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Y3 Medicine > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What are the most common causes of an upper gi bleed?

A

Peptic ulcers and oesphageal varcies.
Other causes inc gastritis/ erosions, erosive duodenitis, portal hypertensive gastropathy, malignancy, mallory- weiss tear, vascular malformation

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2
Q

Give 3 risk factors for peptic ulcers

A

alcohol abuse, renal failure, NSAID use, older age, anticoagulants, steroids

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3
Q

Give 3 risk factors for oesphageal varices

A

advanced liver disease, continued alcohol intake, anticoagulants

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4
Q

How do upper GI bleeds present?

A
  • Epigastric pain
  • haematemesis (active bleeding)
  • coffee ground vomit (bleeding has stopped or is mild)
  • malaena
  • haematochezia (profuse UGIB or colonic bleeding)
  • features of blood loss (shock, syncope, faint, dizziness, pale, cold, thready pulse, confusion, dehydration, oligourea, prolonged caprefill)
  • features of underlying disease (dyspepsia, weight loss, jaundice, ascites, spider naevi, hepatic flap)
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5
Q

Describe the management of someone with an upper GI bleed who is haemodyanamicaly unstable

A
  • stop +/- reverse anticoagulants
  • activate major haemorrhage protocol (get O- blood, cross match)
  • 2x large bore cannula
  • secure airway and use suction
  • run 500ml saline over 10 mins in one and blood in other
  • platelets, FFP, vit K, prothombin complex may be needed
  • arrange urgent endoscopy
  • call 2222/ senior if severe or not improving
  • consider catheter
  • 15 mins obs until stable then hrly
  • FBC U&E, LFT, clotting, cross match
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6
Q

What drug can be used if oesophageal varcies cause the UGIB?

A

Terlipressin IV 1-2mg/ 6hr - also give IV abx

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7
Q

When a pt with an UGIB is haemodynamically stable, what intervention do they need?

A

Endoscopy

They also need 2x large bore cannula, cross matched blood if hb<7, terlipressin, fluids etc

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8
Q

What can be done if endoscopy fails to stop an UGIB?

A

Surgery or emergency mesenteric angiography/ embolisation

Sengstaken- blakemore tube can be used for oesphgeal varcies

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9
Q

What scoring system can be used to assess need for an endoscopy? What is accounted for in it? (8)

A

Blatchford score

Urea level, Hb, systolic BP, HR, malaena, syncope, liverfailure, cardiac failure

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10
Q

What scoring system is used after and before endoscopy for assessing risk of rebleeding and death? What is involved in it?

A

Rockall score

Age, comorbity (heart failure, IHD, renal and liver failure), shock, source of bleed, stigmata of bleeding

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11
Q

What interventions can be done during endoscopy to stop a bleed? (4)

A
  • Clips
  • Adenaline injections (not alone)
  • Fibrin or thombin injections
  • band ligation or transjugular intrahepatic portosystemic shunts for oesphageal varices
  • cauterisation
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12
Q

How is H. pylori identified and treated?

A

Identified with ureas breath test

Cured with 7 day course of PPI plus amoxicillin 1g and either clarithromycin 500mg or metronidazole 400mg all TDS

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13
Q

Describe differences in presentation between UC and crohns

A
  • C younger pts more commonly, non blood diarhoea, smoking increase risk, perianal disease (skin tags, abcesses, fistula), mouth ulcers
  • UC strong genetic link also, bloody diarrhoea, smoking protects,
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14
Q

Describe similarities in UC and crohns presentations

A

peak at 15-25 and 55-60, chronic diarrhoea with flares, colicky abdopain, urgency, tenesmus, systemic symptoms (malaise, anorexia, fever), abdo tenderness

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15
Q

Give 4 extraintestinal manifestations of IBD

A
  • clubbing
  • erythema nodosum
  • pyoderma gangrenosum
  • conjunctivitis
  • iritis
  • uvieitis (more in UC)
  • episcleritis (more in CD)
  • large joint arthritis
  • anklyosing spondylitis
  • fatty liver
  • granulomata of skin
  • kidney stones
  • primary sclerosing cholangitis (more in UC)
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16
Q

