Peer teachings Flashcards

1
Q

What type of hypersensitivity is SLE

A

3 and 2

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2
Q

Triad of lupus

A

Fever, joint pain, rash in woman of child bearing age

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3
Q

What is needed for SLE diagnosis

A
4/11
Malar rash
Discoid rash
Photosensitivity
Mouth/nose ulcers
Serositis (pleuritis/pericarditis)
Polyarthritis
Renal
Neurological (siezures)
Haematologic
Antinuclear antibodies
Other antibody (anti-smith, anti dsDNA, antiphospholipid)
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4
Q

What can pANCA differentiate

A

Crohns and UC. UC has it. Crohns doesnt.

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5
Q

Parkinsons genes

A

Normally not genetic but: PINK1, Parkin, alpha synuclein

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6
Q

What is present in the substantia nigra of those with parkinsons

A

Lewy bodies (eosinophilic with alpha synuclein)

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7
Q

Clinical features of parkinsons

A

Pill roll resting tremor, Cog wheel rigidity, Bradykinesia, Hypokinesia, Akinesia (from difficulty initiation movements), postural instability

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8
Q

What doesnt parkinsons cause

A

Weakness

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9
Q

How does the tremor differ between parkinsons and cerebellar disease

A

Parkinsons is resting, cerebellar is intention

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10
Q

Other dopaminergic dysfunction leads to

A

Depression, dementia, sleep disturbances, difficulty smelling.

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11
Q

Parkinsons treatment

A

Levodopa, Ropinirole (dopamine agonist). Selegiline (MAO-B inhibitor, early on), Entacapone (COMT inhibitor, later on). Deep brain stimulation.

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12
Q

What is the role of Th1

A

Helps macrophages produce an immune response. IL2, IFN gamma

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13
Q

What is the role of Th2

A

Helps B cells produce immunoglobulins. IL4,5,10

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14
Q

Requirements for Obstructive spirometry

A

Reduced FEV1 (<80% normal), Reduced FEV1:FVC ratio (<0.7), reduced peak flow

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15
Q

Requirements for restrictive spirometry

A

Reduced FVC and FEV1. Normal ratio and peak flow

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16
Q

Interstitial lung disease examples

A

Sarcoidosis, IPF, Asbestosis, Goodpastures, GPA (Wegeners granulomatosis)

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17
Q

Define asthma

A

Chronic respiratory condition associated with airway inflammation and hyperresponsiveness

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18
Q

3 pathophysiological changes in asthma

A

Airway inflammation, airway obstruction and bronchial hyperresponsiveness

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19
Q

Which drugs can make asthma worse

A

NSAIDs, Aspirin and beta blockers

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20
Q

What causes the second wave of inflammation in asthma

A

Leukotriene release from mast cells

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21
Q

Symptoms of asthma

A

Tachypnoea, wheeze, cough

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22
Q

Signs of asthma

A

Expiratory polyphonic wheeze, hyperinflation, cyanosis, use of accessory muscles, hyperresonant, reduced air entry

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23
Q

Investigations for asthma

A

FeNO (>40ppb), Spirometry (FEV1/FVC <0.7), bronchodilator reversibility (>12%/200ml), peak flow meter (diurnal variation)

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24
Q

1st line asthma

A

Short acting B2 agonist (salbutamol) as needed

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25
Q

2nd line asthma

A

Low dose inhaled corticosteroid (beclametasone)

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26
Q

3rd line asthma

A

Low dose ICS + LABA (salmeterol)

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27
Q

4th line asthma

A

+Leukotriene receptor antagonist (Montelukast) then pred

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28
Q

What is used for asthma monitoring

A

Peak flow and asthma control test

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29
Q

What is the asthma control test

A
Past 4 weeks
How often has it affected your work
How often were you SOB
How often nocturnal waking
How often use rescue inhaler
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30
Q

What does unable to complete sentences suggest

A

Acute asthma. Give high flow O2, salbutamol nebs and prednisolone. Do ABG and CXR. Can add MgSO4

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31
Q

Causes of acute asthma

A

Infections esp viral, pneumothorax, triggers

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32
Q

PEF for severity of acute asthma

A

Moderate = 50-75
Severe= 33-50/ cant complete sentence
Life threatening= below 33 or altered conscious

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33
Q

Define COPD

A

A common preventable and treatable disease characterised by persistent airflow limitation that is usually progressive and associated with an enhance chronic inflammatory response

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34
Q

What is CREST

A
Limited cutaneous systemic sclerosis.
Calcinosis cutis
Raynauds phenomenon
oEsophageal dysmotility
Sclerodactyly
Telangiectasis
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35
Q

What causes wheeze

A

Air thorugh mucus

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36
Q

What cuases crackles

A

Alveoli opening

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37
Q

COPD signs

A

Exertional breathlessness, chornic cough, regular sputum production, wheeze, frequent winter bronchitis

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38
Q

What are signs of COPD

A

Use of accessory muscles, pursed lip breathing, barrel chest, tar staining on fingers, cyanosis, weight loss form prolonged hypoxaemia, wheeze and reduced breath sounds

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39
Q

COPD v Asthma histologically: cells

A

COPD neutrophils, CD8 T cells and many macrophages. Asthma mast cells, eosinophils, CD4 T cells and macrophages

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40
Q

COPD v Asthma histologically: mediators

A

Asthma: Histamine, IL-4, IL5, some ROS. COPD: IL8 TNFa, many ROS

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41
Q

COPD v Asthma histologically: effects

A

Asthma: all airways, little fibrosis, epithelial shedding. COPD: Peripheral airways, lung destruction, fibrosis and squamous metaplasia.

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42
Q

COPD v Asthma response to steroids

A

Asthma is very responsive, COPD isnt

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43
Q

What is the classification for airflow limitation

A
GOLD. FEV1% Predicted
1, mild= >80%
2, moderate= 50-79%
3, severe= 30-49%
4, very severe= <30%
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44
Q

COPD investigations

A

Spirometry and CXR to rule out pathology

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45
Q

What tool is used for COPD prognosis

A

BODE index. BMI, airflow Obstruction, Dyspnoea, Exercise capacity index

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46
Q

Non inhaler management of COPD

A

Smoking cessation and pulmonary rehabilitation. Physiotherapy and dornase alfa for sputum clearance. Influenza and pneumococcal vaccinations

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47
Q

Step one COPD

A

LAMA (Tiotropium bromide) with rescue SABA

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48
Q

Step two COPD FEV1 >50%

A

+ LABA (Salmeterol)

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49
Q

Step two COPD FEV1<50%

A

+LABA (Salmeterol) and ICS (hydrocortisone)

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50
Q

What PaO2 is needed to get oxygen therapy

A

PaO2<7.3kPa

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51
Q

What is the gene in alpha 1 antitrypsin deficiency

A

SERPINA 1

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52
Q

Management of acute asthma

A

Salbutmaol Nebs, Oxygen then prednisolone and IV hydrocortisone

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53
Q

Causes of COPD exacerbations

A

Community: Haemophilus influeza B, Strep Pneuominae Hospital: Psuedomonas Aeurginosa

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54
Q

Define pneuomothorax

A

Air in the pleural cavity resulting in collapse of the lung on the affected side.

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55
Q

What increases your risk of smoking

A

Marfans, tall young man smoker

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56
Q

Secondary causes of pneumothoarx

A

CF, COPD, Sarcoidosis

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57
Q

Catamenial pneumothorax

A

During menstruation

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58
Q

What is tension pneumothorax

A

1 way valve of air entering

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59
Q

Presentation of pneumothorax

A

Dyspnoea, pleuritic chest pain, hyperresonant on percussion + decreased breath sounds on affected side, reduced chest expansion

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60
Q

What are the additional signs of tension pneumothorax

A

Deviated trachea, mediastinal shift, hyperexpanded chest, tachypnoea and hypotension

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61
Q

Investigations of pneumothorax

A

CXR unless tension which is an emergency

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62
Q

Management of tension pneumothorax

A

100% O2, Large bore IV cannula 2nd intercostal space in mid clavicular line, chest drain

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63
Q

Management of non tension pneumothorax

A

observation if small, needle aspiration if bigger, chest drain tube if more severe

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64
Q

Define pleural effusion

A

Abnormal collection of fluid in the pleural space

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65
Q

Transudate pleural effusion

A

Changes in osmotic pressure, CCF Cirrhosis Nephrotic syndrome, low protein levels

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66
Q

Exudate pleural effusion

A

Inflammation/malignacy leads to increased vascular permeability. Sepsis, malignancy, TB, infections. high protein levels.

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67
Q

Pleural effusion signs and symptoms

A

Pleuritic chest pain, SOB, cough, reduced chest expansion and breath sounds, stony dull percussion.

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68
Q

Criteria for exudative pleural effusion

A

Lights criteria 2/3

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69
Q

Pleural effusion investigations

A

chest xray and diagnostic aspiration

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70
Q

Management of pleural effusion

A

Treat underlying cause, drain if symptomatic, pleuroectomy if mesothelioma

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71
Q

Define bronchiectasis

A

Thickening and permanent dilatation of the airways

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72
Q

Causes of bronchiectasis

A

HIV TB
SLE
CF, foreign body

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73
Q

Presentation of bronchiectasis

A

cough with purulent sputum, wheeze, recurrent infections, clubbing, bilateral coarse crackles

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74
Q

Investigations of bronchiectasis

A

Gold standard= CT chest. CXR= tram track sign, spirometry= obstruction defect, sputum culture

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75
Q

Management of bronchiectasis

A

Smoking cessation exercise, chest physiotherapy, mucoltics (dornase alfa), prophylactiic abx, pneumococcal and flu vaccination

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76
Q

CF inheritance pattern and gene and chromosome

A

Autosomal recessive, mutation in cystic fibrosis transmembrane conductance regulator chromosome 7

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77
Q

Pulmonary CF presentation

A

cough with purulent sputum, wheeze, recurrent infections, clubbing, bilateral coarse crackles

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78
Q

Extra pulmonary CF manifestations

A

Pancreas= steatorrhea, diabetes, pancreatitis
GI: Distal intestinal obstruction syndrome, cirrhosis
GU: Lack of vas deferens and amenorrhea

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79
Q

Respiratory complications of CF

A

Pneumothorax and respiratory failure

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80
Q

Diagnosis of CF

A

In the presence of symptoms, sweat test for children, CF gene test for adults and IRT test for babies

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81
Q

What is the heel prick test for CF in babies

A

immunoreactive tripsinogen

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82
Q

CF complications from malabsorption

A

Underweight, fat soluble vitamin deficiency, reduced bone mineral density, distal intestinal obstruction syndrome

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83
Q

Chronic complications of CF

A

Cirrhosis, infertility diabetes

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84
Q

Respiratory management of CF

A

Exercise, stop smoking, physio, mucolytics (dornase alfa), prophylactic abx (azithromycin), pneumococcal and flu vacinations

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85
Q

GI management of CF

A

ADEK supplementaion, pancreatic enzyme replacement therapy, ursodeoxycholic acid for liver disease

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86
Q

CF screening

A

All babies in UK, immunreactive trypsinogen and sweat test and genetic testing to confirm

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87
Q

Describe ARDS

A

Acute onset, bilateral infiltrates on XRay, small pulmonary wedge pressure. Caused by release of acute phase proteins and inflammatory mediators. Causing pulmonary oedema

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88
Q

Causes of ARDS

A

Pneumonia, gastric aspiration, smoke inhilation, trauma, DIC, Pancreatitis

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89
Q

Pulonary signs/symptoms of interstitial lung diseases

A

Dry cough, SOB, progressive dyspnoea on exertion, infective exacerbations, inspiratory crackles

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90
Q

Systemic signs/symptoms of interstitial lung diseases

A

Lasting tiredness, weight loss, clubbing

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91
Q

Sarcoid treatment

A

Prednisolone and methotrexate can try infliximab. SERUM ACE IS HIGH

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92
Q

Sarcoid signs penumonic

A

Skin - erythema nodosum
Arthritis- feet and hands
Resp- bilateral hilar lymphadenopathy and pulmonary infiltrates
Cardio- Heart block, VT, HF
Occular- uveitis
Intracranial- chronic meningitis, neuropathy, seizures
Derangement of liver and renal function

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93
Q

IPF treatment

A

Best supportive care, transplant, exacerbations (antibiotics, steroids, oxygen, ventilation)

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94
Q

Consequences of occupational lung disorders

A

Risk of unemployment, loss of earnings, chronic ill health

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95
Q

What type of hypersensitivity is extrinsic allergic alveolitis

A

3

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96
Q

Treatment for EAA

A

Avoid allergens, steroids, best supportive care

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97
Q

Ix for EAA

A

FBC (inflammatory markers and WBC), Antibody titre, CXR, Spirometry

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98
Q

Asbestosis

A

Blue is worse. Pleural plaques lead to pleural thickening and mesothelioma

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99
Q

Rheumatoid antibodies

A

antiCCP, antidsDNA, ANA

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100
Q

Bradford hill criteria of causality

A

Temporarlity, reversibility, exposure-response, strength of association, specificity, consistency, analogy, biological plausability

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101
Q

Granulomatosis with polyangitis (Wegeners) signs

A

Saddle nose deformtiy, rash, malaise, diarrhoea, weight loss, joint pain/swelling, nose bleeds

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102
Q

wegeners diagnosis

A
CXR= cavitating lung lesions
FBC= anaemia
U&amp;E= ESR and CRP high
Urine= blood and protein
cANCA
Biopsy
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103
Q

Treatment of wegeners

A

Severe= steroids, cyclophosamide, biologics

No organ damage= prednisolone, methotrexate

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104
Q

Microscopic polyangitis

A

Small vessel vasculitis like wegeners but pANCA. Fatigue, fever, breathlessness, wheeze, cough, haemoptysis

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105
Q

ANCA associated vasculitis treatment

A

Prednisolone, rituximab, cyclophosamide

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106
Q

Rheumatoid arthritis risk factors

A

Women, caucasian, rheumatiod factor, HLA DR4, Other autoimmune conditions, stress, smoking

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107
Q

Symptoms and signs of RA

A

Symmetrical inflamed joint, nodules, episcleritis, carpal tunnel, lymphadenopathy, anaemia, RA nodules and pleural effusions, pericarditis, amyloidosis

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108
Q

RA diagnosis

A

Aspirate joint, FBC (Anaemia), ESR/CRP (high), RF, antiCCP (cyclic citrullinated peptic), XRay

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109
Q

RA on Xray

A

Soft tissue swelling
joint space narrowing
periarticular erosions

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110
Q

RA treatment

A

Methotrexate and sulfasalazine. Pred injections an option

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111
Q

Methotrexate pharmacology

A

Inhibits dihydrofolate reductase which is needed for replication and DNA synthesis, coprescribe folic acid

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112
Q

Methotrexate side effects

A

Mucosal damage, GI upset, nausea, teratogenic

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113
Q

Goodpastures syndrome features

A

Pulmonary haemorrhage and rapidly progressive glomerulonephritis

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114
Q

What type of hypersensitivity reaction is goodpastures

A

Type two

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115
Q

What is the cause of goodpastures

A

antiglomerular basement membrane (anti-GBM) IgM form to T4 collagen

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116
Q

Symptoms of goodpastures

A

Cough, dyspnoea, crackles, increased JVP and haematuria

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117
Q

Investigations in goodpastures

A

Abnormal U&Es, urinalysis (high protein and haemturia), renal biopsy (crescentric GN), CXR (Patchy bilateral symmetrical consolidation)

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118
Q

Goodpastures treatment

A

Plasma exchange and steroids

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119
Q

Define PE

A

Embolic blockage of pulmonary artery, usually from DVT. Means lung tissue is ventilated but not perfused

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120
Q

Clinical presentation of PE

A

Sudden onset unexplained dyspnoea, pleuritic chest pain, cough, haemoptysis with previous leg pain/swelling

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121
Q

Diagnosis of PE

A

Gold= CT pulmonary angiogram. Risk assessment using Well’s Score. Bloods, baseline clotting, D-Dimer, ECG, ABG

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122
Q

Immediate management of PE

A

100% O2 and IV analgesia and enoxaparin

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123
Q

Define pneumonia

A

Inflammation of the lung parenchyma usually secondary to infection of the alveoli and surrounding tissue

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124
Q

Bacterial causes of penumonia

A
Strep Pneumonia (80%)
H. Influenzae (COPD exacerbations)
Klebsiella pneumoniae (alcoholics hobo)
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125
Q

Atypical causes of pneumonia

A

Mycoplasma pneumonia, legionella pneumophilia, chlamydophila pneumoniae, chlamydophila psittaci

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126
Q

Viral causes of pneumonia

A

Influenza virus A/B

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127
Q

Fungal causes of pneumonia

A

Pneumocystis jiroveci (HIV)

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128
Q

Signs and symptoms of pneumonia

A

Cough, SOB, fever, rigors, chest pain, tachycardia, low sats, crackles, reduced breath sounds

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129
Q

Diagnosis of pneumonia

A

Clinical examination, Bloods (high WCC, neutrophils and CRP), XRay (areas of opacification) Microbiology

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130
Q

How do you do microbiology for pneumonia

A

Sputum gram stain, culture and snesitivity
Urine serology: legionella antigen
Bronchoscopy/ bronchoalveolar lavange

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131
Q

Consequence of CURB 0-1 score

A

Outpatient amoxicillin

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132
Q

Consequences of CURB 2 score

A

Hospital admission. Amoxicillin and clarithromycin PO

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133
Q

Consequences fo CURB score over 3

A

Urgent admission, consider ITU, IV coamoxiclav and clarithromycin

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134
Q

Define TB

A

Chronic granulomatous infectious disease caused by mycobacterium tuberculosis

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135
Q

Risk factors for TB

A

Poverty/cramped conditions, poor hygiene, Immunosuppression, smokers, foreign travel

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137
Q

Clinical presentation of TB

A

Weight loss, night sweats, malaise, cough, haemoptysis, SOB, chest pain.

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137
Q

What is the test for latent TB

A

Mantoux test, injection of PPD

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138
Q

Diagnosis of TB

A

Sputum tst x3, . CXR opacities.

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139
Q

How long do you give TB drugs for

A

RIPE for 2 months, continue with R and I for 4 more

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140
Q

Pyrazinamide side effects

A

Arthralgia and hepatitis

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141
Q

Describe small cell tumours

A

15%. Highly associated with smoking. Neuroendocrine tumours. Rapid growth, highly malignant, poor prognosis

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142
Q

Which hormones are secreted by small cell lung cancers

A

5-HT, ACTH, ADH

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143
Q

Name three non small cel lung cancers in order of prevalence

A

Squamous cell, large cell, adenocarcinoma

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144
Q

Common sites of metastasis for bronchial carcinoma

A

Lymph, brain, bone

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145
Q

Symptoms of bronchial carcinoma

A

Cough with haemoptysis, weight loss, SOB, chest pain, Sx of mets (bone pain, seizures)

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146
Q

Do you get osteoporosis from inhaled corticosteroids

A

No

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147
Q

Diagnosis of bronchial carcinoma

A

CXR/ Chest CT and biopsy

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148
Q

Treatment of bronchial carcinoma

A

Surgery, chemo, radiotherapy

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149
Q

Define mesothelioma

A

Aggressive tumour of mesothelial cells which usually occurs in the pleura

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150
Q

Symptoms of mesothelioma

A

SOB, chest pain, weight loss, fatigue, signs of pleural effusion

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151
Q

Diagnosis of mesothelioma

A

CXR/ Chest CT and pleural biopsy

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152
Q

Treatment for mesothelioma

A

Surgery, chemo, radio

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153
Q

AIDS defining infections

A

Candidiasis oesophageal, mycobacterium TB, persistent herpes simplex, pneumocystis jirovecci penumonia, recurrant bacterial pneumonia

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154
Q

AIDS defining neoplasms

A

Kaposis carcinoma, NonHodkins lymphoma

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155
Q

Direct HIV effect conditions

A

HIV dementia

HIV associated wasting

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156
Q

Causes of acute breathlessness

A

Asthma, pneumonia, PE, pneumothorax, hyperventilation

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157
Q

CV causes of clubbing

A

Cyanotic congenital heart disease
Right to left defect
IE

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158
Q

GI causes of clubbing

A

IBD, PBC, Cirrhosis

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159
Q

Endo causes of clubbing

A

Acromegaly and graves acropachy

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160
Q

What do leads I, aVL, V5 and V6 represent

A

Lateral region, circumflex

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161
Q

What do leads II, III and aVF represent

A

Inferior, right coronary artery

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162
Q

What do leads V1-4 represent

A

Septal and anterior. LAD

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163
Q

Define ischaemic heart disease

A

Myocardial demand for oxygen/nutrients greater than delivery via coronary arteries

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164
Q

Causes of IHD from occlusion

A

Atherosclerosis, thrombosis, spasm, embolus, arteritis

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165
Q

Causes of IHD from reduced oxygen delivery

A

Anaemia and hypotension

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166
Q

Causes of IHD from increased oxygen requirements

A

Thyrotoxicosis, aortic stenosis

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167
Q

Non modifiable IHD risk factors

A

Age, male gender, family history

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168
Q

Modifiable IHD risk factors

A

Smoking, alcohol, poor diet, obesity, lack of exercise

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169
Q

Clinical IHD risk factors

A

Hyperlipidaemia, diabetes, hypertension

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170
Q

Psychosocial IHD risk factors

A

Work stress, lack of social support, depression

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171
Q

Define angina

A

Chest pain arising from the heart due to myocardial ischaemia

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172
Q

Describe the pain of angina

A

Heavy central (+retrosternal, radiates to arms and jaw), exertional with no clinical signs usually

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173
Q

Angina investigations

A

Exercise ECG showing ST depression, angiogram if uncertain or intervention likely

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174
Q

Acute management of angina

A

GTN spray, regular nitrates, beta blockers, CCB, revascularisation

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175
Q

Secondary prevention of angina

A

Lifestyle change, control risk factors, aspirin and a statin

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176
Q

How do you differentiate NSTEMI and unstable angina

A

Measure the serum troponin level at 12 hours. Will be positive in MI but not in unstable angina

