Gastroenterology Flashcards

Question

Mx of variceal bleeding

Answer 1

Terlipressin and prophylactic abx given to pts at presentation ( prior to endoscopy). Band ligation and injections of sclerosing agents. TIPS ( transjugular intrahepatic portosystemic shunt) if bleeding not controlled with above measures).

Answer 2

Presence of RFs Diarrhoea Abdominal pain Fever N&V Abdominal distention / tenderness *A Raised WCC is characteristic & be aware severe toxic megacolon may develop.

Answer 3

Mild - normal wcc Moderate - raised WCC but under 15, 3-5 loose stools/ day Severe - WCC > 15 or acute creatinine rise > 50% above baseline. T > 38.5 or evidence of severe colitis ( abdominal or radiological signs). Life threatening - Hypotension, partial or complete ileus, Toxic megacolon or CT evidence of severe disease/

Answer 4

Detection of C Diff Toxin in stool CDT C diff antigen positivity only shows exposure to bacteria rather than a current infection.

Answer 5

1st line - oral vancomycin 10 d 2nd line - oral fidaxomicin 3rd line - oral vanc +/- IV metronidazole Life threatening - Oral vancomycin AND IV metronidazole. Other therapy: Monoclonal antibody Bezlotoxumab ( NICE not currently supporting). Faecal microbiota transplant - in those who have had two or more episodes. Recurrent episode - occurs in 20% of pts, increasing to 50% if 2nd infection. If reccurence before 12 weeks - oral fidaxomicin. After 12 weeks - oral vanc or fidaxomicin.

Answer 6

Low Na/ mg Osteoporosis - increased risk fractures ( malabsorption of mg and Ca) Microscopic colitis Increased risk of C diff infection Can mask symptoms of gastric cancer.

Answer 7

Metoclopramide is a DR receptor antagonist. Has prokinetic actions and is useful in the mx of nausea, diabetic gastroparesis, and in mx of nausea from migraine. SE: Exyrapyramidal effects - acute dystonia and oculogyric crisis. Tardive dyskinesis, parkinsonism, hyperprolactinaemia. Avoid in bowel obstruction

Answer 8

First-line investigations for coeliac disease should include a serum immunoglobulin IgA tissue transglutaminase antibody (tTGA) and total IgA. Testing for specific IgA antibodies must be done alongside a total IgA level, as if the patient has an IgA deficiency, the results may be falsely negative. Selective IgA deficiencies are also more common in people with coeliac disease.

Answer 9

Treating mild - moderate UC : Proctitis - Rectal aminosalicylate ( mesalazine). If remission not achieved in 4 weeks add oral aminosalicyate. If still not achieved add topical or oral steroid. Proctosigmoiditis / L sided UC - Topical aminosalicylate. If remission not achieved in 4 weeks switch to high dose oral aminosalicylate and topical steroid. If still not achieved offer oral steroid. Extensive disease - topical rectal aminosalicylate PLUS oral. IF remission not achieved in 4 weeks stop topical and offer high dose oral + steroid. Severe UC - Hospital admission, IV steroid 1st line. IV ciclosporin if steroid CI. If after 72 hours unsuccessful then consider adding IV ciclosporin to IV steroid or consider surgery.

Answer 10

Following mild- mod flare of UC: Proctitis & proctosigmoiditis - Topical rectal aminosalicylate alone OR oral aminosalicylate plus topoical OR oral aminosalicylate alone. Left sided and extensive UC - Low dose oral aminosalicylate. Following severe relapse or >= 2 exacerbations / yr then oral azathioprine or oral mercaptopurine.

Answer 11

The severity of UC is usually classified as being mild, moderate or severe: mild: < 4 stools/day, only a small amount of blood moderate: 4-6 stools/day, varying amounts of blood, no systemic upset severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

Answer 12

A-E - rescucitation, correct clotting and tranfusions ( FFP/Vit K/ platelets) Terlipressin ( causes vasoconstriction of the splanchnic circulation reducing bleeding) Prophylactic IV abx - Quinolones Endoscopy - bang ligation, sclerotherapy, TIPSS if above fails.

Answer 13

Propanolol - reduced rebleeding and mortality Endoscopic band ligation ( superior to sclerotherapy). Performed at two weekly intervals until all varices have been eradicated. PPI cover given to prevent EVL induced ulceration.

