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fourth year > medicine 2 > Flashcards

medicine 2 Flashcards

1
Q

commonest type of non-small cell lung cancer is

A

squamous

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2
Q

what type of cancer is small cell lung cancer

A

neurosecretory

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3
Q

signs and symptoms of lung cancer

A 
Shortness of breath
Cough
Haemoptysis (coughing up blood)
Finger clubbing
Recurrent pneumonia
Weight loss
Lymphadenopathy – often supraclavicular nodes are the first to be found on examination
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4
Q

CXR findings of lung cancer include

A

Hilar enlargement
“Peripheral opacity” – a visible lesion in the lung field
Pleural effusion – usually unilateral in cancer
Collapse

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5
Q

Ix for lung cancer

A

CXR, CT contract enhanced, PET-CT, bronchoscopy with US and histological diagnosis

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6
Q

first line option for non-small cell lung cancer

A

surgery: lobectomy, segmentectomy and wedge resection

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7
Q

other options for lung cancer treatment

A

RT +Chemo

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8
Q

small cell lung cancer Tx

A

RT + chemo

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9
Q

palliative options for lung cancer

A

endobronchial debulking or stents

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10
Q

extra pulmonary manifestations of lung cancer

A

recurrent laryngeal palsy (hoarse voice), phrenic nerve palsy (SOB), SVC obstruction, horner’s syndrome

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11
Q

SVC obstruction presentation

A

facial swelling, difficulty breathing and distended veins in the neck and upper chest.

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12
Q

“Pemberton’s sign” is

A

SVC obstruction: raising the hands over the head causes facial congestion and cyanosis.

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13
Q

horner’s syndrome presentation

A

riad of partial ptosis, anhidrosis and miosis.

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14
Q

horner’s syndrome arises from obstruction too

A

sympathetic ganglion.

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15
Q

paraneoplastic presentations in small cell lung cancer

A

Syndrome of inappropriate ADH (SIADH)
Cushing’s syndrome
Limbic encephalitis.
Lambert-Eaton myasthenic syndrome.

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16
Q

Syndrome of inappropriate ADH (SIADH) presents with what biochemical abnormality

A

hyponatraemia

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17
Q

squamous cell carcinoma paraneoplastic syndrome

A

Hypercalcaemia

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18
Q

limbic encephalitis presentation

A

memory impairment, hallucinations, confusion and seizures.

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19
Q

limbic encephalitis is associated with

A

anti-Hu antibodies.

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20
Q

Lambert-Eaton Myasthenic Syndrome presents with

A

leads to weakness, particularly in the proximal muscles but can also affect intraocular muscles causing diplopia (double vision), levator muscles in the eyelid causing ptosis and pharyngeal muscles causing slurred speech and dysphagia

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21
Q

Lambert-Eaton Myasthenic Syndrome is the result of

A

antibodies produced by the immune system against small cell lung cancer cells. These antibodies also target and damage voltage-gated calcium channels sited on the presynaptic terminals in motor neurones

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22
Q

presentation of pneumonia

A

Shortness of breath
Cough productive of sputum
Fever
Haemoptysis (coughing up blood)
Pleuritic chest pain (sharp chest pain worse on inspiration)
Delirium (acute confusion associated with infection)
Sepsis

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23
Q

signs of pneumonia

A 
Tachypnoea (raised respiratory rate)
Tachycardia (raised heart rate)
Hypoxia (low oxygen)
Hypotension (shock)
Fever
Confusion
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24
Q

characteristic chest signs of pneumonia

A

bronchial breathing, focal course crackles and dullness to percussion

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25
Q

CURB 65 stands for

A

C – Confusion (new disorientation in person, place or time)
U – Urea > 7
R – Respiratory rate ≥ 30
B – Blood pressure < 90 systolic or ≤ 60 diastolic.
65 – Age ≥ 65

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26
Q

CURB score of what would indicate hospital admission

A

> 2

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27
Q

common causes of pneumonia include

A 
Streptococcus pneumoniae (50%)
Haemophilus influenzae (20%)
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28
Q

CF is associated with what other pneumonia bugs?

A

Pseudomonas aeruginosa
Staphylococcus aureus
Moraxella catarrhalis

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29
Q

atypical pneumonias are usually treated with

A

macrolides (e.g. clarithomycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline).

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30
Q

legionella pneumophilia usually presents with what biochemical abnormality

A

hyponatraemia (low sodium)

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31
Q

mycoplasma pneumoniae presentation is with

A

erythema multiforme characterised by varying sized “target lesions” formed by pink rings with pale centres. It can also cause neurological symptoms

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32
Q

Chlamydophila pneumoniae. presentation

A

a school aged child with a mild to moderate chronic pneumonia and wheeze.

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33
Q

Coxiella burnetii AKA “Q fever”. presentation

A

exposure to animals and their bodily fluids. The MCQ patient is a farmer with a flu like illness.

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34
Q

Chlamydia psittaci. presentation

A

This is typically contracted from contact with infected birds.

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35
Q

Atypical pneumonias are

A

“Legions of psittaci MCQs”

M – mycoplasma pneumoniae
C – chlamydydophila pneumoniae
Qs – Q fever (coxiella burnetii)

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36
Q

what pneumonia commonly occurs in the immunocompromised

A

Pneumocystis jiroveci (PCP) pneumonia

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37
Q

presentation of pneumocystis jiroveci pneumonia is with

A

subtly with a dry cough without sputum, shortness of breath on exertion and night sweats.

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38
Q

Tx of pneumocystis jiroveci is

A

co-trimoxazole (trimethoprim/sulfamethoxazole)

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39
Q

patients with a low CD4 count receive what prophylaxis against PCP?

A

co-trimoxazole

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40
Q

in hospital the minimum Ix for pneumonia are

A

Chest xray
FBC (raised white cells)
U&Es (for urea)
CRP (raised in inflammation and infection)

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41
Q

in severe cases of pneumonia Ix

A

Sputum cultures
Blood cultures
Legionella and pneumococcal urinary antigens (send a urine sample for antigen testing)

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42
Q

mild pneumonia Tx

A

5 day course of oral antibiotics (amoxicillin or macrolide)

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43
Q

mod-severe pneumonia Tx

A

7-10 day course of dual antibiotics (amoxicillin and macrolide)

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44
Q

FEV1 refers too and reflects

A

forced expiratory volume in 1 second. if reduced then obstruction likely.

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45
Q

FVC refers too and reflects

A

forced vital capacity. if reduced then restriction likely.

