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Medicine Flashcards

Rheum ✔ Resp ✔ Gastro - Renal - Cardio ✔ Endo ✔ Infectious -

1
Q

Describe Paget’s disease

A

Excessive, uncoordinated bone turnover
-Increased osteoblast activity
-Increased osteoclast activity
Results in scleritic and lytic lesions (high and low density).

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2
Q

What are the signs of Paget’s disease on bloods and imaging?

A

Raised ALP
Xray- bone enlargements and deformity, osteoporosis circumscripta, cotton wool skull, v shaped lytic defects in long bones

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3
Q

What are the complications of Paget’s disease?

A

Bone pain and deformities
Pathological fractures
Hearing loss
Heart failure(due to hypervascularity of the abnormal bone)
Osteosarcoma
Spinal stenosis and spinal cord compression

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4
Q

Mainstay management of Paget’s?

A

Bisphosphonates (alt is calcitonin)

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5
Q

How do you diagnose osteoporosis?

A

T score <-2.5 on DEXA scan

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6
Q

Risk factors for osteoporosis

A

Older age
Post menopausal
Reduced activity and mobility
Low BMI
Low calcium or vit D intake
Alcohol and smoking
Personal or family hx of fractures
Chronic diseases e.g. CKD
Meds- long term steroids, PPIs, SSRIs, anti epileptics, anti oestrogens

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7
Q

Pathophysiology of osteomalacia(simple)

A

Low vit D= low calcium and phosphate
Low calcium= defective bone mineralisation
Low calcium= increased PTH= increased reabsorption of calcium from bone

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8
Q

Risk factors for osteomalacia

A

Darker skin
Reduced sun exposure
Malabsorption disorders
IBD etc
CKD

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9
Q

Management of osteomalacia?

A

Cholecalciferol

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10
Q

Management of rheumatoid arthritis?

A

Methotrexate long term
Steroids acutely

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11
Q

Joints affected and NOT affected by RA

A

Spares DIP
Small joints- wrist, MCP, PIP, MTP

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12
Q

Classic hand signs of RA

A

Boutonniere’s へ-
Swan neck _/\
Z shaped thumb

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13
Q

What scoring system is used to monitor RA?

A

DAS 28

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14
Q

What is the specific auto antibody for RA?

A

anti-CCP antibodies

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15
Q

What gene is associated with RA?

A

HLA DR4

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16
Q

Classic presentation of reactive arthritis?

A

Can’t see, can’t wee, can’t climb a tree
(anterior uveitis, urethritis/ dysuria/balanitis, knee joint swollen)

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17
Q

What conditions are linked to the HLA B27 gene?

A

Reactive arthritis
Ankylosing spondylitis

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18
Q

What are the triggers of reactive arthritis?

A

infection- chlamydia or gastroenteritis

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19
Q

What are the xray changes in psoriatic arthritis?

A

Osteolysis
Periostitis
Ankylosis
Dactylitis
Pencil in a cup (arthritis mutilans)

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20
Q

Psoriatic arthritis management?

A

NSAIDs
Steroids
DMARDs

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21
Q

What is the test for ankylosing spondylitis?

A

Schober’s test, <20cm is abnormal

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22
Q

What are the associations of ankylosing spondylitis?

A

5 A’s:
Anterior uveitis
Aortic regurgitation
AV block
Apical lung fibrosis
Anaemia of chronic disease

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23
Q

What is enteropathic Arthritis?

A

Arthritis that occurs in conjunction with IBD

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24
Q

Gout vs pseudo gout, PC Ix and Mx

A

PC
Gout: toe or thumb
Pseudo: knee, over 65
Ix
Gout: monosodium- needle, neg bifringent
Pseudo: calcium- rhomboid, +ve bifringent
Mx
Gout: NSAIDs, colchicine
Pseudo: same

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25
Q

Gout vs pseudogout xray

A

Gout: maintained joint space, lytic lesions, punched out erosion
Pseudo: (LOSS) loss of joint space, osteophytes, subarticular sclerosis, subchondral cysts

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26
Q

Septic arthritis joint aspiration result and culture

A

White cells
Staph aureus or gonorrhoea on culture

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27
Q

Classic presentation of polymyalgia rheumatica?

A

Proximal muscle pain and stiffness, worse with rest

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28
Q

How to investigate and treat PMR

A

Treat with steroids(15mg pred OD), and assess response. Likely to be on steroids for 1-2 years, need to know ADRs, sick day rules, steroid dependency card etc.

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29
Q

Difference between PMR and polymyositis?

A

Polymyositis is weakness without pain. PMR has both.

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30
Q

What is the specific autoantibody for myositis?

A

Anti Jo 1

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31
Q

What blood result is raised in myositis?

A

CK

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32
Q

Management of myositis?

A

Steroids
Methotrexate
IV IG
Biologics

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33
Q

What are the skin changes in dermatomyositis?

A

Gottron lesions
Heliotrope rash
Periorbital oedema
Photosensitive rash

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34
Q

Management of SLE?

A

Hydroxychloroquine, NSAID, steroids
DMARDs

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35
Q

Sensitive and specific autoantibodies in SLE?

A

ANA
Anti dsDNA

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36
Q

Specific auto antibody for diffuse systemic sclerosis?

A

Anti Scl 70

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37
Q

Specific auto antibody for limited systemic sclerosis?

A

Anti centromere

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38
Q

What is CREST syndrome?

A

Group of conditions occurring in SS:
Calcinosis
Raynaud’s phenomenon
Oesophageal dysmotility
Sclerodactyly
Telangiectasis

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39
Q

What medication can be given for Raynaud’s?

A

Nifedipine

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40
Q

Typical presentation of Sjogren’s, in one word?

A

DRY
mouth, eyes, vagina.
plus joint pain and stiffness

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41
Q

Specific autoantibodies in Sjogren’s?

A

Anti Ro
Anti La

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42
Q

Unique test for Sjogren’s?

A

Schirmer test
<10mm support dx

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43
Q

Management of Sjogren’s

A

Lubricants, eye drops etc
Pilocarpine
Hydroxychloroquine

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44
Q

Complications of Sjogren’s?

