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Y3 Medicine > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

what are the main differences between Crohns and UC?

A

Crohns:

  • can affect anywhere for mouth to anus
  • skip lesions
  • transmural inflammation
  • fissuring ulcers
  • lymphoid and neutrophil aggregates
  • non caseating granulomas
  • increased incidence in smokers

UC:

  • affects rectum and extends to proximally varying distances
  • continuous
  • mucosa and sub mucosal inflammation only
  • crypt abscesses
  • decreased incidence in smokers
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2
Q

what are the investigations done to diagnose IBD? and what would the likely positive results be?

A
  • blood tests: FBC (anaemia, raised platelets), U&Es (deranged electrolytes or AKI) , CRP (raised)
  • stool tests: stool cultures, faecal calprotectin
  • simple imaging: AXR
  • endoscopy: flexibel sigmoidoscopy, colonoscopy, capsule endoscopy
  • cross sectional imaging: CT abdo, MRI enterography, MRI rectum for perianal disease
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3
Q

what is the treatment for IBD? (long term and in emergencies)

A

steroids: suppositories or enemas, prednisolone orally or hydrocortisone IV

IV hydrocortisone 100mg qds if admitted to hospital

rescue therapy: ciclosporin, biologics or surgery in UC and biologics or surgery in Crohns

mesalazine also used to maintain remission in UC, azathioprine and biologics used to maintian remission in Crohns

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4
Q

what are the symptoms of coeliac disease?

A
  • bloating
  • abdo pain/cramps
  • weight loss
  • dermatitis herpetiformis
  • loose stool s
  • wind
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5
Q

what are some complications of coeliac disease?

A

small bowel lymphoma, small bowel cancer, osteoporosis, neurological complications (gluten ataxia, neuropathy)

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6
Q

what investigations are done to diagnose coeliac disease?

A
  • tissue transglutaminase (tTG) is raised BUT NOT a diagnostic test
  • OGD and duodenal biopsies is diagnostic test - see villous atrophy and intra epithelial lymphocytosis
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7
Q

what investigations are done in a patient with dyspepsia and reflux?

A

PPI test +/- test for H pylori
if any red flag symptoms, atypical symptoms, associated dysphagia, or weight loss or new onset at an older age then investigations need to be done and consider OGD

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8
Q

what are teh cuases of oesophagela dysphagia?

A

physical obstruction: tumour, benign stricture, inflammation from oesophagitis

neuromuscular problem: achalasia, dysmotility, prebyoesophagus

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9
Q

what investgiations need to be done when a patient presents with dysphagia?

A

if oesophageal:

  • OGD to exlcude obstructive cause
  • Barium swallow or oesophageal manometry looking for neuromuscular problems

if oropharyngeal:

  • examine cranial nerves and obtain speech therapy assessment on swallow
  • video fluroscopy
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10
Q

what is the treatment fro dysphagia?

A

TREAT UNDERLYING CAUSE:
- dilatation for benign strictures and surgery or stenting for cancers
for oropharyngeal: alter consistencies of food and fluid and if still unsafe then enteral feeding tube needed

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11
Q

what are eh causes for oro-pharyngeal dysphagia?

A

difficulty getting food to leave the mouth due to problems coordinating he muscles that move bolus to back of mouth due to NEUROLOGICAL disease (e.g. stroke)

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12
Q

what are teh mian functions of the liver?

A
  • nutrition.metabolic
  • bile salts
  • bilirubin
  • clotting factors
  • detoxification
  • immune function
  • manufactures proteins
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13
Q

what are teh risk factors for liver diseasE?

A
  • blood transfusion prior to 1990 in UK
  • IVDU
  • operations/vaccination with dubious sterile procedures
  • sexual exposure
  • medications
  • FH of liver disease
  • obesity and other features o fmetbolic syndrom e
  • alcohol
  • foreign travel
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14
Q

what are the main indications to determining acute from chronic liver disease?

