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Pass Medicine > Gastrointenstinal (medicine) > Flashcards

Gastrointenstinal (medicine) Flashcards

1
Q

Gastroenteritis causes (common)

A

Viral
Campylobacter spp.
Salmonella spp.
Cholera (developing countries)

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2
Q

Gastroenteritis causes (rare but important)

A

E. coli O157
Staphylococcus aureus
Clostridium botulinum
Vibrio para-haemolyticus

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3
Q

Management of gastroenteritis

A

Oral rehydration
Abx if septicaemia (ciprofloxacin)

Colonoscopy if lasts >3 weeks

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4
Q

Chronic gastrointestinal infections

A

Giardiasis:
Treat with tinidazole or metronidazole

TB:
Treat as if for pulmonary TB

Amoebiasis:
Metronidazole + diloxanide furoate

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5
Q

GORD

A

Caused by laxity of the lower sphincter leading to episodic reflux into the oesophagus

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6
Q

What exacerbates GORD

A

Lifestyle factors:
Obesity (higher intra abdominal pressure)
Smoking
Stress
Dietary factors (fatty foods, pastry, alcohol, chocolate)
Postural (e.g. eating at night)

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7
Q

Features of GORD

A 
Marked postural element to symptoms
Chest pain (reflux precipitated oesophageal spasm)
Heartburn and nausea
Belching
Effortless regurgitation
Transient dysphagia
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8
Q

GORD management

A

Can have an upper GI endoscopy

Lifestyle management
Antacids (over the counter) - gaviscon etc
PPI for 1-2 months

Pro-kinetics (domperidone) - if more regurgitation

Surgery - Nissen’s fundoplication

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9
Q

Barrett’s oesophagus

A

Barrett’s epithelium is present in 15% of GORD sufferers

Metaplasia of the lower oesophageal mucosea from squamous epithelium to columnar epithelium

Potentially a premalignant condition (lower third oesophageal adenocarcinoma risk)

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10
Q

Barrett’s oesophagus treatment

A

PPI, high dose

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11
Q

What other condition do you sometimes get with GORD

A

Hiatus hernia

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12
Q

Peptic ulcer disease types

A

Duodenal ulcer

Gastric ulcer

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13
Q

Features of peptic ulcer disease

A

GI haemorrhage
Dyspepsia
Vomiting
Perforation (with peritonitis)

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14
Q

Ix in duodenal ulcer

A

Endoscopy (first-line)

H. pylori testing

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15
Q

H. pylori tests

A

Serology - IgG
Urease breath test
CLO test (campylobacter-like-organism test)
Faecal antigen testing

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16
Q

Duodenal ulcers

A

Where gastric acid production exceeds the buffering capacity of the alkali
Strong association with H. pylori
Pain relieved by eating

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17
Q

H. pylori

A

Gram negative bacteria associated with 95% of duodenal ulcers, 75% of gastric ulcers)

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18
Q

Gastric ulcer

A

Epigastric pain worse after eating

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19
Q

Management of peptic ulcer disease

A

If gastric - endoscopy and biopsy (to ensure not malignant), you probably also do this in duodenal but these are less likely to be malignant

Treatment:
PPIs only if H. pylori negative (4-6 weeks)
H. pyolori positive - triple therapy (PPI, amoxicillin, clarithromycin)

Note - metronidazole can replace amoxicillin in H. pylori eradication

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20
Q

Complications of peptic ulcer disease

A

Vomiting
Bleeding (haematemesis/malaena)
Perforation
Pyloric stenosis

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21
Q

Diverticular disease

A

Herniation of colonic mucosa through the muscular wall of the colon (forming out pouches)

