3A Gastro Flashcards

(108 cards)

1
Q

What is Gilbert’s syndrome?
Inheritance?
Blood test?
Symptom?

A
  • Metabolic disorder, where liver does not properly process bilirubin
  • Autosomal recessive
  • Isolated raised bilirubin (> 17 µmol/L)
  • Intermittent jaundice (often precipitated by illness, exercise or stress eg fasting).
  • No treatment needed
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2
Q

What is this?

A

Barrett’s oesophagus
pearly pink - squamous epithelial mucosa
red- columnar intestinal mucosa

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3
Q

How much hydrochloric acid produced by stomach over day?

Causes of damage to stomach mucosa

A

1.5 litres

H. Pylori, NSAIDs, reflux smoking, alcohol, shock, ischaemia.

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4
Q
  1. Parietal cells produce? location?
  2. Chief cells produce?
  3. Goblet cells produce?
  4. G cells produce?
  5. ECL cells produce?
  6. D cells produce?
A
  1. HCl hydrochloric acid. Gastric body. and Intrinsic Factor (important for absorption of vitamin B12)
  2. Pepsinogen. (Once pepsinogen meets with acid it’s converted to pepsin → breaks down protein). and leptin.
  3. Muscous
  4. Gastrin. Gastric antrum. Increases acid.
  5. Histamine. Gastric body.Increases acid.
  6. Somatostatin. Whole stomach. Decreases acid.

Parietal cells make acid
Gastrin, cholinergic, histamine all inout into parietal cell activity

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5
Q

Gaviscon - how does it work

A

Alginic raft

The medicine works by forming a protective layer that floats on top of the contents of your stomach. This stops stomach acid escaping up into your food pipe. Gaviscon also contains an antacid that neutralises excess stomach acid and reduces pain and discomfort.

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6
Q

H2 receptor antagonists
- Give examples
- Reduce _____ secretion
- Side effects?

A
  1. Cimetidine, nizatidine, etc. (formerly ranitidine). Reduce acid secretion and pepsin secretion. Increase rate of peptic ulcer healing (4-8 weeks). Short half life. Extensive 1st pass metabolism. Few side effects.
    Side effects:
    cimetidine: anti-androgen, gynaecomastia
    inhibits p450, enhances warfarin, theophylline, tolbutamide.
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7
Q

Proton pump inhibitors
- Name examples
- How do they work
- Side effects

A

Irreversibly inhibit the final common pathway of H+ secretion
eg. omeprazole (pro-drug), lansoprazole, pantoprazole, rabeproazole, Esomeprazole (S-isomer, slower metabolism).
Inhibit acid secretion by 90%. Covalently inhibit proton pump. Dose matters little. Most metabolised by p450 system in liver.

Side effects - not many, Diarrhoea. Higher risk of c.diff, salmonella. (Stop PPI if patient on broad spectrum abx in hospital). Bacterial overgrowth - can’t keep small bowel sterile. Microscopic colitis.
Impaired calcium and magnesium absorption. Slight increase in osteoporosis.

Route - usually oral, IV if critically ill. Prevent stress ulcers in ITU.

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8
Q

GORD treatments
- Medication? (3)
- Name of surgery?

A

Gaviscon
PPI
H2RA
Laparoscopic fundoplication

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9
Q

Drugs to treat gastric/duodenal ulcers

  1. Misoprostol side effect?
  2. Sucralfate side effect?
A
  1. Diarrhoea. Uterine contractions (miscarriage /abortion)
  2. Constipation. (how it works -Coats stomach and duodenum)
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10
Q

Gastrin
Production stimulated by low _____ levels in the _______. Stimulates _______ cells to produce _______________. High _____ levels swtiches off __________ production at ___ cells.

Somatostatin - produced by ___ cells. Switches _____ ______ production.

A

Gastrin - production stimulated by low acid levels in stomach. Action - stimulates parietal cells to produce HCl. High acid levels switches off gastrin production at G cells.

Somatostatin - D cells.
Switches off acid production.
‘Somatostatin always switches things off’

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11
Q

What is another name for gastrinoma?

A

Zollinger-Ellison syndrome

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12
Q

Which diseases are associated with too little stomach acid?

A
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13
Q

Reflux red flags

A

Dysphagia
weight loss
Vomiting blood
Doesn’t respond to PPIs

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14
Q

GORD diagnosis

DD

Investigations

Management

A

Clinical - 8 week trial of PPI (take 30-45 mins before food)

Differential Diagnosis -
Hiatus hernia,
Reflux hypersensitivity
Functional heartburn.
H Pylori
Gastric ulcer - pain worse after food
Duodenal ulcer - pain better after food (DU better - Mayank!)
Secondary to asthma, pregnancy, food/drink, alcohol, stress, smoking, medications.

Investigations
- 24 hr pH monitoring - fine probe down nose to oesophagus
- HRM - high resolution manometry- assess swallow with colour picture
- Endoscopy

Treatment
- Risk reduction / Lifestyle management: alcohol, smoking, diet, elevate with pillows, avoid food before bed.
- OTC antacids
- PPI
- Ranitidine alternatives
- Surgery eg. nissan fundoplication

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15
Q

Oesophageal cancer
- Most common type? 1 & 2
- Causes
- Symptoms
- Investigations
- Staging
- Treatment

A

Most common type
1. Adenocarcinoma
2. SCC. Squamous cell carcinoma.

Smoking, alcohol, dietary, HPV, low socioeconomic status, head and neck ca.

Adenocarcinoma (columnar epithelium) lower third oesophagus - male, middle aged, secondary to GORD. - gastrooesophageal junction. Obese, smoking, Barret’s oesophagus (metaplasia).
SCC - anywhere.

Symptoms - progressive dysphagia (is cancer until proven otherwise)!
Persistent reflux not responding to PPI.
Weight loss
Pain
GORD

Investigations:
- OGD
- Barium swallow (obsolete, OGD much better)

Staging
- Upper GI endoscopy with biopsies
- CT scan (chest, abdo, pelvis)
- other investigations if needed eg CT-PET. Labelled deoxyglucose, Metabolically active lights up yellow.

