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Year 3 Medicine > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What are the distinguishing features of Chrohns vs UC?

A
  • Chrohs:
    • Cobblestone appearance
    • Rosethorn ulcers
    • Discontinuous/ skip lesions
    • Transmural - Obstructucted bowel
    • Narrowing of intestinal lumen
    • Skip lesions and strictures
    • Ileocaecal valve: RIF pain
  • UC:
    • Rectum mainly - LIF pain
    • Continuous
    • Crypt abscesses
    • Submucosa and mucosa mainlt
    • Loss of haustra > lead pipe colon
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2
Q

What is UC?

A
  • US is a relapsing and remitting IBD of the colonic mucosa.
  • It may affect just the rectum
  • Can extend to part of the colon (left-sided colitis) or the entire colon (pancolitis, in ~30%).
  • ‘Never’ spreads proximal to the ileocaecal valve
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3
Q

What is the pathophysiology of UC?

A
  • Hyperaemic/haemorrhagic colonic mucosa ± pseudo-polyps formed by inflammation.
  • Punctate ulcers deep into the lamina propria—
  • Continuous inflammation of mucosa
  • Mucosa and submucosa - NOT transmural
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4
Q

What are some of the symptoms of UC?

A
  • Episodic or chronic diarrhoea (± blood & mucus)
  • Crampy abdominal discomfort
  • Systemic symptoms: fever, malaise, anorexia, ↓weight.
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5
Q

What are some of the extra intestinal signs of UC?

A
  • Fingers: Clubbing
  • Mouth: Aphthous oral ulcers
  • Skin: Erythema nodosum, Pyoderma gangrenosum
  • Eyes: Conjunctivitis; episcleritis; iritis
  • Bones: Large joint arthritis; sacroiliitis; ankylosing spondylitis; psc (p[link]); nutritional deficits.
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6
Q

What investigations are used to for diagnosing IBD?

A
  • Blood tests: FBC (anaemia, leukocytosis, or thrombocytosis); UE (AKI due to GI losses); CRP; ESR, LFT
  • Stools: stool cultures; faecal calprotectin (do not do in presence of blood); c. diff
  • Simple imaging: AXR (less frequent but use for toxic megacolon): dilated loops with air-fluid level secondary to ileus; free air is consistent with perforation; in toxic megacolon, the transverse colon is dilated to ≥6 cm in diameter
  • Endoscopy:
    • Flexible sigmoidoscopy (safest in bloody diarrhoeah)
    • Colonoscopy (proximal disease)
    • Capsule endoscopy (small bowel mucosa:
  • Biopsy
  • Cross sectional imaging
    • CT abdomen
    • MRI enterography
    • MRI rectum
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7
Q

What are some of the complications of UC?

A
  • Toxic dilatation of colon (toxic megacolon)
  • Venous thromboembolism
  • Colonic cancer
  • Perforation
  • Infection
  • Stricture/ pseudopolyps
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8
Q

How is IBD (maintaining remissions) treated?

A
  • UC:
    • Mesalazine 5-asa (PR or PO)
    • Hydrocortisone: Topical steroid foams pr
  • Chrohns:
    • Azathioprine
    • Biologics: Anti-tnfα‎ infliximab and adalimumab; Anti-integrin etc.
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9
Q

How is acute (moderate - severe) IBD managed?

A
  • UC
    • Moderate: oral prednisolone 40mg/d for 1wk; then maintain on mesalazine
    • Severe: IV Hydrocortisone 100mg/6h; iv hydration/electrolyte replacement
      • If symptoms dont improve 3-5 days: cyclosporin
      • Or biologics: infliximab
      • Then surgery
  • Chrohns:
    • Same as above
    • Severe: IV Hydrocortisone 100mg/6h, NBM, metranidazole
      • Biologics: Anti-TNFα‎; Anti-integrin
      • Surgery: ~20% subtotal colectomy + terminal ileostomy
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10
Q

What is Chrohns?

A

A chronic inflammatory disease characterized by transmural granulomatous inflammation affecting any part of the gut from mouth to anus

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11
Q

What are some of the symptoms of Chrohns?

