabes dorsales, Argyll - Robertson Pupil

295
Q

Features of Congenital Syphilis?

A
  • blunted upper incisor teeth (Hutchinson’s teeth), ‘mulberry’ molars
  • rhagades (linear scars at the angle of the mouth)
  • keratitis
  • saber shins
  • saddle nose
  • deafness
296
Q

How does pneumocystis jiroveci present?

A

This is a fungal infection which classically affects patients with HIV. It classically presents with a dry cough, exercise-induced desaturations and the absence of chest signs.

297
Q

What are high-risk tetanus prone wounds?

A
  • heavy contamination with material likely to contain tetanus spores e.g. soil, manure
  • wounds or burns that show extensive devitalised tissue
  • wounds or burns that require surgical intervention
298
Q

What are the tetanus rules?

A

Patient has had a full course of tetanus vaccines, with the last dose < 10 years ago

  • no vaccine nor tetanus immunoglobulin is required, regardless of the wound severity

Patient has had a full course of tetanus vaccines, with the last dose > 10 years ago

  • if tetanus prone wound: reinforcing dose of vaccine
  • high-risk wounds (e.g. compound fractures, delayed surgical intervention, significant degree of devitalised tissue): reinforcing dose of vaccine + tetanus immunoglobulin

If vaccination history is incomplete or unknown

  • reinforcing dose of vaccine, regardless of the wound severity
  • for tetanus prone and high-risk wounds: reinforcing dose of vaccine + tetanus immunoglobulin

In short.

Grade 2 wound = tetanus booster.

Grade 3 wound = Add Immunoglobulin

If vaccination history is unknown then your threshold is lowered by 1.

Grade 1 wound = tetanus booster

Grade 2 wound = add Immunogloblin

I you have had vaccine in the last 10 years then you need no extra intervention.

299
Q

What causes kaposi’s sarcoma?

A

caused by HHV-8 (human herpes virus 8)

300
Q

What are the features of leptospirosis?

A

Leptospirosis - conjunctival suffusion plus muscle tenderness (localised in the calves and possibly the paraspinal muscles)

301
Q

What are the features of typhoid/paratyphoid?

A
  • initially systemic upset as above (fever, headache, arthralgia)
  • relative bradycardia
  • abdominal pain, distension
  • constipation: although Salmonella is a recognised cause of diarrhoea, constipation is more common in typhoid
  • rose spots: present on the trunk in 40% of patients, and are more common in paratyphoid
302
Q

Features of legionella

A

Features

  • flu-like symptoms including fever (present in > 95% of patients)
  • dry cough
  • relative bradycardia
  • confusion
  • lymphopaenia
  • hyponatraemia
  • deranged liver function tests
  • pleural effusion: seen in around 30% of patients
303
Q

Features of mycoplasma pneumonaie

A

Haemolytic anaemia and thrombocytopenia

Erythema multiforme

Ecephalitis / GBS

Peri/myocarditis

Bullous myringitis

304
Q

What is treatment for diarrhoea?

A

Invasive diarrhoea (bloody diarrhoea + fever) then give ciprofloxacin, otherwise give clairithromycin

305
Q

What is the most common cause of viral meningitis?

A

Coxsackie

306
Q

Cellulitis treatment if allergic to penicillin

A

clarithromycin, erythromycin (in pregnancy) or doxycyline

307
Q

What are the complications of mycoplasma pneumoniae

A
  • cold agglutins (IgM): may cause an haemolytic anaemia, thrombocytopenia
  • erythema multiforme, erythema nodosum
  • meningoencephalitis, Guillain-Barre syndrome and other immune-mediated neurological diseases
  • bullous myringitis: painful vesicles on the tympanic membrane
  • pericarditis/myocarditis
  • gastrointestinal: hepatitis, pancreatitis
  • renal: acute glomerulonephritis
308
Q

What is the most common cause of viral meningitis?

A

Herpes simplex virus

309
Q

What does hookworm show on blood tests?

A

Iron deficiency anaemia

Eosinophilia

310
Q

How do you treat legionella and mycoplasma pneumoniae

A

Macrolides (clari)

311
Q

How can trimethoprim affect the kidneys?

A

Trimethoprim can cause tubular dysfunction, leading to hyperkalaemia and increased serum creatinine

312
Q

The antibiotic always used in pregnancy

A

Erythromycin

313
Q

Incubation period of salmonella typhi

A

10-20 days

314
Q

What is UTI management in pregnant women?

A

Nitro

Amoxicillin or cefalexin if near term

315
Q

What is Mrizzi syndrome?

A

Mirizzi syndrome described common hepatic duct obstruction by an impacted gallstone.

316
Q

What are the types of renal stones?

A

Calcium oxalate

Cystine

Uric acid

Calcium phosphate

Struvite (staghorn calculi)

Xanthine

317
Q

What are risk factors for calcium oxalate stones?

A

Hypercalciuria

Hyperoxaluria

Hypocitraturia

318
Q

What are risk factors for uric acid stones?

A

urinary pH low

Extensive tissue breakdown

319
Q

What are risk factors for calcium phosphate stones?

A

Renal tubular acidosis (1 and 3)

High pH

320
Q

What is a risk factor for struvite stones?

A

Urease producing bacteria

321
Q

Which stones are opaque/semi-opaque/lucent?

A

Opague:

  • Calcium oxalate
  • Calcium phosphate

Lucent:

  • Uric Acid

Others:

Struvite = slightly radiolucent

Cystine = radiodense

322
Q

Symptomatic AAA have high rupture risk and should undergo endovascular repair (EVAR)

A
323
Q

What is the triad of turp syndrome?

A

Hyponatraemia

Fluid overload

GLycine toxicity

324
Q

Ultrasound findings for liver cysts

A

Haemangioma = hyperechoic

Liver abscess = hyperechoic

Liver cell adnoma = mixed echoity and heterogeneous texture

Cystadenoma = anechoic

Amoebic abscess = fluid filled structure with poorly defined boundaries

Hyatid cysts = septa, hyatid sand or daughter cysts

325
Q

Features of haemangioma

A

Incidental finding

Hyperechoic

326
Q

What are the features of liver cell adenoma?

A

3-5th decade

Women

Link with OCP

327
Q

What are the features of liver abscess?

A

fever, right upper quadrant pain. Jaundice may be seen in 50%

Ultrasound will usually show a fluid filled cavity, hyperechoic walls may be seen in chronic abscesses

328
Q

Features of ameobic abscess in liver?

A

Fever

RUQ

(this is a mimic of cholecystitis)

FLuid filled structure with poorly defined borders

Anchovy paste consistency

Metronidazole

329
Q

Features of hyatid cysts?

