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Gastroenterology Flashcards

0
Q

What is the normal range for transaminases?

A

Normal is <19 in females, and <30 in males

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1
Q

What liver tests are there?

A

Most liver tests are not tests of liver function. Tests include: bilirubin, AST and ALT (transaminases), GGT and ALP ( cholestatic enzymes), albumin, and INR. Only bilirubin, albumin, and INR are tests of liver function.

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2
Q

What is bilirubin?

A

Bilirubin is the breakdown product of RBCs after conjugation in the liver and secretion in the biliary system secretion.

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3
Q

What are the three catorgories of abnormal LFTs?

A

Hepatocellular (ALT and AST)
Cholestatic (predominant ALP elevation)
Infiltrative/mixed

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4
Q

What category of liver disease has an elevated bilirubin?

A

All categories of liver disease can have an elevated bilirubin

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5
Q

What are the causes of isolated hyper bilirubinaemia?

A

Congenital syndrome( eg Gilbert’s), RBC source ( eg heamolysis, intrabdominal bleeding)

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6
Q

What are the causes of an abnormal LFT test with raised ALTs and ASTs?

A

This is a predominantly hepatocellular pattern. It can be caused by: EtOH related liver diseases (acute and chronic), viral hepatitis, other infections (CMV, HIV, HSV, EBV, TB)’ non alcoholic hepatic steatosis, heamochromotosis, Wilson’s disease, alpha 1 anti trypsin deficiency, autoimmune hepatitis, drugs/toxins, cardiovascular pathology(including hypertension), drugs/toxins, HELLP syndrome, acute fatty liver of pregnancy, cardiac or muscular source.

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7
Q

What are the causes of predominantly cholestatic or infiltrative pattern of abnormal LFTs?

A

This presents with raised ALP. It can be caused by choledocholithiasis, malignancy (hepatocellular carcinoma, lymphoma, liver mets, biliary or pancreatic ca), primary biliary cirrhosis, primary sclerosing cholangitis, intrahepatic cholestatic of pregnancy, HIV, granulomatous disease (eg TB), drugs/toxins, non hepatic source (eg bone, renal, or intestinal source)

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8
Q

What causes dysphagia that has difficulty swallowing both liquids and solids from the start?

A

If there is difficulty swallowing liquids and fluids from the start then there motility disorder (achalasia, neurological)or pharyngeal causes.

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9
Q

What are the possible causes of dysphagia that first affect solids and then liquids?

A

Suspect a stricture (benign or malignant)

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10
Q

What sort of conditions make it difficult to make a swallowing movement in dysphagia?

A

Bulbar palsy makes it difficult to make the swallowing movement, and may also cause a cough on swallowing.

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11
Q

What conditions cause odynophagia (painful swallowing) in dysphagia?

A

Cancer, oesophageal ulcer or spasm can cause odynophagia on swallowing.

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12
Q

What sort of conditions cause intermittent dysphagia? What sort of conditions constant and worsening dysphagia?

A

Intermittent dysphagia should be suspected to be oesophageal spasm. Constant and worsening dysphagia should be suspected to be a malignant stricture.

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13
Q

What condition would cause the neck to bulge or gurgle on drinking in dysphagia?

A

One must suspect a pharyngeal pouch.

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14
Q

What investigations should be ordered in someone who is experiencing dysphagia?

A

FBC to check for aneamia, EUC to check for signs of dehydration, CXR to check the mediastinal fluid level, whether there is an absent gastric bubble, and signs of aspiration. Upper GI endoscopy plus or minus biopsy is usually the first investigation. Barium swallow plus or minus video fluoroscopy is useful to diagnose high dysphagia or dysmotility. Further investigations include oesophageal manometry (if normal barium swallow) ENT opinion if suspected pharyngeal cause.

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15
Q

What is achalasia?

A

Achalasia is when the lower oesophageal sphincter fails to relax ( due to degeneration of the myenteric plexus). Achalasia causes dysphagia, regurgitation, substernal cramps, and decreased weight. On barium swallow there is a dilated tapered oesophagus. Achalasia is treated using an endoscopic ballon dilatation and the proton pump inhibitors.

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16
Q

What is a benign oesophageal stricture?

A

A benign oesophageal stricture is caused by gastro oesophageal reflux disease, corrosives, surgery, or radiotherapy.

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17
Q

What is dyspepsia?

A

Dyspepsia is a symptom or a combination of symptoms that alerts a clinician to the presence of an upper GI problem. Typical symptoms include epigastric pain and burning, early satiety, and post prandial fullness, belching, bloating, nausea, or discomfort in the upper abdomen.

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18
Q

Which structures occur retroperitoneally?

A

SADPUCKER Suprarenal glands, Aorta/IVC, DuoDenum (second and fourth segments), pancreas (tail is intraperitoneal) Ureters, Colon (ascending and descending parts), Kidneys, Esophagus, Rectum

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19
Q

How long is the oesophagus?

A

25 cm long

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20
Q

What is the purpose of the duodenum?

A

The duodenum neutralises acid components entering from stomach via secretin and bicarbonate secretion.the duodenum also acts to stimulate bile secretin via cholecystokinin release.

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21
Q

What is the purpose of the jejunum?

A

The jejunum is responsible for the absorption of salt, water, and nutrients ( proteins, carbohydrates, fat, frolic acid, vit BCADEK

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22
Q

What is the purpose of the ilium?

A

The ileum is important as it absorbs water, salt, and nutrients. The ilium absorbs bile salt and is the only source of vitamin B12 absorption.

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23
Q

Whatbarenthe two sources of blood supply to the liver?

