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Year 5 > Respiratory & Gastroenterology > Flashcards

Respiratory & Gastroenterology Flashcards

1
Q

Stepwise management of asthma in adults

A

1) SABA
2) SABA + ICS
3) SABA + ICS + leukotrine receptor antagonist
4) SABA + ICS + LABA
5) Switch ICS/LABA fr MART that includes low dose ICS e.g, fostair

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2
Q

Severe asthma attack signs

A

PEFR 33-50%
RR >25
HR >110
Struggle to complete full sentences

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3
Q

Life threatening asthma attack signs

A 
PEFR <33%
O2 Sats <92%
Silent chest
Cyanosis 
Normal CO2 - as feeble respiratory effort
Bradycardia
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4
Q

Management of asthma attack

A

Nebulised salbutamol
Oral prednisolone - continued for 5 days

Nebulised ipratropium bromide - if severe or life threatening
IV magnesium sulphate - if severe of life threatening
IV aminophylline - considered by seniors if severe
Intubation and ventilation - for patients who fail to respond

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5
Q

Criteria for discharge following asthma attack

A

Stable for 12-24 hours - on no nebulisers or oxygen
Inhaler technique checked
PEF >75% predicted

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6
Q

COPD CXR Signs

A

Hyperinflation
Flat hemidiaphragm
Bullae - large bullae may mimic pneumothorax

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7
Q

Staging of COPD

A 
Based on FEV1 (of predicted)
Stage 1  >80%
Stage 2  50-80%
Stage 3  30-50%
Stage 4  <30%
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8
Q

What vaccinations do COPD patients get?

A

Annual influenza

One off pneumococcal

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9
Q

Medical management of COPD

A 
1st line - SABA or SAMA 
2nd line:
- no steroid responsiveness - LABA + LAMA
- steroid responsiveness - LABA + ICS
3rd line - theophylline
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10
Q

What features suggest steroid responsiveness in COPD?

A

Hx of asthma
High eosinophil count
Substation variation of FEV1 over time
Substation variation of PEF over time

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11
Q

What is the most common infective organisms for exacerbation of COPD

A

Haemophilus influenza

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12
Q

Management of COPD Exacerbation

A

Increased bronchodilator use, consider using nebs
Prednisolone 30mg for 5 days
Abx course - if sputum present or clinical signs of pneumonia (Amoxiciilin, clarithromcycin or doxycycline)
BIPAP - if type II respiratory failure develops

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13
Q

Which abx is given as oral prophylactic therapy in COPD?

A

Azithromycin (given either every day or 3x a week)

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14
Q

Which COPD pt’s are considered for Long term oxygen therapy

A 
FEV1 <30%
Cyanosis 
Polycythemia 
Peripheral oedema
Raised JVP
Sats <92% on room air 
Two ABGs showing pO2 <7.3kPa
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15
Q

Which is the most common causative organism of community acquitted pneumonia?

A

Streptococcus pneumonia

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16
Q

Which causative pneumonia organism is more common in diabetics and alcoholics?

A

Klebsiella

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17
Q

Which causative pneumonia organism is more common in immunocompromised patients

A

Pneumocystis jirovecii

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18
Q

CURB65 scoring points

A 
C - confusion 
U - urea >7
R - resp >30
B - BP <90/60
65 - AGE >65
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19
Q

In what CURB65 score would you admit to hospital?

A

1-2 intermediate risk
3-5 high risk

Both in hospital

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20
Q

Investigations for pneumonia

A 
Bloods - FBC, U&Es, LFTs, CRP
CXR
Blood and sputum cultures
ABG?
Pneumococcal and legionella urinary antigen tests
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21
Q

Medical management of pneumonia

A

Low risk - amoxicillin 5 day course

Moderate/high risk - amoxicillin + clarithromycin 7-10 day course

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22
Q

How long after pneumonia can patients take to feel back to normal

A

Up to 6 months

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23
Q

Two types of pneumothorax

A

Primary - no background of lung disease

Secondary - background of lung disease e.g, COPD

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24
Q

Primary pneumothorax management

A

<2cm - discharge and review

>2cm - aspirate (chest drain if aspirate doesn’t clear symptoms)