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177
Q

Describe the pain in ACS

A

Severe central crushing, radiates to arms and jaw. Not relieved by nitrates or rest. Breathless, nausea, sweating, pale, sense of impending doom

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178
Q

Investigations for ACS

A

ECG, troponin, FBC

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179
Q

ECG changes in STEMI

A

Q waves, >1mm broad and 2mm deep, negative deflection at start of QRS, Normal in AVR and V1, ST elevation, T wave inversion

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180
Q

ECG changes in NSTEMI

A

No Q waves, deep ST depression, T wave inversion

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181
Q

Acute management of STEMI

A

ABCDE, MONA (Morphine, oxygen, nitrates, aspirin), Emergency PCI or thrombolysis

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182
Q

Which drugs are used for thrombolysis

A

Streptokinase or alteplase

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183
Q

Name two nitrates

A

Isosorbide mononitrate and glyceryl trinitrate

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184
Q

Long term management of ACS

A

Aspirin, beta blocker, statin, ACE inhibitor, optimise risk factors, no driving for 1 month

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185
Q

Early complications of MI

A

Arrythmias, sudden death, pericarditis, heart failure, cardiogenic shock, mitral regurgitation, VSD, cardiac dilatation

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186
Q

Late complications of MI

A

DVT, PE, Mural thrombus, cardiac aneurysm, Dressler syndrome

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187
Q

What is dressler syndroms

A

Post MI. Fever, chest pain, pericarditis

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188
Q

Causes of primary HTN

A

Idiopathic, genetic factors, fetal factors, obesity, alcohol,, salt intake, stress

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189
Q

Secondary causes of HTN

A

Renal, Endocrine (Conns, adrenal hyperplasia, phaeochromocytoma, cushings, acromegaly), coarctation, OCP, Steroids, NSAIDs, pregnancy

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190
Q

Stage 1 hypertension

A

Clinic 140/90, ambulatory 135/85

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191
Q

Stage 2 hypertension

A

clinic 160/100, ambulatory 150/95

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192
Q

Severe HTN

A

Clinic 180/110, Ambulatory 180/110

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193
Q

Diabetes HTN target

A

130/80

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194
Q

Investigations in HTN

A
Looking for end organ damage
Urine dipstick for protein + blood
Serum creatinine, electrolytes and eGFR
12 lead ECG (LVH or CHD signs)
Echocardiography
Fasting glucose, fasting serum total and HDL
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195
Q

Who do you treat in HTN

A

Over 80, stage1 +target organ damage or disease

Everyone with stage 2

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196
Q

Target BP under 80

A

140/90

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197
Q

Target BP over 80

A

150/90

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198
Q

Examples of ACE inhibitors

A

Rampiril, lisinopril, enalapril

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199
Q

Examples of Angiotensin II receptor antagonists

A

Losartan, candesartan

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200
Q

Examples of betablockers

A

Atenolol, bisoprolol

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201
Q

Examples of calcium channel blockers

A

Amlodipine, nifedipine

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202
Q

Examples of thiazide diuretics

A

Bendoflumethiazide

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203
Q

First line <55

A

Ramipril

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204
Q

First line Black or >55

A

Amlodipine

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205
Q

What to give instead of CCB if intolerant or high risk of heart failure

A

Bendroflumethiazide

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206
Q

Resistant hypertension

A

Consider adding low dose spironolactone or higher dose thiazide and refer

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207
Q

Define heart failure

A

The heart is unable to maintain sufficient cardiac output to provide a physiologically normal circulation

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208
Q

What two systems are involved in heart failure

A

RAAS and sympathetic

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209
Q

What is the sympathetic heart failure physiology

A

Reduced cardiac output, baroreceptor activation, tachycardia, cardiotoxicity, heart failure

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210
Q

What is the RAAS heart failure physiology

A

Reduced cardiac output, activated RAAS, vasoconstriction and sodium retention, increased peripheral resistance and increased venous pressure, heart failure

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211
Q

Left heart failure causes

A

IHD, cardiomyopathy, hypertension, aortic/mitral valve disease, arrythmias, congenital heart disease

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212
Q

Clinical features of left heart failure

A

Fatigue, SOBOE, Orthopnoea, Paroxysmal nocturnal dyspnoea, tachycardia, fine crackles at lung base

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213
Q

What is orthopnea

A

Shortness of breath which occurs when lying down

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214
Q

Right heart failure causes

A

Cor pulmonale, PE, pulmonary HTN, left to right shunts, tricuspid regurgitation

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215
Q

Clinical features of right heart failure

A

Fatigue, anorexia/nausea, GI upset, raised JVP, pitting oedema, ascites, pleural effusion, hepatomegaly

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216
Q

Investigations of heart failure

A

Chest XRay (ABCDE), ECG (for underlying cause), FBC, LFTs, U&Es, glucose, TFTs, Serum BNP (always high), Echocardiogram (ejection fraction below 0.45)

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217
Q

Signs of heart failure on XRay

A
Alveolar oedema
Kerly B lines (interstitial oedema)
Cardiomegaly
Dilated upper lobe vessels
pleural Effusion
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218
Q

Non drug treatment of heart failure

A

Education, lifestyle measures, optimise risk factors, correct aggravating features like anaemia, pneumococcal and influenza vaccines, driving unrestricted

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219
Q

Drugs for heart failure

A
ACE-i
Bisoprolol
Candesartan
Digoxin
Diuretics
Spironolactone
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220
Q

Surgical treatment of heart failure

A

CABG, Valve replacement, pacemaker, heart transplant

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221
Q

Causes of congenital heart disease

A
Maternal factors
-maternal rubella
-foetal alcohol syndrome
-maternal SLE
Genetic
-trisomy 21
-turners syndrome
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222
Q

Acyanotic congenital heart diseases with shunts

A

ASD, VSD, PDA

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223
Q

Acyanotic congenital heart diseases without shunts

A

Coarctation of the aorta, congenital aortic stenosis

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224
Q

Cyanotic congenital heart disease with shunts

A

Tetralogy of fallot, transposition of the great arteries

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225
Q

Cyanotic congenital heart disease without shunts

A

Severe pulmonary cyanosis

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226
Q

common consequences of congenital heart disease

A

Central cyanosis, congestive heart failure, pulmonary hypertension, polycythaemia, eisenmengers syndrome

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227
Q

Signs of ASD

A

Mid systolic ejection murmur in pulmonary area, fixed splitting of S2.

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228
Q

Symptoms of right heart overload

A

Dyspnoea, fatigue, exercise intolerance

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229
Q

Investigations for ASD

A

CXR- dilated pulmonary artery
ECG- right axis deviation
Echo- hypertrophy and dilation of right heart

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230
Q

Management for ASD

A

Conservative or surgery

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231
Q

Signs of VSD

A

Pansystolic murmur at left lower sternal edge, systolic thrill left parasternal heave

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232
Q

Consequence of small VSD

A

Loud murmur, asymptomatic

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233
Q

Consequences of a large VSD

A

Pulmonary hypertension, breathless, poor feeding

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234
Q

Investigations for VSD

A

CXR, ECG, Echo

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235
Q

Management of VSD

A

Conservative or surgery

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236
Q

What is patent ductus arteriosus

A

Bypass from the pulmonary artery to the aorta

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237
Q

Causes of PDA

A

90% isolated, 10% from maternal rubella

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238
Q

What is QRISK2

A

Used to calculate the risk of CVD event in the next ten years. Age, Sex, Ethnicity, Smoking, RA, Diabetes, CKD, AF, angina

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239
Q

Signs of PDA

A

Usually asymptomatic, continuous machinery murmur, pulmonary HTN

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240
Q

PDA management

A

Percutaneous devices, endocarditis prophylaxis

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241
Q

4 features of tetralogy of fallot

A

RV outflow obstruction
Large VSD
R ventricular hypertrophy
Overriding aorta

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242
Q

Tetralogy of fallot symptoms

A

Cyanosis, feeding difficulty, failure to thrive

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243
Q

Tetralogy of fallot signs

A

Clubbing, loud harsh ejection sysolic murmur at lower left sternal edge. Hyper cyanotic spells.

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244
Q

Investigations for tetralogy of fallot

A

CXR, ECG, Echo

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245
Q

Management of tetralogy of fallot

A

Initially medical, surgery at 6 months

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246
Q

Descibe coarctation of the aorta

A

Narrowing of the aorta at the ductus arteriosus.
Sever: collapse and heart failure
Mild: raised BP and mid-late systolic murmur

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247
Q

Symptoms of coarctation of the aorta

A

headaches, nose bleeds and claudication

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248
Q

Signs of coarctation of the aorta

A

Radio-femoral delay, BP higher in arm than leg. Poor peripheral pulses

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249
Q

Management of coarctation of the aorta

A

Surgery

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250
Q

Causes of aortic stenosis

A

Calcification
Congenital (bicuspid)
Rheumatic fever
Outflow obstruction- hypertrophic obstructive cardiomyopathy

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251
Q

Symptoms of aortic stenosis

A

exercise induced angina, syncope, breathlessness. Sudden death

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252
Q

Signs of aortic stenosis

A

Slow rising pulse, sustained apex beat, systolic thrill in aortic region

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253
Q

Aortic stenosis heart sounds

A

Ejection systolic murmur in aortic area, radiated to the carotid, soft second heart sound, fourth heart sound

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254
Q

Investigations for aortic stenosis

A

ECG - LV Hypertrophy (depressed ST, T wave invert)

Echo is diagnostic

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255
Q

Management of aortic stenosis

A

Conservative, valve replacement if severe/symptomatic

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256
Q

Acute causes of aortic regurgitation

A

Acute rheumatic fever, IE, aortic dissection

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257
Q

Chronic causes of aortic regurgitation

A
Rheumatic fever
Marfans
Syphilis
Autoimmune
Bicuspid aortic valve
Severe hypertension
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258
Q

Symptoms of aortic regurg

A

Asymptomatic until LV fails
Palpitations
Angina/ dyspnoea

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259
Q

Signs of aortic regurgitation

A

Left ventricular failure
Quinckes sign (pulsating nailbeds)
de mussets sign (head nodding with heart beat)
waterhammer pulse
Pistol shot femoral (sharp bang on ausculation)

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260
Q

Aortic regurgitation heart sounds

A

Displaced hyperdynamic apex beat
Soft early diastolic murmur at left sternal edge
Accentuated when patient sits forward
Severe= austin flint murmur

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261
Q

Aortic regurgitation investigations

A

Chest XRay
ECG- LV hypertrophy
Echo

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262
Q

Management of aortic regurgitation

A

Mild= vasodilators and diuretics

Valve replacement

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263
Q

Causes of mitral stenosis

A

Rheumatic fever

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264
Q

Symptoms of mitral stenosis

A

Only in severe, breathlessness, paroxysmal nocturnal dyspnoea, haemoptysis, recurrant chest infections

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265
Q

Signs of mitral stenosis

A
Malar rash
Small-volume pulse
Atrial fibrillation
Tapping apex beat
Signs of RV failure
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266
Q

Mitral stenosis heart sounds

A

Loud first heart sound, opening snap, rumbling mid diastolic murmur at apex with patient on their left

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267
Q

Mitral stenosis investigations

A

Chest XR
ECG= bifid P WAVE
RV hypertrophy
Echo

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268
Q

Mitral stenosis management

A

Diuretics, digoxin, anticoagulation, valvotomy, replacement

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269
Q

Mitral regurgitation causes

A
Mitral valve prolapse
Rheumatic fever
Infective endocarditis
IHD
Cardiomyopathy
SLE/Marfans/ Ehlers-Danlos
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270
Q

Symptoms of mitral regurg

A

Palpitations, dyspnoea, orthopnoea, fatigue, right heart failure

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271
Q

Signs of mitral regurg

A

Cardiac failure, laterally displaced apex, hyperdynamic, systolic thrill

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272
Q

Mitral regurg heart sounds

A

Soft first heart sound, loud pansystolic murmur at apex radiating to axilla, third heart sound

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273
Q

Mitral regurg investigations

A

Chest XR- left atrial and ventricular enlargement

Echo

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274
Q

Management of mitral regurg

A

Echo monitoring, endocarditis prophylaxis, valve replacement

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275
Q

Define pericarditis

A

Inflammation of the pericardium

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276
Q

Viral causes of pericarditis

A

Coxsackie B, echovirus (EBV, HIV)

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277
Q

Bacterial causes of pericarditis

A

Pneumococcal, staphylococci, gram-ve organisms, TB

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278
Q

Non infective causes of pericarditis

A

Dresslers syndrome, autoimmune (Rheumatic fever, SLE, RA)

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279
Q

Symptoms of pericarditis

A

Chest pain (worse on breathing and lying flat, relieved by sitting forward, may radiate to neck and shoulders) malaise

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280
Q

Signs of pericarditis

A

Fever, tachycardia, pericardial friction rub, dyspnoea

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281
Q

Investigations of pericarditis

A

Bloods, ECG, CXR, Echo

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282
Q

Bloods of pericarditis

A

Raised WCC, CRP/ESR, Blood cultures, cardiac enzymes

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283
Q

ECG of pericarditis

A

Widespread shaddle shaped ST elevation

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284
Q

Treatment of pericarditis

A

Treat cause, analgesia, NSAIDs, rest, manage complications ie pericardial effusion

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285
Q

Define cardiomyopathy

A

Disease of the myocardium that effects the mechanical or electrical function of the heart

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286
Q

Types of cardiomyopathy

A

Hypertrophic, dilated, restrictive, arrythmogenic

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287
Q

Define hypertrophic cardiomyopathy

A

Marked ventricular hypertrophy in the absence of abnormal loading conditions

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288
Q

What is teh effect of hypertrophic cardiomyopathy

A

Impaired diastolic filling, reduces stroke volume, most common cause of sudden death in young people. Most causes are familial and autosomal dominant

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289
Q

Symptoms of hypertrophic cardiomyopathy

A

Asymptomatic, breathless, angina syncope, sudden death

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290
Q

Signs of hypertrophic cardiomyopathy

A

Atrial and ventricular arrythmias, jerky carotid pulse, ejection systolic murmur, pansystolic murmur

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291
Q

Investigations of hypertrophic cardiomyopathy

A

ECG always abnormal
Echo shows ventricular hypertrophy
Genetic analysis

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292
Q

Management of hypertrophic cardiomyopathy

A

Amiodarone (reduces arrythmias and sudden death), if high risk then implantable cardioverter defibrillator. Beta blocker for symptoms

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293
Q

Define dilated cardiomyopathy

A

Dilated left ventricle which contracts poorly

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294
Q

Causes of dilated cardiomyopathy

A
Autosomal dominant familial disease
Alcohol
Post pregnancy
Hypertension
Valvular heart disease
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295
Q

Clinical features of dilated cardiomyopathy

A

SOB mainly, can present with embolism, arrythmia or proggressive heart failure

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296
Q

Dilated cardiomyopathy investigations

A

CXR (cardiac enlargement)
ECG
Echo

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297
Q

Management of dilated cardiomyopathy

A

Treat HF and AF, Implantable cardiac defibrilator, cardiac transplant

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298
Q

Define peripheral vascular disease

A

Disease which occurs when there is significant narrowing of the arteries distal to the arch of the aorta, most commonly due to atherosclerosis

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299
Q

Fontane classification for PVD

A

I asymptomatic
II intermittent claudication
III rest pain
IV necrosis/gangrene

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300
Q

Why is there fixed splitting of S2 in atrial septal defects

A

Because the pulmonary valve closes after the aortic

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301
Q

What has a boot shaped heart on XRay

A

Tetralogy of fallot

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302
Q

When is PCI contraindicated

A

When it is too late or they have already had it

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303
Q

Define intermittent claudication

A

Exertional discomfort mainly in the calf, relieved by rest

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304
Q

Define rest pain

A

Unremitting pain in the foot, stops patient from sleeping, relieved by dangling foot over the bed

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305
Q

Signs of PVD

A

Cold dry skin, diminshed pulses, ulceration

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306
Q

Investigations in PVD

A

Pulse, Ankle-Brachial pressure index, duplex ultrasound

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307
Q

ABPI results

A

1 or more= symptom free
0.9-0.5= intermittent claudication
<0.5= critical limb ischaemia

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308
Q

Management fo PVD

A

Aggressive risk factor management, statin, aspirin

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309
Q

The 6Ps of acute limb ischaemia

A
Pain
Pallor
Pulselss
Paraesthesia
Paralysis
Perishingly cold
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310
Q

Causes of acute limb ischaemia

A

Can by embolic or thrombotic

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311
Q

Management of acute limb ischaemia

A

Heparin, if embolic long term warfarin, bypass graft

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312
Q

Define arrythmia

A

Abnormality of cardiac rhythm

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313
Q

Symptoms of. arrythmias

A

Asymptomatic, palpitations, dizziness, syncope, sudden death

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314
Q

What causes sinus arrythmia

A

Fluctuations in the autonomic tone results in changes in the sinus discharge rate

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315
Q

Extrinsic to heart causes of bradycardia

A

Drugs, hypothyroid, hypothermia, cholestatic jaundice, raised ICP

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316
Q

Intrinsic to heart causes of bradycardia

A

Ischaemia, infarction, fibrosis of atrium and sinus node

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317
Q

Treatment of bradycardia

A

Pacemaker if symptomatic

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318
Q

Causes of sinus bradycardia

A

Normal during sleep and athletes

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319
Q

Causes of neurally mediated bradycardia

A

Carotid sinus syndrome, vasovagal attacks

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320
Q

Common causes of heart block

A

Coronary artery disease, cardiomyopathy, fibrosis in conducting tissue

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321
Q

Causes of AV block

A

Block in the AV node or bundle of his

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322
Q

First degree AV block ECG

A

Delayed AV conduction, prolonged PR interval. No change in HR and no treatment needed

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323
Q

Second degree AV block cause

A

Some atrial impulses fail to reach the ventricle

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324
Q

Mobitz type 1 ECG

A

Progressive PR prolongation until fails to conduct

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325
Q

Mobitz type 2 ECG

A

Intermittent non conducted P waves without progressive prolongation of the PR interval

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326
Q

Third degree AV block

A

All atrial activity fails to conduct to the ventricles, atria and ventricles contact independently. No association between P waves and QRS on ECG

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327
Q

What is bundle branch block

A

Complete block of a bundle branch leads to abnormal conduction and widening of QRS >120ms

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328
Q

Right bundle branch block ECG

A

RBB no longer conducts impulse, spread of impulse from left to right. Secondary R wave in V1, slurred S wave in V6

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329
Q

Left bundle branch block ECG

A

Deep, wide S in V1, Secondary R wave in V6

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330
Q

What is sinus tachycardia

A

Physiological response to exercise or excitement. Occurs with fever, anaemia, HF, thyroid, PE, hypovolaeia and drugs

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331
Q

What is AV node reentrant tachycardia

A

The most common SVT, P waves arent visible or are seen directly before or after QRS. Narrow QRS complexes

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332
Q

What is Atrioventricular reciprocating tachycardia

A

Wolff-Parkinson-White syndrome, short PR interval, narrow QRS complexes

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333
Q

Supraventricular tachycardia symptoms

A

Rapid, regular palpitations, abrupt onset, sudeen termination. Dizziness, dyspnoea, central chest pain, syncope, aggravated by exercise, caffeine and alcohol

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334
Q

Treatment of unstable patient SVT

A

Emergency cardioversion, O2, electrolyte abnormalities corrected

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335
Q

Treatment of stable patient SVT

A

Vagal stimulation, adenosine, long term= ablation

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336
Q

Causes of atrial arrythmias

A

IHD, rheumatic disease, thyrotoxicosis, cardiomyopathy, pneumonia, ASD, pericarditis, alcohol use, cardiac surgery

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337
Q

Define atrial fibrillation

A

Uncoordinated rapid continous activation of the atria, leading to mechanically innefective contraction

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338
Q

What is the pulse like in atrial fibrillation

A

Irregularly irregular pulse

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339
Q

Presentation of atrial fibrillation

A

Asymptomatic, palpitations, reduced exercise tolerance, heart fialure, embolic events, irregularly irregular pulse

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340
Q

Investigations for AF

A

ECG: No P waves, irregular rapid QRS rhythm

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341
Q

Management of AF

A
Rate control
-beta blockers or CCBs
Rhythm control
-if young, symptomatic or HF
-electrical DC cardioversion then beta blockers
-or with amiodarone
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342
Q

What score is used to determie the coagulation for AF

A

CHADS2VASc determines the risk of stroke

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343
Q

What does a score of 1 need

A

Aspirin

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344
Q

What does a score of 2 need

A

Warfarin

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345
Q

How do you calculate CHADS2VASc

A
Congestive heart failure
Hypertension
Age
-65-74
-75=2
Diabetes mellitus
Stroke of TIA=2
Vacular disease
Sex female
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346
Q

Atrial flutter

A

Atrial rate of 300bpm and ventricular rate of 150bpm

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347
Q

Investigations of atrial flutter

A

Sawtooth F waves on ECG

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348
Q

Define aortic aneurysm

A

A permanent and irreversible dilation of a blood vessel by atleast 50% of normal

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349
Q

Risk factors for aortic aneurysm

A

Severe atherosclerotic damage, family history, smoking, male, increasing age, hypertension, COPD, hyperlipidaemia

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350
Q

Presentation of aortic aneurysm

A

Pain in back, abdomen, loin to groin. Pulsatile abdominal swelling. If ruptures then sever and sudden pain. Syncope, shock or collapse

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351
Q

Aortic aneurysm on examination

A

Pulsatile, expansible mass

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352
Q

Aortic anurysm investigations

A

Ultrasound, ct, mri angiography

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353
Q

Management of aortic aneurysm

A

Anti HTN, Statin, smoking cessation.

