Gastro Flashcards

Question

Exotoxins

Answer 1

enerally released by Gram positive bacteria with the notable exceptions of Vibrio cholerae and some strains of E. coli

Answer 2

diphtheric membrane' on tonsils caused by necrotic mucosal cells. Systemic distribution may produce necrosis of myocardial, neural and renal tissue.

Answer 3

lead to acute gastroenteritis, toxic shock syndrome and Staphylococcal scalded skin syndrome

Answer 4

causes activation of adenylate cyclase leading to ↑ in cAMP levels, which in turn leads to ↑ chloride secretion.

Answer 5

ABC: patients should ideally be resuscitated prior to endoscopy * Correct clotting: FFP, vitamin K * Vasoactive agents: terlipressin is currently the only licensed vasoactive agent. It has been shown to be of benefit in initial hemostasis and preventing rebleeding. It acts by Constriction of the splanchnic vessels (contraindicated in IHD, use Octreotide as alternative) * Prophylactic antibiotics have been shown in multiple meta-analyses to ↓ mortality in patients with liver cirrhosis

Answer 6

Propranolol: ↓ rebleeding and mortality compared to placebo * Endoscopic variceal band ligation (EVL) is superior to endoscopic sclerotherapy. It should be performed at two-weekly intervals until all varices have been eradicated. Proton pump inhibitor cover is given to prevent EVL-induced ulceration

Answer 7

efers to the metaplasia of the lower esophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium. There is ↑ risk of esophageal adenocarcinoma, estimated at 50-100 folds.

Answer 8

Histological features: the columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)

Answer 9

Management * Endoscopic surveillance with biopsies * Low grade dysplasia: high-dose proton pump inh

Answer 10

24hr esophageal pH monitoring is gold standard investigation in GERD

Answer 11

* Age > 55 years * Symptoms > 4 weeks or persistent symptoms despite treatment * Dysphagia * Relapsing symptoms * W eight loss

Answer 12

typical of esophageal candidiasis, a well documented complication of inhaled steroid therapy

Answer 13

Dysphagia may be associated with weight loss, anorexia or vomiting during eating Past history may include Barrett's esophagus, GERD, excessive smoking or alcohol use Oesophagitis

Answer 14

here may be a history of HIV or other risk factors such as steroid inhaler use

Answer 15

Dysphagia of both liquids and solids from the start Heartburn Regurgitation of food - may lead to cough, aspiration pneumonia etc

Answer 16

More common in older men Represents a posteromedial herniation between thyropharyngeus and cricopharyngeus muscles Usually not seen but if large then a midline lump in the neck that gurgles on palpation Typical symptoms are dysphagia, regurgitation, aspiration and chronic cough. Halitosis may occasionally be seen

Answer 17

Other features of CREST syndrome may be present, namely Calcinosis, Raynaud's phenomenon, Esophageal dysmotility, Sclerodactyly, Telangiectasia

Answer 18

Other symptoms may include extraocular muscle weakness or ptosis Dysphagia with liquids as well as solids

Answer 19

May be history of anxiety Symptoms are often intermittent

Answer 20

Dysphagia of BOTH liquids and solids * Typically variation in severity of symptoms * Heartburn * Regurgitation of food - may lead to cough, aspiration pneumonia etc * Malignant change in small number of patients * 7% ↑ in risk of squamous cell carcinoma

Answer 21

osophageal manometry

Answer 22

Loss of peristalsis in distal esophagus, failure of LOS to relax during swallowing and (i.e ↑ residual relaxing pressure) Loss of peristalsis in distal esophagus BUT ↓ resting LOS p

Answer 23

Loss of peristalsis in distal esophagus BUT ↓ resting LOS pressure

Answer 24

Manometry: excessive LOS tone which doesn't relax on swallowing - considered most important diagnostic test * Barium swallow shows grossly expanded esophagus, fluid level * CXR: wide mediastinum, fluid level

Answer 25

Treatment * Intra-sphincteric injection of botulinum toxin * Heller cardiomyotomy * Balloon dilation * Drug therapy has a role but is limited by side-effects

Answer 26

Features: * Complete transmural (full-thickness) laceration or perforation of the esophagus, distinct from Mallory-Weiss syndrome, a nontransmural esophageal tear also associated with vomiting. * Perforation is almost always on Left side of Lower esophagus. * Gastric contents enter the mediastinum and pleural cavity, if one were to perform a pleural fluid aspirate; one is likely to aspirate gastric contents! * ♂ > ♀ and typically between 50-70 years old * Other clinical features that may suggest the diagnosis include odynophagia and surgical emphysema in the neck

Answer 27

Causes: * Vomiting (against a closed glottis) in eating disorders such as bulimia * Rarely: Extremely forceful coughing - Obstruction by food

Answer 28

Diagnosis: * Radiographs show mediastinal gas, effusion, and later pneumothorax. Esophagram is used to confirm leak, first with water-soluble contrast, then barium if no leak demonstrated.

Answer 29

Early operation after appropriate resuscitation offers the best chance of survival.