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25
Q

Secondary pneumothorax management

A

<1cm and asymptomatic - admit and given oxygen and watch
1-2cm and asymptomatic - aspirate (chest drain if fails)
>2cm - chest drain
Symptomatic - chest drain
>50 years old - chest drain

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26
Q

Signs of tension pneumothorax

A

Hx of trauma
Trachea deviation to opposite side
Hyper-resonance on affected side
Signs of shock - reduced BP

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27
Q

Features of idiopathic pulmonary fibrosis

A 
Restrictive pattern on spirometry 
Progressive dyspnoea 
Bibasal fine end inspiratory crackles 
Dry cough 
Clubbing
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28
Q

CXR findings of idiopathic pulmonary fibrosis

A

Interstitial shadowing - irregular peripheral opacities (ground glass)

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29
Q

CT findings of idiopathic pulmonary fibrosis

A

Honeycombing

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30
Q

Management of idiopathic pulmonary fibrosis

A

Pulmonary rehabilitation
Supplementary oxygen
Prognosis poor and may require lung transplant

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31
Q

What is extrinsic allergic alveolitis (EAA)?

A

Known as hypersensitivity pnemonitis. Immune complex mediated tissue damage in responsive to inhaled organic particles

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32
Q

Types of extrinsic allergic alveolitis

A

Bird fanciers lung - avian proteins from bird droppings
Farmers lung - spores from wet hay
Malt workers lung - Aspergillus clavatus
Mushroom workers lung - termophilic actinomycetes

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33
Q

What is alpha-1 antitrypsin deficiency?

A

Deficiency in A1AT
Enzyme which is usually produced by liver and acts to protect cells from neutrophil elastase enzymes which break down elastin

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34
Q

Pathogenesis of kartagener’s syndrome

A

Dynein arm defect results in immotile cilia

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35
Q

Features of kartagener’s syndrome (primary ciliary dyskinesia)

A 
Dextrocardia (or complete sinus inversus) - quiet heart sounds 
Bronchiectasis 
Recurrent sinusitis 
Subfertlity 
Diabetes
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36
Q

How is pleural fluid aspiration carried out

A

Using 21G needle and 50ml syringe

USS guidance

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37
Q

What is pleural fluid tested for once aspirated?

A 
PH
Protein 
Lactate dehydrogenase (LDH)
Cytology 
Microbiology
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38
Q

What are the two types of causes for pleural effusion and how can you tell the difference by protein content

A

Exudates - protein level >30g/L

Transudate - protein level <30g/L

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39
Q

When is lights criteria used?

A

If protein content in pleural effusion is between 25-30

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40
Q

How can you determine if pleural fluid is exudate using lights criteria?

A

Pleural fluid protein: serum protein ratio >0.5
Pleural fluid LDH: serum LDH ratio >0.6
Pleural fluid LDH more than 2/3rd the upper limits of normal LDH

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41
Q

Causes of transudate pleural effusion

A

Congestive heart failure
Liver cirrhosis
Hypoalbuminaemia
Nephrotic syndrome

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42
Q

Causes of exudate pleural effusion

A 
Malignancy 
Infection 
Trauma 
Pulmonary infarction 
Pulmonary embolism
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43
Q

When would you insert chest drain for pleural effusion?

A

If fluid is turbid/cloudy

If pH is <7.2 - as this suggest an empyema is forming

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44
Q

What is sarcoidosis?