Answer 14

NICE guidance advises that we should not routinely offer H. pylori re-testing, however we can consider re-testing if: There has been poor compliance to eradication therapy Aspirin or NSAID is indicated There is a family history of gastric malignancy The person requests re-testing They advise that re-testing should ideally be done 8 weeks after initial eradication therapy and the carbon-13 urea breath test should be used first-line.

Answer 15

Autoimmune condition with progressive inflammation & damage to the cholangiocytes lining the intrahepatic ducts. Leads to obstruction of bile flow and cholestasis. Ultimately leads to liver fibrosis , cirrhosis and liver failure.

Answer 16

Typically affects females 40- 60 yrs often asymptomatic on initial presentation then picked up with abnormal LFTs. Bile acids , bilirubin and cholesterol normally excreted via bile ducts build up in the blood. Bile acids cause itching, bilirubin causes jaundice. Lack of bile acids leads to malabsorption of fats and greasy stools, lack of bilirubin excretion leads to pale stools and dark urine. Raised cholesterol leads to deposits in the skin called xanthelasma & xanthomas in skin or tendons ( large cholesterol deposits in tendons). Increased risk CV disease. Symptoms: Fatigue Itching Abdo pain / RUQ pain Jaundice Pale greasy stools Dark urine Examination: Xanthoma and xanthelasma Excoriation Hepatomegaly Signs of liver cirrhosis ( splenomegaly and ascites) Clubbing

Answer 17

LFTs --> ALP raised initially. progressed to full obstructive picture raised bilirubin. Antibodies : Antimitochondrial antibodies ( AMA ) m2 - Present in 98% & highly specific Smooth muscle antibodies in 30% of patients Raised serum IgM ( ANA also 30% not specific) Imaging - required before diagnosis to exclude extrahepatic duct biliary obstruction ( RUQ USS or MRCP).

Answer 18

1st line --> Ursodeoxycholic acid ( slows disease progression and improves symptoms) ( Ursodeoxycholic acid is a hydrophilic bile acid that protects cholagiocytes from inflammation and damage). Pruritus --> cholestyramine Immunosuppression - steroids Fat soluble (DAKE) vitamin supplementation Liver transplant end stage disease

Answer 19

Liver cirrhosis most importantly Deficiency DAKE Osteoporosis Hyperlipidaemia --> increased CV risk factor Associated with other AI disease: Sjogrens Systemic sclerosis Thyroid disease RA

Answer 20

Urgent: 2WW for all patients with: 1) Dysphagia 2) upper abdominal mass ( consistent with stomach ca) 3) > 55 yrs with WL & one of: upper abdo pain, reflux or dyspepsia Non urgent: 1) Haematemesis Patients > 55 yrs with: 2) treatment resistant dyspepsia 3) upper abdo pain with low Hb or raised platelet count ( and N/V/WL/Reflux/ dyspepsia/ upper abdominal pain 4) N/V with WL/reflux/dyspepsia/ upper abdo pain

Answer 21

NAFLD - excessive fats and triglycerides in liver cells that interfere with hepatocyte function. Stages: NAFLD ( fat within the liver ) Non alcoholic steatohepatitis ( fat with inflammation) Fibrosis Cirrhosis Risk factors : Middle age onwards Obesity Poor dit / low exercise T2DM High cholesterol HTN Smoking Sudden WL and starvation * Associated with metabolic syndrome which is the triad of HTN, obesity and diabetes. *

Answer 22

IX: LFT's - Raised ALT > AST Increased echogenicity on Liver USS confrim diagnosis of hepatic steatosis ( fat within liver) ELF ( enhanced liver fibrosis) blood test is 1st line for assess for fibrosis in NAFLD. Measures three markers ( HA PIINP & TIMP-1) and uses algorithm to indicate if there is advanced fibrosis. > 10.51 or above - advanced fibrosis under 10.51 - unlikely advanced fibrosis. Recheck 3 yrs. IF ELF + ve then transient elastography / fibroscan can be used to assess stiffness of the liver using high freq uSS. If ELF unavailable there are two other scoring systems available - FIB4 score or NAFLD fibrosis score. Both use AST : ALT ratio to assess severity of fibrosis. Normal ratio less than 1, ratio > 0.8 in NAFLD suggests fibrosis. Used with Fibroscan - good accuracy in fibrosis. Patients likely to have advanced fibrosis should be referred to liver specialist. Liver biopsy may be required to confirm diagnosis and is gold standard test.

