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Year 3 > GI > Flashcards

GI Flashcards

1
Q

what is proctitis

A

where inflammation is limited to the rectum

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2
Q

microscopic aetiology of UC

A

involves only the mucosa
formation of crypt abscesses and a coexisting depletion of goblet mucin cells (they secrete mucin and create protective mucus layer)

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3
Q

2 classifications of UC

A

left sided colitis -> inflammation up to the splenic flexure
extensive colitis -> inflammation beyond the splenic flexure

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4
Q

Key diagnostic factors of UC

A

Presence of risk factors (FH of IBD, being HLA-B27 positive)
Rectal bleeding
Diarrhoea
Blood in stool

Other diagnostic factors:
abdominal pain
arthritis
malnutrition
abdominal tenderness

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5
Q

Describe mild UC rectal bleeding

A

confined to the rectum (proctitis) or rectosigmoid (distal colitis) area, often have insidious presentation with intermittent rectal bleeding associated with the passage of mucus and development of diarrhoea with <4 loose stools a day

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6
Q

what is tenesmus

A

feeling like you need to pass stools although your bowel is empty

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7
Q

First order investigations for UC

A
  • Stool studies for infective pathogens
    • Look for infective cause as patients with IBD are higher risk of infection
    • Result → Negative culture and C. diff toxins A and B; WBC present
  • Faecal calprotectin
    • Elevated if there is bowel inflammation and correlates with endoscopic and histological gradings of disease severity
  • FBC
    • May show leukocytosis, thrombocytosis and anaemia
      • Leuko → because of inflammation
      • Anaemia → because of bleeding
  • Comprehensive metabolic panel (including LFTs)
    • LFTs should be checked every 6-12 months to check for primary sclerosing cholangitis
    • Result → hypokalaemic metabolic acidosis; elevated sodium and urea; elevated alkaline phosphatase, bilirubin, aspartate aminotransferase; hypoalbuminaemia
    • Inflammation reduces the absorption of sodium, chloride, and calcium
  • ESR
    • Variable degree of elevation (>30mm/hour is suggestive of a severe flare up)
  • CRP
    • Persistently raised CRP > 45mg/L during a severe flare up and following 3 days of IV hydrocortisone suggests that unless treatment is changed, surgery may be necessary
  • Plain abdominal radiograph
    • Ulcerated colon usually contains no solid faeces
    • Result → dilated loops of air-fluid secondary to ileus; free air is consistent with perforation
  • Flexible sigmoidoscopy
    • does not require sedation
    • Can be done during surgery
    • Findings → same as in colonoscopy, examination is limited to distal colon
  • Colonoscopy
    • Requires full bowel preparation and sedation
    • Used in patients with UC who are not responding well to treatment to rule out infections and to evaluate need for surgery
    • result → rectal involvement, continuous uniform involvement, loss of vascular marking, diffuse erythema, mucosal granularity, fistulas (rarely seen), normal terminal ileum
  • Biopsies
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8
Q

Some differentials to consider with someone presenting with UC

A
  • Crohns disease
    • Similar signs and symptoms to those with UC
    • Often has perianal involvement, rectal sparing, and a tendency to form fistulae
    • Investigations → distinguished from UC by inflammation that extends deep to the muscularis mucosal, presence of granulomata, and relative lack of depletion of goblet cells
      • Crohns can often affect upper GI tract including the small bowel
  • Infectious colitis
    • History of recent exposure or travel
    • Usually self - limiting (resolves without treatment)
  • Diverticulitis
    • Signs/symptoms → older age, fever, nausea, diarrhoea, or constipation
    • Investigations → Leukocytosis, CT scan
      → CT scan can show evidence of colitis which is different from diverticulitis→ sigmoidoscopy and barium studies are contraindicated in acute diverticulitis because of perforation
  • IBS
    • Patients may have an normal laboratory results and normal levels of inflammatory markers
    • Endoscopy and biopsy are normal
  • Mesenteric ischaemia
    • Older age, history of CVS disease
    • CT scan/endoscopy → typical finding of thickening of bowel wall in segmental pattern
    • Endoscopic findings → pale mucosa with petechial bleeding. Bluish haemorrhagic nodules
  • Vasculitis
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9
Q

Treatment of acute severe UC

A
  • Hospital admission and IV corticosteroid
    • Plus: Supportive measures
      • Such as blood transfusions, fluids and electrolyte replacement
  • Ciclosporin or infliximab
    • If patients do not respond to corticosteroid in 3 days
  • Surgery
    • Any patient with intractable symptoms or intolerable medicine adverse side effects
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10
Q

Treatment of moderate to severe UC

A
  • Oral corticosteroid
    • Prenisolone or budesonide
  • Biological agent
    • infliximab, (anything ending with mab)
  • CONSIDER: immunomodulator
    • azathioprine or methotrexate
  • 2nd line: Tofaitnib
  • 3rd line: colectomy
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11
Q

Treatment of mild UC

A

Proctitis → topical (rectal) aminosalicylate
- Mezalasine rectal

Left-sided colitis → Oral aminosalicylate and topical aminosalicylate
- consider oral budesonide

Extensive colitis → Oral aminosalicylate (mezalasine, anything ending with zine)
- Consider oral corticosteroid (prednisolone)

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12
Q

Complications of UC

A
  • Colorectal cancer
  • Osteoporosis
    • Because of prolonged corticosteroid use
  • Primary sclerosing cholangitis
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13
Q

What is Bacillus cereus?

A

Gram positive rod
commonly associated with consumption of reheated rice contaminated with its toxin
symptomatic management is carried out

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14
Q

What is Campylobacter jejuni

A

gram negative
can cause bloody diarrhoea, and treatment is usually symptomatic

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15
Q

What is Escherichia coli

A

Gram negative
diarrhoea can range from mild to bloody but management is exclusively supportive

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16
Q

What is Giardia lamblia

A

a parasite
causes smelly diarrhoea and cramps

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17
Q

A 27-year-old man with a 3-month history of rectal bleeding and diarrhoea is referred for evaluation. Laboratory tests show mild anaemia, a slightly elevated erythrocyte sedimentation rate, and the presence of white blood cells in stool. Stool culture is negative. Colonoscopy shows continuous active inflammation with loss of vascular pattern and friability from the anal verge up to 35 cm, with a sharp cut-off. The colonic mucosa above 35 cm appears normal, as does the terminal ileum. Biopsy specimens show active chronic colitis.

A

Ulcerative colitis

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18
Q

Complication of coeliac disease?
anal cancer
epilepsy
hyposplenism
pyoderma gangrenosum
toxic megacolon

A

Hyposplenism is a complication of coeliac disease. Hyposplenism is clinically significant as around 1/3 of people with coeliac disease will develop it. Patients with this complication are less equipped to combat infections, leaving them at greater risk of an overwhelming infection which may result in morbidity/mortality.

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19
Q

What is an adhesion

A

Bands of scar like tissue that form between two surfaces inside the body and cause them to stick together

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20
Q

What is a stricture

A

an area of narrowing in the intestine C

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21
Q

A 25-year-old white man presents to his general practitioner with cramping abdominal pain for 2 days. He reports having loose stools and losing 6.8 kg over a 3-month duration. He also reports increased fatigue. On physical examination, his temperature is 37.6°C (99.6°F). Other vital signs are within normal limits. Abdomen is soft with normal bowel sounds and moderate tenderness in the right lower quadrant, without guarding or rigidity. Rectal examination is normal and the stool is guaiac positive. The rest of the examination is unremarkable.

A

Crohns disease

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22
Q

A 16-year-old girl presents to emergency care with perianal pain and discharge. She reports a 2-year history of intermittent bloody diarrhoea with nocturnal symptoms. On examination, she is apyrexial with normal vital signs. Her abdomen is soft and slightly tender on palpation in the left lower quadrant. Rectal examination is difficult to perform due to pain, but an area of erythematous swelling is visible close to the anal margin, discharging watery pus from its apex. Several anal tags are also present.

A

Crohns disease

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23
Q

Management of acute admission peptic ulcer disease

A

ABC approach as with any upper GI haemorrhage
IV PPI
First-line treatment is endoscopic intervention
if this fails then: urgent interventional angiography with transarterial embolisation or surgery

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24
Q

Retroperitoneal structures

A

Duodenum (2nd, 3rd and 4th parts)
Ascending colon
Descending colon
Pancreas
Kidneys
Ureters
Aorta
Inferior Vena Cava

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25
Q

Intraperitoneal structures

A

Stomach
duodenum (1st part)
Jejunum
Ileum
transverse colon
Sigmoid colon

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26
Q

Most common cause of small bowel obstructions

A

adhesions

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27
Q

What would an abdominal radiograph show in bowel perforation

A

signs of penumoperitoneum
classically the double wall/ Riglers sign

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28
Q

What bowel obstruction is diverticular disease most likely to cause

A

large bowel obstruction

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29
Q

Features of small bowel obstruction

A

diffuse, central abdominal pain
nausea and vomiting (typically bilious vomiting - yellow greenish)
constipation with complete obstruction and lack of flatulence
abdominal distention may be apparent
tinkling bowel sounds in early obstruction

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30
Q

Abdominal X-ray findings in small bowel obstruction

A

usually first line in suspected small bowel obstruction
distended bowel loops with fluid levels
(consider dilated if >3mm diameter)

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31
Q

Management of small bowel obstruction

A

Initial steps:
NBM
IV fluids
Nasogastric tube with free drainage
(some settle with conservative management but otherwise will require surgery_

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32
Q

What deficiencies is coeliac disease associated with

A

iron
folate
B12

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33
Q

First line test for coeliac disease

A

Anti-TTG

anti-TTG antibodies are IgA, so if the patient has an IgA deficiency they can appear falsely low or normal. If anti-TTG levels are low or normal and IgA levels are low, we should retest the patient but with the IgG version of anti-TTG.