A
  • Diarrhoea (more mucus filled than blood unlike UC)
  • Abdominal pain (RIF)
  • Weight loss
  • Systemic symptoms: fatigue, fever, malaise, anorexia.
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12
Q

What are some of the intraintestinal signs of Chrohns?

A
  • Bowel ulceration
  • Abdominal tenderness/mass
  • Perianal abscess/fistulae/skin tags
  • Anal strictures
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13
Q

What are some of the small bowel complications of Chrohn’s?

A
  • Toxic dilatation of colon
  • Abscess formation (abdominal, pelvic, or perianal)
  • Fistulae: entero-enteric, colovesical (bladder), colovaginal, perianal
  • Colon cancer
  • Malnutrition.
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14
Q

What tests should be performed for Crohns?

A
  • Bloods: FBC (anaemia), ESR, CRP (elevated), U&E, LFT, INR, ferritin B12, folate - may be low (anaemia)
  • Stool: faecal calprotectin, C.diff
  • Imaging: plain abdo x ray, CT
  • Specialist: colonoscopy, tissue biopsy, ?OGD (if disease extensive)
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15
Q

What is Charcot’s triad?

A

RUQ, Fever, Jaundice

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16
Q

What is Reynald’s Pentad?

A
  • Charcots triad
    • shock (tachycardia, hypotensive, shock)
  • Indicated serious infection of biliary tree
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17
Q

What is Mirizzi syndrome?

A

Obstructive jaundice from common bile duct compression by a gallstone impacted in the cystic duct, often associated with cholangitis

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18
Q

How is Biliary Colic treated?

A
  • Conservative: lifestyle, weight loss, reduced fat
  • Pharmacological:
    • Analgesia: morphine
    • Anti emetic: metacloperamide?
  • Surgery: elective lap cholecystectomy in 6 wks of presentation
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19
Q

What is Calot’s triangle?

A
  • Calot’s triangle (cystohepatic triangle) is a small anatomical space in the abdomen.
  • It is located at the porta hepatis of the liver – where the hepatic ducts and neurovascular structures enter/exit the liver.
  • The borders are as follows:
    • Medial – common hepatic duct.
    • Inferior – cystic duct.
    • Superior – inferior surface of the liver.
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20
Q

What is the surgical relevance of Calots triangle?

A
  • Clinical importance during laparoscopic cholecystectomy
  • Triangle is dissected by surgeon, and its contents and borders identified.
  • Permits safe ligation and division of the cystic duct and cystic artery.
  • Right hepatic artery is important – this must be identified by the surgeon prior to ligation of the cystic artery.
  • If Calot’s triangle cannot be found ( e.g. inflammation), the surgeon may perform a subtotal cholecystectomy, or open surgery.
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21
Q

What is Coeliac disese?

A
  • Immunological response to the Gladin fraction of gluten
  • Immune activation in the small intestine leads to villous atrophy, hypertrophy of the intestinal crypts, and increased numbers of lymphocytes in the epithelium and lamina propria
  • Suspect this if diarrhoea + weight loss or anaemia (esp. if iron or b12 ↓)
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22
Q

What is the prevalence of Coeliac?

A
  • 1 in 100–300 (commoner if Irish).
  • Peaks in childhood and 50–60yrs ♀:♂ >1:1.
  • Risk in 1st-degree relatives
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23
Q

What are the symptoms of Coeliacs?

A
  • Stinking stools/steatorrhoea
  • Diarrhoea
  • Abdominal pain
  • Bloating; nausea + vomiting
  • Mouth: Aphthous ulcers and angular stomatitis
  • ↓weight
  • Fatigue
  • Weakness
  • Bones: Osteomalacia
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24
Q

What are some of the complications of Coeliac?

A
  • Anaemia
  • Dermatitis herpetiformis
  • Osteopenia/osteoporosis
  • GI t-cell lymphoma
  • ↓weight
  • ↑risk of malignancy (lymphoma, gastric, oesophageal, colorectal)
  • Neuropathies
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25
Q

How is Coeliac diagnosed?