A

The hepatic artery (20-25%) of blood. The portal vein (70-75%)

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24
Q

What s the function of the pancreas?

A

The pancreas has both an endocrine and exocrine function. The endocrine function involve the islets of langerhan that produce insulin ( beta cells), glucagon (alpha) and somatostatin (delta cells). The exocrine function consists of digestive enzymes that include amylase, peptidase, lipase, carboxypeptidase, and chymotrypsin.

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25
Q

What is the differential diagnosis for nausea and vomiting that is accompanied by abdo pain that is not relived by vomiting?

A

Gallbladder disease, pancreatitis, myocardial infarction, hepatitis, infectious gastroenteritis.

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26
Q

What is the differential diagnosis of abdominal distension?

A

The differential diagnosis for abdominal distension can be summarised with the 6Fs. Fat, foetus, flatus, feces, fluid, fatal growth.

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27
Q

What are the causes of GORD?

A
  • Inappropriate transient relaxations of the lower oesophageal sphincter
  • low basal LES sphincter tone (especially in scleroderma)
  • delayed oesophageal clearance, delayed gastric emptying, increased intrabdominal factors
  • acid hyper secretion( such as in zollinger Ellison syndrome, rare)
    Nb: a hiatus hernia worsens oesophageal reflux, but does not cause it
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28
Q

What are the symptoms or GORD?

A

Heartburn ( pyrosis), and acid regurgitation, bitter regurgitation/ waterbrash

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29
Q

What treatment is used for GORD?

A

GORD is most successfully treated with proton pump inhibitors(eg omeprazole) . It can also be treated with H2 receptor blockers and antacids (MG(OH)2), Al(OH)2), aliginate). Weightloss and diet can help
, as well as elevating the head of the bed.

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30
Q

What are the complications of GORD?

A

Barretts oesophagus, oesophageal adenocarcinoma, oesophageal stricture disease, ulcer, bleeding.
NB gastroscope is recommended for patients with chronic GORD and symptoms suggestive of complicated disease ( anorexia, weightloss, bleeding, dysphagia)

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31
Q

What is Barrets oesophagus?

A

Barrets oesophagus is a condition caused by the metaplasia of the normally squamous oesophageal to columnar epithelium. The metaplasia is thought to be caused by longstanding GORD. Diagnosis is made on an endoscopic biopsy. It is important to diagnose as Barrets predisposes to malignant transformation.

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32
Q

How is Barrets oesophagus treated?

A

Barrets oesophagus is treated with proton pump inhibitors. It can also be treated using radio frequency ablation techniques, preventative surgery, or oesophagectomy.

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33
Q

What is eosinophilic oesophagitis?

A

Eosinophilic oesophagitis is an inflammatory condition with the prominence of eosinophils upon biopsy. It is more common in children but can be found in adults. It causes dysphagia of solids, allergies are common, and first presentation may be to emergency with food impaction. Treat with corticosteroid spray ( eg fluticasone) or leukotriene inhibitors.

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34
Q

What is shatzki’s ring?

A

Shatzki’s ring is a mucosal ring at the squamo columnar junction above a hiatus hernia. It causes intermittent dysphagia with solids. Treatment involves disrupting the ring with endoscopic bougie.

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35
Q

What is infectious oesophagitis?

A

Infectious oesophagitis is a severe mucosal inflammation and ulceration as a result of viral or fungal infection. Risk factors for reflux oesophagitis include diabetes, malignancy, and immunocomprimised states. Symptoms include odynophagia and dysphagia. De is via endoscopy and biopsy. It is commonly caused by candida, herpes, or CMV

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36
Q

What do parietal cells secrete? What stimulates them?

A

Parietal cells secrete gastric acid (HCl) and intrinsic factor. They are stimulated by histamine, Ach and gastric.

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37
Q

What do chief cells secrete?

A

Chief cells secrete pepsinogin, which is stimulated by vagal input and local acid.

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38
Q

What is gastritis?

A

Gastritis is defined as the inflammation of the stomach mucosa. There are many different types of gastritis and there are many different causes, such as EtOH, Helicobacter pylori, aspirin, NSAIDS, bile, radiation injury, bacteria, viruses, coeliac disease etc. gastritis can be acute or chronic,

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39
Q

What is peptic ulcer disease?

A

Peptic ulcer disease consists of ulcers that penetrate the muscularis mucosa and can result in scarring, as opposed to erosion ( which is superficial to the muscularis mucosa this no scarring). Peptic ulcer disease includes defects located in the stomach and the duodenum.

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40
Q

What are the causes of peptic ulcer disease?

A

h pylori, NSAIDs, idiopathic, zollinger Ellison syndrome

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41
Q

What is the most common presenting symptom of peptic ulcer disease? What are the 6 classical features of duodenal ulcers? How do gastric ulcers present?

A

The most common px symptom is dyspepsia, but only 20% of patients with dyspepsia have ulcers. Duodenal ulcers present with epigastric pain, burning, develops 1-3hours after meals, relieved by eating and antacids, interrupts sleep, periodic it’s ( tends to occur in clusters over weeks with subsequent periods of remission).

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42
Q

What are the possible presenting complications of peptic ulcer disease?

A

Bleeding ( particularly severe if associated with the gastroduodenal artery), perforation (usually occurs in anterior ulcers), gastric outlet obstruction, penetration ( posterior) may cause pancreatitis.

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43
Q

What tests would you order on someone presenting with peptic ulcer disease?

A

Helicobacter breath test or stool test, upper GI gastroscope with histology and biopsy urease test ( to check for h pylori and malignant transformation), stool heme test, and FBC if pt looks aneamia or has signs of blood loss.