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46
Q

obstructive lung disease diagnosis requires

A

FEV1 is less than 75% of FVC (FEV1:FVC ratio < 75%)

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47
Q

restrictive lung disease diagnosis requires

A

FEV1 and FVC are equally reduced and FEV1:FVC ratio > 75%

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48
Q

presentation of asthma

A

Episodic symptoms
Diurnal variability. Typically worse at night.
Dry cough with wheeze and shortness of breath
A history of other atopic conditions such as eczema, hayfever and food allergies
Family history
Bilateral widespread “polyphonic” wheeze

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49
Q

1st line Ix in asthma

A

Fractional exhaled nitric oxide

Spirometry with bronchodilator reversibility

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50
Q

further Ix in asthma includes

A

Peak flow variability measured by keeping a diary of peak flow measurements several times per day for 2 to 4 weeks
Direct bronchial challenge test with histamine or methacholine

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51
Q

ICS example

A

beclometasone

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52
Q

LABA example

A

salmeterol

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53
Q

LAMA example

A

tiotropium

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54
Q

LAMA mechanism

A

these block the acetylcholine receptors. Acetylecholine receptors are stimulated by the parasympathetic nervous system and cause contraction of the bronchial smooth muscles. Blocking these receptors leads to bronchodilation.

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55
Q

NICE guidelines for asthma Tx

A
  1. Add short-acting beta 2 agonist inhaler (e.g. salbutamol) as required for infrequent wheezy episodes.
  2. Add a regular low dose inhaled corticosteroid.
  3. Add an oral leukotriene receptor antagonist (i.e. montelukast).
  4. Add LABA inhaler (e.g. salmeterol). Continue the LABA only if the patient has a good response.
  5. Consider changing to a maintenance and reliever therapy (MART) regime.
  6. Increase the inhaled corticosteroid to a “moderate dose”.
  7. Consider increasing the inhaled corticosteroid dose to “high dose” or oral theophylline or an inhaled LAMA (e.g. tiotropium).
  8. Refer to a specialist.
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56
Q

additional managment for asthma includes

A

Each patient should have an individual asthma self-management programme
Yearly flu jab
Yearly asthma review
Advise exercise and avoid smoking

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57
Q

acute asthma presentation

A

Progressively worsening shortness of breath
Use of accessory muscles
Fast respiratory rate (tachypnoea)
Symmetrical expiratory wheeze on auscultation
The chest can sound “tight” on auscultation with reduced air entry

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58
Q

moderate acute asthma

A

PEFR 50 – 75% predicted

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59
Q

severe acute asthma

A

PEFR 33-50% predicted
Resp rate >25
Heart rate >110
Unable to complete sentences

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60
Q

life threatening asthma

A 
PEFR <33%
Sats <92%
Becoming tired
No wheeze. This occurs when the airways are so tight that there is no air entry at all. This is ominously described as a “silent chest”.
Haemodynamic instability (i.e. shock)
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61
Q

moderate acute asthma Tx

A

Nebulised beta-2 agonists (i.e. salbutamol 5mg repeated as often as required)
Nebulised ipratropium bromide
Steroids. Oral prednisolone or IV hydrocortisone. These are continued for 5 days
Antibiotics if there is convincing evidence of bacterial infection

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62
Q

severe acute asthma Tx

A

Oxygen if required to maintain sats 94-98%
Aminophylline infusion
Consider IV salbutamol

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63
Q

life threatening asthma Tx

A

IV magnesium sulphate infusion
Admission to HDU / ICU
Intubation in worst cases – however this decision should be made early because it is very difficult to intubate with severe bronchoconstriction

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64
Q

ABG pattern in acute asthma

A

Initially patients will have a respiratory alkalosis as tachypnoea causes a drop in CO2. A normal pCO2 or hypoxia is a concerning sign as it means they are tiring and indicates life threatening asthma. A respiratory acidosis due to high CO2 is a very bad sign in asthma.

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65
Q

salbutamol has an effect on what ion?

A

serum potassium causing tachycardia

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66
Q

presentation of COPD

A

long term smoker presenting with chronic shortness of breath, cough, sputum production, wheeze and recurrent respiratory infections,

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67
Q

Dx of COPD

A

clinical presentation and spirometry (FEV1/FVC ratio <0.7)

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68
Q

Ix for COPD

A

CXR, BMI, sputum culture, ECG, ECHO, CT thorax, serum alpha 1-antitrypsin, transfer factor for carbon monoxide.

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69
Q

step 1 for long term managment

A

pneumococcal and annual flu vaccine, SABA or short acting anti muscarinic

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70
Q

Step 2 for long term management

A

LABA or LAMA, long term oxygen therapy

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71
Q

indications for LTOT in COPD

A

chronic hypoxia, polycythaemia, cyanosis or heart failure

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72
Q

ABG signs of acute exacerbation of COPD

A

Low pO2 indicates hypoxia and respiratory failure
Normal pCO2 with low pO2 indicates type 1 respiratory failure (only one is affected)
Raised pCO2 with low pO2 indicates type 2 respiratory failure (two are affected)

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73
Q

Ix in acute exacerbation of COPD

A

CXR, ECG, FBC, U+E’s, sputum culture and blood culture

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74
Q

what mask do you use to deliver specific percentages of oxygen

A

venturi masks

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75
Q

if retaining CO2 in COPD aims for sats of

A

88-92%

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76
Q

medical treatment of acute exacerbation of COPD in community

A

Prednisolone 30mg once daily for 7-14 days
Regular inhalers or home nebulisers
Antibiotics if there is evidence of infection

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77
Q

hospital Tx of acute exacerbation of COPD

A

Nebulised bronchodilators (e.g. salbutamol 5mg/4h and ipratropium 500mcg/6h)
Steroids (e.g. 200mg hydrocortisone or 30-40mg oral prednisolone)
Antibiotics if evidence of infection
Physiotherapy can help clear sputum

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78
Q

non invasive ventilation can be

A

BIPAP (bilevel positive airway pressure) or CPAP (continuous positive airway pressure)

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79
Q

BIPAP is typically used for

A

type 2 respiratory failure

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80
Q

CI to BIPAP is

A

untreated pneumothorax.

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81
Q

high resolution CT of interstitial lung disease will show what appearance

A

ground glass

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82
Q

idiopathic pulmonary fibrosis presentation

A

insidious onset of shortness of breath and dry cough over more than 3 months. It usually affects adults over 50 years old.

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83
Q

signs of idiopathic pulmonary fibrosis

A

bibasal fine inspiratory crackles and finger clubbing

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84
Q

Tx for idiopathic pulmonary fibrosis

A

Pirfenidone is an antifibrotic and anti-inflammatory

Nintedanib is a monoclonal antibody targeting tyrosine kinase

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85
Q

drug induced pulmonary fibrosis may be caused by

A

Amiodarone
Cyclophosphamide
Methotrexate
Nitrofurantoin

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86
Q

Hypersensitivity Pneumonitis is what type of hypersensitivity reaction

A

type III hypersensitivity reaction

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87
Q

hypersensitivity pneumonitis. bronchial lavage will reveal

A

raised lymphocytes and mast cells

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88
Q

Cryptogenic organising pneumonia aetiology

A

this can be idiopathic or triggered by infection, inflammatory disorders, medications, radiation or environmental toxins or allergens.

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89
Q

Cryptogenic organising pneumonia presentation

A

similar to infectious pneumonia with shortness of breath, cough, fever and lethargy. It also presents on similarly to pneumonia on a chest xray with a focal consolidation.

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90
Q

Cryptogenic organising pneumonia Tx

A

systemic steroids

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91
Q

exudative effusion is

A

a high protein count (>3g/dL)

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92
Q

transudative effusion is

A

protein count (<3g/dL).

