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GASTRO > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

A 40-year-old asymptomatic man presents for a routine visit with elevated alanine aminotransferase (ALT) level (55 international units [IU]/mL). His mother died of hepatocellular carcinoma and he has a middle-aged sister with “hepatitis B infection”. He has a normal physical examination and has no stigmata of chronic liver disease.
Likely cause?

A

Hepatitis B presentation

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2
Q

A 42-year-old man is referred to the liver clinic with mild elevation in aminotransferases for several years. He has a medical history significant for obesity, hypertension, and hypercholesterolaemia. He does not smoke or drink alcohol and there is no high-risk behaviour. He has a family history of premature cardiac disease. He is taking a diuretic and, because of his elevated liver tests, was recommended to discontinue his statin medication several months ago. Other than complaints of mild fatigue, the patient feels well. Examination is notable for a BMI of 37 kg/m², truncal obesity, and mild hepatomegaly.
Likely cause?

A

NAFLD

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3
Q

Abdominal signs for Crohns?

A
  • Aphthous ulcers
  • glossitis
  • Abdominal tenderness
  • RIF mass
  • Perianal abscesses, fistulae, tags
  • Anal/rectal stricture
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4
Q

Abdominal signs for UC?

A
  • Fever
  • Tender, distended abdomen
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5
Q

Abdominal symptoms presentation in Crohns?

A
  • Diarrhoea (not bloody mostly)
  • Abdominal pain
  • Weight loss more prominent
  • Extra-intestinal signs
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6
Q

Abdominal symptoms presentation in UC?

A
  • Diarrhoea
  • Blood ± mucus PR
  • Abdominal discomfort
  • Tenesmus, faecal urgency (more rectally)

Nocturnal diarrhoea and incontinence are typical features of IBD.

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7
Q

Acute complications of acute severe ulcerative colitis

A
  • Perforation
  • Bleeding
  • Toxic Megacolon (>6cm)
  • VTE

Later on - DALM lesion can lead to metasitic disease.

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8
Q

Acute pancreatitis?

A

Hypocalcaemia = saponification of fats. As lipase leaks out of damaged pancreas = breaks down fat into triglyceride + fatty acid. These combine with calcium to make soap.

Amylase does not correlate with disease severity.

Serum lipase is more sensitive and specific.

Assessment of severity
- Glasgow, Ranson scoring systems and APACHE II

Predicts severe attack with 48hrs
= Clinical impression of severity
- Body mass index >30
- Pleural effusion
- APACHE score >8

24hrs = Clinical impression of severity
APACHE II >8
Glasgow score of 3 or more
Persisting multiple organ failure
CRP>150

48hr
= Glasgow Score of >3
CRP >150
Persisting or progressive organ failure

  • Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy.
  • Patients with obstructed biliary system due to stones should undergo early ERCP.
  • Patients who fail to settle with necrosis and have worsening organ dysfunction may require debridement, fine needle aspiration is still used by some.
  • Patients with infected necrosis should undergo either radiological drainage or surgical necrosectomy. The choice of procedure depends upon local expertise.
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9
Q

AIH Presentation?

A

Teens and early 20s (25%)
- Constitutional: fatigue, fever, malaise
- Cushingoid: hirsute, acne, striae
- Hepatitis
- HSM (hepatosplenomegaly)
- Fever
- Amenorrhoea
- Polyarthritis
- Pulmonary infiltration
- Pleurisy

Post/peri-menopausal
- Present insidiously with chronic liver disease

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10
Q

Alcoholic ketoacidosis?

A

Alcoholic ketoacidosis is a non-diabetic euglycaemic form of ketoacidosis. It occurs in people who regularly drink large amounts of alcohol. Often alcoholics will not eat regularly and may vomit food that they do eat, leading to episodes of starvation. Once the person becomes malnourished, after an alcohol binge the body can start to break down body fat, producing ketones. Hence the patient develops a ketoacidosis.

It typically presents with a pattern of:
Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration

The most appropriate treatment is an infusion of saline & thiamine. Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis.

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11
Q

Amoebic abscess?

A

Entamoeba Histolytica Liver abscess is the most common extra-intestinal manifestation of amoebiasisBetween 75 and 90% lesions occur in the right lobePresenting complaints typically include fever and right upper quadrant pain. - profuse, bloody diarrhoeathere may be a long incubation periodstool microscopy may show trophozoites if examined within 15 minutes or kept warm (known as a ‘hot stool’)treatment is with metronidazoleUltrasonography will usually show a fluid filled structure with poorly defined boundariesAspiration yield sterile odourless fluid which has an anchovy paste consistencyTreatment is with metronidazole

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12
Q

Antibodies for PBC

A

AMA

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13
Q

Antibodies for PSC

A

ANCA, ANA

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14
Q

Are Crohns or UC patients younger?

A

Crohns = 20s
UC = 30s

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15
Q

As part of portal hypertension - you can get splenomegaly

A

Splenic congestion
- Hypersplenism: decreased WCC, decreased platelets.

Massive splenomegaly - CML, Myelofibrosis, Visceral leishmaniasis, Malaria.

Mild: Infections: IE, EBV, CMV, amyloidosis, sarcoidosis, SLE, RA(Felty’s).

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16
Q

Ascitic tap that indicates SBP?

A

PMN > 250mm indicates SBP, whether or not culture has grown.

Most common organism = E.coli

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17
Q

ASSESSMENT FOR UGIB

A
  • A-E and patient NBM
  • optomise airway and breathing
  • insert 2 wide bore cannula for fluids
  • Bloods:
  • FBC with serial assessment of Hb ever 6 hrs + assessment of platelet levels
  • Group and Save (crossmatch 4-8 units where necessary)
  • Coagulation profile
  • Lfts +U&Es (acute organ injury + underlying cause)
  • urine output needs monitoring
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18
Q

Assessment of a severe attack of Crohns?

A
  • Increased temp, increased HR, increased ESR, increased CRP, increased WCC, decreased albumin
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19
Q

Associated disease of PBC?

A
  • Thyroid
  • RA, Sjogrens, scleroderma
  • Coeliac
  • Renal tubular acidosis
  • Membranous GN
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20
Q

Associated diseases with AIH?

A
  • Autoimmune thyroiditis
  • DM
  • Pernicious anaemia
  • PSC
  • UC
  • GN
  • AIHA (Coombs +ve)
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21
Q

Associated diseases with PSC?

A
  • 3% of those with UC have PSC
  • 80-100% of those with PSC have UC/Crohns
  • Crohns much raiser
  • AIH
  • HIV
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22
Q

At what level is jaundice visible?

A

50uM (3x upper limit of normal)

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23
Q

Autoimmune Hepatitis pathophysiology

A
  • Inflammatory disease of unknown cause characterised by Abs directed vs hepatocyte surface antigens
  • Predominately young and middle-aged women
  • Classified according to Abs
    T1 = Adult, SMA+ (80%), ANA+ (10%), Increased IgG
    T2 = Young, LKM+
    T3 = Adult, SLA+
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24
Q

Barrett’s oesophagus

A

Metaplasia of the lower oesophagus mucosa - squamous being replaced with columnar epithelium.

  • Increased risk of adenocarcinoma.

Barrett’s can be subdivided into short (<3cm) and long (>3cm).

Management
- Endoscopic surveillance with biopsies
- High dose PPI: whilst this is commonly used in patients with Barrett’s the evidence .

Endoscopic surveillance
- Metaplasia endoscopy is recommended every 3-5 years

If dysplasia of any grade is identified endoscopic intervention is offered
- Endoscopic mucosal resection
- Radiofrequency ablation

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25
Q

Benign mechanical mural causes of dysphagia?

A

Plummer-Vinson (Web),
Oesophagitis
Trauma (GORD)
Pharyngeal pouch

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26
Q

Blatchford score

A
  • determine if admission + endoscopy is needed

- patient can go home pre-endsocpy if score <0

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27
Q

Blood effects of alcoholism?

A

Increased MCV
Folate deficiency –> anaemia

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28
Q

Blood transfusion post UGIB indications

A
  • if Hb<7 in vatical bleed
  • If HB<8 in non-variceal bleed
  • if patient lost >30% of blood volume
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29
Q

Calprotectin?

A

Gut inflammation as part of workup for inflammatory bowel disease.

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30
Q

Carcinoid tumours pathology?

A

Neuroendocrine tumours of enterochromaffin cell origin capable of producing 5HT.
- May secrete 5-HT, VIP, gastrin, glucagon, insulin, ACTH.
- Carcinoid syndrome suggest bypass of first-pass metabolism and strongly assoc with metastatic disease.
- 10% part of MEN1

  • Sites
    :Appendix: 45%, Ileum 30%, Colorectum 20%, Stomach 10%, Elsewhere in GIT and bronchus.
    Consider all as malignant.
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31
Q

Cardiac effects of alcoholism?

A

Arrhythmias: e.g AF
Dilated cardiomyopathy (completely reversible)
Increased BP

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32
Q

Cause of a chronic diarrhoea alternating with constipation?

> 14 days.

A

> 3 loose stools per day for more than 4 weeks.
IBS

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33
Q

Causes of bloody diarrhoea?

A

Vascular: Ischaemic Colitis
Infection: Camyplobacter jejuni, Shigella, Salmonella, E.coli (enterotoxigenic E.coli).
Inflammatory: UC, Crohn’s
Neoplastic: Colorectal Cancer, Polpys

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34
Q

Causes of cholangiocarcinoma?

A
  • Flukes (clonorchis)
  • PSC
  • Congenital biliary cysts
  • UC

(intrahepatic from cirrhosis + Hep B + C.

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35
Q

Causes of Chronic Diarrhoea

A
  • Ulcerative Colitis
  • Crohns
  • Drug Effect
  • Coeliac Disease
  • Faecal Impaction (overflow Diarrhoea)
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36
Q

Causes of decompensation

A

AScites, jaundice, encephalopathy

Alcohol

Sedatives: Benzos and opiates

NSAIDS - worsen renal failure
- Excess diuretics

  • Hypokalaemia - results in decreased renal ammonia.

Excess diuretics
- Hypokalaemia - results in decreased renal ammmonia

Constipation
- Any source of increased protein/nitrogen: GI bleed, renal failure.

Infections: SBP (E.coli is commonest)

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37
Q

Causes of gynaecomastia

A

Verapamil
Cimetidine
Spironolactone
Digoxin
Cannabis
Conns

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38
Q

Causes of HCC?

A
  • Viral hepatitis
    Hepatitis B most common cause in world
    Hepatitis C most common cause in Europe
  • Screening with ultrasound (+/- alpha-fetoprotein) for high risk groups.
  • Patients liver cirrhosis secondary to hepatitis B and C or haemochromatosis.
  • Men with liver cirrhosis secondary to alcohol
  • Cirrhosis: EtOH, HH, PBC
  • Aflatoxins (produced bu aspergillus
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39
Q

Causes of malabsorption?

A
  • Common in UK: Coeliac, Chronic pancreatitis, Crohn’s (3 Cs)
  • Rarer:
    decreased bile: PBC, ileal resection, colestyramine
    Pancreatic insufficiency: ca, CF, chronic pancreatitis
  • Small bowel: resection, tropical sprue, metformin
  • Bacterial overgrowth: spontaneous, post-op, blind loops, DM, PPIs

Infection: Giardia, Strongyloides, Cryptoparvum, Whipples (Fever, arthritis + steatorrhoea.

PAS Positive macrophages. T.whipplei

Hurry: post-gastrectomy dumping

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40
Q

Causes of mucus with diarrhoea?

A

IBS
Colorectal Cancer
Polyps

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41
Q

Causes of portal hypertension?

A

Pre-hepatic - portal vein thrombosis (pancreatitis)
Hepatic - cirrhosis or schisto (worldwide)
Post-hepatic - Budd-Chiari, RHF, constrictive pericarditis, TR

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42
Q

Causes of pus mixed with diarrhoea?

A

IBD
Diverticulitis
Abscess

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43
Q

Child’s Pugh Classification

A

A - Albumin
B - Bilirubin
C - Clotting - Prothrombin
D - Ascites
E - Encephalopahty

MELD
- Combination of patient’s bilirubin, creatinine, and INR gives mortality 3 month score.

  • Model end stage liver disease
  • Takes into account aetiology
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44
Q

Cholangiocarcinoma is a malignancy of what?

A
  • Biliary tree malignancy
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45
Q

Chronic Pancreatitis Cause?

A

AGITS
- Alcohol
- Genetic (CF, HH, Hereditary pancreatitis)
- Immune (Lymphoplasmacytic sclerosing pancreatitis (increased IgG4)
- Triglycerides increased
- Structural (Obstruction by tumour or Pancreas divisum)

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46
Q

Chronic phase in Hep B facts?

A

Carriers = 10%. HBsAg +ve > 6 months.
- Chronic hepatitis: 10%
Cirrhosis: 5%

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47
Q

Chronic phase in Hep C facts?

A

Carrier: 80% - HCV RNA+ve > 6 months.
Chronic hepatitis: 80%
Cirrhosis: 20%

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48
Q

Clinical features of Hereditary Haemochromaosis?

A

Early signs: Fatigue, erectile dysfunction and arthralgia.

iron MEALS

-Myocardial:restricted then dilated cardiomyopathy, arrhythmia

-Endocrine:
- Pancreas (DM),
- pituitary (hypogonadism -> amenorrohea, infertility), - parathyroid (hypocalcaemia, osteoporosis)

The menses delay presentation due to reducing iron.

  • Arthritis: 2nd and 3rd MCP joints, knees and shoulders
  • Liver: Chronic liver disease -> cirrhosis -> HCC and hepatomegaly
  • Skin: slate grey discolouration
  • tan + cirrhosis + pseudogout + RCM/DCM + hypogonadism + DM.
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49
Q

Clues to CLD

A

Tatoos/IVDU - viral
Xanthelasma - PBC
- Tan - haemachromatosis
Parotid swelling, neuropathy, gout, cerebellar - alcohol
- BM Stix - NASH
- Afro-caribbean = Sarcoidosis
- Dysarthria, tremor - Wilson’s
Female, vitilgo - autoimmune
- Barrel chest, urse lip breathing

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50
Q

CNS effects of Alcoholism?

A
  • Poor memory/cognition
  • Peripheral polyneuropathy (mainly sensory)
  • Wernicke’s encephalopathy: confusion, ophthalmoplegia (nystagmus, LR (6th nerve palsy - eye cannot turn outwards, looking in slightly), ataxia. –> Mamillary bodies.
  • Korsakoff’s: amnesia –> Confabulation
  • Fits, Falls
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51
Q

Coeliac disease epidemiology

A

Prev: 0.5-1%
Age: any, bimodal: infancy and 50-60yr
Sex: F>M
Geo: Increased in Ireland and N.Africa

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52
Q

Coeliac Pathophysiology

A

HLA-DQ2 and DQ8
CD8+ mediated response to gliadin in gluten

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53
Q

Common causes of cirrhosis?

A

Chronic ETOH
Chronic HCV
NAFLD/NASH

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54
Q

Common causes of hepatomegaly?

A
  • Cirrhosis: if early disease, later liver decreases 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
  • viral hepatitis
  • glandular fever
  • malaria
  • abscess: pyogenic, amoebic
  • hydatid disease
  • haematological malignancies
  • haemochromatosis
  • primary biliary cirrhosis
  • sarcoidosis, amyloidosis
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55
Q

Complications for UC

A
  • Toxic megacolon = Diameter >6cm - Risk of perforation
  • Bleeding
  • Malignancy
    : CRC in 15% with pancolitis for 20yrs
    : cholangiocarcinoma
  • Strictures –> obstruction
  • Venous thrombosis
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56
Q

Complications of achalasia

A

Chronic achalasia –> Oesophageal primary squamous cell carcinoma.

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57
Q

Complications of chronic pancreatitis?

A
  • Pseudocyst
  • DM
  • Pancreatic cancer
  • Biliary obstruction
  • Splenic vein thrombosis - splenomegaly
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58
Q

Complications of Crohn’s surgery?

A

Stoma complications
Enterocutaneous fistulae
Anastomotic leak or stricture

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59
Q

Complications of Crohn’s?

A

Fistulae
- Entero-enteric/colonic –> diarrhoea
- Enterocutaneous = intestine to skin (high or low) output. Can be duodenal/jejunal fistulae which excoriates skin. Colo-cutaneous fistulae leak faeculent material.

  • Enterovesical –> frequency as it goes to bladder.

Investigate with Pelvic MRI to categorise course of fistula.

Management
- Heal provided no underlying IBD.
- When skin involvement = protect underlying skin with stoma bag.
- Nutritional complications may require need for TPN.
- Crohns perianal fistula requires drainage through use of setons.

UTI
- Enterovaginal
- Perianal –> Pepperpot anus.
Abscesses
- Abdominal, anorectal
Malaborption
- Fat –> Steatorrhoea, gallstones
- B12 –> megaloblastic anaemia
- Vit D –> osteomalacia
- Protein –> Oedema

Toxic megacolon and Ca may occur (< cf UC)

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60
Q

Complications of GORD?

