Gastrointestinal Flashcards

Question

Generate a management plan for alcohol withdrawal

Answer 1

First line = long acting benzodiazepines - diazepam (oral if mild, if moderate or severe then i.v.) or clomethiazole Supportive treatment to prevent relapse and relieve symptoms. Phenobarbital if patient needs large benzodiazepine dose Vitamin supplementation (thiamine, magnesium). If severe AWS with or without benziodiazepine-resistance, ICU admission.

Answer 2

Oversedation from treatment Delirium tremens Alcohol-withdrawal seizures - less than 3% of these progress to status epilepticus

Answer 3

Some patients experience persistent insomnia and autonomic symptoms for few months. 50% remain abstinent for a year.

Answer 4

Inflammatory liver injury caused by chronic heavy alcohol intake.

Answer 5

``` Histopathology shows: Steatosis Ballooning and necrosis of hepatocytes Mallory bodies (cytoplasmic inclusions in hepatocytes). Neutrophilic inflammation Cholestasis Giant mitochondria ``` One of the THREE forms of liver disease caused by excessive alcohol intake - the spectrum consists of: Alcoholic fatty liver (steatosis) Alcoholic hepatitis Chronic cirrhosis

Answer 6

Excessive alcohol intake for 10-15 years | Presence of hepatitis C

Answer 7

Occurs in 10-35% of heavy drinkers

Answer 8

``` Rapid onset jaundice Nausea Malaise Anorexia RUQ pain Drowsiness, confusion Fever Abdominal distension (ascites) Swollen ankles GI bleeding ```

Answer 9

``` Febrile Tachycardia Jaundice Bruising Encephalopathy Ascites Hepatomegaly Splenomegaly Palmar erythema Dupuytren’s contracture Spider naevi Gynaecomastia ```

Answer 10

Bloods - FBC: low Hb, high MCV, high WCC, low platelets - LFTs: high AST + ALT, high bilirubin, high ALP + GGT, low albumin - U&Es: low urea and K+ - Clotting: prolonged PT Ultrasound - exclude malignancy, abscess etc Upper GI Endoscopy - investigate varices Liver Biopsy EEG - slow-wave activity indicates encephalopathy

Answer 11

Acute: - IV Thiamine, Vit C and multivitamins - Monitor and correct K, Mg and glucose abnormalities - Ensure adequate urine output - Treat encephalopathy: oral lactulose and phosphate enemas - Treat ascites: diuretics, paracentesis - Treat hepatorenal syndrome: glypressin, N-acetylcysteine Nutrition - Oral or nasogastric feeding (high protein diet) - Vitamin supplementation (IV then oral B vitamins, thiamine, folic acid) Note: if have encephalopathy then protein restriction Steroid therapy - 40mg/day for 4 weeks Long term - Stop drinking/reduce alcohol intake

Answer 12

The development of renal failure in patients with advanced chronic liver disease

Answer 13

Hepatorenal syndrome Cirrhosis Acute liver decompensation

Answer 14

Mortality in the first month = 10% Mortality in the first year = 40% If alcohol intake continues, most will progress to cirrhosis within 1-3 years.

Answer 15

The accumulation of misfolded proteins known as amyloid in organs and tissues. Amyloid demonstrates apple green birefringence under polarised light with Congo red stain. Amyloid deposition is disruptive to tissues and so amyloidosis manifests its clinical sequelae by the dysfunction of those organs in which it deposits

Answer 16

``` Primary amyloidosis (AL): Produce immunoglobulin light chains that are inherently prone to misfolding into an insoluble beta-pleated sheet configuration. Primary target organ = kidney (disruption of glomerular basement membrane) Also deposits in heart (conduction abnormalities) and nerves (vasa nervorum) ``` ``` Secondary amyloidosis (AA): Improper processing of serum amyloid A protein - not broken down enough. Affects kidney, GI tract, thyroid. ```

