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Phase 2 > General Medicine > Flashcards

General Medicine Flashcards

1
Q

What diseases does Raynaud’s present in?

A

SLE
Poly myosotis
Dermatologists

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2
Q

What diseases are associated with ankylosing spondylitis?

A

Crohn’s

Ulcerative colitis

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3
Q

What are the differentials for a monoarthritis?

A

Septic
Crystal
OA
Trauma

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4
Q

Which conditions can cause an asymmetrical arthritis?

A

Reactive

Psoriatic

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5
Q

When should you aspirate a joint?

A

Any monoarthritis

Apart from inflamed/potentially infected skin e.g. Psoriatic plaque

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6
Q

How does a diagnosis of RA affect lifespan?

A

Women - 7y decrease

Men - 4y decrease

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7
Q

Why is RA associated with a decreased lifespan?

A

Cardiovascular risk
Infections
Lymphoma

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8
Q

What is the genetic link of RA?

A

Increased incidence in 1st degree relatives

Polymorphism of HLA Class II genes

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9
Q

How does RA lead to inflammatory arthritis?

A

Immune response triggers inflammation
Local production of inflammatory cytokines (esp. TNF-alpha and IL-1) causes amplification of inflammation
Synovial tissue proliferates and erodes the joint causing pannus formation
Activated macrophages in pannus produce collagenases & proteinases
Cartilage is eroded and this leads to joint instability and deformity

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10
Q

In what order are joints commonly affected in RA?

A

Small joints first - hands and feet

Larger joints later

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11
Q

What does the presence of rheumatoid nodules indicate?

A

Severe arthritis and risk of extra-articulate disease

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12
Q

What are the X-Ray features of RA?

A

Symmetrical. Spares DIPJs
Early: soft tissue swelling and osteopenia
Strophic bone erosions - peri articulate bare areas
Later: joint space narrowing

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13
Q

What is the imaging method of choice in early arthritis?

A

Ultrasound or MRI

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14
Q

What is DAS in RA?

A

Disease Activity Score

Incorporates ESR/CRP, counts of swollen/tender joints, fatigue, radio graphic findings and limitation of function

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15
Q

What are the diagnostic criteria for RA?

A 
Need at least 4 of...
Morning stiffness
Arthritis of 3 or more joints
Arthritis of hand joints
Symmetrical
Rheumatoid nodules
Serum Rheumatoid Factor
Radiographic changes
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16
Q

What is Rheumatoid Factor?

A

Antibody directed against IgG

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17
Q

What is anti-CCP?

A

Antibody, binds to CCPs in synovial and has a pathogenic role

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18
Q

What are the principles of management of RA?

A

Symptomatic relief
Modification of underlying disease
Adjunctive therapy with steroids (flare-ups)
Biological agents

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19
Q

What are the indications for DMARD use?

A

Persistent/progressive disease despite regular NSAIDs

Erosive disease on X-Ray

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20
Q

How long do DMARDs take to work?

A

2-3 months

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21
Q

What is the range of doses of methotrexate?

A

7.5 - 25mg per week

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22
Q

What are the side effects of methotrexate?

A 
Myelosuppression
Pneumonitis
Pulmonary fibrosis
Mucositis
Diarrhoea, nausea, vomiting
Hepatotoxicicity
Teratogenic
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23
Q

What is the diagnosis when TSH is raised but T4 is low?

A

Hypothyroidism

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24
Q

What is the differential when TSH and T4 are both raised?

A

Thyroid-secreting tumour

Thyroid hormone resistance

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25
Q

What is the diagnosis when TSH is low but T4 & T3 are both normal?

A

Sub clinical hyperthyroidism

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26
Q

What is sick euthyroidism?

A

Thyroid tests may be abnormal

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27
Q

What monitoring is required with methotrexate?

A

Regular FBC, LFT, UEs and creatinine

Baseline CXR

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28
Q

What are the effects of sulfasalazine on T cells?

A

Inhibits proliferation

Inhibits IL-2 production

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29
Q

What are the effects of sulfasalazine on neutrophils?

A

Reduced chemotaxis and degranulation

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30
Q

What are the side effects of sulfasalazine?

A 
Nausea
Headache
Dizziness
Rash
Infrequent: myelosuppression and heptatoxicity
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31
Q

Which DMARDs are safe in pregnancy?

A

Sulfasalazine

Hydroxychloroquine

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32
Q

What conditions is hydroxychloroquine used to treat?

A

RA and SLE

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33
Q

What is hydroxychloroquine?

A

Anti-malarial

Inhibits toll-like receptors to reduce inflammation

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34
Q

What are the side effects of azathioprine?

A

Myelosuppression
Infrequent hepatotoxicity
Flu-like illness at onset of therapy

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35
Q

Name 2 anti-TNF agents

A

Infliximab

Etanercept

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36
Q

Name an anti B cell agent

A

Rituximab

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37
Q

Which patients are currently eligible for treatment with biological agents?

A

Clinically active RA
Failure of standard therapy with at least 2 DMARDs

Withdrawn if ADR or no response at 6 months

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38
Q

How does psoriatic arthritis present?

A

Asymmetrical large joint oligoarthritis

Skin lesions/psoriatic nail changes
Dactylitis

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39
Q

How is the Achilles affected in psoriatic arthritis?

A

Enthesitis seen on USS or MRI

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40
Q

How is psoriatic arthritis managed?

A

NSAIDs
Physio/OT
Dermatologists - methotrexate may be helpful when skin is badly affected
Anti-TNF

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41
Q

What is the epidemiology of ankylosing spondylitis?

A

Typically

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42
Q

How does ankylosing spondylitis present?

A

Low back pain & stiffness, improved with exercise and not relieved by rest
SIJ tenderness
Fatigue, weight loss & low grade fever

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43
Q

What are the key investigations for ankylosing spondylitis?

A

CRP/ESR - raised in half of patients
HLA B27 - Not a screening test as 8% all British makes carry it. Only 20% of those with B27 have ank spond

MRI, CT or x-Ray affected area

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44
Q

How is ankylosing spondylitis managed?

A

Exercise and physio
NSAIDs
DMARDs if peripheral synovitis

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45
Q

What are the types of diabetic retinopathy?

A

Macular
Pre-proliferation
Proliferative

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46
Q

What is a reactive arthritis?

A

An aseptic inflammatory arthritis

Precipitated by a distant infection

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47
Q

What infections commonly cause reactive arthritis?

A 
Non-bonobo cal urethritis/cervicitis
Acute diarrhoea
Chlamydia trachomatis
Campylobacter
Salmonella
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48
Q

What is Reiter’s syndrome?

A

Classic triad…
Urethritis
Conjunctivitis
Arthropathy

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49
Q

How do you manage reactive arthritis?

A

Bed rest
Intra-articulate steroids
NSAIDs

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50
Q

Define osteoporosis

A

Quantitative decrease in bone matrix components

I.e. Too little bone, but what there is is normal

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51
Q

What are the risk factors for osteoporosis?

A 
Smoking
Alcohol
Steroid use
Sedentary lifestyle
Family history
Lean body type
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52
Q

What endocrine disorders cause osteoporosis?

A 
Gonadal insufficiency
Hyperparathyroidism
Hyperthyroidism
T1DM
Crushing's
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53
Q

What GI disease can cause osteoporosis?

A 
IBD
Chronic liver disease
Eating disorders
Coeliac disease
Malabsorption
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54
Q

When is bone protection required with steroids?

A

Prednisolone >5mg daily for >3 months

& either over 65 or T score

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55
Q

What are the indications for DEXA scanning?

A

Predict fracture risk
Confirm diagnosis of osteoporosis where there is evidence of osteopenia on radiographs
Planned steroid use >5mg for >3 months and age >65

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56
Q

What is the T score?

A

Number of standard deviations away from the mean of a young person of the same gender and ethnicity

Measures risk of future fractures

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57
Q

How is the T score used to define osteoporosis?

A
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58
Q

What is the Z score?

A

Number of standard deviations away from an age, gender and weight-matched population

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59
Q

What is the FRAX tool?

A

Gives probability of hip/major osteoporotic fractures integrating clinical factors and Bone mineral density

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60
Q

What is the action of bisphosphonates?

A

Reduce osteoclasts function and ultimately cause their apoptosis

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61
Q

What is Fosamax?

A

Alendronate (bisphosphonate)

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62
Q

How can you pharmacologically stimulate bone formation?

A

Give synthetic PTH analogue e.g. Teriparatide

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63
Q

What is the most common cause of osteomalacia in the UK?

A

Calcium or Vitamin D deficiency

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64
Q

What are the causes of calcium and vitamin D deficiency?

A

Dietary
Poor sun exposure
Gastrectomy
Malabsorption

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65
Q

What are the biochemistry results like for someone with osteomalacia?

A 
Low phosphate
Low calcium
Raised alk phos
Low vit D
High PTH
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66
Q

What is responsible for Gout?

A

Monosodium urate monohydrate crystals

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67
Q

How does urate affect gout?

A

Hyperuricaemia increases risk of attacks

Normal urate levels during an attack don’t exclude gout

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68
Q

What are the risk factors for gout?

A 
Family history
Excess alcohol
Diuretics
Renal disease
Ciclosporin and tacrolimus
Chemotherapy for malignancy
Diet
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69
Q

What joints does gout commonly affect?

A 
MTPJs
Mid foot
Ankles
Knees
Olecranon bursa
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70
Q

What are the diagnostic criteria for gout?

A 
At least 2 of...
Typical history
Tophi
Raised serum urate
Crystals in joint during attack
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71
Q

What do urate crystals look like?

A

Needle-shaped

Strongly negatively birefringent

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72
Q

What are the X-Ray features of gout?