A
  • From excess acid = Oesophagitis
  • Oesophagitis can cause ulceration
  • Chronic oesophagitis can cause strictures + dysphagia
  • Furthermore, Barrett’s oesophagus and oesophageal adenocarcinoma.

GORD is single strongest risk factor for development of Barrett’s oesophagus.

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61
Q

Complications of liver failure?

A
  • Bleeding: Vit K, platelets, FFP, Blood.
  • Sepsis: Tazocin (avoid gen: nephrotoxicity)
  • Ascites: fluid + salt restriction, spironolactone (K+ sparing), furosemide, tap, daily weight.
    Hypoglycaemia: Regular BMs, IV glucose if <2mM
  • Encephalopathy: avoid sedatives, lactulose ± enemas, rifaximin.
    Seizures: lorazempam
    Cerebral oedema: mannitol
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62
Q

Complications of post-op liver transplant?

A
  • Acute rejection (T-cell mediated)
    50% @ 5-10 days
    Pyrexia, tender hepatomegaly
    increased or change immunosuppressants
  • Sepsis
  • Hepatic artery thrombosis
  • CMV infection
  • Chronic rejection (6-9 months): shrinking bile ducts
  • Disease recurrence (e.g HBV)
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63
Q

Complications of PSC

A
  • Bacterial cholangitis
  • Increased cholangiocarcinoma
  • Increased risk of colorectal carcinoma
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64
Q

Complications of pseudomembranous colitis?

A
  • Paralytic Ileus (obstruction of the intestine due to paralysis)
  • Toxic Dilatation –> Perforation
  • Multi-organ failure
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65
Q

Contraindications of liver transplant?

A
  • Extra-hepatic malignancy
  • Severe cardiorespiratory disease
  • Systemic sepsis
  • HIV infection
  • Non-compliance with drug therapy
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66
Q

Contraindications to bulking laxatives?

A

Obstruction or faecal impaction.

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67
Q

Correcting clotting abnormalities for UGIB

A
  • platelets <50–> platelet tranfusion
  • Warfarin–> prothrombin complex concentrate +vitamin K
  • DOACs–> praxbind for Dabigatran and PCC for others
  • Coagulopathy for other reason (Ex. Cirrhosis)–> Vit K +- FFP
  • Low fibrinogen (<1g)–> cryoprecipitate
  • Stop anticoagulants and anti-platelets
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68
Q

Cyanocobalamin B12

A

Glossitis –> Sore tongue
Peripheral neuropathy
- Paraesthesia
- Early loss of vibration and proprioception –> ataxia
SCDC (subacute cord degeneration)
- Dorsal and corticospinal tracts
- Sensory loss and UMN weakness
OVerall mixed UMN and LMN signs with sensory disturbance
- Extensor plantars + absent knee and ankle jerks.

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69
Q

Definition of dysphagia?

A

Difficulty swallowing

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70
Q

Difference in a cholestatic picture and a hepatocellular picture?

A

Cholestatic: Bili, ALP, GGT
Hepatocellular: Bili, AST, ALT.

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71
Q

Distribution of Crohns

A

Skip lesions

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72
Q

Distribution of UC

A

Contiguous

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73
Q

Drug causes of diarrhoea?

A

Lactulose abuse
Antibiotics
PPI, Cimetidine (H2 Antagonist)
NSAIDS
Digoxin

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74
Q

Drug-induced cholestasis picture (+/- hepatitis)

A
  • combined oral contraceptive pill
  • antibiotics: flucloxacillin, co– amoxiclav, erythromycin*
  • anabolic steroids,
  • testosterones
  • phenothiazines:
  • chlorpromazine,
  • prochlorperazine
  • sulphonylureas
    fibrates
    rare reported causes: nifedipine
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75
Q

Drug-induced liver disease - hepatocellular picture?

A
  • paracetamol
  • sodium valproate, phenytoin
  • MAOIs
  • halothane
  • anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
  • statins
  • alcohol
  • amiodarone
  • methyldopa
  • nitrofurantoin
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76
Q

Drugs to avoid in Liver failure?

A
  • Avoid: Opiates, oral hypoglycaemics, Na-containing IVI. Effect of warfarin effects increased.
  • Hepatotoxic drugs: paracetamol, methotrexate, isoniazid, salicylate, tetracycline.
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77
Q

Duration of chronic diarrhoea?

A

-More than 4 weeks
->3 loose stools per day
-Waking at night with symptoms (less likely to be functional)

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78
Q

During the icteric phase what distinguishes Hep A from Hep B?

A

Hep B has extrahepatic features (serum sickness syndrome):
- Urticaria or vasculitis rash
- Cryoglobulinaemia
- PAN (polyarteritis nodosa)
- GN (glomerulonephritis)
- Arthritis

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79
Q

Elective Surgery in UC Indications?

A
  • Chronic symptoms despite medical therapy
  • Carcinoma or high-grade dysplasia
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80
Q

Enema Procedure?

A
  • 1 hr before leaving home for day of examination
  • Place unopened enema bottle into jug of warm water for 5 mins.
  • Lie down on bed with knees to chest
  • Insert length of nozzle into your bottom, and squeeze bottle until it is empty.
  • Hold for 15 min until urge to open bowels.
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81
Q

Epidemiology of alpha1-Antitrypsin Deficiency?

A
  • Prevalence: 1/4,000; 10% are carriers
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82
Q

Epidemiology of PBC?

A

Prev: <4/100,000
Sex: F»M = 9.1 (90% womeN)
Age: 50

Middle age woman with liver failure - signs of rheum/autoimmune conditions.

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83
Q

Epidemiology of PSC?

A

Epidemiology
- Age: 30-50yr
- Sex: M>F = 2: 1

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84
Q

Example of a suppository?

A

Glycerol (stimulant)

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85
Q

Examples of bulking laxatives?

A

Bran
Ispaghula husk (Fybogel)
Methylcellulose

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86
Q

Examples of Osmotic laxatives?

A

Lactulose
MgSO4 (rapid)

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87
Q

Examples of stimulant laxatives?

A

Senna
Bisacodyl PO or PR (10mg)
Sodium picosulphate

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88
Q

Examples of stool softeners?

A

Docusate sodium (500mg daily)

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89
Q

Exclusion criteria for IBS

A

> 40 yrs
Bloody stool
Anorexia
Weight loss
Diarrhoea at night

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90
Q

Explain the procedure of the Nissen fundoplication

A

Aim: prevent reflux, repair diaphragm.
- Normally laparoscopic
- Mobilise gastric fundus + wrap around lower oesophagus.
- Close any diaphragmatic hiatus
- Complications: Gas-bloat syndrome: inability to belch/vomit.
- Dysphagia if wrap too tight.

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91
Q

Extra-abdominal manifestations in IBD? Eyes

A

Eyes
- Iritis
- Episcleritis
- Conjunctivitis

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92
Q

Extra-abdominal manifestations in IBD? Joints?

A
  • Arthritis (non-deforming, asymm) (related to disease activity - if asymmetrical)
  • Sacroiliitis
  • Ank Spondylitis
  • Osteoporosis (related to disease activity)

HPB
- PSC + cholangiocarcinoma (mainly UC). UC has PSC - (not related to disease activity) Primary sclerosing cholangitis
- Gallstones (esp. Crohn’s)
- Fatty liver

Other
- Amyloidosis
- Oxalate renal stones (esp. Crohns)- due to reduced bile acid reabsorption

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93
Q

Extra-abdominal manifestations in IBD? Skin?

A

Skin
- Clubbing
- Erythema nodosum
- Pyoderma gangrenosum (not related to disease activity)

Perianal skin tags in Crohns

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94
Q

Extra-mural mechanical causes of dysphagia?

A

Lung Cancer
Rolling hiatus hernia
Mediastinal LN (Lymphoma)
Retrosternal goitre
Thoracic aortic aneurysm

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95
Q

Faecal occult blood?

A

Concerns about bowel malignancy

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96
Q

Fibrosis in which IBD?

A

Crohns

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97
Q

Fistulae in which IBD?

A

Crohns

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98
Q

Frequency of liver flap

A

1Hz. Need 30 second to check for liver flap.

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99
Q

Gastric cancer Risk factors

A
  1. H.pylori,
  2. blood group A: gAstric cancer
  3. Pernicious anaemia (lemon tinge and parasthesia)
  4. Gastric adenomatous polyps
  5. Smoking and alcohol
  6. high salt/nitrates diet
  7. family hx (E-cadherin abnormality)
  8. Lynch syndrome 2
    - M>F
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100
Q

Genetic relations of alpha1-Antitrypsin Deficiency?

A

Autosomal recessive, Chromosome 14
Homozygotes have PiZZ phenotype

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101
Q

Giardia diarrhoea?

A

Giardia causes fat malabsorption, therefore greasy stool can occur.
Resistant to chlorination, hence risk of transfer in swimming pool.

Floats in water therefore steatorrhea.

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102
Q

GIT effects of alcoholism?

A
  • Gastritis, erosions
  • PUD
  • Varices
  • Pancreatitis
  • Carcinoma
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103
Q

Globus Hystericus

A
  • History of anxiety
  • Intermittent and relieved by swallowing
  • Persistent sensation of having a ‘lump in the throat’ when there is none.
  • Usually painless - presence of pain should warrant further investigation.
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104
Q

Granulomas in which IBD?

A

Crohns

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105
Q

Gridiron

A

Oblique incision centered over McBurneys point- usually appendicectomy (less cosmetically acceptable than Lanz

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106
Q

H pylori Tx

A

H Pylori Tx:
• First line:
◦ 7 day course of PPI + amoxicillin(500mg BD)/clarithromycin + metronidazole (500mg BD)
◦ if allergic to penicillin –> use clarithro
‣ if there is previous exposure to clarithromycin
• PPI+metronidazole+tetracyclin +bismuth
• 2nd line
◦ PPI + metro +levofloxacilin
‣ use if allergic to penicilin and no previous exposure to fluoroquinolone
◦ PPI +metro+bismuth+tetracycline
◦ PPI + amox + metro/clarithro
◦ PPI + amox + tetracycline

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107
Q

<p>H. Pylori associations</p>

A

<p>1. B-cell Lymphoma of MALT tissue<br></br>2. atrophic gastritis<br></br>3. Peptic ulcer disease<br></br>4. Gastric carcinoma</p>

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108
Q

H. Pylori associations

A
  1. B-cell Lymphoma of MALT tissue2. atrophic gastritis3. Peptic ulcer disease4. Gastric carcinoma
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109
Q

H.pylori eradication therapy (penicillin allergic)

A
  • PPI: Lansoprazole 30mg BD
  • Metronidazole 400mg BD
  • Clarithromycin 250mg BD

Note that PPIs cause hyponatraemia, osteoporosis (increased risk of fractures), microscopic colitis. Increased risk of C.diff infections.

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110
Q

Hep +ve doesnt know which one. Rash on his hand which look vasculitis and he has clinically got signs of CLD>

A

Hepatitis C

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111
Q

Hepatic effects of alcoholism?

A

Hepatic: Fatty liver –> hepatitis–> cirrhosis
AST: ALT >2, increased GGT.

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112
Q

Hepatic encephalopathy

A

Diural sleeping pattern disturbance
Asterixis
Bradykinesia
Decerebrate then coma

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113
Q

Hepatitis C presentation

A

A 60-year-old man presents with several months of gradually worsening abdominal swelling, intermittent haematemesis, and dark stool. He denies chest pain or difficulty breathing. Past medical and family history are not contributory. Past surgical history is significant for back surgery requiring blood transfusion in 1990. Social history is significant for occasional alcohol use. BP is 110/80 mmHg. Physical examination is significant for spider angiomata on the upper chest, gynaecomastia, caput medusae, and a fluid wave of the abdomen. The rest of the examination is normal.

A 62-year-old man presents for a routine initial visit in New York. He has occasional arthralgia or myalgia, and takes an ACE inhibitor and a thiazide diuretic for hypertension. A retired accountant and non-smoker, he drinks 1 or 2 beers per week and denies current drug use. Physical examination is normal except for being overweight. Routine blood chemistries are normal, but a screening hepatitis C virus (HCV) antibody test is positive. At follow-up, the patient is concerned about whether he will develop liver problems. He had heard on television that new oral medications are easier to take than older regimens that used injections and asks about the next diagnostic and treatment steps.

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114
Q

Hepatitis D?

A

Think about Hep B patient with IVDU.

Superinfecetion: A hep B surface antigen positive patient subsequently develops Hep D. LEads to fulminant hepatitis, chronic hep status and cirrhosis.

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115
Q

Hepatocellular carcinoma epidemiology?

A
  • Rare in west, common in china and sub-saharan africa
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116
Q

How is PBC managed?

A
  • Bile acid analogues - ursodeoxycholic acid.
  • Prednisolone: 20-30mg
  • Antipruritic: colestyramine
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117
Q

How to calculate units in alcohol?

A

Alcohol units = volume x ABV/1,000.

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118
Q

How to induce remission in mild/moderate disease in Crohns?

A

OPD treatment
- Supportive = High fibre diet, vitamin supplements.

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119
Q

How to manage a severe UC patient that is not improving

A

Rescue therapy?
- On day 3: Stool frequency >8, or CRP >45: Predicts 85% chance of needing a colectomy during the admission.
- Discussion between patient, physician and surgeon.
Medical: cyclosporin, infliximab, visiliuzumab (anti-T)
Surgical

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120
Q

How to manage an improving acute flare up UC patient?

A
  • Switch to oral pred + a 5-ASA
  • Taper pred after full remission
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121
Q

How would you manage new onset dyspepsia?

A
  • OGD >60 or ALARMS
  • Consider conservative measures for 4 weeks
  • stopping NSAIDS/CCBs, stop smoking/ decrease ETOH, weight loss.
    Try OTC Antacids/Alginates (Gaviscon).
    1st line: If no alarming features do breath test or stool test for H/Pylori.
    -Breath test = drink C12, measure level of urea as it is broken down by H.pylori. Ensure patient has not had any antibiotics, no antisecretory drugs (PPI) in past 2 weeks. Other: Rapid urease test (CLO test) - biopsy with urea + pH indicator. Serum antibody: positive after eradication. Culture of gastric bipsy Gastric biopsy +ve H.Pylori = 7 day 2x daily Amoxicillin and Clarithromcyin or Metronidazole. -ve Result = PPI (Esomeprazole/Omeprazole/Lansoprazole
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122
Q

Hydatid cyst

A

Seen in cases of Echinococcus infection - A parasitic Tapeworm. Typically an intense fibrotic reaction occurs around sites of infectionThe cyst has no epithelial liningCysts are commonly unilocular and may grow to 20cm in size. The cyst wall is thick and has an external laminated hilar membrane and an internal enucleated germinal layerTypically presents with malaise and right upper quadrant pain. Secondary bacterial infection occurs in 10%.Liver function tests are usually abnormal and eosinophilia is present in 33% casesUltrasound may show septa and hyatid sand or daughter cysts.CT is best to investigate hydatid cyst. Percutaneous aspiration is contra indicated = this is due to risk of anaphylaxis and seeding of daughter cysts through abdomen. Treatment is by sterilisation of the cyst with mebendazole and may be followed by surgical resection. Hypertonic swabs are packed around the cysts during surgery

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123
Q

Hydatid cyst management?

A

Hydatid cysts are endemic in Mediterranean and Middle Eastern countries. They are caused by the tapeworm parasite Echinococcus granulosus. An outer fibrous capsule is formed containing multiple small daughter cysts. These cysts are allergens which precipitate a type 1 hypersensitivity reaction.

Clinical features are as follows:
Up to 90% cysts occur in the liver and lungs
Can be asymtomatic, or symptomatic if cysts > 5cm in diameter
Morbidity caused by cyst bursting, infection and organ dysfunction (biliary, bronchial, renal and cerebrospinal fluid outflow obstruction)
In biliary ruputure there may be the classical triad of; biliary colic, jaundice, and urticaria

CT is the best investigation to differentiate hydatid cysts from amoebic and pyogenic cysts.
Surgery is the mainstay of treatment (the cyst walls must not be ruptured during removal and the contents sterilised first).

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124
Q

IBS Diagnostic criteria?

A

ROME criteria
- At least 1 day per week in the last 3 months, with onset at least 6 months previously, of recurrent abdominal pain or discomfort.
- Associated with 2 or more of the following:
- 1) Improvement with defecation
- 2) Onset associated with change in frequency of stool;
- 3) Onset associated with a change in form of stool

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125
Q

If patient remains shocked after initial resuscitation in UGIB?

A

Blood Group specific or O- until cross-matched.

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126
Q

Imaging for UC?

A

AXR: megacolon (>6cm) wall thickening (also caused by C.diff, ameobosis)
CXR: Perforation
CT
Ba/gastrograffin enema
- Lead-pipe: no haustra
- Thumbprinting: mucosal thickening
- Pseudopolyp: regenerating mucosal island
- Ileocolonoscopy + regional biopsy: Baron Score
= Minimum of two biopsies from at least 5 sites along the colon, including the rectum and terminal ileum.