A
  • Bloods: General:↓Hb↓b12, ↓ferritin, consider blood smear
  • Antibodies:
    • IgA-tTG - not a diagnostic test in adult patients - above normal
    • Endomysial antibody
  • Imaging:
    • Endoscopy and duodenal biopsy while on a gluten-containing diet:
      • Subtotal villous atrophy
      • ↑Intra-epithelial wbcs
      • Crypt hyperplasia
  • Others: HLA, skin biopsy (dermatitis herpetiformis), gluten challenge
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26
Q

How is Coeliac disease treated ?

A
  • Gluten free diet
  • Bisphosphonates for osteoporosis
  • Pneumococcal vaccine + booster every 5 years + influenza on a case by case basis
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27
Q

What is dysphagia?

A

Dysphagia is difficulty in swallowing and should prompt urgent investigation to exclude malignancy

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28
Q

What are some of the causes of dysphagia?

A

Oral, pharyngeal, or oesophageal? Mechanical or motility related?

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29
Q

What are the key history questions to ask re dysphagia?

A
  1. Was there difficulty swallowing solids + liquids from the start?
    • Yes: motility disorder (eg achalasia, cns, or pharyngeal causes).
    • No: Solids then liquids: stricture (benign or malignant).
  2. Is it difficult to initiate a swallowing movement?
    • Yes: bulbar palsy, especially if patient coughs on swallowing
  3. Is swallowing painful (odynophagia)?
    • Yes: ulceration (malignancy, oesophagitis, viral infection or Candida in immunocompromised, or poor steroid inhaler technique) / spasm.
  4. Is the dysphagia intermittent or is it constant and getting worse?
    • Intermittent: oesophageal spasm.
    • Constant and worsening: suspect malignant stricture
  5. Does the neck bulge or gurgle on drinking?
  • Yes: Suspect a pharyngeal pouch
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30
Q

What are some of the signs of dysphagia?

A
  • Is the patient cachectic or anaemic?
  • Examine the mouth
  • Feel for left Virchow’s node—intra-abdominal malignancy)
  • Signs of systemic disease eg systemic sclerosis
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31
Q

What are some of the tests for dysphagia?

A

Bloods: FBC (anaemia); U+E (dehydration).

  1. OGD ± biopsy
  2. Barium swallow - pharyngeal pouch
  3. Oesophageal manometry - dysmotility.

(Video fluoroscopy may help identify neurogenic causes)

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32
Q

What are the symptoms and investigations for diffuse oesophageal spasm?

A
  • Sx: intermittent dysphagia ± chest pain.
  • Contrast swallow/manometry: abnormal contractions
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33
Q

What is Achalasia?

A

Achalasia is an oesophageal motor disorder of unknown aetiology, characterised by oesophageal aperistalsis and insufficient lower oesophageal sphincter (LOS) relaxation in response to swallowing

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34
Q

What are the sx of achalasia?

A
  • Dysphagia
  • Regurgitation
  • ↓Weight
  • Retrosternal pressure and pain
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35
Q

How is achalasia investigated and what is found?

A
  • Upper GI endoscopy: mucosa obscured by retained saliva with frothy appearance; in advanced cases oesophagus may be dilated and tortuous and contain food debris (sigmoid oesophagus)
  • Manometry: incomplete relaxation of LOS with wet swallows and oesophageal aperistalsis; typically high resting lower oesophageal pressure
  • Barium swallow: bird beak-like narrowing at the gastro-oesophageal junction
    *
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36
Q

How is achalasia treated?

A
  • Pharmacological:
    • PPIs
    • CCBs: nifedepine
    • Nitrates: isosorbide dinitrate
  • Surgical:
    • Botulinum toxin injection (non-invasive procedure)
    • Endoscopic pneumatic balloon dilatation
    • Laparoscopic Heller’s cardiomyotomy
37
Q

When should dyspepsia be referred?

A
  • Dysphagia OR
  • >55 yo + persistent symptoms OR
  • ALARM signs
38
Q

What are the alarm’s symptoms?

A
  • Anaemia
  • Loss of weight
  • Anorexia
  • Recent onset/ progressive symptoms
  • Malaena/ haematemesis
  • Swallowing/ difficulty
39
Q

In addition to ALARMS, what are the other symptoms experienced?

