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PACES > PACES Station 1 > Flashcards

PACES Station 1 Flashcards

1
Q

Causes of Cirrhosis

A

Alcohol
Viral: HepB/C
Autoimmune: PBC, PSC, Autoimmune hepatitis
Metabolic: NASH, Haemochromatosis, alpha1antitrypsin, wilsons, CF
Drugs: methotrexate, isoniazid, amiodarone, phenytoin

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2
Q

Features of alcohol misuse

A

Cachexia, tremor, parotid enlargement, dupuytrens, cerebellar syndrome, peripheral neuropathy, myopathy

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3
Q

Classification of Hepatic Encephalopathy

A

Grade 1: Insomnia, reversal of sleep
Grade 2: Lethargy, disorientation
Grade 3: Confusion, somnolence
Grade 4: Coma

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4
Q

Childs-Pugh Cirrhosis Severity and Prognosis

A

Bilirubin, ascites, encephalopathy, PT, albumin

Grade A 5-6: 90% 5 yr survival
Grade B 7-9: 80% 5 yr survival
Grade C >10: 33% 1 yr mortality

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5
Q

Strategy of Management of Cirrhosis

A

Treat underlying cause to stop or slow disease
Prevent superimposed liver damage
Prevent complications: surveillance, 6 monthly US and alphafetoprotein, endoscopy,
Transplant

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6
Q

Causes of Ascites

A 
Cirrhosis
Malignancy
Heart Failure
TB
Pancreatitis
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7
Q

SAAG

A

Serum albumin-ascites gradient
>11g/L suggests transudate
<11g/L suggests exudate

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8
Q

Pathophysiology of ascites and oedema in cirrhosis

A
  1. Disruption of portal flow in liver causing fluid to accumulate in peritoneum
  2. Vasodilation of splanchnic circulation
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9
Q

Hepatorenal Syndrome

A

Systemic vasodilation causes progressive decrease in effective circulation volume leads to RAS activation which reduces renal blood flow

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10
Q

Causes of Hepatomegaly

A 
Malignancy
RHF
Infection: viral hepatitis, toxoplasma, hydatid cyst
Infiltration: amyloid, sarcoid
Vascular: budd-chiari, sickle cell
Polycystic liver
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11
Q

Benign Liver Tumours

A

Cavernous haemangiomas (women of child bearing age)
Hepatic adenoma
Focal nodular hyperplasia

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12
Q

Causes of Splenomegaly

A 
Portal HTN
Myelofibrosis
Haematological malignancy - CML, lymphoma
Infection
Congestion
Splenic vein thrombosis
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13
Q

Cytogenetics of CML

A

Philadelphia translocation chr 9:22
bcr-abl oncogene
tyrosine kinase activity

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14
Q

Causes of hyposplenism

A 
Splenic infarction - vasculitic, sickle
Splenic artery thrombosis
Infiltrative condition - amyloid, sarcoid
Coeliac
Autoimmune disease
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15
Q

Haemochromatosis - genetics

A

Autosomal recessive
HFE gene on chr 6
Leads to raised transferrin saturations >50%

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16
Q

Complications of haemochromatosis

A 
Liver failure 
HCC
Diabetes
Skin pigmentation
Arthropathy
Dilated or restrictive cardiomyopathy
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17
Q

PBC management

A 
ADEK supplements
Treat bone disease
Treat high cholesterol
Treat liver disease with urso
Manage pruritus with cholesytramine but this inhibits absorption of urso
Manage fatigue - naltrexone
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18
Q

How to present renal abdomen

A
  1. Current mode of RRT
  2. Previous modes of RRT
  3. Adequacy of RRT - uraemia and volume
  4. Complications of renal failure e.g. anaemia/bone disease
  5. Complications of immunosuppressive drugs
  6. Aetiology if possible
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19
Q

Problems with haemodialysis

A 
Time
Washout - removal of too much fluid, feel fatigued, cramps, low BP
Bacteraemia - staph
Bleeding - heparin
Amyloidosis
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20
Q

Problems with peritoneal dialysis

A

Peritonitis
Diabetes - glucose in dialysate
Ultrafiltration failure - peritoneal sclerosis
Local hernia, infection, fluid leak

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21
Q

Manifestations of renal oseteodystrophy

A

Osteitis fibrosa - increase bone turnover due to secondary hyperparathyroidism, can cause bone pain and cysts (brown tumours)
Osteomalacia - decreased mineralisation of bone due to aluminium deposition