Treatment
- localised disease: Perioperative chemotherapy (FLOT) x4, then surgery, then more chemotherapy x4.

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16
Q

Gastric cancer
1. Main cause?
2. Symptoms x3
3. Diagnostic procedure?
4. Treatments

A

Junctional cancers or non-junctional

  1. Cause - Heliocobacter pylori (90%) - colonises gastric body and antrum
    Gram negative bacillus - antibiotics
    Chronic atrophic gastritis first then cancer

Symptoms - early satiety, weight loss, anaemia, supraclavicular mass, haematemesis/malaena ( GI bleed)

Male, obese, older age, obesity, smoking, salted foods, FH: CDH1 gene, Menetries disease.

Diagnosis - endoscopy (ulcerated mass). 8x biopsies. you must biopsy gastric ulcer!

Treatment - stage, CT scan with contract (chest, abode, pelvis)
Staging laparoscopy yo check for peritoneal disease (3-6 months survival)
Biopsy.
Surgery - rooftop incision (open). Subtotal gastrectomy or Total gastrectomy(Roux-en-Y). Peritoneal stripping, HIPEC (heated intraperitoneal chemotherapy).
Chemo 4x before and 4x after.

Palliative care - stent, drain, palliative chemotherapy.

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17
Q

Oral candida
1. prevention?
2. treatment?

  1. Dental caries - causative organism?
  2. Complication?
  3. Ludwig’s angina - causative organism?
  4. Streptococcus pharyngitis - causative organism?
A
  1. Oral hygiene
  2. Nystatin, Fluconazole (treatment),
  3. Dental caries - Streptococcus mutans
  4. Complication - Endocarditis
  5. Ludwig’s angina - Streptococcus viridans, Staphylococcus epidermis, and Staphylococcus aureus
  6. Streptococcus pharyngitis - group A strep. Sore throat. (no cough, sneeze, runny nose, conjunctivitis → viral). Streptococcus pyogenes, hard to treat as has capsule.

Raised CRP - bacterial.
Raised neutrophils - bacterial?
Treatment - Ampicillin, amoxicillin, erythromycin,
Penicillin allergy - clindamycin (switches off toxin production?), cephalexin, azithromycin.

Treponema pallidum -syphillis. always pathological in oral cavity.

EBV - do not give amoxicillin (immune mediated rash).

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18
Q

Helicobacter pylori
- Symptoms
- Diagnosis
- Treatment

A

Sx - weight loss, stomach ache, pain, nausea,

Diagnosis
- stool sample
- HP antigen test
- HP PCR

Treatment
- Tripe therapy: PPI (any) plus 2 ABX (amoxicillin + clarithromycin/metronidazole) . Oral treatment for 1 week.

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19
Q

Diarrhoea
- History questions to ask?
- Causes of acute diarrhoea
- Causes of chronic osmotic diarrhoea
- Causes of chronic secretory diarrhoea

A

Patient history - ask
- Frequency (what’s normal for them)
- Consistency (Bristol stool chart)
- Dysentery? Bloody diarrhoea.
- Acute (<14 days) /persistent/chronic (>30 days)

Causes umbrellas
- increased water into lumen
- decreased water adsorption from lumen

Acute - infection
Chronic
- Osmotic. Lactose intolerance, magnesium supplements, osmotic laxatives, coeliac, Crohn’s, bile salt malabsorption- may be a cause of IBS (terminal ileum).

  • Secretory. C. diff, cholera, stimulant laxatives (eg Senna), hormones (g. hyperthyroidism), bile acid malabsorption,
    Ulcerative colitis, rectal villous adenoma (polyp).
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20
Q

Diarrhoea
- Treatments?

A
  • Treat underlying disorder eg. coeliac, UC, drugs
    -Opiates eg. codeine, loperamide (beware IBD - can cause toxic megacolon).
  • Anti-secretory drugs eg. octreotide (somatostatin analogue) can help with varices.
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21
Q

Constipation - causes?

A

Normal less than 3x day, more than 3x week.

Constipation - problem with evacuation or slow transit. Shapes study.

  • Endocrine eg. Hypothyroidism
  • Metabolic eg. Hypercalcaemia
  • Neurological eg anxiety.
  • Neuromuscular eg. MG
  • Physiological eg. dehydration
  • Mechanical eg. tumour, FB, adhesions.
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22
Q

Constipation treatments
- Lifestyle measures?
- Medications?

A

General measures eg. mobilising, hydration, increase dietary fibre. Stop aggravating medications.

Medications
- Bulk forming laxatives eg. fybogel/ispaghula.
- Stimulant laxative eg. Senna, bisocodyl.
- Stool softeners eg. sodium docusate.
- Osmotic laxatives eg. lactulose, Mg salts.
- 5HT4 agonist - prucalopride. For IBS (pain, other meds not worked).
- Naloxegol - works on opiate receptors in gut but not elsewhere on body - good if opiate caused constipation.

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23
Q

IBD
- Ulcerative Colitis
- Crohn’s

A

History -Symptoms, FH, Travel history, abx, smoker, saids, appendicectomy.

Pathophysiology - Crohn’s: T cell mediated

Tests - FBC (anaemia of chronic disease), B12/folate absorption, thrombocytosis = inflammation, CRP, hypoalbuminaemia (albumin goes down as inflammation goes up).
PCR.
5 things to do: AXR, LMWH, stool chart, stool cultures. ?

DD - Many eg. appendicitis, diverticulitis. Infective, non-infective.

Ulcerative colitis. Colon only.
Proctitis - UC limited to rectum
Pseudomemranous colitis - secondary to c.diff - yellow edges

Tests - Abdominal XR.
Treatment - Steroids urgently. Inpatient methylprednisolone (avoid in children - polymeric diet instead). IV fluids. Daily AXR. May eat and drink. LMWH (inflammation is pro-thrombotic state).