A

Multisystemic disorder characterised by non caseating granulomas

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45
Q

What are the features of sarcoidosis

A 
Erythema nodosum 
Bilateral lymphadenopathy 
Dyspneoa 
Polyarthralgia 
Systemic symptoms - malaise, weight loss, 
Lupus pernio (on skin)
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46
Q

What is acute respiratory distress syndrome (ARDS)

A

Increased permeability of alveolar capillaries leading to fluid accumulation in alveoli

(Non cardiogenic pulmonary oedema)

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47
Q

Causes of acute respiratory distress syndrome

A 
Sepsis 
Pneumonia 
Massive blood transfusion 
Smoke inhalation 
Acute pancreatitis
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48
Q

Management of acute respiratory distress syndrome

A

Managed in ITU

Oxygenation/ventilation

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49
Q

What is the common lung pathology that occurs postoperatively

A

Atelectasis - occurs 72 hours postoperatively

Airways become obstructed by bronchial secretions

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50
Q

Management of atelectasis

A

Position patient upright

Chest physiotherapy

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51
Q

Different types of ectopic production in small cell lung cancers and what they cause

A

ADH - causing hyponatraemia
ACTH - cushings
Lambert-Eaton syndrome - muscle weakness

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52
Q

What is the gold standard for diagnosis in mesothelioma?

A

Thorascopic biopsy

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53
Q

What are the causes of complete white on on CXR where the trachea is pulled toward the Opicification

A

Pneumonectomy

Complete lung collapse

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54
Q

What are the causes of complete white out on CXR where the trachea is central?

A

Consolidation
Pulmonary oedema
Mesothelioma

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55
Q

What are the causes of a complete white out on the CXR where the trachea is pushed away from Opicification?

A

Pleural effusion
Diaphragmatic hernia
Large thoracic mass

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56
Q

What are the two drugs licensed for use in smoking cessation

A

Varenicline - nicotinic partial agonist

Bupropion - norepinephrine and dopamine reuptake inhibitor

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57
Q

How can you distinguish Lambert Eaton syndrome from myasthenia gravis?

A

Lambert Eaton - weakness is often relieved temporarily after exertion or physical exercise

Myasthenia gravis - weakness is worse with activity

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58
Q

What are the common causes of lobar collapse?

A

Lung cancer
Asthma - due to mucous plugging
Foreign body

59
Q

What are the signs of lobar collapse on CXR?

A

Tracheal deviation towards side of collapse
Mediastinal shift towards side of collapse
Elevation of the hemidiaphragm

60
Q

Which lobe is aspiration pneumonia most likely to occur in?

A

Right lower lobe - as this is more vertically orientated

61
Q

What is the histopathology of coeliac disease?

A

Sensitivity to gluten protein

Repeated exposure to gluten leads to villous atrophy which in turn causes malabsorption

62
Q

Which diseases are associated with coeliac disease?

A

Autoimmune thyroid disease
Dermatitis herpetiformis
IBS
Type 1 diabetes

63
Q

Symptoms of coeliac disease

A

Unexplained gastro symptoms e.g, diarrhoea, nausea, vomiting
Abdominal pain, cramping or distention
Iron deficiency anaemia
Weight loss

64
Q

Which cancer is associated with coeliac disease?

A

Enteropathy-associated T cell lymphoma of the small intestine (EATL)

65
Q

Which antibodies are associated with coeliac disease?

A

TTG

IgA

66
Q

Why must patients continue taking gluten diet while being tested for disease

A

So they can produce antibodies which can be screened for

67
Q

Management of coeliac disease

A 
Gluten free diet 
Pneumococcal vaccine (every 5 years) - as patients with coeliac disease have a degree of functional hyposplenism
68
Q

Which medications increase risk of peptic ulcers?

A

NSAIDs
SSRIs
Corticosteroids
Bisphosphonates

69
Q

What is Zollinger-Ellison syndrome?

A

Rare gastrin secreting tumour

Increases risk of peptic ulcer disease

70
Q

Difference between gastric and duodenal ulcers?

A

Gastric - pain worse by eating

Duodenal - pain relieved by eating

71
Q

What is H-Pylori eradication therapy?

A

Omeprazole

Amoxicillin + clarithromycin

72
Q

Test for H-Pylori

A

Urea breath test

Stool antigen test

73
Q

What is Gilbert’s syndrome?