Answer 30

* NSAIDs * Bisphosphonates * Steroids The following drugs may cause reflux by reducing lower esophageal sphincter (LOS) pressure * Calcium channel blockers* * Nitrates* * Theophyllines

Answer 31

Chronic gastrointestinal bleeding * Progressive unintentional weight loss * Progressive difficulty swallowing * Persistent vomiting * Iron deficiency anemia * Epigastric mass * Suspicious barium meal

Answer 32

Recent in onset rather than recurrent and * Unexplained (e.g. New symptoms which cannot be explained by precipitants such as NSAIDs) and * Persistent: continuing beyond a period that would normally be associated with self-limiting problems (e.g. Up to four to six weeks, depending on the severity of signs and symptoms)

Answer 33

Gram negative bacteria associated with a variety of gastrointestinal problems, principally peptic ulcer disease

Answer 34

H. pylori eradication 7 day course of: * PPI + amoxicillin + clarithromycin, or * PPI + metronidazole + clarithromycin

Answer 35

Peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers) * Gastric cancer * B cell lymphoma of MALT tissue (eradication of H pylori 80% causes regression) * Atrophic gastritis

Answer 36

Patients consume a drink containing carbon isotope 13 (13C) enriched urea * Urea is broken down by H. pylori urease * After 30 mins patient exhale into a glass tube * Mass spectrometry analysis calculates the amount of 13C CO2 * Sensitivity 95-98%, specificity 97-98% * Used to confirm eradication

Answer 37

Rapid urease test (e.g. CLO test) * Biopsy sample is mixed with urea and pH indicator * Color change if H pylori urease activity * Sensitivity 90-95%, specificity 95-98%

Answer 38

Serum antibody * Remains positive after eradication * Sensitivity 85%, specificity 80%

Answer 39

Histological evaluation alone, no culture * Sensitivity 95-99%, specificity 95-99%

Answer 40

AD autosomal dominant condition characterized by numerous hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles.

Answer 41

Autosomal dominant * Responsible gene encodes serine threonine kinase LKB1 or STK11

Answer 42

* Hamartomatous polyps in GI tract (mainly small bowel) * Pigmented lesions on lips, oral mucosa, face, palms and soles * classical histological appearance of smooth muscle “arborisation” * Intestinal obstruction e.g. Intussusception * Gastrointestinal bleeding

Answer 43

Until recent time esophageal cancer was most commonly due to a squamous cell carcinoma but the incidence of adenocarcinoma is rising rapidly. Adenocarcinoma is now (since 2010) the most common type of oesophageal cancer and is more likely to develop in patients with a history of gastro-esophageal reflux disease (GERD) or Barrett's. The majority of tumours are in the middle third of the esophagus.

Answer 44

Risk factors: * Smoking * Alcohol * Achalasia * Plummer-vinson syndrome * Rare: coeliac disease, scleroderma * Sensetive to radiotherapy

Answer 45

GERD * Barrett's esophagus

Answer 46

Epidemiology * Overall incidence is decreasing, but incidence of tumors arising from the cardia is increasing * Peak age = 70-80 years * More common in Japan, China, Finland and Columbia than the west * More common in ♂s, 2:1

Answer 47

* H. pylori infection (although it is protective against esophageal cancer) * Blood group A: gAstric cAncer * Gastric adenomatous polyps * Pernicious anemia * Smoking * Diet: salty, spicy, nitrates * May be negatively associated with duodenal ulcer

Answer 48

Diagnosis: endoscopy with biopsy * Staging: CT or endoscopic ultrasound - endoscopic ultrasound has recently been shown to be superior to CT

Answer 49

Most cancers develop from adenomatous polyps therefore a screening program could theoretically ↓ mortality * Main techniques being evaluated are faecal occult blood (FOB) testing, sigmoidoscopy and colonoscopy * Fecal occult blood testing is the only method to have been proven to ↓ mortality (by about 20%) in trials. Sensitivity can be ↑ by DNA analysis for the APC gene

Answer 50

2-10%: cancer (colorectal cancer, gastric cancer) * 20-30% adenoma or polyps * Bleeding peptic ulcer * Angiodysplasia of the colon

Answer 51

The Dukes staging system is widely employed for classifying colorectal cancers and is a useful predictor of survival. Tumour grade and depth of penetration are also important: * Duke A (Stage I) defines a tumour confined to the bowel wall (i.e. mucosa and submucosa). * Duke B (Stage II) invades through the muscle wall. * Duke C (Stage III) involves lymph nodes. * After this the patient presents with metastatic disease at distant sites (Stage IV).

Answer 52

Poorly differentiated histological type. * Tumour adherence to adjacent organs. * Bowel perforation. * Colonic obstruction at the time of diagnosis. * Venous invasion by the tumour.

Answer 53

* Surgical excision of a colonic carcinoma is the main treatment * Adjuvant chemotherapy (5-fluorouracil and folinic acid) is warranted in high-risk stage II Causes for a positive fecal occult blood testing are: * 2-10%: cancer (colorectal cancer, gastric cancer) * 20-30% adenoma or polyps * Bleeding peptic ulcer * Angiodysplasia of the colon The Only MRCP Notes You’ll Ever Need 214 / 546 www.sudamedica.com colonic carcinomas and all stage III colonic carcinomas. * The addition of oxaliplatin has been shown to improve survival in these patients in a large multicentre trial (MOSAIC study), but the additional drug can cause a severe peripheral neuropathy. * Adjuvant radiotherapy is used in rectal carcinomas. This is combined with chemotherapy in stage II and III rectal carcinomas to reduce the risk of local as well as metastatic relapse.

Answer 54

eries of genetic mutations. For example, more than half of colon cancers show allelic loss of the adenomatous polyposis coli (APC) gene. It is believed a further series of gene abnormalities e.g. activation of the K-ras oncogene, deletion of p53 and DCC tumour suppressor genes lead to invasive carcinoma

Answer 55

utosomal dominant condition, is the most common form of inherited colon cancer. Proximal colon cancer

Answer 56

At least 3 family members with colon cancer * The cases span at least two generations * At least one case diagnosed before the age of 50 years

Answer 57

* Colonoscopy every 2 years from 20 to 40 years age then annually * Check mutation in DNA or mismatched repair gene.

Answer 58

rare autosomal dominant condition which leads to the formation of hundreds of polyps by the age of 30-40 years mutation in a tumour suppressor gene called adenomatous polyposis coli gene (APC), located on chromosome 5. =total colectomy with ileo-anal pouch formation in their twenties.