A

Soft tissue swelling

Opacities due to Tophi

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73
Q

How do you treat acute attacks of gout?

A

NSAIDs
Colchicine - reduces neutrophil chemotaxis
Corticosteroids

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74
Q

What are the indications for prophylaxis of attacks in gout?

A

2-3 acute episodes per year
Tophi and erosions present
Renal impairment/stones

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75
Q

What is used as prophylaxis in gout?

A

Allopurinol

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76
Q

What is the mechanism of action of allopurinol?

A

Xanthippe oxidase inhibitor - prevents conversion of purine to uric acid

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77
Q

What is responsible for pseudogout?

A

Calcium pyrophosphate dehydrate

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78
Q

What areas are commonly affected in pseudogout?

A

Knees
Wrists
Shoulders
Hips

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79
Q

How do you manage pseudogout?

A 
Aspiration
Injection
NSAIDs
Colchicine
No prophylaxis
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80
Q

What comprises mixed connective tissue disease?

A

Systemic sclerosis & SLE & vascular disease

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81
Q

What does systemic sclerosis consist of?

A

Scleroderma (skin fibrosis) & vascular disease

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82
Q

What is CREST syndrome?

A 
Calcinosis
Raynaud's
oEsophageal & gut dysmotility
Sclerodactyly
Telangiectasia
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83
Q

What is diffuse cutaneous systemic sclerosis?

A

Whole body may be involved
Organ fibrosis occurs early
Lots of skin fibrosis

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84
Q

How do you manage systemic sclerosis?

A

No cure
Immunosuppression if there is organ involvement or progressive skin disease
Control BP
Monitor renal function

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85
Q

What is Sjögren’s syndrome?

A

Inflammation and fibrosis of exocrine glands

Affects tear production, salivation plus other systemic features

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86
Q

What are the systemic features of Sjögren’s syndrome?

A 
Polyarthritis
Raynaud's
Lymphadenopathy
Vasculitis
Lung, liver and kidney involvement
Peripheral neuropathy
Myosotis
Fatigue
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87
Q

What are the signs of dermatomyositis?

A 
Macular rash
Heliotrope rash
Nail fold erythema
Gottron's papules on knuckles and elbows
Subcutaneous calcification
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88
Q

How does polymyositis present?

A

Progressive symmetrical proximal muscle weakness
Myalgia & arthralgia
Can lead to dysphagia, dysphonia or resp muscle weakness

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89
Q

How does SLE typically present?

A

Non-specific: malaise, fatigue, myalgia and fever

Can mimic other systemic diseases

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90
Q

What parameters are used to monitor SLE disease activity?

A

Anti-dsDNA titres
Decreased C3 and C4
ESR raised (CRP normal in SLE)

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91
Q

How do you diagnose fibromyalgia?

A

Pain >3 months, both left and right sides occurring above and below the waist

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92
Q

What are the symptoms of giant cell arteritis?

A 
Headache
Temporal artery and scalp tenderness
Jaw claudication
Amaurosis fugax
Sudden blindness
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93
Q

What is the treatment for GCA?

A

Mostly steroids - start immediately if GCA suspected to prevent irreversible blindness

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94
Q

What is Wegener’s granulomatosis?

A

Granulomatosis with polyangitis

Vasculitis of small/medium sized vessels

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95
Q

In what disease are anti-Jo antibodies found?

A

Polymyositis

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96
Q

What disease is found in 50% of patients with GCA?

A

Polymyalgia rheumatica

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97
Q

What are the features of Polymyalgia rheumatica?

A

> 50y
Shoulders and proximal limb muscles: aching, tenderness, morning stiffness
NO weakness
Fever, weight loss, fatigue, anorexia and depression

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98
Q

What are the blood results like in PMR?

A

Raised CRP and ESR

CK levels normal

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99
Q

What are the 5Rs of IV fluid therapy?

A 
Resuscitation
Routine maintenance
Replacement
Redistribution
Reassessment
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100
Q

What is fluid resuscitation?

A

Fluids given urgently to restore circulation in hypovolaemia or fluid and electrolyte loss

E.g. Bleeding, dehydration, sepsis

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101
Q

When if IV fluid used for routine maintenance?

A

When patients can’t take fluids orally or enterally but have no deficits or ongoing losses

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102
Q

When is fluid replacement needed?

A

Not urgent but required on top of routine maintenance to correct losses or meet abnormal ongoing losses

E.g. GI losses, fever, burns

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103
Q

When is IV fluid required for redistribution?

A

When there are marked internal distribution changes or abnormal fluid handling

E.g. Sepsis, post-op, cardiac, liver or renal comorbidity

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104
Q

What proportion of body weight is water?

A

60%

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105
Q

How is total body water affected by obesity?

A

Lower % of body weight is water as adipose contains less water than lean tissue

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106
Q

How is body fluid divided between intra- and extra cellular compartments?

A

One thirds extracellular

Two thirds intracellular

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107
Q

What ions are mainly responsible for ECF osmolality?

A

Sodium
Chloride
Bicarbonate

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108
Q

What proportion of the ECF is intravascular?

A

A quarter

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109
Q

What is the intravascular volume dependent on?

A

Plasma on comic pressure - mainly due to albumin

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110
Q

What is the normal range for plasma albumin?

A

35-52g/L

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111
Q

What is the starling effect?

A

Hydrostatic pressure in capillaries drives fluid out

Oncotic pressure of plasma proteins draws fluid back in

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112
Q

What is the internal fluid balance?

A

Constant flow of fluid and electrolytes between the ECF and the GI tract

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113
Q

How much water is required per kg per day?

A

25 ml / kg / day

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114
Q

What is the physiological osmolality of plasma?

A

280 - 290 mOsm/kg

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115
Q

What is the volume obligatoire?

A

The minimum amount of urine needed to excrete waste products

About 500ml

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116
Q

How much does ECF need to be expanded by before oedema becomes an issue?

A

2 - 3 L

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117
Q

What is the urine : plasma urea ratio?

A

Osmolality ratio

Measure of the concentrating capacity of the kidney, in the presence of a water deficit

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118
Q

What is the normal range for plasma potassium?

A

3.5 - 5.3 mmol/L

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119
Q

How does hypokalaemia lead to further electrolyte disturbances?

A

Renal H+ reabsorption impaired to increase K+
Causes alkalosis
Decreased ability to excrete Na+ causes hypernatraemia

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120
Q

How is ADH affected by disease?

A

Levels increased

Retention of water

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121
Q

How much sodium is in normal saline?

A

154mmol/L

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122
Q

By what proportion does normal saline expand blood volume?

A

A quarter to a third

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123
Q

What are glucose solutions useful for doing?

A

Providing free water as it is distributed throughout total body water

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124
Q

What is the risk with giving too much glucose solution?

A

Hyponatraemia if too much given too quickly

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125
Q

Name a commonly used synthetic colloid

A

Hydroxymethyl starch (HES)

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126
Q

How do you give fluid resuscitation?

A

Rapid infusion (in less than 15mins) of 500ml boluses

Repeat as necessary until markers of volume status improve

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127
Q

How much glucose is used for routine maintenance?

A

50-100g per day

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128
Q

Who should you prescribe 20-25ml/kg/day fluid to?

A

Elderly/frail
Renal impairment/cardiac failure
Malnourished - at risk of referring syndrome

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129
Q

How do you assess fluid status clinically?

A 
Blood pressure
Fluid balance chart
Peripheral/pulmonary oedema
CRT
Skin turgor
Heart rate
Resp rate
Mucous membranes
UEs
JVP
Thirst
EWS
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130
Q

What are the indications for fluid resuscitation?

A

Systolic 90
Cap refill >2s
RR >20
EWS >5

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131
Q

How should you calculate fluid requirements for an obese patient?

A

Based on their ideal weight not their actual weight

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132
Q

How should you aim to increase sodium in a hyponatraemic patient?

A

No more than 3-5mmol/day

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133
Q

What is the normal range for blood glucose?

A

3.3 - 6 mmol/L

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134
Q

What is melaena?

A

Passage of black, tarry, foul-smelling stools

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135
Q

What is haematochezia?

A

Blood in the stools

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136
Q

What are the causes of pale stools?

A

Hepatitis
Gallbladder disorders
Malabsorption conditions

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137
Q

What is steatorrhea?

A

Fatty stool
Sticky and difficult to flush

Malabsorption syndromes

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138
Q

How should you investigate iron deficiency anaemia?

A

1st colonoscopy - more sinister potential causes

Upper GI endoscopy next if nothing found

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139
Q

What are the indications for an abdominal X-ray?

A

Acute abdominal pain
Small or large bowel obstruction
Acute exacerbation of IBD
Renal colic

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140
Q

What diameters show bowel obstruction?

A

Small bowel >3cm
Large bowel >6cm
Caecum >9cm

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141
Q

What is the difference between Haustra and valvulae conniventes?

A

Haustra are in the large bowel and only go part way across the wall

VCs are small bowel and go all the way across the wall

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142
Q

What is the main cause of small bowel obstruction?

A

Adhesions

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143
Q

What is the main cause of large bowel obstruction?

A

Colorectal cancer

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144
Q

How do you tell if the ileocaecal valve is competent on AXR and why is it significant?

A

If there is gas in the small bowel as well when the large bowel is obstructed

Perforation more likely if valve is competent: pressure higher in the large bowel if gas can’t flow back into the small bowel too

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145
Q

What is the coffee bean sign on abdominal X-ray?

A

Sigmoid volvulus starting in left iliac fossa and extending towards the right upper quadrant

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146
Q

What is the main indication for AXR in inflammatory bowel disease?

A

Suspected toxic mega colon

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147
Q

What is lead-pipe colon?