Answer 23

WL & healthy diet Exercise Avoidance EtoH & Smoking Control of DB / HTN/ High Chol Referral of those with fibrosis to liver specialist Specialist management may include medications that sensitive to insuline ( pioglitazone) , bariatric surgery or transplantation.

Answer 24

Often diagnosed late and poor prognosis. Vast majority are adenocarcinomas & mostly occur in the head of the pancreas leading to compression of the bile ducts and obstructive jaundice. Tend to metastasise early especially to the liver, peritoneum, lungs and bones. Presentation: Painless, obstructive jaundice * key differential is cholangiocarcinoma*. ( Yellow sclera/skin/ pale stool/ dark urine/ itching & cholestatic LFTs) Upper abdominal pain or back pain Unintentional WL N& V Anorexia Palpable masses in epigastric region ( 3rd ) / hepatomegaly (1st)( liver mets) / palpable gallbladder (2nd) Change in BH Loss of exocrine function --> steatorrhoea Loss of endocrine function --> New onset diabetes or worsening of T2DM ** key sign ** Migratory thrombophlebitis ( Trousseau sign)

Answer 25

Bloods: Deranged LFTs with cholestatic picture CA 19.9 - tumour marker raised in pancreatic cancer and cholangiocarcinoma. Imaging: Abdominal USS HR CT - Ix of choice if the diagnosis is suspected. May show " double duct" sign with dilation of common bile and pancreatic duct. Staging CT TAP - usd to look for metastasis and other cancers. MRCP to assess biliary system in detail and assess obstruction & ERCP to stent and relieve obstruction. Special tests: Biopsy ( percutaneous / USS guided or CT guided or during ERCP)

Answer 26

Decided at HPB MDT Surgical if small tumour isolated in head of pancreas. Total / distal pancreatectomy OR whipples procedure ( removal of pylorus of stomach, pancreas, duodenum, gall bladder and bileducts & LNs) . Modified whipples keeps pylorus. Adjuvant chemotherapy often after surgery. Most cases curative surgery is not possible. Palliative treatment may involve: - Stent to relieve obstruction - Surgery to bypass obstruction - Palliative chemo or radiotherapy - EOL care

Answer 27

Peutz Jeghers syndrome is an autosomal dominant condition. characterised by numerous hamartomatous polyps in the gastrointestinal tract, also associated with pigmented freckles on the lips, face, palms and soles. polyps themselves don't have malignant potential, around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years. Features 1) hamartomatous polyps in the gastronintestinal tract (mainly small bowel) 2) small bowel obstruction is a common presenting complaint, often due to intussusception 3) gastrointestinal bleeding 4) pigmented lesions on lips, oral mucosa, face, palms and soles Management conservative unless complications develop

Answer 28

No blood or mucus ( PR bleeding less common) Entire GI tract ( mouth to anus) Skip lesions & strictures Transmural inflammation / terminal ileum most affectd Smoking risk factor ( do not set nest on fire) ( nSAID/COCP weak evidence of worsening)

Answer 29

Lifestyle - stop smoking Inducing remission: 1) Steroids 1st line - oral prednisolone or IV hydrocortisone. Budesonide is an alternative but is less effective. 2) enteral nutrition is an alternative ( particularly if concerns around steroids affecting growth). Enteral nutrition involves specially formulated diet either orally or NG that replaces pts usual diet. Enteral nutrition induces remission by: - treating nutritional deficiencies -Improving gut microbiome - Removing inflammatory foods 3) Mesalazine ( 5 ASA) -2nd line drug . 4) Azathioprine or mercaptopurine are add on drugs 5) methotrexate alternative to purines in those that cannot tolerate or poor Thiopurinemethyltransferase activity ( TPMT) 5) TNF a i - Infliximab used in refractory disease and fistulating disease. ( Typically continue azathioprine or mercaptopurine) . ( Other TNFa inhibitors adalimumab, ustekinumab, vedolizumab) 6) metronidazole for isolated perianal disease Maintaining remission: Azathioprine and mercaptopurine 1st line to maintaining remission ( Methotrexate can be used who cannot tolerate purines or had methotrexate to induce remission)

Answer 30

TPMT ( Thiopurine methyltransferase) levels need to be tested before starting pt on azathioprine or mercaptopurine as deficiency can lead to bone marrow suppression.