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44
Q

What is the biggest difference for prognosis between gastric ulcers and duodenal ulcers?

A

Gastric ulcers must always be biopsies to rule out malignancy whereas duodenal ulcers are rarely malignant.

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45
Q

What test would you use to detect zollinger Ellison syndrome?

A

A fasting gastric measurement can be used if zollinger Ellison is suspected

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46
Q

How do you treat gastric ulcer?

A

Stop all NSAIDs and aspirin and put patient on proton pump inhibitors. If there is an active bleed it can be treated via endoscopy ( with the injection of adrenaline) or via surgery. If h pylori is present it should be eradicated.

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47
Q

Hw should Helicobacter pylori be eradicated?

A

There are a number of different therapy regimes, such as triple therapy or quadruple therapy. One treatment regime consists of using a PPI, with metronidazole and tetracycline.you may also want to consider using bismuth.

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48
Q

What types of diseases are more likely to produce small amounts of diarrhoea, and what types are more likely to produce large amounts?

A

Small volume diarrhoea (tablespoons of stool) are typical of clonic disease, whereas large volumes of stool (>1/2cup) are typical of small bowel disease.

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49
Q

What types of classifications are important to make when assessing diarrhoea?

A

Acute vs chronic
Small volume vs large volume
Watery vs steathorrea vs bloody
Secretory (persists with fasting) vs osmotic ( continues with fasting)

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50
Q

What are important questions to ask someone presenting with diarrhoea?

A

Those fads wilt. Travel, homosexual contacts, outbreak, seafood, extra intestinal signs of IBD, family history, antibiotics, diet, steatorrhoea, weightloss, immunosuppressed, laxatives, tumour history.

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51
Q

What is inflammatory diarrhoea?

A

Inflammatory diarrhoea can be due to a viral, bacterial, or parasitic cause. Inflammatory diarrhoea can also be caused by ischeamia, radiation damage, or inflammatory bowel disease. Inflammatory diarrhoea is associated with tenesmus, mucoid and bloody stool, fever, and abdominal pain.

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52
Q

What is non inflammatory diarrhoea?

A

Non inflammatory diarrhoea is associated with large and frequent volumes of watery diarrhoea. Due to the high volume and frequency of the bowel movements, loss of fluid/dehydration is possible. There is no fever, blood in the stool, or fecal leukocytosis in non inflammatory diarrhoea. Non inflammatory diarrhoea can be divided into osmotic and secretory.

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53
Q

What is secretory diarrhoea?

A

Secretory diarrhoea is when there is there is an altered flow of ions across the intestine resulting in an increase in secretion and decrease in absorption of fluids and electrolytes across the GI tract, especially in the small bowel. Secretory diarrhoea tends not to decrease by fasting. It can be caused by hormonal agents, enterotoxins, intestinal resection, laxative abuse, hyperthyroidism, colitis, and carcinoid tumours.

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54
Q

What can cause steatorrhoea?

A

Pancreatic insufficiency, giardiasis, coeliac disease, or liver disease

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55
Q

What is a schillings test and how is it performed?

A

A schillings test is used to test for causes of B12 malabsorption. An injection of vitamin b12 is given to saturate depleted stores of B12 in the liver. Then, radioactively labelled B12 is given.the amount of radioactive b12 in the urine output is measured. It is considered low if it is less than 10%. The test is then repeated with intrinsic factor ( pernicious aneamia), antibiotics ( bacterial overgrowth), or pancreatic enzymes (pancreatic insufficiency).

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56
Q

What is coeliac disease?

A

Coeliac disease is abnormal small intestine mucosa due to an autoimmune reaction to alpha gliadin, a component of gluten

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57
Q

What are the possible complications of coeliac disease?

A

Complications of untreated disease include gastrointestinal symptoms, malabsorption, increased GI malignancies, and increased overall mortality

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58
Q

What is dermatitis herpatiformis?

A

Dermititis herpatiformis is an intensely pruritiic vesiculopapular rash that occurs symmetrically over the extensor surfaces of the arms and legs, buttocks, trunk, neck, and scalp. Occurs in people with coeliac disease.

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59
Q

Whist are the possible presenting symptoms of coeliac disease?

A

Abdominal pain/discomfort, bloating, diarrhoea, igA deficiency, iron deficiency aneamia, dermatitis herpatiformis, fatigue, weight
Loss, failure to thrive.

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60
Q

What genes are associated with coeliac disease?

A

HLA DQ2 and HLA DQ 8 are both associated with coeliac disease. However, lots of healthy people have these genes without having coeliac disease. A negative HLADQ2 and HLaDQ8 test can be used to rule out the presence of coeliac disease.

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61
Q

What tests would you order in someone you suspected of being a coeliac?

A

FBC and blood smear ( to check for aneamia, iron and B12 deficiency), IGA transglutaminase titre (IgA-tGT, titres above normal range). May also consider a skin biopsy on any presentations of dermatitis herpatiformis. Small bowel enters copy with histology. May also do slider HLA genotyping.

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62
Q

What are the different types of inflammatory bowel disease?

A

Types of inflammatory bowel disease include Crohn’s disease, ulcerative colitis, indeterminate disease, microscopic and collagenous colitis.

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63
Q

Compare the location of Crohn’s disease to the location of ulcerative colitis.

A

Crohn’s disease affects any part of the GI tract. It may be the small bowel and colon, the colon only, or the small bowel Bly. Ulcerative colitis only involves the colon ( large bowel) hence its name.ulcerative colitis always involves the rectum, and may progress proxy ally.

64
Q

Would you expect rectal bleeding in ulcerative colitis, or Crohn’s?