A

Eye- Keratoconjunctivitis sicca and corneal ulcers
Oral - Dental cavities and candida infection
Vaginal - Sexual dysfunction and candida infection
Plus, systemic, altho rarely.

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45
Q

What is the specific autoantibody for drug induced lupus?

A

Anti histone

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46
Q

Typical GCA presentation

A

Female >50 with PMR
Jaw claudication
Temporal scalp tenderness
Amaurosis fugax

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47
Q

GCA management

A

Prednisolone 60mg

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48
Q

Takayasu’s arteritis typical presentation

A

Asian woman
Brachial pulse difference(pulseless disease)
Limb claudication
Headache /syncope

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49
Q

Most common treatment of vasculitis? And exceptions

A

Steroids
Exceptions- Buerger’s, HSP, Kawasaki

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50
Q

Diagnosis of Kawasaki disease

A

5 or more days with fever

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51
Q

Polyarteritis nodosa pathognomonic presentation and renal angiography sign

A

Multisystemic disease, lungs spared
String of beads

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52
Q

Classic presentation of Buerger’s

A

Male smoker
Limb ischaemia/ulcers
Raynaud’s

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53
Q

Management of Buerger’s

A

Smoking cessation
Nifedipine

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54
Q

Granulomatosis with polyangiitis
vs
Eosinophilic granulomatosis with polyangiitis
presentation and autoantibodies

A

GP: Epistaxis, LRTI, nephritic syndrome -c ANCA
EGP: Late onset asthma, mononeuritis complex -p ANCA

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55
Q

HSP presentation

A

Post infection:
Purpura 100%
Joint pain 75%
Abdo pain 50%
Renal 50%

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56
Q

What is the spirometry result in obstructive respiratory disease?

A

FEV1:FVC <0.7
Normal FVC

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57
Q

What spirometry and peak flow results indicate a diagnosis of asthma?

A

Obstructive ratio <0.7
Reversibility, FEV1 inc >12%
Peak flow variability >20%

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58
Q

Stepwise management of asthma?

A

SABA
+ICS
+LABA (maintenance or MART)
Inc ICS or +LRTA
Specialist- oral steroids, theophylline

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59
Q

Emergency management of acute asthma/life threatening?

A

Nebs (SABA, ipratropium bromide)
Steroids
Oxygen
IV (MgSO, SABA, aminophylline)

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60
Q

How to classify severity of COPD

A

FEV1:
mild >80%
moderate 50-80%
severe 30-50%
very severe <30%

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61
Q

MRC dyspnoea scale

A

Grade 1- SOB on strenuous exercise
Grade 2- SOB on walking uphill
Grade 3- SOB that causes slowed walking on flat
Grade 4- Can walk max. 100m on flat
Grade 5- Unable to leave house

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62
Q

Stepwise management of COPD and specialist options

A

1: SABA or SAMA
2:(no asthmatic features): LABA and LAMA
2:(asthmatic features): LABA and ICS
3: LABA, LAMA, ICS
Specialist options:
-Nebulisers
-Oral theophylline
-Oral mucolytic agent e.g. carbocisteine
-Prophylactic abx
-Oral steroids
-LTOT
-Lung volume reduction surgery
-Palliative care

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63
Q

Management of acute exacerbation of COPD

A

Nebulisers (SABA and ipratropium)
Steroids
IV aminophylline
NIV
Intubation and ventilation with admission to ITU
Doxapram (May be used as a respiratory stimulant where NIV or intubation is no appropriate )

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64
Q

What are the indication in a COPD pt for NIV, and when is NIV contraindicated

A

Indications: persistent respiratory acidosis despite max medical tx, potential to recover, acceptable to pt
C/I: pneumothorax

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65
Q

What is cor pulmonale?

A

Right sided HF caused by respiratory disease

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66
Q

What does the pharynx connect?

A

Oral and nasal cavity, to the larynx and oesopahgus

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67
Q

Describe the route of the right and left recurrent laryngeal nerve

A

R RLN travels under the subclavian artery
L RLN travels under the arch of aorta
They both then ascend to innervate the larynx

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68
Q

What is the typical spirometry result in ILD?

A

FEV1 and FVC reduced
FEV1:FVC >0.7

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69
Q

What drugs and conditions can cause secondary pulmonary fibrosis?

A

Drugs:
Amiodarone
Cyclophosphamide
Methotrexate
Nitrofurantoin
Conditions:
Alpha 1 antitrypsin deficiency
RA
SLE
Systemic sclerosis
Sarcoidosis

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70
Q

What are the names of some of the hypersensitivity pneumonitis conditions?

A

Bird fancier’s lung
Farmer’s lung
Mushroom worker’s lung
Malt worker’s lung

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71
Q

What is cryptogenic organising pneumonia and how is it treated?

A

Focal area of inflammation in the lung tissue
Steroids

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72
Q

What cancer specifically is caused by asbestos?

A

Mesothelioma

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73
Q

What medications are used in idiopathic pulmonary fibrosis

A

Pirfenidone
Nintedanib

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74
Q

What is the classic clinical presentation of idiopathic pulmonary fibrosis? (Hx + o/e)

A

Insidious onset of dry cough >3months and SOB
Bibasal fine end inspiratory crackles
Finger clubbing

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75
Q

Describe bronchiectasis

A

Permanent dilatation of the bronchioles
Leading to mucus and organism build up

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76
Q

What are some of the causes of bronchiectasis?

A

Idiopathic
Pneumonia
Whooping cough
TB
A1AT deficiency
Connective tissue disorders
E.g. RA
CF
Yellow nail syndrome (Triad: yellow nail, lymphoedema, bronchiectasis)

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77
Q

What conditions are associated with bronchiectasis?

A

Young’s syndrome
Hypogammaglobulinaemia

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78
Q

Classic signs of bronchiectasis on cxr and ct?

A

CXR- tram track opacities
HRCT- signet ring

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79
Q

How to treat a LRTI in a pt with bronchiectasis?