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354
Q

How does the size of aneurysm alter the treatment

A

Ultrasound and. surgery if big >5cm

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355
Q

Describe aortic dissection

A

Results from a tear in the intima, blood under high pressure seperates the aortic wall layers creating a false lumen. False lumen can obstruct the true lumen.

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356
Q

Risk factors for aortic dissection

A

Hypertension, smoking, hyperlipidaemia, aortic disease, bicuspid aortic valve, history of cardiac surgery

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357
Q

Inherited risks of aortic dissection

A

Marfans, Ehlers Danlos. Familial thoracic aneurysm type 1 and 2.

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358
Q

Aortic dissection presentation

A

Sudden tearing central pain which radiated to the back and moves as dissection progresses.

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359
Q

Investigation for aortic dissection

A

ECG, CXR, Imaging= CT, TOE, MRI

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360
Q

Management of aortic dissection

A

IV access, intensive care, aggressively control BP (<120sys with BB), blood, surgery

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361
Q

What do you call it when someone can speak but is making no sense

A

Expressive aphasia

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362
Q

Define transient ischaemic attack

A

Brief episode of neurological dysfunction due to temporary focal cerebral or retinal sichaemia without infarction, usually lasting seconds or minutes with complete recovery

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363
Q

Differential diagnosis of TIA

A
Hypoglycaemia
Migraine aura
Focal epilepsy
Cerebral amyloid angiopathy
Hyperventilation
Retinal bleeds
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364
Q

Causes of tia

A

Atherothromboembolism (from carotid)
Cardioembolism- mural thrombus post MI or in AF, valve disease or prosthetic valve
Hyperviscosity- polycythaemia, sickle cell, myeloma
Vaculitis- SLE, syphilis, GCA

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365
Q

TIA anterior circulation

A

Amaurosis fugax, aphasia (brocas), hemiparesis or hemisensory loss

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366
Q

TIA posterior circulation

A

Diplopia, vertigo, vomiting, choking, dysarthria, ataxia, hemianopic visual loss, tetraparesis

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367
Q

What score is used for the risk of stroke within two days of TIA

A

ABCD2

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368
Q

How do you work out ABCD2 score

A
Age >60=1
BP >140/90=1
Clinical features,
-unilateral weakness=2
-speech disturbance without weakness=1
Duration of symptoms
->60mins =2
- 10-59mins=1
Diabetes=1
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369
Q

Which ABCD2 score requires urgent investigation and. secondary prevention

A

> 4 or two recent TIAs

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370
Q

Investigations for TIA

A

Bloods, CXR, ECG and Echo, Carotid doppler and angiography, CT

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371
Q

Management of TIA

A

Control cardiovascular risk factors, antiplatelets, warfarin and carotid endarterectomy

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372
Q

How does clopidogrel work

A

It is a ADP receptor blocker

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373
Q

How does dipyridamole work

A

Increases cAMP and reduces thromboxane A2

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374
Q

Which antiplatelets would you use in TIA

A

Aspirin then Clopidogrel and dipyridamole together

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375
Q

Define stroke

A

A syndrome of rapid onset neurological defecit caused by focal, cerebral, spinal or retinal infaction. Tissue injury is confirmed by neuroimaging

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376
Q

Modifiable stroke risk factors

A

Hypertension, smoking, hyperlipidaemia, Diabetes mellitus, heart disease, increased alcohol, pill and hrt

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377
Q

Non modifiable stroke risk factors

A

Age, male, afrocarribean, previous vascular event, family history

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378
Q

Causes of ischaemic stroke

A

Thrombotic, large artery stenosis, small vessel disease, cardioembolic, hypoperfusion

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379
Q

Causes of haemorrhagic stroke

A

Intracerebral haemorrhage, subarachnoid haemorrhage. Other (arterial dissection, venous sinus thrombosis, vasculitis)

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380
Q

What classification is used for ischaemic stroke presentation

A

Bamford classification

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381
Q

What is the presentation of. an ischaemic stroke

A

Acute onset of negative symptoms indicating focal deficits in brain function such as weakness, sensory loss, dysphasia and visual loss

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382
Q

Anterior cerebral artery stroke symptoms

A

Leg weakness, sensory disturbance in legs, gait apraxia, incontinence, drowsiness, akinetic mutism

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383
Q

Middle cerebral artery stroke symptoms

A

Contralateral arm and leg weakness, contralateral sensory loss, hemianopia, aphasia or dysphasia, facial droop, neglect syndromes

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384
Q

Which ABCD2 score strongly predicts a stroke

A

> 6

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385
Q

Posterior cerebral artery symptoms

A

Contralateral homonymous hemianopia, cortical blindness, visual agnosia, prosopagnosia, anomic aphasia (colour naming and discrimination problems), unilateral headaches

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386
Q

Primary causes of intracerebral haemorrhage

A

Hypertensive- rupture of charcot bouchard aneurysms
Cerebral amyloid angiopathy
-lobar, recurrant, associated with alzheimers

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387
Q

Secondary causes of intracerebral haemorrhage

A

Tumour
Arterovenous malformations
Anticoagulants
Venous infarctions

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388
Q

Clinical features of intracerebral haemorrhage

A

Similar to ischaemic but more associated with severe headache and coma from raised intercranial pressure

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389
Q

Investigations in intracerebral haemorrhage

A

CT imaging

MRI and MR angiography for AVM or aneurysms

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390
Q

Management of ischaemic stroke

A

Frequent monitoring of GCS and signs
Reverse anticoagulation (vitamin K)
BP control

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391
Q

Where are berry aneurysms common

A

Between posterior communicating and ICA

Between anterior communicating and anterior cerebral

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392
Q

Consequence of posterior communicating aneurysm pressing on neighbouring structure

A

3rd nerve palsy

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393
Q

Causes of subarrachnoid haemorrhage

A

Berry aneurysm rupture, arteriovenous malformation

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394
Q

Clinical features of subarachnoid haemorrhage

A

Sudden severe thunderlap headache with lasts for housrs. Often associated with vomitting, HTN, neck stiffness or pain. Kernigs sign and budzinskis sign

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395
Q

What is kernigs sign and when is it present

A

Patient cant extend leg when hip flexed. SAH and meningitis

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396
Q

What is brudzinskis sign and when is it present

A

Neck pulled forward causes knee flexion. SAH and meningitis

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397
Q

Investigations of SAH

A

CT

If CT negative then 12 hours later do a LP if no CI and it will be Xanthochromic

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398
Q

Management of SAH

A

Urgent neurosurgery referral, regular CNS examination, hydration and antihypertensives, nimodipine for 3 weeks

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399
Q

Why is Nimodipine given in SAH

A

It is a CCB and reduces vasospasm

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400
Q

Cause of subdural haemorrhage

A

Rupture of bridging veins, caused by head injury and in the elderly, alcoholics and babies

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401
Q

Cause of extradural haemorrhage

A

Skull fracture tearing a branch of the middle meningeal artery

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402
Q

Time frame for subdural haematoma

A

Days weeks or months after

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403
Q

Time from for extradural haematoma

A

Lucid interval of hours or days

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404
Q

Presentation of subdural haematoma

A

Fluctuating conciousness, headache, personality change, unsteadiness, hemiparesis, focal sensory loss, seizures, unequal pupils

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405
Q

Extradural haematoma presentation

A

Low GCS as severe headache, vomitting, confusin, seizures, hemiparesis. Brisk reflexes, upgoing planter reflex. Coma, ipsilateral pupil dilation and irregular breathing

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406
Q

Subdural haematoma on CT

A

Crescent shaped with midline shift

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407
Q

Extradural haematoma on CT

A

Biconvex shape and midline shift

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408
Q

Treatment of subdural haematoma

A

Close attention, neurosurgery burr hole drill of craniotomy. Can resolve itself.

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409
Q

Treatment of extra dural haematoma

A

Neurosurgery, clot evacuation and ligation of bleeding vessel

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410
Q

What does it need to be to have thrombolysis

A

Clinical ischaemic stroke diagnosis
Assessed by experienced team
Within 4.5hours

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411
Q

What is alteplase

A

Tissue plasminogen activator used in thrombolysis

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412
Q

What can a space occupying lesion lead to

A

brain herniation and death

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413
Q

What is used to combat anticoagulants

A

Beriplex and Vitamin K

Beriplex is quicker

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414
Q

What are lacunar infarcts

A

Subcortical infarcts

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415
Q

What is a watershed infarct

A

Infarct at the border of arterial supplies caused by severe cerebral hypoperfusion

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416
Q

Why is extradural haemorrhage biconvex

A

As ararchnoid granulations restrict spread

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417
Q

Very painful eye movements. Bilateral internuclear opthalmoplegia

A

Multiple sclerosis

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418
Q

Define multiple sclerosis

A

Chronic autoimmune T cell mediated inflammation of the CNS. Plaques of demyleination occur thorughout the brain and spinal cord sporadically over years

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419
Q

Who gets MS

A

Women, 20-40, genetics, further from equator (VitD), can be triggered by viruses like EBV

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420
Q

Types of MS

A

Relapsing remitting
Secondary progressive
Primary progressive
Progressive relapsing

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421
Q

Describe relapsing remitting MS

A

Clearly defined disease relapses with full or partial recovery. Periods between disease relapses characterised by a lack of disease progression

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422
Q

Describe secondary progressive MS

A

Initial relapsing remitting pattern is followed by progressive disability allowing for occasional remission and relapses

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423
Q

Describe primary progressive MS

A

Disease progression from onset with occasional plateaus and temporary improvement allowed

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424
Q

Clinical presentation of MS

A

Optic neuritis, brainstem demyelination, spinal cord lesions

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425
Q

What are the symptoms of brainstem legions in MS

A

diplopia, vertigo, facial numbness/weakness, dyarthria and dysphasia. Bilateral internuclear opthalmoplegia

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426
Q

What are the symptoms of spinal cord lesions in MS

A

Thoracic or cervical lesions can lead to assymetric walking difficulty or numbness in limbs. Paraparesis develops over days or weeks.

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427
Q

Common symptoms in MS

A
Visual change
Sensory symptoms
Clumsy hand or limb
Ataxia or unsteadiness
Bladder hyperreflexia
Neuropathic pain
Fatigue
Spascitiy
Temperature sensitivity
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428
Q

What is uhthoff’s pnenomenon

A

Temperature sensitivity in MS

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429
Q

What is Lhermittes sign

A

Neck flexion leads to electric shock sensation

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430
Q

Late stage MS

A
Severe disability 
Spastic tetraparesis
Optic atrophy
Brainstem signs
Urinary incontinence
Pseudobulbar palsy
Cognitive Impairment (often frontal lobe)
Usually 15 years to needing walking aids and 25 to a wheelchair.
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431
Q

Diagnosis of MS

A

2 or more attacks disseminated in time and space, McDonald criteria

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432
Q

Investigations of MS

A

MRI brain + spinal cord
CSF= oligoclonal IgG bands
Blood tests to exclude other inflammatory disorders

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433
Q

Who can diagnose MS

A

Only consultants

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434
Q

Long term management of MS

A

No cure, education, MDT (physio, OT, counsellor), prevent infections with nonlive vaccinations

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435
Q

How to treat acute relapses of MS

A

Methylprednisolone

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436
Q

Disease modifying drug for MS

A

Beta interferon

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437
Q

Treatment for very aggressive RRMS

A

Immunomodulatory drugs- Natalizumab

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438
Q

Drug for spasticity

A

Baclofen or gabapentin

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439
Q

Drug for emotional lability

A

Amitriptyline

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440
Q

Drug for pain in MS

A

Amitriptyline

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441
Q

Drug for tremor in MS

A

Beta blockers or botulinum toxin A type

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442
Q

Urinary urgency/ frequency in MS treatment

A

Intermittent self catheterisation

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443
Q

Signs of meningism

A

Headache, neck stiffness, photophobia, Kernigs and Brudzinskis

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444
Q

Immediate signs of Bacterial meningitis

A

Fevers, rigors, severe headache, photophobia and vomitting

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445
Q

Signs of bacterial menigitis that appear within hours

A

Neck stiffness and positive Kernig’s sign

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446
Q

Signs of viral meningitis

A

Self limiting, headache, high fever

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447
Q

Causes of viral meningtis

A

Coxsackie, HSV, EBV, HIV mumps

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448
Q

Causes of bacterial meningitis in neonates

A

Ecoli, Group B strep, Listeria

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449
Q

Causes of bacterial meningitis in infants

A

Neisseria meningitidis, haemophilus influenzae, strep pneumoniae

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450
Q

Causes of bacterial meningitis in adults

A

Neisseria meningitidis, strep pneumonia

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451
Q

Causes of bacterial meningitis in the elderly

A

Strep pneumoniae, neisseria meningitidis, listeria

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452
Q

Investigations in meningtisi

A

Lunbar puncture, blood culture, nose and throat swabs, stool sample

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453
Q

What does non blanching petechial rash suggest

A

meningococcal septicaemia

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454
Q

Treatment for N.meningitidis in the community

A

IM Benzyl penicillin

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455
Q

Meningitis with no signs of sepsis or raised ICP treatment

A

Blood culture, lumbar puncture, IV dexamethasone. Then Ceftriaxone, fluids bloods

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456
Q

Meningitis with riased ICP management

A

Oxygen, blood culture, IV dexamethasone, delay LP. Give IV cefriaxone. CT imaging. Then bloods

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457
Q

Meningitis with severe sepsis or evolving rash managament

A

Oxygen, blood cultures, fluids. Delay LP. IV ceftriaxone, bloods

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458
Q

When wouldnt you lumbar puncture

A

Severe sepsis or rapidly evolving
Severe respiratory or cardiac compromise
Significant bleeding risk
Signs of raised ICP (need CT)

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459
Q

Migraines with aura diagnostic criteria

A
1 aura symtopm
-visual, zigzags, spots
-unilateral sensory, tingling, numbness
-speech
-motor weakness
2 out of
-aura spreads gradually over >5mins or theres 2 aura symptoms
-aura symptom lasts 5-60mins
- an aura symptom is unilateral
-headache follows aura within an hour
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460
Q

Migraine without aura criteria

A
>5 attacks lasting 4 to 72 hours
2 of
-unilateral, pulsating, moderate/severe pain, aggravated by exercise
1 of 
-nausea/vomitting
-photophobia and phonophobia
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461
Q

Triggers for Migraine

A

Sleep- too much or too little
Stress
Oestrogen for women
Eating- skipping meals and big meals, alcohol
Bright lights, loud noises, physical exercise

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462
Q

Mild migraine management

A

Aspirin + metoclopramide

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463
Q

Name an antiemetic

A

metoclopramide

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464
Q

Severe migraine management

A

Triptan + Paracetamol

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465
Q

Migraine preventative measures

A

Propanolol, acupuncture, amitriptyline

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466
Q

Describe tension headache

A

30mins to 7 days. Bilateral pressing mild/moderate pain. No associated symptoms. Take paracetamol

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467
Q

Describe cluster headache

A

15-180mins, unilateral retroorbital boring severe pain. With autonomic symptoms on the same side of the face. Take sumatriptan and 100% O2

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468
Q

Describe trigeminal neuralgia

A

Lasts seconds, unilateral electric severe pain with many triggers. No associated symptoms. Treat with carbamazepine

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469
Q

More than 50, jaw claudiaction, visual distrbance, tender and pulseless temporal arteries

A

Giant cell arteritis

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470
Q

Severe eye pain, red eyes, cloudy cornea, dilated and unresponsive pupil

A

Acute glaucoma

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471
Q

Headache worse on bending over

A

Sinusitis

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472
Q

Sudden onset thunderclap

A

Subarachnoid haemorrhage

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473
Q

Worse on lying down, exercise or valsalva

A

increased ICP

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474
Q

Fever fits and altered consciousness

A

Encephalitis

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475
Q

Define epilepsy

A

Paroxysmal event in which changes of behaviour, sensation or cognitive processes are caused by excessive hypersynchronous neural discharges in the brain

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476
Q

Are ischaemic or haemorrhagic strokes painful

A

Haemorrhagic

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477
Q

Temporal lobe seizure with awareness (simple partial)

A

Deja vu,, fear, olfactory, gustatory or auditory hallucinations

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478
Q

Ocipital lobe seizure with awareness (simple partial)

A

Visual phenomena such as zigzags

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479
Q

Frontal lobe seizure with awareness (simple partial)

A

Adversion seizures, jacksonian march

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480
Q

What is aura

A

A sensation percieved by a patient that preceds a condition affecting the brain

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481
Q

Temporal seizures with impaired awareness (complex partial)

A

Automatisms, auras, behaviour arrest, 1-2 minutes. Then post ictal confusion

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482
Q

Frontal seziures with impaired awareness (complex partial)

A

Complex movements like bicylce movement of legs, repeated words or phrases. Post ictal confusion

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483
Q

Gneralised absense seizure

A

loss of awareness and vacant expression for less than 10 seconds. Children

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484
Q

Myoclonic generalised seizure

A

Sudden, breif jerking of a limb face or trunk

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485
Q

Tonic generalised seizure

A

Body becomes stiff, can fall to the ground

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486
Q

Tonic clonic generalised seizure

A

Tonic phase (LOC increased tone) Clonic hase (synchronous jerking). Eyes open tongue biting. Postical confusion

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487
Q

Atonic generalised seizure

A

Sudden collapse with loss of muscle tone and consciousness

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488
Q

Epilepsy triggers

A

Sleep deprivation, missed doses, alcohol and recreational drug (withdrawal), exhaustion, intercurrent illness or metabolic disturbance

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489
Q

Which children and teenagers get epilepsy

A

Genetic, perinatal and congenital disorders

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490
Q

Which young adults get epilepsy

A

Trauma, drugs and alcohol

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491
Q

Which older adults get epilepsy

A

Vascular disease and neoplasms causing mass legions

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492
Q

Epilepsy investigations

A

Bloods, ECG, MRI, EEG, VIDEO telemetry DIAGNOSTIC

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493
Q

Management of focal seizures

A

Carbamazepine (lowers effectiveness of pill)

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494
Q

Management of general seizures

A

Sodium valproate (teratogenic)

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495
Q

How do you treat status epilepticus (seizure >5mins)

A

Airway, O2, IV access. Diazepam. Rectal in community, IV in hospital

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496
Q

Describe epilepsy

A

Aura, common from sleep, less than 2mins, rhythmical jerking, eyes open, tongue biting, incontinence, breathing stops, recovery slow

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497
Q

Describe non epileptic attack disorder

A

Aura, common in medical situations, more than 2 mins, thrashing movements, hip thrusting, respiration fast, eyes closed no tongue biting or incontince

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498
Q

Describe syncopy

A

Nausea, sweating, visual grey out, prolonged standing or on stnading. Less than 2 mins, occasional limb jerks, eyes closed no tonuge biting. Normal breathing, fast recovery

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499
Q

Ascending weakness, fasciculations, no sensory sphincter or eye loss, 50-70

A

MND

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500
Q

Define MND

A

Neurodegenerative condition caused by progressive loss of upper and lower motor neurones in the spinal cord, cranial nerve nuclei and motor cortex

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501
Q

Familial cause of MND

A

SOD1 gene mutation

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502
Q

Describe upper motor neurone legion

A

Weakness, increased reflexs, plantar and tone. No fasciculations or atrophy

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503
Q

Describe lower motor neurone lesions

A

Weakness atrophy fasciculation. Reduced reflexes, plantars, tone

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504
Q

What are the four clinical patterns of MND

A

Amyotrophic lateral sclerosis
Progressive muscular atrophy
Progressive bulbar palsy
Primary lateral sclerosis

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505
Q

Amyotrophic lateral sclerosis

A

UMN and LMN

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506
Q

Progressive muscular atrophy

A

LMN

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507
Q

Progressive bulbar palsy

A

CN 9-12

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508
Q

Primary lateral sclerosis

A

UMN

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509
Q

Over 40, stumbling spastic gait, footdrop, weak grip, weak shoulder abduction, aspiration pneumonia

A

MND

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510
Q

Diangosis of MND

A

Clinical
Electromyography confirms LMN
Brain/cord MRI for excluding other things
Diagnosis confirmed by steady progression over time

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511
Q

MND management

A

Specialist MDT. Non invasive ventilatory support and feeding (gastronomy. Riluzole

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512
Q

What drug is used in MND and what does it do

A

Riluzole, sodium channel blocker, inhibites glutatmate rlease

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513
Q

Define parkinsonism

A

Clinical syndrome characterised primarily by bradkinesia, rigidity, resting tremor and loss of postural reflexes

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514
Q

Describe the pathophysiology of parkinsons

A

Loss of dopaminergic neurones in the substantia nigra pars compacta and Lewy bodies leads to breakdown of the striatum pathway and decreased output tothe cortex

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515
Q

Describe spasticity

A

There is increased tone at the start of motion but this tops through the range of motion

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516
Q

3 cardinal features of parkinsons

A
Bradykinesia (button problems, micrographia, expressinoless face, dysphonia, dysdiadochokinesia) 
Resting tremor (unilateral pill rolling)
Rigidity (paian, cog weel, stooped posture)
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517
Q

Characteristic gait of parkinsons

A

Slow to start walking, rapid short stride length, festination, reduced arm swing, impaired balance on turning

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518
Q

Not movement features of PD

A

Depression, phobias, anxiety, dementia, autonomic (constipation, increased urinary frequency. Not incontinence)

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519
Q

Parkinsons drugs to increase dopamine availability

A

Cocarledopa, levodopa and carbidopa(reduces SE from increased dopamine). These treat bradkyinesia and rigidity

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520
Q

Dopamine agonists used in parkinsons treatment

A

Ropinirole

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521
Q

Drugs which inhibit the enzymatic breakdown of dopamine in the treatment of parkinsons

A

Entacapone (COMT) Selegilene (MAO-B)