A

Rectal bleeding is uncommon in Crohn’s, but is very common in ulcerative colitis.

65
Q

What is the difference between the abdominal pain in ulcerative colitis to the abdominal pain in Crohn’s disease?q

A

Pain in Crohn’s disease tends to be colicky and post prandial. Pain in ulcerative colitis tends to have ore defecatory urgency.

66
Q

Compare the complications of Crohn’s disease and ulcerative colitis.

A

Crohn’s disease produces strictures, fistulae, perianal disease, and increased risk of colon cancer. Ulcerative colitis may develop toxic mega colon, and also has an increased risk of colon cancer.

67
Q

What are the endoscopic and histology all features of Crohn’s disease?

A

Endoscopic features of Crohn’s disease includes discrete aphthous ulcers, patchy lesions, and pseudopolyps. Histological features include transmural distribution with skip lesions with focal inflammation. On radiology there is a cobblestone

68
Q

What is Crohn’s disease?

A

Crohn’s disease is a chronic transmural inflammatory disorder potentially affecting the entire gut from mouth to perianal region. Onset is generally before age 30, but there is a second peak at age 60.

69
Q

How would you manage an upper oesophageal bleed?

A

Stabilise patient (cannulas, fluids, monitor)
Send blood for FBC, cross match, platelets, PT PTT, electrolytes, cr, LFTs
Keep NPO, consider NG tube to determine upper vs lower
OGD endoscopy to estblish bleeding site and treat lesion. Can tx by injecting adrenaline and thermal haemostasis, or by clips.

70
Q

What are oesophageal varices?

A

Oesophageal varices are dilated collateral blood vessels that develop in patients with liver cirrhosis due to partial hypertension. The liver cirrhosis is often caused by alcoholic liver disease or by hepatitis.

71
Q

What is a Mallory Weiss tear?

A

A Mallory Weiss tear is a longitudinal laceration in the gastric mucosa that occurs after a long episode of vomiting at the lesser curvature of the gastroesophgeal junction. It results in non variceal heamatemesis. 80 -90% of tears are self resolving but cal lead to fatal heamatemesis

72
Q

What are the causes of lower gastrointestinal bleeding?

A 
CHAND
Colitis (ulcerative, radiation, infection, ischeamic, Crohn's)
Haemorrhoids and fissures
Angiodysplasia
Neoplasm
Diverticular disease
73
Q

What are the features of lower gastrointestinal bleeding?

A

Heamatochezia, aneamia, occult blood in stool, rarely maleana.

74
Q

If a colorectal cancer produces blood in the stool, how do you tell if it is left or right sided?

A

Right sided cancers cause maleana left sided causes heamatochezia

75
Q

What is an adenoma?

A

An adenoma is a benign tumour of glandular origin

76
Q

What are the symptoms of colorectal cancer?

A

Change in stool pattern ( generally increased frequency), blood in stools, family history, increased age, hx of syndromes ( Gardners, HNPCC/lynch , inflammatory bowel), rarely palpable abdominal mass or rectal mass.

77
Q

Carcinoembryonic antigen

A

CEA is produced in foetuses. It can be used to monitor the progress of certain cancers. It is mainly related to colorectal cancer. But can also be high in melanoma, gastric, pancreatic, lung, and breast cancers. It is also high in COPD, IBD, hepatitis and other chronic illnesses as well as in smokers.

78
Q

What are the two shapes of colorectal polyps?

A

Colorectal polyps are small mucosal outgrowths into the lumen of the colon or the rectum. Sessile means flat, pedunculated means on a stalk.

79
Q

What is FAP?

A

Familial adenomatous polyposis is an autosomal dominant mutation in the APC gene on 5q. It has hundreds to thousands of colonic adenomatous by an average age of 40. Extra colonic manifestations include carcinoma of the small bowel, stomach, bile duct, pancreas, thyroid, adrenals, and congenital hypertrophy of retinal pigment epithelium. 100% lifetime risk of colon cancer.

80
Q

What are the different variants of FAP?

A

Gardners syndrome and turcots syndrome. Gardners is FAP plus extra intestinal lesions such as bone or Desmond tumours), turcots syndrome is FAP/HNPCC with CNS lesions.

81
Q

What is HNPCC?

A

Heridatary non polyposis colorectal carcinoma is an autosomal dominant mutation in DNA mismatch resulting in genomic instability manifesting as ‘micro satellite instability’ . Diagnosis is based on suspicion due to family history and age of diagnosis, and confirmed with molecular diagnosis. Feature colorectal cancer with an early age of onset, rapid evolution of normal mucosa to cancer. Mean age of cancer is 44years, lifetime risk is 70 -80%. Also known as lynch syndrome. If someone has HNPCC also screen for endometrial cancer.

82
Q

How do you treat fap?

A

Total proctocolectomy, or surveillance if patient doesn’t want surgery.

83
Q

What does prothrombin time tell you about liver function?

A

PT (prothrombin time, or INR) is a marker of hepatic protein synthesis. It is increased by impaired hepatic protein synthesis (>80%) (including all coagulation factors except VIII). It is also increased by vitamin K deficiency. Hence PT is only a reliable marker of liver function if vitamin K is ruled out.

84
Q

Which clotting factors are exclusively synthesised in the liver?

A

All clotting factors Are synthesised in the liver except for factor VIII and von willebrand factor

85
Q

Apart from hepatic dysfunction, what else could cause decreased serum albumin?

A

Serum albumin level is a marker of hepatic protein synthesis. Low albumin due to malnutrition, renal or GI losses must be excluded.