During acute flares endoscopic examination should be limited to flexible sigmoidoscopy without bowel prep, due to increased risk of perforation.

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127
Q

Immune response in UC/Crohns?

A

UC = TH2 mediated
Crohns = Th1/Th17 mediated

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128
Q

Immunoglobulins in AIH?

A

Increased IgG = AIH
Increased IgM = PBC

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129
Q

Indication for a phosphate enema?

A

Preparation for a flexible sigmoidoscopy
Constipation

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130
Q

Indications for Crohn’s?

A

Disease pattern in Crohns ends in terminal ileal disease - ileocaecal resection.

Emergency
- Failure to respond to medical management
- intestinal obstruction or perforation
- Massive haemorrhage

Elective
- Abscess or fistula
- Perianal disease
- Chronic ill health
- Carcinoma

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131
Q

Indications for emergency surgery in UC?

A
  • 20% need surgery
  • Toxic megacolon
  • Perforation
  • Extensive haemorrhage
  • Failure to respond to medicine
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132
Q

Indications for Platelet/ FFP transfusion in UGIB

A
  • platelet –> if actively bleeding with platelets<50

- FFP –> if fibrinogen<1g/l or PT/INR or APTT>1.5x normal

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133
Q

Indications of liver transplant?

A
  • Advanced cirrhosis
  • HCC
  • Cholangiocarcinoma
  • Alpha-1 antitrypsin deficiency.
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134
Q

Inducing a remission in mild/moderate disease in an OPD-basis?

A

Oral -
1st line: 5-ASAs (mesalazine) - 1000mg once daily at bedtime for 3-6 weeks.
2nd line: prednisolone (30-40mg)

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135
Q

Inflammatory bowel disease - which is more common?

A

UC = 100-200/100,000
Crohns = 50-100/100,000.

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136
Q

Inflammatory causes of dysphagia?

A

Tonsilitis,
pharyngitis,
oesophagitis (GORD),
Oral candidiasis,
Aphthous ulcers.

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137
Q

Initial management after resus of patient with variceal bleed?

A
  • Terlipressin IV (splanchnic vasoperssor)
  • 2mg stat followed by 2mg every 6 hours for 72 hours
  • Prophylactic Abx: e.g ciprofloxacin 1g/24hr
  • Early endoscopy is indicated with variceal band ligation or TIPPS (last line TIpps may worsen encephalopathy)
  • Balloon tamponade (sengstaken-blakemore tube) can be used acutely if uncontrolled haemorrhage
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138
Q

Interaction with clarithromycin and warfarin

A

Can increase effect of warfarin

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139
Q

Investigations for achalasia (BBBBM)

A

Bedside Obs: HR, O2, BP, RR.
Bloods: FBC (Anaemia), U+E (Electrolytes), (TFTs)
Barium swallow: See a dilated tapering oesophagus (Bird’s Beak). Better in older patients.
Manometry: Checking functioning of the oesophageal valve
CXR: Widened mediastinum
OGD: To exclude malignancy and is usually first line.

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140
Q

Investigations for AIH?

A
  • Increased LFTs
  • Increased IgG
  • Auto Abs: SMA, LKM, SLA, ANA
  • Decreased WCC + decreased platelets due to hypersplenism
  • Liver Biopsy
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141
Q

Investigations for alpha1-Antitrypsin Deficiency?

A
  • Blood - reduced serum a1AT levels
    -Liver biopsy: PAS+ve, diastase-resistant globules
    -CXR: emphysematous changes
    -Spirometry: obstructive defect
    -Prenatal Dx: possibly by CVS
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142
Q

Investigations for Crohn’s Disease?

A

Bloods (top 3 are severity markers)
- FBC: decreased Hb, increased WCC
- LFTs: decreased albumin
- increased CRP/ESR
- Haematinics: Fe, B12, Folate
- Blood cultures

Stools
- MCS: exclude Campy, Shigella, Salmonella
- CDT: C.diff may complicate or mimic

Imaging
- AXR: obstruction, sacroileitis
- CXR: perforation
- MRI: assess pelvic disease and fistula. Assess disease severity
- Small bowel follow-through or enteroclysis (liquid passing through)
Shows: Skip lesions, rose thorn ulcers, cobblestoning: ulceration + mural oedema
- String sign of kantor

Endoscopy
- Ileocolonoscopy + regional biopsy: Ix of choice
- Wireless capsule endoscopy
- Small bowel enteroscopy

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143
Q

Investigations for diarrhoea?

A

Bloods:
- FBC: Increased WWC, Anaemia
- U+E: Decreased K, Dehydration (raised urea)
- Increased ESR: IBD, Oncological
- Increased CRP: IBD, Infection
- Coeliac Serology: Anti-TTG or Anti-Endomysial Abx

Stools:
- MCS and C.Diff

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144
Q

Investigations for dysphagia?

A

Bloods: FBC, U+E
CXR
OGD (Upper GI Endoscopy) - Stop PPI 2 weeks before an upper GI endoscopy.
Barium Swallow ± Video fluroscopy

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145
Q

Investigations for GORD?

A
  • If isolated no need for further investigations –> trial of PPI
  • Bloods: FBC
  • CXR: Hiatus Hernia may be seen.
  • OGD if: >55 yrs old, symptoms >4 weeks, Dysphagia, persistent symptoms, Weight Loss.
  • Barium Swallow (rule out other causes): Hiatus hernia or dysmotility
  • 24 pH testing ± manometry (pH <4 for > 4hrs). Pre-operative workup for patients. Measures pressures within the lower oesophageal sphincter and helps with diagnosis.
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146
Q

Investigations for Hepatitis C?

A
  • Enzyme immunoassay or Hep C antibodies (Exposure to Hep C)
  • NAATs (active infection)
  • Viral genotyping (predicts response to antiviral therapy)
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147
Q

Investigations for Hereditary Haemochromaosis?

A
  • Bloods: increased LFT, ferritin (>55) , iron, LOW TIBC, glucose, genotype

Transferrin = protein that iron binds to for transport. INcreased iron so more available to bind to transferrin so saturation goes up. Ferritin is the intracellular storage form of iron therefore going up.
TIBC - binding sites on transferrin - less capacity so low.

-XR - chondrocalcinosis (cartilage calcification)

-ECG, ECHO (heart failure)

-Liver biopsy - Pearl’s stain to quantify Fe and severity

-MRI liver- can estimate iron loading

Screening - General population: transferrin saturation > ferritin

Family members: HFE genetic testing

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148
Q

Investigations for IBS?

A
  • Bloods: FBC, ESR, LFTs, Coeliac serology, TSH
  • Colonoscopy: if >60yrs or any features of organic disease.
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149
Q

Investigations for liver tumours

A

Bloods: LFTs, Hepatitis serology, AFP (HCC)
Imaging: US or CT/MRI ± guided diagnostic biopsy
ERCP + biopsy in suspected cholangiocarcinoma
- Biopsy (seeding may occur along tract)
- Find primary e.g colonoscopy, mammography

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150
Q

Investigations for Malabsorption?

A

Coeliac Tests
Stool Microscopy
Faecal elastase
Hydrogen breath test
MRI/CT
ERCP (chronic pancreatitis )
Small bowel endoscopy

ELEVATED FOLATE - bacterial overgrowth.

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151
Q

Investigations for PBC?

A

LFTs: very high ALP, very high GGT, moderately high AST/ALT.

Abs: AMA + (98%)
Increased IgM
Increased Cholesterol
± Increased TSH
US to exclude extra-hepatic cholestasis
Liver biopsy: non-caseating granulomatous inflammation

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152
Q

Investigations for peptic ulcer disease?

A
  • Obs: RR, HR, O2, BP
  • Bloods: FBC (anaemia/maleana), urea (increased in haemorrhage)
  • C13 breath test.
  • OGD (Stop PPIs >2 weeks before). Initially order if patient >60. Urease test for H.Pylori. Take biopsies to check for malignancy.
  • Gastrin (Hypergastrinaemia) levels if Zollinger-Ellison suspected.

Forrest Score: on endoscopy
- GBS - (Rockall is old) - Glasgow Blatchford.

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153
Q

Investigations for PSC?

A
  • LFTs: increased ALP initially, then increased BR
  • Abs: pANCA, ANA and SMA may be +ve
  • MRCP: beaded appearance of ducts (beads on string) is standard to diagnose primary sclerosing cholangitis.
  • Can use ERCP if MRCP is contra-indicated.

They are the investigation of choice for diagnosing PSC.

Biopsy: fibrous, obliterative cholangitis

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154
Q

Investigations for pseudomembranous colitis/C.diff?

A

Bloods
- FBC (increased WCC), U+E (increased CRP, dehydration), LFTs (decreased Albumin).
- Stool Culture/PCR
- Abdo X-ray
- Sigmoidoscopy (consider)

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155
Q

Investigations in hepatitis B?

A
  • FBC,
  • LFTs (Raised ALT/AST), Alk phos,
  • HBsAg for more than >6 months = chronic HBV infection. Implies ongoing infection - either acute or chronic if present >6 months.
  • Serum anti-HBs = Provides life-long immunity, suggests resolved infection and is also detectable in those immunised with HBV vaccine.

Therefore positive HBs and negative anti-HBs means no immunity and hence means that patient is chronically infected.

  • Serum anti-HBc = IgM anti-HBc may be only way of diagnosing acute HBV infection. Anti IgM is acute.
  • Serum anti-HBc (IgM + IgG) = IgM anti-HBc appears during acute or recent hep B and present for 6 months. Positive in acute infection, chronic infection. Single best test for screening household contacts of HBV infection.
  • Serum HBeAg = indicates high likelihood of developing chronic HBV infection with HIGH viral replication.
  • clotting

Ground glass appearance of the cytoplasm of hepatocytes.

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156
Q

Investigations of carcinoid tumours?

A
  • Increased urine 5- hydroxindoleacetic acid
  • Increased chromogranin A
  • CT/MRI: find primary
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157
Q

Investigations of chronic pancreatitis?

A

increased glucose
decreased faecal elastase
US: pseudocyst
AXR: speckled pancreatic calcification
CT: pancreatic calcification

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158
Q

Investigations of Coeliac’s Disease?

A
  • Bloods: FBC, LFTs (decreased albumin), INR, VitD and bone, red cell folate, serum B12.

Iron in proximal, Then folate in jejunum, and then B12 in the terminal ileum.

Likely to be deficient in iron, folate, V12.

  • Ab: Anti-endomysial IgA (95% specificity)

1st line: Anti-TTG IgA - Both above decreased with exclusion diet
Anti-Gliadin IgG persists with exclusion diet.
Patient must eat gluten for at least 6 weeks before they are tested.

IgA increased in most but may have IgA deficiency. Need to look for selective IgA deficiency, which would give a false negative coeliac result. Cannot interpret TTG without looking for IgA total.

Stools
- Stool cysts and antibody: exclude Giardia

OGD and duodenal biopsy
- Subtotal villous atrophy
- Crypt hyperplasia
- Intra-epithelial lymphocytes

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159
Q

Investigations of pancreatic cancer?

A
  • Bloods: cholestatic LFTs, increased Ca19-9, increased Ca.
  • Imaging: US: pancreatic mass, dilated ducts, hepatic mets allow biopsy
  • Can consider CT - HRCT for diagnosis
    - HRCT gold standard
    - can show double duct sign ( both CBD and pancreatic duct dilated)

-EUS: better than CT/MRI for staging

  • ERCP
  • Shows anatomy. Allows Stenting and biopsy
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160
Q

Investigations of Wilson’s Disease?

A
  • Bloods: decreased copper, decreased caeruloplasmin.

Caeruloplasmin is an acute-phase protein + may be high during infection. May be low protein states: nephrotic syndrome or malabsorption

  • Increased 24hr urinary copper
  • Liver Biopsy: increased hepatic copper
  • MRI: basal-ganglia degeneration
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161
Q

Investigations to order in alcohol withdrawal?

A
  • Serum urea (in case it is renal)
  • Serum Creatinine
  • Liver function (hepatic dysfunction)
  • Electrolytes (Na/K)
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162
Q

Ischaemia to the lower GI tract, which part most likely to be affected?

A
  • Acute mesenteric ischaemia (sudden, sharp pain from mostly likely superior mesenteric artery, with a history of AF)
  • Chronic mesenteric ischaemia
  • ischaemic colitis
  • Mesenteric ischaemia
    (small bowel, embolism, sudden onset, urgent surgery, high mortality).
  • Ischaemic colitis
    (Large bowel, multifactorial, less severe symptoms, bloody diarrhoea, thumbprinting, conservative management.

Will see high lactate and metabolic acidosis with low bicarb.

  • Ischaemic colitis = acute but transcient compromise in blood flow to large bowel. More likely to occur in watershed areas, such as splenic flexure. Located at the borders of the territory supplied by superior and inferior mesenteric arteries.
    See Thumbprinting on AXR.

Surgery in a minority of cases if conservative measures fail.

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163
Q

Ischaemic hepatitis?

A

Diffuse hepatic injury resulting in acute hypoperfusion (shock liver). Usually has a inciting event + marked increased ALT levels 50x normal. Associated with AKI

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164
Q

Kochers’ scar

A

Incision under right subcostal margin e.g. Cholecystectomy (open)

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165
Q

Less common causes of cirrhosis?

A

Genetic: Wilson’s, a1ATD, HH, CF
AI: AH, PBC, PSC
Drugs: Methotrexate, amiodarone, Methylodopa, INH
Neoplasm: HCC, Mets
Vasc: Budd-Chiari, RHF, constrictive pericarditis

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166
Q

Liver Abscess?

A

Biliary sepsis is a major predisposing factor
Structures drained by the portal venous system form the second largest source
Common symptoms include fever, right upper quadrant pain. Jaundice may be seen in 50%
Ultrasound will usually show a fluid filled cavity, hyperechoic walls may be seen in chronic abscesses

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167
Q

Liver cirrhosis drugs?

A

Methotrexate
Methyldopa
Amiodarone

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168
Q

Liver Tumours pathology?

A

90% are 2ndry mets
-primary in men: stomach, lung colon.
- primary in women: breast, colon, stomach, uterus
- Less common: pancreas, leukaemia, lymphoma
90% of primary tumours are HCC

  • Benign tumours: haemangiomas = reddish purple hypervascular lesion. Hyperechoic on US.
  • Liver adenomas = Linked to OCP. Solitary lesion sharply demarcated. Mixed echoity, hypodense.

cyst.

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169
Q

Macroscopic location of Crohn’s?

A

Mouth to anus esp terminal ileum

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170
Q

Macroscopic location of UC?

A

Rectum + colon + backwash ileitus

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171
Q

Maintaining remission in Crohn’s Disease?

A

1st line: azathioprine or mercaptopurine. Ensure you check the thiopurine methyltransferase activity. Leads to greater risk fo severe side effects.
2nd line: methotrexate
3rd line: infliximab/adalimumab

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172
Q

Maintaining Remission in UC?

A

1st line: 5-ASA PO- sulfasalazine or mesalazine.

Can lead to Mesalazine > Sulfasalazine in terms of pancreatitis.

(Topical Rx may be used in proctitis)
2nd line - beclometasone dipropionate.

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173
Q

Malabsorption

A
  • Diarrhoea/Steatorrhoea
  • Weight loss
  • Lethargy
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174
Q

Malignant mechanical mural causes of dysphagia?

A

Malignant stricture:
1) Pharynx
2) Oesphagus
3) Gastric

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175
Q

Malnutrition definition?

A

BMI <18.5
Weight loss >10% within last 3-6 months unintentially
BMI <20 and unintentional weight loss >5% within 3-6 months.

Screening with the MUST (Malnutrition Universal Screen Tool).
- Done on admission or if there is concern - pressure sores.
- Takes into account BMI
- Categorises patients into low, medium and high risk.

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176
Q

Management for achalasia?

A

Intra-sphincteric injection of botulinum toxin

First line: Pneumatic dilation - - Air inflated balloons are used to apply mechanical stretch to the lower oesophageal sphincter to tear its muscle fibres (Rigiflex or Witzel)
- Surgical cardiomyotomy (open or endo)

Poor surgical candidate?
- Medical - CCB (nifedipine or verapamil) or nitrates. (to lower oesophageal sphincter pressure.
- Botox - inhibits the release of acetylcholine from nerve terminals. Done endoscopically

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177
Q

Management for IBS?

A
  • Exclusion diet can be tried (low FODMAP). Try to have regular meals, avoid missing meals, drink 8 cups of water, restrict tea + coffee to 3 cups a day.

According to predominant symptom

pain: antispasmodic agents (merebavine)
constipation: laxatives but avoid lactulose (Linaclotide)

diarrhoea: loperamide is first-line. An opioid receptor agonist which does not have systemic effects.

2nd line:
- Amitriptyline may be helpful. (abdo pain)
- CBT

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178
Q

Management for proven GORD causes dyspepsia?

A

Lansoprazole 30mg, Omeprazole (20-40mg), Rabeprazole 20mg.