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22
Q

Prevalence of diverticular disease

A

5% at 40 y.o

50% at 80 y.o

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23
Q

Diverticulitis

A

Impacted faeces within a diverticulum causing inflammation

May evolve into an abscess

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24
Q

Where are diverticula found

A

Almost always in sigmoid colon

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25
Q

Symptoms of diverticular disease

A

Intermittent abdominal pain (LLQ)
Bloating
Constipation/diarrhoea

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26
Q

Diverticulitis symptoms

A

Severe abdominal pain in LLQ
Nausea and vomiting
Change in bowel habit (const > diarrhoea)
Urinary frequency
PR bleeding
Pneumaturia/faecaluria - colovesical fistula

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27
Q

Diverticulitis signs

A

Pyrexia
Tachycardia
Tender LIF (20% have a mass)
Guarding/rigidity if perforation

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28
Q

Ix findings in diverticulitis

A

Raised WCC
Raised CRP
Erect CXR - pneumoperitoneum if perforation
AXR - dilated bowel loops/obstruction/abscesses
Colonoscopy - don’t perform initially - high risk of perforation

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29
Q

Management of diverticulitis

A

Oral abx
Liquid diet
Analgesia

If symptoms don’t resolve <72hrs or if symptoms sever: hospital admission for IV abx

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30
Q

Diverticulosis

A

Presence of diverticula without symptoms

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31
Q

Where is iron absorbed

A

Proximal small intestine

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32
Q

Causes of iron deficiency

A

Reduced absorption

  • Coeliac disease
  • Duodenal bypass

Chronic blood loss

  • Menstrual bleeding
  • GI neoplasia
  • Intestinal angiodysplasia
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33
Q

Blood tests in iron deficient anaemia

A 
FBC
Haemotinics
TTG
Faecal occult blood
Colonoscopy
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34
Q

Management of iron deficiency anaemia

A 
Treat cause
Iron replacement (oral)
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35
Q

Virchow’s node

A

Supplied by lymph vessels in the abdominal cavity and there is swollen in abdominal cancers

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36
Q

Ulcerative colitis

A

Always present in the rectum
Extends proximally
Continuous, limited to the mucosa (superficial, one layer)

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37
Q

Ulcerative colitis features

A 
Bloody diarrhoea
Urgency
Tenesmus
Abdominal pain, LLQ
Extra-intestinal features
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38
Q

What is tenesmus

A

Feeling of incomplete rectal emptying

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39
Q

Extra-intestinal features of UC

A 
Arthritis (most common feature)
Erythema nodosum
Episcleritis
Uveitis
Primary sclerosing cholangitis
Pyoderma gangrenosum
Osteoporosis
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40
Q

What is the scoring system for UC

A

Truelove-Witt’s criteria

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41
Q

Ix in UC

A 
Rectal biopsy
Flexible sigmoidosocopy/colonoscopy
Abdo x-ray (toxic dilation)
Stool culture (to exclude infective causes)
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42
Q

Management of UC flare

A

Either topical (rectal) aminosalicylate (e.g. mesalazine) or add oral corticosteroid

IV steroids if severe
IV ciclosporin can be used if steroids contraindicated

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43
Q

Maintaining remission in UC

A

Topical or oral aminosalicylates

Can then move onto azathioprine or mercaptopurine

Infliximab

Surgery

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44
Q

Crohn’s disease

A

Affects entire GI tract - mouth to anus
Inflammation has skip lesions
Deep and transmural (involves all layers)

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45
Q

Clinical features of Crohn’s disease

A 
Weight loss
Lethargy
Diarrhoea (bloody if colitis)
Abdominal pain
Skin tags/ulcers
Extra intestinal features
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46
Q

Extra-intestinal features of Crohn’s

A

Arthritis
Erythema nodosum
Episcleritis
Pyoderma gangrenosum

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47
Q

Ix in Crohn’s

A

ESR/CRP
Colonoscopy (ulcers, skip lesions, abscesses)
Small bowel enema

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48
Q

Management of Crohn’s flares

A 
Steroids (first line)
Enteral feeding
Mesalazine/other 5-ASAs
Inflixmab
Metronidazole
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49
Q