A

Echinococcus infection

Malaise and RUQ

Eosinophilia

Do not aspirate

Mebendazole followed by surgical resection

330
Q

Pain after eating with increased lactate

A

Mesenteric ischaemia

331
Q

How long is PSA elevated for

  1. prostate biopsy
  2. proven UTI
  3. DRE
  4. vigorous exercise
  5. ejaculation
A
  1. 6 weeks of a prostate biopsy
  2. 4 weeks following a proven UTI
  3. 1 week after DRE
  4. 48 hours after vigorous exercise
  5. 48 hours after ejaculation
332
Q

What causes acute epididymo orchitis

A

Acute epididymo-orchitis is most commonly caused by Chlamydia

E. coli is the most common cause of epididymo-orchitis in men over 35 years of age.

333
Q

What type of chemotherapy is used in patients with breast cancer node+

A

FEC-D

334
Q

What is Stauffer syndrome / paraneoplastic hepatic dysfunction syndrome?

A

Cholestasis

Hepatosplenomegaly in response to increased levels of IL-6

335
Q

What is the treatment for renal cell carcinoma?

A

alpha-interferon and interleukin-2 have been used to reduce tumour size and also treat patients with metatases

receptor tyrosine kinase inhibitors (e.g. sorafenib, sunitinib) have been shown to have superior efficacy compared to interferon-alpha

336
Q

What is the parkland fluid formula?

A

The Parkland formula for fluid resuscitation in burns is:

  • Volume of fluid = total body surface area of the burn % x weight (Kg) x 4ml
  • 50% given in first 8 hours
  • 50% given in next 16 hours
337
Q

Abdominal signs of pancreatitis

A

periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare - acute pancreatitis.

338
Q

What is the retinopathy assocaited with pancreatitis?

A

ischaemic (Purtscher) retinopathy - may cause temporary or permanent blindness

339
Q

Investigations for acute pancreatitis vs chronic pancreatitis

A

Acute = can usually be made clinically (raised amylase, lipase)

Ultrasound may be used to determeine cause

Contrast enhanced CT is another option

Chronic = Abdo CT showing pancreatic calcification

Faecal elastase may be used to determine exocrine function

340
Q

Systemic complication of pancreatitis?

A

ARDS

341
Q

What is the glasgow score for pancreatitis?

A
342
Q

What type of drugs are etomidate and propofol?

A

Sedation agents

343
Q

What type of drug is suxamethonium

A

Depolarising muscle relaxant.

Short lasting

Rapid action

344
Q

What type of drug are vecuronium and atracurium

A

Non-depolarizing muscle relaxant

345
Q

What are the side effects of suxamethonium

A

Side effects. Side effects include malignant hyperthermia, muscle pains, acute rhabdomyolysis with high blood levels of potassium, transient ocular hypertension, constipation and changes in cardiac rhythm, including slow heart rate, and cardiac arrest.

346
Q

What is the reversal agent for non-depolarising muscle relaxants?

A

Neostigmine

347
Q

How is local anaesthetic toxicity treated?

A

20% lipid emulsion

348
Q

If a UC patient needs a panproctocolectomy, but is systemically unwell, what is the surgical alternative?

A

Ileoanal pouch with defunctioning ileostomy

Subtotal colectomy

349
Q

What are complications of SAH?

A

Complications of SAH:

  • Re-bleeding
  • happens in around 10% of cases and most common in the first 12 hours
  • if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged
  • associated with a high mortality (up to 70%)
  • Vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
  • Hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
  • Seizures
  • Hydrocephalus
  • Death
350
Q

How do we prevent vasospasm in SAH?

A

Nimodipine

351
Q

What type of breast lump mimics cancer and can have teathering

A

Fat necrosis

352
Q

When would you perform:

  1. Anterior resection
  2. Hartmann’s
  3. Abdominoperineal excision of the rectum?
A

Mid/high rectal tumours can be managed with anterior resection. Hartmann’s procedure is generally for sigmoid tumours, and abdominoperineal excision of rectum is for low rectal or anal tumours.

353
Q

Boas sign

A

Cholecystitis

Hyperaesthesia between 9th and 11th ribs on posterior right side

354
Q

What diabetic medications require changing in preparation for surgery (not insulin for this question)

A

Metformin

Sulfonylureas

SGLT-2 inhibitors

355
Q

What change is required to insulin in preparation of surgery?

A

Lantus/levemir = 20/20/20

Novomix / Humilin M3 = 0/halve/halve

356
Q

Strongest risk factor for anal cancer

A

HPV infection

357
Q

What are the features of renal adenocarcinoma?

A

Hypertension, haematuria, polycythaemia and renal mass = renal adenocarcinoma

358
Q

Renal pelvis = transitional cell carcinoma

A
359
Q

What is subfalcine herniation?

A

Displacement of the cingulate gyrus under the falx ceribri

360
Q

Describe central herniation

A

Downwards displacement of the brain

361
Q

Describe transtentorial/uncal herniation

A

Displacement of the uncus of the temporal lobe under the tentorium cerebelli. Clinical consequences include an ipsilateral fixed, dilated pupil (due to parasympathetic compression of the third cranial nerve) and contralateral paralysis (due to compression of the cerebral peduncle)

362
Q

Describe tonsillar herniation

A

Displacement of the cerebellar tonsils through the foramen magnum. This is called ‘coning’. In raised ICP this causes compression of the cardiorespiratory centre. In Chiari 1 malformation, tonsillar herniation is seen without raised ICP

363
Q

Describe transcalvarial

A

Occurs when brain is displaced through a defect in the skull (e.g. a fracture or craniotomy site)

364
Q

What are the signs of lateral cutaneous nerve lesion

A

Burning over anterior thigh which worsens on walking, positive tinel sign over inguinal ligament

365
Q

Inability to dorsiflex foot after total hip replacement?

A

Sciatic nerve injury

366
Q

Signs of ilioinguinal nerve injury?

A

Pfannelstein incision + pain over inguinal ligament, and tenderness when inguinal nerve is compressed

367
Q

Femoral nerve lesion

A

Weak hip flexion, weak knee extension, impaired quadriceps reflex, sensory deficit over anterior-medial aspect of thigh.

368
Q

What are the 6 tests for brain death?

A
  • Fixed pupils which do not respond to sharp changes in the intensity of incident light
  • No corneal reflex
  • Absent oculo-vestibular reflexes - no eye movements following the slow injection of at least 50ml of ice-cold water into each ear in turn (the caloric test)
  • No response to supraorbital pressure
  • No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation
  • No observed respiratory effort in response to disconnection of the ventilator for long enough (typically 5 minutes) to ensure elevation of the arterial partial pressure of carbon dioxide to at least 6.0 kPa (6.5 kPa in patients with chronic carbon dioxide retention). Adequate oxygenation is ensured by pre-oxygenation and diffusion oxygenation during the disconnection (so the brain stem respiratory centre is not challenged by the ultimate, anoxic, drive stimulus)
369
Q

When should women be prescribed cyclical combined HRT?

A

If their last menstrual period was less than 1 year ago

370
Q

When should continuous combined HRT begin?

A

if they have:

  • taken cyclical combined for at least 1 year or
  • it has been at least 1 year since their LMP or
  • it has been at least 2 years since their LMP, if they had premature menopause (menopause below the age of 40)
371
Q

effect of antiphospholipid syndrome on APTT?