Answer 59

A variant of FAP called Gardner's syndrome can also feature osteomas of the skull and mandible, jaw osteomas which give a "cotton-wool" appearance to the jaws, as well as multiple odontomas, Congenital Hypertrophy of the Retinal Pigment Epithelium (CHRPE)

Answer 60

Patients > 40 years old, reporting rectal bleeding with a change of bowel habit towards looser stools and/or ↑ stool frequency persisting for 6 weeks or more * Patients > 60 years old, with rectal bleeding persisting for 6 weeks or more without a change in bowel habit and without anal symptoms * Patients > 60 years old, with a change in bowel habit to looser stools and/or more frequent stools persisting for 6 weeks or more without rectal bleeding * Any patient presenting with a right lower abdominal mass consistent with involvement of the large bowel * Any patient with a palpable rectal mass * Unexplained iron deficiency anemia in men or non-menstruating women (Hb < 11 g/dl in men, < 10 g/dl in women)

Answer 61

s condition characterized by excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas. 30% MEN 1

Answer 62

typically presents with multiple gastroduodenal ulcers causing abdominal pain, diarrhea and malabsorption. High-dose proton pump inhibitors are needed to control the symptoms.

Answer 63

Fasting gastrin levels, the single best screen test: done in 3 different days as the gastrin secretion is pulsatile * Secretin stimulation test: considered +ve if there is ↑ in gastrin >200 pg/mL after secretin injection (Normally Secretin supresses gastrin, but in ZE, it simply shows that the source of gastrin is not the stomach and it is somewhere else like pancresae)

Answer 64

* If not mets, surgical resection is the cure * Octreotide can be used to alleviate symptoms with interferon and chemotherapy to attempt cure non respectable tumor * PPI is used to control symptoms in actute stages

Answer 65

Associated with H. pylori infection in 95% of cases * Good prognosis * If low grade then 80% respond to H. pylori eradication * Paraproteinemia may be present

Answer 66

VIPoma * 90% arise from pancreas * Large volume diarrhea (secretory type due to enterocytes stimulatioin) * W eight loss * Dehydration * Hypokalemia, hypochlorhydria (refers to states where the production of gastric acid is low)

Answer 67

* Source: small intestine, pancreas * Stimulation: neural * Actions: stimulates secretion by pancreas and intestines, inhibits acid and pepsinogen secretion

Answer 68

aortic stenosis The association between angiodysplasia and aortic stenosis is thought to be caused by von Willebrand factor (vWF) being proteolysed in the turbulent blood flow around the aortic valve. vWF is most active in vascular beds with high shear stress, such as angiodysplasia, and deficiency of vWF increases the bleeding risk from such lesions

Answer 69

Diagnosis * Colonoscopy * Mesenteric angiography if acutely bleeding Management * Endoscopic cautery or argon plasma coagulation * Antifibrinolytics e.g. Tranexamic acid * Estrogens may also be used

Answer 70

Gallstones * Ethanol * Trauma * Steroids * Mumps (other viruses include Coxsackie B) * Autoimmune (e.g. Polyarteritis nodosa), Ascaris infection * Scorpion venom * Hypertriglyceridemia, Hyperchylomicronemia**, Hypercalcemia, Hypothermia * ERCP * Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate) * ↑ Degree burn of large skin area with significant inhalation injury

Answer 71

Ischemic (Purtscher) retinopathy (cotton wool spots seen on fundoscopy) - may cause temporary or permanent blindness. This condition may be seen following head trauma and in conditions such as acute pancreatitis, fat embolisation, amniotic fluid embolisation, and vasculitic diseases.

Answer 72

* Age > 55 * WBC > 16 * Urea > 16 * Glucose > 11 * Alb < 30 * ALT > 250 * Ca+ < 1 * LDH > 350 * PO2 < 8 * Hematocrit ↓ >10% * Base deficit > 4 * Fluid loss > 6L

Answer 73

Around 80% of cases are due to alcohol excess with up to 20% of cases being unexplained. Features of chronic pancreatitis: * Pain is typically worse 15 to 30 minutes following a meal * Steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain * Diabetes mellitus develops in the majority of patients. It typically occurs more than 20 years after symptom begin

Answer 74

nvestigation * Abdominal x-ray shows pancreatic calcification in 30% of cases * CT is more sensitive at detecting pancreatic calcification * Functional tests: pancreolauryl and Lundh tests may be used to assess exocrine function if imaging inconclusive

Answer 75

* Pancreatic enzyme supplements * Analgesia * Antioxidants: limited evidence base - one study suggests benefit in early disease

Answer 76

ncommon complication of acute pancreatitis and are localised collections of pancreatic fluid and debris, usually in the lesser sac. They are initially contained within a fragile wall of granulation tissue which eventually forms a fibrous capsule.

Answer 77

iagnosis: they cannot be diagnosed until more than 6 weeks after the acute attack, and may present with: * Abdominal pain or a mass. * Fever * Persistently raised amylase and liver function tests. Management: * Small pseudocysts usually resolve spontaneously * > 6cm in diameter seldom disappear spontaneously and may lead to complications such as hemorrhage and infection. They are usually managed by endoscopic or percutanous drainage or surgical intervention.

