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Year 6 > GI > Flashcards

GI Flashcards

1
Q

Define Porphyria

A

A spectrum of disorders arising from abnormalities in haem synthesis pathway

Can be classified as acute or non-acute

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2
Q

What are the most common examples of acute porphyrias?

A

Acute intermittent porphyria and variegate porphyria

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3
Q

What are triggers for acute porphyrias?

A
  • Abx = rifampicin, isoniazid, nitrofurantoin
  • Anaesthetic agents = ketamine, etomidate
  • Sulphonamides
  • Barbiturates
  • Antifungal agents
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4
Q

Acute porphyria features

A
  • Abdo pain
  • Nausea
  • Confusion
  • Hypertension
  • Seizures
  • Purple/red urine
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5
Q

Acute porphyria investigations

A

urinary porphobilinogen levels - make sure to protect the sample from light to prevent breakdown of the compound

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6
Q

Acute porphyria management

A

Mainly supportive, but can give haem arginate IV to replenish haem levels and reduce disease severity

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7
Q

Alcohol withdrawal features

A

Simple withdrawal (6-12 hours after last drink):
- Insomnia
-Tremor
- Anxiety
- Agitation
- N&V
- Sweating
- Palpitations

Alcohol hallucinosis (12-24 hours after last drink):
- Hallucinations of visual, tactile or auditory origins

Delirium tremens (72 hours after last drink)
- Delusions
- Confusion
- Seizures
- Tachycardia
- HTN
- Hyperthermia

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8
Q

What are the indications for inpatient treatment of Alcohol withdrawal?

A
  • Pt drinks >30 units per day
  • Score >30 on SADQ score
  • High risk of withdrawal seizures
  • Concurrent withdrawal from benzo’s
  • Psychiatric or medical comorbidities
  • Vulnerable pt
  • Pt under 18
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9
Q

Alcohol withdrawal management

A
  • Chlordiazepoxide in a reducing regimen
  • Rapid acting benzo’s (e.g. IV lorazepam) for withdrawal seizures
  • Pabrinex
  • Oral lorazepam is 1st line for treating DT, w/ parenteral loraz/diazepam 2nd line
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10
Q

What are the stages of Alcoholic liver disease?

A

1) Fatty liver disease = reversible w/ abstinence
2) Alcoholic hepatitis
3) Cirrhosis

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11
Q

Alcoholic liver disease features

A

1) Fatty liver disease = asymptomatic, may have some hepatomegaly
2) Alcoholic hepatitis = jaundice, fever, tender hepatomegaly, N&V, malaise
3) Cirrhosis = jaundice, ascites, hepatic encephalopathy, bleeding tendencies, spider naevi, palmar erythema

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12
Q

Alcoholic liver disease management

A

Conservative:
- Abstinence
- Nutritional support

Medical:
- Alcoholic hepatitis = 1-3 months of oral prednisolone for severe cases (Maddery’s DF > 32)
- Cirrhosis = manage complications

Surgical:
- Liver transplant for cirrhotic pts

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13
Q

What is Maddrey’s discriminant function?

A

A function which predicts prognosis in alcoholic hepatitis and identifies pts who would benefit from treatment w/ steroids

Can be found online

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14
Q

Alpha-1 antitrypsin deficiency definition

A

Genetic deficiency in the alpha-1 antitrypsin deficiency enzyme which usually inhibits neutrophil elastase

This results in emphysema and liver cirrhosis

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15
Q

Alpha-1 antitrypsin deficiency features

A
  • COPD in pts 30-40
  • Neonatal jaundice
  • Deranged LFTs in adults w/ no other identifiable cause and cirrhosis
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16
Q

Alpha-1 antitrypsin deficiency investigations

A
  • Spirometry shows obstructive picture
  • Alpha-1 antitrypsin deficiency levels are low
  • Genotyping
  • CXR shows emphysema
  • Liver biopsy = Periodic acid Schiff +ve globules
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17
Q

Alpha-1 antitrypsin deficiency management

A
  • Smoking cessation
  • IV A1AT (not widely used due to cost)
  • Liver transplant
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18
Q

What causes of nausea is Cyclazine (H1 receptor antagonist) best for?