A

Extended course of ab, 7-14 days
Ciprofloxacin most commonly, esp if pseudomonas aeruginosa

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80
Q

What are the parameters in CURB65

A

Confusion
Urea >7 mmol/L
RR>/=30
BP <90/60
65 or older

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81
Q

Most common causative organisms of typical pneumonia, and abx choice

A

Strep pneumoniae
H. influenzae (most common cause in COPD pts)
Abx of choice (gram positive cover): amoxicillin

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82
Q

What are the atypical causes of pneumonia? And what abx covers them

A

Legionella pneumophila (infected water, travel hx)
Chlamydia psittaci
Mycoplasma
Chlamydia pneumoniae
Coxiella burnetii
Macrolides- clarithromycin

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83
Q

What is the MoA of macrolides?

A

Inhibits protein synthesis

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84
Q

What investigation is done 6 weeks after d/c for pneumonia?

A

CXR- to check no underlying malignancy has been missed

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85
Q

What is lights criteria? (pleural effusion)

A

Exudative if:
Protein pleural:serum >0.5
LDH pleural:serum >0.6
Pleural fluid LDH more than 2 thirds, of the normal upper limit, of serum LDH

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86
Q

Causes of exudative pleural effusion?

A

Infection
CTD
Cancer
Pancreatitis
PE
Dressler’s syndrome
Yellow nail syndrome

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87
Q

Causes of transudative pleural effusion?

A

HF
Hypalbuminaemia (liver, nephrotic, malabsorption)
Hypothyroidism
Meigs syndrome

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88
Q

What investigations should be sent for with a pleural fluid sample from aspiration?

A

LDH, glucose, pH, protein, blood
Cytology
Microbiology

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89
Q

What are the long term management options for recurrent pleural effusions?

A

Pleurodesis
Indwelling pleural catheter

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90
Q

What is empyema?

A

Infected pleural effusion

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91
Q

What is the typical pc of empyema?

A

Improving pneumonia but new or ongoing fever

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92
Q

What pressure is used to define pulmonary hypertension?

A

Mean pulmonary arterial pressure >20mmHg

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93
Q

Causes of pulmonary hypertension?

A

Idiopathic
CTD
Left HF e.g. COPD or fibrosis
Peripheral vasc disease e.g. PE
Others- sarcoidosis, haem disorders, glycogen storage disease

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94
Q

ECG changes of pulmonary HTN?

A

P pulmonale- peaked P waves
Tall R waves in V1+2, Deep S waves in V5+6- R ventricular hypertrophy
Right axis deviation
RBBB

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95
Q

What is sarcoidosis?

A

Chronic granulomatous disorder

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96
Q

What are the pulmonary manifestations of sarcoidosis?

A

Mediastinal lymphadenopathy
Pulmonary fibrosis
Pulmonary nodules
Pulmonary hypertension(more of a complication)

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97
Q

What are the systems involved (except respiratory) in sarcoidosis?

A

Eyes
CNS
Skin
Lymph nodes
Heart
Liver
Kidneys
Bones
PNS

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98
Q

What are some extrapulmonary manifestations of sarcoidosis?

A

Erythema nodosum - raised, red, painful nodules on shins
Lupus pernio- raised, purple, on cheeks and nose
Liver cirrhosis, cholestasis
Uveitis, conjunctivitis, optic neuritis
Bundle branch block, heart block, myocardial muscle involvement
Kidney stones, nephritis
Diabetes insipidus (pituitary involvement), encephalopathy
Facial N palsy
Arthralgia, myopathy, arthritis
SYSTEMIC- fever, weight loss, fatigue

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99
Q

What is the screening test if you suspect sarcoidosis?

A

ACE will be raised. Calcium is sometimes raised.

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100
Q

Classic HRCT appearance in sarcoidosis?

A

Hilar lymphadenopathy and pulmonary nodules

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101
Q

How is sarcoidosis managed?

A

Spontaneously resolves in 50% of cases within 2 years.
Oral steroids are first line.
Methotrexate second line.

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102
Q

Acute management of a simple pneumothorax, if:
1.Asymptomatic, <2cm air
2.Symptomatic or >2cm air

A
  1. No medical intervention, follow up in 2-4 weeks
  2. Aspiration and reassess. If aspiration fails twice, chest drain is done
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103
Q

What is the main complication in tension pneumothorax?

A

Mediastinal shift can kink vessels in the mediastinum and cause cardiorespiratory arrest

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104
Q

Where is a large bore cannula inserted to aspirate the chest?

A

Second intercostal space, midclavicular line

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105
Q

Where is a chest drain inserted?

A

5th intercostal space
Triangle of safety (borders- inferior nipple line, Lats lateral edge, pec major lateral edge

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106
Q

When doing a chest drain, you should insert the needle above or below the rib and angle in what direction?

A

Above the rib and angle down to avoid the neurovascular bundle

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107
Q

Risk factors for PE?

A

Immobility
Recent surgery
Long haul travel
Pregnancy
Hormone therapy with oestrogen (COCP or HRT)
Malignancy
Polycythaemia
SLE
Thrombophilia

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108
Q

What are some of the categories in the Wells PE score?

A

Signs of dvt
Tachycardia
Recent immobilisation
Recent surgery in previous 4 weeks
Haemoptysis
Malignancy

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109
Q

How to use Wells PE score, and how to use PERC?

A

If no PERC criteria is met, PE is ruled out.
If clinically PE is suspected:
Wells says unlikely- do D dimer
Wells says likely- do CTPA or V/Q (and treat)

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110
Q

What results on ABG and CXR indicate PE?

A

ABG- respiratory alkalosis and hypoxia
CXR- normal or Fleischner sign or Westermark’s sign

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111
Q

What is the first line management for PE, alternative and tx if antiphospholipid syndrome

A

Treatment dose DOAC
Alt is LMWH
Warfarin for antiphospholipid, target INR 2-3n

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112
Q

What is the duration of treatment for PE?

A

> 3 months if unprovoked
3 months if provoked and can remove cause e.g. long haul flight

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113
Q

What is ARDS?