Answer 78

Incidence in the West: 9 cases per 100 000 and it’s increasing over the last 20 years. * 60% are ♂ * 5-year survival rate: 2% * K-ras is the most common oncogene in this condition * Insulinomas are the commonest form of endocrine tumours of the pancreas * Majority of cases occur in patients over the age of 60

Answer 79

Smoking (with a twofold increase in incidence) * Diabetes * Chronic pancreatitis * Hereditary pancreatitis * Hereditary non-polyposis colorectal carcinoma * Multiple endocrine neoplasia * Peutz-jeghers syndrome * BRCA2 * Dysplastic naevus syndrome

Answer 80

Contrast CT is used for diagnosis and assessment of invasion * ERCP restricted to palliative care * CA 19-9 * U/S abdomen is less reliable when the tumor is in the body or tail

Answer 81

defect in the PTEN tumour suppressor gene. - Hamartomatous polyps of the GI tract(1st) - oral mucosal papillomas, palmoplantar keratoses and trichilemmomas (benign tumours of hair follicles)

Answer 82

- PSC - Colorectal Ca

Answer 83

No inflammation beyond submucosa (unless fulminant disease) - inflammatory cell infiltrate in lamina propria * neutrophils migrate through the walls of glands to form crypt abscesses * LOSS of goblet cells and mucin from gland epitheli

Answer 84

nflammation always starts at rectum and never spreads beyond ileocaecal valve * Continuous disease * Associated with pANCA antigen

Answer 85

Barium enema * loss of haustrations * superficial ulceration, 'pseudopolyps' * long standing disease: colon is narrow and short -'drainpipe colon'

Answer 86

Lesions may be seen anywhere from the mouth to anus * Skip lesions may be present * Associated with ASCA (Anti- Saccharomyces Cerevisiae Antibodies

Answer 87

Inflammation in all layers from mucosa to serosa * goblet cells * granulomas

Answer 88

high sensitivity and specificity for examination of the terminal ileum * strictures: 'Kantor's string sign' * proximal bowel dilation * 'rose thorn' ulcers * fistulae

Answer 89

Treatment depends on the extent and severity of disease * Rectal aminosalicylates or steroids: for distal colitis rectal mesalazine has been shown to be superior to rectal steroids * Oral aminosalicylates or steroids * Severe colitis should be referred to hospital

Answer 90

Oral aminosalicylates e.g. Mesalazine

Answer 91

colonic cancer, and it is recommended that they be screened annually with colonoscopy.

Answer 92

Stool frequency >6/day * ESR > 30 mm/hr * HR > 90 bpm * Temp > 37.8°C in 2 out of 4 days * Anemia (Hb <75% predicted)

Answer 93

Disease duration > 10 years * Patients with pancolitis * Onset before 15 years old * Unremitting disease * Poor compliance to treatment

Answer 94

Mesalazine: whilst evidence base is limited widely used in active disease * Steroids (oral, topical or intravenous) * Azathioprine is used as a second-line treatment in active disease * Mercaptopurine (also called 6-mercaptopurine, 6-MP) * Methotrexate is used in patients intolerant of azathioprine or refractory disease. Usually given intramuscularly, but not effective in maintaining remission. Significant anemia is a contra- indication for methotrexate. * Infliximab is useful in refractory disease and fistulating crohn's. Patients typically continue on azathioprine or methotrexate

Answer 95

rare multi-system disorder caused by Tropheryma whippelii infection. It is more common in those who are HLA-B27 positive and in middle-aged men

Answer 96

Malabsorption: diarrhea, weight loss * Large-joint arthralgia (seronegative arthropathy) * Lymphadenopathy * Skin: hyperpigmentation and photosensitivity * Pleurisy, pericarditis * Neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus

Answer 97

Investigation * Jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff (PAS) granules * ↑ CRP and ESR * Hypoalbuminemia

Answer 98

1. Watery diarrhea 2. Normal colonoscopy 3. ↑ Inflamation of the lamina propria of the colon.

Answer 99

NSAIDs * Omeprazole, Lansoprazole * Ticlopidine * Cimetidine

Answer 100

Pain: antispasmodic agents * Constipation: laxatives but avoid lactulose * Diarrhea: loperamide is first-lin Second-line pharmacological treatment * low-dose tricyclic antidepressants (e.g. amitriptyline 5-10 mg) are used in preference to selective serotonin reuptak

Answer 101

s caused by sensitivity to the protein gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption.

Answer 102

nclude dermatitis herpetiformis (a vesicular, pruritic skin eruption) and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis). It is strongly associated with HLA-DQ2 (95% of patients) and HLA-B8 (80%) as well as HLA-DR3 and HLA-DR7

Answer 103

? Chronic or intermittent diarrhea ? Failure to thrive or faltering growth (in children) ? Persistent or unexplained gastrointestinal symptoms including nausea and vomiting ? Prolonged fatigue (‘tired all the time’) ? Recurrent abdominal pain, cramping or distension ? Sudden or unexpected weight loss ? Unexplained iron-deficiency anemia, or other unspecified anemia ? Recurrent mouth ulcers

Answer 104

* Anemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease) * Hyposplenism * Osteoporosis * Lactose intolerance * Enteropathy-associated T-cell lymphoma of small intestine * Subfertility, unfavourable pregnancy outcomes * Rare: esophageal cancer, other malignancies

Answer 105

Combination of immunology and jejunal biopsy. Villous atrophy and immunology normally reverses on a gluten-free diet.

Answer 106

Tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE * Endomyseal antibody (IgA) * Anti-gliadin antibody (IgA or IgG) tests are NOT recommended by NICE * Anti-casein antibodies are also found in some patients

Answer 107

* Villous atrophy * Crypt hyperplasia * ↑ in intraepithelial lymphocytes * Lamina propria infiltration with lymphocytes

Answer 108

this disease is most common in the Carribbean and the Far-East. It is characterized by a picture of small intestinal malabsorption and the cause is thought to be infectious in origin.

Answer 109

Diagnosis: * Jejunal biopsy reveals: o Mild villous atrophy o ↑ villous crypts o Mononuclear cellular infiltrates o Enlarged epithelial cells o Large nuclei caused by folate and/or vitamin B12 deficiency.