A

Chronic ulcerative colitis leading to loss of normal architecture

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148
Q

What is thumb-printing on abdominal X-ray?

A

Really thick haustra

Can result from anything causing oedema of the colon, but is classic of IBD

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149
Q

What is the flaciform ligament sign?

A

Indicates perforation - you only ever see the flaciform ligament when there’s gas either side of it

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150
Q

How many calories are there in 1g of protein?

A

4kcal

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151
Q

How many calories are there in 1g of carbohydrate?

A

4kcal

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152
Q

How many calories are there in 1g of fat?

A

9kcal

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153
Q

What is the daily calorie requirement per kg?

A

25kcal per kg

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154
Q

What does vitamin A deficiency lead to?

A

Blindness - vit A needed for retina

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155
Q

What is vitamin C needed for?

A

Immune system

Collagen synthesis

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156
Q

What is vitamin D needed for?

A

Calcium absorption

Bones

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157
Q

How does starvation cause malnutrition?

A

Hormone levels drop and lipase levels rise

Burn fat for energy - so lose fat

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158
Q

How does illness cause weight loss?

A

No time to adjust and increase lipase levels
All glucose and glycogen used first
Muscle broken down to provide glucose
So you lose muscles

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159
Q

What are the daily fluid requirements for an average person?

A

25 ml/kg/day

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160
Q

What does TPN provide?

A

Macro and micronutrients
Minerals
Fluid

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161
Q

How many calories does 1unit of alcohol provide?

A

56kcal

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162
Q

What are the causes of scurvy?

A

Vitamin C deficiency

Poor, pregnancy or strange diet

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163
Q

What are the signs of scurvy?

A 
Anorexia & cachexia
Gingivitis
Loose teeth
Smelly breath
Bleeding from gums, nose, hair follicles
Muscle pain and weakness
Oedema
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164
Q

What is Beriberi disease?

A

Vitamin B1 / thiamine deficiency

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165
Q

How do you treat beriberi?

A

Give thiamine urgently

May lead to wernicke’s encephalopathy

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166
Q

What is pellagra disease?

A

Lack of nicotinic acid

Triad: diarrhoea, dementia, dermatitis

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167
Q

What is xerophthalmia?

A

Vitamin A deficiency

Dry conjunctivae
Corneas cloudy and soft

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168
Q

How does malabsorption present?

A 
Diarrhoea
Weight loss
Lethargy
Steatorrhea
Bloating
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169
Q

What are the main causes of malabsorption in the UK?

A

Coeliac disease
Chronic pancreatitis
Crohn’s disease

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170
Q

What is the prevalence of coeliac disease?

A

1 in 300-1500

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171
Q

What is the pathophysiology of coeliac disease?

A

T-cell mediated autoimmune
Affects small bowel
Prolamin intolerance

Causes villous atrophy and malabsorption

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172
Q

When are the peaks in incidence of coeliac disease?

A

Infancy

50-60y

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173
Q

How do you diagnose coeliac disease?

A

Low Hb, B12 and ferritin

Antibodies: alpha-gliadin, transglutaminase, anti-endomysial

Duodenal biopsy

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174
Q

What are the complications of coeliac disease?

A 
Anaemia
Lactose intolerance
GI T-cell lymphoma
Increased risk of malignancy
Myopathies/neuropathies
Hyposplenism
Osteoporosis
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175
Q

What are the causes of chronic pancreatitis?

A 
Alcohol
Haemochromatosis
Pancreatic duct obstruction
Hyperparathyroidism
Congenital
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176
Q

How does chronic pancreatitis present?

A 
Epigastric pain radiating to back
Relieved by sitting forward or hot water bottles
Bloating
Steatorrhea
Weight loss
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177
Q

What is the medical management of chronic pancreatitis?

A 
Analgesia
Lipase
Creon (enzymes)
Fat-soluble vitamins
? Insulin requirements

Diet: no alcohol and low fat

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178
Q

When is surgery indicated for chronic pancreatitis?

A

Unremitting pain
Narcotic abuse
Weight loss

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179
Q

What are the complications of chronic pancreatitis?

A 
Pseudocyst
Diabetes
Biliary obstruction
Aneurysm
Splenic vein thrombosis
Gastric varices
Pancreatic carcinoma
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180
Q

What is the most common cause of upper GI bleeding?

A

Peptic ulcer disease

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181
Q

What are the common causes of upper GI bleeding?

A 
Peptic ulcer disease
Gastroduodenal erosions
Oesophagitis
M-W tear
Varices
Malignancy
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182
Q

How can you tell if a patient is shocked following upper GI bleed?

A

Cool/clammy with decreased capillary refill
Pulse over 100
Systolic BP lower than 100
Urine output less than 30ml/h

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183
Q

What is the mortality rate from upper GI re bleeding?

A

40%

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184
Q

What are the alarm symptoms related to dyspepsia?

A 
Anaemia
Loss of weight
Anorexia
Rapid onset
Melaena/haematemesis
Swallowing difficulty
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185
Q

What are the risk factors for developing a duodenal ulcer?

A

H.pylori infection

Drugs e.g. NSAIDs, steroids, SSRIs

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186
Q

When is pain from a duodenal ulcer worst?

A

Before meals or at night, i.e. When the stomach is empty

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187
Q

How do you manage peptic ulcers?

A
  1. Lifestyle - reduce smoking, alcohol and aggravating foods
  2. H.pylori eradication (triple therapy)
  3. Drugs to reduce acid secretion: PPIs or H2 antagonist
  4. Surgery
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188
Q

What are the potential complications of peptic ulcers?

A

Bleeding
Perforation
Malignancy
Gastric outflow obstruction

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189
Q

Define GORD

A

Reflux of stomach contents causing symptoms of heartburn, with more than 2 episodes per week

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190
Q

Give some causes of GORD

A 
Hiatus hernia
Abdo obesity
Smoking or alcohol
Overeating
H.pylori
Gastric acid hypersecretion
Pregnancy
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191
Q

What are the potential complications of GORD?

A 
Oesophagitis
Ulcers
Benign stricture
Iron deficiency
Barrett's oesophagus
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192
Q

What can cause oesophagitis?

A 
Corrosives
NSAIDs
Herpes
Candida
Duodenal or gastric ulcer
Cardiac disease
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193
Q

What are the conservative management measures for GORD?

A 
Raise whole bed
Weight loss
Smoking cessation
Small, regular meals
Avoid hot/fizzy drinks, spicy food
Don't eat within 3hours of going to bed
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194
Q

What is a sliding hiatus hernia?

A

Gastro-oesophageal junction slides up into chest

Acid reflux may accompany

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195
Q

What is a rolling hiatus hernia?

A

Junction remains in abdomen
Bulge of stomach herniated into chest alongside oesophagus

Acid reflux uncommon (junction remains competent)

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196
Q

What type of hiatus hernia should be surgically repaired?

A

Rolling

This can strangulate so repair prophylactically

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197
Q

What is the treatment for C.difficile colitis?

A

Metronidazole 400mg/8h

Stop causative antibiotics

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198
Q

When is colectomy required for c.diff colitis?

A

Toxic megacolon
Raised LDH
Rapidly deteriorating

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199
Q

Define extensive UC

A

Extending beyond the splenic flexure

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200
Q

How does smoking affect ulcerative colitis?

A

Decreases incidence

May induce remission

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201
Q

How does smoking affect Crohn’s?

A

Increases incidence

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202
Q

What are the cardinal symptoms of ulcerative colitis?

A

Bloody diarrhoea
Urgency
Tenesmus

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203
Q

Define mild ulcerative colitis

A

Fewer than 4 stools per day

No systemic features

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204
Q

Define severe ulcerative colitis

A

More than 6 stools per day
+ blood
+ systemic features

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205
Q

What are the extra-intestinal features of UC that are related to the disease activity?

A

Erythema nodosum
Aphthous ulcers
Episcleritis
Acute Arthropathy

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206
Q

What are the extra-intestinal features of UC that are unrelated to the disease activity?

A

Sacroileitis
Ank spond
PSC

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207
Q

What are the aims of treatment in ulcerative colitis?

A

Induce remission in acute disease
Maintain remission
Improve quality of life
Decrease risk of colorectal cancer

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208
Q

Why do UC patients get heparin?

A

IBD flares cause a prothrombotic state which can be severe

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209
Q

How are steroids used in UC?

A

Induce remission

No role in long term therapy due to side effects

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210
Q

Why is important to slowly weane off steroids in UC?

A

Doing it too quickly can cause flare up

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211
Q

How is azathioprine used in UC?

A

Steroid-sparing
Maintenance of remission
Takes at least 6 weeks to work

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212
Q

What are the side-effects of azathioprine?

A 
Flu-like
GI upset
Leukopenia
Hepatitis
Pancreatitis
Rash
Infections
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213
Q

How is ciclosporin used in UC? What is its mechanism of action?

A

Salvage therapy in severe refractory colitis

Calcineurin inhibitors

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214
Q

When are laxatives used in UC?

A

Proximal constipation

Relieving this can induce remission in left-sided disease

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215
Q

What are the indications for surgery in UC?

A

Perforation
Massive haemorrhage
Toxic dilatation
Failed medical therapy

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216
Q

How are platelet measurements useful in IBD?

A

High platelets indicates severity of disease

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217
Q

What is the prevalence of Crohn’s disease?

A

0.5-1 per 1000

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218
Q

When is the peak age for Crohn’s to present?

A

20 - 40y and 60 - 70y

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219
Q

What are the symptoms of Crohn’s?

A 
Diarrhoea and urgency
Abdo pain
Weight loss
Fever
Malaise
Anorexia
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220
Q

What are the examination signs of Crohn’s?