A
  • Epigastric pain often related to hunger
  • Specific foods, or time of day,
  • Fullness after meals
  • Heartburn (retrosternal pain)
  • Tender epigastrium.
40
Q

One of the most common causes of dyspepsia, is H.Pylori. How is this tested and treated?

A
  • 2 abx + PPI -
    • Lansoprazole 30mg/12h po
    • Clarithromycin 250mg/12h po
    • Amoxicillin 1g/12h po for 1wk.
  • Refer for urgent endoscopy - dysphagia, + ≳55 with alarm symptoms / with treatment-refractory dyspepsia
41
Q

What is the incidence of duodenal vs peptic ulcer?

A

4-fold commoner than GU

42
Q

What are the major minor RFs for duodenal ulcers?

A
  • Major: H.pylori (90%); drugs (nsaids; steroids; ssri).
  • Major: ↑Gastric acid secretion; ↑gastric emptying (↓duodenal pH); blood group o; smoking.
43
Q

What are the signs/ symptoms of duodenal vs gastric ulcers?

A
  • Gastric: eating exacerbates rather than relieves pain
  • Duodenal: pain is relieved by food but occurs 2-3 hr after a meal
44
Q

What is the diagnosis for duodenal ulcer?

A
  • Upper gi endoscopy.
  • Test for H.pylori
  • Measure gastrin concentrations when off ppis - Zollinger–Ellison syndrome
45
Q

Where and to whom to gastric ulcers occur?

A
  • Stomach - lesser curve.
  • Elderly
  • Ulcers elsewhere are more often malignant.
46
Q

What are the risk factors for gastric ulcers?

A
  • H.pylori (~80%)
  • Smoking
  • NSAIDs
  • Reflux of duodenal contents
  • Delayed gastric emptying
  • Stress, eg neurosurgery or burns (Cushing’s or Curling’s ulcers).
47
Q

How are gastric ulcers diagnosed?

A
  • Upper gi endoscopy to exclude malignancy
  • Multiple biopsies from ulcer rim and base (histology, H.pylori).
  • Repeat endoscopy after 6–8 weeks to confirm healing and exclude malignancy.
48
Q

What are the functions of the liver?

A
49
Q

What is Wernicke’s encephalopathy?

A
  • Caused by B1 (thiamine) deficiency secondary to alcohol miuse
  • Presents: confusion, ataxia, nystagmus
50
Q

What are the risk factors to be asked for patients with liver disease?

A
  • Blood transfusions <1990 UK
  • Ops/ Vaccinations
  • IVDU
  • Sexual exposure
  • Medications
  • FH (liver disease, diabetes, IBD)
  • Obesity
  • Alcohol
  • Foreign travel
51
Q

When do acute and chronic liver disease arise?

A

Acute:

  • No existing liver condition
  • Resolves in 6 months: Hep A, E, CMV, EBV, DILI

Chronic:

  • Starts with acute
  • Effects beyond 6mo
  • Cirrhosis and complications: alcohol, Hep C, NASH, autoimmune (PBC,PSC, AIH)
52
Q

What are the signs of chronic liver diease?

A
  • Spider naevi
  • Finger clubbing
  • Palmer erythema
  • Ascites
  • Hepato/splenomegaly
  • Hepatic encephalopathy
  • Coagulopathy
  • Jaundice
  • Hepatic flap
  • Aphraxia
53
Q

What investigations are used in liver disease and what do they look for?

A
  • Bloods: FBC, UE, coagulopathy( thrombocytopenia), Bilirubin/ Albumin, glucose, paracetemol, Hep ABC, CMV + EBV serology, ferritin, a1 anti trypsin deficiency, LFT:
    • îALT: Hepatocytes
    • îALP: + îGGT - Bile ducts disease + some liver conditions (post hepatic)
      • î​ALP alone - bone disease
    • îLFT showing cholestatic abnormality –> USS (dilated ducts/ cirrhosis)
  • Microbiology: urine and blood cultures, ascitic tap (SBP)
  • Imaging: CXR, USS, doppler of veins
54
Q

What is included in the liver screen?

