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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
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27
Q

Define Spontaneous bacterial peritonitis

A

Bacterial infection of ascitic fluid - a serious complication of ascites

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28
Q

Spontaneous bacterial peritonitis investigations

A

Ascitic tap showing neutrophils >250

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29
Q

Spontaneous bacterial peritonitis management

A

Acute = IV Tazocin

Prophylactic = ciprofloxacin - given if ascitic protein is high

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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

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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

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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
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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

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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

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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

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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

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37
Q

Budd-Chiari syndrome features

A

Range from asymptomatic to fulminant liver failure:

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

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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
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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

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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
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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
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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
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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
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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
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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
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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
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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
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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
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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

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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

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52
Q

Dermatitis herpetiformis management

A

Dapsone

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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

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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

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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

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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

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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

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58
Q

How do Phosphate enemas work?

A

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

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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

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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

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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

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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

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63
Q

Perianal abscess management

A
  • IV ceftriaxone + metronidazole
  • Incision and drainage under GA - wound heals by secondary intention (edges not brought together)
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64
Q

Which drugs are Cytochrome P450 inducers?

A

CRAP GPS induces rage:
- Carbamazepine
- Rifampicin
- Alcohol
- Phenytoin
- Griseofulvin
- Phenobarbitone
- Sulphonylureas

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65
Q

Which drugs are Cytochrome P450 inhibitors?

A

SICKFACE.COM:
- Sodium valproate
- Isoniazid
- Cimetidine
- Ketoconazole
- Fluconazole
- Alcohol and grapefruit juice
- Chloramphenicol
- Erythromycin
- Sulphonamides
- Ciprofloxacin
- Omeprazole
- Metronidazole

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66
Q

What common drugs are metabolised by Cytochrome P450 enzymes?

A

Clopidogrel, statins, warfarin, OCP

There doses need to be reduced if taking inhibitors, and increased when taking inducers

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67
Q

Define Dyspepsia

A

A constellation of upper GI symptoms, such as epigastric pain, bloating, belching, early satiety and nausea, w/out evidence of structural or biochemical abnormalities

It requires assessment for ALARM symptoms

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68
Q

What are ALARM symptoms in dyspepsia?

A
  • Anaemia
  • Loss of weight
  • Anorexia
  • Recent onset of symptoms
  • Melaena/haematemesis
  • Swallowing difficulties
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69
Q

Dyspepsia management

A

Conservative:
- Smoking cessation
- WL
- Avoiding trigger foods
- Smaller meals

Medical:
- Stop offending medications = alpha/beta blockers, anticholinergics, aspirin, CCBs, corticosteroids, NSAIDs, TCA’s, bisphosphonates

Medical:
- PPI trial for 1 month

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70
Q

What are the causes of Dysphagia?

A

Neuro:
- Cerebrovascular disease
- Parkinson’s disease
- MND
- Myasthenia gravis
- Bulbar palsy

Motility disorders:
- Achalasia
- Diffuse oesophageal spasms
- Systemic sclerosis

Mechanical causes:
- Benign strictures
- Malignancy
- Pharyngeal pouch
- Lung cancer
- Mediastinal lymph nodes
- Retrosternal goitre

Other:
- Oesophagitis
- Globus
- Plummer-Vinson syndrome

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71
Q

Define Plummer-Vinson syndrome

A

A complication of long-term iron def anaemia where there are small web-like growths of tissue which partially block the oesophagus

Causes dysphagia

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72
Q

Define Enteric fever

A

Infection w/ salmonella typhi or salmonella paratyphi

Symptoms appear 6-30 days after exposure

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73
Q

Enteric fever features

A
  • High fever
  • Weakness
  • Myalgia
  • Relative bradycardia
  • Abdo pain
  • Constipation
  • Headaches
  • Vomiting (not usually severe)
  • Skin rash w/ rose-coloured spots
  • Confusion (if severe)
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74
Q

Enteric fever management

A
  • A-E for acutely unwell pts
  • Azithromycin or ceftriaxone
  • Typhoid is a notifiable disease
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75
Q

GORD management

A
  • For Pts <40 w/ typical symptoms and no red flags = 8 wks of PPI + lifestyle changes
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76
Q