A

Recessive condition - defective bilirubin conjugation due to lack of enzyme
Results in increase in unconjugated hyperbilirubinaemia
Jaundice may only be seen during intercurrent illness, exercise or fasting

74
Q

Diagnosis of liver cirrhosis

A

Fibroscan

75
Q

Causes of decompensated liver disease

A 
Constipation - due to accumulation of toxic products 
Infection 
Dehydration 
Upper GI bleed
Increased alcohol uptake
76
Q

What is spontaneous bacterial peritonitis?

A

Form of peritonitis usually seen in patients with ascites secondary to liver disease

Ascitic fluid infection

77
Q

Features of spontaneous bacterial peritonitis

A

Ascites
Abdominal pain
Fever

78
Q

Diagnosis of spontaneous bacterial peritonitis

A

Paracentesis - neutrophil count >250 cells

79
Q

Most common organism causing spontaneous bacterial peritonitis?

A

E.Coli

80
Q

Management of spontaneous bacterial peritonitis

A

IV cefotaxime

81
Q

Which patients with liver cirrhosis should be given prophylactic abx for spontaneous bacterial peritonitis?

A

Previous episode fo SBP
Ascitic fluid protein <15
Child-Pugh score >0
Hepatorenal syndrome

82
Q

3 types of antibodies in autoimmune hepatitis

A

ANA - anti neutrophilic antibodies
SMA - anti smooth muscle antibodes
LKM1 - anti liver/kidney type 1 antibodies

83
Q

Management of autoimmune hepatitis

A

Steroids
Immunosupression e.g, azathioprine
Liver transplantation

84
Q

What is Wilson’s disease

A

Excessive copper deposition in tissues

Due to defect in ATP7B gene on chromosome 13

85
Q

What age does Wilson’s disease usually present?

A

Aged 10-25

86
Q

Clinical features of Wilson’s disease

A

Liver symptoms - hepatitis/cirrhosis
Neurological symptoms - behavioural and psychiatric problems
Eye signs - green/brown rings in eyes due to copper accumulation (Kayser-fleischer rings)
Kidney symptoms - renal tubular acidosis (esp. fanconi syndrome)

87
Q

Diagnostic investigation in Wilson’s disease

A

Reduced serum caeruloplasmin - 95% of copper is carried by this so as it is used up it is lower in serum levels

88
Q

Management of Wilson’s disease

A

Penicillamine - this chelates copper

89
Q

What is hepatorenal syndrome?

A

Kidney failure seen in people with severe liver damage
Due to vasoactive mediators which cause splanchnic vasodilation - this results in less blood flow to the kidneys and causes kidney decline

90
Q

Two types of hepatorenal syndrome

A

Type 1 - rapidly progressive, very poor prognosis

Type 2 - slowly progressive, still poor prognosis but patients live longer

91
Q

Management of hepatorenal syndrome

A

Terlipressin - causes vasoconstriction of splanchnic circulation

Transjugular intrahepatic portosystemic shunt - connects the inflow portal vein to the outflow hepatic vein

92
Q

What is budd-chiari syndrome?

A

Hepatic vein thrombosis

Due to obstruction to hepatic venous outflow

93
Q

Causes of budd chairi syndrome

A

Coagulopathy (causing hyper coaguloble state which causes thrombosis in hepatic vein and reduced outflow) - e.g, polycythaemia rubra vera, thrombophillia, antiphospholipid syndrome

Obstructive cause (physical obstruction to hepatic vein) - e.g, tumour compressing on hepatic vein

94
Q

Triad of budd-chiari syndrome

A

Abdominal pain - severe sudden onset
Ascites
Tender hepatomegaly

95
Q

What is achalasia?

A

Failure of relaxation of the lower oesophageal sphincter

Usually due to the degenerative loss of ganglia from auerbach’s plexus (myenteric plexus in oesophageal wall)

96
Q

Clinical presentation of achalasia

A

Dysphagia to both liquids and solids from beginning
Heartburn
Regurgitation of food

97
Q

What does a barium swallow show in patients with achalasia?