A
  • Hepatitis BC
  • IRON: ferritin/ transferring
  • AutoABs (AMA/SMA), Ig
  • CAEROPLASMIN
  • Alpha-a-antitrypsin
  • Coeliac
  • TFT, lipids, glucose
55
Q

How do you manage liver failure?

A
  • NG tube/ cathetar
  • Nutritional supplements: thiamine + folate
  • Steroids
  • 10% glucose to avoid hypoglycaemia
  • Treat the cause: e.g. paracetemol - N-acetylcysteine
  • Ascites: furosemide + spironolactone
  • Bleeding: vitamin K
  • Encephalopathy: lactulose 30–50mL/8h(aim for 2–4 soft stools/d + Rifaximin
  • Seizures (+alcohol withdrawal): diazepam + lorazepam
  • Liver transplant
56
Q

What criteria is used for determining liver transplantation

A

King College Criteria for Liver Transplantatio

57
Q

Which conditions lead to chronic liver disease which could lead to cirrhosis. Which ones are more common in men and females?

A
  • Non alcoholic steatohepatis hepatitis
  • Viral hepatitis B+C
  • Women: PBC, autoimmune hepatitis
  • Men: PSC, associated with IBD, haemachromatosis
  • Adolescents/ young adults: Wilsons, anti LKM autoimmune hepatitis
58
Q

What is liver Cirrhosis?

A
  • Cirrhosis is the pathological end-stage of any chronic liver disease and most commonly results from chronic hepatitis B and C, alcohol-related liver disease, and non-alcoholic fatty liver disease
  • Irreversible liver damage.
  • Histologically: fibrosis and conversion of normal liver architecture to structurally abnormal nodules known as regenerative nodules
59
Q

What are some of the signs of liver cirrhosis?

A
  • Leuconychia: white nails with lunulae undemarcated, from hypo-albuminaemia
  • Hands: Palmar erythema, Dupuytren’s contracture; spider naevi
  • Xanthelasma
  • Gynaecomastia
  • Atrophic testes
  • Loss of body hair
  • Parotid enlargement
  • Portal hypertension: Hepato (small in late liver)/ splenomegaly, Ascites
60
Q

Who should you suspect liver cirrhosis for?

A
  • Patients with thrombocytopenia
  • Clinical stigmata of chronic liver disease
61
Q

What investigations are used for Cirrhosis

A
  • Imaging: - splenomegaly, course texture, nodularity
  • Fibroscan: quicker and more specific
  • Endoscopy: for varices
62
Q

What are the complications of Cirrhosis and how are they investigated and treated?

A
  • Oesophageal varices: Endoscopy: Primary prophylaxis
  • Splenomegaly, liver fibrosis, nodules, sclerosis, hepatomagaly​: USS: (+fibroscan, liver biopsy)
  • Ascites: Spirinolactone > paracentesis
  • Spontaneous bacterial peritonitis: Ascitic tap
  • Hepatocellular carcinoma: alpha-fetoprotein, USS every 6 months
63
Q

What questions should be asked when nutritional assessment is considered

A
  • Appetite
  • Diet history
  • Changes in oral intake
  • Changes in weight
  • MUST tool - Malnutrition Universal Screening tool
64
Q

How do you provide nutritional support conservatively?

A
  • Food and encouragement
  • Avoid interruptions
  • Encourage high quality options
  • Assist with eating
  • Provide appropriate cutlery
  • Teeth
  • Dietitician - nutritional supplements
65
Q

What options provide nutrition when they have a non functioning GI tract or unsafe swallow?

A
  • NG tube
  • PEG/ RIG?PEGJ/RIGJ
  • Paraenteral nutrition
66
Q

What is an NG tube and what are its benefits?

A
  • Short term access and provide all of the nutritional and fluid requirements
  • On top of pt oral intake
  • Check pH to ensure tip is in stomach (not lungs) - pH can be affected by PPI
  • Use CXR to confirm position
  • Can < risk of aspiration, but they can still aspirate through saliva
67
Q

What is an PEG/RIG/PEGJ/RIGJ and what are its benefits?