Maintaining remission in Crohn’s

A

Stop smoking
Azathioprine or mercaptopurine first line
Methotrexate second line
Mesalazine if they have had previous surgery

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50
Q

Complications of Crohn’s

A

Strictures
Abscesses
Fistulae
Small bowel cancer risk increased 40 times
Colorectal cancer increased by 2
Osteoporosis (guessing from the steroids)

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51
Q

Coeliac’s disease

A 
Most common cause of small bowel malabsorption
Peak incidence at 20-40 y.o
Immune reaction to gluten
Villous atrophy
HLA-DQ2 and DQ8 associations
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52
Q

Features of coeliac’s disease

A 
Iron deficiency
Malabsorption symptoms - diarrhoea, weight loss, oedema
Dermatitis herpetiformis (characteristic bleeding eruption)
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53
Q

Investigations in coeliac’s disease

A 
Endoscopy and distal duodenal biops
Tissue-transglutaminase (TTG)
Endomyseal antibody (IgA)
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54
Q

Findings on biopsy in coeliac’s disease

A

Usually in distal duodenum:

Villous atrophy
Crypt hyperplasia
Increase in intrapeithelial lymphocytes
Lamina propria infiltration with lymphocytes

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55
Q

Management of coeliac’s

A

Gluten-free diet
Vitamin and iron replacement
Osteopenia

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56
Q

Pancreatitis causes

A

Alcohol (40%)
Gallstones (50%)
Idiopathic (10%)

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57
Q

Features of pancreatitis

A

Abdominal pain (sudden, epigastric, radiates to the back)
Hypovolaemia/shock
Vomiting
Jaundice

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58
Q

Jaundice in pancreatitis

A

Suggests the presence of an associated cholangitis

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59
Q

Scoring system in pancreatitis

A 
Modified glasgow score
PaO2 <8kPa
Age >55
WBC >15
Calcium <2mmol
Urea >16mmol
AST >200 or LDH >600
Albumin <32g
Blood glucose >10
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60
Q

Mneumonic for glasgow score

A 
PANCREAS
P PaO2
A Age
N Neutrophils
C Calcium
R Renal - Urea
E Enzymes AST/LDH
A Albumin
S Sugar
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61
Q

Ix for pancreatitis

A 
Raised amylase (75% of patients)
Investigate for underlying cause (ultrasound)
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62
Q

Chronic pancreatitis causes

A

Recurrent acute pancreatitis
Alcohol
Idiopathic

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63
Q

Features of pancreatitis

A

Pain
Exocrine pancreatic insufficiency (steatorrhoea/weight loss)
Endocrine pancreatic insufficiency (diabetes)

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64
Q

Ix in chronic pancreatitis

A 
Faecal elastase (chrymotrypsin)
Abdominal CT (pancreatic calcification)
MRCP (demonstrates pancreatic duct irregularity)
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65
Q

Management in chronic pancreatitis

A

Pancreatic enzyme replacement (creon/pancrex)
May need insulin for the pancreatic exocrine insufficient
Opioid pain management

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66
Q

Pancreatic cancer risk factors

A

Smoking
High fat meat diet
Afro/Caribbean
Male gender

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67
Q

Ix in pancreatic cancer

A

Abdo CT
MRCP
Endoscopic US
ERCP

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68
Q

What is first line for painless jaundice?