Answer 17

AL: MGUS, Multiple myeloma. No underlying genetic, environmental or occupational risk factors. AA: Inflammatory polyarthropathies - RA, psoriatic arthritis, ankylosing spondylitis Chronic infections - bronchiectasis, TB, osteomyelitis IBD – Crohn’s Malignancy - Hodgkin’s lymphoma, renal cell carcinoma Castleman's disease - lymphoproliferative disorder

Answer 18

Rare, more common in males, median age of diagnosis is 64, potentially twice as common in black people than white

Answer 19

Depends on where amyloid deposits Cardiomyopathy/heart failure - Fatigue - Weight loss - SOBOE - Raised JVP - Oedema - Postural hypotension GI involvement - Nausea - Abdominal cramps - Change in bowel habit - Weight loss - Hepatomegaly Nephrotic syndrome - Fatigue - Oedema - Postural hypotension Neurological - Peripheral neuropathy (paraesthesia) - Autonomic neuropathy (bladder/bowel dysfunction) - Carpal tunnel syndrome Other - Periorbital purpura/eyelid petechiae (raccoon eyes) - Macroglossia (AL only) - Shoulder pad sign (enlarged shoulders)

Answer 20

Serum and urine immunofixation - presence of monoclonal antibody, light chain protein in urine indicative of multiple myeloma and amyloidosis Immunoglobulin free light chain assay - abnormal kappa to lamda ratio Bone marrow biopsy - would find clonal plasma cells

Answer 21

A painful tear in the squamous lining of the lower anal canal

Answer 22

``` Idiopathic IBD Constipation/passage of hard stool Opiate analgesics (can cause constipation) Pregnancy ``` Rare: syphillis, herpes, trauma, anal cancer, psoriasis

Answer 23

Affects both sexes equally Can occur at any age but most often 15-40 year olds Incidence around 1 in 350 adults

Answer 24

Tearing pain on defecation - described as passing broken glass Fresh PR bleeding Anal spasm Anal itching (pruritus ani)

Answer 25

Visible tear in squamous lining of anus Anal spasm Sentinel pile (harmless growth hanging off skin around outside of anus)

Answer 26

Examine the anus - inspection only as DRE is too painful Anal manometry - patients with resistant fissures have low resting pressure Anal ultrasound - check for anal sphincter defects

Answer 27

Conservative management - High fibre diet - Increased fluid intake - Topical analgesia: lidocaine ointment - Laxatives Medical - GTN ointment (relaxes anal sphincter and promotes healing) - Diltiazem ointment (relaxes anal sphincter and promotes healing) - Botulinum toxin injection if chronic Surgical - Lateral subcutaneous internal sphincterotomy - 2nd line = anal advancement flap

Answer 28

Chronic anal fissure Recurrence Perianal abscess or anal fistula in IBD Incontinence after surgery

Answer 29

60% of fissures heal in 6-8 weeks 30% require a surgical intervention

Answer 30

Acute inflammation of the appendix

Answer 31

Lumen obstruction by faecolith, normal stool, infective agents or lymphoid hyperplasia Gut organisms then invade appendix wall Leads to oedema, ischaemic necrosis and perforation

Answer 32

Can occur at any age but less likely in extremes Most common between 10 and 20 years old Males slightly more likely

Answer 33

``` Periumbilical pain which moves to RIF Anorexia Nausea and vomiting Constipation Diarrhoea Fever ```

Answer 34

``` Fever Tachycardia McBurney’s sign - RIF tenderness Rosving’s sign - palpation of LIF causes more pain in RIF than in left RIF guarding and rebound tenderness Tender mass Psoas sign - pain on extending the hip Cope sign - pain in flex ion and internal rotation of the hip Diminished bowel sounds Fetor ```

Answer 35

Bloods FBC - high white cell count CRP - high ``` CT abdo and pelvis - appendix diameter more than 6mm Urine pregnancy test Abdominal ultrasound Urinalysis - negative Abdo and pelvic MRI if pregnant ```

Answer 36

IV fluids Prompt appendicectomy Antibiotics - cefoxitin and metronidazole

Answer 37

``` Perforation Appendix mass when appendix becomes covered with omentum Appendix abscess Peritonitis Surgical wound infection ```