A

Paradoxical rise

372
Q

Triad of disseminated gonococcal disease

How does this compare to reactive arthritis

A

Triad of tenosynovitis, migratory polyarthritis and dermatitis

Whereas reactive arthritis is urethritis, arthritis and conjunctivitis. Can’t see, pee or climb a tree

373
Q

Bone disease with isolated ALP?

A

Pagets disease

374
Q

Gout vs pseudogout crystals

A

Gout- monosodium urate crystals that are needle-shaped that are negatively birefringent under polarised light

Pseudogout- calcium pyrophosphate crystals are rhombic/brick shaped that are positively birefringent under polarised light

375
Q

Buttock claudication and impotence (not cauda equina!)

A

Leriche syndrome

Also has atrophy of the legs

376
Q

Behcets disease features?

A

Behcet’s disease is an autoimmune small vessel vasculitis that targets venules. It is a type 3 hypersensitivity reaction induced by immune complex deposition in small vessels. Its main clinical presentation is with recurrent oral and genital ulcers, anterior uveitis, and skin lesions (such as erythema nodosum). It is most commonly seen in people of East Mediterranean descent. Flares may be precipitated by parvovirus or herpes simplex virus.

377
Q

What is the Garden system?

A

Grades hip facture severity

Type I: Stable fracture with impaction in valgus

Type II: Complete fracture but undisplaced

Type III: Displaced fracture, usually rotated and angulated, but still has boney contact

Type IV: Complete boney disruption

Just remember that 3 is displaced but with bony contact

378
Q

What is management for intracapsular fracture - undisplaced?

A

Internal fixation

Hemiarthroplasty if unfit

379
Q

What is management of intracapsular hip fracture displaced?

A

Total hip replacement

Hemiarthroplasty if unfit

380
Q

Management of extracapsular fracture intertrochanteric?

A

Dynamic hip screw

381
Q

Management of extracapsular subtrochanteric fracture?

A

Intramedullary device

382
Q

Osteomalacia findings

  1. Calcium
  2. Phosphate
  3. ALP
  4. PTH
A
  1. Calcium - decreased
  2. Phosphate - decreased
  3. ALP - increased
  4. PTH - increased
383
Q

Osteoporosis findings

  1. Calcium
  2. Phosphate
  3. ALP
  4. PTH
A

All normal

384
Q

Primary Hyperparathyroidism findings

  1. Calcium
  2. Phosphate
  3. ALP
  4. PTH
A
  1. Calcium = High
  2. Phosphate = Low
  3. ALP = High
  4. PTH = High
385
Q

Secondary Hyperparathyroidism findings

  1. Calcium
  2. Phosphate
  3. ALP
  4. PTH
A
  1. Calcium = Low
  2. Phosphate = High
  3. ALP = High
  4. PTH = High
386
Q

What test should be done prior to starting hydroxychloroquine?

A

Ophthalmic examination

387
Q

What does hyperparathyoidism predispose you to?

A

Pseudogout

Chondrocalcinosis

388
Q

Inflammatory arthritis involving DIP swelling and dactylitis points to a diagnosis of psoriatic arthritis

A
389
Q

Which two tendons are affected by de-quervains tenosynovitis?

A

De Quervain’s tenosynovitis is a common condition in which the sheath containing the extensor pollicis brevis and abductor pollicis longus tendons is inflamed

390
Q

When does scaphoid fractures become more susceptible to AVN?

A

More proximal

391
Q

How to tell the difference between meralgia paraesthetica and trochanteric bursitis?

A

present very similarly with pain over the anterior aspect of the thigh. However, with meralgia paraesthetica you can also get numbness/paraesthesia.

Meralgia paraesthetic is the same is lateral cutaneous nerve of thigh lesion

(Burning over anterior thigh which worsens on walking, positive tinel sign over inguinal ligament)

392
Q

First line investigation for suspected osteoporotic vertebral fracture?

A

X-ray

393
Q

Salter Harris scoring system

A

Physis = 1 point

Metaphysis = 1 point

Epiphysis = 2 points

5 = crush

394
Q

Function of the following nerves

  1. Femoral
  2. Obturator
  3. Lateral cutaneous nerve of thigh
  4. Tibial
  5. Common peroneal
  6. Superior gluteal
  7. Inferior gluteal nerve
A
  1. Femoral = hip flexion and knee extension
  2. Obturator = thigh adduction
  3. Lateral cutaneous nerve of thigh = Lateral and posterior surfaces of the thigh
  4. Tibial - Plantarflexion and inversion
  5. Common peroneal = dorsiflexion and eversion (and extensor hallucis longus)
  6. Superior gluteal = Hip abduction
  7. Inferior gluteal nerve = Hip extension and lateral rotation
395
Q

What nerve is damaged after anterior hip dislocation?

A

Obturator nerve

396
Q

What nerve injury would a popliteal laceration/posterior knee cause?

A

Tibial nerve

397
Q

What causes damage to the common peroneal nerve?

A

Injury often occurs at the neck of the fibula
Tightly applied lower limb plaster cast

Injury causes foot drop

398
Q

What things can damage the superior gluteal nerve?

A

Misplaced intramuscular injection

Hip surgery

Pelvic fracture

Posterior hip dislocation

399
Q

What nerve injusry would result in a positive trendelenberg sign?

A

Superior gluteal nerve

400
Q

What nerve is commonly injured alongside the inferior gluteal nerve?

A

Sciatic nerve

401
Q

What is the manifestation of injury of the inferior gluteal nerve?

A

Injury results in difficulty rising from seated position. Can’t jump, can’t climb stairs

402
Q

What movement is associated with anterior shoulder dislocation?

A

External rotation and abduction

403
Q

What injuries is the anterior shoulder dislocation assocaited with?

A

Greater tuberosity fracture

Bankart lesion

Hill-Sachs deformity

404
Q

What signs are seen on posterior shoulder dislocation?

A

Rim’s sign, light bulb sign.

Associated with Trough sign

405
Q

What is a hill-sachs deformity vs bankart lesion

A

Hill-Sachs = Compression fracture of posterolateral humeral head due to compression against glenoid

Bankart lesion = labral tear on anterior inferior glenoid

406
Q

Description of anterior vs posterior shoulder x-ray

A

Anterior dislocation description:

On examination, the right arm is abducted and externally rotated, and she resists all movement. The acromion appears prominent. The humeral head is seen in a subcoracoid position in anteroposterior view on X-ray

Posterior dislocation = arm held in internal rotation

407
Q

Crystals seen in osteoarthritis vs rheumatoid arthritis?

A
  • Osteoarthritis- calcium phosphate crystals associated with degeneration of cartilage, coffin-lid shaped with no birefringence
  • Rheumatoid arthritis- cholesterol crystals, these are rhombic/brick-shaped with a negative birefringence
408
Q

Adverse effects of phenytoin?