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34
Q

what is coeliac disease

A

autoimmune condition caused by sensitivity to protein gluten

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35
Q

Conditions associated with coeliac disease

A

dermatitis herpetiformis (cluster of itchy bumps that can be easily confused with acne or eczema) and autoimmune disorders (T1DM and autoimmune hepatitis)
Autoimmune thyroid disease
IBS

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36
Q

Signs and symptoms of coeliac disease

A

-chronic or intermittent diarrhoea
-failure to thrive (children)
-persistent or unexplained GI symptoms including nausea and vomiting
-prolonged fatigue
-recurrent abdominal pain, cramping or distention
-sudden or unexplained weight loss
-unexplained iron-deficiency anaemia or other unspecified anaemia

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37
Q

Complications of coeliac disease

A

Anaemia (iron, folate, B12)
Hypersplenism
osteoporosis/osteomalacia
lactose intolerance
sub fertility
rare: oesophageal cancer, other malignancies

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38
Q

What does hormone gastrin do

A

increases acid secretions by gastric parietal cells, pepsinogen and IF secretion
increases gastric motility , stimulates parietal cell maturation

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39
Q

Source of Gastrin hormone

A

G cells in antrum of the stomach

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40
Q

Stimulus for gastrin hormone

A

distention of the stomach, vagus nerve (mediated by gastrin-releasing peptide), luminal peptides/amino acids

inhibited by: low antral pH , somatostatin

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41
Q

Source of CCK hormone

A

I cells in upper small intestine

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42
Q

Stimulus of CCK hormone

A

partially digested proteins and triglycerides

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43
Q

Action of CCK hormones

A

Increases secretion of enzyme rich fluid from pancreas
contraction of the gallbladder and relaxation of the sphincter of Oddi
Decreases gastric emptying
Trophic effect
induces satiety (feeling full)

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44
Q

Source of Secretin hormone

A

S cells in upper small intestine

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45
Q

Stimulus of secretin hormone

A

acidic chyme
fatty acids

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46
Q

Action of secretin hormone

A

Increases secretions of bicarbonate rich fluid from pancreas and hepatic duct cells
decreases gastric acid secretion
trophic effect on pancreatic acinar cells

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47
Q

Source of VIP hormone

A

Small intestine
pancreas

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48
Q

Stimulus of VIP hormone

A

neural

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49
Q

Action of VIP hormone

A

Stimulates secretion by pancreas and intestines
Inhibits acid secretion

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50
Q

Source of somatostatin

A

D cells in the pancreas and stomach

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51
Q

Stimulus fo somatostatin

A

Fat
bile salts
glucose in the intestinal lumen

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52
Q

Action of somatostatin

A

Decreases acid and pepsin secretion
decreases gastrin secretion
decreases pancreatic enzyme secretion
decreases insulin and glucagon secretion
inhibits trophic effects of gastrin
stimulates gastric mucous production

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53
Q

What is primary biliary cirrhosis

A

chronic liver disorder typically seen in middle aged females
thought to be an autoimmune condition

Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis

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54
Q

Condition associations with primary biliary cirrhosis

A

Sjorgens syndrome
Rheumatoid arthritis
Systemic sclerosis
Thyroid disease

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55
Q

Clinical features of primary biliary Cirrhosis

A

Early: may be asymptomatic (raised ALP on LFTs) or fatigue, pruritus
Cholestatic jaundice
Hyperpigmentation especially on pressure points
Around 10% have RUQ pain
xanthelesma, xanthomata
Also: clubbing, hepatosplenomegaly
Late: may progress to liver failue

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56
Q

How to diagnose PBC

A

Immunology:
anti-mitochondrial antibodies (AMA)
Smooth muscle antibodies
raised serum IgM

Imaging:
Usually MRCP to exclude extra hepatic biliary obstruction

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57
Q

Management of PBC

A

First line : Ursodeoxycholic acid
(slows disease progression and improves symptoms)
Pruritus: cholestryamine
fat soluble vitamin supplements
liver transplantation: If bilirubin > 100

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58
Q

Complications of PBC

A

Cirrhosis -> portal hypertension -> ascites, variceal haemorrhage
osteomalacia/osteoporosis
20 fold risk of hepatocellular carcinoma

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59
Q

Hepatomegaly with a history of malignancy what do you think?

A

Think liver metastasis

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60
Q

Common causes of hepatomegaly

A

Cirrhosis if early disease associated with a non tender firm liver (later disease the liver reduces in size)

Malignancy: metastatic spread or primary hepatoma, associated with a hard irregular liver edge

Right heart failure: firm, smooth, tender liver edge, may be pulsatile

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61
Q

what anti-emetic do you avoid in bowel obstruction

A

metoclopramide
(it promotes gastric emptying

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62
Q

What is Budd-Chiari syndrome also known as

A

hepatic vein thrombosis

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63
Q

Features of Budd-chiari syndrome

A

classically a triad of
Abdominal pain - severe and sudden onset
Ascites -> abdominal distention
tender hepatomegaly

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64
Q

With GI bleeds what does high urea indicate

A

indicates that its an upper GI bleed rather than a lower one

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65
Q

Oesophageal causes of Upper GI bleed

A

Oesophageal varices
Oesophagitis
Cancer
Mallory weiss tear

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66
Q

Gastric causes of GI bleed

A

Gastric ulcer
Gastric cancer
Dieulafoy lesion
Diffuse erosive gastritis

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67
Q

Duodenal causes of upper GI bleed

A

Duodenal ulcer
Aorto-enteric fistula

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68
Q

Management of variceal bleed

A

Terlipressin and prophylactic antibiotics should be given at presentation
Band litigation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures

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69
Q

What is the blatchford score used for

A

risk scoring tool used to predict the need to treat patients presenting with upper gastrointestinal bleeding.

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70
Q

What does the gastroduodenal artery supply

A

pylorus of the stomach
superior part of duodenum
head of the pancreas

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71
Q

What does the inferior mesenteric artery supply

A

hindgut, comprising the distal third of the colon and the rectum superior to the pectinate line

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72
Q

First line antibiotic in patients with C. Diff infection

A

vancomycin

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73
Q

Risk factors for developing C.diff

A

Antibiotics
Proton pump inhibitors

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74
Q

Features of a C.diff infection

A

diarrhoea
abdominal pain
raised WCC (characteristic of infection)

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75
Q

What is Gilbert’s syndrome

A

autosomal recessive condition of defective bilirubin conjugation due to deficiency of UDP glucuronosyltransferase

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76
Q

Features of Gilberts syndrome

A

Unconjugated hyperbilirubinaemia (i.e. not in urine)
Jaundice only to be seen during incurrent illness, exercise or fasting

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77
Q

Investigation and management of Gilberts syndrome

A

investigation -> rise in bilirubin following prolonged fasting or IV nicotinic acid
No treatment required

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78
Q

Strongest risk factor for development of Barrets oesophagus

A

GORD

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79
Q

What is Barrets oesophagus

A

Metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium

Increased risk of oesophageal adenocarcinoma 50-100 fold

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80
Q

Histological features of barrets oesophagus

A

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

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81
Q

Risk factors for Barrets oesophagus

A

GORD (single strongest factor)
Male gender (7:1 ratio)
Smoking
Central obesity

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82
Q

Management of Barrets oesophagus

A

Endoscopic surveillance and biopsies (every 3-5 years)

High dose PPI

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83
Q

What is acute pancreatitis usually due to?

A

alcohol and/or gallstones

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84
Q

Features of acute pancreatitis

A

Severe epigastric pain that may radiate through to the back
Vomiting is common
Examination may reveal epigastric tenderness, ileus and low grade fever
Periumbilical discolouration (cullens sign) and flank discolouration (grey turners sign) is described but rare

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85
Q

Investigations for acute pancreatitis

A

Amylase -> raised in 75% patients >3 times the normal limit
levels do not correlate with disease severity

lipase -> More sensitive and specific than amylase
has a longer half life so may be useful for later presentations

Imaging -> U/S to asses for aetiology
diagnosis can be made without if characteristic pain and amylase/lipase >3 times normal limit

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86
Q

Reasons why serum amylase could be high

A

Pancreatitis
Pancreatic psuedocyst
mesenteric infarct
perforated viscus
acute cholecystitis
DKA

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87
Q

How to diagnose IBS

A

has had the following for the past 6 months:
Abdominal pain and/or
Bloating and/or
Change in bowel habit

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88
Q

Type A gastritis

A

Autoimmune
Circulating antibodies to parietal cells, causes reduction in cell mass and hypochlorhydria
loss of parietal cells = loss of intrinsic factor = B12 malabsorption
Absence of antral involvement
Hypochlorhydria causes elevated gastrin levels- stimulating enterochromaffin cells and adenomas may form

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89
Q

Type B gastritis

A

Antral gastritis
Associated with infection with helicobacter pylori infection
Intestinal metaplasia may occur in stomach and require surveillance endoscopy
Peptic ulceration may occur

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90
Q

Reflux gastritis features

A

Bile refluxes into stomach, either post surgical or due to failure of pyloric function
Histologically, evidence of chronic inflammation, and foveolar hyperplasia
May respond to therapy with prokinetics

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91
Q

Erosive gastritis

A

Agents disrupt the gastric mucosal barrier
Most commonly due to NSAIDs and alcohol
With NSAIDs the effects occur secondary to COX 1 inhibition

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92
Q

Stress ulceration features

A

This occurs as a result of mucosal ischaemia during hypotension or hypovolaemia
The stomach is the most sensitive organ in the GI tract to ischaemia following hypovolaemia
Diffuse ulceration may occur
Prophylaxis with acid lowering therapy and sucralfate may minimise complications

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93
Q

Menetreirs disease features

A

Gross hypertrophy of the gastric mucosal folds, excessive mucous production and hypochlorhydria
Pre malignant condition

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94
Q

Risk factors for gastric cancer

A

H pylori (triggers inflammation of the mucosa -> atrophy and intestinal metaplasia
Atrophic gastritis
Diet (salt and salt-preserved foods, nitrates)
Smoking
blood group

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95
Q

Features of gastric cancer

A

Abdominal pain (typically vague, epigastric pain, may present as dyspepsia)
Weight loss and anorexia
Nausea and vomiting
Dysphagia (if cancer arises above proximal stomach)
Overt upper GI bleeding (rare)
If lymphatic spread then: Virchows node (left supraclavicular lymph node) and Sister Mary Joseph nodule (Periumbilical nodule)