A

MRCP

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69
Q

Pancreatic cancer symptoms

A 
Painless jaundice (due to biliary tree obstruction)
Abdominal pain
Weight loss
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70
Q

Most likely place for pancreatic cancer

A

Tumour of the head of the pancreas

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71
Q

What type of cancer is common in the pancreas

A

Adenocarcinoma

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72
Q

Management of pancreatic cancer

A

90% die within a year, 98% within 5 years

Surgery - Whipple’s resection (pancreaticoduodenectomy) for head of pancreas cancers

Chemotherapy

Palliative - ERCP with stenting

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73
Q

Gallstone disease

A

From precipitation of cholesterol crystals in supersaturated bile
Stones ultimately contain calcium salts

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74
Q

Risk factors for gallstone disease

A 
4 F's:
Fat - obesity (cholesterol synthesis)
Female - 2/3 times more likely due to oestrogen increasing HMG-CoA
Fertile - pregnancy
Forty

DM
Crohn’s
Rapid weight loss
Drugs - fibrates/COCP

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75
Q

Pathophysiology of biliary colic

A

Increase in cholesterol
Decrease in bile salts
Biliary stasis
Pain is due to contracting of the gall bladder against a stone lodged in the cystic duct

76
Q

Features of biliary colic

A 
Colicky pain in the RUQ
Worse postprandially
Worse after fatty foods
Nausea and vomiting common
Can radiate to right shoulder/interscapular region
77
Q

Acute cholecystitis

A

Describes inflammation of the gallbladder

Develops secondary to gallstones in 90%, or alcalculous cholecystitis

78
Q

Features of cholecystitis

A

RUQ pain (may radiate to right shoulder)
Fever and signs of systemic upset
Murphy’s sign on examination
Mildly deranged LFT’s

79
Q

Murphy’s sign

A

Ask the patient to breathe out
Place hand below costal margin on right side (where gallbladder is)
Breathe in
If the patient winces/catches breath, the test is positive

80
Q

Investigating cholecystitis

A

US

If not found on US, do a cholescintigraphy (HIDA) scan

81
Q

Treating cholecystitis

A

IV abx

Laparoscopic cholecystectomy

82
Q

Where is the stone in cholestatic jaundice or ascending cholangitis

A

The common bile duct

83
Q

What is ascending cholangitis

A

A bacterial infection (typically by e. coli) of the biliary tree
Usually gallstones is a cause

84
Q

What is Charcot’s triad

A

A triad of symptoms for ascending cholangitis:
Fever
RUQ pain
Jaundice

85
Q

Management of ascending cholangitis

A

IV abx

Endoscopic retrograde cholangiopancreatography (ERCP)

86
Q

What is Mirizzi syndrome

A

Common hepatic duct obstruction caused by extrinsic compression from an impacted stone in the cystic duct or gallbladder

87
Q

Mirizzi syndrome symptoms/treatment

A

Jaundice
Pain etc.

Cholecystectomy

88
Q

Hepatitis A

A

Common cause of transient hepatitis

Faecal-oral transmission

89
Q

Features of hep A

A

2-4 week incubation period
Flu-like prodome

Acute hepatitis
Fatigue
Malaise
Anorexia
Nausea
Cholestatic phase - jaundice
90
Q

Investigations in viral hepatitis A

A

AST rise (most marked)
Bilirubin rise
ALP rise

HAV IgM serology (diagnostic of acute infection)

91
Q

Management of hepatitis A

A

Usually symptomatic
Evidence of liver failure requires admission (encephalopathy, coagulopathy)

Rare to have complications

92
Q

Immunisation in hep A

A

Initial dose should be followed by a booster dose 6-12 months later

Vaccinations should be for:
Haemophiliacs
Chronic liver disease
MSM
IVDU
HIV patients
93
Q

Hep B

A

Most common cause of chronic liver disease and hepatoma
Double-stranded DNA hepadnavirus

More common in IVDU, sex workers and

94
Q

Clinical features of hep B

A

Fever
Jaundice
Elevated liver transaminases

95
Q

Complications of hep B

A 
Chronic hepatitis
Fulminant liver failure
Hepatocellular carcinoma
Glomerulonephritis
Polyarteritis nodosa
Cryoglobulinaemia
96
Q

Hep B serology

A 
HBsAg - ongoing infection
HbeAg - active viral replication (able to spread, ie infectious)
HBsAb and HBcAb - previous infection
HBsAb alone - vaccine induced immunity
HBV DNA - continued infectious state
97
Q