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22
Q

Definition of nephrotic syndrome

A

Proteinuria > 3g/24hr
Hypoalbumaemia <30g/L
Oedema

(thrombosis and hyperlipidaemia often seen)

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23
Q

Complications of nephrotic syndrome

A 
Oedema - diuretics and salt restrict
HTN - ACEi
High cholesterol 
Thrombosis
Infection - pneumovax and meningoccal vaccination
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24
Q

PCKD genetics

A

Autosomal dominant, most cases chr 16, some chr 4

Screen in over 20s with relative

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25
Q

Extra renal manifestations of PCKD

A

Cerebral aneurysms
Liver cysts
Splenic and pancreatic cysts
Mitral valve prolapse and aortic regurgitation

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26
Q

von-Hippel Lindau syndrome

A

Autosomal dominant condition on chr 3
Cerebellar, retinal and spinal haemangioblastomas
Cysts on liver, kidney, spleen
Increased risk of RCC (bilateral) and phaeochromocytoma

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27
Q

Clinical Features of Interstitial Lung Disease

A 
Clubbing
Features of rheumatoid disease
Reduced expansion and TVF
End inspiratory crackles
Pulmonary HTN: raised JVP, parasternal heave, peripheral oedema
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28
Q

Causes of Interstitial Lung Disease

A 
IPF/CFA
Rheumatological: RA, SS, SLE, AS, Sj
Eosinophilic: ABPA
Inhaled: EAA, silicosis, asbestosis
Drugs: amiodarone, nitrofurantoin, methotrexate, bleomycin
Vasculitis: wegeners, C-S, Goodpastures
Sarcoid
Radiation
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29
Q

Respiratory Causes of Clubbing

A 
Interstitial Lung Disease
Ca Lung
Mesothelioma
Cystic fibrosis
Bronchiectasis
Lung abscess/empyema
TB
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30
Q

Investigations for ILD

A

Bloods: FBC, ESR, Ig, ANA, ENA, ANCA, antiGBM, CK, RhF, Serum ACE
ABG - T1RF
CXR - bilateral reticulonodular infiltrates
PFTs - restrictive pattern + reduced gas transfer
HRCT
MRI
BAL/Biopsy

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31
Q

Apical Pulmonary Fibrosis

A 
Inhaled agents: EAA, berylliosis, silicosis
Radiation 
Sarcoidosis
ABPA
Ank SPond
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32
Q

Basal Pulmonary Fibrosis

A

IPF/CFA
Most rheum disease/CTD
Drugs

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33
Q

Complications of Pulmonary Fibrosis

A 
Rest Failure
Chest infection
Pulmonary HTN
Cor pulmonale
Carcinoma of lung
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34
Q

Management of ILD

A

General measures: stop smoking, remove exposures, treat infection promptly, education
Immunosuppressive therapy - trial of steroids
Surgery - single or double lung transplant option

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35
Q

Clinical Features of COPD

A 
Audible wheeze
Nicotine staining
Prolonged expiratory phase
Tracheal tug
Accessory muscles of Rs
Hyper resonant
Quiet breath sounds
NOT clubbing
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36
Q

Definition of COPD

A

Umbrella term for obstructive airway disease including

  • Chronic Bronchitis - cough for 3 months during 2 consecutive years leading to inflammation
  • Emphysema - histological diagnosis of abnormal and permanently enlarged small airspaces leading to loss of elastic recoil
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37
Q

Spirometry in COPD

A 
FEV1<80% predicted +
FEV1/FVC:
 < 70% mild
30-50 moderate
<30 severe
Plus do reversibility testing
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38
Q

MRC Dyspnoea scale

A
  1. Only breathless during strenuous exercise
  2. SOB when hurrying or up slight incline
  3. Walks slower than contemporaries on flat
  4. Stops every 100m
  5. Too breathless to leave house
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39
Q

Management of Acute IECOPD

A 
Controlled O2
Nebuliser bronchodilators
Antibiotics
Steroids
Consider IV aminophyline
NIV in T2RF with pH<7.35
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40
Q

Most common pathogens in IECOPD

A

Streptococcus pneumonia
Haemophilus influenzae
Moraxella catarrhalis

41
Q

LTOT Criteria for COPD

A 
Stopped smoking
paO2 <7.3 when well 
OR 7.3-8 plus
- secondary polycythaemia
- pulmonary HTN
- peripheral oedema
- nocturnal hypoxaemia (sats <90% for >30% of time )