  • Full dose PPI 1 -2months.
  • Then, low dose PPI PRN.

Adverse effects
- Hyponatraemia
- Osteoporosis
- Microscopic Colitis
- Increased risk of C.diff

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179
Q

Management for proven PUD?

A
  • Full dose PPI for 1-2 months?

What is that again?
- H.pylori eradication if positive
- Endoscopy to check for resolution if GU
- Then, low-dose PPI PRN

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180
Q

Management if patient doesn’t improve after rescue therapy in Crohns?

A
  • Discuss with patient physician and surgeon
  • Medical: methotrexate ± infliximab
  • Surgical
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181
Q

Management of a bleeding ulcer?

A

A-E assessment as with UGIB

  • 1st line Endoscopy ± blood transfusion. IV PPI reduces rebleeding (omeprazole 80). Discontinue NSAIDs.
  • Endoscopical Tx :
    1. Sclerotherapy (fibrin or thrombin injection) with adrenaline
    2. mechanical therapy with adrenaline
    3. thermal coagulation with adrenaline

Surgery is indicated in patients with ongoing acute bleeding despite repeated endoscopic therapy.
- 2nd line: Surgery or embolisation (interventional angiography with transarterial embolisation)

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182
Q

Management of a hiatus hernia?

A

Conservative: Lose weight
Medical: Management of reflux?
Surgical: Only if medical treatment is unmanageable. - NB should repair a rolling hernia as it can strangulate.

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183
Q

Management of Acute Severe ulcerative colitis?

A
  • Resus: Admit, IV hydration, NBM
  • Hydrocortisone: IV 100mg QDS + PR. (IV ciclosporin can be used if steroids are contraindicated). If after 72hrs no improvement, consider ciclosporin IV + steroids or surgery.
  • Transfuse if required
  • Thromboprophylaxis: LMWH
  • Monitoring
    Bloods: FBC, ESR, CRP, U+E
    Vitals + stool chart
    Twice daily examination
    ± AXR
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184
Q

Management of AIH?

A

Immunosuppression
- Prednisolone
- Azathioprine as steroid-sparer
Liver Transplant (disease may recur)

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185
Q

Management of alcoholic hepatitis?

A
  • Stop ETOH
  • Management of withdrawal
  • High Dose B vitamins: Pabrinex
  • Optimise nutrition (BCAA)
  • Immunisation - Pneumo, influenza, Hep A/B.
  • Daily weights, LFTs, U+E, INR
  • Mx complications of liver failure
  • Corticosteroids for severe alcoholic hepatitis. HDF valve >32.
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186
Q

Management of alpha1-Antitrypsin Deficiency?

A

Mostly supportive for pulmonary and hepatic complications
-Quit smoking
-Can consider a1AT therapy from pooled donors

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187
Q

Management of an acute flare of Crohns

A
  • Resus: Admit, NBM, IV hydration
  • Hydrocortisone: IV + PR if rectal disease. Budesonide is an alternative if cannot be tolerated. 5ASA - Mesalazine is second line. - Azathioprine + mercaptopurine is add-on.

If 5 days without improvement - add:
- Infliximab as refractory disease.
- Abx: metronidazole PO or IV
Thromboprophylaxis: LMWH

  • Dietician Review
    Elemental diet: liquid prep of amino acids, glucose and fatty acids. Consider parenteral nutrition.
  • Monitoring
    Vitals + stool chart
    Daily examination
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188
Q

Management of ascites

A
  • Daily weight aiming for <0.5kg/d reduction
  • Fluid restrict <1.5L/d and low Na diet (
  • Spironolactone + frusemide
  • Therapeutic paracentesis with albumin infusion) 100ml 20%/L drained. - Respiratory compromise, pain/discomfort, renal impairment.

Need to give albumin
-To avoid PICD - Paracentesis-Induced Circulatory Dysfunction
- Refractory ascites?: TIPSS.

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189
Q

Management of carcinoid tumours?

A

Symptoms: octreotide or loperamide
Curative: Resection (tumours are v.yellow, give octreotide to avoid carcinoid crisis)

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190
Q

Management of cholangiocarcinoma?

A

30% resectable
- Consider neoadjuvant chemo or chemoradiotherapy.
- Palliative stenting: percutaneous or ERCP

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191
Q

Management of chronic pancreatitis?

A

Drugs
- Analgesia: may need coeliac plexus block
- Creon (Enxymes) /Pancreatin
- ADEK vitamins
- DM management

Diet
- no ETOH
- decreased fat, increased carb

Surgery
- Ind: Unremitting pain, weight loss
- Pancreatectomy

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192
Q

Management of Coeliac Disease?

A

Lifelong gluten free diet,
- Avoid barley, rye, oats, wheat
- OK: Maize, soya, rice
- Verify diet by endomysial Ab test
Pneumovax for HYPOSPLENISM
Dermatitis herpetiformis: dapsone

Annual blood test - FBC, Ferritin, TFTs, LFTs, B12, Folate.

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193
Q

Management of constipation > 3 months?

A

> 3 months
- Treat underlying cause
- Diet + lifestyle advice (fibre and water)

Medical laxatives
- Bulk Laxatives (ispaghula) or methylcellulose.
- 2nd line - Osmotic Laxatives (lactulose, macrogols, magnesium citrate)
- 3rd line - Osmotic laxatives + diet + lifestyle + stimulant laxatives (senna or bisacodyl)

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194
Q

Management of diarrhoea?

A
  • Treat Cause
  • Oral or IV rehydration
  • Codeine Phosphate or Loperamide (4mg orally, then 2mg after each unformed stool) after each loose stool
  • Anti-emetic if associated with n/v e.g prochlorperazine
  • Abx (e.g ciprofloxacin 750mg) in infective diarrhoea –> systemic illness
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195
Q

Management of encephalopathy?

A
  • Nurse 20 degrees head up
  • Correct any precipitants
  • Avoid sedatives
  • Lactulose ± PO4 enemas to decreased nitrogen-forming bowel bacteria –> 2-4 soft stools/d
  • Consider rifaximin PO to kill intestinal microflora.
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196
Q

Management of HCC?

A
  • Resection of solitary tumours improves prognosis (13–> 59%), but 50% have recurrence
  • Also: Chemo, percutaneous ablation and embolisation (transarterial chemoembolisation).

Sorafenib: mutlikinase inhibitor.

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197
Q

Management of Hep B?

A

Acute HBV infection?
- Supportive care
- Some patient suitable for antiviral (Lamivudine, entecavir)

Chronic HBV infection:
- Entecavir, tenofovir, peginterferon alpha.

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198
Q

Management of Hep C?

A

Acute HCV
- Monitor or decide to start treatment

Chronic infection
- Ribavirin, NS3 protease inhibitor, sofosbuvir.

199
Q

Management of hepatorenal failure?

A
  • IV albumin + splanchnic vasoconstrictors (terlipressin)
  • Haemodialysis as supportive management
  • Liver Transplant is management of choice
200
Q

Management of liver failure?

A
  • Manage in ITU
  • Rx of underlying cause: NAC in paracetamol OD
  • Good nutrition: e.g. via NGT with high carbs.
  • Thiamine supplements
  • prophylactic PPI vs stress ulcers
201
Q

Management of NAFLD?

A
  • Diet + Exercise
  • Control HTN, DM, Lipids
  • Consider surgery (Roux en Y)
202
Q

Management of non-bleeding H.pylori negative ulcer?

A

Conservative (Treat underlying cause) : Lose weight/Stop smoking + decrease ETOH. Avoid hot drinks + spicy food. Stop drugs such as NSAIDS, Steroids.
+ Medical:
1st line: Give PPI for 4-8 weeks (lansoprazole 15-30mg OD)
2nd line: H2 Antagonist (Famotidine and Cimetidine 150mg)

For patients who need NSAIDS: Misoprostol 100-200microgram 4x OD.

203
Q

Management of non-bleeding H.pyloti positive ulcer

A
  • Eradication therapy
    (triple = PPI, Clari, Amox or Metro)
    (Quad = PPI, Tetracycline, Metronidaole, bismuth)
204
Q

Management of pancreatic cancer?

A

Surgery:
- Fit, no mets, tumour <3cm (<10% of patients)

  • Whipple’s pancreatoduodenectomy
  • Post-op chemo delays progression
  • 5yrs = 5-14%

Palliation

  • Endoscopic/percutaneous stenting of CBD
  • Palliative bypass surgery
  • Pain relief: may need coeliac plexus block
205
Q

Management of PBC?

A

Symptomatic:
- pruritis: cholestyramine, naltrexone
- Diarrhoea: Codeine phosphate
- Osteoporosis: bisphosphonates

Specific
- ADEK vitamins
- Ursodeoxycholic acid: decreased LFTs but no effect on mortality or need for transplant
- Immunomodulatory therapy: Prednisolone 20-30mg orally once daily intially. Can consider azathioprine or mycophenolate mofetil.

Liver transplant
- End stage disease or intractable pruritis
- Recurrence occurs in 20% but doesn’t usually lead to graft failure.

206
Q

Management of post-op Liver transplant?

A
  • 12-24hr on ITU
  • Immunosuppression
    : Ciclosporin/Tacrolimus +
    Azathioprine/Mycophenolate Mofetil +
    Prednisolone
207
Q

Management of PSC?

A
  • No curative medical therapy: transplant needed
  • Symptomatic:
    Pruritus: colestyramine, naltrexone
    Diarrhoea: codeine phosphate
  • Specific
    ADEK vitamins
    Ursodeoxycholic acid improves cholestasis only
    Abs
  • Screening
    Cholangiocarcinoma: US + Ca19-9

CRC: colonoscopy
Transplant
- Recurrence occurs in 30%

High risk

208
Q

Management of refractory UC?

A

1st line = Mercaptopurine (2-2.5mg/kg) / Azathioprine
2nd line - TNF-alpha inhibitor = infliximab, adalimumab
3rd line
- vedolizumab or tofacitinib
(Janus Kinase inhibitor)
4th line - Ciclosporin
5th line - Colectomy

209
Q

Management of Wilsons

A
  • Conservative: Diet = Avoid high Cu foods: liver, chocolate, nuts.
  • Medical: Penicillamine lifelong (Cu Chelator). SE: Nausea, rash, decreased WCC, decreased Hb, decreased plats, lupus haematuria. Monitor FBC and urinary Cu excretion.
  • Liver Tx if severe liver disease
  • Screen siblings
210
Q

Management once patient improves from an acute flare in Crohns?

A
  • Switch to oral pred (40mg/d)
211
Q

McEvedy’s

A

Groin incision e.g. Emergency repair strangulated femoral hernia - NOW OBSOLETE

212
Q

Mechanical luminal causes of dysphagia?

A

Mechanical block:
- Luminal: (FB, Large food bolus),

213
Q

Mechanism of action of osmotic laxatives?

A

Retain fluid in the bowel

214
Q

Mechanism of Zenker’s Diverticulum?

A

Defect usually posteriorly, but swelling usually bulges to left side of neck.
Therefore food debris, then pouch expansion and dysphagia.

Upper GI endoscopy is potentially hazardous and may result in iatrogenic perforation.

215
Q

Medical causes of diarrhoea?

A

Increased T4
Autonomic Neuropathy (DM)
Carcinoid
Pancreatic Insufficiency

216
Q

Mesalazine

A

A delayed released forms of 5-ASA

mesalazine is still however associated with side-effects such as GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis

217
Q

Metabolic complications of surgical treatment of PUD

A

Dumping syndrome

  • Abdominal pain, flushing + N/V
  • Early pain (10-30 mins) = Osmotic hypovolaemia
  • Late: (2-3 hrs) Reactive hypoglycaemia due to rapid increase in insulin due to excess sugar in intestine.

Also during gastric surgery.

Blind loop syndrome –> Malabsorption, Diarrhoea

  • Overgrowth of bacteria in duodenal stump
  • Anaemia: FB + B12
  • Osteoporosis

Weight loss: Malabsorption of decreased calories intake

218
Q

Microbiological investigations of liver failure?

A
  • Hep, CMV, EBV serology
  • Blood and urine culture
  • Ascites MCS + SAAG
219
Q

Microscopic inflammation of Crohns?

A

transmural
- Granulomas
- Increased goblet cells

220
Q

Microscopic inflammation of UC?

A

Mucosal
Crypt Abscesses

221
Q

Mnemonic of Wilson’s clinical symptoms

A

CLANKAH
- Cornea
- Liver
- Arthritis
- Neurology
- Kidney - Fanconi’s syndtome
- Abortions
- Haemolytic anaemia - Coombs negative

222
Q

MOA Chlorpromazine and promethazine

A

Dopaminergic receptors, used as antipsychotic agents.

223
Q

MOA Dimenhydrinate

A

Histamine H1 receptor antagonist

224
Q

MOA Ondansetron

A

5HT-3 serotonin receptor

225
Q

Monitoring in liver failure?

A

Fluids: urinary and central venous catheters.
Bloods: Daily FBC, U+E, LFTs, INR
Glucose: 1-4hrly + 10% dextrose IV 1L/12hrs.

226
Q

Most likely causes of acute diarrhoea? <14 days.

A

Suspect Gastroenteritis and ask about travel history, their diet and any sick contacts.
- Rotavirus
- Norovirus
- Enteric Adenovirus

Could also be Diverticulitis, antibiotic therapy, constipation overflow.

227
Q

Motility disorders causing dysphagia?

A

Local:
- Achalasia
- Diffuse oesophageal spasm
- Nutcracker oesophagus
- Bulbar/pseudobulbar palsy (CVA, MND)

Systemic:
- Systemic sclerosis/CREST
- MG

228
Q

NAFLD presentation?

A
  • Typically asymptomatic
  • Obesity, insulin, diabetes, hyperlipidaemia, HTN, metabolic syndrome.
  • Absence of alcohol use
  • Fatigue and malaise
  • Hepatosplenomegaly
  • truncal obesity
  • Right upper quadrant abdo discomfort
229
Q

Name the types of Viral hepatitis, their spread and cause?

A

Type A = Faeco-Or, by seafood (especialyl abroad).
Type B = IV, from blood, body fluids, babies (vertical)
Type C = IV, mainly blood, less vertical.
Type D, IV = Dependent on prior Hep B infection
Type E = FO - Developing world.

230
Q

Niacin deficiency (B3)

A

Pellagra - Think about Vegans
- Diarrhoea, Dermatitis, Dementia. Leads to sunburn-like dermatitis rash.

  • Also, neuropathy, depression, ataxia
  • Causes: dietary, isoniazid, carcinoid syndrome
231
Q

NICE Diagnosis of IBS?

A

Consider in anyone who has 6 months of:
- Abdo pain
- Bloating OR
- Change in bowel habit.

Diagnosis if a person has abdo pain which is:
- related to defection
- Associated with altered stool frequency (more or less)
- Altered stool form or appearance.

232
Q

Nutritional deficiences Vitamin A?

A
  • Xerophthalmia
  • Dry conjunctivae, develop spots (Bitots spots)
  • Corneas become cloudy then ulcerated
  • Night blindness –> total blindness

Taken in excess can be teratogenic

233
Q

Oesophageal malignancy most common type

A

SCC

-adenocarcinoma rising rapidly

234
Q

Once resuscitation and maintenance have occured, what is the next part of treatment for an UGIB?

A

Urgent Endoscopy: All patients with suspected Upper GI bleed require an endoscopy within 24hrs of admission.

  • Haemostasis of vessel or ulcer:
    Adrenaline injection
    Thermal/laser coagulation
    Fibrin glue
    Endoclips
  • Variceal bleeding
    : 2 of:
    1st line banding, 2nd line sclerotherapy,

adrenaline, coagulation
Balloon tamponade with

Sengstaken-Blakemore tube
- Only used if exsanguinating haemorrhage endoscopic therapy failure.

  • TIPPS if bleeding can’t be stopped endoscopically.
    Transjugular intrahepatic portosystemic shunt
  • TIPS procedure connects the hepatic vein and the portal vein.
235
Q

Oral therapy to induce remission in Crohns?

A
  • 1st line ileocaecal = budesonide
  • 1st line colitis = sulfasalazine
  • 2nd line: prednisolone (tapering) (or with methotrexate)
  • 3rd line: methotrexate
  • 4th line: infliximab or adalimumab
236
Q

Other presentations of Coeliacs?

A

Lymphoma and carcinoma
- Enteropathy - associated T cell lymphoma
- Adenocarcinoma of small bowel
Other Ca: breast, bladder

Immune Associated
- IgA deficiency
- T1DM
- PBC

Anaemia
- Increased or decreased MCV
- Hyposplenism: Howell-Jolly bodies, target cells

Dermatological
- Dermatitis herpetiformis: Everyone: Symmetrical vesicles, extensor surfaces - Esp elbows
V.itchy
responds to gluten-free diet or dapsone
Biopsy: granular deposition of IgA
Aphthous ulcers

237
Q

Outline the primary management of an Upper GI Bleed

A
  • Resuscitate
  • (consider blood/terlipressin)
  • Maintenance
  • Urgent Endoscopy
  • Management after endoscopy
238
Q

Outline the resuscitation of a patient with an Upper GI bleed?