Answer 31

80% of pts with crohns disease will eventually have surgery. 1) Stricturing terminal ileal disease --> ileocaecal resection 2) segmental small bowel resection 3) stricuroplasty Perianal fistula: Inflammatory tract connection between anal canal and skin. MRI ix of choice - determine if there is an abscess or fistula is complex ( high fistula passing through all muscle layers) or simple ( low fistula ) - Oral metronidazole for pts with symptomatic fistulas Anti TNF - infliximab for closing and maintaining closure of perianal fistulas. Draining seton used for complex fistula ( surgical thread used to keep fistula open and allow drainage, prevent abscess formation). Perianal abscess - needs I & D + Abx.

Answer 32

small bowel cancer (standard incidence ratio = 40) colorectal cancer (standard incidence ratio = 2, i.e. less than the risk associated with ulcerative colitis) osteoporosis

Answer 33

Paracetamol Sodium valproate and phenytoin ( AEDs) MAOI's ( Antidepressants) Anti TB drugs ( RIPE) Statin Alcohol Amiodarone Methyldopa ( antihypertensive) Nitrofurantoin

Answer 34

COCP Steroids Abx - co-amoxiclav, flucloxacillin, erythromycin Antipsychotics - chlorpromazine, prochlorperazine Sulphonylureas Fibrates

Answer 35

MAM Methotrexate Amiodarone Methyldopa ( antihypertensive)

Answer 36

Haemochromatosis is an Autosomal Recessive disorder. ( require 2x copies to inherit disorder). Mutations in human haemochromatosis protein ( HFE) gene on chromosome 6, gene important in regulating iron metabolism. ( Encodes for a gene that regulates the expression of iron regulating hormone hepcidin, get low expression of hepcidin therefore uncontrolled duodenal absorption of iron). Iron accumulates in multiple organs including liver, heart, anterior pituitary, pancreas & joints. Presentation: * often later presentation in women due to iron loss with menses, typical age > 40 yrs men, later for W * Chronic tiredness Joint pain Pigmentation ( bronze skin) Anterior pit signs: Testicular atrophy and erectile dysfunction Amenorrhoea Cognitive symptoms - memory and mood disturbance Hepatomegaly

Answer 37

1) Serum ferritin is the initial investigation ( marker of total amount of iron in the body) 2) If high need full iron studies - focus on transferrin saturation. Typical iron study profile in patient with haemochromatosis transferrin saturation > 55% in men or > 50% in women raised ferritin (e.g. > 500 ug/l) and iron low TIBC 3) HFE genetic testing 4) LFTs 5) Liver biopsy with PERLs stain ( less common) only if evidence of cirrhosis 5) MRI to quantify liver and cardiac iron

Answer 38

Iron accumulation in multiple organs: Pituitary - hypogonadism, testicular atrophy, ED, amenorrhoea Thyroid - hypothyroid Cardiac - arrythmias and cardiomyopathy Liver - cirrhosis & hepatocellular carcinoma Pancreas - T1 DBM Chondrocalcinosis

Answer 39

Venesection - regularly removing blood to remove excess iron ( weekly initially) Monitoring serum FERRITIN & TRANSFERRIN SATURATION ( ferritin as a measure of total iron stores and transferrin saturation as a measure of how much iron bound to protein in the blood)

Answer 40

Adenocarcinoma is now the most common type of oesophageal cancer and is more likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett's. Key RFs - male, increasing age, smoking & alcohol, barretts , GORD, hiatus hernia , FHX, Low SE status Non white race - higher risk SCC

Answer 41

Dysphagia Odynophagia ( pain on swallowing) WL Anorexia Vomiting Hoarseness ( Recurrent LN involvement) Hiccups ( phrenic nerve) Cough ( local invasion of tumour to trachea) Malaena

Answer 42

Upper GI endoscopy with biopsy Endoscopic USS for local regional staging. CT CAP - initial staging PET CT - to detect occult metastases if none found on CT Treatment: Operable disease only if T1NOMO - surgical resection with oeosphagectomy or endoscopic therapy ( only superficial low risk lesions). + Adjuvant chemotherapy If not suitable for surgery --> definitive chemoradiotherapy Palliation if metastatic - palliative chemotherapy & best supportive care

