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Medicine - Year 3 > Medicine - Gastrointestinal System > Flashcards

Medicine - Gastrointestinal System Flashcards

1
Q

What is Leukonychia and what is it a sign of?

A

White spots on nails - low Albumin, CLD

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2
Q

What is Koilonychia and what is it a sign of?

A

Bent-up nails, sign of iron deficiency anaemia

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3
Q

What is finger clubbing a sign of?

A

IBD, Cirrhosis, Coeliac disease

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4
Q

What is Dupuytren’s contracture a sign of?

A

CLD

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5
Q

What is the top right hand corner of the abdomen referred to as?

A

Right Hyopchondrium

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6
Q

Nutrition
What scoring system is used to evaluate malnutrition?
What are the indications for an NGT?
What are the contraindications for an NGT?
What pH must be reached for the correct placement of an NGT?
What are the indications for PEG insertion?
What are the contraindications for PEG insertion?
TPN indications

A

Scoring: MUST

NGT Indications: Functioning gut, inability to meet nutritional requirement via food, unintentionally lost >10% body weight, anorexic

NGT Contraindications: Basal skull fracture, pharyngeal pouch, hiatus hernia, oesophageal varices

pH: 5.5

PEG Indications: Enteral feed >3 weeks, SALT assessment, long-term care required, capacity

PEG Contraindications: Pregnancy, cardiac or respiratory disorders, gastric surgery, hiatus hernia

TPN indications: Non-functioning gut, unsafe intake

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7
Q

What ions are affected in re-feeding syndrome?

A

Magnesium, Phosphate, Potassium

Will need IV Thiamine prior to feeding

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8
Q

Upper GI Bleeds
List 5 causes of upper GI bleeds:
What investigations would you do in query upper GI bleed?
What scoring systems are used and what do they assess?
What management would you give to someone with an acute upper GI bleed?

A

Causes: Peptic ulcer disease, varices, Mallory-weiss tear/Boerhaave’s, Upper GI Malignancy, Gastritis perforation, Epistaxis

Investigations: OGD, CT angio (if needed), FBC + U&Es, Urea, Liver Ultrasound

Scoring: ROCKALL - chance of adverse outcome
Glasgow-Blatchford - identify if needs intervention

Management: Drip and suck, Oxygen, PPIs IV, Endoscopic therapy
If Varices: Terlipressin IV, Minnesota-Sengstaken tube

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9
Q

Varices
Where are the 3 locations of variceal bleeding?
Pathophsyiology:
What prophylactic drug is given to prevent bursting of varices?
What are the treatments for active oesophageal varices bleeding?
How is the liver linked to the umbilicus?

A

Locations: Oesophageal, Umbilical, Anorectal

Pathophysiology: Liver cirrhosis leads to portal hypertension, leading to venous congestion - this then causes it to exit via systemic anastomoses

Prophylactic drug: Beta-blocker

Treatment: Transjugular intrahepatic portosystemic shunt (TIPS), Terlipressin

Liver is linked to the umbilicus via the ligamentum teres

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10
Q

Lower GI bleeds

Causes:

A

Causes: Diverticulitis, Colitis, Colorectal Cancer, Haemorrhoids, Anal fissure, Colorectal cancer, UC, Angiodysplasia, Shigella/Campylobacter

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11
Q 
Crohn's Disease
Name 5 unique features to Crohn's:
Name 5 extra-intestinal features:
Investigations:
Gross Pathological changes seen:
Management:
Complications:
A

Unique: Skip lesions, distal ileum affected, transmural, perianal disease/fistulas

Extra-intestinal: Erythema nodosum, pyoderma gangrenosum, uveitis, nail clubbing, enteropathic arthritis

Investigations: Faecal calprotectin, Colonoscopy with biopsy, abdo X-ray to rule out toxic megacolon

Gross Pathological changes: Skip lesions, cobblestone appearance, fistulae, strictures, mucosal oedema, transmural inflammation

Management: Oral Prednisolone, Azathioprine to maintain remission and induce
TPMT levels low, then given Methotrexate instead of Azathioprine

Complications: Fistula formation, Strictures, Perianal abscess, Malignancy risk, Malabsorption

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12
Q

Ulcerative Colitis
Name 7 unique features to Ulcerative Colitis:
Name 4 extra-intestinal manifestations of UC:
Investigations:
Management:
Complications:

A

Unique: Starts in rectum, crypt abscesses, continuous pattern of inflammation, mucosal inflammation only (superficial), can cause toxic megacolon and perforations (acute exacerbations are fatal), tenesmus, painful red eye

Extra-intestinal: Enterohepatic arthritis, erythema nodosum, pyoderma gangrenosum, uveitis