A
  • Head down
  • 100% O2, protect airway
  • 2 x 14G cannulae + IV crystalloid infusion up to 1L (orange/Grey)
  • give Jesus fluids using 500mgl 0.9% NaCl boluses aiming for SBP=100
  • consider activation of major haemorrhage protocol if indicated
239
Q

Pancreatic cancer risk factors?

A

SINED

  • Smoking
  • Inflammation: chronic pancreatitis, liver cirrhosis
  • Nutrition (high fat diet, high protein)
  • EtOH
  • DM
  • HNPCC
  • MEN
  • BRCA2
  • male, age >65, afro-carribean
240
Q

Pathology of pancreatic cancer?

A
  • Mostly ductal adenocarcinoma
  • Metastasis early, present late
  • 60% head
  • 25% body
  • 15% tail
  • Endocrine tumours are rare
241
Q

Pathophysiology of alpha1-Antitrypsin Deficiency?

A

alpha1-Antitrypsin (a1AT) is a serpin involved in control of inflammatory cascade inhibiting neutrophil elastase

a1AT is synthesised in liver and comprises 90% of sea10globulin on electrophoresis

242
Q

Patient with no abdo pain, jaundice but has palpable gallbladder.

A

Courvoisier’s law states that painless, enlarged gallbladder unlikely to be gallstones.

Pancreatic Cancer
- RF = Age, Smoking, Diabetes, Chronic Pancreatitis, HNPCC, BRCA2

  • Classically painless jaundice, loss of exocrine function (steatorrhoea), loss of endocrine function, Trousseau’s sign = migratory thrombophlebitis
  • Investigations = US, High resolution CT

Management

  • Whipple’s resection (pancreaticoduodenectomy)
  • Adjuvant chemo
  • ERCP with stenting
243
Q

Patient with T1DM should also be screened for what?

A

Coeliac’s
- Villous atrophy = malabsorption
- Associated with dermatitis herpetiformis (vesicular, pruritic skin eruption and AI disorders T1DM and Hepatitis). Associated with HLA-DQ2

Complications of Coeliac’s
- Anaemia = Iron, folate, Vit B12.
- Hyposplenism
- Osteoporosis
- EATL
- Subfertility

244
Q

Perianal disease in Crohn’s, inducing remission?

A

Occurs in ~50%
Ix: MRI + EUA
Rx
- Oral antibiotics: metronidazole
- Immunosuppression ± infliximab
- Local Surgery ± seton insertion

245
Q

Physical complications of Surgical treatment of PUD

A

Physical complications
- Duodenal stump leakage
- Abdominal fullness
- Reflux or bilious vomiting (improves with time)
- Stricture formation

246
Q

Poor prognostic factors for liver failure?

A
  • Grade 3/4 hepatic encephalopathy
  • > 40 yrs old
  • Albumin <30g/L
  • Increased INR
  • Drug-induced liver failure
247
Q

Presentation of alpha1-Antitrypsin Deficiency?

A

Variable
- Neonatal and childhood hepatitis
- 15% adults develop cirrhosis by 50 Y
-75% adults have emphysema (especially smokers)

248
Q

Presentation of carcinoid syndrome? 5HT?

A
  • Flushing: Paroxysmal, upper body ± wheals
  • Intestinal: diarrhoea
  • Valve fibrosis: tricuspid regurg and pulmonary stenosis –> affected the right side of the heart.
  • Wheeze: Bronchoconstriction
  • Hepatic involvement: bypassed 1st pass metabolism
    therefore only when liver mets have occured will you get serotinin syndrome.
  • Tryptophan deficiency –> Pellagra (3Ds)

May also present with some classic Cushingoid features - moon-face, central fat accumulation and bruising. Cortisol causes hypokalaemia and hypernatraemia.

249
Q

Presentation of carcinoid tumours locally?

A
  • Appendicitis
  • Intussusception or obstruction
  • Abdo pain
250
Q

Presentation of cholangiocarcinoma?

A

Fever, malaise
Abdo pain, ascites, jaundice
Increased bilirubin, increased ALP

Diagnosis
- Obstructive picture with liver function tests-
-Ca 19-9^^, CEa, CA125
- CT/MRI and MRCP

251
Q

Presentation of chronic pancreatitis?

A
  • Epigastric pain (bores through to back, relieved by sitting back or hot water bottle –> Erythema ab igne)
  • exacerbated by fatty food ot EToH.
  • Steatorrhoea
  • Weight loss
  • DM
  • Epigastric mass: pseudocyst
252
Q

Presentation of Liver

A

Mr J has evidence of fingernail clubbing conjunctival jaundice, palmar erythema and evidence of digital clubbing.

The jugular venous pressure was elevated and there were mutliple spider naevi in the distribution of the SVC. The abdomen is distended with dilated veins which fills away from the umbilicus suggestive of caput medusae.

I noted 8 finger breadth of smooth-non tender heptaomgealy extending below the right costal margin, There is no associated splenomegaly.

He has a distended abdomen with shifting dullness in keeping with ascites which is non-tense. There is peripheral oedema likely from hypoalbuminaemia.
These finding would be most consistent with a diagnosis of cirrhosis liver disease with some evidence of decompensation.

To complete my examination
- Examine the CVS system to look for underlying valvular heart disease.
- Perform a urine dip to look for glucosuria, as diabetes is a risk factor for NASH
- examine external genitalia looking for loss of secondary sexual characteristics

Perform a DRE to look for melaena as a sign of decompensation
Request a URine dip
Neuro exam for cerebellar ataxia and peripheral neuropathy.

253
Q

Presentation of pancreatic cancer?

A

Typically male >60
Head: painless obstructive jaundice
- with dark urine + pale stools
Body/Tail: epigastric pain
- Radiates to back, relieved sitting forward
Anorexia and weight loss
Acute pancreatitis
Sudden onset DM in the elderly

254
Q

Presentation of PBC

A

THe M rule of Primary Biliary Cholangitis - Anti-Mitochondrial antibodies, middle aged females, IgM.

  • Often asymptomatic and Dx incidentally (Increased ALP)
  • Jaundice occurs LATE
  • Pruritis and fatigue - occurs first.
  • Pigmentation of face
  • Bones: osteoporosis, osteomalacia (decreased VIt D)
  • Big organism: hepatosplenomegaly
  • Cirrhosis and coagulopathy (decreased Vit K)
  • Cholesterol increased: xanthalasma, xanthomata
  • Steatorrhoea
255
Q

Presentation of PSC?

A

May be asyptomatic and diagnosis incidentally (increased ALP).

256
Q

Prevention (not stopping once) of a primary UGIB?

A

Betablockers (propranolol), repeat endoscopic banding

257
Q

Prevention of secondary UGIB?

A

Betablockers (propranolol), repeat banding, TIPSS.

258
Q

Primary sclerosing cholangitis - what is it?

A

Inflammation, fibrosis of strictures and intra- and extra-hepatic ducts. Chronic biliary obstruction –> 2ndry biliary cirrhosis –> liver failure

259
Q

Procedure for UC in emergency?

A

Emergency presentation - Subtotal colectomy.

This is because removal of the rectum is not always conducted in an emergency setting. End ileostomy is created and rectum is stapled off or left in situ.

Elective = Curative
- proctocolectomy with permanent ileostomy
- proctocolectomy with continent ileostomy

restorative option
- ileal-pouch anal anastomosis (IPAA) ( J pouch) = restorative option. Only when rectum is in situ and cannot usually be underaken

  • Panproctocolectomy + permanent end ileostomy (removal of entire colon, rectum and anal canal)
260
Q

Procedures in Crohn’s?

A

Primary remove most of the bowel as Crohns can recur if just segmental. Surgery is NOT a cure.

Severe perianal or rectal = proctectomy (pouch not recommended)

  • Limited resection: e.g ileocaecal.

Extensive small bowel resections may result in short bowel syndrome and localised stricturoplasty may allow preservation of intestinal length.

261
Q

Procedures in elective surgery in UC Indications?

A
  • Panproctocolectomy with end ileostomy or IPAA (J pouch)
  • Total colectomy with IRA
262
Q

Prognosis of AIH?

A
  • Remission in 80% of patients
  • 10yr survival 80%
263
Q

Prognosis of carcinoid tumours?

A
  • Median survival is 5-8yrs (~3 yrs if mets present)
264
Q

Prognosis of Hereditary Haemochromaosis?

A
  • Venesection returns life expectancy to normal if non-cirrhotic and non-diabetic
  • Cirrhotic patients have >10% chance of HCC
265
Q

Prognosis of liver transplant in CLD?

A

Depends on disease aetiology
60-90% 5 yrs.

266
Q

Prognosis of pancreatic cancer?

A

Mean survival <6 months
5yrs = <2 %.

267
Q

Pseudopolyps in which IBD?

A

Ulcerative Colitis

268
Q

Pyridoxine B6

A

Peripheral sensory neuropathy
- Causes: PZA

269
Q

Radiological investigations of liver failure?

A
  • CXR
  • Abdo US + portal vein duplex. (US is preffered).
  • For patients with suspected cholangitis, cholecystitis, pancreatitis = CT study.
270
Q

Refeeding syndrome

A
  • Refeeding syndrome describes the metabolic abnormalities which occur on feeding a person following a period of starvation. It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism. The metabolic consequences include:
  • hypophosphataemia
  • hypokalaemia
  • hypomagnesaemia: may predispose to torsades de pointes
  • abnormal fluid balance

Patients are considered high-risk if one or more of the following:
BMI < 16 kg/m2
unintentional weight loss >15% over 3-6 months
little nutritional intake > 10 days
hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

Levels are already depleted due to malnutrition. Carbohydrate ingestion causes insulin release which causes rapid intracellular shift of potassium, magnesium and phosphate

271
Q

Risk factors for GASTRIC ulcers?

A
  • Lifestyle: Smoking, DECREASED gastric emptying
  • Infection: H.pylori
  • Drugs: NSAIDS, Steroids, SSRI, bisphosphonates
  • Stress:
    Cushing’s Ulcer due to intracranial disease? Increased vagal stimulation, Increased stomach acid
    Curling’s ulcer: Burns, Sepsis, Trauma (reduced plasma volume)
272
Q

Rooftop

A

Upper abdomen access for Whipple’s

273
Q

Rooftop scar?

A

Liver transplant
Whipples

274
Q

Rutherford Morrison

A

Hockeystick scar
- Kidney Surgery

275
Q

Rutherford Morrison

A

Extraperitoneal approach to left or right lower quadrants. Gives excellent access to iliac vessels and is the approach of choice for first time renal transplantation.

276
Q

Score for prognosis of alcoholic hepatitis?

A

Maddrey score - Looks at Prothrombin, thrombin and bilirubin.
- Mild: 0-5% 30 day mortality
- Severe: 50% 30d mortality
- 1yr after admission: 40% mortality

277
Q

Severity of UC assessment?

A

Truelove and Witts Criteria
- Motions (<4), (4-6), <6
- PR bleed (small, moderate, large)
- Temp (aprexic) or (>37.8)
- HR (>70), >90
- Hb (>11) (<10.5)
- ESR <30 >30

278
Q

Short gut syndrome?

A

<1-2m small bowel
- Features:
Steatorrhoea, ADEK and B12 malabsorption
Bile acid depletion –> gallstones
-Hyperoxaluria –> renal stones

Rx
- Dieticians
- Supplements or TPN
- Loperamide

279
Q

Signs of dysphagia?

A

Cachexia
Anaemia
Virchow’s node (+ve = Troisier’s sign)
Neurology
Signs of systemic disease

280
Q

Signs of liver tumorus

A
  • Hepatomgealy: smooth, hard or irregular
  • Signs of chronic liver disease
  • Abdominal mass
  • hepatic bruit (HCC)
281
Q

Signs of pancreatic cancer?

A
  • Epigastric mass
  • Jaundice
  • Palpable gallbladder
  • Thrombophlebitis migrans (Trousseau Sign) - episodes of vessel inflammation due to blood clot
  • Splenomegaly: PV thrombosis –> Portal HTN
  • Ascites
282
Q

Signs of PSC?

A
  • Jaundice: dark urine, pale stools
  • Hepatosplenomegaly
283
Q

Signs of severity

A

Cachexia
Organ failure
- Bruising from coagulopathy
- Peripheral oedema (hypoalbuminuria)
- Fetor hepaticus (portosystemic shunting - varices)
- Portal HTN - splenomegaly, ascites, caput medusa + varices.

284
Q

Small Bowel Bacterial overgrowth syndrome

A

Risk factors for SBBOS
- Neonates with congenital gastrointestinal abnormalities
- Scleroderma
- Diabetes Mellitus

Presents with chronic diarrhoea, bloating, flatulence, abdominal pain

Diagnosis
- Hydrogen breath test
- Small bowel aspiration and culture: this is used less often as invasive and results are often difficult to reproduce
- Clinicians may sometimes give a course of antibiotics as a diagnostic trial. Rifaximin is now treatment of choice.

285
Q

Smoking with IBD?

A

UC is protective
Crohns increased risk

286
Q

Specific management for HCV?

A
  • Interferon-a/Oral antiviral = Sofosbuvir, Elbasvir
287
Q

Specific management for SBP?

A
  • IV Cefotaxime 2g every 8-12 hrs + Vancomycin 500-1000mg
  • Prophylaxis given to patient who have had an episode of SBP
  • Patients with fluid protein <15 and either a Child-Pugh score of at least 9 or hepatorenal syndrome.
  • Offer oral cipro or norfoxacin prophylaxis for people with cirrhosis + ascites.
288
Q

Staging of HCC?

A

Staging = Liver MRI, chest abdo and pelvic CT. Check testes.

BCLC - 0A, B, C,D.
A = Liver transplantation alongside TACE (transarterial chemo-embolisation and/or radiofrequency ablation bridging therapy.
B = TACE + percutaneous ablation
C = sorafenib or lenvatinib - oral multikinase inhibitors.
D = Hospice care (± liver transplant)

289
Q

Success rate of eradication therapy?

A

95%.
Failure due to poor compliance.
Bismuth can be used for resistance to clarithromycin but gives stools tarry black colour.

290
Q

Sulphasalazine

A

Sulphapyridine and 5-ASA

Many side-effect are due to the sulphapyridine moiety: rashs, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis.

Other side-effects are common to 5-ASA drugs.

291
Q

Surgery in Crohn’s?

A

50-80% need >1 operation in their life
Never curative
Should be as conservative as possible

292
Q

Surgical complications of UC?

A

Abdominal
- Small bowel obstruction
- Anastomotic stricture
- Pelvic Abscess

Stoma complications: Retraction, stenosis, prolapse, dermatitis
Pouch
- Pouchitis (50%):
- metronidazole + ciprofloxacin
- Decreased female fertility
- faecal leakage

293
Q

Surgical treatment of PUD - Antrectomy with vagotomy

A

Removal of the distal half of stomach + anastomosis:
- Directly added to duodenum: Biliroth 1
- To small bowel loop with duodenal stump oversewn: Biliroth 2 or Polya.

294
Q

Surgical treatment of PUD - Subtotal gastrectomy with Roux-en-Y

A

Sometimes performed for Zollinger-Ellison

295
Q

Surgical treatment of PUD - Vagotomy?

A

Rarely used today.
- Vagotomy:
Truncal (must be included with a pyloroplasty (open opening to duodenum) or gastroenterostomy)
- Selective: Vagus nerve only denervates where it supplies lower oesophagus. (Nerves of Laterjet)

296
Q

Symptoms of liver tumours?

A
  • Benign tumours usually asymptomatic
  • Systemic: fever, malaise, weight loss, anorexia
  • RUQ pain: stretching of Glisson’s capsule
  • Jaundice is often late except in cholangiocarcinoma
  • May rupture –> intraperitoneal haemorrhage
297
Q

Symptoms of PSC?

A
  • Jaundice
  • Pruritus
  • Fatigue
  • Abdo pain
298
Q

Symptoms of SBP?

A
  • Frequently encountered bacterial infection in patients with cirrhosis, most commonly seen in patients with end-stage liver disease.
  • Key symptoms = abdo pain, fever, vomiting, altered mental status and GI bleeding. However can also present asymptomatically.
299
Q

Systemic symptoms presentation of IBD

A

Fever
Malaise
Anorexia
Weight Loss

300
Q

The majority of C.dff infections are caused by what?

A
  • Abx associated Diarrhoea
  • 100% of Abx associated pseudomembranous colitis
301
Q

Thiamine deficiency (B1)

A

Beri Beri
- Wet: heart failure + oedema
- Dry: Polyneuropathy
- Wernicke’s: ophthalmoplegia, ataxia, confusion

302
Q

Treatment of Hereditary Haemochromaosis?