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522
Q

How do you treat the tremor in parkinsons

A

Anticholinergics- amantadine

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523
Q

Motor complications of late stage PD

A

Wearing off, on dyskinesias, off dyskinesias, freezing

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524
Q

Hyperkinetic movements, deranged liver function tests, kayser fleischer rings

A

Wilsons disease

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525
Q

Magnetic gait, incontience, dementia

A

Normal pressure hydrocephalus

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526
Q

Signs of cauda equina syndrome

A

Bilateral sciatica, bilateral flaccid leg weakness, saddle anaesthesia, bladder/bowel dysfunction, erectile dysfunction, areflexia

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527
Q

Causes of cauda equina syndrome

A

Herniated lumbar disc, lumbar spinal stenosis, inflammatory conditions, osteomyelitis, tumours/neoplasms, trauma

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528
Q

Diagnosis of cauda equina syndrome

A

MRI spine

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529
Q

Treatment of cauda equina syndrome

A

Surgical decompression by lumbar laminectomy

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530
Q

Describe the pathology of huntigntons

A

Autosomal dominant conditions. more than 39 repeats of the CAG triplet of the huntingtin gene. Striatum atrophy and depletion of GABA. Increased dopamine and increased movement

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531
Q

Clinical features of huntingtons

A

Irritability, depression, self neglect,behavioural problems
Chorea and rigidity
Dementia

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532
Q

How do you treat huntingtons

A
Chorea= sulpride
Depression= SSRI
Aggression= risperidone
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533
Q

What does anticipation in huntigntons mean

A

The symptoms get more severe and onset is earlier as the condition is passed from one generation to the next

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534
Q

Define myasthenia gravis

A

Autoimmune disease against nicotinic acetylcholine receptors in the neuromuscular junction

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535
Q

Presentation of myasthenia gravis

A

Painless, fatiguable muscle weakness particularly
-proximal limbs
-extra occular muscles
-bulbar and facial muscles
Worse at night, respiratory symptoms= cirsis
Stairs, chairs, hair

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536
Q

What is lambert eaton myasthenic syndrome

A

Paraneoplastic from small cell lung cancer. Defective Ach release but improves with exercise

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537
Q

Investigations for myasthenia gravis

A

Look for antiAChR and if negative look for antiMusk

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538
Q

Treatment for myasthenia gravis

A

Pyridostigmine (anticholinesterase), oral prednisolone

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539
Q

Define guillain barre syndrome

A

Acute inflammatory demyelinating ascending polyneuropathy affecting the peripheral nervous system following URT or GI infection

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540
Q

How do you treat guillain barre

A

IV immunoglobulin and enoxaparin

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541
Q

How does guillain barre present

A

Symmetrical ascending muscle weakness 1-3 weeks post infection

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542
Q

Carpal tunnel

A

Median nerve compression at the wrist. Tinnels or Phalens signs may be positive. Splinting and corticosteroid injections treatment

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543
Q

Clinical features of encephalitis

A

LOC, Confusion, seizures, headache and fever

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544
Q

Investigations of encephalitis

A

MRI, EEG, LP

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545
Q

Viral causes of Encephalitis

A

mumps, rabies, EBV

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546
Q

Define herpes zoster

A

Reactivation of varciella zoster virus in the dorsal root ganglia due to decreased immunity

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547
Q

Treatment of herpes zoster

A

Oral acyclovir. Post herpetic neuralgia=amitryptilline

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548
Q

Where do secondary brain tumours come from

A

Lungs, breast, melanoma, renal, GI

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549
Q

Glial cell tumours can be

A

Atrocytic or oligodendroliomas

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550
Q

Classification of astrocytomas

A

I Pilocytic
II premalginant
III anaplastic
IV diffuse glioblastoma multiforme

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551
Q

What causes the conversion to malginant

A

Isocitrate dehydrogenase 1

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552
Q

Presentation of brain tumours

A

Headache, papilloedema, seizures, progressive neurologicla deficit

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553
Q

Investigations of brain tumours

A

MRI/CT

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554
Q

Treatment of brain tumours

A

Debulking surgery, radiotherapy, chemo and dexamethasone

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555
Q

Define dementia

A

A syndrome caused by a number of brain disorders which causes memory loss, difficulty thhinking, problem solving or language and difficulties with activites of dailly living

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556
Q

Types of dementia

A

Alzheimers, vascular, lewy body, frontotemporal

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557
Q

What causes alzheimers

A

Accumulation of beta amyloid peptide causes progressive neuronal damage, neurofibrillary tangles, amyloid plaques and loss of ACH

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558
Q

5 Key features of alzheimers

A
Short term memory loss.
Disintegration of personality and intellect
Decline in language
Decline in visuosptail skills
Agnosia
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559
Q

Medication for alzheimers

A

Acetylcholinesterase inhibitors- donepezil

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560
Q

Antibiotics which cause C.dificle

A

Clindamycin, ciprofloxacin, coamoxiclav, cephalosporins

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561
Q

What is a mallory weiss tear

A

Linear tear in mucosa were the oesophagus meants the stomach

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562
Q

What does painless cholestatic jaundice suggest

A

Pancreatic cancer

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563
Q

What are varices

A

Distended veins from portal hypertension

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564
Q

What are the U+Es like in upper GI bleed

A

Only urea is raised and this is because of breakdown of blood

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565
Q

How do you treat mallory weiss tear

A

Minor=fluids

Major= banding

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566
Q

How do you treat varices

A

Banging and propanolol

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567
Q

Prehepatic cause of portal hypertension

A

Portal vein thrombosis

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568
Q

Hepatic cause of portal hypertension

A

Primary biliary cirrhosis, cirrhosis, buddchiari

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569
Q

Post hepatic cause of portal hypertension

A

Constrictive pericarditis, IVC obstruction

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570
Q

Causes of upper GI bleed

A

Mallory weiss tear, grastic and duodenal ulcer, varices

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571
Q

Causes of upper GI motility probelms

A

Achalasia and systemic sclerosis

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572
Q

How do you detect upper Gi motility problems

A

barium swallow

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573
Q

What are teh signs of limited systemic sclerosis

A
Calcinosis
Raynauds phenomenon
Esophageal dysfunction
Sclerodactyly
Telangiectasis
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574
Q

How do you detect systemic sclerosis

A

Anit nuclear antibodies

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575
Q

How do you treat upper GI motility disorders

A

Omeprazole, antacids and surgery

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576
Q

Define GORD

A

Excessive entry of gastric contents into the oesophagus through the gastrooesophageal junction

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577
Q

Risk factors for GORD

A

NSAIDs, large meals, hiatus hernia, obesity, prengancy, alcohol, coffee

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578
Q

Symptoms of GORD

A

Reflux, indigestion, heart urn, acid tast, bloatin, belching, discomfort, odynophagia

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579
Q

Diangosis of GORD

A

History and improvement with PPI

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580
Q

Managemtn of GORD

A

Weight loss, reduced alcohol, smoking cessation, avoid large or bedtime meals. Omeprazole and ranitidine (H2 antagnoist)

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581
Q

Define barrets oesophagus

A

Change in the lower oesophagus from squamous to columnar epithelium - metaplasia

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582
Q

Peptic ulcer disease investigation

A

H pylori testing and endoscopy only if over 55 or red flags

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583
Q

Treatment for PUD

A

Stop smoking, treat cause

  • omeprazole, clarithromycin and amoxicillin
  • stop NSAIDs
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584
Q

Wchich artery do posterior duodenal ulcers go into

A

Gastroduodenal artery

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585
Q

Which artery do gastric ulcers go into

A

Left gastric artery

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586
Q

What relieves pain in gastric

A

Vomitting, antacids and milk

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587
Q

What relieves pain in duodenal

A

Intake of food and anatacids and milk

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588
Q

Describe gastric ulcers

A

Occur in the stomach, epigastric pain 1-2hours after eating, cause haematemesis or melena, heart burn, chest discomfort and early satiety are ofetn seen. Can cause gastric carcinoma

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589
Q

Describe duodenal ulcers

A

Occurs in the duodenum, epigastric pain 2-5 hours after eating, cases melena or blood in stools. Pain may awaken patient during the night

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590
Q

Name 3 things H pylori can cause

A

Peptic ulcers, atopic gastritis, cancer

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591
Q

Investigations for H pylori

A

Endoscopy and biopsy for ulcers, C13 breath test

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592
Q

Dyspepsia features

A

Postprandal fullness, early satiation, epigastric burning

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593
Q

Causes of dyspepsia

A

GORD, IBS, PUD, lactose intolerance, anxiety or depression

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594
Q

Red flags in upper GI

A

Unexplain weight loss, anaemia, GI blood loss, dysphagia, upper abdo mass, persistent vomitting

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595
Q

early post prandial pain

A

GORD or gastritis

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596
Q

late post prandial pain

A

duodenal

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597
Q

Risk factors for oesophageal metaplasia

A

Obestiy, reflux, age

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598
Q

Risk factors for oesophageal squamous cell carinoma

A

Alcohol, smoking, east asia

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599
Q

Treatmetn of oesophagel cancer

A

Resection if fit, stent, chemo radio, palliative

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600
Q

Diangostic testing in oesophagel

A

Endoscopy, CT, PET

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601
Q

2 week wait for endoscopy if

A

Dysphagia or over 55 and upper abdo pain or reflux or dyspepsia

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602
Q

Non urgent endoscopy if

A

Haematemsis, over 55 with upper abso pain and anaemia, raised platelets, symptoms of GI cancer

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603
Q

Define coeliac disease

A

Systemic autoimmune disease trigerred by dietary gliadin

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604
Q

Describe the pathophysiology of coeliac disease

A

Autoimmune reaction, antiendomysial antibodies attack tissue transglutaminase enzyme which breaks down gluten

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605
Q

Risk factors for coeliac

A

HLA DQ2/8. T1D, AI addisons and gravves

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606
Q

Histoloical findings in the small intestine in coeliac

A

Increased lymphocytes in the epithelium and lamina propria, crypt hyperplasia, villous atrophy

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607
Q

Symptoms of coeliac disease

A

Abdo pain, bloating, diarrhoea, steatorrhea, weight loss

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608
Q

Signs of coeliac

A

dermatitis hepetiformis, anaemia, osteoporosis, failure to thrive

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609
Q

Where is iron absorbed

A

First part of the duodnum

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610
Q

Where is folate absorbed

A

jejunum

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611
Q

Where is B12 absorbed

A

Terminal ileum

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612
Q

What is dermatitis hepatiformis

A

Rash on the extenosr surfaces of the arms

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613
Q

Coeliac diagnosis

A

Tissue transglutaminase antibodies (IgA) (and endomysial antibodies. Bloods for serology, FBC and ferritin. Endoscopy and diagnosis is by small bowel biopsy

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614
Q

What would you see on a coeliac endoscopy

A

Atrophy and scalloping of mucosal folds, nodularity and mosaic pattern of mucosa

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615
Q

General symptoms of IBD

A

abdo pain, chronic diarrhoea (+- blood and mucous), weight loss

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616
Q

Describe UC

A

Continous inflammation that begins at the rectum to the ileocaecal valve. Cardinal symptom bloody diarrhoea. HLAB27

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617
Q

Describe crohns

A

Transmural and granulomatous inflammation from mouth to anus. Has skip legions. Mouth ulcers and perianal disease are classic. Smoking worsens symptoms

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618
Q

Investigations of IBD

A
Bloods:
anaemia, FBC, increased CRP B12/Folate deficency, Stool MC&amp;S, TFTs.
Sigmoidoscopy
Colonoscopy
Diagnosed with biopsy
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619
Q

How do you differentiate IBD and IBS

A

IBD has increased faecal calprotectin

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620
Q

UCR v crohns histology

A

UC: not beyond submucosa, neutrophils migrate to form crypt abscesses, reduced goblet cells and mucin
Crohns: Non caseating granuloma, transmural inflammation, lymphocytic infiltration

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621
Q

UC v Crohns endoscopically

A

UC: uniform inflammation and pseudopolyps
Crohns: Skip lesions and cobblestone appearnace, commonly affects terminal ileum

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622
Q

UC v crohns long term complications

A

UC: haemorrhage, toxic megacolon, marked increase in colon cancer risk
Crohns: Fistula, abscess, obstruction, slight increased colon cancer risk

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623
Q

IBD extra intestinal manifestations

A

Erythema nodosum, pyoderma gangrenosum, irritis, conjunctivits, episcleritis, large joint arthrits, ank spond

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624
Q

How do you treat relapses of IBD

A

Prednisolone then mesalazine maintenance

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625
Q

What is mesalazine

A

5-aminosalicylic acid

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626
Q

Prophylactic treatment for severe IBD first and second line

A

Azathiopine then metronidazole

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627
Q

Diarrhoea which is winter, hospital outbreaks, selflimiting

A

Rotavirus

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628
Q

Undercooked meat

A

Campylobacter jejuni

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629
Q

Poor food hygeine

A

Staph aureus

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630
Q

Watery travellers diarhoea

A

Enterotoxigenic E Coli

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631
Q

Bloody diarrhoea

A

Eneterohaemorrhagic Ecoli (0157)

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632
Q

Parasitic causes fo diarrhoea

A

Giardia lamblia and schistosomiasis

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633
Q

Investigations for infective diarrhoea

A

Basic obs, bloods, U&Es stool sample

634
Q

What do you do with the stool sample in infective diarrhoea

A

3 samples, 1 immmediately and 2 more 3 days apart. Culture, ova&parasites, serotyping/PCR

635
Q

Mnagement of infective diarrhoea

A

Exclude from work, rehydration, anitemetic, analgesia, notify public health england (food,bloody or cholera)

636
Q

Complication of infective diarrhoea

A

Haemolytic uraemic syndrome (microangiopathic, haemolytic anemia, thrombocytopenia, AKI)

637
Q

Indirect inguinal hernia

A

Protrusion of abdo/pelvic contents thorugh the internal inguinal ring lateral to epigastric vessels

638
Q

Direct inguinal hernia

A

Protrusion of abdo/pelvic contents thorugh the abdominal wall into the inguinal canal medial to epigastric vessels

639
Q

Define appendicitis

A

Acute inflammation of the appendix usually caused by obstruction of the appendix (usually by faecolith)

640
Q

Complications of appendicitis

A

Rupture and gangrene leading to peritonitis

641
Q

Presentation of appendicitis

A

Generalised pain which moves to mcburneys point, diarrhoea, vomitting

642
Q

Signs of appendicitis

A

Pyrexial,guarding and rebound tenderness in the right illiac fossa

643
Q

Investiagtions of appendicitis

A

Diagnosis with abdo CT or USS, increased WCC, rule out ectopic

644
Q

Mangement of appendicitis

A

Nil by mouth, IV fluids, Abx, laparoscopic appendectomy

645
Q

Causes of small bowel obstruction

A

Post op adhesions, strangulated hernia volvulus (children)

646
Q

Casues of large bowel obstruction

A

Malignancy, sigmoid/caecal volvulus

647
Q

What is ileus

A

Bowel ceases to function and there is no peristalsis, caused by post op and opioids

648
Q

What is volvuls

A

Complete twisting of a loop of intestina around its mesenteric attachment

649
Q

How are bowel obstructions classified

A

Site, extent mecahnism pathology

650
Q

Small bowel v large bowel presentation

A

Constipation early in SBO, LBO has faeculent vomitting and later contipation

651
Q

Cardinal signs of bowel obstruction

A

N+V, colicky abdo ppain, abdo distension, contipation, tinkling bowel sounds, hyperresonant or absent bowel sounds

652
Q

Ivestigation of obstruction

A

Bloods, erect CXR (exclude perforation) abdo XR (dilated bowel loops and kidney bean sign(volvolus)

653
Q

Mangement of obstruction

A

IV fluis, analgesia, antiemetics and monitor then surgery

654
Q

Define diverticulum

A

Outpouching of gut wall

655
Q

Primary peritonitis

A

Spontaneous bacterial peritonitis, ascites, immunoompromised. Diagnose via ascitic tap. Broad spectrum Abx, dont need surgery

656
Q

Secondary peritonitis

A

Appendicitis, ectopic pregnancy, bowel ischaemia, PUD

657
Q

Bacteria for peritonitis

A

Ecoli or spneumoniae (children). Post dialysis gets Staph aureus

658
Q

Signs of ascending cholangitis

A

Ecoli. Charcots triad

  • RUQ pain
  • Fever
  • Jaundice
659
Q

Acute cholecystits signs

A

RUQ pain, fever, raised inflammatory markers

660
Q

Treatment of ascending cholangitis

A

Fluids, metronidazole, ERCP stenting, laparoscopic cholecystectomy

661
Q

Typhoid antibiotic

A

Ciprofloxacin

662
Q

Describe haemorrhoids

A

swolen veins, disrupted and dilated anal cushions. Band ligation. Get them in strainging pregancy, portal HTN and CCF. Fresh blood

663
Q

Describe anal fissure

A

tear in skin around anal canal.Pain on defecation. Inspect. Hard faeces, IBD, anal cancer

664
Q

Desribe anal fistula

A

Abnormal communication between anal canal and perianal skin. Crohns, Tb rectal carcinoma.

665
Q

Pilondial sinus describe

A

Infected tract under skin between buttocks. Men sedentary obese. Hygeine

666
Q

Functions of the liver

A

Glucose and fat metabolism, detoxification and excretion, protein synthesis, defense against infection

667
Q

Screening for bowel cancer

A

Every 2 years 60-74. Faecal occult blood

668
Q

Familial causes of bowel cancer

A

Familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer(aggressive)

669
Q

Risk factors for bowel cancer

A

Age 50, red meat low fibre, IBD, FHx, smoking alcohol and obesity

670
Q

Red flag symptoms for bowel cancer

A

Abdominal pain, change in bowel habit, unexplained weight loss, chronic diarrhoea, Fe deficiency anaemia, rectal mass

671
Q

Diagnosis of bowel cancer

A

Colonscopy and biopsy with histology

672
Q

Staging of bowel cancer

A

TNM/ Dukes classification

673
Q

Management of bowel cancer

A

Surgery, chemo, radio

674
Q

Dukes A

A

Muscularis mucosae

675
Q

Dukes B

A

Extension through the muscularis mucosa not lymph

676
Q

Dukes C

A

Involvement of regional lymph nodes

677
Q

Dukes D

A

Distant metastases

678
Q

Causes of acute liver disease

A

Viral, drug, alcohol, congestion, obstruction

679
Q

Causes of chronic liver disease

A

Alcohol, viral, autoimmune, metabolic

680
Q

Presentation of acute liver disease

A

Malaise, nausea, anorexia, myalgia, abdo pain, bleeding, liver pain (=malignancy or obstruction). Ecephalopathy

681
Q

Waht is hepatic encephalopathy

A

Liver flap, confusion, coma

682
Q

Presentation of chronic liver failure

A

Ascites, oedema, haematemesis, malaise, anorexia, wasting, easy bruising, itching, hepatomegaly, abnormal LFTs, hypoglycaemia

683
Q

Liver disease observations

A

Weight loss, scratching/itching, alcohol smell/withdrawal, encephalopathy

684
Q

Liver disease hands

A

Clubbing, dupuytrens contracture, leuconychia, brusing, flapping tremor, palmar erythema

685
Q

Liver disease face

A

Jaundice, spider naevi, parotid swelling, xanthelasma

686
Q

Liver disease chest

A

Loss of body hair, spidernaevi, gynaecomastia

687
Q

Liver disease abdomen

A

Ascites, caput medusae, hepatomegaly, spenomegaly, palpable gall bladder, hepatic bruit, tumour

688
Q

Liver disease legs

A

Brusing oedema

689
Q

Investigating chronic liver disease

A

Viral serology, immunology, biochemistry, Ultrasound scan

690
Q

Initial test for alcoholic liver disease

A

Liver function tests. AST is higher than ALT, high MCV

691
Q

Initial test for NASH

A

LFTs then confirm with liver biopsy

692
Q

Initial test for chronic hep B

A

HBsAg

693
Q

initial test for chronic hep C

A

HCV antibody

694
Q

Initial test for primary biliary cirrhosis

A

Antimitochondrial antibody

695
Q

Initial test for primary sclerosing cholangitis

A

Mangetic resonance cholagiopancreatography

696
Q

Initial test for haemochromatosis

A

Transferrin and ferritin levels then confirm with HFE gene test

697
Q

Initial test for wilsons disease

A

Caeruloplamin then confirm with 24hr urinary copper

698
Q

Initial test for a1 antitrypsin

A

a1 antitrypsin level then confirm with genotype testing

699
Q

Which serum liver enzymes are cholestatic

A

ALP and Gamma GT

700
Q

Which serum live enzymes are hepatocellular

A

Asparate transaminase and alanine transaminase

701
Q

What is ALP

A

Alkaline phosphatase produced by liver, bile duct and bone. If it is raised and GGT is not, it suggests a bone problem

702
Q

When is ALT higher than AST

A

Chronic liver disease

703
Q

When is AST raised higher than ALT

A

Cirrhosis and alocholic hepatitis

704
Q

Which liver enzyme suggests and alcoholic cause

A

Aspartate transaminase

705
Q

Causes of isolated rise in ALP

A

Bony mets, vitamin D defieincy, recent bone fracture, renal osteodystrophy

706
Q

Causes of decompensation in chronic liver disease

A

New drugs, constipation, GI bleed, infetion, low sodium, pottasium or sugar, alcohol withdrawal

707
Q

Consequences of liver dysfunction

A

Malnutrition, variceal bleeding, encephalopathy, ascites, infection, coagulopathy, endocrine changes, hypoglycaemia

708
Q

How do you treat malnutrition

A

NG tube

709
Q

how do you treat ascites

A

Fluid/salt restriction, diuretcs, paracentesis

710
Q

Which haematology changes do you get from liver dysfunction

A

Vit K deficiency, impaired clotting factors, thrombocytopenia

711
Q

Which endocrine changes do you get from liver failure

A

Gynaecomastia, impotence,, amenorrhea

712
Q

Signs of alcoholic hepatitis

A

Mallory bodies and giant mitochondria

713
Q

Stages of alcoholic liver disease

A

Fatty liver, hepatitis and cirrhosis

714
Q

Describe steatosis

A

Acute reversible flat globules in the cytoplasm. FBC will be macrocytic if alcoholic

715
Q

Describe hepatitis histopathology

A

Neutrophil infiltration, mallory bodies (hyalin aggregates), giant mitochondria

716
Q

Symptoms of hepatitis

A

Jaundice, ascites, pain, hepatosplenomegaly

717
Q

Tests for alcoholic hepatitis

A
Luecocytosis on FBC
LFTs
-ast/alt raised
alk P raised
prothrombin time longer
Low albumin
718
Q

Alcoholic cirrhosis histopathlogy

A

Mallory bodies, infiltration neutrophils

719
Q

Symptoms of cirrhosis

A

Liver failure, portal hypertension, ascites, pain, varices, encephalopathy

720
Q

Tests for cirrhosis

A
FBC= raised bilirubin adn leucocytosis
U&amp;E= low sodium, high creatitine 
LFT= deranged, long PT
721
Q

Investigations for alcoholic liver disease

A

Blood tests, imaging, biopsy, ascitic tap

722
Q

Management of ALD

A

Fatty liver=abstinence
Hepatitis= abstinence, supplements, steroids
Cirrhosis= manage complications

723
Q

Alcohol withdrawal and managemtn

A

Tremors, hallucinations, agitation, delirium tremens. Give Chlorodiazepoxide

724
Q

Treatment for alcohol dependence

A

Naltrexone and disulfiram

725
Q

Describe paracetamol overdose.