A 
Apthous ulcers
Abdo tenderness
Perinatal abscess, fistulae
Clubbing
Skin, joint and eye problems
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4
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221
Q

Why is albumin low in Crohn’s?

A

The liver switches protein synthesis to favour inflammatory proteins eg CRP

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222
Q

What are the indications for surgery in Crohn’s?

A 
Failure of medical management
Perforation
Obstruction by stricture
Fistula
Abscess
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223
Q

What is the incidence of IBS?

A

10-20% population

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224
Q

What symptoms should make you think of something other than IBS?

A 
Older than 40
Less than 6 month history
Anorexia and weight loss
Waking at night with pain or diarrhoea
Mouth ulcers
Abnormal CRP, ESR, Hb or coeliac serology
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225
Q

Why is ispaghula better than lactulose to relieve constipation in IBS?

A

Lactulose ferments so can exacerbate bloating

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226
Q

How do you treat bloating?

A

Mebeverine 135mg QDS

This is an antispasmodic

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227
Q

At what point does hyperbilirubinaemia cause visible jaundice?

A

> 60umol/L

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228
Q

Why do you get dark urine and pale faeces alongside jaundice?

A

Conjugated bilirubin enters urine, darkening it

Less conjugated bilirubin reaches the gut, so there is less in faeces and they are pale

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229
Q

What do pale stools and dark urine commonly indicate?

A

Chile stasis

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230
Q

How does drug-induced jaundice present?

A

DRESS:

Drug Rash with Eosinophilia and Systemic Symptoms

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231
Q

What does decompensated liver disease mean?

A

Signs and symptoms present and patient generally unwell

232
Q

What are the 2 main pathological processes leading to the clinical features of chronic liver disease?

A

Reduced hepatocyte mass

Portal hypertension

233
Q

What clinical features are caused by reduced hepatocyte mass?

A

Encephalopathy
Loss of lean body mass
Coagulopathy

234
Q

What clinical features are caused by portal hypertension?

A

Varices
Ascites
Splenomegaly

235
Q

What are the features of hepatic encephalopathy?

A 
Reduced attention span
Reversed sleep pattern
Metabolic flap
Constructional dyspraxia
Coma
236
Q

What does cirrhosis mean?

A

Irreversible liver damage

Loss of normal architecture plus modular regeneration

237
Q

What are the causes of cirrhosis?

A 
Chronic alcohol abuse
HBV or HCV infection
Genetic disorders
Non-alcoholic fatty liver
Autoimmune eg PBC
Drugs
238
Q

How does cirrhosis lead to kidney problems?

A

Reduced hepatic clearance of immune complexes
Means they become trapped in the kidney
Commonly IgA nephropathy

239
Q

What are the signs of chronic liver disease found in the hands?

A

Clubbing
Palmar erythema
Leuconychia

240
Q

What are the causes of decompensation of chronic liver disease?

A 
Drugs (eg alcohol)
Electrolyte disturbance
Sepsis
GI bleed
Hepatoma
241
Q

How is encephalopathy graded?

A

I altered mood
II drowsy
III stupor
IV coma

242
Q

What is fulminant hepatic failure?

A

Massive necrosis of liver cells

Leads to severe liver function impairment

243
Q

What is the most common cause of fulminant hepatic failure?

A

Paracetamol

244
Q

What emergencies should you look out for in hepatic failure?

A

Sepsis
Hypoglycaemia
GI bleeds/varices
Encephalopathy

245
Q

How do you treat cerebral oedema?

A

20% mannitol IV

246
Q

How do you treat Ascites?

A

Fluid restriction
Low salt diet
Diuretics

247
Q

What drugs should be avoided in hepatic failure?

A

Constipation drugs
Oral hypoglycaemics
Saline IV
All drugs with hepatic metabolism

NB warfarin’s effects are enhanced in hepatic failure

248
Q

Name 5 hepatotoxic drugs

A 
Paracetamol
Isoniazid
Methotrexate
Azathioprine
Oestrogen
Salicylates
Tetracycline
6-MP
249
Q

How does ammonia cause cerebral oedema?

A

Ammonia builds up as liver fails
Passes into brain - taken up by astrocytes
Convert glutamate to glutamine to clear ammonia
Glutamine has osmotic effect and draws water into astrocytes
Leads to cerebral oedema

250
Q

Define hepatorenal syndrome

A

Cirrhosis + Ascites + Renal Failure

251
Q

Name a screening tool for alcoholism

A

CAGE

252
Q

What is the prognosis for an alcoholic with cirrhosis who keeps drinking?

A

48% 5yr survival

253
Q

What type of anaemia is seen in alcoholism and why?

A

Macrocytic

Marrow depression, GI bleeds, folate deficiency and haemolysis

254
Q

What are the CVS complications of alcoholism?

A

Arrhythmias
Hypertension
Cardiomyopathy
Sudden death due to binges

255
Q

What are the symptoms of alcohol withdrawal?

A 
Tachycardia
Hypotension
Tremor
Convulsions
Fits
Hallucinations
256
Q

How do you manage alcohol withdrawal?

A

Beware of hypotension

Chlordiazepoxide 10-50mg QDS PO for 3 days & gradually wean over 7-10days

Vitamin supplements eg pabrinex

257
Q

What is the effect of disulfiram?

A

Causes acetaldehyde build-up and unpleasant effects when alcohol is consumed

Used to treat chronic alcohol dependence

258
Q

What is Charcot’s triad?

A

Fever, pain and jaundice

Cholangitis

259
Q

Describe the typical pain of biliary colic

A

Central, severe and constant
Radiates to back
Lasts for as long as the stone is stuck
Doesn’t have to be everyday, can be any frequency

NB no abdominal tenderness

260
Q

What are the alarm symptoms related to dyspepsia?

A 
Anaemia
Loss of weight
Anorexia
Rapid onset
Melaena/haematemesis
Swallowing difficulty
261
Q

What are the risk factors for developing a duodenal ulcer?

A

H.pylori infection

Drugs e.g. NSAIDs, steroids, SSRIs

262
Q

When is pain from a duodenal ulcer worst?

A

Before meals or at night, i.e. When the stomach is empty

263
Q

How do you manage peptic ulcers?

A
  1. Lifestyle - reduce smoking, alcohol and aggravating foods
  2. H.pylori eradication (triple therapy)
  3. Drugs to reduce acid secretion: PPIs or H2 antagonist
  4. Surgery
264
Q

What are the potential complications of peptic ulcers?

A

Bleeding
Perforation
Malignancy
Gastric outflow obstruction

265
Q

Define GORD

A

Reflux of stomach contents causing symptoms of heartburn, with more than 2 episodes per week

266
Q

Give some causes of GORD

A 
Hiatus hernia
Abdo obesity
Smoking or alcohol
Overeating
H.pylori
Gastric acid hypersecretion
Pregnancy
267
Q

What are the potential complications of GORD?

A 
Oesophagitis
Ulcers
Benign stricture
Iron deficiency
Barrett's oesophagus
268
Q

What can cause oesophagitis?

A 
Corrosives
NSAIDs
Herpes
Candida
Duodenal or gastric ulcer
Cardiac disease
269
Q

What are the conservative management measures for GORD?

A 
Raise whole bed
Weight loss
Smoking cessation
Small, regular meals
Avoid hot/fizzy drinks, spicy food
Don't eat within 3hours of going to bed
270
Q

What is a sliding hiatus hernia?

A

Gastro-oesophageal junction slides up into chest

Acid reflux may accompany

271
Q

What is a rolling hiatus hernia?

A

Junction remains in abdomen
Bulge of stomach herniated into chest alongside oesophagus

Acid reflux uncommon (junction remains competent)

272
Q

What type of hiatus hernia should be surgically repaired?

A

Rolling

This can strangulate so repair prophylactically

273
Q

What is the treatment for C.difficile colitis?

A

Metronidazole 400mg/8h

Stop causative antibiotics

274
Q

When is colectomy required for c.diff colitis?

A

Toxic megacolon
Raised LDH
Rapidly deteriorating

275
Q

Define extensive UC

A

Extending beyond the splenic flexure

276
Q

How does smoking affect ulcerative colitis?

A

Decreases incidence

May induce remission

277
Q

How does smoking affect Crohn’s?

A

Increases incidence

278
Q

What are the cardinal symptoms of ulcerative colitis?

A

Bloody diarrhoea
Urgency
Tenesmus

279
Q

Define mild ulcerative colitis

A

Fewer than 4 stools per day

No systemic features

280
Q

Define severe ulcerative colitis

A

More than 6 stools per day
+ blood
+ systemic features

281
Q

What are the extra-intestinal features of UC that are related to the disease activity?

A

Erythema nodosum
Aphthous ulcers
Episcleritis
Acute Arthropathy

282
Q

What are the extra-intestinal features of UC that are unrelated to the disease activity?

A

Sacroileitis
Ank spond
PSC

283
Q

What are the aims of treatment in ulcerative colitis?

A

Induce remission in acute disease
Maintain remission
Improve quality of life
Decrease risk of colorectal cancer

284
Q

Why do UC patients get heparin?

A

IBD flares cause a prothrombotic state which can be severe

285
Q

What is the normal range for blood glucose?

A

3.3 - 6 mmol/L

286
Q

What are the symptoms of hyperglycaemia?

A 
Polyuria
Polydipsia
Weight loss
Visual blurring
Genital thrush
287
Q

What are the normal actions of insulin on glucose metabolism?

A

Inhibits liver glycogen breakdown
Enhances glucose uptake by liver
Enhances glucose uptake by muscle and adipose

288
Q

What is the pathophysiology of type 1 diabetes?

A

Autoimmune destruction of beta cells

Causes absolute insulin deficiency

289
Q

What proportion of all diabetes is type 1?