ABG taken when well on 2 occasions at least 3 weeks apart

42
Q

Alpha 1 antitrypsin deficiency

A

Autosomal dominant chr 14
encodes alpha 1 antitrypsin which is enzyme that inhibits neutrophil elastase
Multiple phenotypes M (medium), S (slow), Z (very slow)

43
Q

Management of COPD

A

General measures: stop smoking, immunise
Stepwise bronchodilators/antiinflammatory
Mucolytics
LTOT
Diuretics for cor pulmonale
Pulmonary rehab - MDT programme - education, nutrition, psychological support, physical training

44
Q

Role of surgery in COPD

A

Bullectomy, lung volume reduction surgery, transplantation

45
Q

Stepwise therapies in COPD

A
  1. SABA
  2. FEV1>50% add LAMA or LABA, FEV1<50% add LABA+ICS or LAMA
  3. Add in the other one

Always educate and use spacer

46
Q

Clinical Features of Pleural Effusion

A

Reduced chest expansion,
Stony dull percussion note
Reduced TVF
Diminished breath sounds

47
Q

Causes of Pleural Effusion

A

Exudate >30g/L:
Neoplasm: Ca lung, mesothelioma, lymphoma
CTD: Ra, SLE
Infection: pneumonia, TB
Sub-diaphragmatic: pancreatitis, abscess
Drugs: methotrexate, nitrofurantoin, bromocriptine
Other: asbestosis, sarcoid, dresslers, trauma, yellow nail syndrome

Transudate <30g/L
CCF
Constrictive pericarditis
Low albumin
Nephrotic syndrome
Cirrhosis
Dialysis
Uraemia
Hypothyroidism
48
Q

What volume of pleural fluid can be detected on CXR?

A

180ml would show was loss of costophrenic angle

49
Q

Pathophysiology of a Pleural Effusion

A

Inflammatory causes lead to altered permeability of membrane
Reduced oncotic pressure in low albumin
Increased hydrostatic pressure in CCF
Reduced lymphatic drainage in malignancy

50
Q

Causes of low glucose in pleural fluid

NB also causes of low pH (assuming patient has normal ABG)

A 
Malignancy
Empyema
TB
RA
Oesophageal rupture
SLE
51
Q

What is the significant of low pH in context of malignant pleural effusion (<7.3)?

A

More extensive pleural involvement
Higher yield on cytology
Decreased success of pleurodesis
Shorter life expectancy

52
Q

Complications of pleural fluid drainage

A

Pneumothorax
Haemothorax
Hypovolaemia
Unilateral pulmonary oedema (reexpansion)

53
Q

Indications for pleurodesis

A

Recurrent malignant effusion

Recurrent pneumothoraces

54
Q

Clinical Features of Bronchiectasis

A 
Productive cough (sputum pot)
Inspiratory coarse creps which alter after coughing
Clubbing
Sometimes wheeze
Often no features of pulmonary HTN
55
Q

Causes of Bronchiectasis

A

Childhood resp infection: pertussis, measles, TB
Bronchial obstruction: foreign body, chronic aspiration, endobronchial tumour
Long standing fibrosis
Mucociliary clearance problem: CF, kartageners
Immunodeficiency: hypogammaglobulinaemia, AIDS
ABPA
Autoimmune disease: RA, IBD, Sjogrens
Congenital abnormality
Idiopathic

56
Q

Pathophysiology of Bronchiectasis

A

Abnormal bronchial wall dilatation, destruction and transmural inflammation caused by destruction of muscular and elastic components of bronchial wall leading to inflammation, oedema and scarring
Impaired clearance of secretions leads to colonisation and infection causing further damage

57
Q

Complications of Bronchiectasis

A 
Pneumonia
Pneumothorax
Empyema
Collapse
Metastatic cerebral abscess
Respiration failure
Pulmonary HTN
Amyloidosis
58
Q

Anatomical distribution of Bronchiectasis and aetiology

A

Infection - lower lobes
ABPA & TB - upper lobes
Obstruction - right middle lobe

59
Q

Diagnosis of Bronchiectasis

A

HRCT - signet ring sign - bronchial diameter greater than adjacent vessel
Spirometry - may be normal, may have obstructive pattern, may be restrictive in advanced disease

60
Q

Most common pathogens in bronchiectasis

A 
Staphylococcus aureus
Haemophilus influenzae
Pseudomonas
Streptococcus pneumoniae
Klebsiella
Aspergillus
61
Q