A

Phenytoin adverse effects:

P= p450 interactions

H = hirsutism

E= enlarged gums

N = nystagmus

Y= yellow skin ie jaundice

T = teratogen

O = osteomalacia

I = intereference with b12 metabolism - causing megaloblastic anaemia

N = neuropathies

Can also cause DUPYTREN’s

409
Q

Elderly people becomming clumsy with their hands

Positive hoffmans sign?

A

Degenerative cervical myelopathy

410
Q

Definition of orthostatic hypotension?

A

a. A drop in systolic BP of 20mmHg or more (with or without symptoms)
b. A drop to below 90mmHg on standing even if the drop is less than 20mmHg (with or without symptoms)
c. A drop in diastolic BP of 10mmHg with symptoms (although clinically much less significant than a drop in systolic BP).

411
Q

What does the drug memantine act on?

A

NMDA receptor antagonist

412
Q

What is involved in a confusion screen?

A

B12/folate: macrocytic anaemias, B12/folate deficiency worsen confusion

TFTs: confusion is more commonly seen in hypothyroidism

Glucose: hypoglycaemia can commonly cause confusion

Bone Profile (Calcium): hypercalcaemia can cause confusion

413
Q

What type of dementia is assocaited with motor neurones disease?

A

Frontotemporal

414
Q

How does respiratory alkalosis impact calcium?

A

Hypocalcaemia can be seen secondary to respiratory alkalosis as the higher pH lowers the amount of ionised calcium seen in the blood

415
Q

What are the first line drugs for spasticity in MS?

A

Baclofen

Gabapentin

416
Q

How can syringe drivers be used to manage respiratory secretions and bowel colic?

A

Syringe drivers: respiratory secretions & bowel colic may be treated by hyoscine hydrobromide, hyoscine butylbromide, or glycopyrronium bromide. If bowel colic, assume it’s an obstruction - use hyoscine butyl bromide. Metoclopramide is contraindicated in bowel obstruction.

417
Q

What is pellagra?

A

Niacin deficiency

Vitamin B3

  • Pellagra
  • dermatitis
  • diarrhoea
  • dementia
418
Q

What are the features of vitamin B6 deficiency?

A

Anaemia, irritability, seizures

B6 is called pyridoxine

419
Q

What are the features of B7 deficiency?

A

Dermatitis

Seborrhoea

B7 is called biotin

420
Q

What is vitamin B9 called

What does deficiency in this vitamin cause?

A

Folic acid

Megaloblastic anaemia, deficiency during pregnancy - neural tube defects

421
Q

What is the name for vitamin B12?

A

Cyanocobalamin

Megaloblastic anaemia, peripheral neuropathy

422
Q

What is ascorbic acid?

A

Vitamin C

Scurvy

gingivitis

bleeding

423
Q

What is the name of vitamin E

What does deficiency of this vitamin cause?

A

Tocopherol, tocotrienol

Mild haemolytic anaemia in newborn infants, ataxia, peripheral neuropathy

424
Q

What is the name of vitamin K?

A

Naphthoquinone

425
Q

What are risk factors for placental abruption?

A

Abruption previously;

Blood pressure (i.e. hypertension or pre-eclampsia);

Ruptured membranes, either premature or prolonged;

Uterine injury (i.e. trauma to the abdomen);

Polyhydramnios;

Twins or multiple gestation;

Infection in the uterus, especially chorioamnionitis;

Older age (i.e. aged over 35 years old);

Narcotic use (i.e. cocaine and amphetamines, as well as smoking)

426
Q

Risk factors for endometrial cancer

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
427
Q

When does the Moror reflex dissappear?

A

4 months

428
Q

Risk factors for DDH

A
  • female sex: 6 times greater risk
  • breech presentation
  • positive family history
  • firstborn children
  • oligohydramnios
  • birth weight > 5 kg
  • congenital calcaneovalgus foot deformity
429
Q

Difference between lichen planus and lichen sclerosus

A

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

430
Q

What do fibroids look like on ultrasound?

A

Hypoechoic mass

431
Q

What does beads on a string refer to?

A

Chronic salpingitis

432
Q

What sign is assocaited with ovarian torsio non ultrasound?

A

Whirlpool sign

433
Q

Sensitising events:

Potentially sensitising events in pregnancy:

  • Ectopic pregnancy
  • Evacuation of retained products of conception and molar pregnancy
  • Vaginal bleeding < 12 weeks, only if painful, heavy or persistent
  • Vaginal bleeding > 12 weeks
  • Chorionic villus sampling and amniocentesis
  • Antepartum haemorrhage
  • Abdominal trauma
  • External cephalic version
  • Intra-uterine death
  • Post-delivery (if baby is RhD-positive)
A
434
Q

When do you use antibiotics in mastitis?

A

an infected nipple fissure, symptoms not improving after 12-24 hours despite effective milk removal and/or breast milk culture positive.

If antibiotics are indicated, first line would be flucloxacillin for 10-14 days or erythromycin or clarithromycin if penicillin allergic.

435
Q

Risk factors for PPH

A
  • previous PPH
  • prolonged labour
  • pre-eclampsia
  • increased maternal age
  • polyhydramnios
  • emergency Caesarean section
  • placenta praevia, placenta accreta
  • macrosomia
  • ritodrine (a beta-2 adrenergic receptor agonist used for tocolysis)
436
Q

Management of PPH

A

1st line (physical method)

  • bimanual uterine massage
  • empty bladder (catheter)

2nd line

  • oxytocin/syncitocin
  • carboprost
  • ergimetrine (not in hypertension)

3rd line (surgical)

  • balloon tamponade (do this first in surgical method)
  • B-Lynch suture
  • ligation of the uterine arteries or internal iliac arteries

Last option

hysterectomy

437
Q

When are grommets used?

A
  • recurrent acute otitis media
  • otitis media with effusion in both ears 3 months or one ear for 6 months
  • In patients with speech delays
438
Q

What are the common causative organisms in acute otitis media?

A

whilst viral upper respiratory tract infections (URTIs) typically precede otitis media, most infections are secondary to bacteria, particularly Streptococcus pneumonaie, Haemophilus influenzae and Moraxella catarrhalis

439
Q

When should antibiotics be prescribed for acute otitis media?

A

Antibiotics should be prescribed immediately if:

  • Symptoms lasting more than 4 days or not improving
  • Systemically unwell but not requiring admission
  • Immunocompromise or high risk of complications secondary to significant heart, lung, kidney, liver, or neuromuscular disease
  • Younger than 2 years with bilateral otitis media
  • Otitis media with perforation and/or discharge in the canal
440
Q

According to NICE guidance ‘a woman of reproductive age who has not conceived after 1 year of unprotected vaginal sexual intercourse, in the absence of any known cause of infertility, should be offered further clinical assessment and investigation along with her partner.’

A
441
Q

What factors exacerbate psoriasis?

A

trauma

alcohol

drugs: beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs and ACE inhibitors, infliximab

withdrawal of systemic steroids

442
Q

How to tell the difference between bullous pemphigoid and pemphigus vulgaris?