A

5-10%

290
Q

Why are ketones produced?

A

Ketone production normally suppressed by insulin

In starvation or insulin deficiency, ketone production is activated

291
Q

What hormones antagonise the action of insulin?

A

Cortisol
Growth hormone
Glucagon
Adrenaline

292
Q

How do you manage cardiovascular risk in diabetics?

A 
Target other risk factors e.g.
Hypertension
Smoking
Obesity
Hyperlipidaemia
293
Q

What is DAFNE?

A

Dose adjustment for normal eating

Course to educate diabetics on insulin doses

294
Q

What is the most effective time for lifestyle intervention in type 2 diabetes?

A

Phase of impaired glucose tolerance

295
Q

What does HbA1c measure?

A

Average glucose levels over the past 8 weeks

296
Q

What are the microvascular complications of diabetes?

A

Nephropathy
Neuropathy
Retinopathy

297
Q

What are the macrovascular complications of diabetes?

A

Cerebrovascular
Peripheral vascular
Cardiovascular

298
Q

What is the mechanism of action of metformin?

A

Decreases hepatic gluconeogenesis
Increases muscle glucose metabolism
Mild anorexic

299
Q

What are the side effects of Metformin?

A

GI upset

Rarely lactic acidosis

300
Q

What are the contraindications for Metformin?

A

Renal failure

Hepatic impairment

301
Q

Give an example of a sulfonylurea

A

Gliclazide

302
Q

What is the mechanism of action of sulfonylureas?

A

Increased insulin release from beta cells

Binds and closes K+ channels to depolarise the cell

303
Q

What are the side effects of sulfonylureas?

A

Weight gain

Hypoglycaemia

304
Q

Give an example of a thiazolidinedione

A

Pioglitazone

305
Q

What is the mechanism of action of Pioglitazone?

A

Activates PPAR-alpha to stimulate transcription of glut-1 and -4

306
Q

What is the mechanism of action of acarbose?

A

Inhibits carbohydrate digestion to reduce glucose absorption

307
Q

What are the side effects or acarbose?

A

Bloating

diarrhoea

308
Q

What is exenatide?

A

GLP-1 receptor analogue

Stimulates insulin release
Inhibits glucagon release

309
Q

What is the mechanism of action of dapagliflozin?

A

Inhibits SGLT2 to inhibit renal glucose reabsorption

310
Q

What are the side effects of dapagliflozin?

A

UTI
Genital thrush
Hypoglycaemia
Increased urination

311
Q

Give 2 examples of ultra-fast insulin

A

Humalog

Novorapid

312
Q

Give an example of a mixed insulin preparation and its content

A

NovoMix

30% short acting
70% long acting

313
Q

Give 2 examples of long-acting insulin

A

Glargine

Insulin detemir

314
Q

When is glargine taken?

A

Bedtime

315
Q

What is a QDS insulin regime?

A

Before meals: ultrafast

Bedtime long-acting

316
Q

What is a good starter regime for T2 diabetics switching from tablets to insulin?

A

Once-daily long-acting insulin at bedtime

Can retain Metformin

317
Q

How are insulin requirements affected by illness?

A

Insulin requirement increases despite eating less

318
Q

What is the target blood pressure for diabetics?

A

Less than 140/80mmHg

319
Q

What is the target BP for diabetics with CKD?

A

Less than 125/75 mmHg

320
Q

What is the pathophysiology of diabetic retinopathy?

A

Capillary basement membrane thickening leads to leaky vessels, occluded vessels and macular oedema

321
Q

Why are diabetics screened for retinopathy?

A

Allows laser photo coagulation to be used
Stops production of angiogenesis factors from is ischaemic retina

Blindness is preventable!

322
Q

How does pre-proliferative retinopathy look?

A

Cotton-wool spots
Haemorrhages
Venous bleeding

323
Q

How does proliferative retinopathy look?

A

New vessels have formed (they are likely to bleed)

Haemorrhages

324
Q

How do you treat macular oedema?

A

Intra-vitreal steroids

Prompt laser treatment

325
Q

Why do diabetics get cataracts?

A

Acute hyperglycaemia induces osmotic changes in the lens

Reversed when blood glucose returns to normal

326
Q

What is the increased cardiovascular risk for diabetics?

A

MI 4 times more likely

Stroke twice as likely

327
Q

What is the pathophysiology of diabetic foot disease?

A

Peripheral vascular disease
Peripheral neuropathy
Increased susceptibility to infection

328
Q

What are the consequences of diabetic foot?

A

Ulceration
Infection
Gangrene
Charcot’s foot

329
Q

What are the features of diabetic ketoacidosis?

A 
Gradual drowsiness
Vomiting
Dehydration
Abdo pain
Polyuria/polydipsia/weight loss
Ketotic breath
Coma
Deep breathing
330
Q

How do you diagnose DKA?

A

Blood pH

331
Q

What are the potential complications of DKA?

A

Cerebral oedema
Aspiration pneumonia
Hypokalaemia/magnaesemia/phosphataemia
Thromboembolism

332
Q

How do you treat DKA?

A

50units actrapid insulin in 50ml 0.9% saline

Continue their long-acting insulin

333
Q

What is the target decrease in blood ketones in DKA?

A

0.5mmol/L/h

334
Q

What are the common triggers of DKA?

A 
Infection
Surgery
MI
Pancreatitis
Chemotherapy
Antipsychotics
Poor insulin dosing or non-compliance
335
Q

What is HONK?

A

Hyperosmolar non-ketotic syndrome

Dehydration + blood glucose >35mmol/L

336
Q

How do you treat HONK?

A

Slow rehydration: 110-220mmol/Kg deficit

Use 0.9% NaCl

337
Q

Why should blood glucose be maintained between 10 and 15 mmol/L for the first 24h in HONK?

A

To avoid cerebral oedema

338
Q

How do you treat hypoglycaemic coma?

A

20-30g glucose IV
(Eg 200-300ml 10% dextrose)

Give sugary drinks and meal once conscious

339
Q

Define hypoglycaemia

A

Plasma glucose

340
Q

What are the autonomic symptoms of hypoglycaemia?

A 
Sweating
Anxiety
Hunger
Tremor
Palpitations
Dizziness
341
Q

What are the neuroglycopenic symptoms of hypoglycaemia?

A 
Confusion
Drowsiness
Visual disturbance
Seizures
Coma
342
Q

What is the main cause of fasting hypoglycaemia?

A

Insulin or sulfonylurea treatment

Increased activity, missed meal or an overdose

343
Q

What are the causes of hypoglycaemia in non-diabetics?

A 
EXPLAIN:
EXogenous drugs
Pituitary insufficiency
Liver failure
Addison's disease
Islet cell tumours
Non-pancreatic neoplasms
344
Q

How do you manage hypoglycaemia?

A

Oral sugary drink and long-acting starch (eg sandwich)

If can’t swallow: IV 25-50ml 50% glucose

If no IV access: 1mg IM glucagon

345
Q

What are the risks of gestational diabetes?

A 
Miscarriage
Pre-term labour
Pre-eclampsia
Congenital malformations
Macrosomia
346
Q

What are the risk factors for gestational diabetes?

A 
Older than 25
Family history
Overweight
Non-Caucasian
HIV
Previous GDM
347
Q

What proportion of patients with gestational diabetes go on to develop T2DM later in life?

A

50%

348
Q

What % of pregnancies are complicated by gestational diabetes?

A

3.5%

349
Q

What blood glucose level should be maintained in the peri operative period?

A

6-11mmol/L

350
Q

How long should VRII be maintain postop?

A

Until eating and drinking normally

351
Q

How is blood glucose affected by being acutely ill?

A

Blood glucose higher due to:
Cortisol, adrenaline and growth hormone release
Physical inactivity
Alteration in diet

352
Q

What is the initial management for Hyperlipidaemia?

A

Diet modification

Address other CVS risk factors: smoking, hypertension, excess weight

353
Q

What are the target levels for cholesterol?

A

Total

354
Q

What drugs are used to treat hypercholesterolaemia?

A

Statins
Ezetimibe/fibrates
Bile acid-binding resins

355
Q

What drugs are used to treat hypertriglyceridaemia?

A

Fibrates
Nicotinic acid
Fish oil capsules

356
Q

What are the indications for starting statin therapy?

A

Diabetes mellitus and over 40y
Total cardiovascular disease risk >20% over 10y
2 of: family history, albuminuria, hypertension and smoking
Men with LDL>6.5 despite dietary change
Familial hypercholesterolaemia

357
Q

When are statins indicated for secondary prevention?

A

Coronary artery disease
TIA or strike
Peripheral artery disease

358
Q

What is low dose dexamethasone suppression test used for?

A

Screening for cushing’s

359
Q

What is the high dose dexamethasone suppression test used for?

A

Determining pituitary vs adrenal cause of Cushing’s syndrome

360
Q

What is the synacthen test?

A

Normal response is to cause cortisol release form the adrenals

Test of primary adrenal failure

361
Q

What is the insulin stress test?

A

Should cause cortisol release to >600

Insulin-induced hypoglycaemia

Good test for hypopitutarism as it tests ACTH and GH reserve

362
Q

What are the contraindications for the insulin stress test?

A

Epilepsy

Ischaemic heart disease

363
Q

What is the glucose tolerance test?

A

Should suppress growth hormone

Test for acromegaly
Bonus of glucose will suppress GH in normal people, failure to suppress in acromegaly

364
Q

What are the effects of pituitary tumours?

A

Excess hormone production

Physical effects of lump on surrounding structures

365
Q

What are the features of acromegaly?

A 
Growth of hands and feet
Coarse features
Headache
Sweating
Carpal tunnel syndrome
366
Q

Which hormones are affected by something blocking the pituitary stalk?