A

Vestibular disturbances

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19
Q

What causes of nausea are Domperidone or metoclopramide (D2 receptor antagonist) best for?

A

Post-operative nausea, motion sickness (avoid in bowel obstruction as they also increase gut motility)

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20
Q

What causes of nausea is Ondansetron (5HT3 receptor antagonist) best for?

A

Acute gastroenteritis, post-operative nausea, radiotherapy- or chemotherapy-induced

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21
Q

What causes of nausea is Hyoscine hydrobromide (Anti-muscarinic) best for?

A

Vestibular disturbances, palliative care

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22
Q

Ascites investigation

A
  • Ascitic tap done under US guidance
  • Serum ascites albumin gradient (SAAG)
  • Bloods
  • Imaging
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23
Q

What is Serum ascites albumin gradient (SAAG)?

A

A calculation used to determine the cause of the ascites:

Serum albumin concentration - ascites albumin concentration

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24
Q

What are causes of ascites with a high SAAG (>11 g/L)?

A

High SAAG suggests that the cause is due to raised portal pressure as water is being forced into the peritoneal cavity whilst albumin stays w/in the vessel - results in a higher difference between serum and ascites albumin concentrations

Causes:
- Cirrhosis
- RHF
- Budd-Chiari syndrome
- Constrictive pericarditis
- Liver failure

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25
Q

What are causes of ascites with a low SAAG (<11 g/L)?

A
  • Cancer/mets in the peritoneum
  • Infections = TB, peritonitis
  • Pancreatitis
  • Hypalbuminaemia = nephrotic syndrome, Kwashiorkor (severe protein malnutrition)
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26
Q

Ascites management

A
  • Treat underlying cause
  • High SAAG = salt-restricted diet and fluid restriction
  • Spironolactone = 1st line treatment, add furosemide if it ineffective alone
  • If pt is refractory to medical management - give regular paracentesis’s
27
Q

Define Spontaneous bacterial peritonitis

A

Bacterial infection of ascitic fluid - a serious complication of ascites

28
Q

Spontaneous bacterial peritonitis investigations

A

Ascitic tap showing neutrophils >250

29
Q

Spontaneous bacterial peritonitis management

A

Acute = IV Tazocin

Prophylactic = ciprofloxacin - given if ascitic protein is high

30
Q

Classification of Autoimmune hepatitis

A

3 different types classified by antibodies:

1) ANA +ve w/ anti-smooth muscle abs
2) Anti-liver/kidney mitochondrial type 1 (LKM1) abs - more common in children
3) Anti soluble liver-kidney antigen

31
Q

Autoimmune hepatitis features

A

Can present as acute hepatitis:
- Fever
- Jaundice
- Malaise
- Abdo pain
- Urticarial rash
- Polyarthritis
- Pulmonary infiltrates
- Glomerulonephritis

Can present as chronic liver disease:
- Ascites
- Jaundice
- Leukonychia
- Spider naevi

Other symptoms:
- Fatigue
- Anorexia
- Hepatomegaly
- Splenomegaly

32
Q

Autoimmune hepatitis investigations

A
  • Bloods = deranged LFTs showing a hepatic pattern - raised ALT and bilirubin, normal or mildly raised ALP
  • IgG predominant hypergammaglobulinemia
  • Specific antibody testing
33
Q

Autoimmune hepatitis management

A

1st line = prednisolone for acute flairs and then maintenance w/ azathioprine

2nd line = other immunosuppressants

3rd line = liver transplant

34
Q

Define Barrett’s oesophagus

A

Metaplasia of the distal 1/3 oesophagus from the usual squamous epithelium to columnar epithelium - increases the risk of oesophageal adenocarcinoma 100-fold

Causes by long-term GORD

35
Q

Barrett’s oesophagus management

A

Conservative:
- Manage the GORD
- If there is a short-segment (<3cm) of Barrett’s oesophagus w/out intestinal metaplasia then no further surveillance is required

Surveillance:
- Long-segment (>3cm) Barrett’s oesophagus = repeat OGD every 2-3 years
- Short-segment Barrett’s oesophagus w/ intestinal metaplasia = repeat OGD every 3-5 years
- Indefinite dysplasia = OGD every 6 months