Investigations: Faecal calprotectin, Colonoscopy or Sigmoidoscopy, CXR to check for lead pipe colon or mural thickening, CT for toxi megacolon

Management: Heparinisation (thromboembolic state), Mesalazine rectally, with added oral pred if not working, then Mesalazine as remission + infliximab
Total proctocolectomy is curative

Complications: Toxic megacolon, colorectal carcinoma, osteoporosis

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13
Q

Toxic Megacolon
Pathophysiology:
Symptoms:

A

Complication of C. Diff + UC

Symptoms:

  • Severe abdominal pain
  • Abdominal distension
  • Pyrexia
  • Systemic toxicity
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14
Q

Acute Liver Failure
Causes:
Symptoms:
Grades of hepatic encephalopathy:

A

Causes: Paracetamol toxicity, Hep A/B, Severe alcohol toxicity

Symptoms: Jaundice, Hepatic Encephalopathy, Haemorrhage (variceal) due to loss of clotting factor production, AKI (hepatorenal)

Grades: 1-4: 1 = Poor memory, reversed sleep pattern, slow thought
2 = Lethargy, disorientation, agitation
3 = Drowsy
4 = Coma

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15
Q

Jaundice causes - how can you tell easily if pre/hepatic/post?

A 
Pre = no urine or faecal changes
Renal = urine colour change, no faeces change
Post = urine and faeces colour change (white)
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16
Q

Chronic Liver Disease
Causes:
Signs:
Cirrhosis investigations:

A

Causes: Alcoholic liver disease, Hepatitis B/C, NASH, PBC, PSC, Autoimmune hepatitis, Haemochromatosis, Wilson’s disease

Signs: Ascites, Jaundice, Hepatosplenomegaly. Spider naevi, Hepatic flap, Clubbing, Dupuytren’s, Leukonychia

Investigations: USS scan (fibroscan) of the liver, Liver screen

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17
Q

Jaundice
Pre-Hepatic:
Hepatic:
Post-Hepatic:

A

Pre-Hepatic: Sickle cell, malaria

Hepatic: Cirrhosis, alcoholic/viral hepatitis, pancreatic cancer, PBC, PBS, Haemochromatosis, Wilson’s, Paracetamol OD

Post-Hepatic: Cholecystitis/ Ascending Cholangitis/Malignancy

18
Q

Wilson’s disease
Pathophysiology:
Symptoms:

A

Pathophysiology: Increased copper uptake and reduced secretion -> deposition

Symptoms: Keyser-Fleischer rings, Parkinsonian symptoms and memory loss, abnormal LFTs/jaundice

19
Q

Hereditary Haemochromatosis
Pathophysiology:
Management:

A

Pathophysiology: Increased iron absorption from the small intestine, leading to iron deposition in tissues - “bronze diabetes”

Management: Venesection

20
Q

Primary Biliary Cirrhosis

Pathophysiology:

A

Pathophysiology: Destruction of the intra-hepatic bile ducts, mainly affects women, ANA/Smooth muscle antibodies

21
Q

Primary Sclerosing Cholangitis
Pathophysiology:
Associated conditions:

A

Pathophysiology: Fibrosis of the intra and extra hepatic bile ducts, common in men, ANCA antibodies

Associated with: UC, Cholangiocarcinoma, HCC

22
Q

Gilbert’s Syndrome

Pathophysiology:

A

Pathophysiology: Reduced ability of the liver to process bilirubin, leading to short episodes of jaundice, usually incited by playing sports - self-resolving

23
Q

Alcohol Intake
How many units of alcohol are recommended per week?
How can you calculate the number of units in a drink?
What conditions is alcohol intake associated with?
What condition is alcohol withdrawal associated with?
How is alcohol withdrawal managed?

A

Units: 14 units/ week

Calculated by: Quantity * ABV /1000

Conditions associated: Cirrhosis, Folate/B12 deficiency (Macrocytic anaemia), Mallory-Weiss tear, Delirium Tremens, Hepatic Encephalopathy, Alcoholic fatty liver disease

Withdrawal: Delirium Tremens

Management of alcohol withdrawal: B12, Folate, Thiamine, Benzodiazepine, Do a Clinical Institute Withdrawal Assessment for alcohol (CIWA), give Disulfiram and refer to CBT groups

24
Q

Hepatorenal syndrome

Define the pathophysiology of hepatorenal syndrome

A

Cirrhosis -> Portal Hypertension -> Arterial vasodilation (splanchnic) -> RAAS activation -> Renal artery vasoconstriction (AKI)

25
Q

Hepatitis
How are each of the Hepatitises primary caught?
Which of the hepatitises are chronic, which are mainly acute?