A

Increase in all pituitary hormones

EXCEPT prolactin as this is mainly under inhibitory control by dopamine

367
Q

What is IGF-1?

A

Released from the liver in response to growth hormone

This is the main way growth hormone takes its effect

368
Q

What is the treatment for acromegaly?

A

Somatostatin analogues eg ocreotide

Growth hormone receptor blockers eg pegvisomant

369
Q

How do you distinguish between active and inactive acromegaly?

A

Active: headaches, sweating

Inactive means they have already had treatment, but may still have big features

370
Q

What are the features of Cushing’s syndrome?

A 
Moon fancies
Thinning of skin
Easy bruising
Buffalo hump
Central obesity
Abdominal striae
Hypertension/diabetes
371
Q

How do you do a low dose dexamethasone suppression test?

A

0.5mg dexamethasone QDS for 48h

If cortisol decreases to less than 30nmol/L, it is not true Cushing’s syndrome

372
Q

What are the physical effects of a pituitary tumour?

A

Hypopitutarism

Visual field disturbance (bitemporal hemianopia)

Headache

373
Q

What effect does compression of the pituitary stalk have on prolactin?

A

Causes hyperprolactinaemia

374
Q

What are the features of primary adrenal insufficiency?

A

Hyponatraemia
Hyperkalaemia
Postural hypotension
Increased pigmentation

375
Q

What are the causes of primary adrenal insufficiency?

A 
Autoimmune
TB
Iatrogenic
Sepsis
Infiltrative disease
376
Q

What is the management of a hypo adrenal crisis?

A 
Fluid resuscitation
Glucose
Steroids
Treat sepsis
Find cause
377
Q

What can Addison’s disease mimic clinically?

A

Depression

Often not diagnosed until they have a crisis

378
Q

What are the symptoms of hypothyroidism?

A 
Bradycardia
Slow reflexes
Goitre
Carpal tunnel
Weight gain
Depression
Fatigue
Cold intolerance
Constipation
379
Q

What are the symptoms of hyperthyroidism?

A 
Weight loss despite good appetite
Tremor
Palpitations
Heat intolerance
Diarrhoea
Irritability
Tachycardia
Proptosis
Hyperreflexia
Lid lag
Goitre
380
Q

In what order are hormones affected by hypopituitarism?

A 
Growth hormone
Gonadotrophins
Prolactin
TSH
ACTH
381
Q

What are the usual causes of panhypopituitarism?

A

Irradiation
Surgery
Pituitary tumour

382
Q

What is the most common type of pituitary tumour?

A

Benign adenoma

383
Q

What cranial nerves are affected by pituitary tumours?

A

CN III, IV and VI

384
Q

What is the management of a prolactinoma?

A

Medical therapy with dopamine agonist

385
Q

What is pituitary apoplexy?

A

Rapid bleed into a pituitary tumour

Causes rapid expansion

386
Q

Why does hyperprolactinaemia present earlier in females than males?

A

Causes menstrual disturbance in females

Erectile dysfunction in males

387
Q

Why does hyperprolactinaemia cause hypogonadism, infertility and osteoporosis?

A

Inhibits secretion of gonadotrophin releasing hormone

388
Q

Where is dopamine released from?

A

Hypothalamus

389
Q

What are the causes of hyperprolactinaemia?

A

Excess pituitary production eg prolactinoma
Disinhibition eg compression of pituitary stalk causes reduced local dopamine levels
Dopamine antagonist use

390
Q

What drugs can cause hyperprolactinaemia?

A

Metoclopramide
Haloperidol
Antipsychotics

(Dopamine antagonists)

391
Q

Name a dopamine agonist

A

Bromocriptine

392
Q

Why are free T3 and T4 levels a more useful test than total hormone levels?

A

Total levels are affected by TBG levels, which are increased in pregnancy or HRT

393
Q

What are thyroid function tests like in hyperthyroidism?

A

Raised T4

Low TSH

394
Q

At what time of day are TSH levels lowest and highest?

A

Lowest about 2pm

Highest in the dark

395
Q

What is ‘sick euthyroidism’?

A

Thyroid function tests may be deranged with any systemic illness

Typically all results are low

Retest when recovered

396
Q

Name the thyroid autoantibodies implicated in grave’s and hashimoto’s disease

A

Anti thyroid peroxidase

Antithyroglobulin

397
Q

Which patients should be screened for thyroid abnormalities?

A 
AF
Hyperlipidaemia
DM
Gestational diabetes
Those on lithium and amiodarone
Down's/turner's syndrome
Addison's disease
398
Q

What proportion of thyrotoxicosis is due to Grave’s disease?

A

Two thirds

399
Q

What is the male:female ratio for hyperthyroidism?

A

1:9

400
Q

What is the pathophysiology of Grave’s disease?

A

Circulating IgG antibodies bind to TRH receptors and cause thyroid enlargement and increased hormone production

401
Q

What proportion of patients with Grave’s disease get thyroid eye disease?

A

25-50%

402
Q

Define proptosis

A

Eyes protruding beyond the orbit

Have to look from above to see this

403
Q

How do you treat symptoms of hyperthyroidism?

A

Beta blockers

404
Q

How do you prescribe carbimazole?

A
  1. Titration: start with 20-40mg/day PO for 4 weeks. Reduce depending on TFTs every 1-2 weeks
  2. Block-replace: give carbimazole and thyroxine together
405
Q

What are the side effects of carbimazole?

A

Agranulocytosis: see GP if they get an infection, need FBC

406
Q

What are the contraindications of radio-iodine treatment?

A

Pregnancy

Lactation

407
Q

What structures may be damaged during thyroidectomy?

A

Recurrent laryngeal nerve

Parathyroid glands

408
Q

What are the potential complications of thyrotoxicosis?

A 
Heart failure
Angina
AF
Osteoporosis
Ophthalmopathy
Gynaecomastia
409
Q

What is myxoedema?

A

Hypothyroidism

410
Q

What are the causes of hypothyroidism?

A

Primary atrophic hypothyroidism (common)

Hashimoto’s thyroiditis

Iodine deficiency

411
Q

What is primary atrophic hypothyroidism?

A

Lymphocytic infiltration of thyroid leads to atrophy

No goitre

412
Q

What diseases is hashimoto’s disease related to?

A

Type 1 diabetes
Addison’s disease
Pernicious anaemia

413
Q

What problems can hypothyroidism cause in pregnancy?

A 
Eclampsia
Anaemia
Premature birth
Low birthweight
Stillbirth
Post-Partum haemorrhage
414
Q

What is the treatment for hypothyroidism?

A

Levothyroxine 50-100ug/day

415
Q

What is sub clinical hypothyroidism?

A

TSH raised but T3 and T4 are normal

Asymptomatic

416
Q

What is the effect of amiodarone on the thyroid and why?

A

Can cause hyper or hypothyroidism

Amiodarone is structurally similar to T4 (contains lots of iodine)

417
Q

What types of hormone does the adrenal cortex produce?

A

Steroids:
Mineralocorticoids
Glucocorticoids
Androgens

418
Q

How is cortisol excreted?

A

Urinary free cortisol

419
Q

What is the most common cause of Cushing’s syndrome?

A

Oral steroids

420
Q

What is the most common endogenous cause of Cushing’s syndrome?

A

80% due to increased ACTH

Pituitary adenoma (Cushing’s disease) is the most common cause of this

421
Q

What is the normal range for blood glucose?

A

3.3 - 6 mmol/L

422
Q

What are the symptoms of hyperglycaemia?

A 
Polyuria
Polydipsia
Weight loss
Visual blurring
Genital thrush
423
Q

What are the normal actions of insulin on glucose metabolism?

A

Inhibits liver glycogen breakdown
Enhances glucose uptake by liver
Enhances glucose uptake by muscle and adipose

424
Q

What is the pathophysiology of type 1 diabetes?

A

Autoimmune destruction of beta cells

Causes absolute insulin deficiency

425
Q

What proportion of all diabetes is type 1?

A

5-10%

426
Q

Why are ketones produced?

A

Ketone production normally suppressed by insulin

In starvation or insulin deficiency, ketone production is activated

427
Q

What hormones antagonise the action of insulin?

A

Cortisol
Growth hormone
Glucagon
Adrenaline

428
Q

How do you manage cardiovascular risk in diabetics?

A 
Target other risk factors e.g.
Hypertension
Smoking
Obesity
Hyperlipidaemia
429
Q

What is DAFNE?

A

Dose adjustment for normal eating

Course to educate diabetics on insulin doses

430
Q

What is the most effective time for lifestyle intervention in type 2 diabetes?

A

Phase of impaired glucose tolerance

431
Q

What does HbA1c measure?

A

Average glucose levels over the past 8 weeks

432
Q

What are the microvascular complications of diabetes?

A

Nephropathy
Neuropathy
Retinopathy

433
Q

What are the macrovascular complications of diabetes?

A

Cerebrovascular
Peripheral vascular
Cardiovascular

434
Q

What are the causes of decreased ACTH levels?

A

Adrenal adenoma/cancer

Adrenal modular hyperplasia

Oral steroids

435
Q

What are the symptoms of Cushing’s?

A 
Weight gain
Depression, lethargy, irritability
Psychosis
Proximal weakness
Gonadal dysfunction
Acne
Recurrent Achilles rupture
436
Q

What are the signs of Cushing’s?

A 
Central obesity
Moon face
Buffalo hump neck
Supraclavicular fat distribution
Skin and muscle atrophy
Bruises, purple abdo striae
Osteoporosis
Hypertension
Hyperglycaemia
Increased infection risk and poor healing
437
Q

Why are random cortisol levels not reliable?