A
  • Provide longer term enteral access than an NG tube
  • Stomach - PEG and RIG
  • Small bowel - PEG-J or PEG-J
  • Must be placed endoscopically (PEG) or radiologically (RIG)
  • Do not prevent aspiration as patients may aspirate through their saliva.
68
Q

What is paraenteral nutrition and what are its benefits?

A
  • Provides nutrition and fluid directly into patients veins
  • When GI tract is not accessible (blocked) or not working (short, leaking or diseased)
  • Mix of fluids, micro and macronutritients
  • Dedicated central line required: PICC or Hickman line
  • Risks: sepsis, liver dysfunction
69
Q

What other questions should be asked in a GI bleed history?

A
  • What do they mean by passing blood
  • Haematemesis (fresh vomited blood) ?
  • Coffee ground vomit (altered blood but anything that has been in the stomach)
  • Malaena (black tarry sticky stool)
  • Fresh PR bleeding (lower GI or in a haemodynamically unstable pt it can be upper GI)
  • Risk factors: chronic liver disease, stigmata of chronic liver disease, NSAIDs, anti patelets or anticoagulants?
70
Q

What are some of the common causes of an upper GI bleed?

A
  • Peptic ulcers
  • Mallory-Weiss tear
  • Oesophageal varices
  • Gastritis/gastric erosions
  • Drugs (NSAIDS, aspirin, steroids, thrombolytics, anticoagulants)
  • Oesophagitis
  • Duodenitis
  • Malignancy
  • No obvious cause
71
Q

What are some of the rarer causes of upper GI bleeding?

A
  • Bleeding disorders
  • Portal hypertensive gastropathy
  • Aorto-enteric fistula10
  • Angiodysplasia
  • Haemobilia
  • Dieulafoy lesion11
  • Meckel’s diverticulum
  • Peutz-Jeghers’ syndrome
  • Osler-Weber-Rendu syndrome.
72
Q

What signs indicate an upper GI bleed?

A
  • Malaena
  • Haematemesis
73
Q

How would you manage an acute upper GI bleed?

A
  • ABCDE!
  • A- Protect airway
  • B- High flow o2
  • C - IV access, 2 wide bore cannulae, take bloods (FBC, UE, LFT, clotting, cross match, group and save);
    • IV fluids: If haemodynamically, give group O Rh−ve blood. Avoid saline if cirrhotic/varices
    • Transfuse (with crossmatched blood if needed) if significant Hb drop (<70g/L).
    • Urinary cathetar: Urine Output
    • Consider CVP line to monitor and guide fluid replacement
  • CXR, ECG, ABG
  • Correct clotting abnormalities (vitamin k, ffp, platelets)
  • Specific management: varices - terlipressin iv eg 1–2mg/6h for ≤3d + broad-spectrum iv antibiotic cover.
  • Monitor pulse, bp, and cvp (keep >5cmH2O) at least hourly until stable.
  • OGD
  • If endoscopic control fails, surgery or emergency mesenteric angiography, varices: Sengstaken–Blakemore tube - uses balloons to decompress the varices
74
Q

What tests are used for evaluating Upper GI bleeds?

A
  • Rockall - risk of death by upper GI bleeds and re bleeding
  • Glasgow Blatchford - predicts need for intervention. Spec blood tests required
75
Q

What are the specific management techniques for oesophageal varices?

A
  1. IV access and fluid resuscitation
  2. IV Prophylactic AB (broad spectrum)
  3. Telipressin (if no ischaemic HD/ PVD) + somatostatin analogues
  4. Refer for Upper GI endoscopy.
  5. Surgery
    1. Endoscopic banding
    2. Sengstaken–Blakemore tube - uses balloons to decompress the varices. Used to buy time.
    3. TIPPS (trans jugular intra hepatic porto systemic shunt) - connects portal + hepatic vein.
76
Q

How do you specifically manage Peptic Ulcer?

A
  • Adrenaline, cauterisation, IV PPI omeprazole 80mg
  • H Pylori eraditcation (clarithromycin, amoxicillin, PPI)
  • Urgent upper GI endoscopy
  • Emergency mesenteric embolisation/ Angioembolisation
77
Q

What will blood tests reveal to you in an upper GI bleed?