Ablation:
- Pts w/ dysplasia are eligible for ablation therapy
1 1st line = endoscopic ablation of visualised lesions

36
Q

Define Budd-Chiari syndrome

A

The obstruction of hepatic venous outflow, either due to thrombosis or compression of the hepatic veins and/or the IVC

This obstruction impedes the normal drainage of blood from the liver, leading to increased hepatic sinusoidal pressure causing congestion and ischaemia - eventually leads to fibrosis and cirrhosis

37
Q

Budd-Chiari syndrome features

A

Range from asymptomatic to fulminant liver failure:

  • RUQ pain
  • Hepatomegaly
  • Jaundice
  • Ascites
  • Peripheral oedema
  • Splenomegaly
  • Variceal bleeding
38
Q

Budd-Chiari syndrome investigations

A

Bedside:
- Abdo exam

Bloods:
- LFTs
- FBCs and coagulation
- Serum albumin
- Ascitic tap showing high SAAG due to portal HTN

Imaging:
- Doppler USS = initial test to assess blood flow in the hepatic veins and IVC
- MRI or CT angiography = see extent of obstruction
- Hepatic venography = directly visualize veins and measure pressure

Invasive:
- Liver biopsy = assess degree of liver damage and fibrosis

39
Q

Budd-Chiari syndrome management

A
  • Anticoagulation depending on underlying cause
  • Thrombolytic therapy
  • Angioplasty and stenting
  • Transjugular Intrahepatic Portosystemic Shunt = to reduce portal HTN and improve blood flow
  • Liver transplant if liver failure
40
Q

Define Carcinoid tumour

A

Slow-growing neuroendocrine tumours that typically originate in the appendix and small intestine

5-10% secrete serotonin

Have the potential to become malignant

41
Q

Carcinoid tumour features

A

Symptoms usually only occur when the pts has liver mets which allow the serotonin to enter systemic circulation w/out undergoing metabolism - this is called carcinoid syndrome:

  • Abdo pain
  • Diarrhoea
  • Flushing
  • Wheezing
  • Pulmonary stenosis
42
Q

Carcinoid tumour investigations

A
  • Urine 5-HIAA levels = breakdown product of serotonin
  • Imaging = CT, MRI or octreotide scans
  • Tissue biopsy = definitive diagnosis through histology
43
Q

Carcinoid tumour management

A
  • Octreotide = somatostatin analogue which blocks the production of hormones by the tumour
  • Surgical resection
  • Embolism, radio/chemotherapy based on the extent of disease
44
Q

Cholera features

A
  • Sudden onset watery diarrhoea
  • Abdo cramps
  • N&V
  • Excessive thirst
  • Dry mouth and mucus membranes
  • Oliguria
  • Drowsiness or lethergy
  • Irritability
45
Q

Cholera investigations

A
  • Stool culture = gold standard
  • Rapid diagnostic tests = can give results w/in hrs but less sensitive and specific than stool culture
46
Q

Cholera management

A
  • Aggressive fluid replacement
  • Doxycycline or co-trimoxazole can decrease the volume of diarrhoea by 50% and is recommended in pts w/ moderate to severe dehydration
47
Q

What are risk factors for developing C. diff?

A
  • Abx = clindamycin, ciprofloxacin, 3rd gen cephalosporins (e.g. ceftriaxone), penicillins, Tazocin, carbapenems
  • Long stay in healthcare setting
  • > 65
  • IBD, cancer r kidney disease
  • Immunocompromised
  • Taking a PPI
48
Q

C. diff features

A
  • Watery diarrhoea which can be bloody
  • Painful abdo cramps
  • Nausea
  • Signs of dehydration
  • Fever
  • Anorexia
  • Confusion
  • Pseudomembranous colitis on XR
    Classically has a raised WCC w/ little change in CRP
49
Q

C. diff management

A
  • Stop abx if possible
  • Move to side room immedietly
  • Abdo X-ray looking for megacolon
  • PO vancomycin for first episode
  • If recurrent or persistent - switch to PO fidaxomicin
  • If severe (signs of shock) add IV metronidazole
50
Q