Answer 38

In uncomplicated appendicitis most people recover with no long term complications

Answer 39

Chronic inflammatory disease of the liver of unknown aetiology characterised by autoimmune features, hyperglobulinaemia and the presence of circulating autoantibodies

Answer 40

``` Female HLA-DR3/DR4 Other autoimmune conditions eg pernicious anaemia, thyroiditis, coeliac Measles virus Cytomegalovirus Epstein-Barr virus Hepatitis A, C or D virus Drugs ```

Answer 41

Type 1: Anti-nuclear antibodies, anti-smooth muscle antibodies, anti-actin antibodies, anti-soluble liver antigen Type 2: Anti-liver/kidney microsomes, anti-liver cytosol antigen

Answer 42

Highest among people with northern European ancestry. Can occur in any age group. Type 1 had a bimodal age distribution - between 10-30 and 40-60 years. Type 2 mainly affects children between the ages of 2 and 14 years. Women are affected more frequently than men.

Answer 43

Insidious ``` Malaise Fatigue Anorexia Weight loss Nausea Jaundice Amenorrhoea Epistaxis Pruritis ``` ``` Acute presentation: Fever Anorexia Jaundice Nausea/Vomiting/Diarrhoea RUQ pain Arthralgia Polyarthritis Maculopapular rash ```

Answer 44

Stigmata of chronic liver disease = hepatomegaly, spider naevi, jaundice, splenomegaly Late features = Ascites, oedema, hepatic encephalopathy

Answer 45

Bloods LFTs: high AST, ALT, GGT, ALP, Bilirubin. Low albumin (in severe disease) Clotting: High PT (in severe disease) FBC: Low Hb, platelets and WCC Serum globulin - hypergammaglobulinaemia with presence of ANA, ASMA and Anti-LKM antibodies Liver Biopsy - establish diagnosis and check whether hepatitis or cirrhosis ``` To rule out other causes of liver disease: Viral serology Urinary copper/caeruloplasmin Ferritin and transferrin saturation Alpha-1 antitrypsin Anti-mitochondrial antibodies (PBC) ``` US, CT or MRI of liver and abdomen - visualise structural lesions ERCP - rule out PSC

Answer 46

Metaplastic change in the lower oesophageal mucosa from oesophageal stratified squamous epithelium to intestinal simple columnar epithelium secondary to prolonged acid reflux SQAUMOUS -> COLUMNAR

Answer 47

``` Central obesity Age White ethnicity Male Smoking Family history of Barrett's oesophagus or oesophageal adenocarcinoma GORD Hiatus hernia - makes GORD more likely ```

Answer 48

0.5-2.0% of the general population Rare in children - more prevalent with increasing age More common in white men

Answer 49

``` Same as symptoms of GORD: Heartburn Nausea Water-brash (sour taste in the mouth) Bloating Belching Burning pain when swallowing Dysphagia Regurgitation ```

Answer 50

Nil of note

Answer 51

Upper GI endoscopy with biopsy - violaceous epithelium proximal to the gastro-oesophageal junction. Barium oesophagogram - not diagnostic but can look for mass or stricture before endoscopy if having dysphagia

Answer 52

Non-dysplastic Barrett's oesophagus: - PPI and surveillance - Radiofrequency ablation in high-risk patients - If PPI ineffective, anti-reflux surgery and surveillance Low-grade dysplasia: - Radiofrequency ablation with or without endoscopic mucosal resection if nodular High-grade dysplasia: - Radiofrequency ablation with or without endoscopic mucosal resection and PPI - 2nd line = oesophagectomy

Answer 53

Dysplasia and oesophageal adenocarcinoma | Oesophageal stricture

Answer 54

Adenocarcinomas discovered while screening for Barrett's oesophagus are early-stage lesions and have good prognosis (5-year survival >85%). 5-10% of those with Barrett's oesophagus will develop adenocarcinoma over 10-20 years.

Answer 55

Cancers arising from the bile duct epithelium which are mostly adenocarcinomas

Answer 56