A
  • no mucosal involvement (in exams at least*): bullous pemphigoid
  • mucosal involvement: pemphigus vulgaris
443
Q

One of the main clinical features of polymorphic eruption in pregnancy is periumbilical sparing

A
444
Q

What are the discontinuation symptoms of SSRIs?

A
  • increased mood change
  • restlessness
  • difficulty sleeping
  • unsteadiness
  • sweating
  • gastrointestinal symptoms: pain, cramping, diarrhoea, vomiting
  • paraesthesia
445
Q

What drugs are ototoxic?

A

aminoglycosides (e.g. Gentamicin), furosemide, aspirin and a number of cytotoxic agents

446
Q

When are APGAR scores measured?

A

1,5,10 minutes

447
Q

What are the features of wet age related macular degeneration?

A

Decreasing vision over months with metamorphopsia and central scotoma should cause high suspicion of wet age-related macular degeneration

448
Q

What is the diagnostic threshold for gestational diabetes vs the targets for gestational diabetes?

A

Diagnosis

fasting glucose is >= 5.6 mmol/L

2-hour glucose is >= 7.8 mmol/L

449
Q

When is gestational diabetes screened for?

A

as soon as possible after booking and at 24-28 weeks

450
Q

Summary of managment of gestational diabetes

A

If fasting glucose is less than 7

try exercise - add metformin if needed - add insulin if needed

If over 7 go immediately to insulin

451
Q

How do you manage gestational diabetes?

A
  • weight loss for women with BMI of > 27 kg/m^2
  • stop oral hypoglycaemic agents, apart from metformin, and commence insulin
  • folic acid 5 mg/day from pre-conception to 12 weeks gestation
  • detailed anomaly scan at 20 weeks including four-chamber view of the heart and outflow tracts
  • tight glycaemic control reduces complication rates
  • treat retinopathy as can worsen during pregnancy

Also having diabetes (type 1 or 2) is a high risk factor for pre-eclampsia, therefore women should take aspirin 75-150mg daily from 12 weeks gestation until the birth.

452
Q

Risk factors for pre-eclampsia

A
453
Q

What precipitates pompholyx eczema?

A

Precipitated by humidity and temperature

Pompholyx eczema is a subtype of eczema characterised by an intensely pruritic rash on the palms and soles (basically, if the diagnosis seems like hand foot and mouth but it’s an adult.

454
Q

What do they test during the heel prick of a baby with CF?

A

Newborns with a positive heel prick for CF, i.e. they have a raised immunoreactive trypsinogen (IRT) result, get a sweat test, which will be high if they have CF

455
Q

What is the management of vaginal vault prolapse?

A

Sacrocolpoplexy

456
Q

What is the management of cystocele/cystourethrocele?

A

anterior colporrhaphy, colposuspension

457
Q

Management of uterin prolapse?

A

Hysterectomy

Sacrohysteropexy

458
Q

Management of rectocele

A

Posterior colporrhaphy

459
Q

Management of chickenpox exposure in pregnancy, i.e. post-exposure prophylaxis (PEP)

A

PEP

Woman less than 20 weeks pregnant and has EXPOSURE

  • Check immunity status
  • Give VZIG IMMEDIATELY

Women over 20 weeks pregnant

  • Check iommunity status
  • Give VZIG or Aciclovir 7-14 days after the exposure

Signs of varicella infection:

Give oral aciclovir

460
Q

How do we manage HIV increased risk of CIN?

A

Annual cervical cytology

461
Q

What causes eczema herpeticum?

A

Eczema herpeticum is a primary infection of the skin caused by herpes simplex virus (HSV) and uncommonly coxsackievirus

462
Q

What is the managment of ramsay hunt?

A

Oral aciclovir

Oral steroids

463
Q

When do cord prolapses often happen

A

After articficial rupture of membranes

464
Q

What bacteria causes erythrasma?

A

Corynebacterium minutissimum

Treated with erythromycin

465
Q

What is Samter’s triad?

A

asthma + aspirin sensitivity + nasal polyposis

466
Q

What are the features of dermatomyosits?

A

Skin features

  • photosensitive
  • macular rash over back and shoulder
  • heliotrope rash in the periorbital region
  • Gottron’s papules - roughened red papules over extensor surfaces of fingers
  • ‘mechanic’s hands’: extremely dry and scaly hands with linear ‘cracks’ on the palmar and lateral aspects of the fingers
  • nail fold capillary dilatation

Other features

  • proximal muscle weakness +/- tenderness
  • Raynaud’s
  • respiratory muscle weakness
  • interstitial lung disease: e.g. Fibrosing alveolitis or organising pneumonia
  • dysphagia, dysphonia
467
Q

What are the antibodies assocaited with dermatomyosits?

A
  • the majority of patients (around 80%) are ANA positive
  • around 30% of patients have antibodies to aminoacyl-tRNA synthetases (anti-synthetase antibodies), including:
  • antibodies against histidine-tRNA ligase (also called Jo-1)
  • antibodies to signal recognition particle (SRP)
  • anti-Mi-2 antibodies
468
Q

Features of polymyositis

A
  • proximal muscle weakness +/- tenderness
  • Raynaud’s
  • respiratory muscle weakness
  • interstitial lung disease: e.g. fibrosing alveolitis or organising pneumonia
  • dysphagia, dysphonia
469
Q

Investigations for polymyositis

A
  • elevated creatine kinase - this helps distinguish the condition from PMR
  • other muscle enzymes (lactate dehydrogenase (LDH), aldolase, AST and ALT) are also elevated in 85-95% of patients
  • EMG
  • muscle biopsy
  • anti-synthetase antibodies
  • anti-Jo-1 antibodies are seen in pattern of disease associated with lung involvement, Raynaud’s and fever
470
Q

General mnemonic for antisynthetase syndrome

A

RIM JOB

Reynauds

Interstitial lung disease

Myositis (or mechanics hands with gottrons papules for dermatomyositis)

JOB = jo-1 antibodies

471
Q

What antibodies are assocaited with drug induced lupus?

A

ANA positive in 100%, dsDNA negative

anti-histone

472
Q

What drugs cause drug-induced lupus?

A

Most common causes

procainamide

hydralazine

Less common causes

isoniazid

minocycline

phenytoin

473
Q

Most sensitive and most-specific antibodies for lupus?

A

99% are ANA positive

this high sensitivity makes it a useful rule out test, but it has low specificity

20% are rheumatoid factor positive

anti-dsDNA: highly specific (> 99%), but less sensitive (70%)

anti-Smith: highly specific (> 99%), sensitivity (30%)

also: anti-U1 RNP, SS-A (anti-Ro) and SS-B (anti-La)

474
Q

What is the first line investigation for psoas abscess?

A

Abdominal CT

475
Q

Antiphospholipid syndrome: (paradoxically) prolonged APTT + low platelets

A
476
Q

Which artery is compromised in the fracture of the scaphoid?

A

The dorsal carpal branch of the radial artery is the main neurovascular structure that is compromised in a scaphoid fracture

477
Q

What are the features of scleroderma renal crisis?