A

Acute respiratory distress syndrome:
Increased permeability of alveola capillaries
Fluid accumulates in alveoli
i.e. non cardiogenic pulmonary oedema

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114
Q

What are come causes of ARDS?

A

Infection
Massive blood transfusion
Trauma
Smoke inhalation
Acute pancreatitis
COVID 19
Cardio pulmonary bypass

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115
Q

What is the most common type of lung cancer?

A

Adenocarcinoma

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116
Q

Where are secondary lung ca mets likely to come from?

A

Kidney
Prostate
Breast
Bone
GI
Cervix
Ovary

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117
Q

What are some extrapulmonary manifestations specific to small cell lung cancer?

A

Paraneoplastic syndromes:
SIADH
Cushing’s syndrome
Limbic encephalitis
Others:
Lambert Eaton myasthenic syndrome

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118
Q

What is an extrapulmonary manifestation of a pancoast tumour?

A

Horner’s syndrome
-partial ptosis
-anhydrosis
-miosis

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119
Q

What are some general extrapulmonary manifestations of lung cancer?

A

Recurrent laryngeal nerve palsy
Phrenic nerve palsy
SVCO

120
Q

What is the lung cancer 2ww criteria?

A

40 years old or older and one of:
Haemoptysis
CXR suggestive
Finger clubbing
Recurrent LRTI

40 years old or older and two of:
Smoker
Cough
Fatigue
SOB
Chest pain
Weight loss
Appetite loss

121
Q

What is the immunotherapy sometimes used in ling cancer?

A

Pembrolizumab
PD-1 inhibitor

122
Q

What is the criteria to diagnose DKA?

A

Known DM or glucose >11
Ketones >3
pH <7.3

123
Q

What can cause a raised d dimer?

A

Trauma- surgery, injury etc
Infection
Cancer
Clots

124
Q

What can cause a raised troponin?

A

MI, HF, AF
Sepsis
CKD
Aortic dissection
PE

125
Q

What are the types of shock, and examples of causes?

A

Hypovolaemia e.g. haemorrhage, DKA, burns
Cardiogenic e.g. MI, HB
Distributive e.g. sepsis, anaphylaxis
Obstructive e.g. PE, tension pneumothorax, cardiac tamponade, SVCO

126
Q

Define shock

A

Circulatory insufficiency leads to inadequate tissue perfusion, and thus delivery of O2 to the tissues of the body.
OR,
Oxygen delivery fails to meet oxygen demands- in the context of circulatory insufficiency

127
Q

When would you consider doing a renal tract USS, in acute kidney failure?

A

If there is no obvious explanation for the AKI
If obstructive cause of AKI is suspected
Pyelonephritis suspected- to exclude abscess
If AKI is presumed to be pre renal, but fails to respond to treatment

128
Q

What are the indications for dialysis in kidney failure?

A

(AEIOU-acidosis, electrolyte, intoxication, oedema, uraemia)
Hyperkalaemia refractory to treatment
Severe metabolic acidosis, pH<7.2
Pulmonary oedema refractory to treatment
Uraemia with clinical manifestations e.g. encephalopathy

129
Q

Where does insulin come from and what does it do?

A

Beta islets of langerhans in the pancreas
Primarily induces glucose uptake and glycogen synthesis. Also, uptake of electrolytes esp. potassium and protein synthesis. Inhibits ketogenesis.

130
Q

How is DKA managed?

A

DKA protocol:
Normal saline bolus
Fixed rate insulin
Potassium monitoring and replacement

131
Q

What is the pathophysiology of HHS?

A

High levels of catecholamines and low levels of insulin= reduced peripheral glucose uptake
Glycosuria results in loss of water, causing hyperosmolarity and dehydration. This is worsened further by decreased intravascular volume reducing eGFR and glucose clearance, increasing glucose levels further.

132
Q

What is the M rule and what condition for?

A

PBC:
IgM
Anti mitochondrial antibodies
Middle aged females

133
Q

What are the indications for surgery in bronchiectasis>

A

Uncontrolled haemoptysis
Localised disease

134
Q

What are the classic electrolyte derangements seen in refeeding syndrome?
What ECG abnormality can they cause?

A

Hypophosphatasemia - classic sign
Hypokalemia
Hypomagnesemia

Torsade de pointes (potassium and magnesium, not phosphate)

135
Q

What blood component causes venous eczema?

A

Hemosiderin

136
Q

What are the two most common sites of infection in a patient with liver failure?

A

Abdomen- peritonitis secondary to ascites
Legs- cellulitis secondary to peripheral oedema

137
Q

What is an emergency complication of Scleroderma? How does it present?

A

Scleroderma renal crisis:
AKI
Hypertensive retinopathy
Hypertensive encephalopathy
Seizures
Pulmonary oedema

138
Q

What is the MoA of aminophylline?

A

Non-selective adenosine receptor antagonist and phosphodiesterase inhibitor

139
Q

What is the initial management of temporal arteritis? With and without vision involvement

A

With- IV methylprednisolone
Without- high dose prednisolone

140
Q

How does CKD lead to anaemia?

A

Reduction in erythropoietin levels (produced in the kidneys)

141
Q

What medication can cause nephrogenic diabetes insipidus?

A

Lithium

142
Q

What is a ‘salmon pink rash’ indicative of?

A

Still’s disease

143
Q

What is the classic presentation of primary biliary cholangitis?
What are some other signs and symptoms?

A

Itching in a middle aged woman
RUQ pain
Fatigue, jaundice
Hyperpigmentation
Hepatosplenomegaly
Xanthelasma

144
Q

What is the pathophysiology of PBC?

A

Autoimmune condition
Interlobular bile ducts become damaged by an inflammatory progress
Progresses to cholestasis
Can eventually lead to cirrhosis

145
Q

What conditions are associated with PBC?

A

Sjogrens - most commonly
RA
Systemic sclerosis
Thyroid disease

146
Q

How is PBC managed?

A

Ursodeoxycholic acid - first line
Cholestyramine for pruritus
Vitamin supplementation
Liver transplant if bilirubin > 100

147
Q

What are the complications of PBC?