``` Age >50 years Cholangitis Choledocolithiasis Cholecystolithiasis Structural disorders of biliary tree UC Primary sclerosing cholangitis Liver disease - Cirrhosis, Alcoholic liver disease Hepatitis B or C virus Parasitic infections ```

Answer 57

Mostly between 50-70 years old Males slightly more likely More common in developing world due to increased prevalence of parasitic infections

Answer 58

``` Painless jaundice Weight loss Malaise Anorexia Abdominal pain Obstructive jaundice symptoms: Pruritis, yellow sclera, pale stool, dark urine ```

Answer 59

Palpable gallbladder Hepatomegaly Courvoisier's Law - in the presence of jaundice, a palpable gallbladder (that is non-tender) is unlikely to be due to gallstones (i.e. cancer of the pancreas or biliary tree is more likely)

Answer 60

Bloods: LFTs - high conjugated bilirubin, ALP, GGT, slight increase AST and ALT Clotting screen - increased PT Tumour markers - high CA19-9, CEA, CA-125 Abdo USS - identify malignant vs benign Abdo CT if necessary Abdo MRI MR angiography for staging ERCP/MRCP/PTC to show extent of duct involvement

Answer 61

Acute inflammation of the gallbladder

Answer 62

Complete cystic duct obstruction due to impacted gallstone in gallbladder neck or cystic duct Blockage of bile flow. Gall bladder distension which leads to inflammation within the gallbladder wall.

Answer 63

``` Age Female Fat Diabetes mellitus Drugs (OCP, octreotide) Family history Ethnicity (Caucasian) Pregnancy TPN Terminal ileum disease Female, fat, fertile, fair, forty ``` Pigment Stone Risk Factors (caused by increased bilirubin due to haemolysis): haemolytic disorders (e.g. sickle cell anaemia)

Answer 64

3 times more common in women More common with increasing age 10-15% of adults have gallstones

Answer 65

``` RUQ pain Pain referred to right shoulder Fever Systemically unwell Anorexia Nausea Previous episodes of biliary pain ```

Answer 66

``` Positive Murphy's sign - ask patient to exhale, palpate right costal margin and ask patient to inhale. Patient stops breathing in and winces. Tachycardia Pyrexia RUQ guarding or rebound tenderness Rare: abdominal mass ```

Answer 67

``` Bloods: FBC - high WCC High CRP LFTs - high ALP, GGT and bilirubin Blood cultures Amylase (exclude pancreatitis) ``` Ultrasound - shows gallstones, increased thickness of gallbladder wall, dilatation of biliary tree HIDA if USS shows nothing - shows failure of gallbladder filling AXR Other imaging - to exclude differentials (e.g. erect CXR, ERCP)

Answer 68

Conservative: If only mild biliary colic - low-fat diet ``` Medical: NBM IV fluids Analgesia Anti-emetics Antibiotics (if infection is present) If symptoms persist despite antibiotics, suspect localised abscess or empyema - drainage Urgent biliary drainage by ERCP PTC ``` Surgical: Laparoscopic Cholecystectomy

Answer 69

Perforation Abscess Necrosis Gallstone ileus ``` Cholecystectomy complications: Bile duct injury Bleeding Infection Bile leak ```

Answer 70

Gallstones are usually asymptomatic | Surgery offers an excellent chance of cure if they were to become symptomatic

Answer 71

End-stage of chronic liver damage with replacement of normal liver architecture with abnormal diffuse fibrosis and nodules of regenerating hepatocytes. Decompensation occurs when there is evidence of complications e.g. portal hypertension, varices, encephalopathy, jaundice, ascites

Answer 72

Chronic alcohol misuse - MOST COMMON UK CAUSE Chronic viral hepatitis B/C - MOST COMMON WORLDWIDE CAUSE Autoimmune hepatitis Drugs (e.g. methotrexate, hepatotoxic drugs) Inherited -Alpha1-antitrypsin deficiency -Haemochromatosis -Wilson's disease -Galactosaemia -Cystic Fibrosis Vascular -Budd-Chiari Syndrome -Hepatic Venous Congestion Chronic Biliary Diseases - primary sclerosing cholangitis, primary biliary cirrhosis, biliary atresia Non-Alcoholic Steatohepatitis (NASH)

Answer 73