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93
Q

exudative causes are related too

A

inflammation

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94
Q

exudative causes:

A

Lung cancer
Pneumonia
Rheumatoid arthritis
Tuberculosis

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95
Q

transudative causes are related too

A

fluid shifts

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96
Q

transudative causes:

A

Congestive cardiac failure
Hypoalbuminaemia
Hypothroidism
Meig’s syndrome

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97
Q

CXR signs of pleural effusion

A

Blunting of the costophrenic angle
Fluid in the lung fissures
Larger effusions will have a meniscus. This is a curving upwards where it meets the chest wall and mediastinum.
Tracheal and mediastinal deviation if it is a massive effusion

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98
Q

presentation of pleural effusion

A

Shortness of breath
Dullness to percussion over the effusion
Reduced breath sounds
Tracheal deviation away from the effusion if it is massive

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99
Q

Tx of pleural effusion

A

conservative, pleural aspiration or chest drain

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100
Q

pleural aspiration of empyema reveals

A

pus, acidic pH (pH < 7.2), low glucose and high LDH.

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101
Q

suspect empyema when

A

Suspect an empyema in a patient who has an improving pneumonia but new or ongoing fever.

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102
Q

pneumothorax If no SOB and there is a < 2cm rim of air on the chest xray then

A

no treatment required

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103
Q

pneumothorax If SOB and/or there is a > 2cm rim of air on the chest xray then

A

it will require aspiration and reassessment.

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104
Q

if aspiration of a pneumothorax fails twice, unstable patient or bilateral then

A

chest drain.

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105
Q

signs of a tension pneumothorax

A

Tracheal deviation away from side of pneumothorax
Reduced air entry to affected side.
Increased resonant to percussion on affected side.
Tachycardia.
Hypotension.

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106
Q

Mx of a tension pneumothorax

A

“Insert a large bore cannula into the second intercostal space in the midclavicular line.”

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107
Q

triangle of safety for a chest drain is

A

The 5th intercostal space (or the inferior nipple line)
The mid axillary line (or the lateral edge of the latissimus dorsi)
The anterior axillary line (or the lateral edge of the pectoris major)

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108
Q

the neurovascular bundle runs where in relation to the rib

A

just below

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109
Q

Risk factors for pulmonary embolism

A 
Immobility
Recent surgery
Long haul flights
Pregnancy
Hormone therapy with oestrogen
Malignancy
Polycythaemia
Systemic lupus erythematosus
Thrombophilia
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110
Q

presentation of a pulmonary embolism is

A 
Shortness of breath
Cough with or without blood (haemoptysis)
Pleuritic chest pain
Hypoxia
Tachycardia
Raised respiratory rate
Low grade fever
Haemodynamic instability causing hypotension
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111
Q

high Wells score requires

A

a CT pulmonary angiogram

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112
Q

low wells score requires

A

perform a d-dimer and if positive perform a CTPA

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113
Q

alternative to a CTPA for PE Dx is

A

V/Q scan

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114
Q

PE ABG sign

A

respiratory alkalosis due to high RR

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115
Q

initial managment of PE is with

A

enoxaparin and dalteparin. -> LMWH

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116
Q

long term options for VTE are

A

warfarin, a NOAC or LMWH.

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117
Q

massive PE may require

A

thrombolysis

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118
Q

thrombolytic agents include

A

streptokinase, alteplase and tenecteplase.

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119
Q

pulmonary hypertension signs

A 
SOB and 
Syncope
Tachycardia
Raised JVP
Hepatomegaly
Peripheral oedema.
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120
Q

ECG signs of pulmonary hypertension

A

Right ventricular hypertrophy seen as larger R waves on the right sided chest leads (V1-3) and S waves on the left sided chest leads (V4-6)
Right axis deviation
Right bundle branch block

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121
Q

CXR signs of pulmonary hypertension

A

Dilated pulmonary arteries

Right ventricular hypertrophy

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122
Q

other Ix for pulmonary hypertension

A

A raised NT-proBNF blood test result indicates right ventricular failure
Echo can be used to estimate pulmonary artery pressure

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123
Q

Tx for primary pulmonary hypertension is

A 
IV prostanoids (e.g. epoprostenol)
Endothelin receptor antagonists (e.g. macitentan)
Phosphodiesterase-5 inhibitors (e.g. sildenafil)
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124
Q

20-40 year old black female presenting with a dry cough and shortness of breath. They may have nodules on their shins suggesting erythema nodosum. - what is the diagnosis?

A

sarcoidosis

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125
Q

sarcoidosis is an example of

A

granulomatous inflammatory condition

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126
Q

granulomas are

A

nodules of inflammation full of macrophages

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127
Q

lung symptoms of sarcoidosis

A

Mediastinal lymphadenopathy
Pulmonary fibrosis
Pulmonary nodules

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128
Q

systemic symptoms of sarcoidosis

A

Fever
Fatigue
Weight loss

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129
Q

liver symptoms of sarcoidosis

A

Liver nodules
Cirrhosis
Cholestasis

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130
Q

eye symptoms of sarcoidosis

A

Uveitis
Conjunctivitis
Optic neuritis

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131
Q

skin symptoms of sarcoidosis

A 
Erythema nodosum (tender, red nodules on the shins caused by inflammation of the subcutaneous fat)
Lupus pernio (raised, purple skin lesions commonly on cheeks and nose)
Granulomas develop in scar tissue
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132
Q

Lofgren’s Syndrome, a special presentation of sarcoidosis is a triad of

A

Erythema nodosum
Bilateral hilar lymphadenopathy
Polyarthralgia (joint pain in multiple joints)

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133
Q

differentials for sarcoidosis are

A 
Tuberculosis
Lymphoma
Hypersensitivity pneumonitis
HIV
Toxoplasmosis
Histoplasmosis
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134
Q

blood tests for sarcoidosis will reveal

A

Raised serum ACE. This is often used as a screening test.
Hypercalcaemia (rasied calcium) is a key finding.
Raised serum soluble interleukin-2 receptor
Raised CRP
Raised immunoglobulins

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135
Q

CXR of sarcoidosis will reveal

A

hilar lymphadenopathy

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136
Q

CT of sarcoidosis will reveal

A

hilar lymphadenopathy and pulmonary nodules

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137
Q

MRI of sarcoidosis will reveal

A

CNS involvement

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138
Q

gold standard diagnosis for sarcoidosis is

A

histology of mediastinal lymph nodes

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139
Q

sarcoidosis histology will reveal

A

non-caseating granulomas with epithelioid cells.

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140
Q

tests for other organs in sarcoidosis include

A

U+E’s, urine dipstick, LFT, ophthalmology, ECG, ECHO, US

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141
Q

Tx for sarcoidosis is

A

no treatment, oral steroids , bisphosphonates

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142
Q

severe sarcoidosis may require

A

lung transplant from fibrosis or methotrexate and azathioprine.