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96
Q

Investigations for gastric cancer

A

Diagnosis: endoscopy with biopsy (Signet ring cells)
Staging: CT

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97
Q

Management of gastric cancer

A

Surgical options depend on extent and side but:
endoscopic mucosal resection
partial gastrectomy
total gastrectomy

and chemotherapy

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98
Q

GET SMASHED pneumonic for pancreatitis

A

Gallstones
Ethanol
Trauma

Steroids
Mumps
Autoimmune (e.g. polyarteritis nodosa)
Scorpion venom
Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
ERCP
Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)

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99
Q

Risk factors for femoral hernias

A

Female gender and pregnancy
Increasing age
Increased abdominal pressure -> heavy lifting, chronic cough

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100
Q

Features of a femoral hernia

A

Lump within the groin that is usually mild painful
Femoral hernias are inferolateral to the pubic tubercle
typically non-reducible though can be
Cough impulse is normally absent because of small size of femoral ring

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101
Q

Features of Crohns disease (in comparison to UC)

A

diarrhoea usually non-bloody
weight loss more prominent
Upper GI symptoms: mouth ulcers, perianal disease
abdominal mass usually palpable in RIF

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102
Q

Features of UC (in comparison to crohns)

A

Bloody diarrhoea more common
Abdominal tenderness in LLQ
tenesmus

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103
Q

Extra intestinal manifestations of crohns disease

A

gallstones are more common secondary to reduced bile acid reabsorption
(oxalate renal stones)

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104
Q

Extra intestinal manifestations of UC

A

Primary sclerosing cholangitis more common

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105
Q

Complications of Crohns disease

A

obstruction, fistula, colorectal cancer

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106
Q

complications of UC

A

risk of colorectal cancer higher in UC than in Crohns

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107
Q

Difference in pathology between Crohns and UC

A

Crohns: lesions can be seen anywhere from mouth to anus - skip lesions may be present

UC : inflammation always starts at rectum and never spreads beyond ileocaecal valve (continuous disease)

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108
Q

Endoscopy for Crohns

A

deep ulcers
skip lesions
cobble-stone appearance

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109
Q

Endoscopy for UC

A

Widespread ulceration with preservation of adjacent mucosa which has appearance of polyps (pseudo polyps)

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110
Q

Describe what type of bacteria C.diff is

A

gram positive anaerobic bacillus

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111
Q

What is Murphys sign

A

inspiratory arrest upon palpation of RUQ

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112
Q

3Fs for developing gallstones

A

Fat
Female
Forty

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113
Q

Features of acute cholecystitis

A

RUQ pain - may radiate to right shoulder
Fever and signs of systemic upset
Murphys sign one examination
LFTs typically normal - deranged if Mirizzi syndrome (gallstone impacted in the distal cystic duct causing extrinsic compression fo the common bile duct)

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114
Q

Investigation for acute cholecystitis

A

US first line investigation

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115
Q

Treatment for acute cholecystitis

A

IV antibiotics ( penicillins, cephalosporins, or fluoroquinolones.)
Early laparoscopic cholecystectomy within 1 week of diagnosis

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116
Q

Difference in location between femoral and inguinal hernia

A

inguinal = superior and medial to pubic tubercle
femoral = inferior and lateral to pubic tubercle

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117
Q

What is Oesophageal candidiasis characterised by

A

white spots in oropharynx with extension into the oesophagus

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118
Q

What is oesophageal candidiasis associated with

A

broad spectrum antibiotic usage
immunosuppression
immunological disorders

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119
Q

glasgow prognostic score used for?

A

severity of acute pancreatitis
Remember PANCREAS
P - PaO2 <8kpa
A - Age > 55
N -Neutrophils (WBC >15)
C - calcium <2
R- uRea >16
E - Enzymes (LDH>600 or AST/ALT >200)
A - albumin <32
S- sugar (glucose >10)

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120
Q

What is a Spontaneous bacterial peritonitis (SBP)

A

a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis.

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121
Q

Most common organism found on an ascitic fluid culture (drained from ascites) with someone who has spontaneous bacterial peritonitis (SBP)

A

E. coli

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122
Q

features of spontaneous bacterial peritonitis

A

ascites
abdominal pain
fever

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123
Q

How to diagnose spontaneous bacterial peritonitis

A

Paracentisis -> neutrophil count >250cells/ul

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124
Q

Management of spontaneous bacterial peritonitis

A

IV cefotaxime

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125
Q

Different types of laxatives

A

osmotic laxatives
stimulant
bulk-forming
faecal softners

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126
Q

Examples of osmotic laxatives

A

lactulose, macrogols, and rectal phosphate

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127
Q

Examples of stimulant laxatives

A

Senna, docusate, bisocodyl, and glycerol
co-danthramer should only be prescribed to palliative patients due to its carcinogenic potential

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128
Q

Examples of bulk-forming laxatives

A

examples include ispaghula husk and methylcellulose

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129
Q

Example of faecal softner laxatives

A

include arachis oil enemas
not commonly prescribed

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130
Q

Genetic causes of chronic pancreatitis

A

cystic fibrosis
hereditary haemachromatosis

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131
Q

Features of chronic pancreatitis

A

pain is typically worse 15 to 30 minutes following a meal
steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
diabetes mellitus develops in the majority of patients. It typically occurs more than 20 years after symptom begin

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132
Q

Investigations for chronic pancreatitis

A

abdominal x-ray shows pancreatic calcification in 30% of cases
CT is more sensitive at detecting pancreatic calcification. Sensitivity is 80%, specificity is 85%
functional tests: faecal elastase may be used to assess exocrine function if imaging inconclusive

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133
Q

Management of chronic pancreatitis

A

pancreatic enzyme supplements
analgesia
antioxidants: limited evidence base - one study suggests benefit in early disease

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134
Q

What is Wilsons disease

A

Wilson’s disease is an autosomal recessive disorder characterised by excessive copper deposition in the tissues. Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion. Wilson’s disease is caused by a defect in the ATP7B gene located on chromosome 13.

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135
Q

Features of Wilsons disease

A

result from excessive copper deposition in the tissues, especially the brain, liver and cornea:
Liver -> hepatitis, cirrhosis
Neuro -> basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus
speech, behavioural and psychiatric problems are often the first manifestations
also: asterixis, chorea, dementia, parkinsonism
eyes -> Kayser-Fleischer rings
green-brown rings in the periphery of the iris
due to copper accumulation in Descemet membrane
present in around 50% of patients with isolated hepatic Wilson’s disease and 90% who have neurological involvement
other -> renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails

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136
Q

Investigations for Wilsons disease

A

slit lamp examination for Kayser-Fleischer rings
reduced serum caeruloplasmin
reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
free (non-ceruloplasmin-bound) serum copper is increased
increased 24hr urinary copper excretion
the diagnosis is confirmed by genetic analysis of the ATP7B gene

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137
Q

Management of Wilsons disease

A

penicillamine (chelates copper) has been the traditional first-line treatment

trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future

tetrathiomolybdate is a newer agent that is currently under investigation

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138
Q

what does a serum-ascites albumin gradient (SAAG) > 11g/L indicate

A

indicates portal hypertension

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139
Q

What area is most likely affected in ischaemic colitis

A

the splenic flexure

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140
Q

Common predisposing factors in bowel ischeamia

A

-increasing age
-AF(particularly for mesenteric ischamia)
-Other causes of emboli: endocarditis, malignancy
-CVS risk factors: smoking, HTN, diabetes
-cocaine

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141
Q

Common features of bowel ischaemia

A

-abdominal pain
-rectal bleeding
-diarrhoea
-fever

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142
Q

What structure does a patients bowel have to travel through to be classed as a direct inguinal hernia

A

Hesselbachs triangle

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143
Q

Investigations for carcinoid tumours?

A

Urinary 5-HIAA
Plasma chromogranin A y

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144
Q

What is pernicious anaemia

A

an autoimmune disease caused by antibodies to intrinsic factor +/- gastric parietal cells
Autoimmune destruction of gastric parietal cells take place

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145
Q

What is B12 important in

A

production of blood cells and myelination of nerves -> megaloblastic anaemia and neuropathy

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146
Q

Pernicious anaemia risk factors

A

-More common in females
-Develops middle-old age
-Autoimmune disorders: vitiligo, thyroid disease, T1DM, Addisons, rheumatoid
-More common if blood group A

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147
Q

Features of pernicious anaemia

A
  • anaemia features:
    lethargy
    pallor
    dyspnoea
    neurological features
    -peripheral neuropathy: ‘pins and needles’, numbness. Typically symmetrical and affects the legs more than the arms
    subacute combined degeneration of the spinal cord: progressive weakness, ataxia and paresthesias that may progress to spasticity and paraplegia
    neuropsychiatric features: memory loss, poor concentration, confusion, depression, irritabiltiy
    -other features
    mild jaundice: combined with pallor results in a ‘lemon tinge’
    glossitis → sore tongue
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148
Q

Investigations for pernicious anaemia

A

FBC:
-Macrocytic anaemia
-Hypersegmented polymorphs on blood film
-Low WCC and platelets can be seen
Vit B12 and folate levels
Antibodies:
anti-intrinsic antibodies
anti gastric parietal cell antibodies (not often used clinically)

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149
Q

Management of pernicious anaemia

A

vitamin B12 replacement
usually given intramuscularly
no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections
more frequent doses are given for patients with neurological features

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150
Q

Contents of inguinal canal in men and women

A

men - spermatic cord and ilioinguinal nerve
women - round ligament of uterus and ilioinguinal nerve

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151
Q

sentinel lymph node of the gall bladder

A

Lunds node (cystic lymph node)

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152
Q

Which artery supplies the posterior part of the stomach

A

Splenic artery

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153
Q

What is the 1st part of the duodenum known for (pathologically)

A

peptic ulcers

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154
Q

What can the 3rd part of the duodenum be affected by

A

by superior mesenteric artery syndrome, where the duodenum is compressed between the SMA and the aorta, often in cases of reduced body fat.