86
Q

Which transaminases is more specific to the liver?

A

ALT is more specific to the liver. AST is from multiple sources (especially muscle)

87
Q

If ALT>AST

A

Most causes of hepatitis.

88
Q

If ASL>ALT

A

Alcoholic liver disease or other causes of hepatitis that have progressed to advanced liver cirrhosis.

89
Q

What should you consider if ALP elevation is out of proportion to AST/ALT elevation?

A

You should consider:

  • obstruction of the common bile duct (pancreatic ca, lymphoma, stones, cholangiocarcinoma, sclerosing cholangitis, helminths)
  • obstruction of the microscopic ducts (eg. Primary biliary cirrhosis)
  • bile acid transporters defects (drugs, intrahepatic cholestatic of pregnancy)
  • infiltration of the liver (liver metastasis, lymphoma, granulomas, amyloid)
90
Q

What are the differential diagnoses for hepatomegaly?

A

Congestive heart failure (right heart failure, budd-chiari syndrome),
Infiltrative: malignant (primary, secondary, lymphoproliferative, leukaemia)
Benign ( fatty liver, cysts, heamochromotosis, extramedullary heamatopoiesis, amyloid)
Proliferative: infectious (viral, tuberculosis, abcess, echinococcus)
Inflammatory: sarcoidosis granulomas, histiocytosis )

91
Q

What type of virus is the hepatitis A virus? How is it spread? What is its incubation period? How is it diagnosed? How does it present?

A

RNA virus spread via fecal-oral route with an incubation period of 4 -6 weeks. Dx by elevated transaminases and positive anti-HAV IgM. Children are generally asymptomatic, but adults px with fatigue, nausea, arthralgia, fever, and jaundice. Hep A can cause fulminant hepatic failure and subsequent death. Can relapse but never becomes chronic.

92
Q

Dx if someone has HBsAg -, anti HBs +, HBeAg -, anti HBe - and anti HBc -

A

Immunisation against Hep B

93
Q

Dx if someone has HBsAg +, anti HBs -, HBeAg -, anti HBe +, and anti HBc IgG.

A

Chronic hep B infection with low HBV DNA

94
Q

Dx if someone has HBsAg +, anti HBs -, HBeAg +, anti HBe - anti HBc IgM

A

Acute hep B infection

95
Q

Dx is someone is HBsAg-, anti HBs-/+, HBeAg -, anti HBe -/+, anti HBc IgG

A

Resolved infection of hep B

96
Q

Dx if someone has HBs Ag +, anti HBs -, HBe Ag+, anti HBe -, antimHBc IGG

A

Chronic HBV infection with high HBV DNA

97
Q

What are the four phases of chronic hepatitis?

A

The four phases of chronic hepatitis include immune tolerance, immune clearance, immune control, and immune escape.

98
Q

What is the immune tolerance stage in chronic hepatitis?

A

In the immune tolerance stage there is extremely high HBV DNA (>20,000 IU/mL), HBeAg positive, but normal AST/ALT. this is due to little immune control and minimal immune mediated liver damage.

99
Q

What happens in the immune clearance phase of hepatitis

A

The immune clearance pause is also known as the immunoactive phase. The HBV DNA levels are still elevated but now being to fall. HBeAg is positive due to an immune attack on the virus and immune mediated liver damage. Is a progressive disease that leads to liver fibrosis, sometimes goes on to cirrhosis or hepatocellular carcinoma.

100
Q

What is the stage of immune control in hep B infection?

A

In the immune control phase of the hep B infection there are lower HBV DNA levels (<20,000 IU/mL), HBeAg negativ , anti HBe positive, AST/ALT normal due to immune control without immune mediated liver damage. Risk of re activation of immune clearance especially with immunosupressants.

101
Q

What is the immune escape phase of hep B infection?

A

The immune escape stage has elevated HBV DNA, HBe Ag negative because of pre core or core promoter gene mutation, anti HBe positive, ALT/AST high, characterised by progressive disease without treatment and increasing liver fibrosis (sometimes progressing to cirrhosis and/or hepatocellular carcinoma), likely to benefit from treatment.

102
Q

Wat is hep D

A

Hepatitis D is a defective RNA virus requiring HBs Ag for entry into the hepatocyte, therefore it only infects patients with hepatitis B , and causes a more aggressive disease than hep B alone. Co infection with hep D has a better prognosis than superinfection with hep D. Whilst hep D increases severity of hepatitis it does not increase risk of progression to chronic hepatitis. However, in the context of chronic infection, it does increase risk to cirrhosis.

103
Q

What enzyme metabolises paracetamol? How does paracetamol overdose present? How does it cause fulminant hepatic failure?

A

Paracetamol is metabolised by hepatic cytochrome P450 system. It presents with nausea and vomiting in the first 24 hrs. Then it becomes asymptomatic but ongoing necrosis results in transaminases >1000 U/L followed by jaundice and encephalopathy. High paracetamol doses saturates glucuronidation and sulfation elimination pathways. This means that the reactive metabolite is formed. The reactive metabolite covalently binds to the hepatocyte membrane.

104
Q

What is the therapy for paracetamol overdose?

A

Gastric lavage, oral activated charcoal, N acetyl cysteine can be given PO or IV

105
Q

What is Wilson’s disease?

A

Wilson’s disease is an autosomal recessive defect in copper metabolism (gene ATP7B). Clinical manifestations of Wilson’s disease include: asterixis, basal ganglia degeneration (parkinsonian features in someone young), decreased ceruloplasmin, cirrhosis, corneal deposits (keiser fliescher rings), copper in urine, dementia, acute or chronic hepatitis, fulminant liver failure, kidney stones and fanconis syndrome, arthritis, heamolysis.