EIMs (extra-intestinal manifestations) - Joints, skin, eyes, liver.
mouth aphthous ulcers, episcleritis (Asymp, STERID DROPS), uveitis, erythema nodosum, pyoderma gangrenosum (sp?), arthritis.

Crohn’s - patchy transmural inflammation (vs UC just mucosal) skip lesions. Mouth to anus. Crohn’s colitis - Crohn’s disease affecting colon.

Drugs - aminosalicylates (mesalazine) -not Crohn’s, steroids, immunomodulators, surgery.
Thiopurines eg. azathioprine. Slow onset of action - bridging steroids.
Methotrexate - Crohn’s sometimes.
Ciclosporin(CsA) - if not responsive to steroids.
Infliximab (IFX).
Rescue therapy - IFX or CsA

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24
Q

Oesophageal varices.
1. Prophylaxis
2. Treatment?

A
  1. Propranolol (P=prophylaxis)
    NSBB = non-selective beta blocker
  2. Terlipressin (T=treatment).
    Vasopressin analogue.
    Octreotide may also be used. (somatostatin analogue = synthetic version of hormone somatostatin. Slows down cancer growth, slows down production of hormones)
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25
LFT's Bilirubin 20 µmol/L (3 - 17) ALP 104 u/L (30 - 100) ALT 53 u/L (3 - 40) γGT 58 u/L (8 - 60) Albumin 38 g/L (35 - 50)
26
The combination of cholestatic jaundice, raised IgM and positive anti-mitochondrial antibodies should hint towards the diagnosis of ? what is the 1st line therapy that will slow disease progression?
Primary biliary cirrhosis. Ursodeoxycholic acid (may protect the liver by increasing bile flow through the liver).
27
Colorectal cancer - name 3 symptoms - name 3 risk factors - Name 3 investigations
Symptoms: usually occult. Weight loss, PR bleeding, change in bowel habits (looser stool - cancer either secretes blood or mucus which stimulates increased peristalsis), tiredness, anaemia, abdominal pain, tenesmus, mucus, mass, emergency -blee, obstruction, perforation/peritonitis. Risk factors - increasing age, Western location - diet: high in fat and cholesterol, processed and red meat, too little fibre, obesity, alcohol, diabetes, smoking, genetic, IBD, pelvic radiotherapy, radiation exposure. Bowel screening FIT faecal immunochemical test. Investigations - History, abode exam, digital rectal examination, sigmoidoscopy, colonoscopy, staging CT/MRI (mets to LIVER and LUNGS), blood - CEA tumour marke, assess fitness for surgery.
28
Name 2 genetic causes of bowel cancer
- FAP (familial adenomatous polyposis - hundreds of polyps, over 90% chance cancer by age 70 without surgery - preventative sub-total colectomy plus ileostomy and later reconnection). - Hereditary non-polyposis colorectal cancer (HNPCC) / Lynch syndrome.85% lifetime risk,
29
Coeliac disease - Causative protein - Test - Ax skin disease - Treatment
Reaction to Gliadin - a protein in the gluten of wheat, rye and barley (oats are ok) IgA anti-endomysial antibody Tissue Transglutaminase (TTG) Dermatitis herpetiformis Gluten free diet
30
NAFLD / Metabolic MASLD Metabolic dysfunction associated steatitic liver disease
steatosis - simple fat. non-harmful. steatohepatitis - inflammation fibrosis - scarring cirrhosis - permanent end stage scarring, at risk of cancer Present with other features of metabolic syndrome - comorbidities eg diabetes, PCOS, cardiovascular disease, strokes. Presentation/ Tests - abnormal LGTs (mildly raised ALT or GGT), normal LFTs! Raised ferritin (normal transferrin). AST:ALT ratio. (higher AST 2:1 = alcohol related, Metabolic ALT2:1 NAFLD score (albumin, BMI and platelets), higher. 1:1 ratio can mean fibrosis) Fib4 score. - Ultrasound - steatosis. Picks up change if >30% fatty liver.Unreliable. - Liver biopsy (expensive). Gold standard test for diagnosis ad staging. - Transient Elastography, fibroscan. Scarred liver stiff. Uses ultrasound to produce a shear wave. Less accurate in obesity. Causes - Obesity - Genetics - Disorders of lipid metabolism - TPN - Hepatitis C - Losing weight too quickly eg. gastric surgery. - Medications eg chemo, amiodarone, tamoxifen, met, steroids, HAART - Starvation - Wilson's disease - Coeliac Treatment - lifestyle modification eg. weight loss, healthy diet, exercise, coffee. - Treating other aspects of metabolic syndrome eg control diabetes, stop smoking, statins, control BP, sleep apnoea. - Treat complications - Bariatric surgery (avoid in portal hypertension, varrices, cirrhosis) - Glitazones good, pioglitazone.
31
Alcohol related liver disease
Take a good alcohol history. Bad = > 14 units a week, no alcohol free days, all at once, harm eg injury/accident etc, physical dependence. Normal - alcohol dehydrogenase converts ethanol → acetaldehyde → acetate. Acetate excreted. If heavy alcohol, primary pathway gets saturated, use secondary pathway - ROS reactive oxygen species produced - causes damage. Risk factors - Women (lower levels of alcohol dehydrogenase). - genetic variability, ethnicity - nutrition, low B vitamins - Hepatitis co-infection - Co-exposure to drugs and toxins - Family history of alcoholism - genetically linked. Forms - alcoholic steatosis (simple fat) - alcoholic hepatitis (history of heavy drinking, inflammatory process (AST>x2ALT but less than 300, rising bilirubin, raised PT, hepatomegaly, neutrophilic). Emergency, high fatality. Tx- Steroids, pentoxifylline, alcohol abstinence (crucial). - cirrhosis and its complications. Most don't progress to cirrhosis. Wish of HCC. Abstinance can improve. Transplant can be considered.
32
Viral hepatitis