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155
Q

What is the distal 1/3 of the transverse colon supplied by

A

Inferior mesenteric artery

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156
Q

What does GI mucosa contain

A

muscularis mucosae
lamina propia

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157
Q

What does the GI muscularis externa contain

A

Auerbach’s (myenteric) plexus

158
Q

Quick comparison between ascending cholangitis and biliary colic

A

ascending cholangitis -> RUQ pain, fever, jaundice
Biliary colic -> female, middle-aged, episodic RUQ pain

159
Q

Infective causes of acute abdominal pain

A

gastroenteritis
appendicitis
diverticulitis
pyelonephritis
cholecystitis
cholangitis
pelvic inflammatory disease
hepatitis
pneumonia

160
Q

Inflammatory causes of acute abdominal pain

A

pancreatitis
peptic ulcer disease

161
Q

Vascular causes of acute abdominal pain

A

ruptured abdominal aortic aneurysm
mesenteric ischaemia
myocardial infarction

162
Q

Traumatic causes of acute abdominal pain

A

ruptured spleen
perforated viscus (e.g. oesophagus, stomach, bowel)

163
Q

Metabolic causes of acute abdominal pain

A

renal/ureteric stone
diabetic ketoacidosis

164
Q

Describe mechanism of oemeprazole

A

Irreversible blockade of H+/K+ ATPase

165
Q

Examples of Antagonist of the P2Y12 adenosine diphosphate (ADP) receptor

A

clopidogrel
prasugrel
ticagrelor
ticlopidine

166
Q

Foregut structures and blood supply

A

structure : mouth to proximal half of duodenum
Blood supply: coeliac trunk

167
Q

Midgut structures and blood supply

A

distal half of duodenum to the splenic flexure of the colon
SMA

168
Q

Hindgut structures and blood supply

A

descending colon to the rectum
IMA

169
Q

What is H.Pylori

A

Gram-negative bacteria associated with a variety of GI problems, primarily peptic ulcer disease

170
Q

Associations of H Pylori

A

peptic ulcer disease
95% of duodenal ulcers
75% of gastric ulcers
gastric cancer
B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
atrophic gastritis

171
Q

Management of H pylori

A

eradication may be achieved with a 7-day course of
a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin

172
Q

What is odynophagia

A

a painful sensation in the oesophageal region that occurs in relation to swallowing.

173
Q

Abdominal pain, rectal bleeding, metabolic acidosis in a question is most likely to indicate:

A

Mesenteric ischaemia

174
Q

What is achalasia

A

an oesophageal motor disorder characterised by a loss of oesophageal peristalsis and failure of the lower oesophageal sphincter to relax in response to swallowing.

175
Q

Clinical features of achalasia

A

-Dysphagia of BOTH liquids and solids
-typically variation in severity of symptoms
-Heart burn
-regurgitation of food (may lead to cough, aspiration pneumonia etc.)
-malignant change seen in small number of patients

176
Q

Investigations for achalasia

A

oesophageal manometry:
-excessive LOS (loss of sphincter)tone which doesn’t relax on swallowing
-considered the most important diagnostic test

barium swallow:
-shows grossly expanded oesophagus, fluid level
-‘bird’s beak’ appearance

chest x-ray:
-wide mediastinum
-fluid level

177
Q

Irreversible complications of haemachromatosis

A

Liver cirrhosis**
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy

178
Q

A 20-year-old obese woman with a 2-year history of gallstones presents to the emergency department with severe, constant right upper quadrant (RUQ) pain, nausea, and vomiting after eating fried chicken for dinner. She denies any chest pain or diarrhoea. Three months ago she developed intermittent, sharp RUQ pains. On physical examination she has a temperature of 38°C (100.4°F), moderate RUQ tenderness on palpation, but no evidence of jaundice.

A

Acute cholecystitis

179
Q

A 53-year-old man with a history of hepatitis C presents with a complaint of abdominal distention, fever, vomiting, and blood in his stool. Paracentesis has improved symptoms on the numerous occasions that he has previously presented with abdominal distension.

A

Spontaneous Bacterial peritonitis

180
Q

A 46-year-old woman with a history of long-standing alcoholism and previous episodes of hepatic encephalopathy presents with altered mental status and worsening abdominal distention.

A

Spontaneous Bacterial peritonitis

181
Q

A 34-year-old man presents 2 weeks after returning from a month-long trip to India. He denies attending pre-travel vaccination clinic and did not take prophylaxis of any sort while in India. He reports a 6-day history of malaise, anorexia, abdominal pain, nausea with emesis, and dark urine. He admits to dietary indiscretion and consumed salad at a road-side vendor 3 weeks before onset of symptoms. On examination there is icterus. His alanine transaminase (ALT) is 5660 units/L, and total bilirubin 153.9 micromols/L (9 mg/dL). Serum IgM anti-hepatitis A virus antibodies are detected.

A

Hepatitis A

182
Q

A 40-year-old asymptomatic man presents for a routine visit with an elevated alanine aminotransferase level (55 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.

A

Hepatitis B

183
Q

A 45-year-old woman presents with insidious onset of fatigue, malaise, lethargy, anorexia, nausea, abdominal discomfort, mild pruritus, and arthralgia involving the small joints. Her past medical history includes coeliac disease. Physical examination reveals hepatomegaly and spider angiomata.

A

Autoimmune hepatitis

184
Q

A 40-year-old man with a history of alcohol-misuse is brought to the emergency department by police, who found him lying down by the side of the street. On examination he is somnolent and confused. He has a horizontal gaze palsy with impaired vestibulo-ocular reflexes and severe truncal ataxia in the presence of normal motor strength and muscle stretch reflexes.

A

Wernickes encephalopathy

185
Q

A 30-year-old woman underwent bariatric surgery for Class III (BMI ≥40) obesity. The postoperative course was complicated by a bronchopneumonia, vomiting, and poor oral intake. Four weeks after surgery she complained of vertigo and headache and soon became apathetic and developed vertical nystagmus that was worse on downward gaze.

A

Wernickes encephalopathy

186
Q

A 35-year-old man comes to the emergency department with a history of nausea, vomiting, and watery diarrhoea of 1 day’s duration. The patient and his wife have just returned from a Caribbean cruise, and his wife also has mild diarrhoea. The patient denies any blood or mucus in the stool. He has chills but no fever. On examination, the patient is afebrile and anicteric, but has dry mucous membranes. His heart rate is 95 beats per minute and blood pressure (BP) is 110/70 mmHg. His abdomen is soft and non-tender, with hyperactive bowel sounds.

A

Viral Gastroentertitis

187
Q

A 70-year-old woman is brought to the emergency department from her nursing home with a history of nausea, projectile vomiting, and non-bloody diarrhoea of 1 day’s duration. She also describes generalised body aches, chills, and fatigue. Her roommate in the nursing home has also had diarrhoea for 2 days. Past medical history included hypertension and coronary artery disease. BP on examination is 100/60 mmHg and heart rate is 110 beats per minute. Abdomen is non-distended and is non-tender.

A

Viral Gastroenteritis

188
Q

A 40-year-old man presents to his primary care physician with a 2-month history of intermittent upper abdominal pain. He describes the pain as a dull, gnawing ache. The pain sometimes wakes him at night, is relieved by food and drinking milk, and is helped partially by famotidine. He had a similar but milder episode about 5 years ago, which was treated with omeprazole. Physical examination reveals a fit, apparently healthy man in no distress. The only abnormal finding is mild epigastric tenderness on palpation of the abdomen.

A

Peptic ulcer disease

189
Q

A 42-year-old man presents with a recent history of abdominal pain, distension, and nausea. Urea breath testing for Helicobacter pylori is positive.

A

Gastritis

190
Q

A 58-year-old white woman of North European descent presents with a 2-month history of increasing fatigue, difficulty with ambulation, and memory deficits. Family history is notable for autoimmune disease. Laboratory findings are remarkable for a macrocytic anaemia, a markedly reduced serum vitamin B₁₂, and presence of anti-parietal cell antibodies.

A

Gastritis

191
Q

A 55-year-old man presents with severe dysphagia to solids and worsening dysphagia to liquids. His social history is significant for 40 pack-year cigarette smoking and a 6-pack of beer per day. He has lost over 10% of his body weight and currently is nourished only by milkshake supplements. He complains of some mild odynophagia and is constantly coughing up mucus secretions.

A

Oesophageal cancer

192
Q

An otherwise healthy 45-year-old male executive complains of heartburn. He has tried over-the-counter medications with no relief. He was tried on a course of proton pump inhibitors for 6 weeks, but still has heartburn. He has no weight loss or dysphagia.

A

Oesophageal cancer

193
Q

A 70-year-old man who smokes heavily presents with a 6-month history of intermittent abdominal pain and nausea. He has lost 10 kg of weight in the past 2 months, which he thinks is due to a decreased appetite, and he complains of pruritus. On physical examination there is icterus in the conjunctival sclerae and epigastric tenderness but no abdominal mass or lymphadenopathy. Blood tests demonstrate elevated bilirubin and alkaline phosphatase; the rest of the blood tests are within the normal range.

A

Pancreatic cancer

194
Q

A 45-year-old woman presents to her physician with vague upper abdominal (epigastric) pain. After treatment with proton-pump inhibitors, analgesics, and antacids over a period of 3 months, which were ineffective, the patient also started to experience back pain. This prompted an initial upper gastrointestinal endoscopy, which was normal. Nearly 4 months after initial presentation, an upper abdominal ultrasound reveals a pancreatic mass with liver metastases.

A

Pancreatic cancer

195
Q

A 51-year-old man with moderate obesity (body mass index of 34 kg/m²) is seen in consultation for heartburn and regurgitation. He has a diagnosis of gastro-oesophageal reflux disease and has been treated with proton-pump inhibitors. His heartburn is less severe with the medication, but he is still bothered by regurgitation. His physical examination is unremarkable. A barium oesophagram and upper endoscopy demonstrate a type I (sliding) hiatus hernia, with about one third of the upper stomach in the chest. The patient has free reflux to the level of the cervical oesophagus.

A

Hiatal hernia

196
Q

A 68-year-old retired labourer presents to his primary medical doctor with a 3-week history of a dull dragging discomfort in his right groin toward the end of the day. The discomfort is associated with a lump while standing but disappears when lying supine. He denies any other significant past medical or surgical history. On physical examination, a bulge is present when standing that disappears when supine.

A

Inguinal hernia

197
Q

A 6-month-old healthy girl presents with a bulge at her umbilicus that her parents have noticed since birth. She has no accompanying symptoms and has been growing and developing normally. Physical examination of the abdomen reveals a soft, non-tender bulge at the umbilicus that is easily reduced into the peritoneal cavity with gentle pressure. Reduction allows palpation of the abdominal fascia, revealing an 8 mm fascial defect.