A

1- Abrupt onset of moderate to severe hypertension that is typically associated with an increase in plasma renin activity

2- Acute kidney injury (AKI)

3- Urinalysis that is normal or reveals only mild proteinuria with few cells or casts

478
Q

What is the treatment for scleroderma renal crisis?

A

Ace inhibitors

479
Q

Extra-genital features of behcets

A

Behcet’s syndrome is associated with various dermatological symptoms including aphthous ulcers, genital ulcers, acne-like lesions and erythema nodosum.

480
Q

What is the most common site of metatarsal stress fracture?

A

2nd metatarsal

481
Q

What is the Z score of the DEXA scan adjusted for?

A

Age

Gender

Ethnic factors

482
Q

What is the investigation for osteomyelitis vs septic arthritis

A

Osteomyelitis=MRI

Septic arthritis = joint aspiration/bloodcultures/joint imaging

483
Q

What is CK and ESR in PMR?

A

CK normal

ESR raised

484
Q

filter paper near conjunctival sac to measure tear formation

A

Schirmers test

485
Q

Which medium vessel vasculitis is assocaited with hep-b

A

Polyarteritis nodoa

486
Q

What is the test for meniscal tear?

A

Thelassey’s test

weight bearing at 20 degrees of knee flexion, patient supported by doctor, postive if pain on twisting knee (for meniscal tear)

487
Q

What are causes of avascular necrosis of the hip?

A
  • long-term steroid use
  • chemotherapy
  • alcohol excess
  • trauma
488
Q

What is theinvestigation of choice for avascular necrosis of the hip?

A

MRI

X-ray may show crescent sign

489
Q

Features of OA in hands

A

OA of the hand:

Usually bilateral: Usually one joint at a time is affected over a period of several years. The carpometacarpal joints (CMCs), distal interphalangeal joints (DIPJs) are affected more than the proximal interphalangeal joints (PIPJs). Squaring of thumb

490
Q

Antibodies for scleroderma

A

ANA positive in 90%

RF positive in 30%

anti-scl-70 antibodies associated with diffuse cutaneous systemic sclerosis

anti-centromere antibodies associated with limited cutaneous systemic sclerosis

491
Q

What biochemical marker can be used to measure disease activity in patients with lupus?

A

Low complement = active disease

492
Q

Methotrexate may cause mucositis

A
493
Q

How to tell the difference between osteochondritis dissecans and chondromalacia patella?

A

Osteochondritis dissecans:

= Pain after exercise, swelling, locking, giving way, clunking

Chondromalacia patellae =

Softening of the cartilage of the patella
Common in teenage girls
Characteristically anterior knee pain on walking up and down stairs and rising from prolonged sitting
Usually responds to physiotherapy

494
Q

Why is a chest x-ray important before starting biologics for RA?

A

Look for TB

Biologics can cause re-activation of TB

495
Q

Features of colles fracture?

A

Features of the injury

  1. Transverse fracture of the radius
  2. 1 inch proximal to the radio-carpal joint
  3. Dorsal displacement and angulation
496
Q

Features of smiths fracture

A

Volar angulation of distal radius fragment (Garden spade deformity)

Caused by falling backwards onto the palm of an outstretched hand or falling with wrists flexed

497
Q

Describe bennets fracture

A
  • Intra-articular fracture at the base of the thumb metacarpal
  • Impact on flexed metacarpal, caused by fist fights
    • X-ray: triangular fragment at the base of metacarpal
498
Q

Monteggia fracture

A
  • Dislocation of the proximal radioulnar joint in association with an ulna fracture
  • Fall on outstretched hand with forced pronation
  • Needs prompt diagnosis to avoid disability
499
Q

Galeazzi fracture

A
  • Radial shaft fracture with associated dislocation of the distal radioulnar joint
  • Occur after a fall on the hand with a rotational force superimposed on it.
  • On examination, there is bruising, swelling and tenderness over the lower end of the forearm.
  • X Rays reveal the displaced fracture of the radius and a prominent ulnar head due to dislocation of the inferior radio-ulnar joint.
500
Q

Description of Barton’s fracture

A
  • Distal radius fracture (Colles’/Smith’s) with associated radiocarpal dislocation
    • Fall onto extended and pronated wrist
501
Q

Features of radial head fracture

A
  • Fracture of the radial head is common in young adults.
  • It is usually caused by a fall on the outstretched hand.
  • On examination, there is marked local tenderness over the head of the radius, impaired movements at the elbow, and a sharp pain at the lateral side of the elbow at the extremes of rotation (pronation and supination).
502
Q

longitudinal compression of the thumb = scaphoid fracture

A
503
Q

What can discitis be secondary to?

A

Infective endocarditis

504
Q

what are the ottowa rules for ankle fracture?

A

An ankle x-ray is required only if there is any pain in the malleolar zone and any one of the following findings:

  • bony tenderness at the lateral malleolar zone (from the tip of the lateral malleolus to include the lower 6 cm of posterior border of the fibular)
  • bony tenderness at the medial malleolar zone (from the tip of the medial malleolus to the lower 6 cm of the posterior border of the tibia)
  • inability to walk four weight bearing steps immediately after the injury and in the emergency department
505
Q

What is a potts ankle fracture

A

Bimalleolar ankle fracture

Forced foot eversion

506
Q

What is weber classification of ankle fracture

A

Related to the level of the fibular fracture.

Type A is below the syndesmosis

Type B fractures start at the level of the tibial plafond and may extend proximally to involve the syndesmosis

Type C is above the syndesmosis which may itself be damaged

507
Q

General management of ankle fractures

  1. Weber a / minimally displaced
  2. Displaced
  3. Unstable
  4. Management prior to scan
A
  1. Weber a / minimally displaced = cam boot
  2. Displaced = casted
  3. Unstable / weber c = ORIF
  4. Management prior to scan = reduction

All ankle fractures should be promptly reduced to remove pressure on the overlying skin and subsequent necrosis

508
Q

RA drug therapy

A

NSAIDS

Steroid

DMARDS

509
Q

What are the drug therapies available for RA?

A

Steroids for flares

(IM methylprednisolone, intra-articular steroids, oral prednisolone)

NSAIDs for symptom relief

DMARDs

(methotrexate, sulfasalazine, hydroxychloroquine, leflunomide)

Biologics:

TNF = infliximab, etanercept, adalimumab

Anti-CD20 - rituximab

Anakinra = IL-1

IL-6 = Toclizumab

510
Q

What are the side effects of methotrexate?

A

Pneumonitis

Oral ulcers

Heoatotoxicity

511
Q

How often is methotrexate monitored?

A

Initially monthly then every three months

512
Q

Whar are the side effects of sulfasalazine?

A
  • oligospermia
  • Stevens-Johnson syndrome
  • pneumonitis / lung fibrosis
  • myelosuppression, Heinz body anaemia, megaloblastic anaemia
  • may colour tears → stained contact lenses
513
Q

Side effects of hydroxychloroquine

A

Irreversible retinopathy

514
Q

What are the side effects of leflunomide?