A

acute: no preexisting liver disease, resolves in 6 months (Hep A, E, CMV, EBV, Drug induced lvier disease )
chronic: starts with acute lvier disease, > 6 months, may lead to cirrhosis and complications (Hep C, alcohol, non alcoholic steatohepatitism, autoimmune (PBC, PSC, AIH)), chronic stigmata (spider neava, clubbing, palmar erythema, ascites)

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15
Q

what investigations are done to diagnose liver disease

A

LFTs (ALT rise = hepatocyte damage, ALP rise = duct damage)
thrombocytopenia for liver fibrosis
bilirubin, albumin, INR
US if LFTs show cholestatic cause

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16
Q

if ALT > 500 then what liver diseases woudl you consider?

A

hepatic causes: viral, ischaemia, toxic (e.g. paracetmaol), autoimmune

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17
Q

if ALT is 100-200 then what liver diseases would you consider?

A
  • non alcoholic steatohepatitis
  • autoimmune hepatitis
  • chronic viral hepatitis
  • drug induced liver injury
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18
Q

what diseases would you consider with cholestatic liver disease causes with dilated ducts?

A
  • gallstones

- malignancy

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19
Q

what diseases would you consider with cholestatic liver disease causes without dilated ducts?

A
  • alcoholic hepatitis
  • cirrhosis: PBC, PSC, alcohol
  • drug induced liver injury: antibiotics
20
Q

what are the causes (conditions leading to) of chronic liver disease?

A

most common: ALD, non alcoholic steatohepatitis (NASH), viral hepatitis (C&D)

commoner in men: PSC, heamochromotosis
commoner in women: PBC, autoimmune hepatitis
commoner in younger: Wilsons disease, anti LKM autoimmune hepatitis

21
Q

what is cirrhosis?

A

cirrhosis is the end pathology of chronic liver disease

22
Q

what imaging signs give cirrhosis as a diagnosis?

A

splenomegaly, coarse texture, nodularity

23
Q

what investigations can be used to diagnose cirrhosis?

A

FBC - thrombocytopenia
clinical stigmata of CLD e.g. ascites (diagnostic ascitic tap), spider neava
imaging + fibroscan
presence of varices on endoscopy
DEXA scan to check for osteoporosis (reduced VitD absorption)
alpha feroprotein and USS to check for liver tumour due to cirrhosis

24
Q

what is involved in a nutritional assessment?

A
  1. history - appetitie, diet history, chnages in oral intake, chnages in weight (unplanned), BMI
  2. MUST (malnutrition universal screening tool)
25
Q

what is the first step in nutritional support?

A

FOOD AND ENCOURAGEMENT

  • dont interrupt meal times
  • high calorie food options (without increasing volume)
  • assistance with eating
  • appropriate cutlery
  • make sure teeth are okay (e.g. need dentures?)
  • nutritional supplements
26
Q

what options are available if a patient is unable to swallow/non functioning GI tract/meet nutritional needs

A
  • NG TUBE
  • PEG/RIG/PEGJ/RIGJ (longer term)
  • parenteral nutrition (via picc or hickman line when GI tract not working/not accessible)
27
Q

what are the two assessment scores used to assess GI bleeding?

A

ROCKALL score - assesses upper GI bleeds + risk of death

Blatchford score - assesses whether a patient needs to be admitted to hospital by blood test results

28
Q

what investigations need to be done when a patient is experiencing a GI Bleed?

A

FBC - check haemoglobin and platelet count (thrombocytopenia may suggest CLD)
U&Es - raised urea suggest upper GI bleed
clotting
group & save
LFTs
venous blood gas

29
Q

what is the management for variceal bleeding?

A
  • IV access and fluids given (followed by blood)
  • IV terlipressin and IV ABX
  • upper GI endoscopy urgently
  • definitive treatment: mechanical obstruction of blood outflow - need endoscopic banding/Linton or Sengstaken tube or possibly a TIPSS procedure
30
Q

what is the management for a non variceal bleed?

A
  • IV access and fluid given (followed by bloods)
  • dependent on underlying pathology - endoscopic treatments / radiological embolisation / surgery (possibel PPI use if have ulcers)
31
Q

what are teh signs anf symptoms of acute liver failure?

A
  • jaundice
  • confusion, altered mental status, asterixis (hepatic encephalopathy)
  • oedema and ascites
  • bruising (coagulopathy)
  • GI bleeding
  • hepatomegaly
  • ascites
32
Q

what are the causes of acute liver failure?