Campylobacter gastroenteritis summary

A

From contaminated food

Incubation period = 16-48hrs

Causes bloody diarrhoea

Treated w/ macrolides e.g. clarithromycin

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77
Q

E.coli gastroenteritis summary

A

Most common cause of travellers diarrhoea

From improperly cooked meat

Treated w/ fluids

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78
Q

Salmonella gastroenteritis summary

A

From contaminated poulty, eggs and milk

Incubation period = 16-48 hrs

Causes bloody diarrhoea

Treated w/ fluids

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79
Q

Shigella gastroenteritis summary

A

Faecal-oral route

Incubation period = 1-4 days

Causes severe bloody diarrhoea

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80
Q

Bacillus cereus gastroenteritis summary

A

From contaminated foods - usually reheated rice

Causes vomiting and diarrhoea due to 2 toxins

Incubation period = 0.5-6 hours for vomiting and 8-16 hours for diarrhoea

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81
Q

Staph aureus gastroenteritis summary

A

Causes profuse vomiting w/ mild diarrhoea and abdo pain

Incubation period = <6 hrs

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82
Q

Which parasites cause gastroenteritis, and how do they present?

A
  • Cryptosporidium = prolonged GI symptoms
  • Entamoeba histolytica = ranges from mild-severe dysentery
  • Giardia = explosive watery diarrhoea, constitutional symptoms and bloating - may last a long time

These can be treated w/ metronidazole

83
Q

Define Gastroparesis

A

A chronic medical condition characterised by delayed gastric emptying w/out any mechanical obstruction in the stomach

It arises due to impaired activity of the stomach muscles which causes the stomach to take longer than usual to empty its contents

84
Q

What are the causes of Gastroparesis?

A

Most common = autonomic neuropathy in DM

Other causes = post-surgical complication, meds, Parkinson’s, MS

85
Q

Gastroparesis features

A
  • N&V
  • Early satiety
  • Abdo pain
  • Bloating

Can lead to poor glucose level management in diabetics due to delayed absorption of food

86
Q

Gastroparesis investigations

A

Solid meal gastric scintigraphy (AKA radionucleotide study of gastric emptying)

This allows for visualisation of gastric emptying

87
Q

Gastroparesis management

A
  • Dietary modifications = low fibre diet, smaller but more frequent meals, consumption of pureed food
  • Medical = Prokinetic meds - Metoclopramide (1st line), domperidone or erythromycin
88
Q

Which cause of gastroenteritis can lead to lactose intolerance?

A

Giardiasis

89
Q

Define Gilbert’s syndrome

A

An autosomal recessive disorder where there is decreased activity of the enzyme that conjugates bilirubin

90
Q

Gilbert’s syndrome features

A

intermittent episodes of mild unconjugated jaundice triggered by stress, fasting injections or exercise

91
Q

H. pylori investigations

A

1st line = stool test or carbon-13 urea breath test

If having an OGD, rapid urease test (CLO) can be done

92
Q

How do the different Hepatitis viruses present?

A

Hep A and E = acute hepatitis:
- Prodromal viral illness
- RUQ pain
- Jaundice
- Tender hepatosplenomegaly (due to swelling of the liver capsule)

Hep B or C = chronic hepatitis:
- Jaundice
- Ascites
- Coagulopathy
- Hepatic encephalopathy

Hep D can only occur in individuals who are infected with hep B

93
Q

What is the incubation time of Hepatitis A?

94
Q

What does Hepatitis B surface antigen indicate?

A

Current infection - can persist for up to 6 months

95
Q

What does anti-hep B surface antigen indicate?

A

Immunity from past infection or vaccination

96
Q

What does Hepatitis B e antigen indicate?

A

Acute active viral replication

97
Q

What does Hepatitis B e antibody indicate?

A

Lower viral replication due to seroconversion

98
Q

What does Hepatitis B core antibody indicate?

A

IgM indicates acute infection

IgG indicates past infection or vaccination

99
Q

Hep B investigations

A
  • Hep B antigen testing
  • Biopsy = ground glass hepatocytes
100
Q

Hep B management

A
  • 1st line = Pegylated interferon alpha-2a (doesn’t cure the infection, but stops liver disease)
  • 2nd line = tenofovir and entecavir (antivirals)
101
Q

What additional symptoms can occur in Hep C other than chronic liver disease?