A

Increased BP

Oral ulcers

Hepatotoxicity

Diarrhoea

Male and female teratogenicity

515
Q

What DMARDs are contraindicated in pregnancy?

A

Methotrexate

women should avoid pregnancy for at least 6 months after treatment has stopped

the BNF also advises that men using methotrexate need to use effective contraception for at least 6 months after treatment)

Leflunomide

516
Q

DMARDs that may be used during pregnancy?

A

Sulfasalazine

Hydroxychloroquine

517
Q

What are the drug interactions of methotrexate?

A
  • avoid prescribing trimethoprim or co-trimoxazole concurrently - increases risk of marrow aplasia
  • high-dose aspirin increases the risk of methotrexate toxicity secondary to reduced excretion
518
Q

What is methotrexate co-prescribed with?

A

Folic acid

folic acid 5mg once weekly should be co-prescribed, taken more than 24 hours after methotrexate dose

519
Q

What are the adverse effects of cyclophosphamide?

A
  • Haemorrhagic cystitis
  • myelosuppression
  • transitional cell carcinoma
520
Q

Bleomycin SE

A

Lung fibrosis

521
Q

Anthracyclines (doxorubicin SE)

A

Cardiomyopathy

522
Q

SE of fluoracil

A

Myelosuppression, mucositis, dermatitis

523
Q

SE of cytarabine

A

ataxia

524
Q

SE of vincristine

A

Peripheral neuropathy (reversible) , paralytic ileus

525
Q

SE of docetaxel

A

Neutropenia

526
Q

SE of cisplastin

A

Ototoxicity, peripheral neuropathy, hypomagnesaemia

527
Q

Eye features of third nerve palsy?

A

Third nerve palsy:

Eye will be abducted and depressed

Ptosis

Dilated pupil and absent light reflex - there will be intact consensual constriction

528
Q

What are causes of third nerve palsy

A
  • diabetes mellitus
  • vasculitis e.g. temporal arteritis, SLE
  • Uncal herniation
  • posterior communicating artery aneurysm (often associated pain)
  • cavernous sinus thrombosis
  • Weber’s syndrome: ipsilateral third nerve palsy with contralateral hemiplegia -caused by midbrain strokes
  • amyloid, multiple sclerosis
529
Q

What is autonomic dysreflexia?

A

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

Management of autonomic dysreflexia involves removal/control of the stimulus and treatment of any life-threatening hypertension and/or bradycardia.

530
Q

What are the different types of motor neurone disease?

A

Amytrophic lateral sclerosis

Primary lateral sclerosis

Progressive muscular atrophy

Progressive bulbar palsy

531
Q

What are the features of ALS?

A
  • 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
532
Q

What are the features of primary lateral sclerosis?

A

UMN signs only

533
Q

Signs of progressive muscular atrophy

A

LMN signs only

affects distal muscles before proximal

carries best prognosis

534
Q

Signs of progressive bulbar palsy

A
  • palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
  • carries worst prognosis
535
Q

Adrenaline doses

A
536
Q

Side effects of sodium valproate

A
  • teratogenic
  • P450 inhibitor
  • gastrointestinal: nausea
  • increased appetite and weight gain
  • alopecia: regrowth may be curly
  • ataxia
  • tremor
  • hepatotoxicity
  • pancreatitis
  • thrombocytopaenia
  • hyponatraemia
  • hyperammonemic encephalopathy: L-carnitine may be used as treatment if this develops
537
Q

Side effects of Carbemazepine

A

Adverse effects

  • P450 enzyme inducer
  • dizziness and ataxia
  • drowsiness
  • headache
  • visual disturbances (especially diplopia)
  • Steven-Johnson syndrome
  • leucopenia and agranulocytosis
  • hyponatraemia secondary to syndrome of inappropriate ADH secretion
538
Q

What are the antibodies associated with diabetes?

A

Antibodies associated with diabetes. (Anti-GAD, islet cell antibodies, insulin autoantibodies)

539
Q

Driving advice for type 1 diabetes

A
  • Driving advice for type 1 diabetes:
  • If you have had more than 1 hypo in the last 12 months you must not drive and inform the DVLA
  • If you have had a hypo in the last 12 months you must not drive a lorry and you must notify the DVLA of every severe episode of hypoglycaemia
  • If severe hypoglycaemia occurs whilst driving - stop driving and inform the DVLA
  • Keep glucose treatments in car
  • Check blood glucose before driving and every two hours
  • Blood glucose should be more than 5 in order for you to drive
540
Q

Where is BROCAs and Wernickes?

A
  • Brocas is inferior frontal gyrus. It is typically supplied by the superior division of the left MCA.
  • Wernickes = Due to a lesion of the superior temporal gyrus. It is typically supplied by the inferior division of the left MCA
541
Q

How do acute haematomas compare to chronic haematomas?

A

Acute = hyperdense

Chronic = hypodense

542
Q

How do you diagnose acromegaly?

A

Diagnosis of acromegaly = measure serum IGF1 levels (raised), then do glucose tolerance test - measuring GH (normal patients GH is suppressed to less than 1 microgram/L. Levels higher than this conform acromegaly. MRI of sella turcica needed as well. Remember to screen for other secretory effects of the tumour: They include thyroid stimulating hormone (TSH), gonadotropic hormones (FSH, LH), adrenocorticotropic hormone, and prolactin.

543
Q

Jacksonian movements are a feature of frontal lobe epilepsy.

Temporal lobe seizures are associated with aura, lip smacking and clothes plucking.

Occipital seizures are associated with visual abnormalities.

Parietal seizures are associated with sensory abnormalities.

A
544
Q

Rapid correction of

  1. Hyponatraemia
  2. Hypernatraemia
A
  1. Rapid correction of hyponatraemia can cause osmotic demyelination syndrome
  2. Correction of chronic hypernatraemia too fast predisposes to cerebral oedema
545
Q

What is management for intrapartum pyrexia?

A

Benzylpenizillin, to cover for BGS

Vanc if penicillin allergic

Erythromycin is given for premature rupture of membranes

546
Q

What drugs can cause idiopathic intracranial hypertension?

A

ciclosporin, oral contraceptives, mineralocorticoids, amiodarone, antibiotics (tetracyclines, sulphonamides), retinoic acid

547
Q

What is the most common brain tumour in adults?

A

Glioblastoma multiforme

548
Q

How does glioblastoma look on imaging and histology?

A

Imaging: Central necrotic area, with enhanced rim

Histology: Pleomorphic tumour cells border necrotic areas

549
Q

Where do meningiomas arise from?

A

Dura matter

550
Q

Histology of meningioma

A

Spindle cells in concentric whorls and calcified psammoma bodies

551
Q

Histology of vestibular schwannomas

A

Antoni A or B patterns are seen. Verocay bodies (acellular areas surrounded by nuclear palisades)

552
Q

What is the most common primary brain cancer in children?

A

Pilocytic astrocytoma

553
Q

What are the histological features of astrocytoma?

A

Rosenthal fibres (corkscrew eosinophilic bundle)

554
Q

What is the histology for medulloblastoma?