Tests for liver fibrosis

A

Hepatic elastography

Procollagen II
N-peptide
TIMP-1
Hydraluronidase

98
Q

Management of hep B

A

Pegylated interferon-alpha acutely

Antivirals:
Tenofovir
Entecavir

Screening for HCC

Transplant if decompensated liver cirrhosis

99
Q

Hepatitis C

A

RNA Flavivirus
Incubation period 6-9 weeks

Transmission risk:
IVDU
Vertical
Sex

100
Q

Symptoms in hep c

A

Only 30% get symptoms

Serum aminotransferases rise
Jaundice
Fatigue
Arthralgia

101
Q

Ix in hep C

A 
HCV RNA (acute infection)
Anti-HCV (have cleared the virus)
102
Q

Outcomes of acute hep C

A

Develops into chronic hep C in >50% of cases

103
Q

Chronic hep C

A

Defined as having HCV RNA in your blood for 6 months

104
Q

Complications of chronic hep C

A

Rheum:
Arthralgia/arthritis
Sjogren’s

Hepatocellular cancer
Cryoglobulinaemia
Porphyria cutanea tarda
Membraneous glomerulonephritis

105
Q

How to manage chronic hep C

A

Depends on genotype
Protease inhibitors
Antivirals

Liver transplants

106
Q

Autoimmune hepatitis

A

90% are women
ANA or SMA positive
Elevated globulins + IgG
May present with amenorrhoea

107
Q

Autoimmune hepatitis treatment

A

Steroids
Azathioprine
Liver transplant

108
Q

Does c difficile cause bloody diarrhoea

A

No

109
Q

Primary biliary cholangitis (primary biliary cirrhosis)

A

Chronic liver disorder
Typically seen in middle age females (9:1)
Interlobular bile ductrs become damaged by a chronic inflammatory process
Can lead to cholestasis and eventually cirrhosis

110
Q

Features of PBC

A

Pruritis
Lethargy
Fatigue

Later:
Steatorrhoea
Fat soluble vitamin deficiency (A, D, K)

111
Q

Conditions associated with PBC

A

Sjogren’s (80%)
RA
Systemic sclerosis
Thyroid disease

112
Q

Diagnosis of PBC

A

AMA positive
Cholestatic liver panel
Biopsy shows granuloma

113
Q

Treatment of PBC

A

Ursodeoxycholic acid
Fat soluble vitamin supplementation
Cholestyramine (for itching)

Liver transplant if bilirubin high (>100)

114
Q

Complications of PBC

A

Cirrhosis
Osteomalacia
Ostoporosis
Increased risk of HCC

115
Q

Primary sclerosing cholangitis

A

Inflammation of the intra AND extra hepatic bile ducts

116
Q

PSC associations

A

Male gender

UC (80% of people with PSC have UC)
Crohn’s (less-so)
HIV

117
Q

Features of PSC

A

Cholestasis (jaundice, pruritus)
RUQ pain
Fatigue

118
Q

Ix in PSC

A

ERCP or MRCP
ANCA positive
Liver biopsy (onion skin)

119
Q

Complications

A

Small increase in cholangiocarcinoma and colorectal cancer

Can give ursodeoxycholic acid to help with itching
No specific therapy

120
Q

Non-alcoholic fatty liver disease

A

Most common cause of liver disease in the developed world
Largely associated with metabolic syndrome: T2DM, obesity, HTN, elevated TG
Insulin resistance is underlying mechanism
US shows fatty liver

121
Q

Fulminant liver failure

A

Progression from normal liver to liver failure (ie hepatic encephalopathy) within 8 weeks

122
Q

NAFLD features

A

Usually asymptomatic
Hepatomegaly
ALT > AST
Increased echogenicity

123
Q

Management of NAFLD

A

Lifestyle

Potentially metformin, gastric banding, pioglitazone (not licensed yet I think?)