Answer 43

Antigens / Antibodies: Surface antigen HBsAg - active infection. Normally implies acute disease, if present > 6 months then chronic. Surface antibody (given in vaccination) - HBsAb - implies vaccination, past or current infection. Core antibodies HBcAb - implies past or current infection. IgM implies acure active infection ( develop 1st 6 mths ) whereas IgG indicates past infection ( develops after 6 mnths) if HBsAg is negative. E antigen HBeAg - marker of viral replication and high infectivity ( breakdown product of infected liver cells) HBV DNA - direct count of viral load. When screening, test HBcAB ( detects prev infection) and HBsAg ( for active infection). If positive need to test HBeAg ( infectivity) and HBV DNA viral load.

Answer 44

Irritable bowel syndrome is a functional disorder. This means there is no identifiable bowel disease underlying the symptoms, and the symptoms result from the abnormal functioning of an otherwise normal bowel. Diagnosis of IBS should be considered if patient has the following for at least 6mnths. ABC. Abdominal pain ( relieved by defecation & worse with eating ) Bloating Change in bowel habit & stool form ( constipation/ diarrhoea or fluctuating. Stools - loose, watery or hard stools with associated mucus). A positive diagnosis of IBS should be made if the patient has abdominal pain relieved by defecation or associated with altered bowel frequency stool form, in addition to 2 of the following 4 symptoms: altered stool passage (straining, urgency, incomplete evacuation) abdominal bloating (more common in women than men) symptoms made worse by eating passage of mucus Other symptoms - lethargy, nausea, backache and bladder symptoms. Symptoms may be triggered by Anxiety/ depression / stress Sleep disturbance Illness Caffiene Alcohol Certain foods / medications Red flags : Rectal bleeding WL FHX ovarian or bowel cancer Onset > 60 yrs

Answer 45

FBC - anaemia Inflammatory markers - ESR/CRP Coeliac serology - Anti TTG Faecal calprotectin for iBD CA 125 ovarian cancer

Answer 46

1) lifestyle - Hydration, regualar small meals, adjustment of fibre intake according to BH ( increase for constip, reduce for diarrhoae), limit caffiene, alcohol & fatty foods. LOW FODMAP diet Probiotics Regular exercise & stress mx 2) Medical: Loperamide for diarrhoea Bulk forming laxatives ( isphagula husk) for constipation ( lactulose can cause bloating) Antispasmodics - mebeverine, alverine, hysocine, peppermint oil)

Answer 47

Over 40 yrs with jaundice 2ww Over 60 yrs with WL plus one additional symptom --> referral for a direct access CT abdomen. NICE suggest GP referral for direct access CT abdomen ( or USS if not available) to assess for pancreatic cancer if patient has WL plus one of: Change bowel habit ( D or C) Back pain Abdo pain N or V * New onset diabetes *

Answer 48

Autoantibodies are created in response to gluten which target epithelial cells of the small intestine leading to inflammation. Inflammation leads to atrophy of intestinal villi and malabsorption. Antibodies: tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE endomyseal antibody (IgA) needed to look for selective IgA deficiency, which would give a false negative coeliac result anti-gliadin antibody (IgA or IgG) tests are not recommended by NICE Endoscopic findings: Villous atrophy Crypt hyperplasia Increase in intraepithelial lymphocytes & invasion into lamina propria

Answer 49

Often asymptomatic and under diagnosed. Remember to test all new diagnoses of autoimmune thyroid disease and T1DM. Presentation: Failure to thrive in children Diarrhoea Bloating Fatigue WL Mouth ulcers dermatitis herpetiformis ( itchy blistering rash on abdomen) Anaemia can occur scondary to malabsorption leading to neurological symptoms: peripheral neuropathy, ataxia, epilepsy.