A
  • arthralgia/arthritis
  • Sjogren’s syndrome
  • Cryoglobulinemia
  • Porphyria cutanea tarda
  • Membranoproliferative glomerulonephritis
102
Q

Hep C management

A
  • Nucleoside anologues = sofosbuvir + daclatasvir
  • Antivirals
103
Q

Risk factors for Hepatocellular carcinoma

A

Chronic liver disease and cirrhosis

104
Q

Hepatocellular carcinoma features

A
  • Abdo pain
  • WL
  • Jaundice
  • Ascites
  • Hepatomegaly w/ a craggy liver edge on examination
  • Encephalopathy
105
Q

Hepatocellular carcinoma investigations

A
  • Increased alpha-fetoprotein (AFP) = tumour marker
  • Abdo USS is 1st line imaging
  • Liver biopsy is gold standard for diagnosis
  • CT CAP +/- PET for staging

Pts w/ liver cirrhosis have 6 monthly HCC screening AFPs +/- USS

106
Q

Hepatocellular carcinoma management

A
  • Radical resection if lesion < 3cm
  • Percutaneous radiofrequency ablation and tumour embolisation
  • Liver transplant
  • Palliative for advanced disease
107
Q

Define Hereditary haemochromatosis

A

A genetic disorder of iron metabolism which leads to excessive iron deposition in the heart, liver, joints, pituitary, pancreas and skin

108
Q

Hereditary haemochromatosis features

A
  • Bronze skin
  • T2DM
  • Fatigue
  • Joint pain
  • Liver disease/cirrhosis features
  • Adrenal insufficiency
  • Testicular atrophy
  • Dilated cardiomyopathy
109
Q

Hereditary haemochromatosis investigations

A

Iron studies:
- Raised transferrin saturation (>55% in women, >50% in men)
- Raised ferritin
- Raised iron
- Low total iron binding capacity

Genetic testing
MRI brain and heart to look for iron deposition
Liver biopsy to confirm iron overload

110
Q

Hereditary haemochromatosis management

A
  • Venesection = stimulates erythropoiesis and mobilises iron from parenchymal cells and other storage sites - target transferrin <50%
  • Desferrioxamine = iron chelating agent
111
Q

Define Hiatus hernia

A

Where abdominal contents protrude through an enlarged oesophageal hiatus in the diaphragm

112
Q

What are the 2 types of Hiatus hernia?

A

Sliding (80%):
- Where the gastro-oesophageal junction slides up into the chest
- This results in a less competent sphincter and consequent acid reflux

Rolling (20%):
- Where the gastro-oesophageal junction stays in the abdomen, but a part of the stomach protrudes into the chest alongside the oesophagus
- Requires more urgent treatment since volvulus can occur and lead to ischaemia

113
Q

Hiatus hernia features

A
  • Dysphagia
  • Regurgitation
  • Odynophagia
  • Dyspepsia
  • SOB
  • Chronic cough
  • Chest pain
114
Q

Hiatus hernia investigations

A
  • Barium swallow is most sensitive
  • Endoscopy
  • Oesophageal manometry
115
Q

Hiatus hernia management

A

Conservative:
- WL
- Elevating head of the bed
- Avoidance of alcohol and acidic foods
- Smoking cessation (nicotine relaxes the lower oesophageal sphincter)

Medical = PPI’s for 4-8 weeks before assessing response

Surgical = Nissen’s fundoplication (closing defect by tightening the crura and wrapping the gastric fundus around the LOS)

116
Q

Which drugs most commonly cause iatrogenic diarrhoea?

A
  • Magnesium
  • Abx - esp penicillins
  • Chemo agents
  • PPIs
  • H2 blockers = cimetidine and ranitidine
  • NSAIDs
  • Metformin
117
Q

Which drugs most commonly cause iatrogenic constipation?

A
  • Anti-depressants
  • Anti-psychotics
  • Levodopa
  • Aluminium-based antacids
  • Iron supplements
  • Opiates
118
Q

What are the Manning criteria for diagnosis of IBS?

A

Abdo discomfort or pain relieved by defecation OR associated w/ altered bowel frequency or stool form

AND at least 2 of the following:
- altered stool passage (e.g. straining or urgency)
- Abdo bloating
- Symptoms worsened by eating
- Passage of mucus

119
Q

IBS investigations

A

Rule out organic diseases w/:
- Faecal calprotectin
- FBC, ESR/CRP
- Coeliac serology

120
Q

IBS management

A

Conservative:
- Exercise
- Stress management
- Dietary changes (e.g low-FODMAP diet)

Medical:
- Mebeverine (antispasmodic)
- Laxatives
- Imodium
- Low dose TCA (2nd line)

121
Q

What are the causes of Jaundice?