``` Alcohol misuse IVDU Unprotected sex Blood transfusion Obesity Diabetes Total parenteral nutrition Short bowel syndromes Hyperlipidaemia Drugs (e.g. amiodarone, tamoxifen) ```

Answer 74

Common in alcoholics

Answer 75

``` Early non-specific symptoms: Anorexia Nausea Fatigue Weakness Weight loss ``` Symptoms due to decreased liver synthetic function: Easy bruising Abnormal swelling Ankle oedema ``` Symptoms due to reduced detoxification function: Jaundice and pruritis Personality change Altered sleep pattern Amenorrhoea Galactorrhoea ``` Symptoms due to portal hypertension: Abdominal swelling Haematemesis - coffee ground vomit PR bleeding or melaena

Answer 76

``` Asterixis Bruises Clubbing Dupuytren's contracture Palmar erythema Fetor hepaticus Jaundice Gynaecomastia Leukonychia Parotid enlargement Spider naevi and facial telangiectasia Scratch mark (from cholestatic pruritis) Ascites (Hepatomegaly) - in early phase however shrinks at later phases Testicular atrophy Caput medusae Splenomegaly Liver flap ```

Answer 77

Bloods FBC: low platelets due to hypersplenism as a result of portal hypertension LFTs: high AST, ALT, ALP, GGT and bilirubin, ALT highest. Serum albumin: low Serum sodium: low Clotting: prolonged PT Investigations to determine CAUSE Hepatitis C antibodies Hepatitis B surface antigen Viral serology Alpha-1 antitrypsin Iron studies: serum ferritin, iron, total iron binding capacity (TIBC) - check for haemochromatosis Anti-mitochondrial antibody, ANA, ASMA - chec for autoimmune hepatitis Serum ceruloplasmin - low in Wilson's disease Ascitic Tap MC&S - check for infection Biochemistry (protein, albumin, glucose, amylase) Cytology ASCITIC TAP WITH NEUTROPHILS > 250/mm3 = spontaneous bacterial peritonitis (SBP) US, CT or MRI Endoscopy - To examine varices

Answer 78

Treatment of underlying chronic liver disease Prevent superimposed hepatic injury - avoid alcohol and hepatotoxic drugs e.g. NSAIDs, high doses of paracetamol. Immunisation against hep A and B for susceptible patients, management of metabolic risk factors, maintenance of adequate nutrition, and regular exercise Monitoring for complications Sodium restriction and diuretics for ascites - spironolactone and furosemide if not responding 2nd line = liver transplantation Treatment of complications: 1. Encephalopathy - liver cannot break down ammonia in GI tract so goes to brain and exerts toxic effects Treat infections Exclude GI bleed Lactulose (decrease gut absorption of ammonia) and phosphate enemas Avoid sedation 2. Ascites Diuretics (spironolactone with/without furosemide) Dietary sodium restriction Therapeutic paracentesis (with human albumin replacement) Monitor weight Fluid restrict if plasma sodium < 120 mmol/L Avoid alcohol and NSAIDs 3. Spontaneous Bacterial Peritonitis Antibiotics (e.g. cefuroxime and metronidazole Prophylaxis against recurrent SBP with ciprofloxacin 4. Surgical TIPS (transjugular intrahepatic portosystemic shunt) -reduce portal hypertension

Answer 79

``` Portal hypertension with ASCITES Hepatic encephalopathy Variceal haemorrhage Spontaneous Bacterial Peritonitis Hepato Cellular Carcinoma Renal failure (hepatorenal syndrome) AKI Pulmonary hypertension (hepatopulmonary syndrome ```

Answer 80

The overall median survival of patients with cirrhosis is approximately 10 years Likelihood of transitioning to decompensated cirrhosis within 10 years is 50%. The median survival time in patients with decompensated cirrhosis is approximately 2 years.

Gastrointestinal Flashcards

(104 cards)