A

Glutathione transferase runs out, you get reactive intermediats causing cellular necrosis. Very high ALT. Nausea and vomitting, needs Nacetylcysteine and acid base support

726
Q

Autoimmune hepatitis

A

IgG, ANA, females. Good response to therapy.

727
Q

Primary biliary cirrhosis

A

Chronic autoimmune granulomatous infiltration of interlobular bile ducts.. IgM, antimitochondrial antibodies. HCC

728
Q

Treatment for primary biliary cirrhosis

A

Ursodeoxycholic acid

729
Q

Primary sclerosing cholangitis

A

Primary sclerosing cholangitis, intrand extrahepatic bile ducts. Associated with UC. pANCA and ANA. Obliterative cholangitis and onion skin fibrosis

730
Q

Haemochromatosis who gets it

A

Recessive, C282y. Hepcidin expression disrupted.

731
Q

Symptoms of haemochromatosis

A

Iron deposition in liver heart, pancreas and joints leads to fibrosis. Tired Athralgia, grey skin, DVT, cirrhosis

732
Q

Investigations for haemochromatosis

A

High ferritin, transferrin, serum iron. LFTs raised. Biopsy, genetic testing. Echo

733
Q

Treatmetn of haemochromatosis

A

Venesection. Desferrioxamine iron chelator. tea, coffee, red wine

734
Q

Pathophysiology of a1 antitrypsin

A

Recessive gene condition. Antitrpsin accumulation in liver and emphysema as protein defiency in blood

735
Q

Investiagtions for a1antitrypin

A

Serum a1 antitrypsin low.

Biosy shows globules of alpha 1 antipsyin

736
Q

Wilsons pathology

A

Copper toxicity. Decreased copper incorporation into caeruloplasmin and reuced copper excretion

737
Q

Who gets wilsons

A

Autosomal recessive on 13

738
Q

Symptoms of wilsons

A

Kayser Fleischer ring, grey skin, hypermobile joint. Depression, cirrhosis, tremor

739
Q

Investigations of wilsons

A

Reduced serum copper, high urine copper 24hr, low serum caeruloplasmin. Do a liver biopsy. MRI basal ganglia. Genetinc testing

740
Q

Treatment of wilsons

A

Penicillamine is a copper chelator
Screen family
No liver, chocolate, nuts, muschrooms, legumes

741
Q

COPD and liver cirrhosis

A

Alpha 1 antitrypsin

742
Q

Symptoms of hepatitis

A

General malaise, myalgia, GI upset, abdo pain

743
Q

Hep A

A

Acute only, faecooral, travellers, foodhandlers, shellfish

744
Q

Hep B

A

Blood bourne, needle stick, tattoos, sexual, vertical

745
Q

Hep D

A

Needs HepB, bloody and bodily fluids. IVDU

746
Q

Hep C

A

Blood and bodily fluids, IVDU, blood transfusions, needle stick, MSM

747
Q

Hep E

A

Faecooral

748
Q

Hep Vaccines

A

A100%
B inactivated HBsAg (HBV IgG post exposure)
D hepBvaccine

749
Q

Complications of A and E hep

A

Fulminant hepatitis

750
Q

Hep B C and D complications

A

Cirrhosis, HCC, Cholangiocarcinoma

751
Q

Hep A and E treatment

A

Supportive

752
Q

Hep B, C and D treatment

A

PEG IFN

753
Q

HBsAg suggests

A

Acute or chronic infection. Infectious

754
Q

antiHBs suggests

A

Recovered or has been vaccinated

755
Q

antiHBc suggests

A

Have or recovered (proper infection)

756
Q

Signs of cirrhosis

A
CLAPS
Clubbing
Leukonychia
Ataxia
Palmar erythema
Scratch marks
757
Q

General signs ofcirrhosis

A

Hepatomegaly, jaundice, ascites

758
Q

Describe portal hypertension

A

Blockage leads to 10mmHg, collateral circulation occurs thorugh portosystemic shunt and dilation of gastro-oesophageal veins (varcies)

759
Q

Transudate causes of ascites

A

Potal hypertension (cirrhosis)
BuddChiari
Cardiac failure

760
Q

Exudate causes of acites

A
Pertioneal carcinoma
Peritoneal TB
Pancreatitis
Nephrotic syndrome
Lymphatic obstruction
761
Q

Presenation of ascites

A

Abdominal distension, fullness in teh flanks, shifting dullness. Respiratory distress if tense ascites. Pleural effusion and oedema

762
Q

Investigations for ascites

A

Aspiration. Albumin, Neutrophil (SBP?), MC&S, Cytology, amylase

763
Q

Managemtn of ascites

A

Treat underlying cause, spironolactone
Paracentesis and albumin replacement
Transjugular intrahpeatic portosystemic shunt

764
Q

Spontaneous bacterial peritonitis

A

Ecoli. Cefotaxime and metronidazole

765
Q

Complications of gall stones

A

Biliary colic, ascending cholangitis and acute cholecystis

766
Q

Define gall stones

A

Obstruction in cystic orcommon bile duct by a stone

767
Q

Define ascending cholangitis

A

Infection of the biliary tree caused by obstruction of the common bile duct

768
Q

Define acute cholecystitis

A

Obstruction of the neck of the gallbladder resulting in inflammation of the gall bladder

769
Q

Signs of gall stones

A

Colicking RUQ pain after eating, can radiate to the right shoulder

770
Q

Ascending cholangitis signs

A

Charcots triad: biliary colic, jaundice, fever (hypotension+confusion)

771
Q

Acute cholecystitis signs

A

RUQ pain, fever and nausea, murphys sign

772
Q

What is murphys sign

A

Pain on taking deeep breath when two fingers on RUQ

773
Q

Diagnosis of gallstones

A

Abdominal ultrasound scan

774
Q

Management of gallstones

A

Lithotripsy, ERCP, surgery

775
Q

Describe prehepatic jaundice

A

Dark urine because of urobiliinogen and conjugated. Caused by Gilberts, haemolysis and malaria

776
Q

Describe post hepatic jaundice

A

Dark urine (conjugated) and pale stool, gall stone or stricture

777
Q

Describe heaptic jaundice

A

Hepatitis (all the types), ischaemia, neoplasm. Increased unconjugated

778
Q

Difference between acute and chronic pancreatitis

A

Acute=reversible damage

Chronic=irreversible damage

779
Q

Causes of acute pancreatitis

A
Gallstones
Ethanol
Trauma
Steroid
Mumps
Autimmune
Scorpion venom
Hyperlipidaemia
ERCP
Drugs (azathioprine and sodium valproate)
780
Q

Pancreatitis presentation

A

Severe epigastric pain that may radiate to the back, vomitting, cullens and grey turners

781
Q

What is cullens sign

A

Perimubilical discolouration

782
Q

What is grey turners sign

A

Flank discolouration

783
Q

Pancreatitis investaigtion and diagnosis.

A

CT. Diagnosis= raised serum amylase X3 and serum lipase

784
Q

Define polycythaemia

A

Increase in red blood cell, packed cell volume and haemoglobin concentrations

785
Q

Causes of apparent polycythaemia

A

Beiing overweight, alcohol, diuretics, dehydration, stress

786
Q

Describe primary polycythaemia

A

Polcythaemia vera, JAK2 mutation means the Bone marrow is increasedsensitivity to EPO so more RBC are produced. Peak in 60s

787
Q

Causes of secondary absollute polycythaemia

A

Hypoxia, high altitude, abnormal RBC, tumours, renal artery stenosis

788
Q

Symptoms of polycthaemia

A

Bleeding, bruising, fatigue, itchy skin

789
Q

Signs of polycythaemia

A

Splenomegaly, hypertesnion, red skin, thrombocytosis

790
Q

Polycythaemia puts you at risk of

A

Blood clots, MI, PE

791
Q

Investigations of polycythaemia

A

History, FBC, blood film, genetic testing, U&Es, LFTs, serum EPO and red cell mass studies

792
Q

Treatement of pvc

A

Venesection, hydroxycarbamide, interferon

793
Q

Define pancytopenia

A

A reduction in RBC, WBC, and platelets

794
Q

Causes of pancytopenia,

A

chemo, HIV, SLE, Malignancy

795
Q

Diagnosis of pancytopenia

A

Bone marrow biopsy and FBC

796
Q

How do you detect myeloblasts

A

Myeloperoxidase

797
Q

How do you detect lymphoblasts

A

Tdt

798
Q

Who gets AML

A

70s

799
Q

Who gets AML

A

<p>70s</p>

800
Q

Unique feauters of AML

A

Auer rods, Hepatosplenomegaly and gum hypertophy

801
Q

Who gets ALL

A

3.5yo boys

802
Q

What are ALL and AML linked to

A

Downs

803
Q

Treatment of AML

A

Supportive, chemotherapy, bone marrow transplant

804
Q

Unique presentation of ALL

A

Lymphadenopathy and testicular swelling

805
Q

What are the symptoms of marrow failure

A

Fatigue, infection, bleeding and bruising

806
Q

What should you give in ALL and AML to prevent tumour lysis syndrome

A

Allopurinol

807
Q

What does Philadelphia chromosome cause

A

CML and ALL

808
Q

Treatment of ALL

A

Supportive, chemotherapy and bone marrow transplant

809
Q

Investigations in acute leukaemia

A

FBC, Blood film, BM biopsy, cytogenetics

810
Q

Define CML

A

Uncontrolled proliferation of myeloid cells

811
Q

Define AML

A

Neoplastic proliferation of blast cells derived from marrow myeloid elements

812
Q

Define ALL

A

Malignancy of immature lymphoid cells

813
Q

Who gets CML

A

40-60

814
Q

What causes CML

A

Philadelphia chromosome causes increased tyrosine kinase activity

815
Q

Presentation of CML

A

Constituional symptoms, massive splenomegaly, thrombocytosis

816
Q

Investiagtions in CML

A

FBC, Blood Film, cytogenetics

817
Q

Management of CML

A

Imatinib (tyrosine kinase inhibitor), hydroxycarbamide, bone marrow transplant

818
Q

Define CLL

A

Accumulation of mature B cells which have escaped programmed cell death and undergone cell cycle arrest

819
Q

Presentation of CLL

A

Enlarged rubbery non tender lymph nodes, constitutional symptoms, hepatosplenomegaly

820
Q

Investigations of CLL

A

FBC and Rai staging

821
Q

Treatment of CLL

A

Rituximab, radiotherapy, chemotherapy, stem cell transplant

822
Q

Define myeloma

A

Malignant proliferation of clonal plasma cells

823
Q

Who gets myeloma

A

60-70

824
Q

Presentation of myeloma

A

Calcium, Renal impairment, Anaemia, Bone disease

825
Q

Myeloma findings

A

Constitutional, amyloidosis, hyperviscosity, marrow infiltration, infection

826
Q

Investigations in myeloma

A

FBC, blood film, U&E, urine electrophoresis, bone marrow biopsy, XRay skeletal survey

827
Q

What are the findings on investigation in Myeloma

A

Marrow failure, roleaux formation, bence jones protein in urine and blood. Increased blasma cells in the bone marrow. Lytic lesions and pepperpot skull

828
Q

Complications of myeloma

A

Hypercalcaemia, spinal cord compression, hyperviscosity, AKI

829
Q

Treatment of myeloma

A

Analgesia and bisphosphonates, blood transfusion, IV immunoglobulin. Chemo, stem cell transplant

830
Q

Painless, rubbery nodes which hurt with alcohol

A

Lymphoma

831
Q

Define lymphoma

A

Malignancy of mature lymphocytes that arises in the lymphatic system

832
Q

Define leukaemia

A

Malignancy of lymphocyte precursors that arises in the bone marrow

833
Q

Presentation of lymphoma

A

Painless lymphadenopathy, systemic symptoms, compression syndromes

834
Q

Investigations in lymphoma

A

Blood film, bone marrow and lymph node biopsy, immunophenotyping and cytogenetics

835
Q

Staging of lymphoma

A

Bloods, CT chest/abdo./pelvis

836
Q

Low grade non hodgkins

A

Follicular

837
Q

High grade non hodgkins

A

Diffuse large b cell

838
Q

Very high grade non hodgkins

A

burkitts

839
Q

Define hodgkins lymphoma

A

Malignant proliferation of lymphocytes and reed stern berg cells present

840
Q

Who gets hodgkins lymphoma

A

30s or 70s

841
Q

Risk factors for hodgkins

A

EBV, SLE, post transplant, obesity

842
Q

Staging of hodgkins lymhoma

A

Ann arbor

843
Q

Presentation of hodgkins

A

Painless asymmetrical lymphadenopathy (pain on alcohol), systemic symptoms, anaemia, LDH raised and hepatosplenomegaly

844
Q

Treatment of 1-2a HL

A

Short course chemo then radio

845
Q

Treatment of 2b-4 HL

A

Combination chemo

846
Q

Late effects of HL

A

Cancers, psychological issues

847
Q

Late effects of HL chemo

A

Infertility, cardiomyopathy, lung damage, peripheral neuropathy

848
Q

NHL presentation

A

Bowel obstruction, bone marrow crowding out, spinal cord compression

849
Q

Risk factor for burkitts lymphoma

A

EBV

850
Q

Risk factor for gastric MALT lymphoma

A

H pylori

851
Q

Treatment of NHL

A

Conservative if follicular, chemo, radio, bone marrow transplant

852
Q

Tumour lysis syndrome

A

Large tumour burden and aggressive cancers, release of cellular components overwhelms the kidneys

853
Q

Signs of tumour lysis syndrome

A

Hyperkalaemia, hyperphosphotaemia, hyperuricaemia, hypercalcaemia. Results in AKI, Seizures, death

854
Q

Treatment of tumour lysis syndrome

A

IV fluids, treat high pot

855
Q

Features of febrile neutropenia

A

Fevers, rigors, hypotension

856
Q

How to treat febrile neutropaenia

A

Broad spectrum ab (tazosin), and take blood cultures

857
Q

Signs of malignant cord compression

A

Back pain, spastic paresis, sensory level

858
Q

Treatment of spinal cord compression

A

Dexamethasone, urgent MRI, chemo or R/T surgery

859
Q

Causes of hyperviscosity syndrome

A

Increased immunoglobulins (myeloma), increased blood cells (leukaemia), reduced deformability of RBC (sickle cell)

860
Q

Presentation of hyperviscosity triad

A

Mucosal bleeding, visual change, neurological disturbance

861
Q

Consequences of hyper viscosity

A

Congestive heart failure, MI, pulmonary oedema

862
Q

4 species of malaria

A

P.vivax, ovale, malariae, facilparum

863
Q

What effect does malaria have on cells

A

Haemolysis, RBC sequestration and cytokine release

864
Q

Signs of malaria

A

Anaemia, thrombocytopenia, coma, convulsions, acidosis

865
Q

Diagnosis of malaria

A

Serial thin and thick films

866
Q

Other tests in malaria

A

FBC, Clotting, glucose, ABG, U&E, blood cultures

867
Q

Prophylaxis for malaria

A

Malarone

868
Q

Treatment for malaria

A

Chlorquine, primaquine

869
Q

Which diseases give protection against malaria

A

Sickle cell and G6PD

870
Q

Low Hb, high WCC, platelets normal

A

Autoimmune haemolysis

871
Q

Infection following blood transfusion

A

Probably bacterial as platelets stored at room temperature

872
Q

What is the effect of CKD on blood

A

Lack of EPO therefore anaemia

873
Q

What is the effect of renal cell carcinoma on blood

A

Secondary polycthaemia

874
Q

Types of haemoglobin

A

A2gamma2 switches to a2b2 at 6 months

875
Q

Diagnositc tests for anaemia

A

WCC, platelet count, reticulocyte count, blood film, haematinics, bone marrow biopsy

876
Q

Signs of iron deficiency anaemia

A

Koilonychia, angular cheilosis, atrophic glossitis, post cricoid webs

877
Q

Causes of iron deficiency anaemia

A

Menorrhagia, GI bleeding, hookworm, coeliac

878
Q

General signs of anaemia

A

Breathlessness, tachycardia, fatigue, pallor of mucous membranes, hyperdynamic circulation

879
Q

Appearnace of microcytic anaemia RBC

A

Microcytic and hypochromic

880
Q

Causes of microcytic anaemia

A

Iron deficiency, thalassaemia, sideroblastic anaemia, anaemia of chronic disease

881
Q

Treatment of iron deficiency anaemia

A

Ferrous sulfate for 3 months and treat underlying cause

882
Q

Causes of normocytic anaemia

A

Blood loss, chronic disease, bone marrow or renal failure. Pregnancy and hypothyroid

883
Q

Iron deficiency anaemia in someone without an obvious cause

A

Do oesophagogastroduodenoscopy and colonoscopy for GI bleed and exclude malignancy

884
Q

Causes of anaemia of chronic disease

A

Inflammation, malignancy, infection, renal failure, rheumatoid arthritis

885
Q

Treatment for anaemia of chronic disease

A

Treat underlying cause and give EPO

886
Q

Diagnosis of iron deficiency anemia

A

Low ferritin and serum iron. Total iron binding capacity high. Microcytic with anistocytosis and poikilocytosis. Do stool sample for ova and coeliac serology

887
Q

Causes of sideroblastic anaemia

A

Congenita, cancer, antiTB drugs. Ring sideroblast appearance because of iron deposits. Ferritin increased

888
Q

Describe pernicious anaemia

A

Antiparietal cell and intrinsic factor antibodies. Associated with other AI, Vitiligo and hyporthyroid

889
Q

Diagnosis of pernicious

A

Low Hb, raised MCV, hypersegmented neutrophils on blood film. Megaloblasts on biopsy

890
Q

Treatment of pernicious anaemia

A

IV hydroxycabalamin, oral folate

891
Q

Sources of vitamin B12

A

Meat, fish, dairy

892
Q

Causes of B12 deficiency

A

Dietary, malabsorption, congential metabolic errors

893
Q

Causes of B12 malabsorption

A

Atrophic gastritis causing pernicious anaemia or short gut syndrome preventing uptake

894
Q

Where is B12 absorbed

A

Terminal ileum

895
Q

Where is folate found

A

Green vegetables

896
Q

Where is folate absorbed

A

Duodenum/jejunum

897
Q

Where is iron absorbed

A

First part of the duodenum

898
Q

Causes of folate deficiency

A

Dietary, malabsorption, drugs

899
Q

B12 deficiency features

A

Lemon tinged skin, beefy red tongue, demention, paraesthesia, peripheral neuropathy

900
Q

Increased red cell distribution width

A

Coeliac. Both micro and macrocytic anaemia

901
Q

Clinical features of haemolytic anaemia

A

Anaemia, jaundice, gall stones, hepatosplenomegaly

902
Q

Signs of haemolytic anaemia

A

Anaemia. increased unconjugated bilirubin, increased urobilinogen, increased reticulocytes

903
Q

Glucose 6 phosphate dehydrogenase deficiency

A

X linked, Africa and med, bite and blister cells

904
Q

B thalassaemia

A

First year of life, skull bossing, hepatosplenomegaly, treat with transfusions and splenectomy. Target cells

905
Q

Alpha thalassaemia

A

Cant do without. So die. Bart’s hydrops

906
Q

Hereditary spherocytosis

A

Autosomal dominant, sherical red cells become trapped in spleen and undergo haemolysis

907
Q

Result of thalassaemia

A

Unmatched chains clump together and cause haemolysis and anaemia

908
Q

Result of vessel and platelet disorders

A

Purpura, bleeding, prolonged bleeding

909
Q

Result of coagulation disorders

A

Delayed bleeding into joints and muscles

910
Q

Causes of reduced platelet production

A

Bone marrow failure, aplastic anaemia

911
Q

Casues of destruction of platelets

A

Immune thrombocytopenia and Disseminated intravascular coagulation

912
Q

What makes foetal haemoglobin

A

Liver and spleen

913
Q

What makes adult haemoglobin

A

Bone marrow

914
Q

Describe sickle cell

A

Sickle cell haemoglobin is abnormal and polymerises when deoxygenated

915
Q

How do you diagnose sickle cell

A

Hb electrophoresis

916
Q

Symptoms of a sickle cell crisis

A

Acute chest, dactylitis, stroke, priapism

917
Q

How do you treat sickle cell

A

Hydroxycarbamide

918
Q

What causes an increased prothrombin time

A

Liver disease, warfarin, DIC

919
Q

What causes and increased activated partial thromboplastin time

A

Haemophilia, heparin, DIC

920
Q

What causes an increased thrombin time

A

Heparin and DIC

921
Q

What causes increased D-Dimer

A

DVT and DIC

922
Q

Signs of DIC

A

Purpura and brusing, bleeding from cannula sights. Shistocytes on blood film.