Cystic Fibrosis

A

Autosomal recessive, defect on chr7
CFTR Chloride channel abnormality leads to thick mucus and impaired ciliary clearance. Also causes meconium ileum, gallstones, bile salt malabsorption, arthropathy and fertility problems in men

62
Q

ABPA

A

Allergic bronchopulmonary aspergillosis
Hypersensitivity to aspergillus in patients with asthma or CF. Excess mucus production and ciliary clearance. Immune complex deposition incites type III reaction to damage bronchial wall leading to bronchiectasis

63
Q

General management of bronchiectasis

A

General measures: smoking cessation, immunisations, nutrition, MDT, LTOT if needed
Antibiotics including nebuliser tobramycin in CF
Postural drainage and chest physio - flutter devices
Bronchodilators
Steroids
Surgical resection if localised, transplant in CF

64
Q

Clinical Features of Ca Lung

A 
Cachectic
Productive cough
Clubbing
Palpable LNs
Dull percussion, reduced TVF (may have effusion)
Bronchial breathing above dullness
Pan coast tumour  - reduced sensation C8-T1, wasting of muscles, ipsilateral horners (ptosis, miosis, anhydrosis)
Deviated trachea 
Radiation burns
65
Q

Classification of bronchial Ca

A 
Small cell - 20%, smokers
Non small cell including:
- adenocarcinoma: non-smokers, peripheral
- bronchoalveolar: develops at multisite
- squamous: cavitation, smokers
- large cell: undifferentiated
66
Q

Risk factors for Lung Ca

A 
Smoking
ILD
Radon
Asbestos
Arsenic
Coal tar
Radiation
67
Q

TNM classification of Lung Ca

A 
Tis - in situ
T1 <3cm
T2 >3cm, invasion of pleura/main bronchus
T3 extra pulmonary extension
T4 Extensive extra pulmonary extension

N1 ipsilateral intrapulmonary nodule
N2 ipsilateral mediastinal LN
N3 contralateral nodule or scalene/supraclavicular nodule

M0 - none, M1 mets

68
Q

Paraneoplastic Lung Ca in SCLC

A

Endocrine:
-SIADH ,Cushings, Hypercalcaemia, hypoglycaemia

Neurological:

  • Lambert-Eaton myasthenia - presynaptic Ca channel Abs
  • Cerebellar degeneration - antiYo
  • Sensory neuropathy - anti Hu

MSK

  • dermatomyositis
  • clubbing
  • osteoarthropathy

Skin

  • acanthuses nigricans
  • ichthyosis
69
Q

Pancoast Tumour

A

Apical lung tumour erodes into lower part of brachial plexus (C8-T1) and cervical sympathetics
Ipsilateral wasting of small muscles of hand with dermatomal sensory loss
Ipsilateral horners

70
Q

General Management of Lung Ca

A 
MDT!!!
surgery, chemotherapy, radiotherapy
Analgesia
Anxiolytics
Stents in palliative
Pleurodesis
Psychological support
71
Q

Clinical Features Lobectomy/Pneumonectomy

A 
Deviated trachea
Thoracotomy scar
Reduced chest expansion
Dull percussion
Absent breath sounds/bronchial breathing above
Clubbing - indicates bronchiectasis or malignancy or ILD
Palpable LNs - malignancy
Deformity of chest wall
72
Q

Indications for Lung Lobectomy

A 
Bronchiectasis with uncontrolled symptoms
Malignancy
Solitary pulmonary nodule
CF
TB
73
Q

Indications for Pneumonectomy

A

Bronchiectasis
Malignancy
TB

74
Q

Clinical Features of Old TB

A

Apical fibrosis
Scars from thoracoplasty/pneumonectomy/lobectomy
Phrenic nerve crush - left supraclavicular scar and raised hemidiaphragm

75
Q

Patients at risk of TB

A 
Immigrant population
Immunocompromised
Elderly
Alcoholics
Malnutrition
Homeless
76
Q

Complications of TB

A 
Pneumothorax
Pleural effusion
Empyema
Collapse
Tubulointerstitial nephritis
ARDS
TB meningitis
Miliary TB
Fibrosis
Bronchiectasis
77
Q

Interferon Gamma Testing in TB

A

Allows to distinguish between active TB and someone who has previously had BCG and thus positive tuberculin skin test

78
Q

Indications for chemoprophylaxis in TB

A

All children under 5 in close contact

Patients with previous hx of TB or radiological evidence and starting on immunosuppressive therapy