A

Ascites, variceal haemorrhage
Osteomalacia and osteoporosis
Increased risk of hepatocellular carcinoma

148
Q

What is the pathophysiology of primary sclerosing cholangitis?

A

Mostly unknown
Inflammation and fibrosis of intra and extra hepatic bile ducts

149
Q

What conditions are associated with PSC?

A

UC - most common
Crohns
HIV

150
Q

What is the gold standard for diagnosis of PSC?

A

ERCP or MRCP
Show biliary strictures giving a beaded appearance

151
Q

What are the complications of PSC?

A

Cholangiocarcinoma
Increased risk of colorectal cancer

152
Q

What are the consequences of hypophosphataemia in refeeding syndrome?

A

Muscle weakness
Cardiac muscle= cardiac failure
Diaphragm= respiratory failure

153
Q

What is the pathophysiology of hypophosphataemia in refeeding syndrome?

A

Shift from fat to carbohydrate metabolism.
Activates insulin secretion.
Insulin and increased glucose uptake stimulate the movement of phosphate intracellularly.
Phosphate is in demand for anabolic processes to create ATP.
There are reduced stores of phosphate due to malnutrition.

154
Q

What patients are high risk for refeeding syndrome?

A

One of:
BMI <16
Weight loss >15% over 3-6 months
Little nutritional intake >10 days
HypoK/Mg/PO3 prior to feeding
Two of:
BMI <18.5
Weight loss >10% over 3-6 months
Little nutritional intake >5 days
Alcohol abuse, insulin use, chemo, diuretics, antacids

155
Q

What is melanosis coli associated with?

A

(bowel wall pigmentation) associated with laxative abuse

156
Q

What are the reversible and irreversible complications of haemachromatosis?

A

Reversible:
Cardiomyopathy
Skin pigmentation (bronze skin)
Irreversible:
Liver cirrhosis
DM
Hypogonadotrophic gonadism
Arthropathy

157
Q

What is the inheritance pattern of haemochromatosis?

A

Autosomal recessive

158
Q

What is the first line management of haemochromatosis?

A

Regular venesection to keep tranferrin saturation below 50%

159
Q

What is the inheritance pattern of Wilson’s disease?

A

Autosomal recessive

160
Q

What is the first line management for Wilson’s disease?

A

Penicillamine - chelates copper

161
Q

What renal and neurological complications can arise in Wilson’s disease?

A

Basal ganglia degeneration due to copper deposits. Causing speech, behavioural and psychiatric problems.
Renal- renal tubular acidosis

162
Q

What are the blood and urine investigation findings in Wilson’s disease?

A

Increased 24hr copper urinary excretion
Reduced serum caeruloplasmin
Reduced total serum copper

163
Q

What is Zollinger Ellison syndrome?

A

A condition characterised by excessive levels of gastrin secondary to a gastrin-secreting tumour
Causes peptic ulcers, diarrhoea and malabsorption

164
Q

Why is it important to know about giardiasis?

A

Parasite that causes gastroenteritis, diarrhoea and often lactose intolerance that can persist for months if left untreated (needs metronidazole)

165
Q

What is the tumour marker for hepatocellular carcinoma?

A

AFP

166
Q

What is the main risk factor for hepatocellular carcinoma?

A

Liver Cirrhosis

167
Q

What are the red flag features to enquire about in regards to IBS?

A

Rectal bleeding
Weight loss
FMH bowel or ovarian cancer
Onset over 60 y/o

168
Q

What 3 main symptoms should make you consider a diagnosis of IBS, and how long should they be present?

A

6 months of ABC
Abdo pain
Bloating
Change in bowel habit

169
Q

What is the pathophysiology of hepatorenal syndrome?

A

As a result of liver cirrhosis:
Splanchnic vasodilation reduces systemic vascular resistance, causing hypoperfusion in kidneys.
Juxtaglomerular apparatus then activates the renin-angiotensin-aldosterone system, causing renal vasoconstriction (which is not enough to counterbalance the effects of the splanchnic vasodilation)

170
Q

What is the difference in IBD on histology?

A

Crohns- full thickness inflammation. Increased goblet cells. Granulomas
UC- Inflam limited to submucosa. Crypt abscesses. Depletion of goblet cells. Granulomas less frequent.

171
Q

What is the first line management of hepatic encephalopathy?

A

Lactulose

172
Q

How is ascites (caused by portal hypertension) managed?

A

Fluid restriction and reducing dietary sodium
Aldosterone anatgonists e.g. spironolactone
Drainage if tense ascites
Prophylactic abx to reduce risk of SBP
TIPS may be considered

173
Q

What medication is used in prophylaxis of variceal haemorrhage?

A

Propanolol

174
Q

What medication is used to treat variceal haemorrhage

A

Terlipressin

175
Q

What is Budd Chiari syndrome?

A

Hepatic vein thrombosis

176
Q

What is the triad seen in Budd Chiari syndrome?

A

Sudden onset of:
Abdo pain
Ascites
Tender hepatomegaly

177
Q

What is the Child Pugh classification and what parameters does it consider?

A

Was used to assess severity of liver cirrhosis:
Bilirubin
Albumin
PTT
Encephalopathy
Ascites

178
Q

How is c.diff managed? (1,2,3rd line)

A

1- vancomycin PO 10 days
2- fidaxomicin PO
3- vanc PO +/- IV metronidazole

179
Q

How are pyogenic liver abscesses managed?

A

Percutaneous drainage and abx (amox+cipro+metro)

180
Q

What is the most common cause of an enlarged, pulsatile liver?

A

Right heart failure

181
Q

What are the first 2 medications to be given in status epilepticus? And doses?

A

Benzodiazepines -up to 2 doses, 5 mins apart. E.g. IV loraz 4mg, PR diaz 10mg.
Phenytoin 20mg/kg.

182
Q

What is the typical regime of haemodialysis?

A

4 hours/day, 3 days/week

183
Q

How does haemodialysis work?

A

Blood is taken out of the body and passed through the dialysis machine, along semipermeable membranes.
The concentration gradient between the blood and the dialysate fluid causes water and solutes to diffuse out of the blood and across the membrane.
Anticoagulation with citrate or heparin is necessary to prevent blood clotting in the machine and during the process.