A
  • Iron removal : venesection - aim for Hct <0.5, (transferrin <50) Desferrioxamine is 2nd line
  • General: Monitor DM, low Fe diet
  • Joint x-ray = Chondrocalcinosis
  • Screening: Se ferritin and genotype, screen 1st degree relatives
  • Transplant in cirrhosis
303
Q

Triad of chronic mesenteric ischaemia?

A
  • Colicky post-prandial abdominal pain
  • Weight loss
  • Abdominal bruit
304
Q

Types of Liver transplant in CLD?

A
  • Cadaveric: heart-beating or non-heart beating
  • Live - right lobe
305
Q

Types of liver transplants?

A
  • Cadaveric: heart-beating or non-heart beating
  • Live: right lobe
306
Q

TYPES OF PANCREATIC CANCER

A
  • adenocarcinoma (95%)
  • Acinar carcinoma
  • Cystadenocarcinoma
307
Q

Ulceration in Crohns?

A

Deep, thin, serpiginous –> Cobblestone mucosa

308
Q

Ulceration in UC?

A

Shallow and broad

309
Q

Unconjugated bilirubin converted to conjugated by what enzyme?

A

BR-UDP-glucuronyl transferase in the liver.

310
Q

Vitamin C deficiency

A

Scurvy
- Gingivitis
- Bleeding: gums, nose, hair follicles (petechial)
- Muscle pain/weakness
- Oedema
- Corkscrew hairs

311
Q

Vitamin D –> osteomalacia

A

Bone pain + fractures

312
Q

Vitamin K

A

Decreased factors 2,7,9, 10 C and S
- Bruising: petechiae
- Bleeding: e.g epistaxis, menorrhagia

313
Q

What are liver mets?

A
  • Rx and prognosis vary with type and extent of primary
  • Small solitary CRC mets may be resectable
  • Advanced disease therefore prognosis < 6months.
314
Q

What are oesophageal varices?

A

Portal HTN –> Dilated veins @ sites of porto-systemic anastomosis –> L.gastric and inferior oesophageal veins.
- 30-50% with portal HTN will bleed from varices.
- Overall mortality 25%: increased severity of liver disease.

315
Q

What are prominent Abdominal Veins

A
  • A lot more common than caput medusa. - Blood flow down below towards legs: portal HTN. - Blood flow towards the head: IVC obstruction.
316
Q

What are the 3 classifications of a hiatus hernia?

A

1) Sliding (80%) - Gasto-oesophageal junction SLIDES up into chest. Associated with GORD.
2) Rolling (15%) - Gasto-oesophageal junction remains in abdomen, but a bulge of stomach rolls into chest alongside the oesophagus. LOS remains in abdomen therefore little GORD. Can become strangulated.
3) Mixed

317
Q

What are the 3 overarching causing of jaundice?

A

-Pre-hepatic
- Hepatic
- Post-hepatic

318
Q

What are the antibodies for AIH?

A

AIH: SMA, SLA, LKM, ANA

319
Q

What are the autoimmune, neoplastic and vascular causes of conjugated hepatic jaundice?

A

AI: AIH
Neoplasia: HCC, Mets
Vascular: Budd-Chiari

320
Q

What are the blood investigations for cirrhosis?

A

Bloods:
- FBC:
decreased WCC,
decreased platelets indicate hypersplenism. Thrombocytopenia is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with liver disease.
- Increased LFTs (2.5 increase ratio of AST to ALT). Urea should go down.

  • Increased INR
  • Decreased Albumin
321
Q

What are the blood investigations for ulcerative colitis?

A

Ix
- Bloods:
FBC: decreased Hb, Increased WCC
LFTs: decreased albumin
Increased CRP/ESR (>30 suggestive of a severe flare up)

Faecal calprotectin.- NICE advise the use of faecal calprotectin to differentiate IBS from IBD.

Blood cultures

322
Q

What are the categories defining severe C.Diff Diarrhoea?

A

> 1 of
- Shock
- WCC > 15
- Creatinine >50% above baseline
- Temp >38.5
- Clinical / Radiological evidence of severe colitis.

323
Q

What are the causes fo conjugated hepatic jaundice?

A

Problems with the liver/Hepatocellular dysfunction?
- Congenital
- Infection
- Autoimmune
- Neoplastia
- Vascular

324
Q

What are the causes of Achalasia?

A

Primary/Idiopathic: commonest
Secondary: oesophageal Ca, Chagas’ disease (T.cruzii)

325
Q

What are the causes of Budd-Chiari Syndrome?

A
  • Hypercoagulable state -
  • Myeloproliferative disorders (PV most common), PNH, anti-phospholipid, OCP.
    Local Tumour: HCC
    Congenital: membranous obstruction of IVC
326
Q

What are the causes of decreased hepatic bilirubin excretion leading to a conjugated hepatic jaundice?

A
  • Dubin-Johnson (black liver due to melanin deposits)
  • Rotors
327
Q

What are the causes of drug induced cholestasis and subsequent jaundice?

A
  • Flucloxacillin (weeks after Rx)
  • Co-amoxiclav
  • OCP
  • Sulphonylureas
  • Chlopromazine, prochlorperazine (antipsychotic)
328
Q

What are the causes of drug-induced haemolytic jaundice?

A

Antimalarials - Dapsone

329
Q

What are the causes of drug-induced hepatitis and jaundice?

A
  • Paracetamol OD
  • RMP, INH, PZA
  • Valproate
  • Statins
  • Halothane
  • MAOIs –> Monoamine oxidase
330
Q

What are the causes of dyspepsia?

A

Inflammation: GORD, Gastritis, PUD
Malignancy: Gastric or Oesophageal
Functional: Non-ulcer dyspepsia

331
Q

What are the causes of liver failure?

A

1) Cirrhosis

2) Acute failure due to:
- Infection: Hep A/B, CMV, EBV, Leptospirosis
- Toxin: EtOH, Paracetamol, Isoniazid, halothane
- Vascular: Budd-Chiari
- Other: Wilson’s, AIH
- Obs: Eclampsia, Acute Fatty Liver of pregnancy.

332
Q

What are the causes of portal HTN?

A

Pre-hepatic: Portal vein thrombosis
Hepatic: cirrhosis (80% in UK), schisto (worldwide), sarcoidosis
Post-hepatic: Budd-Chiari (occlusion of hepatic vein), RHF, constrict pericarditis

333
Q

What are the causes of pre-hepatic jaundice?

A
  • Excess bilirubin production
    –> Haemolytic anaemia
    – >Ineffective erythropoiesis (thalassaemia, sickle cell, G6PD)
334
Q

What are the causes of unconjugated hepatic jaundice?

A

Unconjugated?
- Decreased BR uptake due to using up liver’s ability to take it up.
1) Drugs: contrast, Rifampycin
2) Congestive cardiac failure

  • Decreased bilirubin conjugation
    1) Hypothyroidism (decreased movement + conjugation)
    2) Gilbert’s (AD)
    3) Crigler-Najjar (AR)

Neonatal jaundice is both increased production and reduced conjugation.

335
Q

What are the clinical features of Wilson’s Disease

A
  • Cornea - Kayser Fleischer rings (70% may need slit-lamp)
  • Liver disease - Children present with acute hepatitis with necrosis/ cirrhosis
  • Arthritis Chondrocalcinosis/Osteoporosis
  • Neurology - Parkinsonism = Bradykinesia, tremor, chorea, tics. Ataxia + depression, dementia, psychosis.
  • Kidney - Fanconi’s syndrome (T2 RTA) type 2 renal tubular acidosis loss of bicarbonate) Osteomalacia
  • Abortions
  • Haemolytic Anaemia
336
Q

What are the common causes of an Upper GI bleed?

A

1) PUD: 40% (mostly DU)
2) Gastritis/Erosions: 20%
3) Mallory-Weiss tear: 10%
4) Varices: 5%
5) Oesophagitis: 5%
6) Ca Stomach/oesophagus
7) Boerhaave’s

337
Q

What are the complications of cirrhosis?

A
  1. Decompensation –> Hepatic Failure
    - Jaundice (conjugated)
    - Encephalopathy
    - Hypoalbuminaemia –> oedema + ascites
    - Coagulopathy –> bruising
    - Hypoglycaemia
  2. Spontaneous Bacterial Peritonitis
  3. Portal Hypertension
  4. Increasing risk HCC
338
Q

What are the complications of peptic ulcer disease?

A

Start from ulcer:

Bleeding –> Haemorrhage:

  • Haematemesis or melaena
  • Fe deficiency anaemia

Duodenal ulcer bleeds from gastroduodenal artery.

Even more? –> Perforation (check using X-ray–> pneumoperitoneum)

  • Peritonitis
  • can penetrate and form fistula with biliary tree or penetrate left liver lobe

Growing and blocking? –> Gastric Outflow obstruction
- Vomiting, colic, distension

Long term? Malignancy
- Increased risk with H.pylori

339
Q

What are the components for metabolic syndrome associated with NAFLD?

A
  • Central obesity (increased waist circumference) and two of:
  • Increased triglycerides
  • Decreased HDL
  • HTN
  • Hyperglycaemia: DM, IGT, IFG
340
Q

What are the congenital causes of conjugated hepatic jaundice?

A
  • Hereditary Haemochromatosis
  • Wilson’s
  • a1ATD
341
Q

What are the Diabetic GI complications

A

Achalasia
Neurological plexus damage
Gastroparesis
Constipation
Diarrhoea
Gallstones
NASH

342
Q

What are the differential diagnosis for GORD?

A
  • Other causes of oesophagitis: Infection, IBD, burns.
  • PUD
  • Oesophageal cancer
343
Q

What are the differentials for ascites?

A

Serum Ascites Albumin Gradient (SAAG) = Serum albumin - ascitic albumin - SAAG >=1.1g/L = Portal HTN. (pre, hepatic, post), Cirrhosis in 80%. - SAAG <1.1g/dL = other causes. = Neoplasia: peritoneal or visceral = Inflammation: e.g pancreatitis= Nephrotic syndrome = Infection: TB peritonitis

344
Q

What are the differentials for haematemesis?

A
  • VINTAGE- Varices- Inflammation: (Oesophagus, stomach or duodenum).- PUD (DU is most common) - Neoplasia (Oesphageal or gastric Ca) - Trauma: Mallory-Weiss because of vomiting. - Boerhaave’s Syndrome - Full thickness tear 2cm proximal to LOS. - Angiodysplasia + other vascular anomalies Angiodysplasia (vascular malformation), HHT or Osler-Weber-Rendu (hereditary haemorrhagic telangiectasia, Dieulafoy lesion: rupture of large arteriole in stomach or other bowel. - Generalised bleeding diathesis Warfarin, thrombolyticsCRF (chronic renal failure) - Epistaxis
345
Q

What are the differentials for rectal bleeding?

A

DHIPING ARSE
- Diverticulae
- Haemorrhoid
- Infection:
Campy
Shigella
E.coli
C.diff
Amoebic dysentery
- Polyps
- Inflammation (Crohn’s, UC)
- Neoplasia
- Gastric-Upper Bowel Bleeding
- Angio (Ischaemic colitis, HHT, Angiodysplasia)

346
Q

What are the extra-oesophageal symptoms of GORD?

A
  • Chronic cough
  • Laryngitis, sinusitis
  • Nocturnal asthma (chest tightness, SOB, Wheeze)
347
Q

What are the genetic associations of Hereditary Haemochromaosis?

A

Autosomal recessive:
HFE gene (High FE) on chromosome 6 (C282Y)

348
Q

What are the indications for surgery after an UGIB?

A
  • Rebleeding
  • Bleeding despite transfusing 6U
  • Uncontrollable bleeding at endoscopy
  • Initial Rockall score >3 or final >6.
349
Q

What are the infectious causes of conjugated hepatic jaundice?

A
  • CMV
  • Hep A/B/C
  • EBV
350
Q

What are the investigation for post hepatic jaundice?

A
  • Urine: Increased BR ++, no urobilinogen
  • LFTs: Increased CBR, Increased AST, increased ALT, Increased ALP, Increased GGT.
  • Other: Abdo US - Ducts >6mm, ERCP, MRCP, Anti-AMA, ANCA (PSC), ANA.
351
Q

What are the investigations for a hiatus hernia?

A

Bloods: FBC, U+E
CXR: Gas bubble + fluid level within the chest cavity.
Ba Swallow: Diagnosis
OGD: Can help visualise the mucosa but is not diagnostic.
24hr pH + manometry: exclude dysmotility or achalasia

352
Q

What are the investigations for ascites?

A
  • Bloods: FBC, U+E, LFTs, INR, chronic hepatitis screen.
  • US: confirm ascites, liver echogenicity, PV duplex
  • Ascitic tap:
    MCS and AFB
    Cytology
  • Chemistry: albumin, LDH, glucose, protein
  • SAAG = Serum albumin - ascites albumin
  • Liver biopsy
353
Q

What are the investigations for Budd-Chiari?

A

Bloods: FBC, clotting (prolonged prothrombin), LFTs

US + hepatic vein Doppler. Very sensitive and is radiological investigation.

Ascitic Tap: increased protein (>2.5g/dL), with increased SAAG (>1.1g/dL)
Other: JAK2 mutation analysis, RBC, CD55 and CD59 (PND)

354
Q

What are the investigations for hepatic jaundice?

A

Do a PR for melaena

Urine: Increased bilirubin, increased urobilinogen
LFTs: Increased conjugated bilirubin, increased AST:ALT
- If >2 = ETOH
if < 1 = Viral
- Increased GGT (EtoH, Obstruction)
- Increased ALP
- Function: decreased albumin, increased PT.
- Others: FBC = Anaemia
Anti-SMA (AIH), LKM (AIH), SLA (Chronic Hep C), ANA
a1AT, ferritin, caeruloplasmin, Liver biopsy.

355
Q

What are the investigations for NAFLD?

A

BMI
Liver profile: increased (AST: ALT <1)
Glucose
Fasting lipids
Liver biopsy

In patients with incidental finding of NAFLD - typically asymptomatic fatty changes on liver US. Liver Fibrosis blood test should be performed to assess for more severe liver disease.
- Hyaluronic acid + procollagen III + tissue inhibitor of metaloproteinase 1.

Associated with obesity, T2DM, hyperlipidaemia, jejunoileal bypass.
Sudden weight loss/starvation.

356
Q

What are the investigations for pre-hepatic jaundice?

A

Urine: No Bilirubin, increased urobilinogen, increased Hb if intravascular haemolysis
LFTs: increased uBR, increased AST, increased LDH
Others: FBC and film, Coombs Test, Hb Electrophoresis

357
Q

What are the investigations of liver failure?

A

Bloods:
- FBC: infection, GI bleed, decreased MCV (ETOH)
- U+E: Decreased urea, increased creatinine: Hepatorenal syndrome
(urea synthesised in liver so poor test of renal function).

  • LFT:
    AST:ALT >2 = ETOH
    AST:ALT <1 = Viral

Albumin: decreased in chronic liver failure

PT: Increased in acute liver failure.
- Clotting: Increased INR
- Glucose
- ABG: Metabolic acidosis
Causes: Ferritin, a1AT, caeruloplasmin, Abs, paracetamol lvls.

358
Q

What are the oesophageal symptoms of GORD?

A
  • Heart burn that is related to meals, lying down, and gets better with antacids.
  • Belching
  • Acid Brash (salivation due to excess acid)
  • Odynophagia
359
Q

What are the possible precipitants of encephalopathy?

A

Constipation (commonest cause - due to excessive nitrogen load and can lead to Liver decompensation. HEPATICS - Hepatic encephalopathy- Haemorrhage: e.g varices- Electrolytes: decreased K, decreased Na - Poisons: diuretics, sedatives, anaesthetics - Alcohol - Tumour: HCC- Infection: SBP, pneumonia, UTI, HDV- Constipation (commonest cause - due to excessive nitrogen load- Sugar (glucose) decrease: e.g low calorie diet.

360
Q

What are the post-hepatic causes of jaundice?

A
  • Obstruction
    Stones
    Ca Pancreas
    Drugs
    PBC
    PSC
    Biliary Atresia
    Choledochal Cyst
    Cholangio carcinoma
361
Q

What are the risk factors of C diff diarrhoea?

A

Abx:
- Clindamycin
- Cephalosporins
- Augmentin
- Quinolones

  • Increased Age
  • Increased length of stay at hospital
  • Increased contact with C.diff - +ve contact
  • PPIs
362
Q

What are the risk factors of duodenal ulcers?

A

Lifestyle: ETOH, Smoking, increased gastric emptying (damage to duodenum)

Infection: H.pylori (90%)

Drugs: NSAIDS (COX-1 blocks prostaglandins needed for gastric mucosa), Steroids
Also SSRI, steroids, bisphosphonates.

363
Q

What are the risk factors of GORD?

A

Lifestyle: Smoking, ETOH, Obesity
Physiological: Pregnancy
Anatomical: Hiatus Hernia
Iatrogenic: drugs (nitrates, CCB, TCA, anti-ACHm.
Surgical: Heller’s Myotomy

364
Q

What are the signs of alcohol withdrawal?