Answer 110

eatment: * Tetracyclines 250mg qds up to 6 months * Ampicillin may be used as an alternative in patients who are intolerant of tetracyclines. * Folate and B12 deficiencies should also be corrected * Complete recovery is possible with appropriate therapy.

Answer 111

Coeliac disease * Tropical sprue * Hypogammaglobulinemia * Gastrointestinal lymphoma * Whipple's disease * Cow's milk intolerance

Answer 112

Management: * Toxic dilatation can be treated medically for 12-24 hours with IV and rectal hydrocortisone but if there is then no improvement in the triad of o Pulse } o Stool frequency o Colon dilatation THEN urgent colectomy.

Answer 113

resentation: * Diarrhoea * Steatorrhoea * Malabsorption manifestation: Weight loss, anemia, osteoporosis/osteomalacia, electrolyte disturbances and hypovolemia. Management: * In patients with > 100cm of jejunum, oral intake is still possible. Diarrhoea may reduce with lactose exclusion or with a course of metronidazole to eradicate bacterial overgrowth. * In patients with < 100cm of jejunum, total parenteral nutrition is recommended.

Answer 114

disorder of pigmentation of the bowel wall. Histology demonstrates pigment- laden macrophages. It is associated with laxative abuse, especially anthraquinone compounds such as senna

Answer 115

assw liver cirrosis Paracentesis: neutrophil count > 250 cells/ul

Answer 116

ntravenous cefotaxime is usually given * Patients who have had an episode of SBP should be on prophylactic antibiotics Alcoholic liver disease is a marker of poor prognosis in SBP.

Answer 117

irrhosis * Alcoholic hepatitis * Schistosomiasis * Fulminant hepatic failure * Budd–Chiari syndrome * Acute or chronic portal vein obstruction * Cardiac diseases * Spontaneous bacterial peritonitis secondary to cirrhosis.

Answer 118

Nephrotic syndrome Protein losing enteropathy Peritoneal carcinomatosis Tuberculous peritonitis Pancreatic duct leak Biliary ascites.

Answer 119

Bilirubin is derived from the breakdown of heme in the red blood cells within the reticuloendothelial system. o The unconjugated bilirubin then binds albumin and is taken up by the liver. o In the liver it is conjugated which then makes it water-soluble and thus allows it to be excreted into the urine. o Normally total serum bilirubin is measured; however, the unconjugated (indirect bilirubin) and conjugated (direct bilirubin) portions can be.

Answer 120

ALT is more specific to the Liver, as AST is also found in cardiac and skeletal muscle and red blood cells. In chronic Liver disease ALT >AST, once cirrhosis established AST >ALT 􏱏 The extremes of the ratio of AST:ALT can also be helpful: 􏱍 >2 suggests alcoholic liver disease. 􏱍 <1.0 suggests nonalcoholic liver disease.

Answer 121

sensitive marker of hepatic function, but not useful in the acute stages as it has a long half life (20 days).

Answer 122

also related to the bile ducts. Typically elevated in cholestasis (with elevated ALP) but, if ALP normal, suggests induction of hepatic metabolic enzymes (e.g alcohol or enzyme-inducing drugs).

Answer 123

comes mainly from the cells lining bile ducts but also in bone. Marked elevation is typical of cholestasis (often with elevated GGT) or bone disorders (usually normal GGT). Isoenzyme analysis may help identify source. It is physiologically increased when there is increased bone turnover (e.g. adolescence) and is elevated in the third trimester of pregnancy (produced by the placenta).

Answer 124

Cirrhosis: if early disease, but later liver ↓ in size. Associated with a non-tender, firm liver * Malignancy: metastatic spread or primary hepatoma. Associated with a hard, irregular. Liver edge * Right heart failure: firm, smooth, tender liver edge. May be pulsatile

Answer 125

chronic liver disorder typically seen in middle-aged ♀s (♀:♂ ratio of 9:1). The aetiology is not fully understood although it is thought to be an autoimmune condition, with HLA DR3 association. Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis, which may eventually progress to cirrhosis. The classic presentation is itching in a middle-aged woman

Answer 126

Sjogren's syndrome (seen in up to 80% of patients) * Rheumatoid arthritis * Systemic sclerosis * Thyroid disease * Membranous GN * RTA

Answer 127

Clinical features * Early: may be asymptomatic (e.g. Raised ALP on routine LFTs) or fatigue, pruritus * Cholestatic jaundice * Hyperpigmentation, especially over pressure points * Xanthelasmas, xanthomata * Also: clubbing, hepatosplenomegaly * Late: may progress to liver failure

Answer 128

Anti-mitochondrial antibodies (AMA) M2 subtype in 98% of patients and are highly specific. * Smooth muscle antibodies in 30% of patients * Raised serum IgM

Answer 129

Management * Median survival is 7-10 yrs, but ↓ to 2 yrs if jaundice is present * Pruritus: cholestyramine * Fat-soluble vitamin supplementation * Ursodeoxycholic acid * Liver transplantation e.g. If bilirubin > 100 (PBC is a major indication) - recurrence in graft can occur but is n

Answer 130

IgM * Anti-Mitochondrial antibodies, M2 subtype * Middle aged ♀s

Answer 131

biliary disease of unknown aetiology characterized by inflammation and fibrosis of intra and extra-hepatic bile ducts

Answer 132

Associations * Ulcerative colitis: 4% of patients with UC have PSC, 80% of patients with PSC have UC * Crohn's (much less common association than UC) * HIV

Answer 133

* Cholestasis * Hepatomegaly * Intermittent jaundice

Answer 134

Investigation * ERCP is the standard diagnostic tool, showing multiple biliary strictures giving a 'beaded' appearance * MRCP is superior to ERCP * ANCA may be positive * There is a limited role for liver biopsy, which may show fibrous, obliterative cholangitis often described as ‘onion skin’

Answer 135

omplications * Cholangiocarcinoma (in 10%) * ↑ risk of colorectal cancer Management: * Liver transplantation, survival post transplant is 90% although rejection is high. Indication for transplantation:

Answer 136

autosomal recessive disorder characterized by excessive copper deposition in the tissues. Metabolic abnormalities include ↑ copper absorption from the small intestine and ↓ hepatic copper excretion. Wilson's disease is caused by a defect in the ATP7B gene located on chromosome 13.