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143
Q

features of obstructive sleep apnoea

A 
Apnoea episodes during sleep (reported by partner)
Snoring
Morning headache
Waking up unrefreshed from sleep
Daytime sleepiness
Concentration problems
Reduced oxygen saturation during sleep
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144
Q

Tx for sleep apnoea

A

correct reversible factors, CPAP, and surgery

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145
Q

what is the stepwise progression of alcoholic liver disease?

A

alcohol related fatty liver->alcoholic hepatitis->cirrhosis

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146
Q

recommended daily alcohol intake

A

14 units per week

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147
Q

CAGE Q’s

A

C – CUT DOWN? Ever thought you should?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Ever feel guilty about drinking?
E – EYE OPENER? Ever drink in the morning to help your hangover/nerves?

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148
Q

complications of alcohol

A 
Alcoholic Liver Disease
Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
Alcohol Dependence and Withdrawal
Wernicke-Korsakoff Syndrome (WKS)
Pancreatitis
Alcoholic Cardiomyopathy
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149
Q

signs of liver disease

A 
Jaundice
Hepatomegaly
Spider Naevi
Palmar Erythema
Gynaecomastia
Bruising – due to abnormal clotting
Ascites
Caput Medusae – engorged superficial epigastric veins
Asterixis – “flapping tremor” in decompensated liver disease
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150
Q

bloods for liver disease

A 
FBC raised MCV
LFT - raised ALT and AST
Raised GGT
elevated bilirubin in cirrhosis
clotting raised PT
U+E's may be deranged in hepatorenal syndrome
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151
Q

Ix for liver disease

A

CT, MRI, US/fibroscan, endoscopy for varices, liver biopsy if considering steroid treatment

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152
Q

alcohol withdrawal natural history

A

6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delirium tremens”

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153
Q

alcohol stimulated what receptors and inhibits

A

stimulates GABA - relaxing

inhibits glutamate

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154
Q

alcohol withdrawal on the brain causes

A

under functioning GABA and over functioning glutamate = extremely excitable brain with access adrenergic function

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155
Q

presentation of delirium tremens

A 
Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
Hypertension
Hyperthermia
Ataxia (difficulties with coordinated movements)
Arrhythmias
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156
Q

Tx for alcohol withdrawal

A

Chlordiazepoxide (“Librium”) is a benzodiazepine
and
IV high dose B vitamins (pabrinex)

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157
Q

Wernicke-Korsakoff Syndrome (WKS)Wernicke-Korsakoff Syndrome (WKS) is caused by

A

thiamine B1 deficiency

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158
Q

features of Wernicke’s encephalopathy

A

Confusion
Oculomotor disturbances (disturbances of eye movements)
Ataxia (difficulties with coordinated movements)

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159
Q

features of korsakoff’s syndrome

A 
Memory impairment (retrograde and anterograde)
Behavioural changes
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160
Q

four commonest causes of liver cirrhosis

A

Alcoholic liver disease
Non Alcoholic Fatty Liver Disease
Hepatitis B
Hepatitis C

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161
Q

signs of cirrhosis are

A

Jaundice – caused by raised bilirubin
Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
Splenomegaly – due to portal hypertension
Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
Palmar Erythema – caused by hyperdynamic cirulation
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising – due to abnormal clotting
Ascites
Caput Medusae – distended paraumbilical veins due to portal hypertension
Asterixis – “flapping tremor” in decompensated liver disease

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162
Q

bloods for cirrhosis are

A 
LFT
albumin and PT
hyponatraemia 
Urea and creatinine
viral markers or autoantibodies
alpha fetoprotein
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163
Q

first line ix for assessing fibrosis is

A

enhanced liver fibrosis blood test

164
Q

US of a cirrhotic liver may show

A 
Nodularity of the surface of the liver
A “corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow
Enlarged portal vein with reduced flow
Ascites
Splenomegaly
165
Q

severity of cirrhosis scoring is called

A

child-pugh

166
Q

child pugh features that score one

A

bilirubin <34
albumin >35
INR <1.7

167
Q

child pugh features that score two are

A 
bilirubin 34-50
albumin 28-35
INR 17-23
Ascites mild
encephalopathy mild
168
Q

child pugh features that score three are

A 
bilirubin >50
albumin <28
INR >2.3
ascites severe
encephalopathy severe
169
Q

what score system is used for compensated cirrhosis

A

MELD every 6 months

170
Q

complications of cirrhosis include

A

Malnutrition
Portal Hypertension, Varices and Variceal Bleeding
Ascites and Spontaneous Bacterial Peritonitis (SBP)
Hepato-renal Syndrome
Hepatic Encephalopathy
Hepatocellular Carcinoma

171
Q

Mx of cirrhosis is

A 
Regular meals (every 2-3 hours)
Low sodium (to minimise fluid retention)
High protein and high calorie (particularly if underweight)
Avoid alcohol
172
Q

varices occur at

A

Gastro oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall via the umbilical vein (caput medusae)

173
Q

Tx of stable varices include

A

Gastro oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall via the umbilical vein (caput medusae)

174
Q

Resus for a bleeding oesophageal varices includes

A

Vasopressin analogues (i.e. terlipressin)
vit K + FFP
prophylactic broad spectrum antibiotics
ITU
urgent endoscopy with sclerosant injection or band ligation
Sengstaken-blakemore tube

175
Q

Ascites effect on the RAAS system

A

The kidneys sense this lower pressure and release renin, which leads to increased aldosterone secretion (via the renin-angiotensin-aldosterone system) and reabsorption of fluid and sodium in the kidneys. Cirrhosis causes a transudative, meaning low protein content, ascites.

176
Q

Mx of ascites includes

A

Low sodium diet
Anti-aldosterone diuretics (spironolactone)
Paracentesis (ascitic tap or ascitic drain)
Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients with less than 15g/litre of protein in the ascitic fluid
Consider TIPS procedure in refractory ascites
Consider transplantation in refractory ascites

177
Q

presentation of spontaneous bacterial peritonitis

A

Can be asymptomatic so have a low threshold for ascitic fluid culture
Fever
Abdominal pain
Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
Ileus
Hypotension

178
Q

common causes of spontaneous bacterial peritonitis

A

Escherichia coli
Klebsiella pnuemoniae
Gram positive cocci (such as staphylococcus and enterococcus)

179
Q

management of spontaneous bacterial peritonitis includes

A

Take an ascitic culture prior to giving antibiotics

Usually treated with an IV cephalosporin such as cefotaxime

180
Q

Hepatorenal Syndrome refers too

A

hypotension in the kidney and activation of the renin-angiotensin system. This causes renal vasoconstriction, which combined with low circulation volume leads to starvation of blood to the kidney. fatal within a week.

181
Q

Tx for hepatorenal syndrome

A

liver transplant

182
Q

Hepatic Encephalopathy is caused by what toxin

A

ammonia

183
Q

why does ammonia increase in cirrhosis

A

Firstly, the functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products. Secondly, collateral vessels between the portal and systemic circulation mean that the ammonia bypasses liver altogether and enters the systemic system directly.