184
Q

What are the complications of an AV fistula?

A

Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High output HF

185
Q

What are the two ways in which blood is accessed in patients receiving long term haemodialysis?

A

Tunnelled cuffed catheter
AV fistula

186
Q

How does peritoneal dialysis work?

A

A dialysis solution containing dextrose is added to the peritoneal cavity, causing ultrafiltration from the blood to occur, across the peritoneal membrane into the solution.

187
Q

What are the complications of peritoneal dialysis?

A

Bacterial peritonitis
Peritoneal sclerosis
Ultrafiltration failure
Weight gain
Psychosocial implications

188
Q

How is access to the peritoneal cavity gained in peritoneal dialysis?

A

Tenckhoff catheter

189
Q

What is the complication of suddenly dialysing a pt rather than gradually?

A

Disequilibrium syndrome - urea removal causes cerebral oedema

190
Q

What are the complications of renal transplant?

A

Rejection- hyper acute, acute, chronic
Failure
Electrolyte imbalances
From immunosuppressants:
IHD
T2DM (from steroids)
Infections
Non Hodgkins lymphoma
Skin cancer- SCC

191
Q

What infections are post renal transplant pts at risk of?

A

Secondary to immunosuppression:
Pneumocystis jiroveci pneumonia
Cytomegalovirus
TB

192
Q

What type of match do patient and donor kidneys need to have?

A

HLA type- human leucocyte antigen

193
Q

What is Stills disease?

A

A rare inflammatory arthritis with fevers, rash and arthralgia
Has a bimodal age distribution: 15-25 and 35-46 y/o

194
Q

What is the key difference in investigation findings of type 1 or type 4 renal tubular acidosis?

A

Type 1- hypokalaemia
Type 4- hyperkalaemia

195
Q

What is the pathophysiology of type 1 renal tubular acidosis?

A

Distal tubule cannot excrete hydrogen ions

196
Q

What can cause type 1 renal tubular acidosis?

A

Genetic
SLE
Sjogrens
PBC
Hyperthyroidism
Sickle cell anaemia
Marfan’s syndrome

197
Q

What is the pathophysiology of type 4 Renal Tubular Acidosis?

A

AKA hyperkalaemic RTA
Reduced aldosterone.
Causes insufficient potassium and hydrogren ion excretion.
Hyperkalaemia suppresses ammonia production, which normally buffers hydrogen ions in the distal tubules

198
Q

What are the causes of AF?

A

MI
IHD
Thyrotoxicosis
Rheumatic fever
Alcohol
Electrolyte disturbances
Sepsis/pneumonia

199
Q

What are the causes of type 4 Renal Tubular Acidosis?

A

Adrenal insufficiency
Diabetic nephropathy
Medications e.g. ACEi, spironolactone, eplerenone

200
Q

How is renal tubular acidosis treated?

A

Type 1- bicarb
Type 4- treat underlying. Fludrocortisone for aldosterone deficiency. Treat hyperkalaemia.

201
Q

What is the main complication in type 1 Renal Tubular Acidosis?

A

Nephrocalcinosis and renal stones

202
Q

What are the causes of hypoglycaemia?

A

DM
Exogenous insulin
Pituitary failure
Liver failure
Addison’s
Insulinoma
Neoplasm
Exogenous drugs - e.g. quinine for malaria

203
Q

What are the causes of hypercalcaemia?

A

Malignancy
Hyperparathyroidism
Vit D intoxication
Iatrogenic
Sarcoidosis
Dehydration

204
Q

What is the most common causative organism in peritionitis?

A

E.coli

205
Q

What are the most common causes of c.diff?

A

Recent abx treatment
-penicillin
-clindamycin
-ciprofloxacin
-meropenem

206
Q

What are the complications of c.diff?

A

Pseudomembranous colitis
Toxic megacolon
Systemic toxicity and SIRS

207
Q

How does hepatitis A typically present?

A

Flu like prodrome
Abdo pain
Tender hepatomegaly
Jaundice
Deranged LFTs
Can cause cholestasis

208
Q

What is the difference in prognosis in hepatitis A and C?

A

A is most likely to resolve.
C will most likely become chronic if not treated.

209
Q

What is the difference in transmission in hepatitis B and C?

A

B is through intercourse and vertical
C is the same plus IVDU

210
Q

What does the presence of HBsAg, E antigen, core antibodies, anti-HBs, HBsAb indicate?

A

HBsAg- Active infection
E antigen- Infectivity
Core antigen- Past infection
Anti-HBs/HBsAb- Immunity

211
Q

How is malaria diagnosed?

A

Malaria blood film is done with a FBC blood bottle- parasites will be present
3 samples are taken over 3 consecutive days before Malaria can be excluded

212
Q

How is malaria spread?

A

Female anopheles mosquitos

213
Q

What is the most common type of malaria?

A

Plasmodium falciparum

214
Q

What is the characteristic fever caused by malaria?

A

Spikes every 48 hours as the RBC rupture and release merozites- tertian malaria

215
Q

What are the complications of malaria?

A

Cerebral malaria
Seizures
AKI
Pulmonary oedema
DIC
Haemolytic anaemia
Multi organ failure

216
Q

What are the options for treatment or prophylaxis of someone at risk of complications of influenza?

A

Oral oseltamivir
Inhaled zanamivir

217
Q

What is the most common causative organism of UTI?

A

E.coli - gram neg, anaerobic, rod shaped

218
Q

What are the two initial abx therapy for UTI, and what are their cautions?

A

Nitrofurantoin - unless eGFR<45
Trimethoprim - bacterial resistance

219
Q

What is infective endocarditis?

A

Infection of the endothelium of the heart
Commonly affects the heart valves

220
Q

What are the risk factors for infective endocarditis?

A

IVDU
Structural heart pathology
CKD- esp on dialysis
Immunocompromised
PMH of infective endocarditis

221
Q

What is the most common causative organism of IE?

A

Staph aureus

222
Q

What are the key examinations in infective endocarditis?