Answer 137

Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea: * Liver: hepatitis, cirrhosis * Neurological: speech and behavioral problems are often the first manifestations. Also: tremor, chorea * Kayser-fleischer rings → * Renal tubular acidosis (esp. Fanconi syndrome) * Hemolysis * Blue nails

Answer 138

Diagnosis * ↓ serum ceruloplasmin * ↑ 24hr urinary copper excretion * Slit lamp: Kayser-Fleischer ring Management * D-penicillamine: chelates copper 1.5-2g/day in divided dose then 0.75-1.5g/day maintenance * Trientine * Zinc

Answer 139

is an autosomal recessive* condition of defective bilirubin conjugation due to a deficiency of UDP glucuronyl transferase. The prevalence is approximately 1-2% in the general population. Viral infections are common triggers for a rise in the bilirubin in patients with Gilbert's Features * Isolated hyperbilirubinemia * Unconjugated hyperbilirubinemia (i.e. Not in urine) * Jaundice may only be seen during an intercurrent illness Investigation and management * Investigation: rise in bilirubin following prolonged fasting or IV nicotinic acid * No treatment required

Answer 140

is a benign autosomal recessive disorder resulting in hyperbilirubinemia (conjugated, therefore present in urine). It is due to a defect in the canalicular multispecific organic anion transporter (cMOAT) protein. This causes defective hepatic bilirubin excretion. Features: * ↑ of conjugated * NO elevation of liver enzymes (ALT, AST). * Usually asymptomatic but may be diagnosed in early infancy based on laboratory tests. * Liver biopsy shows dark granules in the hepatocytes (thought to be due to melanin deposition) * Prognosis is good, and treatment of this syndrome is usually unnecessary. Most patients are asymptomatic and have normal life spans.

Answer 141

are, relatively benign autosomal recessive bilirubin disorder of unknown origin. It is a distinct disorder, yet similar to Dubin-Johnson Syndrome — both diseases cause an increase in conjugated bilirubin.

Answer 142

s a rare disorder affecting the metabolism of bilirubin, which results in high levels of unconjugated bilirubin and often leads to brain damage in infants.

Answer 143

is a cause of chronic diarrhea. It can result from malabsorption secondary to gastro-intestinal disease or be a primary disorder. Treatment with bile acid sequestrants is often effective. Types: * Type 1: Bile acid malabsorption, secondary to ileal resection, or ileal inflammation (e.g. in Crohn's disease) * Type 2: Idiopathic bile acid malabsorption, Primary bile acid diarrhea * Type 3: Secondary to various gastrointestinal diseases including cholecystectomy, vagotomy, small intestinal bacterial overgrowth, radiation enteropathy, celiac disease, chronic pancreatitis, etc.

Answer 144

Diagnosis: * SeHCAT test (selenium homocholic acid taurine or tauroselcholic acid): nuclear test involves two scans a week apart and only very limited radiation exposure. Retention of SeHCAT at 7 days is normally above 15%. Values less than 15% predict a response to bile acid sequestrants. The SeHCAT test measures multiple cycles of bile acid excretion and reabsorption over 7 days. This test is not licensed in the USA, and is underutilized even where it is available * Fecal bile acid quantfication or the 14C-glycocholic breath test are no longer in routine clinical use.

Answer 145

Hepatitis B: Basics * Incubation period (weeks) = 6-20 * Double-stranded DNA virus * Spread: body fluids + vertical * Chronic disease in 5-10% * Vaccination available

Answer 146

healthcare workers, intravenous drug users, sex workers, close family contacts of an individual with hepatitis B, individuals receiving blood transfusions regularly, chronic kidney disease patients who may soon require renal replacement therapy, prisoners, chronic liver disease patients

Answer 147

Immunization * Contains HBsAg adsorbed onto aluminum hydroxide adjuvant and is prepared from yeast cells using recombinant DNA technology * Most schedules give 3 doses of the vaccine with a recommendation for a one-off booster 5 years following the initial primary vaccination

Answer 148

Indicates adequate response, no further testing required. Should still receive booster at 5 years

Answer 149

Suboptimal response - one additional vaccine dose should be given. If immunocompetent no further testing is required

Answer 150

Non-responder. Test for past or previous infection. Give further vaccine course (i.e. 3 doses again) with testing following. If still fails to respond then HBIG would be required for protection if exposed to the virus

Answer 151

* Chronic infection (5-10%) * Fulminant liver failure (1%) * Hepatocellular carcinoma * GBS * Glomerulonephritis (memberanoproliferative) * Polyarteritis nodosa * Cryoglobulinemia (more with Hepa C than Hepa B)

Answer 152

Management: * Pegylated interferon-alpha used to be the only treatment available. It reduces viral replication in up to 30% of chronic carriers. A better response is predicted by being ♀ < 50 years old, low HBV DNA levels, non-Asian, HIV negative, high degree of inflammation on liver biopsy * However due to the side-effects of pegylated interferon it is now used less commonly in clinical practice. Oral antiviral medication is increasingly used with an aim to suppress viral replication (not in the dissimilar way to treating HIV patients) * Examples include lamivudine, tenofovir and entecavir