184
Q

Tx for hepatic encephalopathy

A

laxatives (lactulose) and antibiotics rifaximin, nutritional support

185
Q

precipitating factors for hepatic encephalopathy

A 
Constipation
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications (particularly sedative medications)
186
Q

RF for NAFLD

A 
Obesity
Poor diet and low activity levels
Type 2 diabetes
High cholesterol
Middle age onwards
Smoking
High blood pressure
187
Q

non-invasive liver screen includes

A

Ultrasound Liver
Hepatitis B and C serology
Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis)
Immunoglobulins (autoimmune hepatitis and primary biliary cirrhosis)
Caeruloplasmin (Wilsons disease)
Alpha 1 Anti-trypsin levels (alpha 1 anti-trypsin deficiency)
Ferritin and Transferrin Saturation (hereditary haemochromatosis)

188
Q

Tx for liver fibrosis may include

A

vitamin E or pioglitazone.

189
Q

hepatitis symptoms

A 
Abdominal pain
Fatigue
Pruritis (itching)
Muscle and joint aches
Nausea and vomiting
Jaundice
Fever (viral hepatitis)
190
Q

biochemical findings of hepatitis is

A

massively raised transaminases (ASt/ALT) proportionally less in ALP

191
Q

hepatitis A type of virus and route

A

RNA: faecal-oral route

192
Q

hepatitis B type of virus and route

A

DNA - blood.

193
Q

natural history of hepatitis A

A

t presents with nausea, vomiting, anorexia and jaundice. It can cause cholestasis (slowing of bile flow through the biliary system) with dark urine and pale stools and moderate hepatomegaly. It resolves without treatment in around 1-3 months.

194
Q

Mx of hepatitis A is

A

notify public health, analgesia and a vaccine is available

195
Q

hepatitis B natural history

A

Most people fully recover from the infection within 2 months, however 10% go on to become chronic hepatitis B carriers. Due to DNA intergration

196
Q

active infection marker for hep B

A

Surface antigen (HBsAg)

197
Q

marker of viral replication and implies high infectivity for hepatitis B

A

E antigen (HBeAg)

198
Q

implies past or current infection for hepatitis B

A

Core antibodies (HBcAb)

199
Q

implies vaccination or past or current infection for hepatitis B

A

Surface antibody (HBsAb)

200
Q

this is a direct count of the viral load for hepatitis B

A

Hepatitis B virus DNA (HBV DNA

201
Q

hepatitis B screen consists of

A

HBcAb (for previous infection) and HBsAg (for active infection).

202
Q

hepatitis C is what type of virus and route

A

RNA and blood

203
Q

disease course in hepatitis C

A

1 in 4 fights off the virus and makes a full recovery
3 in 4 it becomes chronic
Complications: liver cirrhosis and associated complications and hepatocellular carcinoma

204
Q

hepatitis D is what sort of virus

A

RNA but requires infection with hepatitis B

205
Q

hepatitis E is what sort of virus and route?

A

RNA faecal oral route.

206
Q

type 1 autoimmune hepatitis presents in

A

adults

207
Q

type 1 autoimmune hepatitis antibodies

A

Anti-nuclear antibodies (ANA)
Anti-smooth muscle antibodies (anti-actin)
Anti-soluble liver antigen (anti-SLA/LP)

208
Q

type 2 autoimmune hepatitis presents in

A

kids

209
Q

Tx for autoimmune hepatitis is with

A

high dose steroids and immunosuppressants such as azathioprine.

210
Q

Haemochromatosis pathology

A

iron storage disorder that results in excessive total body iron and deposition of iron in tissues.

211
Q

gene responsible for haemochromatosis

A

human haemochromatosis protein (HFE) gene is located on chromosome 6

212
Q

haemochromatosis genetic transmission is

A

autosomal recessive

213
Q

symptoms of haemochromatosis

A

Chronic tiredness
Joint pain
Pigmentation (bronze / slate-grey discolouration)
Hair loss
Erectile dysfunction
Amenorrhoea
Cognitive symptoms (memory and mood disturbance)

214
Q

main diagnostic method for haemochromatosis is

A

serum ferritin level

215
Q

how to differentiate a high serum ferritin from iron overload and inflammation

A

transferrin saturation

216
Q

liver biopsy with what stain for haemochromatosis

A

Perl’s stain

217
Q

liver biopsy with Perl’s stain reveals

A

iron concentration in the parenchymal cells

218
Q

Ix for hemochromatosis

A

CT or MRI

219
Q

complications of haemochromatosis

A

cardiomyopathy, hepatocellular carcinoma, hypothyroidism, chrondocalcinosis/pseudogout

220
Q

Mx of haemochromatosis is with

A

venesection, avoid alcohol and genetic counselling

221
Q

Wilson’s disease is caused by excessive

A

copper

222
Q

wilson’s disease is caused by a mutation in chromosome

A

13

223
Q

the wilson’s disease protein is called

A

“ATP7B copper-binding protein”

224
Q

Wilson’s disease inheritance is

A

autosomal recessive

225
Q

features of wilson’s disease are

A 
Hepatic problems (40%)
Neurological problems (50%)
Psychiatric problems (10%)
226
Q

neuro symptoms of wilson’s disease include

A

dysarthria (speech difficulties) and dystonia (abnormal muscle tone). Copper deposition in the basal ganglia leads to Parkinsonism (tremor, bradykinesia and rigidity). Motor symptoms are often asymmetrical in Wilson disease.

227
Q

slit lamp examination of wilson’s disease will reveal

A

Kayser-Fleischer rings in cornea

228
Q

other possible features of wilson’s disease are

A

Haemolytic anaemia
Renal tubular damage leading to renal tubular acidosis
Osteopenia (loss of bone mineral density)

229
Q

first line Ix wilson’s disease is through

A

serum caeruloplasmin. A low serum caeruloplasmin is suggestive of Wilson disease

230
Q

gold standard diagnosis for wilsons disease is

A

liver biopsy

231
Q

other diagnosis for wilson’s disease includes

A

24-hour urine copper assay

232
Q

Wilson’s disease Mx is with

A

Penicillamine

Trientene

233
Q

elastase is secreted by what cell?

A

neutrophils

234
Q

Alpha-1-antitrypsin (A1AT) role is to

A

inhibit the neutrophil elastase

235
Q

Alpha-1-antitrypsin (A1AT) exists on chromosome

A

14

236
Q

inheritance of Alpha-1-antitrypsin (A1AT) deficiency is by

A

autosomal recessive

237
Q

organs effected byAlpha-1-antitrypsin (A1AT) deficiency

A

Liver and lungs

238
Q

Dx of Alpha-1-antitrypsin (A1AT) deficiency

A

serum alpha 1 antitrypsin, liver biopsy and acid-Schiff-positive staining globules, genetic testing, high resolution CT

239
Q

Alpha-1-antitrypsin (A1AT) deficiency liver Mx

A

stop smoking, organ transplant

240
Q

Primary biliary cirrhosis is a condition where the immune system attacks

A

small bile ducts within the liver. The first parts to be affected are the intralobar ducts, also known as the Canals of Hering. This causes obstruction.