Viral hepatitis screen / liver screen - Hepatitis B - most infectious (100 x more infectious than HIV). Causes cirrhosis, HCC, liver transplant. Vaccinated as babies. Very common STD. IV drug user. Health worker. Mother to baby. Look first for HBsAg - surface antigen - general marker of CURRENT infection. anti-HBc IgM - marker of acute infection (Total) anti-HBc - current or past infection (core total antibody) anti-HBs - recovery or immunity (vaccination) HBeAg - high levels Treatment - pegylated interferon ... IgG = immune? Hepatitis C - most common. no symptoms until late stage 15/20 years. Vaccine. Curable - 2 drugs 8-12 weeks. Causes end stage cirrhosis, HCC, liver transplant. Can come with diabetes, B cell lymphomas. 85% of infections becomes chronic. Causes - IV drug use, harm-dialysis, needle stick injury, sexually transmitted, mother to child, tattoo, blood transfusion. Diagnosis - HCV antibodies. Appears 12 weeks after infection. HCV RNA - acute phase. Treatment - Protease inhibitors eg. telaprevir, NS5A inhibitors, NS5B inhibitors. Hepatitis D - Most severe form of viral hepatitis. Accelerated pathway. High death. Can only infect those with Hep B already. Co-infection or superinfection (bad). sex, drugs. consonants = chronic. Blood borne. Test anyone with HepB. Anti-HDV RNA? Treatment - Buleviritide (entry inhibitor). Hepatits A & E (vowels) - not chronic. Just acute. Enteric route - contaminated water, pork, shellfish. Mild illness. No carriage. Hep E - symptoms week 5-9, high ALT, IgG anti-HEV (immunised or past infection) and IgM anti-HEV (IgM = acute). Hep A - vaccine or Ig for contacts of cases. (both for older). Causes - viral infections as above plus EBV, CMV, HSV, etc., Bacterial infections, drugs, alcohol, poisons, wilson's disease, travel eg. yellow fever. Symptom - jaundice, icterus (eyes), (bilirubin > 20 micro mol) Rise of ALT. (not GGT non-specific) Causes Hepatocellular carcinoma (HCC). Malaise, weak, bleed.
33
Drug metabolism Which drugs reduce effect of OCP? Which drugs can raise INR when on warfarin?
Drug metabolism - liver. First pass metabolism through liver breaks down drug, or activates drug (eg azathioprine to mercaptopurine, levodopa to dopamine). Enzymes act on drug before reaching systemic circulation. eg. swallowing GTN tablet avoids headache after, or change to ISMN which avoids liver breakdown. Drugs w high first pass - nitrates, opioids. Oral bioavailability - (first pass metabolism) Drug excretion - kidney. Water soluble drugs easily eliminated. Fat soluble can't dissolve in urine. Convert first to soluble product in liver. Which drugs reduce effect of OCP? Carbamazepine and phenytoin (breaks down oestrogen)., rifampicin, St John's wort, barbiturates. Which drugs can raise INR when on warfarin? Enzyme inhibitors - ciprofloxacin (quinolones), clarithromycin. less breakdown of warfarin. Carithromycin also causes statin myopathy. Erythromycin, antifungals, SSRIs eg fluoxetine, paroxetine. Food interactions eg. recent TB, unwell after Japanese meal of tuna and mackerel. Flushing, itching, dizzy. Drug - ISONIAZID - histamine inhibitor, treatment for TB (avoid thymine rich eg. mature cheese, herring, marmite, bovril) or histamine rich foods (mature cheese, tuna, mackerel, salmon). Azathioprine - check TPMT genetic testing prior to commencing. Prescribing liver disease, be careful with pro-drugs, sedatives eg benzodiazepines, affect electrolyte and kidney, are metabolised inlayer and have narrow therapeutic range eg. warfarin, theophylline.
34
Problem drugs in renal disease Problem drugs in elderly
Furosemide, NSAIDs (worsen renal failure), metformin (lactic acidosis), insulin (hypos as kidney not clearing inulin), aminoglycosides, morphine. Elderly - opioids and sedatives, postural / orthostatic hypotension.
35
Isolated high bilirubin?
Gilbert's syndrome - a genetic hereditary disorder where slightly higher than normal levels of bilirubin build up in the blood, causing jaundice.
36
ALT AST Alk phos GGT Cholestatic picture?
ALT in cytoplasm - alto first to be affected. AST in mitochondria. Alk phos - liver, bone, metastasis. GGT - cell membrane adjacent to bile tract (means injury to bile tract). Cholestatic picture - high ALT, high bilirubin eg. gallstone. High ALP, ALT, Bili & GGT = liver failure. Also low platelets and albumin. Isolated raised ALT -
37
LFT interpretation - where are they made?
ALT - from hepatocytes, liver. More specific for liver. AST - liver, muscles. ALP.(alkaline phosphatase) - liver, bones, placenta, kidneys, bile ducts. GGT (gamma gt) - bile duct (predominantly) and liver. Albumin - protein, made in liver only. Important from oncotic pressure. INR / PT - clotting factors made in liver.
38
Ratio to remember for alcoholic hepatitis?
AST:ALT ratio. (higher AST 2:1 = alcohol related, Metabolic ALT2:1 NAFLD score (albumin, BMI and platelets), higher. 1:1 ratio can mean fibrosis) Fib4 score. GGT raised in alcohol
39
LFTs for hepatocellular injury Causes
Raised ALT and AST - NAFLD - obesity, diabetes, HTN - Viral hepatitis eg. chronic hep B/C - Ischaemic hepatitis (acute) - older, IHD - Alcohol - high AST to ALT ratio, microcytic anaemia low B12 - Drug induced eg. sodium valproate. - EBV - splenomegaly, sore throat, malaise, fever. - Hepatitis A/E - travel, D&V. - CMV. - Muscle injury (much higher AST than ALT). AST release from muscle injury.
40
LFTs for cholestatic injury
Raised ALP and GGT (more than ALT, AST). - Cholecystitis from gallstones - RUQ pain and fevers. USS. - PBC (primary biliary cholangitis) - itchy, maybe xanthelasma, chronic, antibodies. - PSC (primary sclerosing cholangitis_ - link to IBD. auto antibodies → ANCA. USS. MRCP (shows structuring/beads of bile ducts) - Cancer. Head of pancreas. Weight loss. - Drug induced eg. antibiotics CO-AMOXICLAV. - Sepsis Isolated raised ALP - Prostate cancer metastasised to bone - low Vitamin D
41
All LFTs raised - causes?
All raised but predominantly hepatocellular picture → Drug induced liver injury eg. paracetamol toxicity. (Reversal drug → N-acetylcysteine) Acute liver failure - URGENT ACTION required. Can be fatal.
42
Pancreatitis - causes?
Causes - I GET SMASHED -Idiopathic - Gall stones - Ethanol - Trauma - Steroids - Mumps - Autoimmune - Scorpion stings - Hypertriglyceridemia, hypercalcaemia and hyperparathyroidism - ERCP – endoscopic retrograde cholangiopancreatography - Drugs – such as sodium valproate, azathioprine and sulphonamides
43
Pancreas facts 1. Intra / retro peritoneal? 2. Sits behind the? 3. How to do needle biopies of pancreas? 4. _______ is activated by ______kinase in _________ into ______.