Answer 153

Abnormal ALT in at least 1 occasion * Liver biopsy shows fibrosis * Hepa B viremia >105 HBV DNA copies per mL

Answer 154

first marker to appear and causes the production of anti-HBs * HBsAg normally implies acute disease (present for 1-6 months)

Answer 155

implies chronic disease

Answer 156

immunity (either exposure or immunization)

Answer 157

results from breakdown of core antigen from infected liver cells as is therefore a marker of infectivity (e=infectivity)

Answer 158

Anti-HBc implies previous (or current) infection. IgM anti-HBc appears during acute or recent hepatitis B infection and is present for about 6 months (c=current or recent)

Answer 159

chronic liver disorder typically seen in middle-aged ♀s (♀:♂ ratio of 9:1). The aetiology is not fully understood although it is thought to be an autoimmune condition, with HLA DR3 association. Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis, which may eventually progress to cirrhosis. The classic presentation is itching in a middle-aged woman

Answer 160

Sjogren's syndrome (seen in up to 80% of patients) * Rheumatoid arthritis * Systemic sclerosis * Thyroid disease * Membranous GN * RTA

Answer 161

Clinical features * Early: may be asymptomatic (e.g. Raised ALP on routine LFTs) or fatigue, pruritus * Cholestatic jaundice * Hyperpigmentation, especially over pressure points * Xanthelasmas, xanthomata * Also: clubbing, hepatosplenomegaly * Late: may progress to liver failure

Answer 162

* Anti-mitochondrial antibodies (AMA) M2 subtype in 98% of patients and are highly specific. * Smooth muscle antibodies in 30% of patients * Raised serum IgM The Only MRCP Notes You’ll Ever Need 231 / 546 www.sudamedica.com Management * Median survival is 7-10 yrs, but ↓ to 2 yrs if jaundice is present * Pruritus: cholestyramine * Fat-soluble vitamin supplementation * Ursodeoxycholic acid * Liver transplantation e.g. If bilirubin > 100 (PBC is a major indication) - recurrence in graft can occur but is not usually a problem. 5 y

Answer 163

s a biliary disease of unknown aetiology characterized by inflammation and fibrosis of intra and extra-hepatic bile ducts

Answer 164

Associations * Ulcerative colitis: 4% of patients with UC have PSC, 80% of patients with PSC have UC * Crohn's (much less common association than UC) * HIV

Answer 165

Features * Cholestasis * Hepatomegaly * Intermittent jaundice Investigation * ERCP is the standard diagnostic tool, showing multiple biliary strictures giving a 'beaded' appearance * MRCP is superior to ERCP * ANCA may be positive * There is a limited role for liver biopsy, which may show fibrous, obliterative cholangitis often described as ‘onion skin’

Answer 166

Wilson's Disease is an autosomal recessive disorder characterized by excessive copper deposition in the tissues. Metabolic abnormalities include ↑ copper absorption from the small intestine and ↓ hepatic copper excretion. Wilson's disease is caused by a defect in the ATP7B gene located on chromosome 13.

Answer 167

Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea: * Liver: hepatitis, cirrhosis * Neurological: speech and behavioral problems are often the first manifestations. Also: tremor, chorea * Kayser-fleischer rings → * Renal tubular acidosis (esp. Fanconi syndrome) * Hemolysis * Blue nails

Answer 168

iagnosis * ↓ serum ceruloplasmin * ↑ 24hr urinary copper excretion * Slit lamp: Kayser-Fleischer ring Management * D-penicillamine: chelates copper 1.5-2g/day in divided dose then 0.75-1.5g/day maintenance * Trientine * Zinc

Answer 169

is a benign autosomal recessive disorder resulting in hyperbilirubinemia (conjugated, therefore present in urine). It is due to a defect in the canalicular multispecific organic anion transporter (cMOAT) protein. This causes defective hepatic bilirubin excretion.

Answer 170

ikely to become a significant public health problem in the UK in the next decade. It is thought around 200,000 people are chronically infected with the virus. At risk groups include intravenous drug users and patients who received a blood transfusion prior to 1991 (e.g. hemophiliacs). Hepa C is an RNA virus.

Answer 171

Transmission * Risk of transmission during a needle stick injury is about 2% * The risk of transmitting the virus during sexual intercourse is probably less than 5% * Vertical transmission rate from mother to child is about 6% (high viral load at delivery ↑ risk) * Breast feeding is not contraindicated in mothers with Hepatitis C Features * After exposure to the Hepatitis C virus less than 20% of patients develop an acute hepatitis

Answer 172

Complications * Chronic infection (80-85%) - only 15-20% of patients will clear the virus and will hence the majority will develop chronic hepatitis C * Cirrhosis (20-30% of those with chronic disease) * Hepatocellular cancer * Cryoglobulinemia

Answer 173

is condition of unknown etiology which is most commonly seen in young ♀s. Recognized associations include other autoimmune disorders, hypergammaglobulinemia and HLA B8, DR3. Three types of autoimmune hepatitis have been characterized according to the types of circulating antibodies present

Answer 174

Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA)

Answer 175

Anti-liver/kidney microsomal type 1 antibodies (LKM1)

Answer 176

Soluble liver-kidney antigen

Answer 177

autoimmune hepatitis

Answer 178

Features * May present with signs of chronic liver disease * Acute hepatitis: fever, jaundice etc (only 25% present in this way) * Amenorrhea (common) * ANA/SMA/LKM1 antibodies, raised IgG levels * Liver biopsy: inflammation extending beyond limiting plate 'piecemeal necrosis', bridging necrosis

Answer 179

Management * Steroids, other immunosuppressants e.g. Azathioprine * Liver transplantation

Answer 180

Features: * Increased serum transaminase * Macrocytosis * Thrombocytopenia * Poor hepatic synthetic function * Leucocytosis irrespective of infection * Increased acute phase reactants. * AST/ALT is usually > 2. * Liver enzymes do not exceed 500.