A

Cortisol is a stress hormone so can be increased due to the situation eg illness

438
Q

What are incidentalomas?

A

Non-functioning masses found on imaging
Not the actual cause of Cushing’s

5% have adrenal incidentalomas
10% have pituitary incidentalomas

439
Q

What are the causes of pseudo-Cushing’s?

A

Alcohol excess
Obesity
Depression

440
Q

What is the treatment for Cushing’s disease?

A

Transphenoidal removal of adenoma

441
Q

When can adrenal insufficiency suddenly develop?

A

In those on long-term steroids

Septic individuals

Malignancy

442
Q

What is the main cause of adrenocortical insufficiency?

A

Autoimmune

443
Q

What are the symptoms of Addison’s disease?

A 
Tearful
Tired, weakness
Abdo pain
Vomiting
Anorexia
Dizziness, faints
Flu-like arthralgias/myalgias
Postural hypotension
Pigmented palmar creases
444
Q

How does an Addisonian crisis present?

A

Shock: hypotensive and tachycardic
Fever
Coma

445
Q

What are the electrolyte abnormalities found in Addison’s disease?

A

Hyponatraemia
Hyperkalaemia

Hypoglycaemia
Uraemia
Hypercalcaemia

446
Q

What is the short synacthen test?

A

Do plasma cortisol before and after 250ug IM synacthen

Not Addison’s if cortisol is less than 550nmol/L at 30min

447
Q

What is the treatment for Addison’s disease?

A

Steroids: 15-25mg hydrocortisone daily
Give early in the day to avoid insomnia

Fludrocortisone for postural hypotension and to decrease sodium and increase potassium

448
Q

What are patients with Addison’s given for emergencies?

A

Syringes of IM hydrocortisone

Inject 100mg if vomiting prevents oral intake

449
Q

What is primary hyperaldosteronism?

A

Excess production of aldosterone with no increase in RAAS activity

Leads to increased sodium and water retention and decreased renin release

450
Q

What are the features of primary hyperaldosteronism?

A

Hypertension
Hypokalaemia
Alkalosis
Sodium slightly raised or normal

451
Q

What is Conn’s syndrome?

A

Single aldosterone-producing adenoma

Causes primary hyperaldosteronism

452
Q

How are renin and aldosterone levels affected by primary hyperaldosteronism?

A

Suppressed renin

Raised aldosterone

453
Q

When should the adrenals be MRId?

A

After hyperaldosteronism confirmed

Due to high incidence of incidentalomas

454
Q

What is used to medically manage hyperaldosteronism?

A

Spironolactone

455
Q

What is secondary hyperaldosteronism?

A

High renin levels caused by reduced renal perfusion

456
Q

What is a phaeochromocytoma?

A

Rare tumour usually found in adrenal medulla

Produces catecholamines

457
Q

What is the triad of features found in phaeochromocytoma?

A

Episodic headache
Sweating
Tachycardia

458
Q

Name an alpha blocker and a use

A

Phenoxybenzamine

Preop medical management of phaeochromocytoma

459
Q

What are the actions of parathyroid hormone?

A

Increased osteoclast activity
Increased calcium/decreased phosphate resorption in kidney
Increased production of 1,25-dihydroxyvitamin D

460
Q

What is the overall effect of parathyroid hormone?

A

Increased serum calcium

Decreased serum phosphate

461
Q

What is the main cause of primary hyperparathyroidism?

A

Single adenoma

462
Q

What are the features of hypercalcaemia?

A 
Weak
Tired
Depression
Thirsty
Renal stones
Abdo pain
Pancreatitis
Ulcers
463
Q

Why is alk phos raised in hyperparathyroidism?

A

Increased bone resorption

464
Q

What is the treatment for mild hyperparathyroidism?

A

Increase fluid intake to avoid stones

Avoid thiazides and high calcium/vit D intake

465
Q

What are the complications of removing a parathyroid adenoma?

A

Hypoparathyroidism
Recurrent laryngeal nerve damage
Symptomatic hypocalcaemia

466
Q

How does Cinacalcet work?

A

Increases sensitivity of parathyroid cells to Ca2+
Increases negative feedback effect
Decreases PTH secretion

467
Q

What are the causes of secondary hyperparathyroidism?

A

Reduced Vit D intake

Chronic renal failure

468
Q

What is PTHrP commonly produced by?

A

Squamous cell lung cancers
Breast cancer
Renal cell carcinoma

469
Q

What is the acute management of hypercalcaemia?

A

Correct dehydration with 0.9% saline
Bisphosphonate (max dose 90mg)

Diagnose and treat underlying cause

470
Q

What is primary hypoparathyroidism?

A

Primary gland failure causing decreased PTH secretion and hence hypocalcaemia

471
Q

What are the causes of secondary hypoparathyroidism?

A

Surgery
Radiation
Hypomagnesaemia (needed for PTH production)

472
Q

What are the features of hypocalcaemia?

A 
Spasms
Anxious, irritable, irrational
Seizures
Hypertonic smooth muscle (colic, wheeze, dysphagia)
Dermatitis
Impaired orientation & confusion
473
Q

What is the treatment of mild hypocalcaemia?

A

Calcium 5mmol/6h PO

474
Q

What is the treatment of severe hypocalcaemia?

A

10ml 10% calcium gluconate IV over 30mins

475
Q

What are the causes of hypocalcaemia with increased phosphate levels?

A 
CKD
Hypoparathyroidism
Acute rhabdomyolysis
Vit d deficiency
Hypomagnaesemia
476
Q

What are the causes of hypocalcaemia with normal or decreased phosphate levels?

A

Osteomalacia
Acute pancreatitis
Over hydration
Respiratory alkalosis

477
Q

What are the levels of FSH and LH like in primary Hypogonadism?

A

High

478
Q

What are the levels of FSH and LH like in secondary hypogonadism?

A

Normal or low

479
Q

What chromosomal abnormalities cause hypogonadism?

A

Klinefelter

Turner

480
Q

What are the causes of primary hypogonadism?

A 
Klinefelter/Turner syndrome
Autoimmune eg Addison's
Infection
Haemochromatosis
Surgery on gonads
481
Q

What are the causes of secondary hypogonadism?

A

Hypothalamic or pituitary defect:

Hypothalamic eg kallmann syndrome
Pituitary eg hypopituitarism
PCOS

482
Q

What is the treatment for secondary hypogonadism?

A

Men: testosterone replacement therapy
Women: oestrogen and progesterone replacement

483
Q

How can morbid obesity be managed medically?

A

Orlistat - prevents absorption of fats by inhibiting lipase

484
Q

What are the indications for bariatric surgery?

A

BMI over 40kg/m2
Non-surgical measures failed for at least 6 months
Intensive specialist management
Fit for surgery
Patient commits to need for long-term follow-up

485
Q

When is surgery the 1st line treatment for obesity?

A

Adults with BMI > 50

486
Q

What is MEN?

A

Multiple endocrine neoplasia
Functioning hormone-producing tumours in multiple organs
Autosomal dominant inheritance

487
Q

What are the features of MEN-1?

A

Parathyroid hyperplasia or adenoma
Pancreas endocrine tumours
Pituitary prolactinoma

488
Q

What are the features of MEN-2a?

A

Thyroid carcinoma
Adrenal eg phaeochromocytoma
Parathyroid hyperplasia

489
Q

How is genetic testing used in MEN?

A

MEN-2 gene is a proto-oncogene

Test for it and do prophylactic thyroidectomy before 3 years of age

490
Q

What is the normal range for GFR?

A

70-140ml/min

491
Q

How much of the cardiac output do the kidneys receive?

A

20%

492
Q

How much urine do the kidneys normally produce?

A

50-100ml per hour

493
Q

Where is the urine made acidic?

A

Collecting ducts: whatever sodium resorption that occurs is accompanied by an equivalent excretion of H+ and K+

494
Q

Where does sodium resorption occur?

A

60-70% proximal tubule
20-30% loop
5-8% distal tubule

495
Q

Why is GFR better than creatinine at measuring renal impairment?

A

Creatinine also dependent on muscle mass - so if muscle mass is low, creatinine can be normal despite GFR being reduced

496
Q

What is the MDRD equation?

A 
Estimates GFR from 4 parameters:
Serum creatinine
Age
Gender
Race
497
Q

What is the normal range for pCO2?

A

4.7 - 6 kPa

498
Q

What is the normal range for HCO3-?

A

22-28mmol/L

499
Q

What is the equation for anion gap?

A

(Na+ + K+) - (Cl- + HCO3-)

500
Q

What is the normal range for the anion gap?

A

10-18mmol/L

501
Q

What is the anion gap useful for?

A

Determining the cause of metabolic acidosis

502
Q

What are the causes of metabolic acidosis with an increased anion gap?

A

Lactic acid eg shock, infection, ischaemia
Urate ie renal failure
Ketones (DKA, alcohol)
Drugs/toxins

503
Q

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

A 
Renal tubular acidosis
Diarrhoea
Drugs
Addison's disease
Pancreatic fistula
Ammonium chloride ingestion
504
Q

Why does the anion gap increase in some metabolic acidosis?

A

Increased production or reduced excretion of organic acids
Causes HCO3- to fall
Other organic anions rise

505
Q

What are the causes of metabolic alkalosis?

A

Vomiting
Potassium depletion eg diuretics
Burns
Ingesting base

506
Q

What causes respiratory acidosis?

A

Type 2 respiratory failure of any cause

Most commonly COPD

507
Q

What causes respiratory alkalosis?

A

Hyperventilation

Eg stroke, asthma, anxiety, pregnancy, PE, drugs

508
Q

Give 2 examples of loop diuretics

A

Furosemide

Bumetanide

509
Q

What is the mechanism of action of loop diuretics?