A

Umbilical hernia

198
Q

A 48-year-old woman experiences intermittent diffuse abdominal pain, worse after eating meals. The pain has been present for the previous 6 months, but has worsened recently. She has had significant weight loss since the onset of symptoms. Her past medical history includes systemic lupus erythematosus, which has been difficult to manage medically.

A

Intestinal ischaemia

199
Q

A 54-year-old man presents with 2 days of worsening generalised abdominal pain. He is nauseated and the pain is worse after eating. He was hospitalised last month with acute pancreatitis and was found to have a splenic vein thrombus during that admission.

A

Intestinal ischaemia

200
Q

A man in his early 70s presents with acute-onset, colicky, lower abdominal pain and distension, failing to pass flatus or faeces in the preceding 12 to 24 hours. He reports a recent change in his bowel habit with increased frequency of defecation, some weight loss, and the passage of blood mixed with his stools. On examination he is generally unwell, is pyrexial, and has a distended tympanic abdomen along the distribution of the large bowel, with tenderness in the right lower quadrant. He has an empty rectum on digital rectal examination.

A

Large bowel obstruction

201
Q

A 27-year-old male presents with cramping abdominal pain of sudden onset, emesis, and failure to pass any flatus or stool for 24 hours. The patient has no history of prior surgery. Physical examination reveals peritonitis. Computed tomography reveals the level of the obstruction.

A

Small bowel obstruction

202
Q

A 43-year-old female with a prior history of open cholecystectomy presents with gradual onset of nausea, vomiting, absolute constipation, and abdominal distention. Physical examination does not demonstrate peritonitis. Computed tomography is used to confirm the diagnosis.

A

Small bowel obstruction

203
Q

A 52-year-old man undergoes an elective sigmoid resection with primary colorectal anastomosis for chronic diverticulitis. The operative course is routine. Postoperatively, he starts on a clear-liquid diet and receives morphine via patient-controlled analgesia pump. On the second postoperative day, he has a distended abdomen, is nauseated, and has not passed flatus. He vomits repeatedly and requires nasogastric decompression. CT-scan shows uniform small bowel distention and no evidence of a transition zone between dilated and collapsed bowel (a key indicator of obstruction).

A

Ileus

204
Q

A 34-year-old mother of three presents to her family physician with a 3-week history of abdominal cramping pain in both lower quadrants. She has been having frequent small, soft stools accompanied by some mucus but no blood. Her symptoms are improved with bowel movement or passage of flatus. She has had these symptoms almost monthly since she was in college, but they have been worse recently. Past history is negative except for three normal pregnancies. Family history is negative for colon cancer. A sister has similar symptoms but has not seen a physician. Personal/social history reveals that she is an accountant working long hours. Her firm is about to merge with another, and she fears her job situation is tenuous. She has not lost any weight or had any other constitutional symptoms. On physical examination, the only finding is some mild tenderness in the right lower quadrant. No mass is felt.

A

IBS

205
Q

A 40-year-old housewife complains of recurrent constipation. She has had problems since her 20s, but they are worse now. The constipation is accompanied by abdominal bloating and abdominal pain, and the discomfort is only better when she has a bowel movement. On her gynaecologist’s advice, she has tried more fibre in her diet, including fresh fruits and leafy vegetables, but that has only made the bloating worse. Her past history includes a cholecystectomy and a hysterectomy. Physical examination is entirely normal. Rectal examination reveals normal consistency stool. Stool samples test negative for occult blood.

A

IBS

206
Q

A 42-year-old woman has heartburn after meals and a sour taste in her mouth. For the past 4-6 months she has had symptoms several times per week. Symptoms are worse when she lies down or bends over. Antacids help somewhat. She has no dysphagia, vomiting, abdominal pain, exertional symptoms, melaena, or weight loss. Past medical history and family history are non-contributory. The patient drinks alcohol occasionally and does not smoke. On physical examination, height is 1.63 m, weight 77.1 kg, and blood pressure 140/88 mmHg. The remainder of the examination is unremarkable.

A

GORD

207
Q

A 39-year-old woman presents with a 2-year history of gradually worsening constipation. She complains of bloating, gas, and lower abdominal discomfort with irregular bowel habits. She describes her stool as mostly sausage-shaped, hard, and lumpy. She takes metoprolol for hypertension and lansoprazole for heartburn. She has previously used senna and bisacodyl without improvement of her symptoms. She also increased her daily fibre and fluid intake without relief. Physical examination is unremarkable except for mild abdominal distension and palpable stool in the right and left lower quadrants. Perianal inspection is normal, and the anocutaneous reflex is present in all 4 quadrants. Digital rectal examination reveals a large amount of stool in the rectum. When asked to push and bear down, she shows adequate pelvic descent with normal anal relaxation.

A

Constipation

208
Q

A 50-year-old woman presents with a lifelong history of constipation that has worsened over the past 2 years. She reports decreased stool frequency and straining during defecation. She has a feeling of incomplete evacuation and admits to applying pressure over her posterior vaginal wall during defecation. She describes her stool as separate hard lumps. She has had 2 vaginal deliveries, with no known history of tears. She has had a hysterectomy and bladder suspension surgery. She has used ispaghula and milk of magnesia with limited relief. Examination is unremarkable. Her abdomen is soft and non-distended with no palpable masses. Perianal inspection is normal, and the anocutaneous reflex is present in all 4 quadrants. Digital rectal examination reveals no stool in the rectum. On digital rectal examination, resting anal tone is weak but her squeeze tone is normal. She does not relax the puborectalis muscle or the external anal sphincter when simulating defecation; she also has 2-cm perineal descent with straining.

A

Constipation

209
Q

A 56-year-old man with a remote history of intravenous drug use presents to an initial visit complaining of increased abdominal girth but denies jaundice. He drinks about 2 to 4 glasses of wine with dinner and recalls having had abnormal liver enzymes in the past. Physical examination reveals spider naevi, a palpable firm liver, mild splenomegaly, and shifting dullness consistent with the presence of ascites. Liver function is found to be deranged with elevated aminotransferases (aspartate aminotransferase [AST]: 90 U/L, alanine aminotransferase [ALT]: 87 U/L), and the patient is positive for anti-hepatitis C antibody.

A

Cirrhosis

210
Q

A 60-year-old woman with a past medical history of obesity, diabetes, and dyslipidaemia is noted to have abnormal liver enzymes with elevated aminotransferases (ALT: 68 U/L, AST: 82 U/L), and normal alkaline phosphatase and bilirubin. She denies significant alcohol consumption, and tests for viral hepatitis and autoimmune markers are negative. An abdominal ultrasound reveals evidence of fatty infiltration of the liver and slight enlargement of the spleen.

A

Cirrhosis

211
Q

A 42-year-old man presents to his primary care physician complaining of a 3-month history of lower intestinal bleeding. He describes the bleeding as painless, bright blood appearing on the tissue following a bowel movement. He has had 2 episodes recently where blood was visible in the toilet bowl following defecation. He denies any abdominal pain and any family history of gastrointestinal malignancy. Physical examination reveals a healthy man with the only finding being bright blood on the examining finger following a digital rectal examination.

A

Haemorrhoids

212
Q

A 28-year-old woman presents complaining of rectal pain of 3 days’ duration. She states that on the day before the onset of symptoms she had been moving boxes at her home. She describes the pain as sharp and present constantly, but worse with bowel movements or sitting. She denies any fevers or chills or perianal discharge. Physical examination reveals a 2-cm, painful, bluish lesion adjacent to the anal canal.

A

Haemorrhoids

213
Q

A 77-year-old man presents to his general practitioner with weight loss of 6.8 kg (15 lbs) and a 3-month history of dysphagia and abdominal pain. The only abnormal finding on physical examination is stools positive for occult blood. He is referred for an upper endoscopy, which shows an exophytic, ulcerated mass in the cardia of the stomach. Biopsy reveals moderately differentiated adenocarcinoma.

A

Gastric cancer

214
Q

A 46-year-old obese woman presents with a 6-hour history of moderate steady pain in the right upper quadrant (RUQ) that radiates through to her back. This pain began after eating dinner, gradually increased, and has remained constant over the last few hours. She has experienced previous episodes of similar pain for which she did not seek medical advice. Her vital signs are normal. The pertinent findings on physical examination are tenderness to palpation in the RUQ without guarding or rebound..

A

Gallstones

215
Q

A 57-year-old woman with a history of hypertension and hypercholesterolaemia presents to the accident and emergency department with a 24-hour history of gradually worsening left-lower quadrant abdominal pain associated with nausea and vomiting. Prior to this episode, the patient did not have any significant gastrointestinal (GI) problems, except slight constipation and occasional dyspepsia after heavy meals. She felt feverish but did not take her temperature. Her family history is negative for GI disorders.

A

Diverticular disease

216
Q

A 32-year-old obese, but otherwise healthy, man presents to the accident and emergency department with onset of acute lower abdominal pain of 2-hour duration. He has no fever and there is no history of any previous significant illness, except loud snoring, possible sleep apnoea, and being overweight.

A

Diverticular disease

217
Q

A 32-year-old obese, but otherwise healthy, man presents to the accident and emergency department with onset of acute lower abdominal pain of 2-hour duration. He has no fever and there is no history of any previous significant illness, except loud snoring, possible sleep apnoea, and being overweight.

A

Diverticular disease

218
Q

A 70-year-old man presents to his primary care physician with a complaint of rectal bleeding. He describes blood mixed in with the stool, and a change from his normal bowel habit as he is going more frequently than normal. He has also experienced some crampy left-sided abdominal pain and weight loss. He has previously been fit and well and there is no family history of gastrointestinal disease. Examination of his abdomen and digital rectal examination are normal.

A

Colorectal cancer

219
Q

A 46-year-old woman presents with fatigue and is found to have iron deficiency with anaemia. She has experienced intermittent episodes of mild diarrhoea for many years, previously diagnosed as irritable bowel syndrome and lactose intolerance. She has no current significant gastrointestinal symptoms such as diarrhoea, bloating, or abdominal pain. Examination reveals two oral aphthous ulcers and pallor. Abdominal examination is normal and results of faecal testing for occult blood are negative.