A

Small, blue cells. Rosette pattern of cells with many mitotic figures

555
Q

Where are ependymomas commonly seen

A

4th ventricle

556
Q

What are the histology findings for ependymoma?

A

perivascular pseudorosettes

557
Q

Oligodendroma appearance on histology

A

Calcifications with ‘fried-egg’ appearance

558
Q

Haemangioblastoma histology

A

foam cells and high vascularity

559
Q

Histology of craniopharyngoma

A

Derived from remnants of Rathke pouch

560
Q

Neuroleptic malignant syndrome blood findings

A

raised CK and leukocytosis

561
Q

Squamous vs adenocarcinoma lung cancer location

A

Squamous = central

Adenocarcinoma = peripheral

562
Q

Which cranial nerves are affected in vestibular schwannomas

A

5’7’8

563
Q

What is a marker of medullary thyroid cancer?

A

calcitonin

564
Q

Painful third nerve palsy = posterior communicating artery aneurysm

A
565
Q

Multi-system atrophy is just Parkinson’s symptoms plus autonomic disturbance

A
566
Q

How to manage metastatic bone pain

A

Analgesia

Bisphosphonates

Radiotherapy

567
Q

How do you manage acute hyponatraemia?

A

Hypertonic saline

568
Q

How would you manage chronic hyponatraemia?

A

If a hypovolemic cause is suspected

normal, i.e. isotonic, saline (0.9% NaCl)

this may sometimes be given as a trial

if the serum sodium rises this supports a diagnosis of hypovolemic hyponatraemia

if the serum sodium falls an alternative diagnosis such as SIADH is likely

If a euvolemic cause is suspected

fluid restrict to 500–1000 mL/day

consider medications:

demeclocycline

vaptans (see below)

If a hypervolemic cause is suspected

fluid restrict to 500–1000 mL/day

consider loop diuretics

consider vaptans

569
Q

What type of dementia has fluctuating cognition?

A

Lewy body dimentia

570
Q

Describe progressive supranuclear palsy

A

Parkinson’s plus falls plus vertical gaze palsy

571
Q

What drugs cause SIADH?

A

Carbemazepine

Sulfonylureas

SSRIs

Tricyclics

572
Q

How do you treat hiccups in palliative care?

A

Chlorpromazine or haloperidol

573
Q

Parkinson’s plus dementia think Lewy body

A
574
Q

Drugs for neuropathic pain are typically used as monotherapy, i.e. if not working then drugs should be switched, not added

A
575
Q

If raised afp what testicular cancer is excluded

A

seminoma

576
Q

Which nerves are frequently injured during axillary nerve dissection?

A

The intercostobrachial nerves are frequently injured during axillary dissection. These nerves traverse the axilla and supply cutaneous sensation.

577
Q

How does subacute degeneration of the spinal cord present?

A

dorsal columns and lateral corticospinal tracts are affected. joint position and vibration sense lost first then distal paraesthesia.

578
Q

What is weakness after a seizure called?

A

Todds paresis

579
Q

Which drugs exacerbate myaesthenia gravis

A

The following drugs may exacerbate myasthenia:

  • penicillamine
  • quinidine, procainamide
  • beta-blockers
  • lithium
  • phenytoin
  • antibiotics: gentamicin, macrolides, quinolones, tetracyclines
580
Q

What are the symptoms of digoxin toxicity?

A

gastrointestinal disturbance (nausea, vomiting, abdominal pain)

dizziness

confusion

blurry or yellow vision

arrhythmias.

581
Q

Treatment for trigeminal neuralgia

A

Carbemazepine

582
Q

The patient has a Klumpke’s paralysis involving brachial trunks C8-T1. Classically there is weakness of the hand intrinsic muscles. Involvement of T1 may cause a Horner’s syndrome. It occurs as a result of traction injuries or during delivery.

The patient has an Erb’s palsy involving brachial trunks C5-6.

A
583
Q

Marfan syndrome + headache =

A

Intracranial hypotension

584
Q

What are the side effects of levodopa

A

dyskinesia

dry mouth

anorexia

palpitations

postural hypotension

psychosis

drowsiness.

585
Q

Side effects of bromocriptine and cabergoline?

A

pulmonary, retroperitoneal and cardiac fibrosis.

586
Q

What are causes of hyperkalaemia?

A
  • acute kidney injury
  • drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
  • metabolic acidosis
  • Addison’s disease
  • rhabdomyolysis
  • massive blood transfusion
587
Q

What drug is used to treat magnesium sulphate driven respiratory depression?

A

Calcium gluconate

588
Q

Sudden onset hearing loss management

A

Following referral to ENT, patients with sudden-onset sensorineural hearing loss are treated with high-dose oral corticosteroids

589
Q

Which contraceptive does not interact with enzyme inducers

A

depo-provera

590
Q

Constipation in children management

A

Constipation in children = movicol then add stimulant (Senna), then add osmotic such as lactulose

591
Q

What can be used to promote PDA closure?

A

Indomethacin or ibuprofen

592
Q

Which medical condition contraindicates ulipristal

A

Asthma

Breastfeeding - have to stop for one week after taking ulipristal

593
Q

What drugs most commonly cause TENS/SJS?

A

Penicillins

Quinolones

Sulfonamides

Corticosteroids

NSAIDs

594
Q

What blood test might you need to do before starting SSRI?

A

U and E

SSRI may invoke hyponatraemia, if patient is on a drug like omeprazole which also causes hyponatraemia you need to check U and E before starting SSRI

595
Q

What organism causes tinea capitis?

A

Caused by trichopghyton tonsurans or Microsporum Canis (associated with cats and dogs, and fluoresce under woods lamp). Treatment for trichophyton tonsurans = oral terbinafine. Treatment for microsporum Canis = griseofulvin. Topical ketoconazole shampoo for first two weeks to reduce transmission.

596
Q

What organism causes tinea corporis (ringworm)

A

Tinea corporis = trichophyton rubrum and trichophyton verrucosum. Treated with oral fluconazole. (BMJ says that this is treated with topical terbinafine adjunct is aluminium acetate topical. 2nd line is topical ‘azoles’. 3rd line is oral terbinafine/ oral itraconazole)

597
Q

Antibiotic therapy for PID?

A

oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline + oral metronidazole

598
Q

The first visit is from eight

Check everything with mum is great

Urine, bloods and rhesus state

Give advice and educate

From eleven to thirteen

Is the best time to do the Down’s screen

While you’re at it, check the dates

At sixteen or ten plus six

Do BP and multistix

Second scan is at twenty

To check the fingers and toes

(Make sure there’s plenty(twenty).)

Once again at twenty-eight

Urine, blood and rhesus state

Anti-D if appropriate

Must give anti-D once more

When the week is thirty-four

And plan for the birth, what a chore

Check the lie at thirty-six

If breech offer a quick fix

Last visit at thirty-eight

All that is left it to wait

A
599
Q

Causes of horners

A
600
Q

Keith and Wagener classification of hypertensive retinopathy

A

FINALS (3 decks)

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