A

Block Na/K/Cl cotransporter in thick ascending limb
Prevent reabsorption of sodium, chloride and potassium
Increases amount of solute in filtrate
Reduces water reabsorption

510
Q

What are the uses of loop diuretics?

A 
Acute pulmonary oedema
Peripheral oedema
Ascites
Heart failure
Severe hypercalcaemia
511
Q

What are the side effects of loop diuretics?

A

Hypokalaemic metabolic alkalosis (because they cause H+ and K+ excretion)
Hypovolaemia
Ototoxicity
Allergies

512
Q

Give 2 examples of thiazides

A

Bendroflumethiazide

Metolazone

513
Q

What is the mechanism of action of thiazides?

A

Inhibit NaCl transporter in distal tubule

Decrease NaCl reabsorption to increase water loss

514
Q

How do thiazides affect serum potassium?

A

Cause hypokalaemia

Due to excessive potassium loss

515
Q

What are the uses of thiazides?

A

Hypertension

Long-term oedema eg heart failure

Reduce renal stone formation in hypercalcuria

516
Q

What are the side effects of thiazides?

A 
Hypokalaemia
Hyponatraemia
Hypomagnaesemia
Metabolic alkalosis
Hyperglycaemia
Increased serum lipid
Increased uric acid level
517
Q

Name 2 aldosterone antagonists

A

Spironolactone

Eplerenone

518
Q

Name 4 potassium sparing diuretics

A

Spironolactone and Eplerenone

Amiloride and triameterene

519
Q

What is the mechanism of action of amiloride?

A

Block ENaC in distal tubule to prevent sodium reabsorption

520
Q

What potassium abnormality is common with potassium-sparing diuretics?

A

Hyperkalaemia

They reduce potassium excretion

521
Q

Which works more quickly, Spironolactone or amiloride?

A

Amiloride works in hours

Spironolactone takes days for full effect

522
Q

How can you prevent hyperkalaemia when using potassium sparing diuretics?

A

Use in combination with loop or thiazides diuretic

523
Q

What are the side effects of Spironolactone?

A

Gynaecomastia
GI upset
Hyperkalaemia

524
Q

Name an osmotic diuretic and its mechanism of action

A

Mannitol

Freely filtered but not reabsorbed - stays in lumen and causes less water to be reabsorbed from the proximal tubule

525
Q

What are the uses of mannitol?

A

Reduce brain volume/ICP
Haemolysis
Rhabdomyolysis
Reduce intraocular pressure

526
Q

What are the side effects of mannitol?

A

Headache
Nausea
Vomiting
Hypernatraemia

527
Q

Define hypokalaemia

A

K+

528
Q

What is the most common cause of hypokalaemia?

A

Diuretic therapy

529
Q

What ECG changes appear in hypokalaemia?

A 
Flat T wave
U waves
Long PR
Depressed ST
Tachyarrhythmias
530
Q

What are the symptoms of hypokalaemia?

A 
Weakness
Intestinal ileus
Hypotonia and hyporeflexia
Cramps
Tetany
Palpitations
Light-headedness
Cardiac arrest
531
Q

How do you manage mild hypokalaemia?

A

Oral K+ supplement

Consider changing to potassium-sparing diuretic

532
Q

How do you treat severe hypokalaemia?

A

IV KCl cautiously

No more than 20mmol/h
Not more concentrated than 40mmol/L

533
Q

What is the maximum rate and concentration of potassium that it is safe to give?

A

20mmol per hour

40mmol/L

534
Q

What potassium concentration is an emergency?

A

Above 6.5 mmol/L

535
Q

What are the causes of hyperkalaemia?

A 
Oliguric renal failure
Potassium-sparing diuretics
Rhabdomyolysis
Metabolic acidosis
Excess K+ therapy
Addison's disease
Massive blood transfusion
Burns
Drugs eg ACEi
Artefactual result
536
Q

Why do you get artefactual results stating hyperkalaemia?

A

Commonly from primary care causing delayed analysis

Difficult venue puncture causing haemolysis

Contamination with EDTA in FBC bottle - do UEs first

537
Q

What are the concerning signs in hyperkalaemia?

A 
Fast irregular pulse
Chest pain
Weakness
Palpitations
Light-headedness
538
Q

What are the ECG changes in hyperkalaemia?

A

Tall tented T waves
Small P waves
Wide QRS
VF

539
Q

How do you manage non-urgent hyperkalaemia?

A

Treat underlying cause
Stop precipitating medications

Calcium resonium: binds to K+ in gut to prevent its absorption

540
Q

How do you treat severe hyperkalaemia?

A

> 6.5mmol/L get senior help

IV calcium gluconate 10ml 10% over 2min
Insulin + dextrose IV
Dialysis

541
Q

What is the pathophysiology of rhabdomyolysis?

A

Skeletal muscle breakdown

Release of contents into circulation (myoglobin, potassium, urate, CK)

542
Q

What are the consequences of rhabdomyolysis?

A

Hyperkalaemia

AKI as myoglobin is filtered at glomerulus then obstructs renal tubules

543
Q

What are the causes of rhabdomyolysis?

A 
Post-ischaemia
Prolonged immobilisation
Burns
Crash injury
Excessive exercise
Uncontrolled seizures
Myosotis
Infections
Drugs
544
Q

What is plasma CK like in rhabdomyolysis?

A

Very raised, over 1000iU/L

545
Q

How do you distinguish between rhabdomyolysis and MI?

A

Troponin negative in rhabdomyolysis

546
Q

How do you treat rhabdomyolysis?

A

Treat hyperkalaemia urgently
IV fluids to prevent AKI
Maintain urine output of 300ml/h until myoglobinuria has stopped

547
Q

What is the normal range for plasma sodium?

A

135-145 mmol/L

548
Q

What are the features of hyponatraemia?

A 
Anorexia, nausea, malaise
Headache
Irritability
Confusion
Weakness
Reduced GCS and seizures
Cardiac failure/oedema
549
Q

What are the causes of hyponatraemia with hypovolaemia?

A

Renal loss of sodium : diuretics, Addison’s

Extra renal loss: vomiting, diarrhoea, burns, sweat

550
Q

What are the causes of hyponatraemia with normovolaemia?

A 
Inappropriate IV fluid (eg 5% dextrose)
Hypothyroidism
SIADH
Sickle cell
Drugs eg carbamazepine
551
Q

What are the causes of hyponatraemia with Hypervolaemia?

A 
Renal failure
Cardiac failure
Hepatic failure
Nephrotic syndrome
Inappropriate IV fluid eg excess 0.9% saline
552
Q

How should sodium be replaced in hyponatraemia?

A

Replace sodium and water at the same rate they were lost

553
Q

How do you manage Asymptomatic, chronic hyponatraemia?

A

Restrict fluid intake

Demeclocycline (ADH antagonist) may be needed

554
Q

What are the dangers of correcting hyponatraemia too quickly?

A

Central pontine myelinolysis

555
Q

What is the maximum rate of increase in acute hyponatraemia?

A

1 mmol/h

556
Q

What is the action of vasopressor receptor antagonists?

A

Cause water excretion without losing electrolytes

Effective for hyper/euvolaemic hyponatraemia

557
Q

Define clinical criteria for SIADH

A

Concentration of urine >20mmol/L Na+
Hyponatraemia
Low plasma osmolality

558
Q

What are the causes of SIADH?

A 
Malignancy
CNS disorders
Chest disease eg TB or pneumonia
Endocrine disease eg hypothyroid
Drugs
Porphyria
Trauma
Major abdo/thoracic surgery
559
Q

How do you treat SIADH?

A

Restrict fluid intake and treat cause

If severe, may require salt and loop diuretic

560
Q

Define hypernatraemia

A

Plasma sodium > 145mmol/L

561
Q

What are the features of hypernatraemia?

A 
Lethargy
Thirst
Weakness
Irritability
Confusion
Coma
Fits
Signs of dehydration
562
Q

What is the mechanism of action of cyclizine?

A

H2 receptor antagonist

Used to treat GI causes of vomiting

563
Q

What is the action of metoclopramide?

A

D2 receptor antagonist

564
Q

What is the mechanism of action of ondansetron?

A

5HT3 receptor antagonist

565
Q

How do bulking agents work? Give an example

A

Increase faecal mass to stimulate peristalsis

Ispaghula husk eg fybogel

566
Q

How do stimulant laxatives work? Give an example

A

Increase intestinal motility

Senna

567
Q

How do osmotic laxatives work?

A

Retain fluid in the bowel

Also retain ammonia so used in hepatic encephalopathy

568
Q

Give two examples of osmotic laxatives

A

Lactulose

Macrogol (movicol)

569
Q

What dose of codeine phosphate is used to treat diarrhoea?

A

30mg TDS PO

570
Q

What is the dose of loperamide?

A

2mg PO after each loose stool

Max 16mg per day

571
Q

Define AKI

A

Rapid reduction in renal function over a period of hours to days

572
Q

How is AKI measured?

A

Serum urea and creatinine

573
Q

What are the risk factors for AKI?

A 
Age over 75
CKD
Heart failure
PVD
Chronic liver disease
Diabetes
Drugs
Sepsis
Low fluid intake/increased losses
History of urinary symptoms
574
Q

How is urine output used to diagnose AKI?

A

Less than 0.5ml/kg/h for 6h - stage 1

12h - stage 2
24h - stage 3

575
Q

How is serum creatinine used to define AKI?

A

Stage 1 - >26umol/L increase or 1.5x baseline

576
Q

What are the common causes of pre-renal AKI?

A

Hypo perfusion

Hypotension
Renal artery stenosis
ACE inhibitors

Phase 2 (21 decks)

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