923
Q

Casues of DIC

A

Trauma, malignancy, sepsis, birth

924
Q

Treatment of DIC

A

Replace platelets and give fresh frozen plasma

925
Q

Haemolytic uraemic syndrome

A

After EColi. Triad of AKI, haemolytic anaemia and low platelets

926
Q

Immune thrombocytopenia

A

Antibodies against platelets in children two weeks after infections

927
Q

Vitamin K deficiency

A

Low 2,7,9,10. Caused by anticoagulants, biliary obstruction. Causes increased PTT

928
Q

Vonwillebrand disease

A

Factor 8 problem, increased PTT

929
Q

Haemophilia A

A

X linked, factor 8 deficiency. Raised APTT. Treat with desmopressin and recombinant factor 8

930
Q

Haemophilia B

A

Same but factor 9

931
Q

Risk factors for DVT

A

Immobility, cancer, oestrogen, surgery, thrombophilia

932
Q

Diagnosis of DVT

A

Wells score and D dimer then do ultrasound. If unprovoked look for malignancy.

933
Q

Virchows triad of venous thrombosis

A

Stasis of blood

934
Q

Thrombophilias

A

Clotting problem. Factor V leiden and antiphospholipid syndrome

935
Q

Treatment fo DVT

A

LMWH and warfarin

936
Q

How does LMWH work

A

Inactivates factor Xa and thrombin (IIa)

937
Q

How does warfarin work

A

Vitamin K antagonist

938
Q

How do DOACs work

A

Xa antagonist

939
Q

How to prevent DVT

A

Early mobilisation, compression stockings, leg elevation, LMWH

940
Q

Name a DOAC

A

apXaban

941
Q

Long bleeding time but otherwise normal suggests

A

Von Willebrand disease

942
Q

Anaemic male and nothing wrong suggests

A

Gastroenterology

943
Q

What should you give someone who has gout if they have other things going on like AF and DM

A

Colchicine

944
Q

Symptoms of OA

A

Pain on movement and at end of day

945
Q

Signs of OA

A

Bony swelling: Heberdens (DIPJ), Bouchards (PIPJ)

946
Q

Secondary causes of OA

A

Haemochromatosis, obesity, occupational

947
Q

What causes OA

A

Abnormal stresses or abnormal cartilage lead to compromised cartilage and biophysical and biochemical changes lead to cartilage breakdown

948
Q

Biophysical changes in OA

A

Collagen network fracture and proteoglycan unravelling

949
Q

Biochemical changes in OA

A

Inhibitors are reduced and proteolytic enzymes are increased

950
Q

OA on XRay

A

Loss of joint space

951
Q

Non pharmacological management of OA

A

Weight loss, exercise, aids and devices

952
Q

Pharmacological management of OA

A

Paracetamol then oral NSAID if needed and intrarticular pred

953
Q

Surgical management of OA

A

Joint replacement

954
Q

Should you give NSIADs to people on warfarin

A

No GI bleed risk

955
Q

Should you give steroids to people with diabetes

A

No upsets diabetic control

956
Q

Describe gout crystals

A

Monosodium urate crystals are needle shaped and negatively birefringent under polarised light

957
Q

Describe pseudo gout crystals

A

Calcium pyrophosphate crystals which are rhomboid and positively birefringent under polarised light

958
Q

What causes decreased uric acid secretion

A

Diuretics, CKD, lead

959
Q

What causes increased production of uric acid

A

Leukaemia, cytotoxic drugs, severe psoriasis

960
Q

How does gout present

A

Acute monoarthropathy with severe joint inflammation. Caused by hyperuricaemia resulting in monosodium urate crystal deposition

961
Q

Where is gout most common

A

Metatarsophalangeal joint

962
Q

Causes of gout

A

Hereditary, increased dietary purines, alcohol, diuretics, trauma, leukaemia, surgery, starvation

963
Q

Associations of gout

A

CV disease, DM, CKD

964
Q

Important differential of gout

A

Septic arthritis

965
Q

Investigations in gout

A

Bloods: serum urate

966
Q

Non pharmacological Mangement of acute gout

A

Protect rest, ice, elevate.

967
Q

1st line acute gout

A

NSAID max dose (ibuprofen) w/ppi or colchicine

968
Q

2nd line acute gout

A

Joint aspiration and intrarticular pred

969
Q

3rd line gout

A

Short course oral pred or single IM pred

970
Q

Prevention of gout 1st line

A

Allopurinol

971
Q

Prevention of gout 2nd line

A

Febuxostat

972
Q

How does allopurinol work

A

Xanthine oxidase inhibitor

973
Q

Prevention of gout 3rd line

A

Consider colchicine to prevent acute attacks

974
Q

Presentation of pseudogout

A

Acute monoarthropathy of larger joints. Can be provoked by trauma illness or surgery. Calcium pyrophosphate cystal arthritis

975
Q

Risk factors for pseudogout

A

Old age, hyperparathyroidism, haemochromatosis, hypophosphataemia

976
Q

Investigations of pseudogout

A

Polarised light microscopy of synovial fluid

977
Q

Treatment of acute acute of pseudogout

A

Cool packs, rest aspirate, intrarticular steroids. NSAIDs or Colchicine

978
Q

Treatment of chronic pseudogout

A

Methotrexate

979
Q

RA initial management

A

Methotrexate + Sulfalasalzine + short course of pred

980
Q

Definition of rheumatoid arthritis

A

Chronic systemic autoimmune inflammatory disease characterised by a symmetrical, deforming, peripheral arthritis

981
Q

Define OA

A

Non inflammatory degenerative arthritis

982
Q

Typical presentation of RA

A

Symmetrical, swollen, painful, stiff small joints of the hands and feet. Worse in the mornings. Slowly progressive, affects women more than men.

983
Q

Investigations in RA

A

Bloods, XRay, Ultrasound

984
Q

Blood in RA

A

Rheumatoid factor

985
Q

XRay of RA

A

Periarticular erosions, soft tissue swelling, loss of joint space

986
Q

Ultrasound of ra

A

Synovitis, bony erosion

987
Q

Pathophysiology of RA

A

Synovitis, hypertrophy, T lymphocyte and macrophage proliferation, pannus, malnutrition from cytokine effect, thin cartilage and bone exposure

988
Q

Early signs of RA

A

Inflammatory signs, swollen symmetrical MCP, PIP, wrist or MTP

989
Q

Late signs of RA

A

Ulnar deviation

990
Q

Extraarticular manifestations of RA

A

Vasculitis, pericarditis, raynaud’s, episcleritis, fibrosing alveolitis

991
Q

Conservative management of RA

A

PT, OT, Podiatry, psychological support

992
Q

RA 1st line

A

Methotrexate, sulfasalazine and short term pred

993
Q

RA 2nd line

A

If combination not appropriate, just methotrexate

994
Q

Long term MA management

A

Try and reduce DMARD dose, short term pred for flares. Consider bioligs

995
Q

antiTNF alpha blocker

A

Infliximab, etanercept, adalimumab

996
Q

Anti CD20 blocker

A

Rituximab

997
Q

Tyrosine kinase inhibitor

A

Imatinib

998
Q

Does RA or OA respond to steroids

A

RA better

999
Q

Describe seronegative spondyloarthropathies

A

Test negative for Rheumatoid factor, HLAB27 antigen.

1000
Q

Which joints are involved in seronegative spondyloarthropathies

A

Inflammation of the sacroiliac joint and spine

1001
Q

SPINEACHE acronym for seronegative spondyloarthropathies

A

Sauasage digit (dactylitis)

1002
Q

Ank spond criteria

A

¾ in under 50

1003
Q

Ank Spond on XRay

A

Syndesmophytes, sacroiliitis

1004
Q

Ank Spond bloods

A

FBC, raised ESR and CRP, HLAB27

1005
Q

Management of Ank Spond

A

Exercise and manage CV risk. 1st line NSAIDs, consider bisphosphonates and pred injections

1006
Q

What are the three classic features of reactive arthritis

A

Urethritis, arthritis, conjunctivitis. Cant wee, cant see, cant climb a tree

1007
Q

Define reactive arthritis

A

Sterile large joint arthritis affect the lower limb typically 1-4 weeks after infection

1008
Q

Infections that cause reactive arthritis

A

Urethritis (chlamydia)

1009
Q

Other features of reactive arthritis other than reiters syndrome 3

A

Iritis, mouth ulcers, enthesitis

1010
Q

Reactive arthritis investigations

A

Bloods, culture stool/sexual health review, infectious serology.

1011
Q

Management of reactive arthritis

A

Splint, aspirate, NSAIDs, corticosteroids, antibiotics. If chronic methotrexate

1012
Q

Define psoriatic arthritis

A

Arthritis in patients with psoriasis or a family history of psoriasis.

1013
Q

Presentation of psoriatic arthritis

A

Joint swelling, pain, stiffness, tenderness of joints

1014
Q

Features of psoriatic

A

Dactylitis and onycholysis

1015
Q

Investigations for psoriatic

A

Bloods raised ESR and CRP

1016
Q

Management of psoriatic

A

NSAIDs, sulfasalazine, methotrexate

1017
Q

Triad of septic arthritis

A

Low grade fever, impaired ROM, painful large joint

1018
Q

Risks for septic arthritis

A

RA, DM, immunosuppression, IVDU, over 80

1019
Q

Investigations for septic arthritis

A

Urgent joint aspiration for MC&S, blood cultures

1020
Q

Management of septic arthritis 1st line

A

Flucoxacillin for 6weeks. Splint. If prosthetic then debride

1021
Q

If penicillin allergic and septic arthritis

A

Clindamycin

1022
Q

If gonococcal arthritis which antibiotic

A

Cefotaxime

1023
Q

Definition of septic arthritis

A

Infection of the surface fo cartilage

1024
Q

Definition of osteomylelitis

A

Infection of the bone that can include the periosteum, medullary cavity and cortical bone

1025
Q

Common causative agent of septic arthritis and osteomyelitis

A

Staph Aureus

1026
Q

Who gets septic arthritis

A

Old people

1027
Q

Who gets osteomyelitis

A

Children

1028
Q

Diagnosis of septic arthritis

A

Join aspiration

1029
Q

Diagnosis of osteomyelitis

A

Bone cultures

1030
Q

Management of osteomyelitis

A

Debridement and antibiotics

1031
Q

Define raynauds disease

A

Peripheral digital ischaemia due to vasospasm

1032
Q

Colour changes in raynauds

A

Normal to white to blue to red to normal

1033
Q

Triggers of raynauds

A

Cold and stress

1034
Q

Seconday raynauds causes

A

SLE, RA, occupational, beta blockers

1035
Q

Treatment of raynauds

A

Stop smoking, keep warm, nifedipine, sildenafil

1036
Q

Define systemic lupus erythematosus

A

Inflammatory multisystemic disease with antinuclear antibodies

1037
Q

What is the common presentation of lupus

A

Fatigue, malaise fever

1038
Q

SLE associations

A

Black, women, IBS

1039
Q

Criteria for lupus acronym

A

SOAP BRAIN MD

1040
Q

What does the lupus criteria stand for

A

Serositis

1041
Q

Diagnosis of lupus

A

Clinical, ESR high but CRP low. Skin or renal biopsy

1042
Q

Treatment of SLE

A

Avoid smoking and sunlight. NSAIDs for arthralgia and topical steroids for cutaneous.

1043
Q

Acute severe SLE flare

A

IV prednisolone and cyclophosmaide

1044
Q

Chronic managemtn of SLE

A

NSAIDs and hydroxychloroquine

1045
Q

Define sjorgens

A

Inflammatory autoimmune disorder with lymphocytic infiltration of exocrine glands

1046
Q

Symptoms of Sjorgens

A

Dry eyes, mouth, vagina. Fever, malaise, polyarthralgia

1047
Q

Diagnosis of Sjorgens

A

Schirmers test. Serology ANA, RF, AntiRo and AntiLa. Biopsy showing plasma and lymphocytes

1048
Q

Management of sjorgens

A

Synthetic tears and saliva, lubrication for vagina, NSAID

1049
Q

Complications of Sjorgens

A

Non HL

1050
Q

What symptoms do you get in all autoimmune conditions

A

Fatigue, malaise, polyarthralgia, myalgia

1051
Q

What is the presentation of dermatomyositis

A

Polymyositis and skin involvement. Heliotrope rash, macular rash, subcut calcifications and gottrons papule.

1052
Q

Define polymyositis

A

Inflammation and progressive necrosis of skeletal muscle fibres

1053
Q

Presentation of polymyositis

A

Difficulty squatting, climbing stairs, raising hands above head. Arthralgia, dysphonia, dysphagia, fever, raynauds

1054
Q

What causes polymyositis

A

Cytotoxic T cells

1055
Q

Diagnosis of polymyositis

A

Creatinine kinase and aldolase

1056
Q

Mangement of polymyositis

A

Oral prednisolone

1057
Q

Presentation of limited cutaneous systemic sclerosis

A

Calcinosis

1058
Q

What is the different presentation of diffuse cutaneous systemic sclerosis

A

Earlier organ fibrosis and diffuse cutaneous involvement

1059
Q

Diagnosis of limited cutaneous systemic sclerosis

A

Anti centrome ab

1060
Q

Diagnosis of diffuse cutaneous systemic sclerosis

A

AntiScl 70 and anti-RNA polymerase

1061
Q

Management of diffuse cutaneous systemic sclerosis

A

Control BP, monitor echo spirometry renal function

1062
Q

Complication of systemic sclerosis

A

Malnutrition

1063
Q

What causes systemic sclerosis

A

Collagen deposition

1064
Q

How do you diagnose PE

A

CT pulmonary angiogram

1065
Q

Antiphospholipid syndrome

A

Venous and arterial thrombosis. Phospholipid antibodies. Low dose aspirin treatment

1066
Q

Large cell vasculitis

A

Granulomatous disease. Giant cell arteritis and Takayasu arteritis

1067
Q

Medium vessel vasculitis

A

Polyarteritis nodosa and Kawasaki disease

1068
Q

What will you see on biopsy for GCA, polyarteritis nodosa, wegeners, churgg strauss

A

Granulomas

1069
Q

Consequences of vasculitis

A

Stroke, MI, fever headache

1070
Q

Signs of giant cell arteritis

A

Unilateral headache, scalp tenderness in temporal region, jaw cladication, amaurosis fugax, morning stiff ness

1071
Q

Diagnosis of giant cell arteritis

A

Clinical, bloods.

1072
Q

Management of giant cell arteritis

A

Immediate prednisolone

1073
Q

Define polymyositis

A

Inflammation of striated muscle

1074
Q

How would you differentiate polymyalgia rheumatica from polymyositis

A

PMR gets pain

1075
Q

Key deatures of polyarteritis nodosa

A

Medium arteries. Microaneurysms. HepB. Skin rash and punched out ulcers. No glomerulonephritis or ANCA

1076
Q

Diagnosis of polyarteritis nodosa

A

Renal angiography or biopsy

1077
Q

Management of polyarteritis nodosa

A

Prednisolone and cyclophosamide

1078
Q

Define granulomatosis with polyangiitis

A

Necrotising granulomatous vasculitis nmediated by neutrophils (cANCA)

1079
Q

Symptoms of GPA

A

Cough, sinusitis, haemoptysis, haematuria, ulcers, saddle nose deformity

1080
Q

Diagnosis of GPA

A

History, bloods, cANCA and PR3 ab test. Renal or lung biopsy showing granuloma

1081
Q

Treatment of acute GPA

A

Prednisolone and IV cyclophosamide

1082
Q

Maintenance of gpa

A

Azathioprine

1083
Q

Churg-Strauss syndrome

A

Asthma, eosinophilia and vasculitis. MPO ab, pANCA. Steroids. Then long term rituximab

1084
Q

Microscopic polyangiitis

A

Like wegeners but pANCA and no granuloma

1085
Q

Fibromyalgia treatment

A

CBT and tailored exercise programme

1086
Q

Define fibromyalgia

A

Chronic widespread pain and sensitivity to pressure at 11/18 tender points without inflammation (exclude DDx)

1087
Q

Yellow flags of fibromyalgia

A

Sickness behaviour (extended rest, social withdrawal, low participation in treatment, belief that pain and activities are harmful)

1088
Q

Investigations in back pain

A

Urgent MRI, FBC, U&E, LFT, ESR, CRP serum electrophoresis

1089
Q

Define multiple myeloma

A

Abnormal proliferation of a single clone plasma cell

1090
Q

Prognostic myeloma test

A

Serum Beta2 microglobulin

1091
Q

Osteosarcoma

A

Teenagers and children. Around knee. Chemo and surgery

1092
Q

Ewings sarcoma

A

5-20yo. Leg, pelvis, upper arm, ribs. Chemo and surgery

1093
Q

Chondrosarcoma

A

Malignant tumour of chondrocytes. 40-70, hip pelvis shoulder. Surgery

1094
Q

Secondarys to bone from

A

Breast, lung, thyroid, renal, prostate

1095
Q

Define osteoporosis

A

Progressive systemic skeleteal disease characterised by reduced bone mass and microarchitectural deterioration of bone tissue.

1096
Q

ACCESS for osteoporosis risk

A

Alcohol

1097
Q

What is a T score

A

Score compared to a gender matched individual at peak bone mass

1098
Q

-1 to -2.5

A

Osteopenia

1099
Q

< -2.5 osteoporosis

A

Osteoporosis

1100
Q

LESS THAN -2.5 AND FRACTURE

A

<p>Severe osteoporosis</p>

1101
Q

Management of osteoporosis

A

More exercise, less alcohol, vitamin D supplements. Bisphosphonates.

1102
Q

What does FRAX do

A

Fracture risk assessment tool. Evaluates the 10 year probability of bone fracture.

1103
Q

Name two loop diuretics

A

Furosemide and bumetanide

1104
Q

How do loop diuretics work

A

Act on NaK2Cl in the ascending limb

1105
Q

Adverse effects of loop diuretics

A

Dehydration, hypotension, hypokalaemia so metabolic alkalosis

1106
Q

Name two potassium sparing diuretics

A

Amiloride and spironolactone

1107
Q

How do potassium sparing diuretics work

A

Aldosterone antagonist so acts on ENaC in the DCT

1108
Q

Adverse effects of potassium sparing diuretics

A

GI upset, hyperkalaemia, metabolic acidosis, gynaecomastia

1109
Q

Name a thiazide diuretic

A

Bendroflumethiazide

1110
Q

How do thiazide diuretics work

A

Act on sodium chloride channels in the DCT, longer acting but not as potent as loop

1111
Q

Adverse effects of thiazide diuretics

A

Hypokalaemia, metabolic alkalosis, hypovolaemia, hyponatraemia, hyperglycaemia in diabetics

1112
Q

3 common sites where stones get stuck

A

Pelviureteric junction, pelvic brim, vesicoureteric junction

1113
Q

What are renal stones made up of

A

Calcium oxalate (75%), struvite, uric acid or cysteine. Caused by supersaturation of urine with salt/minerals

1114
Q

What are infection stones made up of

A

Magnesium ammonium phosphate

1115
Q

What causes cysteine stones

A

Cystinuria which is an autosomal recessive condition

1116
Q

How would describe colic

A

Waves of pain

1117
Q

If they have a catheter in and are confused what do you suspect

A

UTI

1118
Q

Renal colic pain presentation

A

Unilateral severe pain, starts in loin and moves to groin. Radiates to ipsilateral testis and labia. There can be periods of relief before it returns again.

1119
Q

What are the other symptoms of renal colic

A

Rigors, dysuria, haematuria, urinary retention, nausea and vomiting

1120
Q

Risk factors for stones

A

Anatomical abnormalities, FHx, hypertension, gout, hyperparathyroidism, immobile, dehydrated

1121
Q

Differentials for renal colic

A

Ruptured AAA, diverticulitis, appendicitis, pancreatitis, testicular torsion, pyelonephritis, MSK

1122
Q

Investigations for renal colic

A

Bloods inc calcium, phosphate urate. Urinalysis, MSU if positive. Non contrast computerised tomography kidney ureter bladder. NCCT KUB gold standard

1123
Q

Management of renal colic

A

Strong analgesic= diplofenac

1124
Q

Management of obstruction and infection

A

Ureteric stent

1125
Q

Prevention of renal stones

A

Drink plenty of water

1126
Q

Define AKI

A

An abrupt sustained rise in serum urea and creatinine due to a rapid decline in GFR leading to a failure to maintain, fluid, electrolyte and acid base homeostasis

1127
Q

3 criteria for AKI

A

Increase in creatinine of more than of 26micromol/L in 48hr

1128
Q

Risk factors for AKI

A

Age, CKD, cardiac failure, PVD, diabetes, drugs, sepsis, dehydration

1129
Q

Prerenal AKI causes

A

Hypoperfusion, hypotension, renal artery stenosis, drugs

1130
Q

Renal AKI causes

A

Acute tubular necrosis, AI, glomerulonephritis, vasculitis

1131
Q

Post renal causes of AKI

A

Urinary tract obstruction. Stones, malignancy, BPH

1132
Q

ACE-I and ARB effect on kidney

A

Results in dilated efferent arterioles, decreasing GFR

1133
Q

NSAIDs effect on kidney

A

Inhibits cyclooxygenase causing excess vasoconstriction of the afferent arterial

1134
Q

Aminoglycosides effect on the kidney

A

Acute tubular necrosis

1135
Q

Investigations of AKI

A

Full screen. Cr, U and E, LFT, clotting, glucose, urine dipstick, autoantibodies (antiGBM, ANCA), Renal USS. U and E is diagnostic

1136
Q

Management of AKI

A

Aim for euvolaemia, stop nephrotoxic drugs, treat cause, manage complications

1137
Q

How do you treat hyperkalaemia

A

Insulin/dextrose, salbutamol, calcium gluconate

1138
Q

Define CKD

A

GFR below 60mL/min/1.73m for more than 3 months, with or without evidence of kidney damage

1139
Q

Causes of CKD

A

Glomerular disease, hypertension, interstitial disease (myeloma, TB, schistosomiasis), PCKD, SLE, Vasculitis

1140
Q

CKD on USS

A

Bilaterally small kidneys

1141
Q

Presentation of CKD

A

Malaise, nocturia and polyuria, itching, NVD, oedema, bruising

1142
Q

What causes itching in CKD

A

High urea levels

1143
Q

Stage one CKD

A

GFR over 90, with evidence of kidney damage. Check for proteinuria and haematuria

1144
Q

Stage two CKD

A

60-89, kidney damage and slightly low GFR. Lower BP and give low protein diet

1145
Q

Stage three A and B CKD

A

30-45,45-60 moderate reduction in GFR. control BP low protein diet

1146
Q

Stage 4 CKD

A

15-29. Severely low GFR. Prepare for dialysis

1147
Q

Stage 5 CKD

A

<15 or dialysis. Kidney failure.