Retroperitoneal organ, sits behind the stomach Lesser sac sits between stomach and pancreas - in pancreatitis the lesser sac can fill with fluid Needle biopsies of pancreas can be done through posterior wall of stomach Proteases are released in inactivated form. Trypsinogen is activated by enterokinase in small bowel into trypsin. Trypsin then activates the zymogens/proteases to their active state. If trypsinogen happens in pancreas it causes acute pancreatitis. Acinar cells make enzymes.
44
Signs of chronic liver disease (ABCDEFGHIJ)
45
46
Causes of abnormal ALT? and how to investigate?
NAFLD Haemochromatosis Auitoimmune hepatitis Viral hepatitis Wilson's disease Alpha-1 antitrypsin deficiancy
47
Normal LFT values?
48
MRCP stands for? What is MRCP? What colour do the following objects appear? 1. Spine vertebra 2. Fat 3. Gallstones Benefits Risks
Magnetic resonance cholangiopancreatography Magnetic resonance imaging (MRI) is a type of scan that uses strong magnetic fields and radio waves to produce detailed images of the inside of the body. An MRI scanner is a large tube that contains powerful magnets. You lie inside the tube during the scan. Special sort of MRI to look at biliary and pancreatic system - liver, gallbladder, bile ducts, pancreas, pancreatic duct. 1. Grey (low intensity) 2. White (high intensity) 3. Black (low intensity) This images show gallstones causing an obstruction at the ampulla Benefits - No radiation - Painless - Clear images of soft tissues - No risk of pancreatitis compared to ERCP - If contrast needed, gadolinium is safer than CT contrast Risks - large body sizes may not fit into scanner - Some medical devices may not be appropriate to go into scannr like cochlear implants, brain aneurysm clips, older pacemakers. - Claustrophobia - MRI scanner is like a doughnut. - Noisy
49
What is ERCP?
Endoscopic retrograde cholangiopancreatography Endoscopic retrograde cholangiopancreatography, or ERCP, is a procedure to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas. It combines X-ray and the use of an endoscope—a long, flexible, lighted tube. Endoscope is no.4 No pathology present
50
What is this test and what does it show?
Test - Plain abdominal Xray. Findings - gallstone, small bowel obstruction, aerobilia (air in the biliary tree) Pathology - gallstone ileus, where gallstone causes small bowel obstruction. This one is lodged at the ileocaecal valve.
51
What test is this? What does it show?
Axial slice of an abdominal CT Aerobilia - air in the biliary tree. Causes - previous ERCP? - Gallstone ileus
52
Acute Pancreatitis - causes - treatment
Increase in ductal pressure inappropriate activation of enzymes Acute - Alcohol - Gall stones / Bile duct stone - Drugs eg. azathioprine, sodium valproate, HIV, some abx, furosemide, thiazides, exenatide. - Trauma eg. seatbelt, bike handlebar - Infection eg. mumps, Hep E, coxsackie virus - Genetic: autosomal dominant mutation in trypsinogen, auto activates in the pancreas, to become trypsin. - Worm - Pancreatic cancer (all unexplained pancreatitis should have CT scan within 6/52) Treatment - Abx only if also has acute cholangitis
53
Acute Pancreatitis - diagnosis - Treatment
Raised amylase - only raised for 48 hours Lipase - 4 days + Don't rush to imaging - CT after 5/7 days Treatment - Fluid resuscitation - Pain relief eg. IV morphine - IV antiemetics - Feeding / NG tube - DVT prophylaxis - if severe, early intensive care review - Abx only if infected or have acute cholangitis
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Chronic pancreatitis - Symptoms - Causes - Tests - Treatment
Irreversible damage to pancreas Symptoms - Pain chronic, epigastric, radiating to back - Steatorrhoea (fatty stool) Causes - Alcohol, smoking, high calcium, high triglycerides - Auto-immune pancreatitis - Obstructive (cystic fibrosis) - sticky secretions in pancreatic duct. Tests - Late CT - damaged ducts, calcium deposits, pancreatic atrophy, pancreatic ductal stones. - USS only for early chronic panc. Treatment - PERT - pancreatic enzyme replacement therapy. eg. CREON (from pork) - Stop smoking / alcohol.
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What is short bowel syndrome? Treatment?
Short bowel syndrome is a condition in which the body cannot absorb enough nutrients from foods because part of the small intestine is missing or damaged. St. Mark's solution double strength dioralyte Loperamide, codeine → slow transit Lanreotide (somatostatin) s/c fluids and electrolytes IV fluids and electrolytes TPN Bowel transplant Nutrition Lecturer neil.bowron@uea.ac.uk
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EDs 1. What should you give before refeeding to prevent Wernicke's encephalopathy? 2. Signs of refeeding syndrome on blood tests? 2. Deadly triad in anorexics?
1. IV pabrinex (B vitamins and thiamine) - give before refeeding to prevent Wernicke's encephalopathy. 2. Refeeding syndrome (happens to nearly all ED patients to some extent , proof the food is going in) - low phosphate (low ATP → stop breathing) - low K - low Mg - thiamine deficiency - sodum and water retention start feeding SLOWLY eg 5 kcal / kg / day? up to 25. 3. Deadly triad in anorexics - low glucose, low temp, low albumin. Can get sepsis with no temp rise, no CRP/WCC rise. Low albumin shows sign. Don't have capacity as cannot weigh up information to make a decision (would rather die than gain weight) Can be fed against will to save life. IV glucose can be given to treat hypo. But restraint not allowed. Section 5(2) to keep in hospital - Section 2, 28 days. Section 3, initially up to 6 months, MEED guideline. - medical emergencies in eating disorders. https://www.rcpsych.ac.uk/improving-care/campaigning-for-better-mental-health-policy/college-reports/2022-college-reports/cr233
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Immunosuppression