A

Pre-hepatic:
- Conjugation disorders = Gilbert’s, Crigler-Naajjar
- Haemolysis
- Drugs = contrast, rifampicin

Hepatic (hepatocellular dysfunction):
- Viruses
- Drugs = paracetamol OD, nitrofurantoin, halothane, valproate, statins, TB treatment
- Alcohol
- Cirrhosis
- Liver mass (abscess or malignancy)
- Haemochromatosis
- AI hepatitis
- Alpha-1 antitrypsin deficiency
- Budd-Chiari
- Wilson’s disease

Post-hepatic:
- PBC
- PSC
- Gallstones in CBD
- Drugs = coamox, flucloxacillin, steroids, sulfonylureas
- Pancreatic malignancy
- Cholangiocarcinoma
- Biliary atresia

122
Q

Jaundice investigations

A

Bedside:
- Urine dip for urobilinogen levels - raised in pre-/hepatic jaundice, but decreased in obstructive jaundice

Bloods:
- FBCs, U&Es, LFTs, split bilirubin
- Synthetic liver function tests (albumin, coag screen)

Imaging:
1st = abdo USS to look for duct dilation
2nd = MRCP
- Liver biopsy may be done

123
Q

Define Liver Cirrhosis

A

Irreversible scarring of the liver w/ loss of normal hepatic architecture

124
Q

What are the causes of Liver Cirrhosis?

A

Common:
- Alcohol
- Hep B and C
- MAFLD

AI:
- AI hepatitis
- PBC
- PSC
- Sarcoid

Genetic:
- Haemochromatosis
- Wilson’s
- A1AT

Drugs:
- Methotrexate
- Amiodarone
- isoniazid

Other:
- Budd-Chiari
- Heart failure
- Tertiary syphilis

125
Q

Liver Cirrhosis features

A

Compensated cirrhosis:
- Fatigue
- Anorexia and cachexia
- Nausea and abdo pain
- Spider naevi
- Gynaecomastia
- Clubbing
- Leukonychia
- Dupuytren’s contracture
- Caput medusae
- Splenomegaly

Decompensated cirrhosis:
- Above features
- Ascites and oedema
- Jaundice
- Pruritus
- Palmar erythema
- testicular atrophy
- Easy bruising
- Hepatic encephalopathy
- Liver flap

126
Q

How is Liver Cirrhosis severity calculated?

A

Charles-Pugh score - is a predictor of mortality and transplant need

127
Q

Liver Cirrhosis management

A

Conservative:
- Good nutrition and no alcohol
- Avoid NSAIDs, sedatives and opiates
- 6 monthly USS and serum AFP to monitor for hepatocellular cardinoma
- OGD for varices every 3 years

Medical:
- Cholestyramine for itching
- Ascites management
- Prophylactic lactulose and rifaximin for encephalopathy
- Prophylactic abx in those at risk of spontaneous bacterial peritonitis

Surgical:
- Liver transplant

128
Q

Define Liver failure

A

The loss of liver function and the development of complications including jaundice, coagulopathy or encephalopathy

It can be:
- Hyperacute = onset <7 days
- Acute = onset 8-21 days
- Subacute = onset 4-26 weeks
- Chronic = on a background of cirrhosis

128
Q

What is the pathology of hepatic encephalopathy?

A

In liver failure, ammonia accumulates in the circulation

It can cross the BBB, and once in the cerebral circulation it is detoxified by astrocytes which form glutamine

The excess glutamine disrupts the oncotic balance and the astrocytes begin to swell, causing cerebral oedema

129
Q

What are the 4 stages of hepatic encephalopathy?

A

1) Altered mood and behaviour, disturbance of sleep pattern and dyspraxia
2) Drowsiness, confusion, slurring of speech and personality changes
3) Incoherency, restlessness, asterixis
4) Coma

130
Q

Management of Hepatic encephalopathy

A
  • Grade the encephalopathy
  • Give lactulose = increases ammonia loss through bowels
  • Rifaximin = abx which reduces nitrogen forming organisms in the gut
  • IV mannitol can reduce the cerebral oedema
131
Q

Define Hepatorenal syndrome

A

A triad of cirrhosis, ascites and renal failure

Occurs due to portal HTN which leads to release of vasoactive mediators and splanchnic vasodilation - this reduces renal perfusion, causing a pre-renal AKI

2 types:
1) Rapidly progressive - treated w/ terlipressin 2
2) Slowly progressive - treated w/ midodrine (alpha agonist)

132
Q

Define Malnutrition

A
  • BMI < 18.5
  • Unintentional WL >10% w/in 3-6 months
  • BMI <20 and unintentional WL >5% w/in 3-6 months
133
Q

Malnutrition classification

A

Undernutrition:
- Marasmus = deficiency in carbs, fats and proteins - causes visible wasting of fat and muscles under the skin
- Kwashiorkor = deficiency in protein - causes bilateral swelling of the extremities and abdomen
- Vitamin deficiencies

Overnutrition:
- Metabolic syndrome

134
Q

Define Metabolic syndrome

A

A group of conditions that together increase a persons risk of CVD, T2DM and stroke.