241
Q

what is usually excreted via the bile ducts

A

Bile acids, bilirubin and cholesterol

242
Q

presentation of PBC

A 
Fatigue
Pruritus
GI disturbance and abdominal pain
Jaundice
Pale stools
Xanthoma and xanthelasma
Signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi)
243
Q

associations with PBC are

A 
Middle aged women
Other autoimmune diseases (e.g. thyroid, coeliac)
Rheumatoid conditions (e.g. systemic sclerosis, Sjogrens and rheumatoid arthritis)
244
Q

diagnosis of PBC is with

A

raised alk P, raised IGM and ESR and Anti-mitochondrial antibodies is the most specific to PBC and forms part of the diagnostic criteria
Anti-nuclear antibodies are present in about 35% of patients and liver biopsy

245
Q

Tx of PBC is with

A

ursodeoxycholic acid and colestyramine, liver transplant

246
Q

Primary sclerosing cholangitis is a condition where the

A

ntrahepatic or extrahepatic ducts become strictured and fibrotic. This causes an obstruction to the flow of bile out of the liver and into the intestines.

247
Q

risk factors or PSC

A

Male
Aged 30-40
Ulcerative Colitis
Family History

248
Q

presentation of PSC is

A 
Jaundice
Chronic right upper quadrant pain
Pruritus
Fatigue
Hepatomegaly
249
Q

LFT cholestatic picture is

A

deranged ALK P, potentially a rise in bilirubin. later deranged transaminases

250
Q

gold standard for PSC is

A

magnetic resonance cholangiopancreatography.

251
Q

Tx for PSC is

A

ERCP, ursodeoxycholic acid, and cholestyramine

252
Q

commonest primary liver cancer is

A

hepatocellular carcinoma

253
Q

other type of liver cancer is

A

cholangiocarcinoma

254
Q

Risk factors for hepatocellular carcinoma is

A

Viral hepatitis (B and C)
Alcohol
Non alcoholic fatty liver disease
Other chronic liver disease

255
Q

cholangiocarcinoma is associated with

A

primary sclerosing cholangitis

256
Q

presentation of liver cancer is with

A 
Weight loss
Abdominal pain
Anorexia
Nausea and vomiting
Jaundice
Pruritus
257
Q

cholangiocarcinoma presentation is with

A

Cholangiocarcinoma often presents with painless jaundice in a similar way to pancreatic cancer.

258
Q

Ix for liver cancer is with

A

AFP, CA19-9 for cholangiocarcinoma, US, CT, MRI and ERCP

259
Q

Tx for hepatocellular carcinoma

A

kinase inhibitors such as sorafenib, regorafenib and lenvatinib or liver transplant

260
Q

Tx for cholangiocarcinoma is

A

early resection of palliation with ERCP

261
Q

Haemangiomas are

A

common benign tumours of the liver

262
Q

Focal nodular hyperplasia is associated with

A

COCP

263
Q

orthotopic transplant refers too

A

dead patient transplant

264
Q

types of transplant

A

orthotopic, split donation or living donor

265
Q

surgery incision for transplant liver is

A

rooftop or mercedes benz

266
Q

presentation for GORD is

A 
Heartburn
Acid regurgitation
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice
267
Q

red flags for GORD are

A 
Dysphagia (difficulty swallowing) at any age gets a two week wait referral
Aged over 55 (this is generally the cut off for urgent versus routine referrals)
Weight loss
Upper abdominal pain / reflux
Treatment resistant dyspepsia
Nausea and vomiting
Low haemoglobin
Raised platelet count
268
Q

PPI examples are

A

Omeprazole

Lansoprazole

269
Q

H2 receptor antagonist example is

A

ranitidine

270
Q

surgery for GORD is

A

laparoscopic fundoplication

271
Q

H.pylori is hat sort of bacteria?

A

gram negative aerobic bacteria

272
Q

H.pylori produces what to neutralise stomach acid?

A

It also produces ammonia to neutralise the stomach acid. this damages the epithelial cells

273
Q

tests for H. pylori

A

Urea breath test using radiolabelled carbon 13
Stool antigen test
Rapid urease test can be performed during endoscopy.

274
Q

triple therapy consists of

A

proton pump inhibitor (e.g. omeprazole) plus 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.

275
Q

barrett’s oesophagus is an example of

A

metaplasia

276
Q

barett’s eosophagus may become

A

adenocarcinoma

277
Q

Tx for barret’s is

A

PPI, or endoscopy with photodynamic therapy, laser therapy or cyrotherapy.

278
Q

what type of GI ulcer is more common?

A

duodenal

279
Q

presentation of an ulcer is through

A

Epigastric discomfort or pain
Nausea and vomiting
Dyspepsia
Bleeding causing haematemesis, “coffee ground” vomiting and melaena
Iron deficiency anaemia (due to constant bleeding)

280
Q

eating effect on ulcers

A

worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.

281
Q

presentation of oesophageal bleed is

A

Haematemesis (vomiting blood)
“Coffee ground” vomit. This is caused by vomiting digested blood that looks like coffee grounds.
Melaena, which is tar like, black, greasy and offensive stools caused by digested blood
Haemodynamic instability

282
Q

suspected upper GI bleed scoring is with

A

glasgow-blatchford score

283
Q

glasgow blatchford score areas

A 
Drop in Hb
Rise in urea
Blood pressure
Heart rate
Melaena
Syncopy
284
Q

why does urea rise in an upper GI bleed

A

lood in the GI tract gets broken down by the acid and digestive enzymes. One of the breakdown products is urea and this urea is then absorbed in the intestines.

285
Q

what is the score system used for risk of recurrent rebleed in an upper GI bleed

A

Rockall score

286
Q

management for an upper GI bleed

A

A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 large bore cannula)
T – Transfuse
E – Endoscopy (arrange urgent endoscopy within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)

287
Q

bloods in an upper GI should be

A 
Haemoglobin (FBC)
Urea (U&amp;Es)
Coagulation (INR, FBC for platelets)
Liver disease (LFTs)
Crossmatch 2 units of blood
288
Q

group and save is for

A

s where the lab simply checks the patients blood group and keeps a sample of their blood saved incase they need to match blood to it.

289
Q

crossmatch is for

A

is where the lab actually finds blood, tests that it is compatible and keeps it ready in the fridge to be used if necessary.