Transplant rejection Prevention of graft vs host disease ITP, vasculitis, IBD, psoriasis etc. Cancer chemo/radio. H1 antagonists NSAIDs/coxibs. Leukotriene receptor antagonists? Glucocorticoids - inhibit cytokine release. Anti-proliferative agents - reduce DNA synthesis of proliferating cells Lymphocyte signal transduction inhibitors eg cyclosporin, inhibitnspecific enzymes. Steroids Methylprednisolone used most widely. Dexamethasone - used in brain tumours Azathioprine is converted to mercaptopurine (don't give allopurinol with aza). Pre-treatment genetic testing now common and advised. IBD, autoimmune hepatitis. Leflunamide - rheum. eg. RA, PA. Met - inhibits dihydrofolate reductase - forms bases for pyridine and purines.Anti-cancer effects.
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Antibodies 1. Anti-smooth muscle antibodies? 2. Anti-mitochondrial antibodies? 2. IgA Anti-endomysial antibodies?
1. Anti-smooth muscle antibodies - auto-immune hepatitis. 2. Anti-mitochondrial antibodies - PBC: primary Biliary Cholangitis 2. Anti-endomysial - coeliac disease (present in 90%)
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Liver screen?
For raised ALT HBsAg & HCV Autoantibodies Ferritin FG / HBA1C Immunoglobulins TTG USS - fatty liver (NAFLD) + alpha-1 antitypsin Can also calculate FIB4 score
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Causes of acute pancreatitis
drugs FATSHEEP look it uo!
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FATSHEEP drugs that cause acute pancreatitis?
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Motivational interviewing
Can use pen and paper for drawing visual scales eg 1-10 readiness to change What are your thoughts about your drinking at the moment? Is there anything you don't like about it? Pros/ Cons. How important is it to you to make a change? (show hand drawn scale and explain) 'There's a part of you thats ready to make a change' Set goals? Any techniques you could use to reduce the number of drinks? Things I've seen people do / work for other people. Do either of these things seem like they'd work for you? So in term of setting the goal ... (repeat) and do this by ... How confident are you that you could make this change? (sad face to happy face scale) So at this point, we've got a goal, a strategy, you're reasonably confident you could make the change. shall we meet again in a few weeks to see how you're getting on?
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Foregut Midd]gut Hindgut what makes up each, and blood supply, and where is pain felt?
Hindgut - suprapubic pain Appendix - initially umbilical pain, then right iliac fossa (migratory)
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Haemorrhoids - symtoms - grading - treatment
Bleeding, prolapse, itching, irritation, ?pain Treatment - conservative management : lifestyle, treat constipation, fibre, fluids etc. Creams, tablets, Band ligation, injections - causes fibrosis of haemorrhoids, surgery - haemorrhoidectomy, HALO, stapled haemorrhoidopexy. (Treat above dentate line as less painful, leave skin bridges surgical site should look like a clover, give laxatives to prevent constipation/pain)
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Anal fissure
Very painful when BO, bleeding, itching. Physical examination (painful). Treatment - diltiazem cream, (relaxes anal tone to allow healing) (1st choice), botox, lateral sphincterotomy. Rule out IBD. Khamis says Vitamin E
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Perianal abscess
Fever, pain, lump/swelling.
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ASA scoring categories 1-6?
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OSCE shared decision making station
Agenda setting Help them make a decision in the station Structure - Strong start (make it explicit its collaborative) 'important I find out your viewpoint, hopefully by the end of it we can come to an agreement about what will work for you' - BRAIN (benefits and risks of recommended / best clinical treatment. BRA is information giving - clear concise, jargon free, chunk and check, summarise) - Strong finish (agree or defer decision). TIPS 1st line treatment - content marks. I Intuition - need to do more. 'are you leaning towards any of the options we've discussed?' 'what are your feelings about the options we've discussed?' N Nothing - don't forget this. keep asking 'what are you thoughts on that?' 'what do you feel about that?'
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OSCE motivational interviewing
TIPS Don't forget the medicine (advise as a doctor) Don't forget agenda setting, clear and concise No time for waffling Use the scale as a tool Use what they tell you to help eg. 'you told me that last time you struggled with cravings when trying to stop smoking, I think nicotine replacement therapy could help with this, shall we discuss this now? As I think this would avoid this problem next time' Aim to progress the patient along the stages of change eg. pre-contemplation to contemplation = win. Pros and cons 'could you tell me what you like about smoking?' 'what don't you like about your smoking?' Acknowledging the hurdles the patient faces. Keep it open and soft. 'What do you understand about the risks of smoking?' OARS Open questions Affirming Reflecting Summarising
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Readiness ruler
eg. if a 4 'great, why are you a bit more ready than a 2? What could give you the confidence to be a 6? How confident are you - use this scale
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Goal setting - Strong end to the consultation
Goals eg reduce smoking from 30 to 28 a day (SMART - specific, measurable, attainable, relevant, timely). Go with the goal that THEY are suggesting. For a win they need to achieve it. Don't suggest other random goals.
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PR examination