These are:
- Excessive abdo fat - waist circumference > 40 inches in men or > 35 inches in women
- Hypertriglyceridemia (>150 mg/dl)
- Low HDL levels
- Raised fasting plasma glucose (>6.1)
- Raised BP - systolic > 135, diastolic > 85

135
Q

Define Melanosis coli

A

A histological condition associated w/ chronic stimulant laxative abuse (esp Senna)

Characterised by the presence of dark brown pigmentation (necrosis and apoptosis) of the macrophages in the lamina propria of the colon - detected by colonoscopy

Not typically harmful, but a useful sign of laxative abuse

136
Q

Define Mucosa-associated lymphoid tissue (MALT)

A

A NHL that usually occurs in the stomach and is associated with H. pylori infection and chronic inflammation

137
Q

Mucosa-associated lymphoid tissue (MALT) features

A
  • Abdo pain
  • N&V
  • Anaemia
  • WL
138
Q

Mucosa-associated lymphoid tissue (MALT) investigations

A
  • Endoscopy and biopsy
  • Immunohistochemistry to identify B cell linage
  • Staging CT/PET
139
Q

Mucosa-associated lymphoid tissue (MALT) management

A
  • H pulori eradication
  • Chemo/radioT if that didnt cure, or if H. pylori -ve
  • Can add rituximab in severe cases
140
Q

What are the stages of Metabolic associated fatty liver disease (MAFLD)?

A

1) Simple steatosis
2) Metabolic associated steatohepatitis (MASH)
3) Fibrosis ad cirrhosis

141
Q

What are the causes of MAFLD?

A
  • Metabolic syndrome
  • Rapid WL or prolonged starvation
  • PCOS
  • Hypothyroidism
  • OSA
142
Q

MAFLD investigations

A
  • Bloods = LFTs, FBC, fasting glucose and lipids, tests to exclude other pathologies
  • Imaging = USS (1st line), Elastography (AKA FibroScan - measures liver stiffness to ass fibrosis), Enhanced liver fibrosis test (blood test assessing markers of fibrosis)
  • Liver biopsy (gold standard)
143
Q

MAFLD management

A

Conservative:
- Lifestyle mods = WL, exercise dietary changes
- Avoid hepatotoxic drugs

Medical:
- Metabolic management = control DM, hyperlipidaemia and HTN

Monitoring:
- Screen for hepatocellular carcinoma in cirrhotic pts

144
Q

Causes of portal hypertension

A
  • Cirrhosis or fibrosis
  • Portal vein thrombosis
  • Schistosomiasis
145
Q

Oesophageal varices features

A

Asymptomatic till they bleed

  • Haematemesis
  • Melena
  • Palpitations
    -Syncope
  • Hypotension
  • Raised urea (digestion of blood)
146
Q

Oesophageal and gastric varices management

A

Acute:-
Resuscitation
- Terlipressin = vasopressin analogue which reduces portal pressure and bleeding
- Broad spectrum abx to reduce the risk of bacteraemia and spontaneous bacterial peritonitis
- Variceal band ligation via endoscopy for oesophageal
- Sclerotherapy for gastric
- For uncontrolled bleeding - insert a Sengstaken-Blakemore tube (NG-like tube which has a balloon which can be inflated to tamponade the bleeding)

Prevention:
- Non-selective beta blockers and band ligation
- If these don’t work, transjugular intrahepatic portosystemic shunt (TIPS)

147
Q

What are the causes of Oesophagitis?

A
  • GORD
  • NSAIDs
  • Infections e.g. candida
  • Allergens = eosinophilic oesophagitis
148
Q

Oesophagitis management

A

PPI for 1 month

149
Q

Oral candida management

A

1st line = oral nystatin

Fluconazole can be given if there is oropharyngeal involvement

150
Q

Define Hairy leucoplakia

A

A benign condition triggered by EBV and is suggestive of underlying HIV

Causes white patches on the tongue which may look hairy and cannot be scraped off

Is a pre-malignant condition

151
Q

Aphthous ulcer management

A

1st line = chlorohexidine mouth wash

If not healing after 3 wks - biopsy and referral to oral surgeon to rule out malignancy