A

10-72hrs after last drink
- Consider in new ward pt (<3 days) with acute confusion
- Signs
= increased HR, decreased BP, tremor
= Confusion, fits, hallucinations: esp formication (DTs).

365
Q

What are the signs of cirrhosis in the abdomen?

A
  • Striae
  • Hepatomegaly (may be small in late disease)
  • Splenomegaly
  • Dilated superficial veins (caput medusa)
  • Testicular atrophy
366
Q

What are the signs of cirrhosis in the face?

A

Pallor: ACD
Xanthelasma: PBC
Parotid enlargement: espc with ETOH

367
Q

What are the signs of cirrhosis in the hands?

A
  • Clubbing (± periostitis)
  • Leuconychia (decreased albumin)
  • Terry’s nails (white proximally, red distally)
  • Palmar erythema
  • Dupuytron’s contracture
368
Q

What are the signs of cirrhosis in the trunk?

A
  • Spider naevi (>5 fill from centre)
  • Gynaecomastia (low albumin - altered sex hormone metabolism
  • Loss of 2ndry sexual hair
369
Q

What are the signs of liver failure?

A

Jaundice
Oedema + ascites
Bruising
Encephalopathy - normally in acute liver failure.
- Aterixis, Constructional apraxia
Fetor hepaticus (sweet breath/thiols pass into lungs)
Signs of cirrhosis/chronic liver disease

370
Q

What are the signs of the prodromal phase of hepatitis A and B.

A
  • Splenomegaly
  • Right upper quadrant pain
  • Posterior cervical adenopathy
  • Bradycardia
371
Q

What are the stool investigations for UC?

A

MCS: exclude campy, shigella, salmonella
CDT: C.diff may complicate or mimic

372
Q

What are the symptoms of ascites?

A
  • Distension –> abdo discomfort and anorexia
  • Dyspnoea
  • decreased venous return
373
Q

What are the three portosystemic anastomoses?

A

Oesophageal varices =
Portal - Left and short gastric veins.
Systemic = Inf. oesophageal veins.

Caput medusae = Peri-umbilical vein. Superficial abdo wall veins.

Haemorrhoid = Super rectal veins. Inferior and middle rectal veins.

374
Q

What are the toxin causes of conjugated hepatic jaundice?

A
  • EtOH
  • Drugs
375
Q

What are the treatments for Budd-Chiari?

A
  • Treat underlying disease
  • Anticoagulate: unless varices present
  • Ascites: fluid and salt restrict, spiro, frusemide, tap, daily weights
  • Other options: Thrombolysis, angioplasty, TIPSS
  • Transplant if fulminant hepatic failure or cirrhosis
376
Q

What are the two types of hepatorenal failure?

A

Type 1: Rapidly deteriorating (survival <2 weeks)
Type 2: Steady deteriorating (survival ~6 months)

377
Q

What cells convert Hb to unconjugated BR?

A

Splenic macrophages

378
Q

What do you see on barium swallow with diffuse oesophageal spasm?

A

Ba Swallow shows corkscrew oesophagus.

379
Q

What does a spontaneous tear of oesophagus from retching suggest? - Vomiting, thoracic pain, subcutaneous emphysema.

A

Boerhaave’s syndrome.

380
Q

What does coffee ground vomiting suggest?

A

More for PUD and makes variceal bleed less likely.

381
Q

What does faecal urgency suggest?

A

Rectal Pathology

382
Q

What does NAFLD stand for?

A

Non-alcoholic Fatty Liver Disease

383
Q

What does the presence of N+V in the setting of melaena suggest?

A

Upper GI bleeding source distal to pylorus.

384
Q

What does TIPSS stand for?

A

Transjugular Intrahepatic Porto-Systemic Shunt

  • connects hepatic vein to portal vein
385
Q

What happens after an urgent endoscopy for an Upper GI bleed?

A
  • Omeprazole IV + continuation PO (decreased re-bleeding). Do not do it before as it may mask the bleeding.
  • Offer Vit K
  • Antibiotic
  • Keep NBM for 24hr –> Clear fluid –> light diet @ 48hr
  • Daily bloods: FBC, U+E, LFTs, Clotting
  • H.pylori testing and eradication
  • Stop NSAIDs, Steroids etc.
386
Q

What imaging is used for cirrhosis?

A

Transient elastography and acoustic radiation force (for patients with NAFLD, enhanced liver fibrosis). This is fibroscan. Measures the stiffness of the liver.

Abdo US + Portal Vein Duplex
- Small liver, nodularity, splenomegaly, increased diameter of the portal vein.
- Reversed portal vein flow
- Ascites

  • Also liver biopsy
387
Q

What investigations may demonstrate a genetic cause of cirrhosis?

A

Ferritin (Haemachromatosis), a1AT, caeruloplasmin (decreased in Wilson’s)

388
Q

What investigations may demonstrate a NASH cause of cirrhosis?

A

Hyperlipidaemia, increased glucose.

389
Q

What investigations may demonstrate an alcoholic cause of cirrhosis?

A

EToH: increased MCV, increased GGT

390
Q

What investigations may demonstrate an infective cause of cirrhosis?

A

Hep C, Hep B, CMV, EBV serology

391
Q

What is a carcinoid crisis?

A

Tumour outgrows blood supply or is handled too much –> massive mediator release
- Vasodilator, hypotension, bronchoconstriction, hyperglycaemia
- Management: High-dose octreotide

392
Q

What is a Dieulafoy Lesion?

A

Tortuous arteriole - located in the upper stomach, which causes an upper GI bleed.

Approximately 6 cm from OG junction.

393
Q

What is a pharyngeal Pouch/ Zenker’s Diverticulum

A

Outpouching of the oesophagus
- Between borders of cricopharyngeus and lower border of inferior constrictor of pharynx.
- Weakness in muscle wall termed Killian’s dehiscence

Management is with Surgery

394
Q

What is a TIPSS procedure?

A
  • IR creates an artificial channel between hepatic vein and portal vein –> Decreased portal pressure
  • Colapinto needle creates tract through liver parenchyma, expand using a balloon and maintained by placement of a stent.
  • Used prophylactically or acutely if endoscopic therapy fails to control variceal bleeding.
395
Q

What is blind loop syndrome?

A

Blind loop syndrome –> Malabsorption, Diarrhoea
- Overgrowth of bacteria in duodenal stump
- Anaemia: FB + B12
- Osteoporosis

396
Q

What is Budd-Chiari Syndrome?

A

Hepatic vein obstruction (from level of small hepatic veins to inferior vena cava) –> ischaemia and hepatocyte damage –> Liver failure or insidious cirrhosis

397
Q

What is C.Diff?

A
  • Gram Positive Spore-forming anaerobe
  • Releases enterotoxins A and B
  • Spores are V.robust and can survive for >40d
398
Q

What is Crigler-Najjar syndrome?

A

Rare auto rec total UDP-GT deficiency
- Severe neonatal jaundice and kernicterus
Rx: liver Tx

399
Q

What is diffuse oesophageal spasm?

A

Intermittent dysphagia ± chest pain.

400
Q

What is first line eradication therapy for H.pylori? (NKDA)

A

PAC 500 (Penicillin)

  • PPI: Lansoprazole 30mg BD
  • Amoxicillin 1g
  • Metronidazole 400g BD

Post eradication investigation is breath test.

401
Q

What is Gilbert’s syndrome?

A
  • Autosomal dominant UDP-GT deficiency
  • 2% of the population
  • Jaundice occurs during intercurrent illness
  • Dx: increase in uBR on fasting, normal LFTs.
402
Q

What is Haematochezia?

A

Fresh blood through the anus, in or with stools.
Different to melaena which is black. More associated with LGIB than UGIB.

403
Q

What is hepatorenal syndrome?

A

-Renal failure in patients with advanced CLF.
- Diagnosis of exclusion

404
Q

What is IBS?

A

Enhanced visceral perception giving bowel symptoms for which no organic cause can be found.

405
Q

What is malignant ascites?

A

Patients with malignancies in the peritoneum which lead to ascites, via increased production of peritoneal fluid + concurrent decreased resorption.

406
Q

What is Melanosis Coli?

A

MElanosis Coli is a disorder of pigmentation of the bowel wall. Histology demonstrates pigment-laden macrophages.

Associated with laxative abuse, especially senna.

407
Q

What is more common, a duodenal ulcer or a gastric ulcer?

A

Duodenal are 4x more common

408
Q

What is NAFLD?

A
  • Cryptogenic cause of hepatitis and cirrhosis associated with insulin resistance and the metabolic syndrome.
  • Non-alcoholic steatohepatitis is most extreme form and –> cirrhosis in 10%.
409
Q

What is nutcracker oesophagus?

A

Increase contraction of smooth muscle with normal peristalsis.

410
Q

What is PBC?

A

Primary Biliary Cholangitis
- Disease of small intrahepatic bile ducts (and eventual loss) occuring in the context of chronic portal tract inflammation. Develops fibrosis, then bile acids remain in the liver, resulting in cirrhosis.

411
Q

What is primary biliary cholangitis?

A

Intrahepatic bile duct destruction by chronic granulomatous inflammation –> cirrhosis

412
Q

What is pseudomembranous colitis?

A
  • Severe systemic symptoms: fever, dehydration.
  • Abdominal pain, bloody diarrhoea, mucus PR
  • Evidence of pseudomembranes (yellow plaques) on a flexible sigmoidoscopy
  • Pseudomembranous colitis is a nonspecific pattern of injury resulting from decreased oxygenation, endothelial damage, and impaired blood flow to the mucosa that can be triggered by a number of disease states.
  • Whilst most patients will have this due to C.diff, there may be other causes.
413
Q

What is SBP?

A
  • Patient with ascites and peritonitic abdomen
  • Caused by E.co.i, Klebsiella, Streps
  • Complicated by hepatorenal syndrome in 30%
  • Ix: Ascites PMN > 250mm + MCS
  • Rx: Tazocin or cefotaxime/vancomycin until sensitivities known
414
Q

What is the 3 fates of urobilinogen in the bile?

A
  • Reabsorbed, returned to the liver, and back into the bile
  • Excreted in the urine
  • into the GIT, converted to sterobilin (brown).
415
Q

What is the Child-Pugh Grading of Cirrhosis?

A

Predicts risk of bleeding, mortality and need for Tx
- Graded A-C using severity of 5 factors.

  • Albumin - 1,2 or 3 points for each.
  • Bilirubin -
  • Clotting -
  • Distension: Ascites
  • Encephalopathy .

Class A = 5-6 points (1yr survival 100%)
Class B = 7-9 points
Class C = 10-15 points (45%)

416
Q

What is the classification of encephalopathy (NICE)?

A

1: Confused - irritable, mild confusion, sleep inversion
2: Drowsy - Increased disorientated, slurred speech, asterixis
3: Stupor - rousable, incoherence
4: Coma - unrousable, ± extensor plantars

417
Q

What is the classification of peptic ulcer disease? (PUD)

A

Acute: Usually due to drugs (NSAIDs, Steroids) or Stress.

Chronic:
Drugs, H.pylori, Hypercalcaemia
Zollinger-Ellison - 1/3 have MEN-1. Parathyroid, pituitary and pancreas.

Zollinger-Ellison is too much gastrin - 30% have MEN-1.
Causes multiple gastroduodenal ulcers, diarrhoea, malabsorption.

Diagnosed with fasting gastrin and secretin.

418
Q

What is the conservative management of GORD?

A
  • Lose weight
  • Raise head of bed
  • Small regular meals at least 3hrs before bed
  • Stop smoking + decreased alcohol intake
  • Avoid hot/spicy food
  • Stop drugs: NSAIDs, Steroids, CCBs, Nitrates.
419
Q

What is the definition of constipation?

A
  • Infrequent bowel motions less than 3/week.
    OR
  • Less often than normal or with difficulty, straining or in pain.
420
Q

What is the definition of dyspepsia?

A

Non-specific group of symptoms:
- Epigastric discomfort
- Bloating
- Heartburn

421
Q

What is the epidemiology of Hereditary Haemochromaosis?

A
  • Prevalence: 1/3,000; 10% are carriers
  • Age of onset - 40-60 years (women later due to menses)
422
Q

What is the glasgow-blatchford bleeding score?

A

First assessment score (candidates for outpatient management)
- Haemoglobin <100 = 6 points.
- Blood urea (think about protein meal)
- Systolic blood pressure = <90 = 3 points.
- Pulse >100/min = 1 point.
- Presentation with melaena = 1 point.
- Presentation with syncope = 2 points.
- Hepatic disease = 2 points
- Cardiac failure = 2 points.
- Sex

423
Q

What is the history for an upper GI bleeding?

A
  • May have had previous bleeds
  • Known ulcers or dyspepsia
  • Dysphagia/Weight loss
  • Liver disease or known varices
  • Drugs and EtOH
  • Co-morbidities

Presenting complaint:
- haematemesis-bright red-highest mortality
- Coffee ground vomit-bleeding has ceased
- Melaena- acute UGIB or bleeding from R colon
- shock-tachy+hypotensive
If there is an iron deficiency anaemia
- Check FBC
- Then if low Hb and low MCV in non-pregnnacy person check the ferritin. Ferritin can be elevated in disease malignancy etc.
- If this is the case consider iron, TIBC, transferrin.

Once confirmed as iron deficiency anaemia = serum ferritin less than 15mcg/L.

424
Q

What is the investigations for alcoholic hepatitis?

A
  • Bloods: increased MCV, Increased GGT, AST: ALT >2, elevated bilirubin, decreased albumin, INR prolonged
  • Ascitic tap
  • Abdo US + PV duplex - fatty liver, hepatomegaly, cirrhosis
425
Q

What is the Kings College Hospital Criteria in Acute Failure?

A

Paracetamol-induced
- pH <7.3 24hr after ingestion.
Or all of:
PT >100s
Cr >300uM
Grade 3/4 encephalopathy

Non-paracetamol
PT >100s
Or 3 out of 5 of:
- Drug-induced
- Age <10 or >40
- >1 week from jaundice to encephalopathy
- PT >50s
- BR >300uM

426
Q

What is the Los Angeles classification for GORD?

A

Grade A = One or more mucosal breaks < 5mm in maximal length.

Grade B = Breaks >5 mm but without continuity across mucosal folds.

Grade C = Mucosal breaks between >2 mucosal folds = less than 75% of oesophageal circumference.

Grade D = Involving more than 75% of oesophageal circumference.

427
Q

What is the management of alcohol withdrawal?

A
  • Tapering regime of chlordiazepoxide PO 50-100mg /lorazepam IM
  • Thiamine
428
Q

What is the management of alcoholism?

A

Group therapy or self-help AA
- Naltrexone (50-100mg) OD: patients still drinking + Decreased pleasure.
- Acamprosate: 666mg TDS. Decreases cravings
- Disulfiram (500mg orally for 1 week then 250mg) : aversion therapy
- Baclofen: decreased cravings

429
Q

What is the management of C.diff Diarrhoea?

A

General
- STOP causative Abx
- Avoid antidiarrhoeals and opiates
- Precautions in the ward

Medical
- 1st line non-severe: metronidazole 500mg 3x OD.

  • 1st line severe: Vancomycin 125mg orally 4x daily. Up to 250mg QDS if no response. (Max = 500mg). 2nd line = Van 125mg
    May require urgent colectomy if toxic megacolon, Increased LDH, Deteriorating condition.

Repeated
- Repeat Vanc on a tapered and pulsed regimen.

430
Q

What is the management of cirrhosis?

A
  • General - Good nutrition,
  • ETOH abstinence: baclofen helps decreasing cravings
  • Colestyramine for pruritus
  • Screening: HCC -US and AFP every 6 months.
  • Oesophageal varices: endoscopy.
431
Q

What is the management of constipation < 3 months?

A

< 3 months?
- Treat underlying cause (medication induced/malignancy).
- Diet + lifestyle + laxatives or prunes/stool softeners.
- Consider Evacuation measures: Enemas, suppositories, macrogols, stimulant laxatives or disimpaction.

432
Q

What is the management of decompensation in cirrhosis?

A

Ascites: fluid and salt restrict, 1st line: spiro
2nd line: fruse, tap, daily weights.
Coagulopathy: vit K, platelets, FFP, blood.

Encephalopathy: avoid sedatives, lactulose ± enemas, rifaximin (used to reduce the recurrence of episodes of overt hepatic encephalopathy - use if refractory to lactulose). Neomycin is another medication licensed for use in hepatic encephalopathy.

Sepsis/SBP: Tazocin? Cefotaxime + Vanc
Hepatorenal syndrome: IV albumin + terlipressin

433
Q

What is the mechanism of action of bulking laxatives?

A

Increases faecal mass –> Increased peristalsis.

434
Q

What is the medical management of GORD?

A
  • OTC: Gaviscon, Mg Trisilicate
  • First line: Full dose PPI for 1-2 months (omeprazole 20mg/lansoprazole 30mg OD)
  • Second line: If no response double dose of PPI BD.
  • Third line: If no response: add H2RA such as ranitidine 300mg ON.
435
Q

What is the medical treatment for Wilson’s?