Coeliac disease features

A

GI:
- Abdo pain
- Distention
- N&V
- Diarrhoea
- Steatorrhea

Systemic:
- Fatigue
- WL or failure to thrive in children
- Signs of vitamin deficiency = bruising (vit K)
- Dermatitis herpetiformis

51
Q

Coeliac disease investigations

A

Serology = 1st line - Anti-TTG IgA antibodies and IgA levels, followed by anti-TTG IgG and anti-endomyseal antibodies

OGD and duodenal/jejunal biopsy is gold standard for diagnosis

Pt needs to have been eating gluten for 6 wks before the tests for them to be valid

52
Q

Dermatitis herpetiformis management

A

Dapsone

53
Q

What are the 2WW criteria for constipation?

A

Constipation (or diarrhoea) w/ WL in pts 60+

Consider urgent CT/US to rule out pancreatic cancer

54
Q

Give an example of a bulk forming laxative, explain how they work and the common side effects

A

Ispaghula husk

Works by increasing faecal mass to stimulate peristalsis

SE = Bloating and flatulence

55
Q

Give an example of a stimulant laxative, explain how they work and the common side effects

A

Senna

Increases intestinal motility for short-term relief

SE = cramps

56
Q

Give an example of a stool softening laxative, explain how they work and the common side effects

A

Macrogol, sodium docusate

Increases water and fat absorbance in the stool to soften it and make it easier to pass

SE = flatulence, nausea

57
Q

Give an example of an osmotic laxative, explain how they work and the common side effects

A

Lactulose

Pulls water into the stool, or stops it being drawn out

SE = abdo discomfort, flatulence, diarrhoea, electrolyte imbalances

1st line in hepatic encephalopathy due to its inhibition of ammonia-forming microorganisms

58
Q

How do Phosphate enemas work?

A

Increases the fluid in the small bowel and causes a motion w/in 1-5 minutes

59
Q

Crohn’s features

A

GI Symptoms:
- Crampy abdo pain
- Non-bloody diarrhoea
- Perianal disease
- WL
- Fever

Dermatological:
- Erythema nodosum
- Pyoderma gangrenosum

Ocular:
- Anterior uveitis
- Episcleritis

MSK:
- Enteropathic arthropathy (symmetrically, non-deforming)
- Axial spondyloarthropathies

Hepatobiliary:
- Gallstones due to reduced bile acid reabsorption and increased Ca loss

Haematological:
- AA amyloidosis
- Renal stones

Signs:
- Anaemic
- Clubbing
- Aphthous ulcers in the mouth
- RLQ tenderness, RIF mass
- PR = skin tags, fistulae, perianal abscess

60
Q

Crohn’s investigations

A

Bedside:
- Stool culture to exclude infection
- Faecal calprotectin (antigen produced by neutrophils - will be raised)

Bloods:
- Raised WCC, CRP, ESR
- Thrombocytosis
- Anaemia
- Low albumin (malabsorption)

Imaging:
- Endoscopy required for diagnosis - will show skip lesions, cobblestone mucosa, transmural inflammation and non-caseating granulomas

61
Q

Crohn’s management

A

Inducing remission (treating flares):
- Monotherapy w/ steroids = oral pred or IV hydrocortisone (if 1st presentation and severe enough to require admission)
- Biologics

Maintaining remission:
- Azathioprine or mercaptopurine if 2 or more flares in 12 month period, or the steroid cannot be tapered
- Methotrexate can be used/added in pts who are intolerant to or uncontrolled on the above drugs
- Biologics (infliximab or adalimumab) in severe cases unresponsive to dual therapy

Surgical:
- Used to control fistulae, resect strictures or rest/defunction the bowel

62
Q

Perianal fistulae management

A

High (trans-sphincter) fistula = drainage seton

Low (submucosal) fistula = fistulotomy (dissecting the superficial tissue and opening the tract)

Cant do a fistulotomy in a high fistula as you cant cut the sphincter

63
Q

Perianal abscess management

A
  • IV ceftriaxone + metronidazole
  • Incision and drainage under GA - wound heals by secondary intention (edges not brought together)

Year 6 (8 decks)

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