152
Q

Oral candida features

A
  • White patches in the mouth which can be scraped off
  • Friable mucosa underneath
  • Satellite lesions
153
Q

Paracetamol OD features

A
  • <24 hrs = asymptomatic, or N&V
  • 24-72 hrs = RUQ pain, hypotension
  • 72-96 hrs = liver and renal failure, metabolic acidosis, encephalopathy, coagulopathy, confusion, drowsiness, oliguria, loin pain, jaundice, bleeding diathesis
154
Q

Paracetamol OD medical management

A
  • Ingestion less than 1 hr ago + dose >150mg/kg = activated charcoal
  • Ingestion 1-4 hrs ago = wait until 4 hrs to take a level and treat w/ N-acetylcysteine (NAC) based on level
  • Ingestion w/in 4-8 hrs + dose >150 mg/kg = NAC immediately if there is going to be a delay of >8 hrs in obtaining paracetamol level, otherwise weight for level and treat if high
  • Ingestion w/in 8-24 hrs + dose >150 mg/kgs = NAC immediately
  • Ingestion >24 hrs ago = NAC immediately if pt has jaundice, RUQ, elevated ALT, INR >1.3 or if paracetamol conc detectable
  • Staggered OD = NAC immediately
155
Q

How is N-acetylcysteine given?

A

Given IV over 2 12 hr infusions

If pt still has deranged LFTs, clotting or renal function, continue infusions and discuss for urgent transplant

156
Q

What are the criteria for urgent liver transplant in paracetamol OD?

A
  • INR >3 at 48 hrs, or >4.5 at any time
  • Oliguric or creatinine > 200
  • pH < 7.3 despite fluid resus
  • Hypotension (systolic < 80)
  • Severe thrombocytopenia
  • Encephalopathy
157
Q

Which type of peptic ulcer is more common?

A

Duodenal are 4x higher

158
Q

What are the causes of duodenal ulcers?

A
  • Primarily H. pylori
  • NSAIDs
  • Chronic steroid use
  • SSRI’s
  • Increased secretion of gastric acid
  • Smoking
  • Blood group O
  • Accelerated gastric emptying
159
Q

What are the causes of gastric ulcers?

A
  • NSAIDs
  • H. pylori
  • Smoking
  • Delayed gastric emptying
  • Severe stress
160
Q

Peptic ulcer features

A

Both:
- Abdo pain
- N&V
- Anorexia
- Unexplained WL
- Coffee ground vomiting

Gastric = pain worse on eating (increased gastric acid)

Duodenal = pain relieved by eating (pyloric sphincter closes so less acid)

161
Q

Peptic ulcer management

A

Conservative:
- Smoking cessation
- Smaller meals, avoid spicy/fatty foods and coffee
- Stress management
- Avoid NSAIDs, steroids, bisphosphonates, K supplements, SSRIs

Medical (H. pylori +ve):
- Associated w/ NSAID use = 8 wks PPI followed by triple eradication therapy for 7 days
- Not NSAID associated = triple therapy for 7 days

Gastric ulcers require a repeat OGD 6-8 wks following PPI treatment to ensure healing and rule out malignancy

Surgical:
- Underrunning of ulcer
- Fixation of perforation

162
Q

Pernicious anaemia pathophysiology

A

1) AI attack = destruction of gastric parietal cells leads to reduced intrinsic factor
2) Intrinsic factor deficiency = leads to impaired B12 absorption
3) B12 deficiency
4) Megaloblastic changes = impaired DNA synthesis in RBC, results in larger RBC which are less effective at at carrying O2 and thus anaemia occurs
5) Haemolysis (sometimes)

163
Q

B12 Deficiency features

A
  • Fatigue
  • Pallor
  • Glossitis
  • Subacute combined degeneration of the cord
  • Jaundice (haemolysis)
  • Cognitive impairment = memory problems, confusion and mood changes
164
Q

Pernicious anaemia management

A

Life long B12 replacement via 3 monthly hydroxocobalamin injections

165
Q

What are the long-term complications of Pernicious anaemia?