1148
Q

AKI v CKD: kidney size

A

Normal v small

1149
Q

AKI v CKD: anaemia

A

No v normochromic normocytic

1150
Q

AKI v CKD: diabetes

A

No v diabetes

1151
Q

AKI v CKD: BP

A

Low v high

1152
Q

AKI v CKD: time span

A

Rapid v slow

1153
Q

AKI v CKD: urine output

A

Oligouria v polyuria and nocturia then oligouria

1154
Q

AKI v CKD: CNS symptoms

A

None v In late disease

1155
Q

Nephrotic disease triad

A

Proteiunuria, hypoalbuminaemia, oedema. Also severe hyperlipidaemia as liver goes into overdrive from albumin loss

1156
Q

Causes of primary nephrotic

A

Minimal change disease, membranous nephropathy, focal segmental glomerulonephritis

1157
Q

Causes of secondary nephrotic

A

Diabetes, hepatitis, malignancy

1158
Q

Cause of nephrotic

A

Injury to podocyte foot processes

1159
Q

What happens in minimal change disease

A

Fusion of footprocesses of podocytes

1160
Q

Investigations of nephrotic

A

Urine dip (high protein), bloods (low albumin and biopsy in adults

1161
Q

Management of nephrotic

A

Steroids in children, diuretics, ACE-I for proteinuria. Treat cause

1162
Q

Complications of nephrotic

A

Infections, thromboembolism, hypercholesterolaemia

1163
Q

Nephritic syndrome 4 things

A

Haematuria (red cell clasts), proteinuria, hypertension, oligouria

1164
Q

Cause of nephritic

A

Immune response to podocytes so pores

1165
Q

Causes of nephritic

A

Spot streptococcal glomerulonephritis, IgA nephropathy, good pastures

1166
Q

What do red cell clasts indicate

A

Glomerular damage

1167
Q

How long after URTI does IgA nephropathy happen

A

Days

1168
Q

How long after URTI foes post strep glomerulonephritis happen

A

Weeks

1169
Q

What happens in IgA nephropathy

A

Abnormal IgA form and accumulate, IgG bind against. These immune complexes get trapped in the mesangium causing type 3 hypersensitivity

1170
Q

Why do you get a proinflammatory response in IgA nephropathy

A

Alternative complement system is activated by immune complexes

1171
Q

How do you diagnose IgA nephropathy

A

Mesangial proliferation

1172
Q

How do you prevent immune complexes

A

Prednisolone

1173
Q

Which bacteria cause post strep GN

A

Group A Beta haemolytic strep

1174
Q

How do you diagnose post strep GN

A

Biopsy shows enlarged glomerular basement membrane then EM shows humps

1175
Q

What hypersensitivity is post strep GN

A

3, immune complex. Then alternative complement.

1176
Q

Management of post strep GN

A

Supportive

1177
Q

Minimal change disease

A

Children, Cytokines damage podocytes making them flattened and lose their negative charge. Nephrotic syndrome. Selective proteinuria

1178
Q

Association of minimal change disease

A

Hodgkins lymphoma

1179
Q

Diagnosis of minimal change disease

A

Fused podocyte processes on EM

1180
Q

Treatment of minimal change disease

A

Prednisolone

1181
Q

Focal segmental glomerulonephritis

A

Hyalinosis leads to sclerosis. Diagnosed by afacement of podocytes on EM. Treat with prednisolone

1182
Q

What is used when the patient is steroid resistant

A

Ciclosporin

1183
Q

Membranous neuropathy

A

Immune complexes against basement membrane. Biopsy= thickened BM and C3 and IgG deposits. Treat with prednisolone

1184
Q

Causes of nephrotic

A

Minimal change disease, membranous neuropathy and focal segmental glomerulonephritis

1185
Q

Causes of nephritic

A

IgA nephropathy, post streptococcal glomerulonephritis, goodpastures

1186
Q

What are the features of nephrotic which nephritic doesn’t have

A

Oedema, hyperlipidaemia and hypoalbuminaemia

1187
Q

Autosomal dominant Polycystic kidney disease

A

PKD1 more common and more severe. PKD2 less common and less severe

1188
Q

Pathophysiology of ADPKD

A

Polycystin 1 and 2 mutations mean unregulated tubular and vascular growth in the kidneys and other organs

1189
Q

Other organ involvement of ADPKD

A

Liver= no affect on function

1190
Q

Presentation of ADPKD

A

Nocturia, loin pain, HTN, bilateral kidney enlargement. Haematuria following trauma. UTI, pyelonephritis, stones more common

1191
Q

Investigations of ADPKD

A

Ultrasound

1192
Q

Management of ADPKD

A

Counselling and support for family, monitor progression, treat HTN, UTI, Stones and colic. Dialysis when needed

1193
Q

What happens in retention

A

The kidneys are still producing urine but the bladder is unable to void

1194
Q

Causes of acute bladder retention

A

Bladder stone, BPH, Prostate cancer, MS, prolapsed disc at S2,3,4

1195
Q

Define BPH

A

Benign proliferation of musculofibrous/glandular tissue of the transitional zone of the prostate

1196
Q

Voiding LUTS

A

Hesitancy

1197
Q

Storage LUTS

A

Frequency

1198
Q

Investigations for BPH

A

DRE smooth and enlarged

1199
Q

Non medical prostatic hyperplasia treatment

A

Lower caffeine and alcohol, bladder training

1200
Q

What is needed for BPH

A

Dihydrotestosterone

1201
Q

1st line medical BPH

A

Alpha blockers, Tamsulosin

1202
Q

2nd line medical BPH

A

5alpha reductase inhibitors, finasteride

1203
Q

Surgical treatment of BPH

A

TURP, TUIP, Retropubic prostatectomy

1204
Q

Side effects of alpha blockers

A

Dizziness, postural hypertension, weight gain

1205
Q

Define prostate cancer

A

Malignant adenocarcinoma of the peripheral zone of the prostate

1206
Q

Symptoms of prostate cancer

A

LUTS, cancer symptoms, bone pains

1207
Q

Risk factors for prostate cancer

A

Family history, high levels of testosterone (obesity not a risk factor but more aggressive form)

1208
Q

Where does prostate met to

A

Adjacent structures, bone lung

1209
Q

Investigations of prostate cancer

A

DRE (hard and irregular), PSA, biopsy, TRUSS, imaging, bone scan

1210
Q

How does gleason grading work

A

20 biopsies. First part is most common, 2nd part the worst.

1211
Q

TNM: T for prostate 1

A

Non palpable

1212
Q

T2 prostate

A

Palpable and confined to prostate

1213
Q

T3 prostate

A

Palpable and through capsule

1214
Q

T4 prostate

A

Palpable and invades other structures

1215
Q

Prostate cancer localised treatment low rise

A

Active surveillance

1216
Q

Prostate cancer progression treatment

A

Radical prostatectomy and radiotherapy

1217
Q

Hormone treatment for prostate

A

LHRH agonist (goserelin) and antiandrogen

1218
Q

Metastatic prostate treatment

A

Surgical castration and palliative care

1219
Q

Side effects of hormone treatment

A

Osteoporosis, gynaecosmastia, sexual dysfunction

1220
Q

Renal cell carcinoma

A

Adenocarcinoma of the PCT, highly vascular

1221
Q

Where does renal cell carcinoma met to

A

Bone, liver lungs

1222
Q

Risk factors for renal cell carcinoma

A

Poor lifestyle, HTN, CKD, horseshoe kidney, haemodialysis

1223
Q

Signs of RCC

A

Abdo mass, haematuria, obstruction

1224
Q

Symptoms of RCC

A

Loin pain, cancer symptoms

1225
Q

Investiagtions of RCC

A

Bloods, urine, USS

1226
Q

Localised RCC treatment

A

Radical nephrectomy

1227
Q

Metastatic RCC treatment

A

Biologics

1228
Q

Symptoms of bladder cancer

A

Painless haematuria

1229
Q

3 types of bladder cancer

A

Transitional cell, squamous, adenocarcinoma

1230
Q

Risk factors for bladder cancer

A

Rubber, azo dyes, schistosomiasis(=squamous). Chronic cystitis, smoking, male

1231
Q

Bladder cancer diagnosis

A

Flexible cystoscopy, biopsy and CT urogram

1232
Q

Where does bladder cancer met to

A

Paraaortic and iliac lymph nodes

1233
Q

Management of T1 bladder cancer

A

Transurerthral resection of bladder tumour. And chemo

1234
Q

Management of T2-3 bladder cancer

A

Radical cystectomy

1235
Q

T4 bladder cancer management

A

Palliative chemo

1236
Q

Testicular pain causes

A

Torsion, sti=epididymoorchitis, renal colic referred pain

1237
Q

Testicular cancer types

A

Seminoma (germ cell) and non seminoma

1238
Q

Risk factors for testicular cancer

A

Undescended testes, infant hernia

1239
Q

Presentation of testicular cancer

A

Painless testicular lump, haematospermia

1240
Q

Testicular cancer diagnosis

A

Scrotal US, biopsy, serum tumour markers

1241
Q

Testicular cancer tumour markers

A

A-fetoprotein, B-human chorionic gonadotrophin, lactate dehydrogenase

1242
Q

Seminoma unique

A

Young. A-fetoprotein and B-HcG

1243
Q

Teratoma unique

A

B-HcG and LDH

1244
Q

Treatment of seminomas

A

Radical orchidectomy and radiotherapy

1245
Q

Treatment of no seminomas (teratoma)

A

Chemotherapy

1246
Q

Staging of testicular

A

1=no mets

1247
Q

Where can TCC occur

A

Bladder, renal pelvis, calyx, ureter, urethra

1248
Q

Wilms tumour

A

Childhood tumour, primitive renal tubules and mesenchymal cells. Abdo mass and haematuria in children.

1249
Q

Penile cancer

A

Irradiation or virus, ulceration and discharge. Give radiotherapy, iridum wired or amputate

1250
Q

Backpain, withdrawn, confused

A

Prostate with mets to bone

1251
Q

What makes testicular cancer more likely

A

Body of testes and cant separate

1252
Q

Epididymal cyst

A

Clear milk fluid, above and behind testes

1253
Q

Hydrocele

A

Can be transilluminated. Fluid in tunica vaginales, caused by patent process vaginales or secondary in older people to Tumour, trauma, infection. Aspirate and surgery if needed.

1254
Q

Varicocele

A

Dilated pampniform plexus, left more than right. Bag of worms. Ligate the gonadal vein

1255
Q

Haematocele

A

Blood in tunica vaginales from trauma, aspirate or surgery

1256
Q

Epidydmoorchitis

A

Sudden onset testicular pain, usually caused by STI

1257
Q

Why is varicocele more common on left

A

RCC invasion of left renal vein causes compression of left gonadal vein

1258
Q

What causes testicular torsion

A

Twisted spermatic cord cuts off blood supply to testes, causing ischaemia

1259
Q

Presentation of testicular torsion

A

Sudden onset testicular pain, inflamed and tender testical, unilateral, abdo pain, Nausea and vomiting

1260
Q

What to do for testicular torsion

A

Refer to urology ASAP, can do scrotal US. Surgery

1261
Q

Testicular lump

A

Cancer

1262
Q

Acute and tender lump

A

Testicular torsion

1263
Q

Definition of UTI

A

Pure growth of more than 10 5 organisms per ml of fresh MSU

1264
Q

Risk factors for UTI

A

Female, intercourse, pregnancy, menopause, UT obstructions, malformations, immunosuppression, catheterisation

1265
Q

What do you find on urine dipstick of UTI

A

Nitrites (bacteria convert nitrate to nitrites)

1266
Q

When is it hard to spot UTI

A

Dementia or children

1267
Q

Why do you get more UTI in diabetes

A

It weakens the immune system

1268
Q

Organisms in UTI

A

Escherichia coli

1269
Q

What is E Coli

A

Gram negative lactose fermenting

1270
Q

What is proteus mirabilis

A

Gram negative, swarming on cultures

1271
Q

What is klebsiella pneumonia

A

Gram negative

1272
Q

What is staphylococcus saprophyticus

A

Gram positive cocci, lactose fermenting, catalase positive, coagulase negative

1273
Q

What is enterococcus

A

Gram positive diplococci

1274
Q

What are upper UTI

A

Pyelonephritis and ureteritis

1275
Q

What are lower UTI

A

Cystitis, urethritis, prostatitis

1276
Q

What are signs and symptoms of UTI

A

Loin/abdo pain, offensive smelling urine, haematuria, fever

1277
Q

Investigations of UTI

A

GOLD= MC&S of MSU

1278
Q

Management of UTI

A

Abx, fluid intake, pain relief

1279
Q

How to prevent UTI

A

Hydrate, void before and after sex

1280
Q

Signs and symptoms of cystitis

A

Suprapubic pain, haematuria, dysuria, frequency, urgency

1281
Q

Uncomplicated UTI treatment

A

Trimethoprim or nitrofurantoin

1282
Q

Complicated UTI treatment

A

Cefalexin

1283
Q

Pyelonephritis signs and symptoms

A

High fever, loin pain, rigors, N and v

1284
Q

Uncomplicated pyelonephritis treatment

A

Ciprofloxacin or coamoxiclav

1285
Q

Complicated pyelonephritis treatment

A

Cefalexin

1286
Q

What do beta cells secrete

A

Insulin

1287
Q

What do alpha cells secrete

A

Glucagon

1288
Q

What do delta cells secrete

A

Somatostatin

1289
Q

Which hormones control glucose levels

A

Insulin, glucagon, cortisol and growth hormone

1290
Q

Actions of insulin

A

-stimulates glucose uptake by insulin dependent tissues

1291
Q

What should blood glucose always be between

A

3.5 and 8mmol

1292
Q

GLUT 1

A

Non insulin stimulated glucose uptake

1293
Q

GLUT 2

A

Low affinity transporter for Beta cells

1294
Q

GLUT 3

A

Non insulin stimulated glucose uptake into brain and placenta

1295
Q

GLUT 4

A

Insulin mediated glucose uptake in muscle and adipose tissue

1296
Q

Symptoms of hypoglycaemia

A

(<3) dizziness, confusion, hunger, convulsions, coma, sympathetic action (tachycardia, sweating, pallor)

1297
Q

Define diabetes mellitus

A

Syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance or both

1298
Q

Secondary causes of DM

A

Pancreatitis, cystic fibrosis, trauma, haemochromatosis, acromegaly, cushings

1299
Q

Diabetes Fasting plasma glucose

A

Over 7mmol/L

1300
Q

Prediabetes fasting plasma glucose

A

5.5-7mmol/L

1301
Q

Diabetes oral glucose tolerance test

A

11.1mmol/L

1302
Q

Prediabetes oral glucose tolerance test

A

7.8-11mmol/L

1303
Q

diabetes HBA1C concentration and percentage

A

47 or 6.4%

1304
Q

Prediabetes HBA1C concentration and percentage

A

42-27 or 6-6.4%

1305
Q

What test would you do if you suspect gestational diabetes

A

OGTT

1306
Q

If you are symptomatic how many positive results do you need

A

Just one

1307
Q

Define diabetes mellitus type one

A

Caused by insulin deficiency from autoimmune destruction of insulin secreting pancreatic beta cells

1308
Q

Which conditions is DMT1 associated with

A

Vitiligo, addisons, pernicious anaemia

1309
Q

Risk factors for DMT1

A

Polygenic,

1310
Q

If theres a thin old person with diabetes and rapid progression to insulin therapy what do they have

A

Latent autoimmune diabetes in adults (LADA)

1311
Q

What are the HLAs of DMT1

A

HLA DR3 DQ2 and HLA DR4 DQ8

1312
Q

Symptoms of DMT1

A

Polydipsia, polyuria, polyphagia, fatigue and weight loss. Diabetic ketoacidosis

1313
Q

Environmental influences of DMT1

A

Diet, enteroviruses, vitamin D deficiency, cleaner environment

1314
Q

Diagnosis of DMT1

A

Measure glycaemic control and find autoantibodies. Diabetic consequences like retinopathy is diagnostic

1315
Q

Treatment of DMT1

A

Dietary control and insulin therapy

1316
Q

Types of insulin therapy

A

Rapid, short, intermediate and long acting insulin

1317
Q

Define DMT2

A

Results from a combination of insulin resistance and less severe insulin deficiency

1318
Q

DMT2 pathology

A

Beta cell mass is greatly reduced, it isn’t a problem with binding. There is hypersecretion of insulin from a depleted cell mass due to higher demand. Amyloid deposition

1319
Q

Does DMT1 or DMT2 have a stronger genetic link

A

DMT2

1320
Q

Risk factors for DMT2

A

South Asian, African, FHx, male, obese central, lack of exercise, hyperlipidaemia, hypertension, alcohol, stress, urban environment

1321
Q

Acute presentation of DMT2

A

Polyuria, polydipsia, weight loss

1322
Q

Subacute presentation of DMT2

A

Lethargy, fatigue, visual blurring, pruritus vulvas

1323
Q

Complications of DMT2

A

Staph skin infections, retinopathy, polyneuropathy, erectile dysfuntion, arterial disease

1324
Q

Treatment of DMT2

A

Patient education, decrease alcohol, regular blood glucose measuring. Identify and manage long term complications

1325
Q

Drug treatment of DMT2

A

Statins and BP drugs

1326
Q

Metformin

A

Reduces gluconeogenesis by the liver and increases glucose sensitivity. It doesn’t cause hypoglycaemia or weight gain

1327
Q

Sulphonylureas

A

Gliclazide or tolbutamide (in elderly), act in beta cells to promote insulin secretion. Only works if beta cell mass, and causes weight gain and hypos

1328
Q

Microvascular DMT2 complications

A

Diabetic retinopathy, diabetic neuropathy, nephropathy

1329
Q

Macrovascular DMT2 complications

A

Increased risk fo CVD, IHD, MI and diabetic foot ulcers

1330
Q

Signs of diabetic retinopathy

A

Haemorrhages, abnormal growth of vessels, aneurysm, cotton wool spots

1331
Q

Who can get diabetic ketoacidosis

A

DMT1 mainly, DMT2 can but very rare

1332
Q

Circumstances of DKA

A

Previously undiagnosed diabetes, interruption of insulin therapy, stress of intercurrent illness

1333
Q

What causes DKA

A

Increased hepatic ketogenesis. Increased peripheral lipolysis means theres more FFA which are converted into acetyl CoA by the liver then into ketone bodies by the mitochondria. More ketone bodies mean more metabolic acidosis, and dehydration so impaired excretion.

1334
Q

Signs and symptoms of DKA

A

N,V Abdo pain. Polyuria, polydipsia, drowsiness, ketone smelling breath, Kussmaul breathing

1335
Q

Describe kussmaul breathing

A

Low deep, sighing inspiration and expiration

1336
Q

Diagnosis of DKA

A

Acidosis, ketonaemia, hyperglycaemia

1337
Q

Treatment of DKA

A

Saline

1338
Q

Cause of sudden CNS decline in DKA

A

Cerebral oedema

1339
Q

What is hyperosmolar, hyperglycaemic state

A

Hyperglycaemia and hyperosmolality. No ketosis or acidosis. Alteration of consciousness.