106
Q

What are the different types of heamochromotosis ?

A

Primary heamochromotosis due to HFE recessive gene that results in ongoing gut absorption despite adequate iron stores.
Secondary heamochromotosis comes from parent earl iron overload eg. Transfusions, chronic haemolytic aneamia (thalasseamia, pyruvate kinase deficiency), excessive iron intake.

107
Q

How does heamochromotosis usually present?

A

Heamochromotosis usually presents with a trivial rise in serum transaminases, liver cirrhosis,media eyes, chronic pancreatitis, bronze or grey skin (due to melanin, not iron), dilated cardiomyopathy, hypo gonadotropin gonodism( impotence, decreased libido, amennorrhoea), arthralgia! Chondricalcinosis,

108
Q

What are the risk factors for non alcoholic fatty liver disease?

A

Risk factors for NAFLD are metabolic syndrome along with type II diabetes, hypertension, and hypertriglyceridemia as well as rapid weight loss or rapid weight gain.

109
Q

Why are the clinical features/investigations of NAFLD?

A

NAFLD is often asymptomatic, but may present with fatigue, malaise, and vague RUQdiscomfort. There is often elevated serum triglyceride and cholesterol levels and insulin resistance. Elevated serum AST, ALT, where AST/ALT<1. Presents with an ec
Hogenic liver texture on ultrasound. The liver biopsy is diagnostic but often only necessary for prognosis.

110
Q

How is NAFLD managed?

A

There is no proven effective therapy other than gradual weightloss. There is some evidence for vitamin E and pioglitiazone if diabetes is concomitantly present. Optimisation of therapy for hyperlipideamia, diabetes, and hypertension.

111
Q

What is chronic hepatitis?

A

Chronic hepatitis is defined by an increase in transaminases for >6 months.

112
Q

What are the causes of chronic hepatitis?

A

Chronic hepatitis is caused by fat (metabolic syndrome, EtOH), viral causes (hepatitis B, C, D), drugs (methyl dopa, isoniazid, amiodarone) autoimmune hepatitis, and genetic diseases (Wilson’s disease, heamochromotosis, and alpha1 antitrypsin deficiency) . The clinical features of chronic hepatitis are raised AST and ALT. treatment involves treating the underlying cause.

113
Q

What is cirrhosis?

A

Cirrhosis is liver damage that is characterised by diffuse distortion of the basic architecture and replacement with scar tissue. Stage 1 cirrhosis is compensated and asymptomatic. It can last for 10 to 20 years with almost normal life expectancy.
Stage 2 cirrhosis is the onset of first decompensation, typically the development of liver failure, ascities, or variceal bleed.

114
Q

What are the causes for cirrhosis?

A

Causes for cirrhosis include fatty liver (EtOH, metabolic syndrome), chronic viral hepatitis, autoimmune hepatitis, heamochromotosis, a1 antitrypsin deficiency, primary biliary cirrhosis, chronic hepatic congestion (cardiac cirrhosis, or hepatic vein thrombosis/budd chiari syndrome), idiopathic, Wilson’s disease, gauchers disease

115
Q

What are the complications of cirrhosis?

A 
VARICES:
Varices
Aneamia
Renal failure
Infection
Coagulooathy
Encephalopathy
Sepsis
116
Q

What is portal hypertension?

A

Portal hypertension is when the pressure gradient between the hepatic vein pressure and the wedged hepatic vein pressure (corrected sinusoidal pressure) is >5mmHg.

117
Q

What are the complications of portal hypertension?

A

Portal hypertension results in GI bleeding from varices in the oesophagus or stomach, ascities, hepatic encephalopathy, thrombocytopenia, renal dysfunction, sepsis, arterial hypoxemia.

118
Q

How do you manage portal hypertension?

A

Beta blockers, nitrates, shunts (eg. Transjugular intrahepatic ports systemic shunt = TIPS)

119
Q

What are the causes of ascities when serum albumin - ascities albumin is >11 g/L?

A

It is portal hypertension related. Ddx includes cirrhosis/severe hepatic hepatitis, chronic hepatic congestion (RHF, budd chiari), massive liver mets, myxoedema.

120
Q

What are the causes of ascities when serum albumin - ascities albumin is <11 g/L?

A

It is non portal hypertension related. This includes peritoneal carcinomatosis, TB, pancreatic disease, serositis, nephrotic syndrome.

121
Q

When is ascities clinically detectable?

A

Ascities is clinically detectable when greater than 500mL

122
Q

How do you treat encephalopathy in cirrhosis?

A

Treat with lactulose

123
Q

What is spontaneous bacterial peritonitis?

A

Spontaneous bacterial peritonitis is a idiopathic complication in approx 10% of ascites. 1/3 of those suffering from it will not show any symptoms so you may need to do a diagnostic parecentesis to find it. For those with symptoms, they experience fever, chills, abdominal pain, ileus, hypotension, and worsening encephalopathy. Gram negatives tend to make up most of the pathogens (e. coli, streptococcus, klebsiella)

124
Q

What are your findings upon investigation for spontaneous bacterial peritonitis?

A

There is a raised neutrophil count and a raised white cell count in the peritoneal fluid. The gram stain might be positive, but only in a small number of patients. The culture may not be positive either.

125
Q

How do you treat spontaneous bacterial peritonitis?

A

Treat with IV cefotaxime (gram negative, not metabolised by the liver) modify if response is inadequate or culture shows resistant organisms.
Also give IV albumin

126
Q

What is jaundice?