A

Coeliac disease

220
Q

A 9-year-old boy presents with vomiting for 5 days. His sister, who has coeliac disease, has had similar symptoms. His growth has been normal and he has not experienced any other possible symptoms of coeliac disease, except for intermittent constipation. Immunoglobulin A-tissue transglutaminase titre is 5 times the upper limit of normal.

A

Coeliac disease

221
Q

A 28-year-old woman presents with a history of severe pain on defecation for the last 3 months. She has noticed a small amount of blood on the stool. The pain is severe and she is worried about the pain she will experience with the next bowel action.

A

Anal fissure

222
Q

A 50-year-old man presents to his general practitioner with complaints of fatigue for 2 months. He also notes distension of his abdomen and shortness of breath beginning 2 weeks ago. His wife reports that the patient has been having episodes of confusion lately. The patient has a significant medical history of chronic heavy alcohol consumption of about half a pint of vodka daily for around 20 years. On physical exam the patient is noted to have scleral icterus, tremors of both hands, and spider angiomata on the chest. There is abdominal distension with presence of shifting dullness, fluid waves, and splenomegaly. Laboratory examination shows low haemoglobin, low platelets, low sodium, aspartate aminotransferase (AST) elevation > alanine aminotransferase (ALT) elevation, and high prothrombin time (PT) and international normalised ratio (INR). Ultrasound of the abdomen shows liver hyperechogenicity, portal hypertension, splenomegaly, and ascites.

A

Alcoholic liver disease

223
Q

A 38-year-old man presents to the emergency department for severe alcohol abuse with nausea and vomiting. He has a significant medical history of chronic heavy alcohol consumption of about one bottle of wine each day for about 5 years until 1 year ago; since then he has had severe intermittent binge alcohol intake. He reports no other significant medical problems. The patient is confused and slightly obtunded, and hepatomegaly is discovered on physical exam. His body mass index is 22. Pertinent positive laboratory values show low haemoglobin, AST elevation > ALT elevation, normal PT and INR, and very high serum alcohol level. Ultrasound of the abdomen shows fatty infiltration in the liver.

A

Alcoholic liver disease

224
Q

A 22-year-old male presents to the emergency department with abdominal pain, anorexia, nausea, and low-grade fever. Pain started in the mid-abdominal region 6 hours ago and is now in the right lower quadrant of the abdomen. The pain was steady in nature and aggravated by coughing. Physical examination reveals a low-grade fever (38°C [100.5°F]), tenderness on palpation at right lower quadrant (McBurney’s sign), and leukocytosis (12 x 109/L or 12,000/microlitre) with 85% neutrophils.

A

Appendicitis

225
Q

A 12-year-old girl presents with sudden-onset severe generalised abdominal pain associated with nausea, vomiting, and diarrhoea. On examination she appears unwell and has a temperature of 40°C (104°F). Her abdomen is tense with generalised tenderness and guarding. No bowel sounds are present.

A

Appendicitis

226
Q

A 53-year-old man presents to the emergency department with severe mid-epigastric abdominal pain that radiates to the back. The pain evolved over 1 hour. He also describes nausea, vomiting, and anorexia, and gives a history of heavy alcohol intake over many years, including this past week. He is tachycardic, tachypnoeic, and febrile with hypotension. He is slightly agitated and confused. He is diaphoretic and tender in the epigastric region with guarding and rebound tenderness.

A

Acute pancreatitis

227
Q

A 47-year-old overweight woman is admitted with generalised abdominal pain. She has been unable to eat or drink due to nausea and vomiting. She states the pain started in the right upper quadrant suddenly 6 hours ago, but is now in the epigastric region. An ultrasound obtained on her last visit to the emergency department revealed gallstones with no inflammation of the gallbladder, and she was told that she should see a surgeon. She looks jaundiced and in distress. She has point tenderness under her ribs on the right, which is worsened with deep palpation. No mass is palpable.

A

Acute pancreatitis

228
Q

A 65-year-old woman presents to the emergency department with a 2-day history of progressive right upper quadrant (RUQ) pain that she rates as 9/10. She reports experiencing fever, and being unable to eat or drink due to nausea and abdominal pain at baseline, exacerbated by food ingestion. Her bowel movements are less frequent and have become loose. Her pain is not relieved by bowel movement and is not related to food. She has not recently taken antibiotics, nor does she use non-steroidal anti-inflammatory drugs or drink alcohol. On examination, she is febrile at 39.4°C (102.9°F); supine BP is 97/58 mmHg; standing BP is 76/41 mmHg; HR is 127 bpm; and respiratory rate is 24 breaths per minute with normal oxygen saturation. Her examination is remarkable for scleral and sublingual icterus, tachycardia, RUQ pain with no rebound, and involuntary guarding on the right side. Faecal occult blood test is negative. Laboratory results show a WBC of 18.0 × 10⁹/L (18,000/microlitre) (reference range 4.8-10.8 × 10⁹/L or 4800-10,800/microlitre) with 17% (reference range 0% to 4%) bands and PMNs of 82% (reference range 35% to 70%). AST is 207 units/L (reference range 8-34 units/L), ALT is 196 units/L (reference range 7-35 units/L), alkaline phosphatase is 478 units/L (reference range 25-100 units/L), total bilirubin is 107.7 micromol/L (6.3 mg/dL) (reference range 3.4 to 22.2 micromol/L or 0.2 to 1.3 mg/dL), and amylase is 82 units/L (53-123 units/L).

A

Acute cholangitis

229
Q

Long term management for bleeding varices

A

Non-cardioselective beta-blocker (e.g. propranolol)

230
Q

Gene mutation assoicated with pancreatic cancer

A

KRAS

231
Q

RIsk factors for Barret’s oesophagus

A

GORD
male gender
smoking
central obesity

232
Q

Management of Barret’s

A

endoscopic surveillance with biopsies (every 3-5 years for patients with metaplasia)
high dose PPI

233
Q

Pathogenesis of acute appendicitis

A

lymphoid hyperplasia or a faecolith → obstruction of appendiceal lumen

234
Q

Courvoisiers law states what

A

states that a palpable gallbladder along with jaundice is unlikely to be gallstones. The cause is likely to be cholangiocarcinoma or pancreatic cancer.

235
Q

Why does HRT need to be stopped before surgery

A

Oestrogen-containing contraception (e.g., the combined contraceptive pill) or hormone replacement therapy (e.g., in perimenopausal women) need to be stopped 4 weeks before surgery to reduce the risk of venous thromboembolism (NICE guidelines 2010).

236
Q

What does Hartmann’s procedure involve

A

removal of rectosigmoid colon with closure of the anorectal stump and formation of a colostomy

237
Q

What does a coffee bean sign on an abdominal xray indicate

A

sigmoid volvulus

238
Q

What are you risking if you give normal saline 0.9%

A

has a concentration of sodium of 154 mmols/L. The normal blood concentration of sodium is 135-145 mmols/L. When you use normal saline, you are adding a lot of sodium into the system, significantly increasing the risk of hypernatraemia. Normal saline also carries a risk of causing metabolic acidosis due to adding so much chloride (hyperchloraemic acidosis)

239
Q

Risk factors for post operative nausea and vomiting

A

Female
History of motion sickness or previous PONV
Non-smoker
Use of postoperative opiates
Younger age
Use of volatile anaesthetics

240
Q

When wouldn’t you give the anti-emetic ondansetron

A

5HT3 receptor antagonist) – avoided in patients at risk of prolonged QT interval

241
Q

When wouldn’t you give dexamethasone as a prophylactic anti-emetic

A

caution in diabetic or immunocompromised patients

242
Q

When wouldnt you give cyclizine as a prophylactic anti-emetic

A

(histamine (H1) receptor antagonist) – caution with heart failure and elderly patients

243
Q

What is an ileus

A

condition affecting the small bowel
where the normal peristalsis temporarily stops
can be called a paralytic or adynamic ileus

244
Q

Causes of ileus

A

injury to the bowel
handling of the bowel during surgery
Inflammation or infection in or nearby the bowel
electrolyte imbalance

245
Q

What is Meckel’s diverticulum

A

malformation of the distal ileum that occurs in around 2% of the population
usually asymptomatic and does not require treatment
however, it can bleed, become inflamed, rupture or causes a volvulus or intussusception
Can mimic the presentation of appendicitis

246
Q

Where is McBurney’s point

A

refers to a specific area one-third of the distance from the anterior superior iliac spine (ASIS) to the umbilicus.

indicative of appendicitis

247
Q

What is Rovsing sign

A

palpation of the left iliac fossa elicits pain on the right iliac fossa

inidicative of appendicitis

248
Q

What acid base disturbance is found in profuse vomiting

A

metabolic alkalosis

249
Q

Tumour marker that is raised in cholangiocarcinoma.

A

CA 19-9 (carbohydrate antigen)

cancer of the head of the pancreas

250
Q

Describe a colostomy bag

A

where large intestine is brought to the skin (usually flush with the skin because solid contents are less irritating than that of an ileostomy)
typically located in the left iliac fossa

251
Q

Describe an ileostomy bag

A

where end portion of small bowel is brought out of the skin
drain more liquid stools
have a spout so content do not touch and irritate surrounding skin
typically located in right iliac fossa

252
Q

When are end colostomies deemed permanent

A

after resection of abdomino-pernieal resection (APR) because the entire anus and rectum have been removed

253
Q

When are end ileostomies deemed permanent

A

after a panprotocolectomy (total colectomy with removal of the large bowel , rectum and anus)
an alternative to this is to create an ileo-anal anastomosis (j-pouch)

254
Q

Describe a J pouch

A

where the ileum is folded back on itself and fashioned into a larger pouch which functions a bit like a rectum
The j pouch is then attached to the anus and collects stools prior to the person passing a motion

255
Q

Describe a loop ileostomy

A

temporary stoma to allow a distal portion of the bowel and anastamosis to heal after surgery
usually reversed after 6-8 weeks
Bowel is partially opened and folded so that there are two openings on the skin side-by-side, attached in the middle

Loop refers to it being the two ends (proximal and distal)
Proximal end is the productive side and is turned inside out to form a spout to the surrounding skin, this is where bowel habits comes out, distal end is flatter

256
Q

Complications of stomas

A

psycho-social impact
local skin irritation
parastomal hernia
loss of bowel length leading to high output, dehydration and malnutrition
constipation (colostomies)
stenosis
obstruction
retraction (sinking into the skin)
prolapse (telescoping of bowel through hernia site)
bleeding
granulomas causing raised red lumps around the stoma

257
Q

Obese 50 year old women presents with pain in RUQ which radiates to interscapular region
apyrexial and not jaundiced

A

think biliary colic

258
Q

What hormones decrease gastric empyting

A

CCK
somatostatin

259
Q

When testing for heb B previous immunisation would show what

A

Anti-Hbs positive
all other negative

260
Q

When testing for hep B previous infection >6months ago and not a carrier wpuld show what

A

anti-HBc positive (mini c = caught, negative if immunised)
HBaAg negative

261
Q

when testing for hep B now a carrier what would it show

A

anti-HBc positive
HBsAg positive

262
Q

What is bilirubin

A

chemical by-product of the breakdown of heme (component of RBCs)

263
Q

when does jaundice appear in terms of bilirubin

A

reaches an excess of 35umol/l

264
Q

What can raised levels conjugated bilirubin result from

A

defective excretion of bilirubin for example Dubin Johnson syndrome or cholestasis

265
Q

define sepsis

A

infection that triggers a particular systemic inflammatory response syndrome (SIRS)
Characterised by body temperature outside 36-38
Hr >90
RR > 20
WBC >12,000 or <4,000

266
Q

What is superior to spleen?
anterior?
Posterior?
Inferior?