Explain & consent - 'I'd like to examine your back passage to check for lumps and bumps and check the colour of your stool. If you're uncomfortable let me know' Chaperone Position - face wall/left side Look - thighs, anus, fissures, swellings, rash (lichen planus), discolouration, anal warts, sexual trauma, haemorrhoids, WARN patient 'I'm going to now insert a finger' Insert lubricated finger, feel for lumps and bumps, feel prostate in males, check collar of stool Get patient to cough? Wipe Thank patient, say they can get dressed. Dispose PPE Wash hands https://geekymedics.com/rectal-examination-pr/
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Types of hernias - name 6 types and location
https://teachmesurgery.com/general/small-bowel/abdominal-hernia/ Epigastric - Between sternum and umbilicus Umbilical - At umbilicus Incisional - at site of previous surgery eg midline Spigelian - Through spigelian fascia, lateral to umbilicus Inguinal - inguinal canal Femoral - below the level of inguinal ligament https://teachmesurgery.com/general/small-bowel/femoral-hernia/ Red flags - weight loss, loss of appetite, signs of bowel obstruction eg vomitting, absolute constipation.
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Hernia
Abnormal protrusion of contents with the abdominal wall Treatments - conservative eg no straining. Truss (support corset). Surgery - Wounds - clean 1%?, contaminated 5%, dirty eg abscess 25% infection rate of surgery Complications : infection. pain, bleeding, chronic pain
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Causes of temp post-op Day 1-2 3-5 5+
wind, water, wound, walking Day 1-2 chest Day 3-5 UTI Day 5+ Wound infection Day 5+ walking (PE/DVT)
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Shock
Inability of body to oxygenate tissues inflammatory mediators cause leaky capillaries sympathetic - raised BP Spinal shock - blood vessels dilate
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Quick facts 1. Alcoholic hepatitis treatment and blood results 2. Epigastric pain relieved by eating 3. Epigastric pain worsens with eating 4. Gastrin secreting tumour 5. Anti-histone antibodies
1. Prednisolone Raised GGT, AST:ALT ratio >2. 2. Duodenal ulcer (pyloric sphincter closes when eating) 3. Gastric ulcer (food stimulates acid production) 4. Zollinger-Ellison syndrome 5. Drug induced lupus
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Primary biliary cholangitis - antibodies? Which Ig? What is it? Symptoms Bloods Management
Primary biliary cholangitis - the M rule IgM anti-Mitochondrial antibodies (98% of patients), M2 subtype Middle aged females Smooth muscle antibodies present 30% patients. Autoimmune - T cells attack bile duct cells. Bile leaks causing inflammation and later, cirrhosis. Sx : jaundice, xanthomas, pruritis, joint pain. Raised ALP, GGT, bilirubin. Management first-line: ursodeoxycholic acid slows disease progression and improves symptoms pruritus: cholestyramine
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Small bowel 1. What's absorbed in the duodenum? 2. What's absorbed in the jejunum? 3. Ileum?
1. Calcium, magnesium and iron 2. Vitamins. Folate. 3. B12, bile salts 'Dude Is Just Feeling Ill Bro' Duodenum-Iron Jejunum-Folate Ileum - B12
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Causes of acute pancreatitis?
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Acute mesenteric ischaemia - PMH? - Investigation? - treatment?
Arteriopath eg AF. CT Laparotomy - resect, usually.
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- What is Charcot's triad? - for what condition? - Bloods? - investigation - Management
1. Pain (RUQ, intermittent) 2. Fever (usually with rigors) 3. Jaundice Acute cholangitis inflammation of biliary duct, obstruction of biliary flow or Ascending cholangitis. Elevated bilirubin MRCP ABC, ERCP +- cholecystectomy https://zerotofinals.com/surgery/general/acutecholangitis/
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Give examples of what causes abdominal pain in each quadrant - Right hypochondriac - Epigastric - Left hypochondriac - Right lumbar - Umbilical - Left lumbar - Right iliac - Hypogastric - Left iliac
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Primary sclerosing cholangitis - what is it? - Diagnosis? - PMH
Damage of medium-large intra hepatic and extra hepatic bile ducts. Diagnosis - MRCP PMH: Ulcerative colitis
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Locations of abdominal pain
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Difference between direct and indirect inguinal hernia?
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Alcoholic liver disease - Typical LFT findings? - Treatment?
Raised GGT AST:ALT ratio > 2:1 Treatment (stop drinking alchohol completely) + 1. Prednisolone 2. Pentoxyphylline
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Revision! Causes of - Microcytic anaemia - Normocytic anaemia - Macrocytic anaemia
NB. Alcohol = macrocytic anaemia
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Types of bowel surgery - name the operations
Anterior resection is the most commonly performed operation for rectal tumours, except in lower rectal tumours https://www.bowelcanceruk.org.uk/about-bowel-cancer/treatment/surgery/types-of-surgery/ (read to prep for info giving osce stations)
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What condition has a symptom triad of dysphagia, glossitis and iron deficiency anaemia?
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What condition has the symptom triad of abdominal pain (sudden onset, severe), shifting dullness (ascites), hepatomegaly?
Budd-chiari syndrome = hepatic vein thrombosis ('liver DVT') Instead of painful swollen leg - painful swollen liver Investigation - Doppler Ultrasound (like a DVT)
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Give an example of a somatostatin analogue and a condition it might treat
Octreotide Neuroendocrine tumours eg carcinoid syndrome
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Antibodies! What antibodies are specific for: 1. Primary biliary cholangitis (PBC) 2. primary sclerosing cholangitis (PSC) 3. Autoimmune hepatitis (AIH) 4. Coeliac disease 5. B12 deficiency