A

New heart murmur
Splinter haemorrhages
Petechiae
Janeway lesions
Osler’s nodes
Roth spots

223
Q

Osler’s nodes vs Janeway lesions?

A

Osler’s- painful. pads of fingers and toes
(Immunological phenomenon)
Janeway- painless. palms of hands and soles of feet
(Vascular phenomenon)

224
Q

What blood test is important in IE?

A

Blood cultures- three samples from different sites, taken 6 hours apart ideally

225
Q

What is the initial imaging done in suspected IE?

A

Transoesophageal echo

226
Q

Briefly, what is the modified Duke criteria? What score gives a diagnosis

A

Used to diagnose IE
One major plus 3 minor, or
Five minor criteria

227
Q

What are the different criteria in Duke’s criteria?

A

Major:
+ve blood cultures (consistently)
Imaging +ve e.g. vegetations
Minor:
Risk factors e.g. IVDU
Fever
Vascular phenomena e.g. janeway
Immunological phenomena e.g. Osler’s
Microbiological phenomena

228
Q

How long are abx given in IE?

A

4 weeks
(6 if prosthetic valve)

229
Q

When is surgery needed in IE?

A

HF relating to valve pathology
Large vegetations or abscesses
Infection not responding to abx

230
Q

What are the complications of IE?

A

Heart valve damage = regurg
HF
Emboli -abscesses, strokes, splenic infarcts
Glomerulonephritis

231
Q

What medication can reduce awareness of hypoglycaemia?

A

B blockers

232
Q

What are the possible ECG changes seen in STEMI?

A

ST segment elevation
New LBBB

233
Q

What are the possible ECG changes seen in NSTEMI?

A

ST segment depression
T wave inversion

234
Q

What are pathological Q waves indicative of?

A

Deep infarction affecting full thickness of heart muscle
Appear 6 or more hours after onset of symptoms

235
Q

What is the initial A-E management of ACS?

A

Morphine
Oxygen
Nitrate - GTN
Aspirin 300mg

236
Q

What are the more definitive management options of STEMI and when are they done?

A

PCI within 2 hours. Preceded by prasugrel with aspirin.
Thrombolysis within 12 hours (streptokinase, alteplase etc) plus antithrombin at same time e.g. fondaparinux

(If bleeding risk, instead of prasugrel or ticagrelor, give clopidogrel)

237
Q

What is the medical management of NSTEMI?

A

If GRACE score indicates medium or high risk, do angiography and PCI. Preceded by prasugrel and aspirin.
Aspirin 300mg and Ticagrelor 180mg stat
Fondaparinux
Morphine and GTN

(If bleeding risk, instead of prasugrel or ticagrelor, give clopidogrel)

238
Q

What is the secondary prevention following ACS?

A

Aspirin
Antiplatelet- ticagrelor or clopidogrel
Atorvastatin
ACEi
Atenolol- B blocker
Aldosterone antag if HF- eplerenone

239
Q

What are the complications of an MI?

A

DREAD
Death
Rupture of septum or papillary muscles
Oedema
Arrhythmia and aneurysm
Dressler’s syndrome

240
Q

What are the causes of pericarditis?

A

Idiopathic
Infection- TB, HIV, EBV
Autoimmune e.g. SLE, RA
Injury e.g. MI or surgery
Uraemia
Cancer
Medications e.g. methotrexate

241
Q

What are the two key presenting feature of pericarditis?

A

Chest pain and low grade fever
Pain is sharp, central, pleuritic and worse lying down

242
Q

What is the key examination finding of pericarditis?

A

Pericardial friction rub on auscultation

243
Q

What does a saddle shaped ST depression indicate? What other signs may be present on ECG?

A

Pericarditis
PR depression

244
Q

How is pericarditis managed?

A

NSAIDs are mainstay
Colchicine long term reduces recurrence

245
Q

What is the pathophysiology of HOCM?

A

Hypertrophic cardiomyopathy
Defect in genes for sarcomere proteins, causing: a disorder of the heart in which the LV becomes hypertrophic, usually asymmetrically affecting the septum of the heart, blocking the outflow of the LV

246
Q

What is the inheritance pattern of HOCM?

A

Autosomal dominant

247
Q

What signs o/e indicate HOCM?

A

Ejection systolic murmur at left lower sternal border
Fourth HS
Thrill at left lower sternal border

248
Q

What are the possible complications in HOCM?

A

Arrythmias e.g AF
Mitral regurg
HF
Sudden cardiac death

249
Q

What is Addison’s disease?

A

When the adrenal glands have been damaged causing primary adrenal insufficiency

250
Q

What is the most common cause of addisons disease?

A

Autoimmune

251
Q

What can cause secondary adrenal insufficiency?

A

Inadequate ACTH:
Pituitary adenomas
Surgery to pituitary
Radiotherapy
Sheehan’s syndrome: PPH = avascular necrosis of pituitary gland
Trauma

252
Q

What is the most common cause of tertiary adrenal insufficiency?

A

Long term oral steroid use suppresses hypothalamus

253
Q

What are the signs of adrenal insufficiency?

A

Bronze hyperpigmentation
Hypotension

254
Q

What is the key biochemical finding in adrenal insufficiency?

A

Hyponatraemia

255
Q

What test is used to diagnose adrenal insufficiency? And then to differentiate primary from secondary?

A

Short synacthen test:
Give synthetic ACTH
Check blood cortisol before and after
It should at least double

Long synacthen test used to be the test, however can now check ACTH level (high in primary or low in secondary)

256
Q

How is Addisonian crisis managed?

A

A-E
IM or IV hydrocortisone 100mg stat, followed by infusion or 6hrly doses
IV fluids
Correct hypoglycaemia with dextrose
Monitor U&Es

257
Q

What can cause an Addisonian crisis?

A

Sudden cessation of steroids
In established adrenal insufficiency:
Infection
Trauma

258
Q

What are the features of Cushing’s syndrome?