290
Q

Crohn’s Crows nest

A

N – No blood or mucus (less common)

E – Entire GI tract

S – “Skip lesions” on endoscopy

T – Terminal ileum most affected and Transmural (full thickness) inflammation

S – Smoking is a risk factor (don’t set the nest on fire)

291
Q

UC Closeup

A

C – Continuous inflammation

L – Limited to colon and rectum

O – Only superficial mucosa affected

S – Smoking is protective

E – Excrete blood and mucus

U – Use aminosalicylates

P – Primary Sclerosing CholangitisC – Continuous inflammation

L – Limited to colon and rectum

O – Only superficial mucosa affected

S – Smoking is protective

E – Excrete blood and mucus

U – Use aminosalicylates

P – Primary Sclerosing Cholangitis

292
Q

presentation of IBD

A

Diarrhoea
Abdominal pain
Passing blood
Weight loss

293
Q

testing for IBD is with

A

routine bloods, thyroid, U+E’s, LFTm faecal calprotectin, endoscopy with biopsy, imaging for complications

294
Q

Crohn’s first line

A

steroids

295
Q

crohn’s second line

A 
Azathioprine
Mercaptopurine
Methotrexate
Infliximab
Adalimumab
296
Q

Crohn’s maintaining remission

A

Azathioprine

Mercaptopurine

297
Q

surgery for crohn’s involves

A

distal ileum, strictures and fistulas

298
Q

inducing remission for UC is with

A

First line: aminosalicylate (e.g. mesalazine oral or rectal)

299
Q

maintaining remission with UC is

A

Aminosalicylate (e.g. mesalazine oral or rectal)
Azathioprine
Mercaptopurine

300
Q

surgery for UC is with

A

(panproctocolectomy) leaving either a ileo-anal anastomosis or j pouch.

301
Q

coeliac disease auto antibodies are

A

anti-tissue transglutaminase (anti-TTG) and anti-endomysial (anti-EMA).

302
Q

coeliac disease particularly effects

A

the jejunum

303
Q

presentation of coeliac is with

A

Failure to thrive in young children
Diarrhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis (an itchy blistering skin rash typically on the abdomen)

304
Q

genetic associations with coeliac disease is

A

HLA-DQ2 gene (90%)

305
Q

biopsy in coeliac disease will show

A

Crypt hypertrophy”

“Villous atrophy”

306
Q

first line for diarrhoea is

A

Loperamide for diarrhoea

307
Q

Gram positive bacteria features

A

have a thick peptidoglycan cell wall that stains with crystal violet stain.

308
Q

bacterial folic acid pathway

A

PABA is then converted to DHFA which is converted inside the cell to THFA then folic acid.

309
Q

gram negative bacteria stain

A

counterstain (such as safranin) which binds to the cell membrane in bacteria that don’t have a cell wall (gram negative bacteria) turning them red/pink.

310
Q

gram positive cocci

A

Staphylococcus
Streptococcus
Enterococcus

311
Q

gram positive rods

A 
Corney – Corneybacteria
Mike’s – Mycobacteria
List of – Listeria
Basic – Bacillus
Cars – Nocardia
312
Q

gram positive anaerobes

A

C – Clostridium
L – Lactobacillus
A – Actinomyces
P – Propionibacterium

313
Q

gram negative bacteria

A 
Neisseria meningitis
Neisseria gonorrhoea
Haemophilia influenza
E. coli
Klebsiella
Pseudomonas aeruginosa
Moraxella catarrhalis
314
Q

atypical bacteria

A 
Legions – Legionella pneumophila
Psittaci – Chlamydia psittaci
M – Mycoplasma pneumoniae
C – Chlamydydophila pneumoniae
Qs – Q fever (coxiella burneti)
315
Q

antibiotics options for MRSA

A 
Doxycycline
Clindamycin
Vancomycin
Teicoplanin
Linezolid
316
Q

ESBLs are resistant too

A

beta lactam antibiotics

317
Q

ESBLs tend to be

A

e.coli or klebsiella

318
Q

ESBLs are sensitive too

A

carbapenems such as meropenem or imipenem.

319
Q

antibiotics that inhibit cell wall synthesis with a beta lactam ring

A

Penicillin
Carbapenems such as meropenem
Cephalosporins

320
Q

antibiotics without a beta lactam ring but inhibit cell wall synthesis

A

Vancomycin

Teicoplanin

321
Q

antibiotics that inhibit folic acid metabolism

A

Sulfamethoxazole blocks the conversion of PABA to DHFA

Trimethoprim blocks the conversion of DHFA to THFA

Co-trimoxazole is a combination of sulfamethoxazole and trimethoprim

322
Q

metronidazole mechanism

A

reduction of metronidazole into its active form only occurs in anaerobic cells. When partially reduced metronidazole inhibits nucleic acid synthesis.

323
Q

antibiotics inhibit protein synthesis by targeting ribosomes

A 
Macrolides such as erythromycin, clarithromycin and azithromycin
Clindamycin
Tetracyclines such as doxycycline
Gentamicin
Chloramphenicol
324
Q

streptococcus, listeria and enterococcus consider which antibiotic?

A

amoxicillin

325
Q

staphylococcus, haemophilus and e. coli consider which antibiotic

A

co-amoxiclav

326
Q

septic shock is defined as

A

Systolic blood pressure less than 90 despite fluid resuscitation

Hyperlactaemia (lactate > 4 mmol/L)

327
Q

risk factors for sepsis

A

Very young or old patients (under 1 or over 75 years)
Chronic conditions such as COPD and diabetes
Chemotherapy, immunosuppressants or steroids
Surgery or recent trauma or burns
Pregnancy or peripartum
Indwelling medical devices such as catheters or central lines

328
Q

neutropenic sepsis is defined as

A

1 x 10*9/L.

329
Q

neutropenic sepsis treatment is with

A

tazocin

330
Q

common cause of chest infection is

A

streptococcus pneumoniae

331
Q

atypical bacterial chest infection Tx

A

Macrolides such as clarithromycin
Quinolones such as levofloxacin
Tetracyclines such as doxycycline

332
Q

lower UTI presents with

A

Dysuria (pain, stinging or burning when passing urine)
Suprapubic pain or discomfort
Frequency
Urgency
Incontinence
Confusion is commonly the only symptom in older more frail patients

333
Q

pyelonephritis presents with

A

Fever is a more prominent feature than lower urinary tract infections.
Loin, suprapubic or back pain. This may be bilateral or unilateral.
Looking and feeling generally unwell
Vomiting
Loss of appetite
Haematuria
Renal angle tenderness on examination

334
Q

duration of simple lower UTI for women Tx

A

3 days

335
Q

what is the classification system for cellulitis

A

Eron classification

336
Q

what antibiotics is very effective against gram positive cocci?

A

flucloxacillin

337
Q

bacterial tonsillitis is commonly caused by

A

Group A Streptococcus (GAS) infections, mainly streptococcus pyogenes.

338
Q

the Centor criteria for tonsillitis is

A

Fever > 38ºC
Tonsillar exudates
Absence of cough
Tender anterior cervical lymph nodes (lymphadenopathy)

339
Q

common causes of intraabdominal infections

A 
Anaerobes (e.g. bacteroides and clostridium)
E. coli
Klebsiella
Enterococcus
Streptococcus
340
Q

co-amoxiclav cover

A

good gram positive, gram negative and anaerobic cover.

341
Q

quinolones cover

A

Ciprofloxacin and levofloxacin provide reasonable gram positive and gram negative cover and also cover atypical bacteria however they don’t cover anaerobes

342
Q

gentamicin coverage

A

This provides very good gram negative cover with some gram positive cover particularly against staphylococcus.

343
Q

vancomycin coverage

A

This provides very good gram positive cover including MRSA.