A

Jaundice yellowing of the sin caused by high levels of bilirubin in the blood that deposits in the skin, sclera, and mucous membranes.

127
Q

What are the causes of unconjugated jaundice?

A

Causes of predominantly unconjugated hyperbilirubeamia

  • Overproduction: heamolysis, ineffective erythropoiesis (megaloblastic aneamias etc)
  • Decreased hepatic uptake: Gilbert’s syndrome, drugs (eg. Rifampicin)
  • decreased conjugation: drug inhibition (eg chloramphenicol), crigler najar syndromes 1 and 2, Gilbert’s syndrome, neonatal jaundice
128
Q

What are the causes of conjugated hyperbilirubeamia due to impaired hepatic secretion?

A

Familial disorders (rotor syndrome, Dublin Johnstone syndrome, cholestasis of pregnancy), hepatocellular disease, drug induced cholestasis (oral contraceptives, chlorpromazine), primary biliary cirrhosis, primary sclerosing cholangitis, sepsis, post operative

129
Q

What are the causes of conjugated hyperbilirubeamia due to extra hepatic biliary obstruction?

A

Intraductal obstruction: gallstones, biliary stricture, parasite, malignancy (cholangiocarcinoma ), sclerosing cholangitis
Extraductal obstruction: malignancy ( pancreatic cancer, lymphoma), metastases in peri portal nodes, inflammation (eg pancreatitis)

130
Q

What is Gilbert’s syndrome?

A

Gilbert’s syndrome is a mild, non conjugated hyperbilirubeamia due to a mild decrease in glucuronyltransferase activity (UDPGT). It is an autosomal dominant inherited disorder that presents in teens and 20s often as an incidental finding. The only manifestation in intermittent jaundice that characteristically develops whilst fasting.

131
Q

What is primary sclerosing cholangitis?

A

Primary sclerosing cholangitis is inflammation of the biliary tree (can be either intra or extra hepatic ducts) that leads to scarring and obliteration. PSC CIA most commonly idiopathic, however it can be caused by chronic choledocholithiasis, cholangiocarcinoma, iatrogenic, contiguous inflammatory process, post ERCP, associated with HIV/AIDS.

132
Q

How does primary sclerosing cholangitis present? What are the findings on invesitgation?

A

Primary sclerosing cholangitis is often insidious, and may present with fatigue and pruritis and may present with episodic bacterial cholangitis secondary to biliary obstruction. On investigation, there is increased ALP (hallmark), less often there is increased bilirubin, there is mildly increased ALT (usually <300U/L), there is P-ANCA in 30-80%, elevated IgM,

133
Q

How do you treat PSC?

A

Image the bile duct using MRCP annually for early detection of cholangiocarcinoma.
Tx with endoscopic sphincterotomy, or a biliary stent.
Use antibiotics to treat any cholangitis, and conduct an emergency drainage of pus for superlative cholangitis
Liver transplant is the best treatment, however, prognosis is unfavourable. Mean survival is 4-10years with eventual death from liver failure or cholangiocarcinoma

134
Q

What is primary biliary cirrhosis?

A

Primary biliary cirrhosis is a condition that is most likely autoimmune and primarily affects,idle aged women. PBS is chronic inflammation and fibrous obliteration of the intrahepatic bile ductules. PBS is often asymptomatic or presents with pruritis and fatigue. Chronically the patient will develop jaundice and melanosis (darkening of the skin) and other signs of cholestasis. End stage there is hepatocellular failure, portal hypertension and ascites. There is also a high incidence of osteoporosis.

135
Q

Compare the differences between primary sclerosing cholangitis and primary biliary cirrhosis.

A

PSC affects males, PBC affects females. PSC is associated with IBD, PBC is associated with other autoimmune disorders (such as sjorgrens CREST, or RA). PSC affects both extra and intra hepatic ducts, PBS only affects intrahepatic. Investigate PSC by ERCP/MRCP as the narrowing and dilatations of the duct can be visualised. Investigate PBC using anti mitochondrial antibodies IgM, increased lipids, liver biopsy (absence of duct narrowing on ERCP)

136
Q

What is ascending cholangitis? What causes ascending cholangitis?

A

Ascending cholangitis is infection of the biliary tree. Ascending cholangitis is caused by stasis in the biliary tract from obstruction or stricture (usually from a previous cholecystectomy). Infection originates in the duodenum or spreads heamatogenously from the portal vein.

137
Q

What are the main infective organisms in ascending cholangitis?

A

E. coli, klebsiella, enterobacter, enterococcus. Co infection with bacteroides and clostridia can occur.

138
Q

How does ascending cholangitis present?

A

Ascending cholangitis presents with ‘Charcots Triad’. This is RUQpain, fever, and jaundice. Reynolds Pentad presents with RUQpain, fever, jaundice, hypotension, and confusion. On investigation the patient has increasedWBCs, increasedALP, ALT, and less often increased bilirubin. They need a blood culture and abdominal ultrasound (CBD dilation,most ones).

139
Q

What are the causes of pancreatitis?

A

Causes of pancreatitis = get smashd
Gallstones, ethanol, trauma/ERCP, steroids/sphincter of oddi dysfunction, mumps, ,mycoplasma and other infections such as EBV, HIV related infections, Autoimmume such as PAN, Scorpion stings, Drugs such as sulfonamides, furosemide, azathiopine, valproic acid.

140
Q

What are the presenting symptoms of pancreatitis?

A

Nausea and vomiting, anorexia, fever, tachycardia, and epigastric pain radiating to the back

141
Q

What are the pancreatic enzymes?

A

Pancreatic enzymes are amylase, lipase, trypsin, chymotrypsin.