A

Round face (known as a “moon face”)
Central obesity
Abdominal striae (stretch marks)
Enlarged fat pad on the upper back (known as a “buffalo hump”)
Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms)
Male pattern facial hair in women (hirsutism)
Easy bruising and poor skin healing
Hyperpigmentation of the skin in patients with Cushing’s disease (due to high ACTH levels)

259
Q

What are the metabolic complications of cushings?

A

HTN
Cardiac hypertrophy
T2DM
Dyslipidaemia
Osteoporosis

260
Q

What are the causes of Cushing’s syndrome?

A

(CAPE)
Cushing’s disease- pituitary adenoma
Adrenal adenoma
Paraneoplastic syndrome
Exogenous steroids

261
Q

What test is done to diagnose Cushing’s? And to determine cause?

A

Dexamethasone Suppression Tests: (to exclude, diagnose and determine cause)

Low dose 48 hr test-
Giving dex should suppress the cortisol, so a normal cortisol is diagnostic.

High dose 48 hr test-
The dex will suppress cortisol if cause is a pituitary adenoma.

262
Q

How does PTH increase serum calcium?

A

Increase osteoclast activity
Increase calcium reabsorption in the kidneys
Increase vit D activity, for more calcium absorption in the intestines

263
Q

What medications can cause drug induced interstitial nephritis?

A

Commonly- penicillin
Diuretics e.g. furosemide
NSAIDs

264
Q

Acute renal failure associated with fever, arthralgia, rash and eosinophils in blood and urine, is characteristic of what condition?

A

Drug-induced interstitial nephritis

265
Q

What are the indications for LTOT in COPD pts?

A

PaO2 <7.3kPa on 2 readings more than 2 weeks apart
Or PaO2 7.3-8 and one of:
-nocturnal hypoxia
-polycythaemia
-peripheral oedema
-pulmonary HTN

266
Q

What bloods, aside from routine, are involved in a confusion screen?

A

Vit B12/folate
Bone profile
Glucose
TFTs

267
Q

What can cause a metabolic acidosis with raised anion gap?

A

Excess production of acids:
DKA, lactic acidosis
Ingestion of acids:
Methanol, ethanol, ethylene glycol
Inability to clear acids:
Renal failure

268
Q

What can cause a metabolic acidosis with normal or decreased anion gap?

A

Loss of bicarbonate:
From GI- diarrhoea
From kidneys- renal tubular acidosis

269
Q

What is a typical picture of aspirin overdose?

A

Initial mild respiratory alkalosis.
Suddenly developing metabolic acidosis.
Complaints of: tinnitus, N+V, epigastric pain, sweating

270
Q

What is measured in suspected aspirin overdose?

A

Plasma salicylate concentration

271
Q

How is an overdose of b blockers managed?

A

Glucagon
Replace calcium if needed

272
Q

What is the antidote to organophsophate poisoning?

A

Atropine

273
Q

What is the antidote to ethylene glycol poisoning?

A

Ethanol
(Fomepizole first line)

274
Q

What is the antidote to benzodiazepine poisoning?

A

Flumazenil

275
Q

What is the criteria for CT head within 1 hour in an adult with hx of trauma?

A

GCS 12 or less on initial assessment
GCS less than 15, 2 hours after event
Suspected skull fracture
Seizure post trauma
Focal neurological deficit
More than on episode of vomiting

276
Q

What is the criteria for CT head within 8 hours in an adult with hx of trauma?

A

Age 65 or over
Current bleeding or clotting disorders
Dangerous mechanism of injury
More than 30 minutes retrograde amnesia of the events immediately before the head injury

277
Q

What are the adverse features that might indicate synchronised DC shock in arrhythmias?

A

HISS
Heart failure
Ischaemia
Shock
Syncope

278
Q

How is torsade de pointes managed in a stable pt, and in an unstable one?

A

Stable- IV magnesium sulphate
Unstable- DC cardioversion

279
Q

What is a c/i to adenosine use?

A

Asthma - can cause bronchospasm

280
Q

What is the initial management of DKA - be specific

A

1L NaCl 0.9% over 1 hour
Then, fixed rate insulin at 0.1 units/kg/hr
Monitor potassium for depletion

281
Q

What is the antibody present in antiphospholipid syndrome?

A

Anti cardiolipin antibodies

282
Q

What is the abnormality on clotting profile, in antiphospholipid syndrome?

A

Prolonged APTT

283
Q

What is high output HF and what can cause it?

A

Normal heart but unable to meet metabolic needs

Anaemia
Thyrotoxicosis
Pregnancy
Paget’s disease

284
Q

What are some causes of HF with preserved ejection fraction?

A

HOCM
Cardiac tamponade

285
Q

What may be seen on an ECG after discharge for an MI?

A

Pathological Q wave
Inverted T wave

286
Q

What may be seen on ophthalmoscopy in a pt with infective endocarditis?

A

Roth spot

287
Q

What are signs of pulmonary fibrosis of CXR?

A

Reticulonodular shadowing
Reduced lung volume
Honeycombing - advance disease

288
Q

What are the causes of bilateral perihilar lymphadenopathy?

A

Sarcoidosis
Lymphoma
TB
Bronchial carcinoma

289
Q

What are the complications of pneumonia?

A

Sepsis
Abscess
AF
Pleural effusion
Resp failure
Empyema

290
Q

What can cause bronchial breathing?

A

Pleural effusion at level of alveoli
Pneumonia
Empyema

291
Q

What are the risk factors for obstructive sleep apnoea?

A

Obesity
Enlarged tonsils
Enlarged adenoids
Nasal polyps
Alcohol

292
Q

What are the causes of rhabdomyolysis?

A

Prolonged immobility
Excessive exercise
Crush injury
Burns
Seizures
Neuroleptic malignant syndrome
Disorders of muscle e.g. Duchenne’s

293
Q

What are the complications of nephrotic syndrome?

A

Susceptible to infections W
Inc risk of VTE
Hyperlipidaemia

294
Q

What is the most common cause of nephrotic syndrome in adults?

A

Membranous glomerulonephropathy

295
Q

What is the pathophysiology of DKA?

A

Uncontrolled lipolysis which results in an excess of free fatty acids that are ultimately converted to ketone bodies

Finals (8 decks)

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