Answer 181

occurs in patients with excessive alcohol consumption with hemolysis and severe hyperlipidemia, abdominal pain, transient mildly raised bilirubin. It usually occurs in males and resolves once alcohol consumption is stopped.

Answer 182

* Steatosis - fat in the liver * Steatohepatitis - fat with inflammation, non-alcoholic steatohepatitis (NASH), see below * Progressive disease may cause fibrosis and liver cirrhosis NAFLD is thought to represent the hepatic manifestation of the metabolic syndrome and hence insulin resistance is thought to be the key mechanism leading to steatosis

Answer 183

Associated factors * Obesity * Hyperlipidemia * T2DM * Jejunoileal bypass * Sudden weight loss/starvation

Answer 184

eatures * Usually asymptomatic * Hepatomegaly * ALT is typically greater than AST * Increased echogenicity on ultrasound

Answer 185

Micronodular cirrhosis is associated with alcohol liver disease. Liver Cirrhosis: * Macronodular cirrhosis is associated with chronic hepatitis. * Granuloma formation is not classically seen in cirrhosis.

Answer 186

Other risk factors include: * Alpha-1 antitrypsin deficiency * Hereditary tyrosinosis * Glycogen storage disease * Aflatoxin Drugs: oral contraceptive pill, anabolic steroids * Porphyria cutanea tarda * ♂ sex * Diabetes mellitus, metabolic syndrome

Answer 187

Features * Drugs: oral contraceptive pill, anabolic steroids * Porphyria cutanea tarda * ♂ sex * Diabetes mellitus, metabolic syndrome * Tends to present late * Features of liver cirrhosis or failure may be seen: jaundice, ascites, RUQ pain, hepatomegaly, pruritus, splenomegaly * Possible presentation is decompensation in a patient with chronic liver disease

Answer 188

creening with ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as: * Patients liver cirrhosis secondary to hepatitis B & C or hemochromatosis * Men with liver cirrhosis secondary to alcohol Management options * Early disease: surgical resection * Liver transplantation * Radiofrequency ablation * Transarterial chemoembolisation * Sorafenib: a multikinase inhibitor

Answer 189

* Deranged clotting (e.g. INR > 1.4) * Low platelets (e.g. < 60 * 109/l) * Anemia * Bile duct obstruction * Hydatid cyst * Hemoangioma * Uncooperative patient * Ascites

Answer 190

* Drainage (needle aspiration or catheter) should always be performed * Amoxicillin + ciprofloxacin + metronidazole * If penicillin allergic: ciprofloxacin + clindamycin

Answer 191

efers to the development of acute renal failure in a patient who has advanced liver disease, who has no identifiable cause of intrinsic renal disease. It usually represents the end-stage of a sequence of reductions in renal perfusion induced by increasingly severe hepatic injury. Splanchnic vasodilatation appears to play an important role in the decline in renal function in hepatic disease.

Answer 192

1. Chronic or acute hepatic disease with advanced hepatic failure and portal hypertension 2. Creatinine > 133 mmol/l that progresses over days to weeks 3. Absence of any other apparent cause for the renal disease, including shock, active sepsis, current nephrotoxic drugs, and the absence of ultrasonographic evidence of obstruction or parenchymal renal disease. It is particularly important to exclude spontaneous bacterial peritonitis, which is complicated with acute renal failure 4. Urine sodium < 10 meq/l (off diuretics) and protein excretion < 500 mg/day 5. Lack of improvement in renal function after volume expansion with 1.5litres of isotonic saline.

Answer 193

* Rapidly progressive * Doubling of serum creatinine to > 221 μmol/L or a halving of the creatinine clearance to less than 20 ml/min over a period of less than 2 weeks * Very poor prognosis

Answer 194

*Slowly progressive *Prognosis poor, but patients may live for longer

Answer 195

are longitudinal or elliptical tears of the squamous lining of the distal anal canal. If present for less than 6 weeks they are defined as acute, and chronic if present for more than 6 weeks. Around 90% of anal fissures occur on the posterior midline

Answer 196

* Dietary advice: high-fiber diet with high fluid intake * Bulk-forming laxatives are first line - if not tolerated then lactulose should be tried * Lubricants such as petroleum jelly may be tried before defecation * Topical anesthetics * Sits baths: hip baths in hot water for 2–5 minutes followed by cold water for 1 minute * Topical steroids do not provide significant relief

Answer 197

The above techniques should be continued * Topical glyceryl trinitrate (GTN) is first line treatment for a chronic anal fissure * If topical GTN is not effective after 8 weeks then secondary referral should be considered for surgery or botulinum toxin

Answer 198

* Increasing age * Atrial fibrillation * Other causes of emboli: endocarditis * Cardiovascular disease risk factors: smoking, hypertension, diabetes

Answer 199

Features * Abdominal pain * Rectal bleeding * Diarrhea * Fever * Bloods typically show an elevated WBC associated with acidosis (low HCO3)

Answer 200

schemic colitis occurs with greater frequency in the elderly, most common form of bowel ischemia causes: Causes of the reduced blood flow can include ↓BP or local factors such as constriction of blood vessels or atheroma in the mesenteric vessels (most common).

Answer 201

Diagnosis: * Barium enema results tend to be abnormal in 90% showing thumbprinting, an indicative of mucosal edema * CT is the single best test after plain radiography * Colonoscopy is the diagnostic tool of choice: it shows petechiae, pallor, hyperemia and necrosis

Answer 202

Riedel's thyroiditis * Previous radiotherapy * Sarcoidosis * Inflammatory abdominal aortic aneurysm * Drugs: methysergide

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