1340
Q

Features of HHS

A

Delerium, focal neurological signs, tremors, fasciculations. Give Saline and insulin

1341
Q

What test is used for acromegaly screening

A

IGF-1

1342
Q

What test is used for acromegaly diagnosis

A

Glucose tolerance test

1343
Q

What do C cells produce

A

Calcitonin

1344
Q

What is released from the hypothalamus that acts of the anterior pituitary for TSH release

A

Thyrotropin releasing hormone

1345
Q

What hormone is released by the anterior pituitary and acts on the thyroid

A

TSH- thyroid stimulating hormone

1346
Q

What is the role of thyroid peroxidase

A

It binds thyroglobulin and iodine, and also couples MIT and DIT to make T3 or T4

1347
Q

What is the role of thyroglobulin

A

Iodine binds to its tyrosine residues

1348
Q

Actions of thyroid hormone

A

Increases metabolic rate, beta adrenergic action on the heart and gut, CNS activation, bone demineralisation

1349
Q

What symptoms of hyperthyroid

A

Sweating

1350
Q

Signs of hyperthyroid

A

Tremor

1351
Q

Causes of hyperthyroidism

A

Graves

1352
Q

Who gets hyperthyroid

A

Women 20-40

1353
Q

Graves disease

A

Autoimmune with

1354
Q

Graves unique skin sign

A

Pretibial myoedema

1355
Q

Thyroid acropachy

A

Digital clubbing, swelling and new periosteal bone formation

1356
Q

Graves ophthalmology

A

Exopthalmos, opthalmoplegia, retroorbital inflammation and swelling of the extraorbital muscles

1357
Q

Hyperthyroid diagnosis

A

High T4 and T3 (more sensitive), thyroid peroxidase and thyroglobulin antibodies

1358
Q

Graves diagnosis

A

TSH receptor stimulating antibodies

1359
Q

Treatment of hyperthyroid

A

Propanolol for rapid symptom control

1360
Q

How does carbimazole work

A

Blocks thyroid hormone biosynthesis

1361
Q

Primary causes of hypothyroidism

A

Hashimotos thyroiditis

1362
Q

Secondary causes of hypothyroidism

A

Iodine deficiency, pituitary failure. Amiodarone

1363
Q

Hypo thyroid symptoms (everything a girl don’t want)

A

Weight gain

1364
Q

Signs of hypothyroid

A

Dry, brittle hair and nails. Bradycardia, macroglossia, hyporeflexia, hoarse voice, alopecia

1365
Q

Hashimotos thyroiditis

A

Lymphocytic infiltration and progressive destruction of the gland

1366
Q

Management of hypothyroid

A

Levothyroxine

1367
Q

Diagnosis of hypothyroid

A

Serum free T4 low

1368
Q

Hormones released by hypothalamus

A

GnRH, CRH, TRH, PRH, GHRH, ADH, Oxytocin

1369
Q

What does Gonadotrophin releasing hormone stimulate

A

FSH/LH release from the anterior pituitary which acts on the gonads

1370
Q

What does Corticotropin releasing hormone stimulate

A

ACTH release from the anterior pituitary which acts on the adrenal cortex

1371
Q

What does Thryotropin releasing hormone stimulate

A

TSH from the anterior pituitary which acts on the thyroid

1372
Q

What does prolactin releasing hormone stimulate

A

Porlactin release from the anterior pituitary which stimulates the mammary gland

1373
Q

What does Growth hormone releasing hormone stimulate

A

Growth hormone release from the anterior pituitary which stimulates the liver

1374
Q

What does antidiuretic hormone stimulate

A

Is released from the posterior pituitary and acts on the kidneys

1375
Q

What does oxytocin stimulate

A

Is released from the posterior pituitary and acts on the mammary gland

1376
Q

Explain the action of ADH

A

Acts on V2 receptors to cause the insertion of aquaporin 2 channels

1377
Q

ADH is increased by

A

Hypovolaemia, hypotension, anaemia, nicotine, adrenaline

1378
Q

ADH is decreased by

A

Hypertension, ethanol, alpha adrenergic stimuli

1379
Q

Define diabetes insipidus

A

ADH deficiency or insensitivity to its action

1380
Q

Clinical features of diabetes insipidus

A

Polyuria, nocturia, compensatory polydipsia, dehydration

1381
Q

Cranial causes of diabetes insipidus

A

Familial, tumours, infection, infiltrations, post surgical, trauma

1382
Q

Nephrogenic causes of diabetes insipidus

A

Renal disease, sickle cell disease, drugs

1383
Q

What can mask DI

A

Cortisol deficiency. So give cortisol and if still happening then its DI

1384
Q

What is clubbing

A

Loss of window between nail beds

1385
Q

Investigations of DI

A

Osmolality, U and E, 24hr urine volumes, waterdeprivation test

1386
Q

Diagnosis of diabetes insipidus

A

Water deprivation test (urine doesn’t concentrate) Low urine osmolality, hypernatraemia, high urine volume

1387
Q

Treatment of cranial DI

A

Demsmopressin which is an ADH analogue

1388
Q

Treatment of nephrogenic DI

A

Thiazide diuretics

1389
Q

What is SIADH

A

Inappropriate ADH secretion leads to retention of water and hyponatraemia

1390
Q

Clinical features of SIADH

A

Confusion, nausea, irritable (kinda like UTI), later fits and coma

1391
Q

Causes of SIADH

A

Tumour: SCLC, prostate

1392
Q

Investigations of SIADH

A

U and E, osmolality, urinalysis

1393
Q

Results of SIADH

A

Dilutional hyponatraemia, low plasma osmolality, urinary Na secretion

1394
Q

Treatment of SIADH

A

Restrict fluid intake

1395
Q

Functions of growth hormone

A

Decreases adipose tissue, increases bone growth and muscle mass

1396
Q

Cause of acromegaly/gigantism

A

Pituitary adenoma (MEN-1 or AIP gene)

1397
Q

Symptoms of acromegaly

A

Snoring, deep voice, increased sweating, reduced libido and arthralgia. Increased weight and size of hands and feet. Headache

1398
Q

Signs of acromegaly

A

Acathosis nigricans, big supraorbital ridge, interdental separation, macroglossia, prognathism. Spade like hands and feet, tight rings

1399
Q

Acromegaly screening

A

Increased IGF-1

1400
Q

Acromegaly diagnosis

A

Imparied glucose tolerance test (high glucose)

1401
Q

Acromegaly other investigations,

A

high calcium, bitemporal hemianopia, MRI for pituitary adenoma. Photos.

1402
Q

Treatment of acromegaly 1st line

A

Transsphenoidal surgery

1403
Q

Treatment of acromegaly 2nd line

A

Somatostatin analogue (IM ocreotide)

1404
Q

What does the hypothalamus produce in response to emotional and physical stresses

A

Corticotropin releasing hormone

1405
Q

What is conns and the cause

A

Excess aldosterone caused by solitary aldosterone producing adenoma

1406
Q

What is the result of conns

A

Increased sodium and water retention

1407
Q

How can conns present

A

Hypokalaemia: Hypertension, alkalosis, weakness, cramps

1408
Q

What is the diagnosis in Conns

A

U and E (low renin, high aldosterone), MRI

1409
Q

What is the treatment of Conns

A

Laparoscopic adrenalectomy and spironolactone

1410
Q

What is Cushings syndrome

A

Chronic glucocorticoid excess

1411
Q

What are the symptoms of cushings syndrome

A

Increased weight, mood changes, weakness, acne, recurrant achilles injury, gonadal dysfunction

1412
Q

Signs of cushings syndrome

A

Moon face, central obesity, buffalo neck hump, bruises, muscle atrophy, purple abdo striae

1413
Q

What are the causes of cushings

A

Pituitary adenoma (cushings disease), adrenal tumour, idiopathic. Taking glucorticoids (hydrocortisone)

1414
Q

What are the investigations in Cushings

A

Bloods= high plasma cortisol

1415
Q

How would you investigate a ACTH independent cause of cushings syndrome

A

CT adrenals

1416
Q

How would you investigate ACTH dependent cushings

A

High dose dexamethasone suppression test

1417
Q

If it is ACTH dependent and cortisol suppressed what do you do

A

MRI pituitary

1418
Q

If it is ACTH dependent and cortisol isn’t surpressed what do you do

A

CT chest and abdo

1419
Q

How do you treat iatrogenic cushings syndrome

A

Stop steroids

1420
Q

How do you treat cushings disease

A

Transsphenoidal surgery

1421
Q

How do you treat adrenal adenoma

A

Adrenalectomy

1422
Q

How do you treat adrenal carcinoma

A

Adrenalectomy and radiotherapy

1423
Q

How do you treat ectopic ACTH

A

Adrenalectomy and chemo

1424
Q

What is Addisons disease

A

Primary hypoadrenalism. Destruction of the entire adrenal cortex leads to mineralocorticoid, glucocorticoid and sex hormone deficiency

1425
Q

What are the causes of addisons

A

AI in Uk

1426
Q

Symptoms of addisons disease

A

Weight loss, anorexia, malaise, weakness, fever, depression, syncope, confusion, myalgia

1427
Q

Signs of addisons disease

A

Pigmentation, postural hypotension, general wasting, dehydration, alopecia

1428
Q

Why do you get hyperpigmentation in addisons

A

Negative feedback means theres increased ACTH which is a melatonin predisposer

1429
Q

Urgent addisons investigation

A

Blood sample cortisol and hydrocortisone

1430
Q

Controlled addisons investigation

A

ACTH stimulation test (impaired response)

1431
Q

What is the ACTH stimulation test

A

Measure plasma cortisol before and after IM Tetracosactide. synACTHen- ACTH analogue. Cortisol remains high 30 mins after

1432
Q

Treatment of acute addisons

A

Saline and hydrocortisone and glucose

1433
Q

Maintenance of addisons

A

Hydrocortisone (gluco-) and fludrocortisone (mineralo-). Wear steroid card

1434
Q

Secondary adrenal insufficiency

A

Iatrogenic, hypothalamic pituitary disease (no pigmentation and mineralocorticoids spared)

1435
Q

Actions of PTH

A

Increased renal uptake of calcium in exchange for phosphate in the PCT

1436
Q

Which hormones affect calcium metabolism

A

Vitamin D, parathyroid hormone and calcitonin

1437
Q

UV-B converts what into vitamin D3 (cholecalciferol)

A

7-dehydrocholesterol

1438
Q

The liver converts vitamin D3 into what

A

25 hydroxyvitamin D. Via Vtiamin D3 25 hydroxylase (using vitamin D3 from diet)

1439
Q

The kidney converse 25 hydroxyvitmain D into what

A

1,25-dihydroxy vitamin D (calcitriol) via 1 alpha hydroxylase

1440
Q

Vitamin D effects

A

Calcium and phosphate release from bone

1441
Q

What is primary hyperparathyroidism and its treatment

A

Raised/normal PTH in the presence of raised calcium. Surgery

1442
Q

What is secondary hyperparathyroidism

A

Physiological PTH increased secretion to compensate for prolonged hypocalcaemia

1443
Q

Causes of secondary hyperparathyroidism

A

Low Vitamin D, malabsorption, CKD, osteomalacia

1444
Q

What is tertiary hyperparathyroidism

A

Development of parathyroid hyperplasia following long standing secondary hyperparathyroidism

1445
Q

Treatment of tertiary hyperparathyroidism

A

Parathyroidectomy

1446
Q

Hypercalcaemia causes

A

Hyperparathyroidism, malignancy

1447
Q

Hypercalcaemia signs and symptoms

A

Bone pain, fractures, osteopenia

1448
Q

If there is high everything but low phosphate what does this suggest

A

Primary

1449
Q

What does just low calcium suggest

A

Secondary

1450
Q

What does everything high suggest

A

Tertiary

1451
Q

What is the investigation of hypercalcaemia

A

Serum calcium level, adjust for albumin

1452
Q

Treatment of hypercalcaemia

A

Calcium, treat underlying cause. Bisphosphonates

1453
Q

Causes of hypocalcaemia

A

Low serum albumin, low magnesium, malabsorption

1454
Q

Symptoms of hypocalcaemia

A

Ventricular arrhythmias

1455
Q

What is chovsteks sign

A

Tap on facial nerve leads to twitching

1456
Q

What is trousseaus sign

A

Inflating Bp above systolic leads to carpal flexion

1457
Q

How do you treat severe hypocalcaemia

A

Calcium gluconate, Cardiac monitoring. MgCl

1458
Q

Definition of hyperkalaemia

A

Serum potassium level above 5mmol/L

1459
Q

Causes of hyperkalaemia DREAD

A

Drugs

1460
Q

Hyperkalaemia ECG

A

Wide flat/absent P

1461
Q

Symptoms of hyperkalaemia

A

Fast irregular pulse, weakness, palpitations, dizziness, cardiac arrest

1462
Q

Treatment of mild hyperkalaemia

A

Dietary potassium restriction and restriction of hyperkalaemia causing drugs

1463
Q

Treatment of severe hyperkalaemia

A

Calcium gluconate

1464
Q

Desribe carcinoid tumours

A

Group of enterochromaffin cell tumours capable of producing serotonin

1465
Q

Where are carcinoid tumours common

A

Appendix, ileum, rectum, bronchioles and testes

1466
Q

What is carcinoid syndrome

A

Symptoms from when the tumour releases serotonin, kinins, histamine and prostaglandins into the circulation

1467
Q

Symptoms of carcinoid tumours

A

Flushing wheezing, watery diarrhoea, abdo pain, cardiac abnormalities

1468
Q

Diagnosis of carcinoid tumours

A

High level of 5-HIAA, liver US confirms

1469
Q

Treatment of carcinoid tumours

A

Ocreotide (somatostatin analogue) and surgery

1470
Q

Layers of the epidermis

A

Stratum corneum

1471
Q

Cells of the epidermis

A

Keratinocytes, melanocytes, Langerhans cells

1472
Q

What is the function of langherhans cells

A

Immunity

1473
Q

Cells of the dermis

A

Fibroplasts, sebaceous and sweat glands, hair follicles, Meissner and Pacinian corpuscles

1474
Q

What sense do meissners corpuscles conduct

A

Light touch

1475
Q

What sense do Pacinian corpuscles conduct

A

Coarse touch and vibration

1476
Q

Hypodermis

A

Subcutaneous fat

1477
Q

Functions of the skin

A

Sensation

1478
Q

Inflammatory skin diseases

A

Acne, psoarisis, eczema

1479
Q

Infections of the skin

A

Cellulitis and necrotizing fasciitis

1480
Q

Neoplasias of the skin

A

BCC, SCC, malignant melanoma

1481
Q

Ulcers of the skin

A

Venous, arterial, neuropathic

1482
Q

Describe acnes vulgaris

A

Inflammatory disease of the pilosebaceous follicles. Affecting face, chest and upper back

1483
Q

Steps in acne pathophysiology

A

Seborrhoea (high sebum production)

1484
Q

What is a papule

A

Small red bump

1485
Q

What is a pustule

A

White/yellow spots

1486
Q

What is a nodule

A

Large red painful bumps

1487
Q

What is a pseudocyst

A

Fluctuant nodules

1488
Q

What is the presentation of acne

A

Papules, pustules, nodules and pseudocysts

1489
Q

What suggest its mild acne

A

Open and close comedones predonminate

1490
Q

What suggests its moderate acne

A

Papules and pustules predominate

1491
Q

What suggests its severe acne

A

Nodules and cysts

1492
Q

What is the treatment of mild acne

A

Topical retinoid or benzoyl peroxide for first line. Azelaic acid if retinoids and Bp poorly tolerated. OCP as contraceptive

1493
Q

Name a topical retinoid

A

Tazarotene gel

1494
Q

What is the treatment for moderate acne

A

Same as above but. Clindamycin too

1495
Q

Severe acne treatment

A

Refer. Isotretinoin and laser treatment

1496
Q

Define eczema

A

Chronic itchy inflammatory condition. Papules and vesicles are present on an erythematous base. Commonly on face and flexure surfaces

1497
Q

Atopic eczema is seen with

A

Hay fever and asthma

1498
Q

What causes eczema

A

Fillagrin abnormalities cause poor barrier function and dry skin. Thinning of the stratum corneum. Allows antigen penetration and hyperreactivity

1499
Q

Triggers of atopic eczema

A

Soaps and detergents, house dust mites, extreme temperatures, pollen, food, stress

1500
Q

Eczema treatment

A

Avoid triggers, cut nails short.

1501
Q

Mild corticosteroid

A

Hydrocortisone

1502
Q

Calcineurin inhibitor

A

Tacrolimus

1503
Q

Moderately potent corticosteroid

A

Clobetasone butyrate

1504
Q

What classes as mild eczema

A

Areas of dry skin and infrequent scratching

1505
Q

What classes as moderate eczema

A

Areas of dry skin, frequent itching and redness

1506
Q

What classes as severe eczema

A

Widespread areas of dry skin, incessant itching and redness

1507
Q

What classes as infected eczema

A

Weeping, crusted or there are pustules

1508
Q

Treatment of severe eczema

A

Potent corticosteroid

1509
Q

Potent corticosteroid

A

Flucionide

1510
Q

Antihistamine

A

Chloramphenamine

1511
Q

Treatment of infected eczema

A

Topical antibiotic, if localised. Generalised then flucloxacillin

1512
Q

Define psoarisis

A

Chronic inflammatory skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration

1513
Q

How would describe the lesions in psoarisis

A

Monomorphic erythematous plaques covered with silvery scales

1514
Q

What are the classic signs of psoarisis lesions

A

-epidermal hyperproliferation

1515
Q

What is the most common form of psoarisis

A

Chronic plaque psoarisis

1516
Q

Psoarisis but no scaling and older

A

Flexural psoarisis

1517
Q

Post streptococcal throat, oval plaques

A

Guttate psoarisis

1518
Q

Psoarisis, thickening of palms and soles

A

Palmoplantar psoarisis

1519
Q

Non skin changes in psoarisis

A

Nail pitting, discolouration and onycholysis

1520
Q

Precipiating factors in psoarisis

A

Trauma, lithium, stress, smoking, alcohol

1521
Q

Proarisis treatment

A

E45, hydrocortisone and Calcipotriol

1522
Q

What if psoarisis resistant

A

UV-B, Methotrexate and infliximab

1523
Q

Where are venous ulcers

A

Medial gaitor region

1524
Q

Where are arterial ulcers

A

Toes, heel and ankle

1525
Q

What are the edges of venous ulcers like

A

Sloping and gradual

1526
Q

What are the edges of arterial ulcers like

A

Punched out and well defined

1527
Q

What is the wound bed of venous ulcers like

A

Covered with slough

1528
Q

What is the wound bed of venous ulcers like

A

Covered with slough and necrotic tissue

1529
Q

What is the size of venous ulcers

A

Large

1530
Q

What is the size of arterial ulcers

A

Small

1531
Q

What is the exudate level of venous ulcers

A

High

1532
Q

What is the exudate level of arterial ulcers

A

Low

1533
Q

What is the pain like in venous ulcers

A

Minimal

1534
Q

What is the pain like in arterial ulcers

A

High

1535
Q

Arterial ulcer risk factors

A

Arterial disease, smoking, cholesterol, dm

1536
Q

What are the symptoms of arterial ulcers

A

Leg pain, worse when elevated

1537
Q

What are the signs of arterial ulcers

A

Cold skin, absent peripheral pulse, shiny pale skin, loss of hair

1538
Q

What are the investigations for arterial ulcers

A

ABPI below 0.8, doppler studies

1539
Q

What is the management of arterial ulcers

A

Vascular reconstruction, ibuprofen, clean and covered, don’t use compression bandages

1540
Q

What are the risk factors for venous ulcers

A

Varicose veins, DVT

1541
Q

What are the symptoms of venous ulcers

A

Pain is minimal, better when elevated

1542
Q

How would you describe a venous ulcer

A

Large, shallow, irregular, exudative

1543
Q

What are the signs of venous ulcer

A

Normal pulses, leg oedema, lipodermatosclerosis

1544
Q

What is the investigation for venous ulcer

A

ABPI normal

1545
Q

What is the management of venous ulcer

A

Compression bandage, antibiotics, ibuprofen

1546
Q

What is the risk factors for neuropathic ulcer

A

DM, Neuropathic disease

1547
Q

How would describe the ulcer in neuropathic ulcers

A

Found at pressure sites, variable size, might have vallus

1548
Q

Signs and symptoms of neuropathic ulcer

A

Warm skin and normal peripheral pulces, associated peripheral neuropathy

1549
Q

Management of neuropathic ulcer

A

Appropriate footwear, diabetic control podiatry

1550
Q

Define cellulitis

A

Bacterial infection of the subcutaneous tissue. Common on the lower leg or arm and may spread proximally

1551
Q

Define erysipelas

A

Bacterial infection of the upper dermis and superficial lymphatics, more common on the face and is sharply demarcated

1552
Q

Causative agents of cellulitis and erysipelas

A

Streptococcus pyogenes and staphylococcus aureus

1553
Q

Presentation of cellutitis and erysipelas

A

Tender confluent areas of inflamed skin, fever and malaise

1554
Q

Risk factors for cellulitis and erysipelas

A

Immunosuppresion, wounds, leg ulcers, trauma, atheltes foot, lymphoedema

1555
Q

Management of cellulitis and erysipelas

A

Flucloxacillin or clarithyromycin

1556
Q

Define necrotising fascitiits

A

Deep seated infection of the subcutaneous tissue that results indestruction of fascia and fat but initially spares skin

1557
Q

Presentation of necrotising fasciitis

A

Severe pain which is out of proportion with the degree of skin inflammation. Systemic upset

1558
Q

Cause of necrotizing fasciitis type 1 and 2

A

1:Mixture of aerobic and anaerobic following abdo surgery or diabetes

1559
Q

Treatment of type 2

A

IV benzylpenicillin and clindamycin

1560
Q

Treatment of type 1

A

Add metronidazole

1561
Q

Which is the most common skin cancer

A

Basal cell carcinoma

1562
Q

Describe basal cell carcinoma

A

Locally invasive, grows slowly, malignant neoplasm of epiderminal keratinocytes. Rarely mets

1563
Q

Risk factors for basal cell carcinoma

A

UV exposure, Skin type 1, ageing

1564
Q

Presentation of BCC (rodent ulcer)

A

Commonly on head and neck, has a pearly appearance with blood vessels

1565
Q

Management of BCC

A

Surgical excision, or radio. Normally completely cured but theres local tissue destruction

1566
Q

Describe squamous cell carcinoma

A

Locally invasive malignant tumour of squamous cells. More aggressive and likely to metastasise but still rare

1567
Q

Risk factors for squamous cell carcinoma

A

UV exposure

1568
Q

Describe the appearance of SCC

A

Scaly and crusty, Ill defined nodules, keratotic and may ulcerate

1569
Q

Management of SCC

A

Surgical excision and radiotherapy if unresectable

1570
Q

Define malignant melanoma

A

Invasive tumour of melanocytes

1571
Q

Risk factors for malignant melanoma

A

UV exposure

1572
Q

Signs of MM abcde

A

Assymetrical shape

1573
Q

Symptoms of MM

A

Bleeding. Itching

1574
Q

Presentation of MM

A

Scaly, cursty, ill defined, may ulcerate

1575
Q

Management of MM

A

Surgical excision, radio if cant. Chemo if metastatic

1576
Q

Name a non conventional therapy for psoarisis

A

Phototherapy

1577
Q

Onycholysis, pitting, thickening, subungal hyperkeratinosis

A

Psoarisis

1578
Q

Deep ulcerated base of skin cancer

A

SCC

1579
Q

Moderate acne 1st line if on back

A

Oral erythromycin

1580
Q

What type of hypersensitivity is contact dermatitis

A

Type IV