A

Superior - diaphragm
anterior - gastric impression
posterior - kidney
inferior - colon

267
Q

What nerve is at risk of damage during varicose vein surgery

A

sural nerve damage
Loss of sensation to the lateral foot and posterolateral leg

268
Q

What nerve is at risk of damage during a posterior triangle lymph node biopsy

A

accessory nerve lesion

269
Q

what nerve is at risk of damage on a thyroidectomy

A

laryngeal nerve

270
Q

What nerve is at risk of damage during an anterior resection of the rectum

A

hypogastric autonomic nerve

271
Q

What nerve is at risk of damage during inguinal hernia repair

A

inguinal nerve

272
Q

What is APC

A

adenomatous polyposis coli (APC) gene is a tumour suppressor gene involved in cell adhesion. Mutation or deletion of this gene can result in familial adenomatous polyposis (FAP), which causes almost inevitable bowel cancer in those affected, by early middle age.

273
Q

Lynch syndrome

A

HNPCC (autosomal dominant gene)
most common form of inherited colon cancer
often proximal colon, poorly differentiated and highly aggressive
Most common genes involved : MSH2, MLH1

274
Q

Diverticulosis

A

common disorder characterised by multiple outpouchings of the bowel wall
most commonly the sigmoid colon

Risk factors:
increasing age
low fibre diet

Diverticular disease - term used for symptomatic patients

275
Q

Classic presentation of diverticulitis

A

LIF pain and tenderness
anorexia, nausea and vomiting
diarhhoea
features of infection (pyrexia, raised WCC and CRP)

276
Q

Management of diverticulitis

A

Mild attacks treated with antibiotics
More significant episodes managed in hospital: patients are NBM, IV fluids and IV antibiotics (cephalosporin + metronidazole)

277
Q

Complications of diverticulitis

A

abscess formation
peritonitis
obstruction
perforation

278
Q

Which antibiotic is associated with C.diff

A

Clindamycin treatment can cause C.diff

279
Q

Metabolic consequences of refeeding syndrome

A

Hypophoshataemia
Hypokalaemia
Hypomagnesaemia
abnormal fluid balance

280
Q

Patients considered high risk of referring syndrome

A

BMI <16kg/m2
unintentional weight loss >15% over 3-6 months
little nutritional intake >10days
hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

281
Q

What is often used for detecting cholangiocarcinoma in patients with primary sclerosing cholangitis

A

CA 19-9 levels

282
Q

Features of chronic pancreatitis

A

pain worse 15-30 mins following a meal
Steatorrhea : develop between 5-25 years after onset of pain
DM occurs 20yrs after symptoms begin

283
Q

Post splenectomy blood film features:

A

Howell- Jolly bodies
Pappenheimer bodies
Target cells
Irregular contracted erythrocytes

284
Q

What is Zollinger-Ellison syndrome

A

condition characterised by excessive levels of gastrin usually from a gastrin secretin tumour of the duodenum or pancreas

285
Q

Features of Zollinger-Ellison syndrome

A

multiple gastroduodenal ulcers
diarrhoea
malabsorption

286
Q

How to diagnose Zollinger-Ellison syndrome

A

fasting gastrin levels : single best screen (will be very high)
secretin stimulation test

287
Q

Pyloric stenosis

A

presents in second - fourth weeks of life with vomiting
caused by hypertrophy of the circular muscles of the pylorus

288
Q

features of pyloric stenosis

A

projectile vomiting typically 30 mins after a meal
constipation and dehydration
palpable mass in upper abdomen
hypochloraemic, hypokalaemic alkalosis due to persistent vomiting

289
Q

Diagnosis and management of pyloric stenosis

A

made by US
Ramstedt pyloromyotomy.

290
Q

Primary biliary cholangitis clinical signs on examination

A

jaundice
xanthelesma
spider naevi
splenomegaly

291
Q

What is used to initially treat primary biliary cholangitis

A

Cholestyramine
ursodeoxycholic acid
fat soluble vitamin prophylaxis

292
Q

Anti-smooth muscle antibodies and anti mitochondrial antibodies are typical of what

A

Autoimmune hepatitis and primary biliary cirrhosis respectively

293
Q

High serum transferrin reflects what

A

iron overload in haemachromatosis

294
Q

What is the combination of steatosis and Mallory’s hyaline on liver biopsy is suggestive of

A

alcoholic hepatitis

295
Q

Jaundice and gilberts syndrome

A

transient jaundice after physiological stress such as exercise and fasting is seen in gilberts syndrome

296
Q

What is pneumobilia

A

air in the gallbladder

297
Q

cholecystoenteric fistula

A

rare and late complication of cholecystolithiasis

Spontaneous tract between an inflamed gallbladder and one or more parts of the surrounding GI tract

298
Q

Retroperitoneal structures

A

SAD PUCKER
S: suprarenal (adrenal gland)#
A: Aorta/IVC
D: Duodenum (2/3 parts)
P: pancreas (except tail)
U: ureters
C: colon (ascending and descending)
K: kidneys
E: oesophagus
R: rectum

299
Q

Retroperitoneal structures

A

SAD PUCKER
S: suprarenal (adrenal gland)#
A: Aorta/IVC
D: Duodenum (2/3 parts)
P: pancreas (except tail)
U: ureters
C: colon (ascending and descending)
K: kidneys
E: oesophagus
R: rectum

300
Q

What brain structure is most affected in wilsons disease

A

most copper is deposited in the basal ganglia

301
Q

Plummer Vinson syndrome

A

oesophageal disorder
triad of: dysphagia (secondary to oesophageal webs)
Glossitis
Iron-deficiency anaemia

302
Q

Mallory weiss syndrome

A

Severe vomiting -> painful mucosal lacerations at the gastroesophageal junction resulting in haematemesis
common in alcoholics

303
Q

Boerhaave syndrome

A

severe vomiting
esophageal rupture

304
Q

Tension pnuemothorax

A

Often laceration to lung parenchyma with flap
pressure develops in thorax
most common cause is mechanical ventilation
symptoms overlap with cardiac tamponae, hyper-resonant percussion suggests pnuemothorax

305
Q

Flail chest

A

chest wall disconnects from thoracic cage
multiple rib fractures
association with pulmonary contusion
abnormal chest motion
avoid over hydration and fluid overload

306
Q

Cardiac tamponade signs

A

Becks triad: low BP, distended JVP, muffled heart sounds
Pulsus paradoxus - pulse pressure decreases during inspiration

307
Q

Pulmonary contusion

A

most common potentially lethal chest injury
ABGs and pulse oximetry important
early intubation within an hour if significant hypoxia

308
Q

Blunt cardiac injury

A

usually occurs secondary to chest wall injury
ECG may show features of MI
Dequelae: hypotension, arrhythmias, cardiac wall motion abnormalities

309
Q

Symptoms of diverticular disease

A

altered bowel habit
rectal bleeding
abdominal pain

310
Q

Complications of diverticular disease

A

diverticulitis
haemorrhage
development of fistula
perforation and faecal peritonitis
perforation and development of abscess
development of diverticular phlegmon

311
Q

How to diagnose diverticular disease

A

colonoscopu
CT cologram
or barium enema

312
Q

Hinchey severity classification

A

for diverticular disease
I - para colonic abscess
II - pelvic abscess
III - purulent peritonitis
IV faecal peritonitis

313
Q

Management of diverticular disease

A

Increase dietary fibre
Mild attacks of diverticulitis managed with antibiotics
peri coloic abscesses should be drained surgically or radiologically

314
Q

Pernicious anaemia

A

autoimmune disorder affecting gastric mucosa that results in vitamin B12 deficiency (symptoms and signs are often subtle and diagnosis is often delayed

315
Q

Risk factors for pernicious anaemia

A

more common in females
associated with autoimmune disorders
more common if blood group A

316
Q

Features of pernicious anaemia

A

Anaemia: lethargy, pallor, dyspnoea
Neurological: peripheral pins and needles(affects arms more than legs), progressive spinal cord weakness, ataxia and [paraesthesias
other: mild jaundice, glossitis

317
Q

Investigations for pernicious anaemia

A

FBC (macrocytic anaemia, hypersegmented polymorphs on blood film, low WCC and platelets)
Vitamin B12 and folate (>200nh/L is normal)
Antibodies (Anti intrinsic factor antibodies and anti gastric parietal cell antibodies

318
Q

Management of pernicious anaemia

A

Vitamin B12 replacement
usually given IM
no neurological features = 3 injections per week for 2 weeks followed by 3 monthly treatments
More frequent doses if they have neurological features
folic acid supplementation may also be required

319
Q

Clinical features Large bowel obstruction

A

absence of passing flatus or stool
abdominal pain
abdominal distention
nausea and vomiting (late symptoms_
peritonism if associated bowel perforation

320
Q

How to differentiate large and small bowel obstructions

A

small bowel would cause vomiting earlier on before constipation
large bowel is would have longer history of constipation and later onset of vomiting

321
Q

How to differentiate large and small bowel obstructions

A

small bowel would cause vomiting earlier on before constipation
large bowel is would have longer history of constipation and later onset of vomiting

322
Q

Peutz Jeghers syndrome

A

Autosomal dominant characterised by numerous hamartomatous polyps in GI tract
associated with pigmented freckles on lips, face, palms and soles
although polyps themselves dont have malignant potential 50% patients have died from GI tract cancer by age of 60

323
Q

Features of peutz jeghers syndrome

A

hamartomatous polyps in GI tract (mainly small bowel)
Small bowel obstruction is common PC
pigmented lesions on lips, oral mucosa, face, palms and soles

Hamartomatous = A benign (not cancer) growth made up of an abnormal mixture of cells and tissues normally found in the area of the body where the growth occurs.