A

Birds beak appearance - due to grossly expanded oesophagus

98
Q

Management of achalasia

A

Intra-sphincteric injection of botulinum toxin

Laproscopic heller cardiomyotomy - surgery in which the sphincter muscle is cut to open passage between oesophagus and stomach

99
Q

What is Barrett’s oesophagus

A

Metaplasia of lower oesophageal mucosa - squamous epithelium leads to columnar epithelium due to repeated exposure to stomach acid

100
Q

How often do patients with Barrett’s Oesophagus undergo endoscopy?

A

Every 3-5 years to check for malignant transformation (dysplasia)

101
Q

Two types of oesophageal cancer and where they are located

A

Squamous cell - upper 2/3rds of oesophagus

Adenocarcinoma - lower 1/3rd of oesophagus

102
Q

Where are the majority of pancreatic cancers located?

A

Head of pancreas - they are adenocarcinomas

103
Q

What is courvoisier’s law?

A

In the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones

104
Q

What is trousseau sign?

A

Migratory thrombophlebitis
Where pancreatic cancer is associated with repeated attacks of multiple thrombosis at different and changing sites due to procoagulant factors formed by cancer cells
This presents as carpopedal spasm (which can be brought on by inflating a sphygmomanometer) - adduction of thumb, flexion of metacarpophalangeal joins, flexion of wrist

105
Q

What is the sign on USS in pancreatic cancer?

A

Double duct sign - simultaneous dilation of common bile duct and pancreatic ducts

106
Q

What is the surgical procedure called used to remove head of pancreas cancers

A

Whipple’s resection (pancreaticoduodectomy)

107
Q

What are the 2 genetic mutations linked to colon cancer and their prevalence?

A

Hereditary non-polyposis colorectal carcinoma (HNPCC) - 5%, due to mutation in MSH2 or MSH1
Familial adenomatous polyposis (FAP) - 1%, due to mutation in APC

108
Q

Histopathology of Crohn’s disease

A

Inflammation across all layers of bowel wall down to serosa
Skip lesions
Can occur anywhere from mouth to anus

109
Q

Stepwise management of inducing remission in Crohn’s disease

A

1st line - glucocorticoids, e.g, prednisolone
2nd line - 5-ASA drugs e.g, mesalazine
3rd line - azathioprine
4th line - infliximab

110
Q

What has to be checked before starting patients on azathioprine

A

Thiopurine methyltransferase (TPMT) activity - as this is responsible for the metabolism of azathioprine

111
Q

Which type of inflammatory bowel disease may smoking help?

A

Ulcerative colitis

Smoking makes Crohn’s disease worse

112
Q

What medications are used to help maintain remission in Crohn’s disease

A

1st line - azathioprine

2nd line - methotrexate

113
Q

Complications of Crohn’s disease

A

Intestinal fistulas
Bacterial overgrown
Perianal disease
Increased risk of small bowel and colorectal cancer

114
Q

Histopathology of ulcerative colitis

A 
Only inner layer of bowel wall 
Loss of haustral markings 
Appearance of psuedopolpys 
Inflammation in continuous 
Never spreads beyond ileocaecal valve
115
Q

Extra-intestinal features of ulcerative colitis

A

Primary sclerosing cholangitis
Uveitis
Arthritis
Erythema nodosum

116
Q

Management of remission of ulcerative colitis

A

1st line - topical (rectal) aminosalicylate e.g, mesalazine
2nd line - oral aminosalicylate e.g, mesalazine
3rd line - oral corticosteroids e.g, prednisolone

117
Q

Flares of ulcerative colitis severity

A

Mild flare - <4 stools a day
Moderate flare - 4-6 stools a day
Severe flare - >6 stools a day, containing blood, systemic disturbance

118
Q

Management of ulcerative colitis flares

A

Mild flare - rectal aminosalicylate e.g, mesalazine +/- oral mesalazine

Severe flare - hospital admission, IV corticosteroids, consider IV ciclosporin if not improving in 72 hours

119
Q

Complications of ulcerative colitis

A

Toxic megacolon - transverse colon >6cm in diameter

120
Q

Risk factors for C.Diff infection

A

Hospital
Antibiotic use
PPIs

121
Q

Management of C.Diff

A

Oral metronidazole - 10-14 day course

Oral vancomycin - if not responding to metronidazole

122
Q

What is small bowel bacterial overgrown syndrome (SBBOS)?