A

A = Faecal oral, usually abroad, immunisation available

B = Blood or sex, immunisation available

C = Blood or IVDU, no immunisation

E = Faecal-oral, unsafe drinking water

Chronicity:
A = Not chronic

B = Mostly acute, rare chance of developing into chronic (1/10) - no treatment

C = Chronic always, Interferon and Ribavirin treatment

E = Not chronic

26
Q

Hepatitis B
Which antigen/antibody implies acute disease?
Which antibody implies immunity?
Which antibody implies a previous or current infection?

A

Acute disease: HBs Antigen

Immunity: Anti-HBs

Previous or Chronic infection: Anti-HBc (IgM acute, IgG late)

27
Q 
GORD
Pathophysiology:
Symptoms:
Risk factors:
Investigations:
Management:
Complications:
A

Pathophysiology: Acid exits the stomach and laps at the oesophagus. Usually limited from doing this due to LOS + Diaphragm + Acute Angle of Entry

Symptoms: Central crushing chest pain, retro-sternal, can radiate to back, worse after meals or bending over/lying down, acid taste in mouth, cough, flatus

Risk factors: Obesity, Male, Pregnancy, Hiatus Hernia, Smoking, Coffee, Alcohol, NSAIDs

Investigations: Clinical diagnosis, check for red flags (dysphagia/weight loss > 55 years old), OGD if PPIs not working, 24-hour pH monitoring

Management: Lifestyle modification, PPIs, Ranitidine, Antacids, fundoplication if hiatus hernia

Complications: Aspiration pneumonia, Barret’s Oesophagus, Oesophagitis

28
Q 
Barrett's Oesophagus
Pathophysiology:
Red Flags:
Risk factors:
Investigations:
Management:
A

Pathophysiology: Stratified squamous undergo metaplasia to simple columnar epithelium -> Adenocarcinoma. Less common than SCC in the UK.

Red flags: Weight loss, Dysphagia, Early Satiety, Loss of appetite, Worsening dyspepsia despite PPI treatment, Anaemia of chronic disease

Risk factors: GORD, Male, Smoking, > 55, Hiatus Hernia, FH

Investigations: OGD with biopsy

Management: High-dose PPIs, stop NSAIDs, regular endoscopy, endoscopic mucosal resection

29
Q 
Gastritis (H Pylori-related)
Pathophysiology:
Causes:
Symptoms:
H Pylori pathogenesis:
H Pylori invasion locations:
Investigations:
Management:
A

Pathophysiology: Inflammation of the mucosal lining of the stomach

Causes: H Pylori, Autoimmune (can lead to pernicious anaemia), Alcohol abuse, NSAIDs

Symptoms: Pain, nausea, vomiting, bleeding, can be asymptomatic (in the case of H Pylori)

H Pylori pathogenesis: Produces urease (urea -> ammonia, increasing pH), releases cytotoxins causing epithelial injury, degrades mucous layer

Invasion locations: Antrum - affects G cells, causing increased gastrin secretion

Investigations: Urease breath test (urea labelled with isotope of carbon taken in, measure if isotope labelled CO2 breathed out, showing urea breakdown), Stool antigen test

Management: Proton pump inhibitor + Amoxicillin + Clarithromycin

30
Q 
Paracetamol Overdose
Symptoms:
Investigations:
Management:
When is it safe to discharge?
A

Symptoms: Nausea, vomiting, sweating, RUQ pain

Investigations: Serum paracetamol level, ALT, ABG, INR for elevated prothrombin time

Management: TOXBASE, N-acetylcysteine - replenishes depleted glutathione reserves in the liver, to protect against NAPQI

Safe discharge: Mental health assessment, LFTs for permanent damage, blood paracetamol levels

31
Q 
Ulcers
Pathophysiology:
Causes:
Symptoms:
Investigations:
Management:
(If bleeding:)
Complications:
A

Pathophysiology: Breach in the gastric or duodenal mucosa that extends through the muscularis mucosa, most commonly in the first quarter of the duodenum

Causes: H pylori, particularly duodenal ulcers, NSAIDs, Alcohol, Smoking (relapses), Acute Gastritis

Symptoms: Epigastric pain, relieved immediately by eating if duodenal, or worse on eating in gastric, anaemia, weight loss, early satiety

Investigations: OGD, Urease Breath Test

Management: Lifestyle modification, H Pylori testing and management (PPI + Amoxicillin + Clarithromycin)

If bleeding: IV Fluids, IV PPI, Stop antiplatelets, OGD

Complications: Pyloric stenosis, Perforation (splenic or gastroduodenal), Haemorrhage, Malignancy

32
Q

Ascitic Tap

What is measured in an ascitic tap?