Answer 50

Pts must continue to eat gluten for 6 weeks prior to ix. 1st line blood tests ---> Total immunoglobulin A levels (to exclude IgA deficiency) Anti-tissue transglutaminase antibodies (anti-TTG) Anti-endomysial antibodies (anti-EMA) are a second-line option where there is doubt (e.g., a borderline result). Patients with a positive antibody test are referred to a gastroenterologist to confirm the diagnosis by endoscopy and jejunal biopsy. Typical biopsy findings are: Crypt hyperplasia Villous atrophy

Answer 51

lifelong gluten-free diet Complications: Nutritional deficiency Anaemia Osteoporosis Hyposplenism Ulcerative jejunitis Enteropathy-associated T-cell lymphoma (EATL) Non-Hodgkin lymphoma Small bowel adenocarcinoma

Answer 52

In liver failure all clotting factors are low except FVIII which is supra-normal. FVIII is synthesised in endothelial cells throughout the body and needs hepatocytes to deactivate it. So whilst there is a bleeding risk ( due to deficiency of all other clotting factors ) there is also a risk of venous thrombosis. This is added to by loss of synthesis of natural anticoagulant proteins Protein C & S and antithrombin.

Answer 53

Erythema nodosum ( presents as painful red or purple nodules on the shins) type of panniculitis, or inflammation of the subcutaneous fat, and it is one of the extra-intestinal manifestations of Crohn's disease that correlates with disease activity.

Answer 54

Primary sclerosing cholangitis - intra and extrahepatic bile ducts become inflamed & damaged developing strictures that obstruct bile flow. Sclerosis - hardening of the ducts and cholangitis - inflammation of ducts. Chronic bile obstruction eventually leads to liver inflammation, fibrosis and cirrhosis. RF: Male 30-40 yrs Ulcerative colitis ( 80% presenting with PSC have UC, 4% with UC will get PSC) Crohns Fhx

Answer 55

Often pts asymptomatic at diagnosis with problem picked up on abnormal LFTs. Male BG UC Abdominal pain ruq Fatigue Jaundice Itching hepatomegaly Splenomegaly Investigation: Deranged LFT - ALP & obstructive picture Autoantibodies LESS helpful , pANCA +Ve (ANA, Anti SMA ) imaging - MRCP diagnostic - showing bile duct strictures " beaded appearance". Limited role for liver biopsy - fibrous, obliterative changes Colonoscopy for ? UC Risks --> increased risk cholangiocarcinoma and colorectal cancer

Answer 56

Pernicious anaemia is an autoimmune disorder affecting the gastric mucosa that results in vitamin B12 deficiency. B12 deficiency --> Atrophic gastritis/ H pylori infection, gastrectomy, malnutrtion, alcoholism . Medications that reduce b12 absorption - ppi & Metformin Pathophysiology: 1) antibodies to intrinsic factor +/- gastric parietal cells 2) intrinsic factor antibodies → bind to intrinsic factor blocking the vitamin B12 binding site 3) gastric parietal cell antibodies → reduced acid production and atrophic gastritis. Reduced intrinsic factor production → reduced vitamin B12 absorption 4) vitamin B12 is important in both the production of blood cells and the myelination of nerves → megaloblastic anaemia and neuropathy

Answer 57

F: M ( 6:1 ) Middle - older age Associated AI disorder ( diabetes , thyroid, RA, vitiligo, addisons) Blood group A

Answer 58

Anaemia symptoms: SOB, tired, pallor , palpitations, headache. Glossitis - sore tongue Neurological --> peripheral neuropathy: 'pins and needles', numbness. Typically symmetrical and affects the legs more than the arms. subacute combined degeneration of the spinal cord: progressive weakness, ataxia and paresthesias that may progress to spasticity and paraplegia neuropsychiatric features: memory loss, poor concentration, confusion, depression, irritability

Answer 59

Investigation 1) full blood count macrocytic anaemia: macrocytosis may be absent in around of 30% of patients hypersegmented polymorphs on blood film low WCC and platelets may also be seen 2) vitamin B12 and folate levels a vitamin B12 level of >= 200 nh/L is generally considered to be normal 3) antibodies anti intrinsic factor antibodies: sensivity is only 50% but highly specific for pernicious anaemia (95-100%) anti gastric parietal cell antibodies in 90% but low specificity so often not useful clinically

Answer 60

Intramuscular hydroxocobalamin is initially given to all patients with B12 deficiency, depending on symptoms: No neurological symptoms – 3 times weekly for two weeks Neurological symptoms – alternate days until there is no further improvement in symptoms. Maintenance depends on the cause: Pernicious anaemia – 2-3 monthly injections for life Diet-related – oral cyanocobalamin or twice-yearly injections

Answer 61

When there is B12 & B9 deficiency together, B12 should be corrected first. Giving patient B9 before B12 can lead to subacute combined degeneration of the spinal cord with demyelination of the spinal cord and severe neurological problems.