A

Disorder characterised by excessive amounts of bacteria in the small bowel resulting in GI symptoms

Caused by anything that slows the bowel movements down so bacteria are able to multiply

123
Q

Risk factors for SBBOS

A 
Congenital GI abnormalties I 
Post surgery 
Divertulosis 
Adhesions 
Amyloidosis 
Scleroderma
Diabetes
124
Q

Management of SBBOS

A

Correct underlying disorder

Antibiotic therapy - rifaximin is sometimes used if diagnosis is unclear to see if this helps

125
Q

What is primary biliary cirrhosis/cholangitis?

A

Autoimmne condition where the interlobular bile ducts become damaged causes progressive cholestasis

This can eventually progress to cirrhosis

126
Q

What is the M rule for primary biliary cirrhosis?

A

IgM antibodies
Anti Mitrochondrial antibodies, M2 subtype
Middle aged females

127
Q

Management of primary biliary cirrhosis

A

Ursodeoxycholic acid

Symptomatic management of pruritis - cholestyramine

128
Q

Which rheumatoid conditions are commonly associated with primary biliary cirrhosis?

A

Sjögren’s syndrome - sicca symptoms occur in 70% of cases
Rheumatoid arthritis
Systemic sclerosis

129
Q

What is primary scleorosing cholangitis?

A

Biliary disease of unknown cause characterised by infalmmation and fibrosis of intra and extra hepatic ducts

130
Q

Main association of primary sclerosing cholangitis

A

Ulcerative colitis

131
Q

Cancer associated with primary sclerosing cholangitis

A

Cholangiocarcinoma

132
Q

Types of bowel Ischaemia and characteristics

A

Acute mesenteric ischaemia - typically caused by embolism occlusion of artery, patients classically have AF, severe abdo pain
Chronic mesenteric ischaemia - intestinal angina, colicky abdo pain
Ischaemic colitis - acute but transient compromise in blood flow to small bowel

133
Q

What can be seen on an abdo X-Ray in patients with ischaemic colitis

A

Thumb printing - due to mucosal oedema/haemorrhage

134
Q

Which type of bowel ischaemia is cocaine use associated with?

A

Ischaemic colitis

135
Q

Management of acute mesenteric ischaemia

A

Urgent surgery

136
Q

Management of Ischaemic colitis

A

Supportive - analgesia, fluids
Thrombolytic therapy
Angioplasty
Maybe surgery

137
Q

What is rosvig’s sign?

A

Appendicitis sign

Palpation in left iliac Fossa causes pain in right iliac fossa

138
Q

What are the metabolic abnormalities in refeeding syndrome?

A

Hypophosphataemia
Hypokalaemia
Hypomagnesaemia

139
Q

Risk factors for refeeding syndrome

A

BMI <18
Unintentional weight loss >10% over 3-6 months
Little nutritional intake for >5 days
History of alcohol abuse, insulin use, chemotherapy, diuretics

140
Q

Which is the only test licensed for use to check that H.Pylori eradication therapy has worked?

A

Urea breath test

141
Q

Precipitating factors for hepatic encephalopathy

A

Infection e.g, spontaneous bacterial peritonitis
GI bleed
Constipation
Post transjugular intrahepatic portosystemic shunt

142
Q

Management of hepatic encephalopathy

A

Lactulose - promotes secretion of ammonia

143
Q

Prophylaxis of hepatic encephalopathy

A

Lactulose

Rifaximin

144
Q

Blood results findings in alcoholic hepatitis

A

Raised GGT

Raised AST:ALT ratio

Year 5 (17 decks)

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