79
Q

Clinical Features of Lung Consolidation

A

Productive cough
trachea pulled to affected side
Increased vocal resonance, coarse creps
Underlying cause: features of malignancy, pneumonia, infarction (PE)

80
Q

Typical Pathogens in CAP

A

Streptococcus pneumoniae
Haemophilus influenzae
Staphylococcus aureus

81
Q

Atypical Pathogens in CAP

A

Mycoplasma
Legionella
Chlaymdia
Coxiella

82
Q

Pathogens in HAP

A

Gram negs: klebsiella, pseudomonas, e.coli
Staph
Anaerobes
Fungi

83
Q

Mycoplasma pneumonia

A 
occurs in epidemics every 3-4 years
children and young adults
prolonged prodromal phase
Neurological manifestations: meningitis, encephalitis, GBS, transverse myelitis
Cardiac: myocarditis, pericarditis
Rheum: arthralgia, myalgia, myositis
Haem: thrombocytopenia, DIC
GI: D&amp;V, hepatitis, pancreatitis
Derm: erythema nodosum, S-JS
Renal: glomerulonephritis
84
Q

ECG features of PE

A 
sinus tachycardia
Tall R in V1
Right ventricular strain
RBBB
TWI V1-V3
S1Q3T3
85
Q

Secondary Causes of Pneumothorax

A

Resp: COPD, CF, Asthma, ILD, TB, Malignancy, Sarcoid
CTD: Marfans, Ehlers-Danlos
Lung cysts: Neurofibromas, tuberous sclerosis
Iatrogenic: pleural aspiration, biopsy, pacemaker insertion, CPR
Trauma

86
Q

Clinical Signs of Tension Pneumothorax

A

Tracheal deviation, away
Mediastinal shift - displaced apex
Raised JVP

87
Q

Management of Spontaneous Primary Pneumothorax

A

If <2cm on CXR repeat in 7-10days, return if develop breathlessness
More than >2cm aspirate and if unsuccessful consider chest drain

88
Q

Role of chest drain suction

A

Added after 48 hrs if persistent air leak or failure of pneumothorax to re-expand

89
Q

Management of Secondary Pneumothoraces

A

Admit all
If <1cm and asymptomatic can observe
If <50, <2cm and asymptomatic can aspirate
All others require drain

90
Q

Main predictor of re-expansion pulmonary oedema

A

greater time the lung has been collapsed the greater the risk

91
Q

Clinical Features of Rheumatoid Lung

A

Inspiratory clicks
Symmetrical deforming arthropathy of hands
Clubbing
Steroid purpura
Fine end inspiratory crackles at bases extending to mid zone, do not alter with coughing
May be some bronchiectatic changes also

92
Q

Respiratory Manifestations of Rheumatoid Arthritis

A 
Pleural effusions
Basal fibrosis: RA, gold, methotrexate
Pneumonitis
Pulmonary nodules
Bronchiectasis
Caplans syndrome
93
Q

Pulmonary nodules in RA

A

histologically similar to subcutaneous nodules
In pleura or lung parenchyma
often do not compromise function but can lead to bronchopulmonary fistula or infection

94
Q

Features of RA pleural effusion

A

Exudate
High protein and LDH
Low glucose and complement
High rheumatoid factor

95
Q

Caplans syndrome

A

pneumoconiosis in patient with RA associated with coal miners

96
Q

Causes of Lung Collapse

A

Obstructive
-malignancy, extrinsic compression, TB, mucus plus, foreign body

Non-obstructive

  • adhesive atelectasis: PE, radiation, ARDS, pneumonia
  • Relaxation atelectasis: pleural effusion, pneumothorax
  • Rounded atelectasis: asbestos
97
Q

Clinical Features of SVC obstruction

A

Upper limb and face oedema
Plethoric
Cyanosed
Conjunctival suffusion
Venous angiomata on undersurface of tongue
Prominent and dilated veins over upper limbs, neck and anterior chest
Firm raised venous pressure
Look for signs of radiation marks/effusions to suggest underlying malignancy

98
Q

Causes of stridor

A 
Inspiratory (mostly):
Acute epiglottis
Croup
Vocal chord dysfunction
Foreign body
Trauma
Neck surgery
Expiratory:
Foreign body
Bronchial Ca
Stricture secondary to TB, sarcoid
Lymphadenopathy

PACES (3 decks)

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