A

Appearance eg. turbidity

SAAG (serum-ascites albumin gradient)

Neutrophil count for SBP

33
Q 
LFTs
What does a liver screen contain?
What does a raised ALT imply?
What does a raised Gamma-GT imply?
What does an ALP + Gamma-GT being raised imply?
A

Liver screen: LFTs, Bilirubin, Albumin, Hepatitis tests, Iron studies, Autoantibodies, Alpha-antitrypsin, Coeliac serology (TTG)

ALT = Viral induced hepatitis, Paracetamol OD, autoimmune

Gamma-GT = Alcoholic liver disease

ALP + Gamma-GT = Cholestatic picture eg. gallstones, pancreatic cancer, PBC, PSC

34
Q 
Diarrhoea
Definition:
Salmonella:
Campylobacter:
Shigella:
ETEC:
Rotavirus:
Norovirus:
Cryptosporidium:
Giardia Lamblia:
Entamoeba Histiolytica:
A

Definition: 3 or more loose stools per day

Salmonella: Gram negative rod, Non-bloody diarrhoea, ingested water/food, lasts 2-3 days

Campylobacter: Faecal oral, Bloody Diarrhoea, Weeks - can lead to Haemolytic uremic syndrome, thrombotic thrombocytopenic purpura, reactive arthritis

Shigella: Infected stools, but also flies due to low infectious dose. Bloody diarrhoea with mucous and cramping, clears within 1 week.

ETEC: Not bloody, traveller’s diarrhoea, days

Rotavirus: Children - non-bloody diarrhoea

Norovirus: Most common gastroenteritis, any age, watery diarrhoea, vomiting

Cryptosporidium: Faecal oral route, swimming pools in particular

Giardia lamblia: From developing countries, can lead to lactose intolerance

Entamoeba histolytica: From developing countries, most cases are asymptomatic - can lead to toxic megacolon, requires anti-protozoals and metronidazole

35
Q 
Constipation
Definition:
Causes:
Risk factors:
Management:
Types of laxative:
A

Definition: Straining/lumpy stools/incomplete evacuation >25% of defecations, or fewer than 3 unassisted bowel movements/week

Causes: Stress, Toxic Megacolon, Hypothyroidism, Diabetes, Parkinson’s, MS, Coffee

Risk factors: Female, Surgery, Increasing age, Low level of physical activity, low fibre diet

Management: Fybogel, Increased fluid intake, Increased fibre, Increased exercise, Laxatives

Laxative types:
Osmotic: Movicol (Macrogols) retain water they went in with), Lactulose (draws water into bowel)
Stimulatory: Sodium docusate/Senna
Bulk forming: Fybogel

36
Q 
Clostridium Difficile
Pathophysiology:
Symptoms:
Management:
Complications:
A

Pathophysiology: Gram positive rod, caused by cephalosporins and broad-spectrum antibiotics - toxins A and B

Symptoms: Watery diarrhoea, abdominal pain, distension, fever, NO vomiting

Management: Stop antibiotics, give fluid, Metronidazole IV, Faecal matter transplant

Complications: Psuedomembranous colitis and Toxic Megacolon

37
Q

Spontaneous Bacterial Peritonitis

Pathophysiology:

A

Pathophysiology: Most commonly seen in patients with end stage liver disease - infection of the ascitic fluid

38
Q

Vitamin B12 deficiency
Pathophysiology:
Causes:

A

Pathophysiology: B12 deficiency leads to megaloblastic (macrocytic) anaemia and neurological symptoms. Absorbed in the terminal ileum once bound by intrinsic factor.

Causes: Pernicious anaemia (lack of intrinsic factor), Crohn’s disease, Vegetarianism

39
Q

Lactose Intolerance

Pathophysiology:

A

Pathophysiology: Lactase enzyme deficiency - acts as an osmotic diarrhoea causer

40
Q 
Coeliac Disease
Pathophysiology:
Symptoms:
Investigations:
Management:
A

Pathophysiology: Immunological response to gliadin, causing: Villous atrophy, lymphocyte infiltrate epithelium, impaired digestion/malabsorption

Symptoms: Diarrhoea, weight loss, flatulence, abdominal pain, anaemia, neurological symptoms

Investigations: tTG antibody testing (cannot diagnose though), Endoscopy + Biopsy looking for villous atrophy/ epithelial lymphocytosis

Management: Diet - gluten free diet

41
Q 
Acute Mesenteric Ischaemia
Pathophysiology:
Symptoms:
Risk factors:
Investigations:
Management:
A

Pathophysiology: Symptomatic occlusion of the blood supply to the GI tract. Acute occlusion, usually in the SMA.

Symptoms: Disproportionate abdominal pain, usually 30 mins after eating

Risk factors: Cardiovascular disease, elderly, female

Investigations: CT angiography, erect CXR to check for perforation

Management: Resection of ischaemic bowel, thrombolysis

Medicine - Year 3 (6 decks)

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