A
  • INFECTION: Hep A/B, CMV, EBV, letpspirosis
  • TOXIN: EtOH, paracetamol, isoniazis, halothane
  • VASC: budd chiari syndrome
  • OTHER: wilsons, AIH
  • OBS: eclampsia, acute fatty liver of pregnancy
33
Q

acute liver failure: investigations??

A
  • blood tests: FBC, U+E’s, LFTs, clotting, BM, ABG
  • paracetamol serum level
  • toxicology screen
  • autoimmune markers
  • viral screen
  • liver and pancreas US
  • CXR
34
Q

acute liver fialure: immediate managment?

A

ITU admission and treat all complications (+ monitor urine output and blood lgucose);

  • encephalopathy: IV mannitol if bad
  • hypoglycaemic: IV glucose (+ sodium chloride to prevent hyponatremia)
  • coagulopathy: IV phytomenadione to prevent bleeding
  • sepsis: culture blood and urine

possible discussion with transplant team

35
Q

what are the common symptoms for a paracetamol overdose?

A
  • N+V
  • anorexia
  • malaise
  • abdo pain
  • confusion
36
Q

paracetamol overdose: investigations??

A

BLOODS

  • FBC
  • U+Es
  • LFTs
  • BM
  • paracetamol levels
  • ABG/VBG

Nomogram to check if N-acetylcysteine needed to treat

37
Q

what are the signs of a paracetamol overdose?

A 
Asterixis
Bruising
Jaundice
Right upper quadrant pain
Oliguria/anuria
Tachycardia/hypotension
Coma

(common signs of acute liver failure)

38
Q

what is the specific treatment for a paracetamol overdose?

A

N-acetylcysteine - increases glutathione concentration to bind to NAPQI and reduce toxicity

39
Q

what are the main complications of cirrhosis?

A
  1. decompensation - hepatic failure: jaundice, encephalopathy, hypoalbuminaemia (oedema, ascites), coagulopathy (bruising), hypoglyceamia
  2. SBP (spontaneous bacterial peritonitis)
  3. portal HTN: (SAVE) Splenomegaly, Ascites, Varices, Encephalopathy
  4. Increased risk of hepatocellular carcinoma
40
Q

management of complications of cirrhosis:

  • decompensation
  • SBP
  • varices
  • HCC
A

decompensation:
- ascites: fluid and salt restrict, spironolactone, furosemide, ascitic tap, daily weight
- coagulopathy: vit K, platelets, FFP, blood
- encephalopathy: avoid sedatives, lactulose + enemas, rifaximin
- sepsis/SBP: tazocin
- hepatorenal syndrome: IV albumin and terlipressin

SBP: cefotaxime/ceftriaxone

Varcies: endoscopic banding and OGD screening

HCC: US and AFP every 3-6 months

41
Q

what is the presentation of a patient with portal HTN?

A

SAVE:

  • splenomegaly
  • ascites
  • varcies
  • encephalopathy
  • asterixis, ataxia
  • confusion
  • dysarthria
  • constructional apraxia
  • seizures
42
Q

what is the managment of the complications of Portal HTN?

A

SBP: cefotaxime or tazocin until sensitivites known (tap and MC+S done)
ascites: daily weight, fluid restriction and low Na diet, spironolactone and furosemide

treatment: TIPSS

43
Q

what is the managment of alcoholic liver disease?

A
  • group therapy and self help
  • disulfiram: aversion therapy
  • baclofen + acamprosate: decrease cravings
  • stop Ethanol intake !!!
  • optimise nutrition
  • manage complications of failure
44
Q

what is the managment of viral hepaititis?

A

supportive: no ethanol, avoid heptotoxic drugs e.g. aspirin

anti-viral: HBV - PEGinterferon, HCV - PEGinterferon + ribavarin

45
Q

what is the management of NAFLD?

A
  • lose weight

- control HTN, DM and lipids

46
Q

what is the managment for hereditary heamochromotosis?

A
  1. iron removal: venesection or desferrioxamine
  2. monitor DM, low Fe diet
  3. screening: serum ferritin and genotype, screen 1st degree relatives
  4. transplant in cirrhosis
47
Q

what is teh management for autoimmune hepatitis?

A

immunosuppression: prednisolone or azathioprine as steroid sparing
liver transplant

Y3 Medicine (9 decks)

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