1. Anti-Mitochondrial antibodies present in 98% of patients. (nb. smooth muscle antibodies present in 30% patients). and raised IgM. 2. pANCA (Perinuclear anti-neutrophil cytoplasmic antibodies) 3. Anti-liver/kidney microsomal type 1 antibodies and anti-smooth muscle antibodies Anti-nuclear antibodies lack specificity and can be elevated in liver conditions including PBC, autoimmune hepatitis, and primary sclerosing cholangitis. 4. First choice - IgA tissue transglutaminase (TTG) antibodies (more sensitive and specific) Second choice - IgA anti-endomysial antibodies are positive in 90% of coeliac patients. 5. Intrinsic factor antibodies are more useful than gastric parietal cell antibodies when investigating vitamin B12 deficiency, given low specificity of gastric parietal cell antibodies
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Refeeding bloods?
Phosphate, potassium, magnesium (all low) Caused by Hugh glucose
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What medication should be given to relieve alcoholic ascites?
Spironolactone (aldosterone antagonists)
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Inheritance of gastro illnesses? 1. HNPCC hereditary non-polyposis colorectal carcinoma / Lynch 2. FAP (familial adenomatous polyposis) which is moire common 1 or 2? 3. Haemochromatosis Other inheritance 1. Marfan's
1. Autosomal dominant (more common than 2) 2. Autosomal dominant 3. Autosomal recessive 1. Autosomal dominant, fibrillin-1.
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Typical symptoms of hepatorenal syndrome? Treatment?
The triad for HRS is: Cirrhosis, Ascites, AKI not attributable to any other cause (significant increase in creatinine). Terlipressin. Hepatorenal syndrome (HRS) = a type of functional kidney impairment that occurs in patients with advanced liver disease. The key features include ascites, low urine output, and a significant increase in serum creatinine. Terlipressin, a vasopressin analogue, is the recommended first-line treatment for HRS according to UK guidelines. It works by inducing splanchnic vasoconstriction which reduces portal pressure and improves renal blood flow.
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H. Pylori eradication?
PPI + amoxicillin + clarithromycin
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Gastro emergencies : symptoms, investigation, treatment. 1. Spontaneous bacterial peritonitis.
1. SBP. S - Ascites, abdo pain, fever. I - Paracentesis. High neutrophils, e.coli. T - IV cefoTaxime (Treat) + then prophylactic oral ciProfloxacin (Prevent).
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Conditions - what is the treatment? 1. Wilson's disease 2. PBC primary biliary cholangitis 3. Haemochromatosis
1. Penicillamine 2. Ursodeoxycholic acid 3. Venesection (first line), desferrioxamine - iron chelating agent (second line) transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
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Cancer markers 1. Hepatocellular carcinoma (HCC) 2. Bowel cancer 3. Pancreatic cancer
1. Alpha feta-protein (AFP) 2. Carcinoembryonic antigen (CEA) 3. CA 19-9
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Gastro Drug interactions 1. Clopidogrel with ?
1. Omeprazole (use lansoprazole instead)
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Normal values for 1. Folate 2. Vitamin B12 3. Albumin 4. Bilirubin
1. 3-20 2. 200-800 roughly 3. 35-50 4. 3-17
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OSCE station - info giving/ SDH hernia repair
What is a hernia? Occurs when there's a weakness in the wall of your tummy or groin and some tissue, commonly fat or bowel, protrudes through the hole. Laparoscopic hernia repair Benefits: Recommended treatment for hernias even if asymptomatic. Small scars. shower recovery time. Best for bilateral and recurrent inguinal hernias. Return to non-manual work after 1-2 weeks. Risks: Complications early: bruising, wound infection late: chronic pain, recurrence Alternatives: - Open hernia repair: Pros: surgeon can get more direct access. Best for unilateral inguinal hernia. Mesh repair : lowest recurrence rate. Cons: - more invasive, bigger scar, longer recovery time. Return to non-manual work after 2-3 weeks. - Hernia truss (if not fit for surgery) Intuition Nothing - most become symptomatic, need surgery anyway, some may not.
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What cancers are linked to the following tumour markers? CA-125 CEA (carcinoembryonic antigen) AFP (alpha fetoprotein) CA19-9 CA15-3
CA-125: Ovarian CEA: Colorectal AFP: Testicular and Hepato CA19-9: Pancreas / bile ducts (cholangiocarcinoma) CA15-3: Breast Mnemonic: At 12 you get periods = ovarian At 15 you grow breasts, and 3 looks like breasts = breast 9 sideways looks like a pancreas Numbers increase as you move down the body: Breasts 15-3 Pancreas 19-9 Ovaries 125
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C Diff treatment
First episode of C. difficile infection first-line therapy is oral vancomycin for 10 days second-line therapy: oral fidaxomicin third-line therapy: oral vancomycin +/- IV metronidazole Recurrent episode recurrent infection occurs in around 20% of patients, increasing to 50% after their second episode within 12 weeks of symptom resolution: oral fidaxomicin after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin Life-threatening C. difficile infection oral vancomycin AND IV metronidazole specialist advice - surgery may be considered
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Drug calculations 1. Codeine to morphine? 2. PO morphine to SC? 3. Prescribed morphine to breakthrough morphine? 4. Oral morphine → subcut diamorphine
1. Divide by 10 eg. 240mg codeine → 24mg morphine. 2. Divide by 2 eg. 10mg morphine PO → 5mg morphine SC 3. Divide by 6 eg. 60mg morphine daily → 10mg morphine for breakthrough. 4. Divide by 3 eg. 120mg morphine PO → 40mg diamorphine SC