A
  • FBC - Hg + platelet count - thrombocytopenia - chronic liver disease
  • UE - Î urea
  • Clotting - abnormal clotting
  • Group + save
  • LFTs - normal LFTs do not exclude chronic liver disease
  • Venous blood gas - Hg result
78
Q

What are the important things to consider when managing non variceal bleeding?

A
  • Causes: ulcer disease, vascular malformations: angiodysplasia
  • More likely to stop bleeding on their own than variceal bleeds
  • Ensure pt is haemadynamically stable before endoscopy
79
Q

How would you immediately manage managing non variceal bleeding?

A
  • IV access
  • Fluid resuscitation
  • Prescription: PPI possible post endoscopy
  • Discuss with GI team.
    • Endoscopy
    • If bleeding does not stop by endoscopy, radiological embolization or surgery may be possible
    • PPI to treat ulcers (maybe)
80
Q

What things should you check with Upper GI bleeding?

A
  • Peripherally cool/clammy; capillary refill time >2s; urine output <0.5mL/kg/h
  • ↓GCS (tricky to assess in decompensated liver disease) or encephalopathy
  • Tachycardia (pulse >100bpm)
  • Systolic BP <100mmHg; postural drop >20mmHg.
  • Calculate the Rockall score
81
Q

What are some of the complications of cirrhosis?

A
  • Hepatic failure: coagulopathy, encephalopathy, hypoalbuminaemia (oedema, leuconychia), liver flap, SBP, hypoglycaemia
  • Portal hypertension: ascites, splenomegaly, oesophageal varices, caput meducae
  • Increased risk of HCC
82
Q

How would you manage liver cirrhosis?

A
  • Conservative: stop drinking and smoking, lose weight, avoid NSAIDs, opiates and other hepatotoxic drugs
  • Pharmacological: symptomatic management
    • Alcohol abstinence: diazepam and chlordiazepoxide
    • Pruritis: colestyramine
    • Ascites: spironolactone + furosemide
    • Wilsons disease: pennicillamine
    • SBP: tazocin
  • Monitor for complications: USS + alpha feotoprotein (HCC) + variceal monitoring
  • Surgery: liver transplant - only definitive management
83
Q

What are the causes of liver cirrhosis?

A
  • Chronic alcohol abuse
  • Infection: HBV + HCV
  • Genetic disorders: hemachromatosis, wilsons disease, a1 anti trypsin deficiency
  • Vascular: budd chiari
  • Autoimmune: autoimmune hepatitis PBC, PSC
  • Drugs: amiodorone, methotrexate, rifampacin, methyldopa
  • NASH
84
Q

What grading systems are used for liver cirrhosis?

A

Child Pugh Grading System or cirrhosis and risk of variceal bleeding.

85
Q

What is the diagnostic criteria for IBS?

A

The diagnosis of IBS should be considered if the patient has had the following for at least 6 months:

  • Abdominal pain, and/or
  • Bloating, and/or
  • Change in bowel habit
86
Q

How is IBS managed?

A
  • Constipation: ensure adequate water and fibre intake and promote physical activity
    • Simple laxatives
  • Diarrhoea: avoid sorbitol sweeteners, alcohol, and caffeine; reduce dietary fibre content; encourage patients to identify their own ‘trigger’ foods
    • Bulking agent ± loperamide 2mg after each loose stool.
  • Bloating: oral antispasmodics: mebeverine 135mg/8h or hyoscine butylbromide 10mg/8h (over the counter)
  • Psychological symptoms/visceral hypersensitivity: CBT, hypnosis, and tricyclics, eg amitriptyline 10–20mg at night
87
Q

What classification system is used for GORD/ oesphagitis?

A

Los Angeles Classification

  1. 1 mucosal break. <5mm
  2. mucosal break >5mm
  3. Mucosal break <75% of oesophageal circumference
  4. Mucosal break >75% of oesophageal circumference
88
Q

If referring for an upper GI endoscopy, what should be done before hand?

A
  • NBM 4 h before
  • PPI stopped 2 wks before
  • Dont drive for 24ht if sedation used
  • Sedation: midazolam, propofol (if stronger needed)
  • Give continuous suction

Year 3 Medicine (11 decks)

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