How should IBD be investigated

A
  • bloods: FBC, LFT, U&E, LFT, ESR, CRP, haematinics, iron studies
  • stool culture and microscopy
  • faecal calprotectin
  • c diff toxin
  • colonoscopy and biospies (2 from 5 sites in distal ileum and rectum for UC)
  • AXR if toxic megacolon suspected (tender, distended abdomen)
  • pelvic MRI if perianal disease which isnt simple fistula
  • TMPT levels for azathioprine treatment
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17
Q

Describe the NICE guidelines for severity of IBD

A

Mild: <4 stools p/day, small blood in stools, no anaemia, HR<90, no fever, normal ESR and CRP
Mod: 4-6 stools, some blood, no anaemia, fever, HR<90, normal ESR and CRP
Severe: >6 stools, visible blood, systemic upset fever, high HR, anaemia, ESR or CRP up)

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18
Q

How are crohns flares managed?

A
  • pred 30-40mg
  • azathioprine added if 2nd flare in 12 months or methotrex if TPMT levels low
  • Infliximab if severe/ refractory
  • Surgery if disease limited to distal ileum
  • Antispasmodics can treat cramps if obstruction excluded
19
Q

How is crohns remission maintained?

A

Azathioprine or mercaptopurine, infliximab if severe
Stop smoking
Lopermide can help reduce diarrhoea in remission but not acute disease

20
Q

How is UC remission induced?

A

Aminosalicylates (mesalazine) in mild to mod disease, presnisolone if severe or this doesnt work
Azathioprine or 6MP if >1 relapse per year
CIclosporin or infliximab for rescue therapy in severe refractory colitis
Surgery last resort

21
Q

Give 4 complications of IBD

A
  • extra intestinal manifestations (ank spond)
  • colorectal cancer, bowel cancer
  • psychosocial and sexual problems
  • osteoporosis due to steds
  • toxic megacolon (usually triggered by opiates, hypokalaemia, anticholinergics, barium enemas)
  • perforation, stricture, fistula
  • iron, folate and B12 deficiency
  • gall and renal stones
22
Q

What is acute liver failure?

A

Appearance of severe complications (coagulopathy and encephalopathy) rapidly after first signs of liver disease. Hyperacute is <1 week, acute= 8-28 days, subacute= 4-12 weeks.

23
Q

Give 4 causes of acute liver failure

A

Infections: viral hepatitis, yellow fever, leptospirosis
Drugs: paracetamol OD, isoniazid
Toxins: types of mushrooms
Vascular: veno- occlusive disease
Other: alcohol, fatty liver, primary billary cholangitis, haemochromatosis, autoimmune hepatitis, a1 antitrypsin deficiency, malignancy

24
Q

How does acute liver failure present?

A
  • rapid onset jaundice, weakness and ascites
  • encephalopathy: confusion, hallucinations, reduced GCS, papillodema, hypertension, bradycardia
  • Coagulopathy: prolonged PR/ INR, thrombocytopenia, bleeding, bruising, DIC
  • Signs of chronic disease: hepatic flap, caput medusa, palmer erythema, dupuytrens contracture
25
Q

How should acute liver disease be investigated?

A
  • FBC (? infection, ? GI bleed), U&E, LFT, clotting, glucose, paracetamol level, virology, CMV and EBV serology, ferritin
  • Blood culture, urine culture, asctitic tap for MC&S
  • CXR, abdo USS, doppler flow studies of portal vein
26
Q

Why does encephalopathy occur in liver disease?

A

Nitrogenous waste (eg ammonia) builds up in circulation and passes to brain. Astrocytes clear it but as they do so produce excess glutamine which causes osmotic shift of fluid into cells- hence causing cerebral odema

27
Q

How is acute liver disease managed? (9)

A
  • beware sepsis, hypos, varices bleeding, encephalopathies
  • urinary and central venous catheters to monitor fluid status
  • monitor obs
  • 10% IV glucose IV 1L/2hrs to avoid hypos
  • treat cause
  • treat malnourishment
  • treat seizures with phenytoin
  • haemodialysis if renal failure develops
  • liase with transplant service
28
Q

List 6 complications of acute liver disease and how you treat them?