Answer 62

Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach's plexus i.e. LOS contracted, oesophagus above dilated. Presentation: Dysphagia to both liquids and solids from the start Typically variation in severity of symptoms Heartburn Regurgitation of food - cough / aspiration Malignant change in small number of pts

Answer 63

IX : Oesophageal manometry - most important diagnostic test, excessive LOS tone. barium swallow - grossly expanded oesophagus, fluid level, " birds beak" appearance. CXR- wide mediastinum and fluid level. Mx: Balloon dilatation 1st line Surgical heller cardiomyotomy if recurrent / persistent sx Intrasphincteric injection of botulinum toxin Drug therapy - nitrates , CCB but limited by SE

Answer 64

Propanolol - non cardioselective BB used. MOA - reduces Cardiac output and BP, and causes splanchnic vasoconstriction ( by blocking b2 receptors) and reducing portal flow.

Answer 65

WD - autosomal recessive disease characterised by excessive copper accumulation in tissues. Mutation in wilson disease protein on Chr 13. (Copper binding protein). Copper binding protein important in removal of excess copper from body via liver. Copper is excreted in bile.

Answer 66

Presenting symptoms result from excessive copper in tissues including the liver, brain and cornea. Uusally presents in teenager or young adult ( 10-25 yrs) , rarely > 40 yrs. Liver problems usually arise first in children, whereas neurological disease in adults. Liver --> hepatitis and later cirrhosis Neurological --> Tremor & parkinsonism ( rigidity, bradykinesia) due to deposition in basal ganglia. Dystonia Speech difficulties Psychiatric --> abnormal behaviour, depression, cognitive impairment and psychosis. Kayser Fleischer rings - deposition in cornea. Haemolytic anaemia Renal tubular damage

Answer 67

1) Slit lamp examination for kayser fleischer rings 2) Serum caeruloplasmin initial screening test: LOW caeruloplasmin suggestive of Wilson's disease & reduced serum copper ( counter intuitive but 95% copper normally bound to caeruloplasmin). Free Copper is increased. 3) increased 24 hr urinary copper excretion 4) Confirmation with genetic analysis ATP7B gene

Answer 68

Copper chelation either with: Penicillamine 1st line Trientine Other tx: Zinc salts - inhibit copper absorption in GI tract Liver transplantation

Answer 69

1) Portal HTN - increase in osmotic pressure pushing fluid into peritoneal cavity 2) Reduced oncotic pressure of the serum due to poor synthetic function of liver ( low albumin states) 3) Activation of RAAS system due to low BP/ Low serum osmolality / redirection of blood flow - increase in Na/H20 retention

Answer 70

Grouped into transudative causes or exudative causes based on the serum albumin to ascitic gradient ( SAAG) SAAG = Serum Albumin - Ascitic fluid albumin > 11g - transudative < 11g - exudative Transudative causes of ascites: ( SAAG > 11g/L) 1) Cirrhosis ( NAFLD/ Alcoholic cirrhosis/ Hep b/c) 2) Acute liver failur 3) liver mets 4) R Heart failure 5) Portal vein thrombosis / Budd chiari ( triad of occlusion of hepatic veins, abdo pain and ascites) Exudative causes: SAAG < 11g/L Hypoalbuminaemia - nephrotic syndrome or severe malnutrition Malignancy - peritoneal mets Infection - TB peritonitis Pancreatitis Biliary ascites Bowel obstruction Post op lymph leak

Answer 71

1) appearance : Clear - liver cirrhosis Cloudy - SBP / pancreatitis Bloody - malignancy / haemorrhagic pancreatitis Milk / chyle - lymhoma, TB or malignancy 2) Biochem: Protein - high in SBP/TB Glucose - lower than serum think TB/Malignancy Amylase ? pancreatitis RBC - high think TB/ malignancy, very high - trauma. WBC > 250/uL abnormal, if raised neutrophils - think SBP 3) SAAG ( serum albumin - ascitic albumin gradient) 4) MCS Other ix: Bloods - LFT/U&E/FBC/Clotting/ Cultures /CRP / NILS Screen Abdominal USS CXR - ? HF/ Pleural effusion