A

Increased risk of gastric cancer and carcinoid tumours

166
Q

Define Pharyngeal pouch

A

AKA Zenker’s diverticulum - a herniation of the pharyngeal mucosa that occurs through a weak point between the thyropharyngeus and cricopharyngeus muscles in the inferior constrictor of the pharynx

167
Q

Pharyngeal pouch features

A
  • Dysphagia
  • Regurgitation of undigested food resulting in halitosis
  • Aspiration
  • Chronic cough
  • WL
168
Q

Pharyngeal pouch investigations

A

Barium swallow test - shows a residual pool of contrast w/in the pouch

AVOID OGD as this can cause perforation

169
Q

Pharyngeal pouch management

A
  • If small and asymptomatic - no treatment required
  • Surgical resection of the diverticulum
  • Incision of the cricopharyngeus
170
Q

Define Primary biliary cholangitis

A

AI scarring and inflammation of the bile ducts

171
Q

Primary biliary cholangitis features

A
  • Asymptomatic
  • Extreme fatigue
  • Pruritus
  • Dry skin (xerosis)
  • Sicca syndrome (dry eyes)
  • RUQ pain
  • Xanthelasma
  • Clubbing
  • Jaundice
  • Late signs = sequalae of chronic liver disease
172
Q

What cancer are pts w/ Primary biliary cholangitis at risk of?

A

Hepatocellular carcinoma

173
Q

Primary biliary cholangitis investigations

A
  • Derranged LFTs w/ a cholestatic picture
  • +ve AMA
  • Raised IgM
  • USS to rule out obstruction
  • MRCP
  • Liver biopsy gold standard for diagnosis = granulomatous inflammation around the bile ducts
174
Q

Primary biliary cholangitis management

A
  • Ursodeoxycholic acid to slow disease progression by promoting bile flow
  • Cholestyramine for pruritus
  • Vitamin supplements
  • Liver transplant once bilirubin > 100 (PBC may reoccur)
175
Q

Primary sclerosing cholangitis definition

A

AI mediated chronic inflammation and fibrosis of the intra and extrahepatic bile ducts

Results in lots of strictures

176
Q

Primary sclerosing cholangitis features

A
  • Hepatomegaly
  • Jaundice
  • RUQ pain
  • Fatigue
  • WL
  • Fevers
  • Sweats
  • Associated w/ UC
177
Q

Primary sclerosing cholangitis investigations

A
  • Deranged LFTs w/ a cholestatic picture
  • +ve anti-smooth muscle antibodies, +ve pANCA
  • MRCP/ERCP = multiple beaded strictures seen
  • Biopsy if diagnosis unclear = fibrosis and obliterative cholangitis (onion skin appearance)
178
Q

Primary sclerosing cholangitis management

A
  • Alcohol avoidance
  • Cholestyramine for pruritus
  • Vit ADEK replacement
  • Strictures may be dilated via ERCP
  • Liver transplant in chronic liver disease or malignancy
179
Q

What cancer are pts w/ Primary sclerosing cholangitis at risk of?

A

Cholangiocarcinoma and colorectal cancer

180
Q

Define Upper GI bleed

A

Any haemorrhage of the GI tract between the oesophagus and the duodenum at the ligament of Treitz

181
Q

What are the causes of Upper GI bleeds?

A

Oesophageal:
- Varices
- Oesophagitis
- Malloy-Weiss tear = tear after severe retching/vomiting
- Oesophgeal cancer

Stomach:
- Peptic ulcers
- Gastric varices
- Gastritis
- Gastic cancer
- Vascular malfortmation = Dieulafoy lesiona dilated submucosal artery that erodes into the GI mucosa resulting in massive bleeding

Duodenum:
= Peptic ulcers
- Aortoenteric fistula

182
Q

What scoring systems are used in Upper GI bleeds?

A

Glasgow-Blatchford score is used on initial assessment to determine how urgently endoscopy is indicated = score of 0 means low risk and can have outpatient OGD

Rockall score is used post-endoscopy to help w/ risk stratification

183
Q

Upper GI bleed features

A
  • Haematemesis
  • Melaena
  • Light-headedness
  • Syncope
  • Abdo pain
  • Anaemia in subacute/chronic bleeds
  • Signs of hypovolaemic shock
184
Q

Upper GI bleed investigations

A

Bedside:
- VBG = for urgent haemoglobin levels
- ECG = cardiac ischaemia can occur in large bleeds

Bloods:
- FBC
- U&Es
- LFTs
- Coagulation
- Group and save
- Cross-match

Imaging:
- OGD
- CXR

185
Q

Upper GI bleed management

A
  • Resuscitate as per major haemorrhage protocol
  • In suspected variceal bleeds - Terlipressin and prophylactic abx
  • Immediate endoscopy = non-variceal bleeding can be clipped w/ thermal coagulation or fibrin/thrombin, variceal bleeding treated w/ band ligation, gastric variceal treated w/ sclerotherapy
186
Q