A
  • cerebral odema: on ITU, 20% mannitol IV and hyperventilate
  • Ascites: fluid restriction, low salt diet, diuretics
  • upper GI bleed: vit K 10mg/d IV for 3 days, platelets, FFP + bloods as needed, endoscopy, terlipressin
  • Infection: ceftriaxone
  • Hypoglycaemia: 50 ml 50% glucose if drops <2 mmol/L
  • Encephalopathy: avoid sedatives, 20 degree head tilt, correct electrolytes, lactulose (causes colonic pH to drop so traps NH3 in colon)
29
Q

What can cause malnutrition?

A
  • neglect
  • poverty
  • dementia
  • severe learning dificulties and mental health problems
  • malignancy
  • renal or heart failure
  • infections (HIV, CMV, hepatitis)
30
Q

What are the 2 clinical syndromes of malnutrition?

A

marasums: inadequate protein and energy, severe muscle wasting
Kwashiorkor: fair- normal energy intake, but inadequate protein leading to odema, usually in children age 1-2

31
Q

How is malnutrition managed?

A
  • NG feeding (enteral) in those with poor intake but functional GI tract or dyspahgia
  • Parenteral nutrition (IV) is used in inadequate intake and non functional GI tract
  • treat cause
  • dietician and social services review
32
Q

What % of normal nutrient requirements are given and for how long in those at risk of refeeding syndrome?

A

50% for 2 days

33
Q

How can malnutrition be assessed?

A

Malnutrition universal score tool.

Looks at BMI, weightloss, illness

34
Q

Describe the clinical features of chronic liver disease

A
  • jaundice
  • ascites
  • hepatomegaly
  • hepatic flap
  • bleeding and brusing
  • deupytrens
  • caput medusa
  • spider naevi
  • encephalopathy
35
Q

What may cause chronic liver disease?

A
  • alcohol is #1
  • non alcoholic steatohepatitis and viral hepatitis are 2nd
  • primary sclerosing cholangitis in men
  • autoimmune hepatitis and primary biliary cholangitis in women
  • haemochromatosis
36
Q

How is cirrhosis managed?

A
  • spironolactone for ascites
  • prophylaxis for oesphageal varices
  • DEXA scan to asses osteoporosis
  • AFP and USS screening for hepatocellar carcinoma
  • platelet infusions if symptomatic thrombocytopenia
37
Q

Give 4 red flags for dyspepsia

A
  • weight loss
  • fhx UGI ca
  • dysphagia
  • age >55 and new onset
  • palpable mass
  • persistant vomiting
  • UGI bleed
38
Q

Describe the clinical features of coeliac disease

A

loose stools, bloating, and abdo cramps worse after eating breads, oats, barley, wheat and rye (gluten)

39
Q

How is coeliac disease diagnosed?

A
  • tTG- raised in most but not diagnostic
  • OGD and biopsies - lamina propria inflammation, villous atrophy and intra epithelial lymphocytosis
  • maintain normal diet during investigations
40
Q

What needs to be monitored for those on TPN?

A
  • Mg, K and PO4 3 times a week
  • zinc weekly
  • weight and fluid balance (they don’t usually need additional fluid)
41
Q

What should you do if a pt on TPN gets a temp?

A
  • think line infection or other cause
  • stop TPN for 30 mins to see if temp drops- if it does then restart it, if temp goes up again then this suggests line infection
  • all pts should get peripheral and central cultures
  • consider chest, urine or wound infections also
42
Q

What are the hickman line / TPN rules?

A
  • dont touch
  • dont take blood
  • don’t stop TPN suddenly as this can cause severe roubound hypoglycaemia (needs to be stopped slowly)
  • don’t give anything otherthan TPN down the line
  • inspect daily (visually) and ask specialist nurse if any concerns
43
Q

what are features of TPN line infection

A
  • pyrexia or rigors with feeding

- muscle pain (suggests staph)

44
Q

What causes high SAAG (<1.1g/L) and low SAAG (<1.1) ascites?

A 
High SAAG: cirrhosis
alcoholic hepatitis
portal vein thrombosis
massive hepatic metastases
heart failure
Low SAAG:peritoneal carcinomatosis
infection (including TB)
pancreatitis
nephrotic syndrome
serositis (including lyphoma)

Y3 Medicine (9 decks)

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