Answer 72

1) Reduce dietary sodium 2) Fluid restriction if Na < 125 mmol 3) Aldosterone antagonists - spironolactone. Can add loop diuretic such as furosemide if above not working. 4) Drainage if tense ascites - therapeutic abdominal paracentesis. Large volume paracentesis requires albumin cover. Removing large vol > 5L can lead to paracentesis induced circulatory dysfunction and hepatorenal syndrome & mortality. 5) Prophylactic Abx in those with Low ascitic protein < 15g then oral ciprofloxacin or norfloxacin until ascites has resolved. 6) TIPS ( transjugular intrahepatic portosystemic shunt) in refractory ascites - Connect portal vein to hepatic vein via a stent bypassing the liver, done in IR under XR guidance.

Answer 73

Alcohol metabolised by 1) Alcohol dehydrogenase ( this pathway promotes fatty infiltration of the liver) 2) Cytochrome P450 which increases free radicals and activates hepatic macrophages. Oxidative stress leads to hepatocyte necrosis and apoptosis & increase in free radicals leads to inflammation and fibrosis. Stages 1) Alcohol releated fatty liver / hepatic steatosis - increase in fat build up in liver, if drinking stops process reverses. 2) Alcoholic hepatitis - inflammation , mild hepatitis reversible with complete abstinence 3) Cirrhosis - irreversible scarring

Answer 74

Hx of excess alcohol consumption Symptoms of liver cirrhosis: Fatigue WL Anorexia N& V Jaundice RUQ pain Signs: Smelling of alcohol Bloodshot eyes Dilated capillaries on face - telangiectasia Tremor Signs of liver cirrhosis: Jaundice Hepatomegaly Splenomegaly Ascites Caput medusa Spider naevi Gynaecomastia & testicular atrophy Palmar erythema & Clubbing Asterixis

Answer 75

FBC - Raised MCV ( B deficiencies, IDA, GI bleed, hypersplenism) Reduced platelets ( hyperspenism) LFTs: Gamma GT characteristically elevated AST: ALT ratio > 2, > 3 strongly suggestive alcoholic hepatitis Raised ALP & bilirubin later in cirrhosis Low albumin due to reduced synthetic function Increased prothrombin time - reduced synthetic function clotting factors U&E's can be deranged in hepatorenal syndrome Liver USS - fatty changes and increased echogenicity. Cirrhosis later. Fibroscan - ? fibrosis Endoscopy for ? varices Liver biopsy used to confirm diagnosis of alcohol related cirrhosis , especially in patients where steroids are being considered.

Answer 76

Stop drinking alcohol permanently (drug and alcohol services are available for support) Psychological interventions (e.g., motivational interviewing or cognitive behavioural therapy) Consider a detoxication regime Nutritional support with vitamins (particularly thiamine – vitamin B1) and a high-protein diet Corticosteroids may be considered to reduce inflammation in severe alcoholic hepatitis to improve short-term outcomes (but not long-term outcomes). Maddreys discriminant function is used , formula basd off prothrombin time and bilirubin. 40 mg prednisilone for 28 days. Pentoxyphylline also sometimes used. (steroids better evidence) . Treat complications of cirrhosis (e.g., portal hypertension, varices, ascites and hepatocellular carcinoma) Liver transplant in severe disease (generally 6 months of abstinence is required)

Answer 77

Chronic hep B is the most common cause worldwide Chronic hep C is the most common cause in Europe Other causes/ RFs: Liver cirrhosis ( alcoholic, NAFLD, ) Alpha 1 antitrypsin Haemochromatosis Primary biliary cirrhosis Diagnosis - Liver USS and alpha fetoprotein performed every 6 months in patients with liver cirrhosis as screening for HCC. Fibroscans done every 2 yrs in pts at risk of cirrhosis: 1) hep B&C 2) heavy etoh / alcoholic liver disease 3) NAFLD & ELF blood test indicating fibrosis

Answer 78

Hypertension in the portal system leads to vessel dilation and reduced vascular resistance. This lads to under filtration of the kidneys. Under filtration activates the RAAS causing vasoconstriction , which combined with a low circulating volume leads to further underfiltration of the kidneys and rapid deterioration in renal function.