Define Backwash ileitis

A

Inflammation of the terminal small bowel in UC when inflammatory mediators are washed passed the ileocecal valve

187
Q

Ulcerative colitis features

A

GI:
- Diarrhoea containing blood or mucus
- Tenesemus or urgency
- Crampy LIF pain

Systemic:
- WL
- Fever
- Malaise
- Anorexia

Extra-intestinal:
- Derm = erythema nodosum, pyoderma gangrenosum
- Ocular = anterior uveitis, episcleritis, conjunctivitis
- MSK = clubbing, enteric arthritis, sacroiliitis
- Hepatobiliary = PSC
- AA amyloidosis

188
Q

Ulcerative colitis investigations

A
  • Faecal calprotectin (raised)
  • Abdo and erect CXR in acute settings to exclude toxic megacolon and perforations
  • Colonoscopy + biopsy + barium enema (diagnostic) - will show continuous inflammation starting at the rectum that does not invade beyond the submucosa, there may be loss of haustral markings, crypt abscesses and pseudopolyps, barium enema will show lead pipe inflammation
189
Q

How is the severity of acute exacerbations of UC assessed?

A

Using Truelove and Witt’s criteria:

Mild:
- <4 bowel movements a day
- Small amount of blood in stool
- No temp, tachycardia or anaemia
- ESR < 30

Moderate:
- 4-6 stools a day
- Mild-severe blood in stool
- No temp, tachycardia or anaemia
- ESR < 30

Severe:
- 6 or more stools per day
- Visible blood in stool
- At least one of; temp, tachycardia or anaemia
- ESR > 30

190
Q

Ulcerative colitis acute management

A

Mild-moderate disease:
- Proctitis or proctosigmoiditis = topical ASA (mesalazine or sulfasalazine) for 4 weeks, of that doesn’t induce remission then escalate to oral ASA, then add oral prednisolone, then add oral tacrolimus
- Left sided or extensive disease = high dose oral ASA for 4 weeks, then add oral prednisolone, then add oral tacrolimus

Severe disease:
Step 1) IV corticosteroids (ciclosporin if contraindicated)
Step2) If no improvement w/in 72 hrs, add IV ciclosporin or consider surgery
Step 3) Trial of etrasimod (selective S1p receptor modulator)

191
Q

What are the surgical options in UC?

A
  • Panproctocolectomy w/ permanent end ileostomy
  • Total colectomy w/ ileorectal anastomosis
192
Q

Scurvy features

A

Causes impaired collagen synthesis resulting in:
- Spontaneous bleeding and bruising (fragile vessels)
- Gingival swelling
- Coiled hairs
- Teeth loss
- Increased risk of intracranial and endocardial haemorrhages

193
Q

Thiamine deficiency features

A
  • Wernicke’s encephalopathy
  • Korsakoff’s syndrome
  • Wet beriberi = HF and cardiomegaly
  • Dry beriberi = peripheral neuropathy (mimics GBS)
194
Q

Pellagra (B3 deficiency) features

A

3 D’s:
- Diarrhoea
- Dermatitis
- Dementia

Treated w/ nicotinamide (vit B3)

195
Q

Vitamin A deficiency features

A
  • Night blindness
  • Xerophthalmia (dry eyes)
  • Complete blindness if severe
196
Q

Define Wipple’s disease

A

A rare disorder caused by the bacterium Tropheryma whipplei

Can affect any part of the body, but most commonly impacts the GI system, joints and nervous system

197
Q

Wipple’s disease features

A
  • Chronic diarrhoea
  • Abdo pain
  • Joint pain
  • WL
  • HF
  • Neurological issues
198
Q

Wipple’s disease investigations

A

Small bowel biopsy = shows acid-Schiff +ve macrophages

199
Q

Wipple’s disease management

A

Long-term course of co-trimoxazole

200
Q

Define Zollinger Ellison syndrome

A

A gastrinoma of the pancreas or duodenum

It uncontrollably releases gastrin resulting in multiple peptic ulcerations

Associated w/ MEN-1

201
Q

Zollinger Ellison syndrome features

A
  • Epigastric pain
  • Diarrhoea
  • GI bleedings
  • Non-responsive to PPI’s
202
Q

Zollinger Ellison syndrome investigations

A
  • Gastrin levels
  • Diagnostic = secretin administration causing extreme gastrin release
  • Somatostatin receptor scintigraphy = imaging choice as CT can miss the tumours
203
Q

Zollinger Ellison syndrome management

A
  • Surgical resection of the tumour
  • PPI’s

Year 6 (12 decks)

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