142
Q

What are the causes increased serum amylase?

A

Increased serum amylase is caused by:

  • Pancreatic disease: pancreatitis, pancreatic duct obstruction (eg ampullary cancer), pseudocyst, abcess, ascites, trauma, cancer
  • Non pancreatic abdominal disease: biliary tract disease, bowel obstruction/ ischeamia, perforated or penetrating ulcer, ruptured ectopic pregnancy, aneurysm, chronic liver disease, peritonitis
  • non Abdominal disease: cancer, salivary glands lesions, bulimia, renal transplant/insufficiency burns, kero acidosis
143
Q

What investigations would you order for acute pancreatitis, and what findings would you expect to see?

A

Serum lipase elevated (more sensitive and specific than amylase), serum amylase >3x normal, AST/ALT ratio (greater than 3 predicts gallstones as cause), urinary amylase, FBC, heamotocrit (predictor of severity of disease), ABGs, plain abdo x ray (may show sentinel loop ( an isolated part of inflated bowel) next to the pancreas, ultrasound may show peri pancreatic stranding, fluid collections or calcifications.

144
Q

How do you treat acute pancreatitis?

A

Make nil by mouth, give IV crystalloids to maintain urine output >30mL per hour to protect kidneys, give anaesthesia and anti emetics. Replace any losses of calcium and magnesium, consider giving insulin.

145
Q

What are the common presenting features of chronic pancreatitis?

A

Dull epigastric pain radiating to back, worse approx 30 minutes post prandial. Diabetes mellitus, steatorrhoea (20%), jaundice (10%).

146
Q

What tests do you get for chronic pancreatitis?

A

Blood glucose may be elevated, calcifications and other changes of the pancreas may be seen in X-ray or ultrasound, or ct

147
Q

What is chronic pancreatitis? What causes it?

A

Chronic pancreatitis is irreversible damage to the pancreas characterised by: pancreatic cell loss (from necrosis), inflammation, fibrosis. It is most commonly caused by EtOH, cystic fibrosis, severe protein calorie malnutrition, hereditary, idiopathic.

148
Q

What is the typical presentation of ulcerative colitis?

A

Ulcerative colitis presents with rectal bleeding, bloody diarrhoea, and gross or occult blood on digital rectal examination. It also presents with abdominal pain, arthritis and spondylitis, malnutrition, abdominal tenderness. Risk factors for ulcerative colitis include family history and positive HLA B27

149
Q

What are the risk factors for Crohn’s disease?

A

Risk factors for Crohn’s disease include white ancestry, age 15-40 or 60-80, or family history

150
Q

What is the typical presentation of someone with Crohn’s disease?

A

Typical presentation of Crohn’s disease includes abdo pain (may be cramps, relieved with defection), non bloody or intermittently bloody diarrhoea, perianal lesions (skin tags, fistulae, abscesses, scarring, or sinuses). It may commonly present with bowel obstruction, fever, fatigue, abdo tenderness,

151
Q

What tests would you order to investigate inflammatory bowel syndrome?

A

Stool studies ( absence of infectious elements, elevated fractal calprotectin)
FBC (aneamia, leukocytosis)
Comprehensive metabolic profile (abnormal electrolytes, hypoalbuminaemia, hypocholestroleaia)
ESR and CRP
Serum folate and b12 in Crohn’s
Flexible sigmoidoscopy with biopsy
Abdo X-ray (dilated loops with air fluid level, free air from perforation, toxic mega colon)
Colonoscopy with biopsy

152
Q

What findings would you see on colonoscopy for Crohn’s disease?

A

Discontinuous skip lesions made of mucousal inflammation and discrete deep superficial ulcers located transversely and longitudinally creating a cobblestone appearance. There is also hyperaemia and oedema.

153
Q

What is found on colonoscopy for ulcerative colitis? What is found on biopsy?

A

Colonoscopy shows rectal involvement that is continuous and uniform. There is a loss of vascular markings, diffuse erythema, mucosal granularity. Biopsy shows that inflammation is confined to the mucosa.

154
Q

What is the treatment for Crohn’s disease?

A

Mild Crohn’s disease can be managed with budesonide or amino salicylate meds ( mesasalazine), antibiotics may also be used if septic complication are suspected. If disease is severe, consider anti TNF therapies ( infliximab) or oral corticosteroids (prednisolone). May also consider IV corticosteroids, immunomodulator therapies, or surgery.

155
Q

What is the definition of upper gastrointestinal bleeding?

A

Upper gastrointestinal bleeding is bleeding before the ligament of treitz. The ligament of treitz is a suspensory ligament where e fourth portion of the duodenum transitions to the jejunum.

156
Q

What are the clinical features of upper gastrointestinal bleeding?

A

In order of decreasing severity: heamatochezia, >heamatemesis > coffee ground emesis >melena >occult stool in the blood

157
Q

What are some of the causes of upper gastrointestinal bleeding?

A

Epistaxis, oesophageal varices, oesophagitis, oesophageal cancer, Malory Weiss tear.
Gastric ulcer, gastritis, gastric cancer
Ulcer in duodenal bulb, aorta enteric fistula ( emergency, usually only after aortic graft perform emergency endoscopy if hx)
Coagulopathy, vascular malformation.

158
Q

What are the different incubation periods for infective organisms that cuase food poisoning?

A
  • 1-6 hrs: Staphylococcus aureus, Bacillus cereus*
  • 12-48 hrs: Salmonella, Escherichia coli
  • 48-72 hrs: Shigella, Campylobacter
  • > 7 days: Giardiasis, Amoebiasi

Medicine (16 decks)

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