A

penicillamine (chelates copper) has been the traditional first-line treatmentTrientine and Zinc 4-6 months.

436
Q

What is the mnemonic for portal hypertension?

A

SAVE
- Splenomegaly
- Ascites
- Varices (Oesophageal varices, caput medusa, worsens existing piles)
- Encephalopathy

437
Q

What is the mnemonic to remember the causes of constipation?

A

OPENED IT
- Obstruction: Mechanical (adhesions, hernia, Ca inflammatory) or Pseudo-obstruction: post-op ileus.
- Pain - Anal Fissure or Proctalgia fugax (sporadic pain)
- Endocrine/Electrolytes: Endo (hypothyroidism), electrolytes (decreased Ca, Decreased K, Uraemia).
- Neuro: MS, Myelopathy (injury to the spinal cord), Cauda equina syndrome.
- Elderly
- Diet/Dehydration
- IBS
- Toxins: Opiods, Anti-mACh

438
Q

What is the MOA of Metoclopramide

A

Dopamine antagonist which may worsen symptoms in patients with Parkinson’s.

Metoclopramide is a D2 receptor antagonist* mainly used in the management of nausea. Other uses include:
gastro-oesophageal reflux disease
prokinetic action is useful in gastroparesis secondary to diabetic neuropathy
often combined with analgesics for the treatment of migraine (migraine attacks result in gastroparesis, slowing the absorption of analgesics)

Adverse effects
extrapyramidal effects: oculogyric crisis. This is particularly a problem in children and young adults
hyperprolactinaemia
tardive dyskinesia
parkinsonism

Metoclopramide should be avoided in bowel obstruction, but may be helpful in paralytic ileus.

439
Q

What is the Nazer score for Wilson’s?

A

The Nazer score is a triage tool on deciding who should receive a liver transplant and those who should receive anti-copper medical therapy. It is based on the severity of abnormality for each of:
- Serum AST
- Bilirubin
- Prothrombin time

0 = Bili <100, AST <100, PT <4

10-12 should be transplanted.
1 - 6 = Medical treatement
7-9 = Evaluated by clinical judgement

440
Q

What is the normal range for normal bilirubin?

A
  • Normal bilirubin = 3-17
441
Q

What is the pathology of gastric ulcers?

A
  • Lesser curve of gastric antrum (medial curve that is smaller)
  • Beware ulcers elsewhere (could be malignant)
442
Q

What is the pathophysiology of achalasia?

A
  • Degeneration of the myenteric plexus (Auerbach’s)
  • Decreased peristalsis
  • Lower oesophageal sphincter fails to relax
443
Q

What is the pathophysiology of ascites?

A
  • back-pressure –> Fluid exudation
  • decreased effective circulating volume –> RAS activation
  • (in cirrhosis): decreased albumin –> Decreased plasma oncotic pressure and aldosterone metabolism impaired.
444
Q

What is the pathophysiology of encephalopathy?

A
  • Decreased hepatic metabolic function
  • Diversion of toxins from liver directly into systemic system.
  • Ammonia accumulates and pass to brain where astrocytes clear it causing glutamate –> Glutamine
  • Increased glutamine –> osmotic imbalance –> cerebral oedema.
445
Q

What is the pathophysiology of GORD?

A

Dysfunction of the lower oesophageal sphincter –> leading to stomach acid reflux up the oesophagus –> oesophagitis.

446
Q

What is the pathophysiology of hepatorenal syndrome?

A
  • Cirrhosis –> Splanchnic arterial vasodilation –> effective hypovolaemia circulatory volume –> RAS activation –> Renal arterial vasoconstriction.
  • This persistent underfilling of renal circulation –> failure.

Systemic trop in PVR causes activation of sympathetic system and vasocontrictiors.

447
Q

What is the pathophysiology of Hereditary Haemochromaosis?

A

Inherited, mutisystem disorder resulting from abnormal iron metabolism

Increased intestinal Fe absoprtion (increased enterocyte DMT + decreased hepatocyte hepcidin) -> deposition in multiple organs

448
Q

What is the pathophysiology of Wilson’s disease?

A
  • Mutations of the Cu transporting ATPase
  • Impaired hepatocyte incorporation of Cu into caeruoloplasmin and excretion into bile
  • Cu accumulation in the liver and in other organs
449
Q

What is the presentation of a duodenal ulcer?

A

Epigastric pain: BEFORE meals, after meals and at NIGHT. Cause pen when hungry and are relieved by eating. Pyloric sphincter contracts when eating.
Relieved by: eating or milk

450
Q

What is the presentation of achalasia?

A

Dysphagia: Liquids and solids at the same time
Arching of neck/standing sitting up straight
Regurgitations
Substernal cramps
Wt Loss

451
Q

What is the presentation of alcoholic hepatitis?

A
  • Anorexia
  • Diarrhoea, vomiting,
  • Tender hepatomegaly,
  • Ascites
  • If severe = Jaundice, varices, encephalopathy
452
Q

What is the presentation of Budd-Chiari?

A

Triad
- RUQ pain: stretching of Glisson’s capsule
- Hepatomegaly
- Ascites: SAAG >1.1g/dL

Jaundice (and other features)

453
Q

What is the presentation of C.difficile? diarrhoea?

A
  • Can be asymptomatic
  • Mild Diarrhoea
  • Colitis w/o pseudomembanes OR
  • Pseudomembranous colitis
  • Fulminant colitis
  • May occur up to 2months after discontinuation of Abx
  • May be due to post-surgery where patients are given antibiotics
  • Clean surgery involving placement of prosthesis or implant
  • clean-contaminated surgery
  • contaminated surgery
  • Dirty or infected wounds.
454
Q

What is the presentation of coeliac’s GI malabsorption?

A

GI malabsorption: fatigue, weakness
- Carbs: N/V/D. Abdo distention + colic, Flatus, weight loss.
- Fat: Steatorrhoea, hyperoxaluria –> Renal stones
- Protein: protein-losing enteropathy
- Haematinic: decreased folate and fe –> Anaemia
- Vitamins: Vit D and ca –> bone pain, osteoporosis
Vit K –> Petechiae and increased INR
B2 (riboflavin)–> angular stomatitis
B1 and B6 –> Polyneuropathy

455
Q

What is the presentation of dysphagia?

A
  • Dysphagia for liquids and solids at start? Motility disorder
  • If not: solids > liquids: Stricture
  • Difficulty making swallowing: bulbar palsy
  • Odynophagia: Ca, oesphageal ulcer, spasm
  • Intermittent: oesophageal spasm
  • Constant and worsening: malignant stricture
  • Neck bulges or gurgles on drinking: pharyngeal pouch
456
Q

What is the presentation of GASTRIC ulcers?

A

Worse ON eating
Relieved by antacids
Weight Loss

457
Q

What is the presentation of the icteric phase in hepatitis?

A
  • Acute jaundice in A>B>C (99, 75, 25%)
  • Hepatitis (abdo pain, hepatomegaly, cholestasis: Dark urine, pale stools.
458
Q

What is the presentation of the prodromal phase of viral hepatitis? Which virus has a prodromal phase?

A

Seen in Hep A and B
- Flu-like, malaise, arthralgia, nausea.
- Distaste for cigarettes in Hep A.
- Ranged between 5-7 days.

459
Q

What is the rockall score?

A
  • done after endoscopy to determine risk of mortality
  • > 6 -surgery needed
  • <3 good prognosis
  • > 8 high risk of mortality
460
Q

What is the Rockall Score?

A
  • Prediction of re-bleeding and mortality
  • 40% of rebleeders die
  • Initial score pre-endosocopy
    –>
    Age (60-79 = +1) (>=80 = +2)
    Shock: BP (SBP <100=1) , Pulse (tachy = 1) ,
    Comorbidities (any = +2, if it is renal, liver or malignancy = +3)
    Diagnosis: Malignancy = +2, All other diagnoses = +1)
    Final score post-endoscopy
  • Final Dx + evidence of recent haemorrhage: Active bleeding, Visible vessel, Adherent clot.
  • Initial score >3 or final >6 are indications for surgery.
461
Q

What is the surgical management of GORD?

A

Nissen Fundoplication
- Indications: Need all 3 of
- Severe symptoms
- Refractory to medical therapy
- Confirmed reflux (pH monitoring)

462
Q

What is the underlying mechanism for hepatic encephalopathy?

A
  • Excessive nitrogen loading
  • Electrolyte or metabolic disturbances
  • Drugs and medication
  • Infection (pneumonia)
463
Q

What is Wilson’s?

A

AR disease - copper accumulation due to enzyme defect in biliary excretion of copper.
Hx: Hepatitis, cirrhosis, hepatic decompensation, psychiatric disorder.
Ix:
- Reduced serum caeruloplasmin
- Reduced serum copper (95% of plasma copper is carried by ceruloplasmin
- Increased 24hr urinary copper excretion
- slit lamp examination, liver biopsy.

464
Q

What key investigations is needed for encephalopathy?

A

increased plasma NH4

465
Q

What maintenance would you give to a patient after resus with a UGIB?

A
  • Crystalloid IV, with transfusion if necessary
  • Catheter + consider CVP (aim for >5cm H20) (central venous pressure)
  • Correct coagulopathy: vit K, FFP, platelets
  • Pabrinex if EtOH
  • Notify surgeons
466
Q

What questions can you ask in an alcoholism history?

A

CAGE
- Cut Down?
- Annoyed by people’s criticisms?
- Guilty about drinking?
- Eye opener?

467
Q

What symptoms alongside dyspepsia are red flags?

A

Urgent :

  1. dysphagia, all patients
  2. upper abdo mass consistent with stomach cancer. 3. Patients aged >55 years who’ve got weight loss and any of the following:
    - upper abdo pain,
    - reflux,
    - dyspepsia.

Non-urgent:

  1. Patients with haematemesis
  2. Patients aged >= 55 years who’ve got:
    • treatment-resistant dyspepsia or
    • upper abdominal pain with low haemoglobin levels or
    • raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
    • nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain

Managing patients who do not meet referral criteria:

This can be summarised at a step-wise approach

  1. Review medications for possible causes of dyspepsia
  2. Lifestyle advice
  3. Trial of full-dose proton pump inhibitor for one month OR a ‘test and treat’ approach for H. pylori

Ensure you rule out coronary artery disease.
Consider ECG, Serum Troponin, exercise stress testing.

ALARM: 
Anaemia/bleeding/Abdo Mass
Loss of Weight 
Anorexia (Appetite) 
Recent onset progressive symptoms
Melaena or haematemesis/vomiting
Swallowing Difficulty
468
Q

What would you see on examination of an Upper GI bleed?

A
  • CLD (jaundice, ascites, encephalopathy, clubbing, spider naevi, Dupuytren’s)
  • PR: Melaena
  • Signs of Shock
    Clammy, cool, CRT >2s
    Decreased BP (<100) or postural hypotension (>20 drop)
    Decreased urine output (<30ml/h)
    Tachycardia
    Decreased GCS.
469
Q

When to avoid 0.9% NS?

A

Uncompensated liver disease (makes ascites worse).
- Use blood or albumin for resus and 5% dextrose for maintenance.

470
Q

Where do you find duodenal ulcers?

A

First part of the duodenum (cap)
More common in males than females.

471
Q

Where is conjugated bilirubin secreted?

A

Into the bile, where it becomes urobilinogen (colourless)

472
Q

Which hepatitis notably has a chronic phase?

A

Hepatitis C and Childhood Hep B
- Can lead to cirrhosis and increased risk of HCC.

473
Q

Which IBD do you get strictures?

A

Crohns

474
Q

Which topical therapies are availabe for mild/moderate UC?

A
  • Mainly for left sided disease

For Mild-to-moderate
- Proctitis: suppositories. Topical, rectal aminosalicylates. For distal colitis rectal masalazine is better. If not improving add oral aminosalicylates. If still not improving give oral steroids.

  • More proximal disease: (proctosigmoiditis + left-sided ulcerative colitis)
    Rectal 5-ASA ± steroids (prednisolone or budesonide)
    If not working switch to high dose oral aminosalicylate or aminosalicylate + steroid.

Extensive (left, transverse and right)
- rectal Aminosalicylate + high-dose oral aminosalicylate.

475
Q

Wilson’s Disease epidemiology?

A

Prevalence: 3/100,000
Age: presents between childhood and 30 (never >56)
Genetics: AR, ATP7B gene on Chr 13

476
Q

RED FLAG SYX FOR 2WW FOR A CT SCAN FOR PANCREATIC CANCER

A

Age>60 w/ weight loss and

  • diarrhoea/constipation
  • Back or abdomen pain
  • N+V
  • New-onset diabetes

Age >40 with jaundice

477
Q

Symptoms of pancreatic cancer

A
  • epigastric pain that radiates to the back and is worse on lying down
  • weight loss/ anorexia
  • Steatorrhoea
  • acute pancreatitis
  • sudden onset DM (if endocrine tumour)
  • Courvoiseir’s law- presence of painless obstructive jaundice and palpable gall bladder that is not tender
  • Migratory thrombophlebitis (Trousseau’s sign)
478
Q

Which type of jaundice is associated with pancreatic cancer

A
  • Obstructive jaundice –> dark urine and pale stools
479
Q

S/E of Whipple’s procedures

A
  1. dumping syndrome

2. peptic ulcer disease

480
Q

Red flag Syx that need 2ww for oesophageal cancer for an endoscopy

A
  1. AGE>55 with weight loss and
    - dyspepsia
    - epigastric pain
    - reflux
    - anaemia
  2. Dysphagia
  3. Dyspepsia in patients with family hx of oesophageal dyspepsia
481
Q

Non-urgent referral for endoscopy for oesophageal cancer

A
  • patients with haematemesis
482
Q

SCC VS Adenocarcinoma for oesophageal cancer

A
483
Q

Plummer Vinson syndrome

A
  1. IDA
  2. Dysphagia
  3. Oesophageal webs
484
Q

Diagnosis of oesophageal cancer

A

Diagnosis
- Upper GI endoscopy is the first line test. Gold standard to take biopsy.

  • Contrast swallow may be of benefit in classifying benign motility disorders but has no place in the assessment of tumours ( can show apple core stricture)
  • Staging is initially undertaken with CT TAP
    - If overt metastatic disease is identified using this modality then further complex imaging is unnecessary
    - If CT does not show metastatic disease, then local stage may be more accurately assessed by use of endoscopic ultrasound (EUS)
    - Staging laparoscopy is performed to detect occult peritoneal disease.
    - PET CT is performed in those with negative laparoscopy.
485
Q

TNM staging for oesophageal cancer

A
486
Q

Tx for oesophageal cancer

A
  • early stage–> endoscopic mucosal resection
  • Locally advanced –> Ivor Lewis oesophagectomy(distal tumour), McKeown (Proximal tumour), transhiatal oesophagectomy (Distal)
  • Adjuvant chemo
  • Palliative –> stenting+- radiotherapy/chemoradiotherapy such as platinum based agents (if hER2+ve can give trastuzumab)
487
Q

S/E of Oesophagectomy

A
  • Anastomotic leak: the single greatest surgical challenge. A leak may result in mediastinitis
  • Recurrent laryngeal nerve injury: proximity of this nerve to the oesophagus places it at risk, either due to invasion of the tumour or iatrogenic injury
  • Delayed gastric emptying: thought to be caused by bilateral vagotomy during the procedure which impairs gastric motility
  • Ivor-lewis oesophagectomy: potentially catastrophic if an anastomotic leak occurs, due to leakage of contents into the thorax (mediastinitis)
  • McKeown oesophagectomy: the complications of a leak are less severe as the anastomosis is in the neck so it does not result in mediastinitis
488
Q

Most common type of gastric cancer

A

adenocarcinoma

  • 2 types: intestinal and diffuse
489
Q

What is the typical pathology finding associated with diffuse adenocarcinomas of the stomach?

A
  • signet ring sign
490
Q

Urgent referral for gastric cancer

A
  1. upper abdo mass
  2. Dysphagia
  3. over 55 with weight loss AND upper abdomen pain/reflux/dyspepsia
491
Q

Non-urgent referral for gastric cancer

A
  • haematemesis
  • > =55 with
    -Treatment-resistant dyspepsia,
    or
    -Upper abdo pain with low hb levels,
    or
    • Raised platelet count with any of the following:
      Nausea,
      Vomiting,
      Weight loss,
      Reflux,
      Dyspepsia,
      Upper abdominal pain,
      or
      -Nausea or vomiting with any of the following:
      Weight loss.
      Reflux.
      Dyspepsia.
      Upper abdominal pain.
492
Q

Signs and Syx of Gastric cancer

A
493
Q

Spread of the gastric cancer

A
  • W/in the stomach –> linitis plastica
  • direct invasion–> pancreas
  • Lymphatic –> Virchows
  • Blood –> Liver, lung
  • Transcoloemic ( ovaries –> Krukenburg tumour or Sister Mary Joseph nodules (umbilical mets))
494
Q

Gastric carcinoma Investigations

A

1.

GASTRO (5 decks)

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