344
Q

common regimes for intra-abdominal antibiotics

A

Co-amoxiclav alone

Amoxicillin plus gentamicin plus metronidazole

345
Q

spontaneous bacterial peritonitis treatment first line

A

tazocin

346
Q

septic arthritis presentation

A

Hot, red, swollen and painful joint
Stiffness and reduced range of motion
Systemic symptoms such as fever, lethargy and sepsis

347
Q

commonest cause of septic arthritis is

A

Staphylococcus aureus

348
Q

In a young patient presenting with a single acutely swollen joint always think of

A

gonococcus septic arthritis

349
Q

differentials for septic arthritis

A

gout, pseudogout, reactive arthritis, haemarthrosis

350
Q

first line antibiotics for septic arthritis

A

Flucloxacillin plus rifampicin is often first line

351
Q

who are offered the Flu vaccine?

A 
Aged 65
Young children
Pregnant women
Chronic health conditions such as asthma, COPD, heart failure and diabetes
Healthcare workers and carers
352
Q

presentation of the flu

A 
Fever
Coryzal symptoms
Lethargy and fatigue
Anorexia (loss of appetite)
Muscle and joint aches
Headache
Dry cough
Sore throat
353
Q

Dx of flu

A

Viral nasal or throat swabs with PCR and send data to public health

354
Q

two treatments for influenza

A

Oral oseltamivir 75mg twice daily for 5 days

Inhaled zanamivir 10mg twice daily for 5 days

355
Q

campylobacter jejuni incubation period

A

2-5 days

356
Q

antibiotics choices for campylobacter jejuni and shigella treatment

A

azithromycin or ciprofloxacin

357
Q

patient develops symptoms soon after eating leftover fried rice that has been left at room temperature. It has a short incubation period after eating the rice and they then recover within 24 hours. What is the likely cause?

A

bacillus cereus

358
Q

frequently affects children causing watery or bloody diarrhoea, abdominal pain, fever and lymphadenopathy after eating undercooked pork what is the likely cause?

A

Yersinia enterocolitica

359
Q

example of antidiarrheal medication

A

loperamide

360
Q

example of antiemetic medication

A

metoclopramide

361
Q

post gastroenteritis complications

A

Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain–Barré syndrome

362
Q

Neisseria meningitidis is what type of bacteria?

A

gram negative diploccous

363
Q

meningococcal septicaemia is the cause of what classic sign?

A

non-blanching rash

364
Q

common causes of bacterial meningitis are

A

Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (pneumococcus).

365
Q

what are the two special tests for meningitis

A

Kernig’s (hip flexed leg straighten) and Brudzinski’s test (chin flex to chest)

366
Q

benzylpenicillin doses for community suspected meningitis

A

< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg

367
Q

what is the prophylactic treatment for meningitis complication

A

dexamethasone

368
Q

post exposure prophylaxis for meningitis is guided by

A

public health

369
Q

Post exposure prophylaxis for meningitis is with

A

ciprofloxacin

370
Q

viral CSF infection

A

clear, mildly raised protein, glucose normal, lymphocytes

371
Q

bacterial CSF

A

cloudy, increased protein, low glucose, neutrophils

372
Q

what type of bacteria is mycobacterium tuberculosis

A

small rod shaped bacillus

373
Q

what stain is required for the acid fastness tuberculosis bacteria

A

Zeihl-Neelsen stain. This turns TB bacteria bright red against a blue background.

374
Q

TB infection and spread via

A

droplets and then via lymphatics and bloods

375
Q

BCG vaccine

A

intradermal live attenuated

376
Q

prior to BCG vaccine they are tested with

A

mantoux test - tuberculin protein.

377
Q

presentation of TB

A 
Lethargy
Fever or night sweats
Weight loss
Cough with or without haemoptysis
Lymphadenopathy
Erythema nodosum
Spinal pain in spinal TB (also known as Pott’s disease of the spine)
378
Q

what are the two tests for immune response to TB

A

mantoux and interferon gamma release assay

379
Q

what is the interferon gamma release assays used for in Tb?

A

diagnosis of latent TB

380
Q

CXR presentation of primary TB

A

patchy consolidation, pleural effusions and hilar lymphadenopathy

381
Q

CXR of reactivated TB

A

patchy or nodular consolidation with cavitation (gas filled spaces in the lungs) typically in the upper zones

382
Q

CXR of disseminated miliary TB

A

millet seeds” uniformly distributed throughout the lung fields

383
Q

cultures for Tb

A

sputum (3*), mycobacterium blood cultures and lymph node aspiration

384
Q

latent Tb Tx

A

Isoniazid and rifampicin for 3 months

Isoniazid for 6 months

385
Q

RIPE treatment for acute pulmonary TB

A

R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for 2 months
E – Ethambutol for 2 months

386
Q

“they are started on R, I, P and E for TB, what should also be prescribed?”

A

pyridoxine.

387
Q

why is pyridoxine prescribed for the Tb regime

A

isoniazid causes peripheral neuropathy and pyridoxine (vitamin B6) is usually co-prescribed prophylactically to help prevent this.

388
Q

patients with active TB should be kept in what rooms in the hospital?

A

negative pressure

389
Q

Side effects of rifampicin

A

can cause red/orange discolouration of secretions like urine and tears.

390
Q

side effects of isoniazid

A

cause peripheral neuropathy. Pyridoxine (vitamin B6) is usually co-prescribed prophylactically

391
Q

Side effects of pyrazinamide

A

hyperuricaemia (high uric acid levels) resulting in gout.

392
Q

side effects of ethambutol

A

colour blindness and reduced visual acuity.

393
Q

what is the specific antigen to test in the blood for HIV

A

p24 antigen

394
Q

end stage HIV/AIDS is defined as

A

Under 200 cells/mm3

395
Q

HIV and breast feeding

A

Breastfeeding is only considered where the viral load is undetectable however there may still be a risk of contracting HIV through breastfeeding.

396
Q

malaria is an infectious disease caused by

A

the Plasmodium family of protozoan parasites.

397
Q

most severe malaria is the

A

plasmodium falciparum

398
Q

malaria is spread via

A

female anopheles mosquitoes

399
Q

freshly injected sporozoites travel to which organ?

A

the liver

400
Q

the sporozoites in the liver mature into

A

merozoites and then infect red blood cells

401
Q

presentation of malaria

A 
Fever, sweats and rigors
Malaise
Myalgia
Headache
Vomiting
402
Q

signs of malaria

A

Pallor due to the anaemia
Hepatosplenomegaly
Jaundice as bilirubin is released during the rupture of red blood cells

403
Q

Dx of malaria

A

blood film in an EDTA bottle . three samples over three days.

404
Q

Treatments for malaria

A

Artesunate. This is the most effective treatment but is not licensed.
Quinine dihydrochloride

405
Q

complications of falciparum

A 
Cerebral malaria
Seizures
Reduced consciousness
Acute kidney injury
Pulmonary oedema
Disseminated intravascular coagulopathy (DIC)
Severe haemolytic anaemia
Multi-organ failure and death
406
Q

antimalarial options

A

proguanil and atovauone (malarone), mefloquine and doxycycline

fourth year (12 decks)

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