324
Q

Secretory diarrhoea

A

involves transformation of what is normally an absorptive gut into a secretory gut via toxins or secretagogues

325
Q

The most common type of pancreatic cancer

A

ductal adenocarcinoma

326
Q

Pancreatic head is supplied by which artery

A

pancreaticoduodenal artery

327
Q

Pancreatic tail is supplied by which artery

A

branches of the splenic artery

328
Q

What is an invagination

A

a cavity or pouch formed by being turned inside out or folded back.

329
Q

What is Intussusception

A

invagination of one portion of bowel into the lumen of the adjacent bowel, most commonly around the ileo-caecal region.

330
Q

Features of intussusception

A

paroxysmal abdominal colic pain
during paroxysm the infant will characteristically draw their knees up and turn pale
vomiting
bloodstained stool - ‘red-currant jelly’ - is a late sign
sausage-shaped mass in the right upper quadrant

331
Q

Investigation for intussusception

A

US

332
Q

Hepatic encephalopathy

A

The aetiology is not fully understood but is thought to include excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut.

333
Q

Features of hepatic encephalopathy

A

confusion, altered GCS (see below)
asterix: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
constructional apraxia: inability to draw a 5-pointed star
triphasic slow waves on EEG
raised ammonia level (not commonly measured anymore)

334
Q

Grading of hepatic encephalopathy

A

Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma

335
Q

Precipitating factors of hepatic enceophalopathy

A

infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)

336
Q

management of hepatic encephalopathy

A

> treat any underlying precipitating cause
NICE recommend lactulose first-line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
lactulose is thought to work by promoting the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
antibiotics such as rifaximin are thought to modulate the gut flora resulting in decreased ammonia production
other options include embolisation of portosystemic shunts and liver transplantation in selected patients

337
Q

contents of the femoral triangle lateral to medial

A

NAVEL
femoral nerve
femoral artery
femoral vein
empty space
lymphatics

338
Q

The presence of what cell confirms gastric adenocarcinoma

A

Signet rings

339
Q

Where are bile salts absorbed

A

in the terminal ileum

340
Q

Function of amylase

A

breaks starch into sugar

341
Q

Function of maltase

A

cleaves disaccharide maltose to glucose + glucose

342
Q

Function of sucrase

A

cleaves sucrose to fructose and glucose

343
Q

Function of lactase

A

cleaves disaccharide lactose to glucose + galactose

344
Q

Terlipressin - method of action

A

constriction of the splanchnic vessels

345
Q

What two structures merge together to form the Ampulla of Vater?

A

Pancreatic duct and common bile duct

346
Q

What does h pylori secrete to survive in the stomach

A

urease

347
Q

Raised urea and upper gi bleed

A

Upper GI bleed can act as a protein meal and cause a temporary disproportionate rise in the blood urea

348
Q

Pharyngeal pouch

A

posteromedial diverticulu through killians dehiscence (triangular area in the wall of the pharynx )
more common in older patients and is 5 times more common in men

349
Q

Features of pharyngeal pouch

A

dysphagia
regurgitation
aspiration
neck swelling which gurgles on palpation
halitosis

350
Q

Investigation for pharyngeal pouch

A

barium swallow combined with dynamic video fluoroscopy

351
Q

Management of a pharyngeal pouch

A

sugery

352
Q

First line treatment for diarrhoea in IBS

A

Loperamide

353
Q

early signs of haemachromatosis

A

fatigue
erectile dysfunction and arthralgia

354
Q

What cancer does pernicious anaemia predispose you to

A

gastric carcinoma

355
Q

What would a severe flare up of UC look like

A

associated with passing >6 stools per day containing blood
patient will also have systemic features (fever)

356
Q

Best way to measure acute liver failure

A

look at prothrombin time and albumin level because ALT does not always accurately reflect function of the liver

357
Q

Associated factors of NAFLD

A

obesity
T2Dm
hyperliidaemia
jejunoileal bypass
sudden weight loss/starvation

358
Q

Features if NAFLD

A

usually asymptomatic
hepatomegaly
ALT is typically greater than AST
increased echogenicity on US

359
Q

Management of NAFLD

A

lifestyle changes (weight loss) and monitoring
on-going research of gastric banding and insulin sensitising drugs

360
Q

Life threatening C.diff infection management

A

ORAL vancomycin and IV metronidazole

361
Q

Viral hepatitis features

A

nausea and vomiting
myalgia
lethargy
RUQ pain
questions may point to risk factors such as foreign travel or IV drug use

362
Q

Gallstone ileus

A

small bowel obstruction secondary to impacted gallstone
may develop if a fistula forms between gangrenous gallbladder and the duodenum
abdominal pain, distention and vomiting are seen

363
Q

features of carcinoid tumours

A

flushing
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis
ACTH and GHRH may also be secreted

364
Q

Investigation and management of carcinoid tumours

A

investigation = urinary 5-HIAA and plasma chromogranin A y
management = somatostatin analogues (octreotide) and for diarrhoea cyproheptadine

365
Q

Variceal haemorrhage management

A

ABC: patients should be resuscitated before endoscopy
2. correct clotting: FFP, vitamin K
3. Vasoactive agents: Terlipressin or octreotide
4. Prophylactic IV antibiotic (typically Quinolones) - both terlipressin and antibiotics should be given BEFORE endoscopy
5. Endoscopic variceal band ligation
6. Sengstaken-Blakemore tube if uncontrolled haemorrhage
7. Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if all other measures fail

366
Q

TIPSS procedure

A

Transjugular Intrahepatic Portosystemic Shunt
Used if everything else fails to control a variceal haemorrhage
connects hepatic vein to portal vein
exacerbation of hepatic encephalopathy is a common complication

367
Q

Prophylaxis of variceal haemorrhage

A

propranolol - reduced rebleeding and mortality
endoscopic variceal band ligation (EVL) at two weekly intervals until all varices have been eradicated

368
Q

What vaccine do people with coeliac disease have every 5 years

A

pneumococcal due to hyposplenism

369
Q

Best test for B12 deficiency

A

intrinsic factor antibodies over gastric parietal cell antibodies

370
Q

Management of pyogenic liver abscess

A

drainage (usually percutaneous) and antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic then ciprofloxacin + clindamycin

371
Q

Management of pyogenic liver abscess

A

drainage (usually percutaneous) and antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic then ciprofloxacin + clindamycin

372
Q

Endoscopic findings supportive of coeliac disease

A

villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes

373
Q

Functions of vitamin A

A

converted into retinal (important visual pigment)
important in epithelial cell differentiation
antioxidant
(teratogenic in high doses)

374
Q

What does an SAAG>11g/L indicate

A

portal hypertension

375
Q

Investigations for ischaemic colitis

A

ABG - metabolic acidosis, elevated lactate
imaging - xray may show thumbprinting but CT is gold stanadard

376
Q

transferrin, ferritin and TIBC for someone with haemachromatosis

A

transferrin high
ferritin high
TIBC low

377
Q

Management for haemachromatosis

A

first line - venesection (transferrin should be kept below 50% and serum ferritin below 50ug/l
second line - desferrioxamine

378
Q

Management of appendicitis

A

appendicectomy
IV prophylactic antibiotics given before

379
Q

Management of hepatic encephalopathy

A

Treat any underlying precipitating cause
first line - lactulose with addition of rifaximin for secondary prophylaxis of hepatic encephalopathy

lactulose (works by promoting excretion of ammonia and increasing metabolism of ammonia by gut bacteria)
rifaximin (modulate the gut flora resulting in decreased ammonia production)

380
Q

How to test for H.pylori post-eradication therapy

A

urea breath test

381
Q

What anaemia can sulphasalazine cause

A

This drug, used in the treatment of ulcerative colitis and rheumatoid arthritis, can cause haemolytic anaemia with Heinz bodies.

382
Q

Adverse effects of metoclopramide

A

extrapyramidal effects (acute dystonia)
diarrhoea
hyperprolactinaemia
tardive dyskinesia
parkinsonism
should be avoided in bowel obstruction but may be helpful in paralytic ileus

383
Q

Red flag symptoms for gastric cancer

A

new-onset dysphagia in a patient >55years
unexplained persistent vomiting
unexplained weight loss
progressively worsening dysphagia
odynophagia
epigastric pain

384
Q

Common source of Hep A infections

A

shellfish

385
Q

Other medication that can cause C.diff

A

omeprazole

386
Q

C.diff recurrent episode management within 12 weeks of symptom resolution

A

treated with oral fidaxomicin

387
Q

features and treatment of a fissure in ano

A

painful bright red rectal bleeding
treatment - stool softners, topicak diltiazem or GTN, botulinum toxin, sphincterotomy

388
Q

Features and treatment of fissure in ano

A

Painful bright red rectal bleeding
treatment - stool softeners, topical diltiazem or GTN, botulinum toxin, sphincterotomy

389
Q

Features and treatment of haemorroids

A

Painless, bright red rectal bleeding occurs following defaecation and bleeds onto the toilet paper and into the toilet pan
treatment - stool softeners, avoid straining, surgery

390
Q

Features and treatment of fistula in ano

A

May initially present with an abscess and then persisting discharge onto the perineum, seperate from the anus

treatment - laying it open (fistulotomy)

391
Q

deficiency in what vitamin causes easy bruising

A

vitamin c

Year 3 (14 decks)

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