124
Q

Hepatic encephalopathy

A 
Occurs in liver failure
Features:
Progressive deterioration in cognitive function
Shortened attention span
Metabolic flap (asterixis)
125
Q

Alcoholic liver disease

A

Occurs due to a:
Fatty liver
Acute alcoholic hepatitis
Cirrhosis

126
Q

Clinical features of alcoholic liver disease

A

If decompensated:
GI bleeding
Ascites

If acute hepatitis:
Sudden jaundice, anorexia, nausea, coagulopathy etc. in a chronic drinker

127
Q

Ix of alcoholic liver disease

A

Clinical history mainly

128
Q

Treatment of alcoholic hepatitis

A

Pentoxifylline

Prednisolone

129
Q

Management of alcoholic liver disease chronically

A

Alcohol cessation
Biopsy for fibrosis
HCC risk so can do surveillance

130
Q

Haemochromatosis

A

Autosomal recessive disorder of iron absorption and metabolism
Results in iron accumulation

131
Q

Precipitating causes of hepatic encephalopathy

A 
Constipation
Diuretics
Infection
Sedatives
GI bleed
132
Q

Ix in hepatic encephalopathy

A

Elevated ammonia (liver can’t remove toxins causing brain damage)

133
Q

Gene in haemochromatosis

A

HFE C282Y

Common in Celtics

134
Q

Features of haemochromatosis

A 
Fatigue
ED
Bronzed skin
Arthralgia (particularly hands)
DM
Liver - stigmata of chronic liver disease (cirrhosis, HCC)
Cardiac
135
Q

Ix in haemochromatosis

A

Raised ALT, though non-specific picture
Iron studies:
Transferrin saturation >80%
Ferritin levels VERY high

136
Q

Treatment of haemochromatosis

A

Venesection (lifelong)
Surveillance for hepatoma
Screen releatives

137
Q

Wilson’s disease

A

Autosomal recessive disorder
Excessive copper deposition in tissues due to failure of biliary excretion
Chromosome 13 ATP7B gene

138
Q

What can be seen in the eyes of patients with Wilson’s

A

Kayser Fleischer rings

139
Q

Presentations of Wilson’s

A

Hepatitis/cirrhosis
Extrapyramidal disturbances/psychosis
Acute intravascular haemolysis
Blue nails

140
Q

How to diagnose Wilson’s

A

Reduced serum caeruloplasmin
Reduced serum copper
Increased 24 hour urinary excretion

141
Q

Management of Wilson’s

A

Penicillamine

Trientine hydrochloride

142
Q

Causes of liver cirrhosis

A

Alcohol
NAFLD
Viral hep B/C

143
Q

How do we investigate for liver cirrhosis

A

Fibroscan (transient elastography)

Measures the ‘stiffness’ of the liver (proxy for fibrosis)

144
Q

What is the worry with liver cirrhosis

A

Progressive scarring can lead to non-function and thus eventually liver failure

145
Q

Symptoms of liver cirrhosis

A

Nausea
Loss of appetite
Loss of sex drive
Tired/weak

Eventually:
Yellowing
Vomiting blood
Itchy skin
Dark tarry stool
Oedema
146
Q

Causes of acute liver failure

A

Paracetamol overdose
Alcohol
Viral hep (A or B)
Acute fatty liver of pregnancy

147
Q

Features of liver failure

A 
Jaundice
Coagulopathy (raised PT time)
Hypoalbuminaemia
Hepatic encephalopathy
Renal failure is common (tubular necrosis)
148
Q

Treatment of fulminant liver failure

A

Airway management
Fluid resus if needed
Nac if paracetamol

149
Q

Portal hypertension features

A

Ascites (free fluid in the peritoneal cavity)
Splenomegaly
Thrombocytopenia
Varices

150
Q

Treatment of portal hypertension

A

Portosystemic shunts

- splenic vein to the left renal vein

151
Q

Ascites groups

A

Serum-ascites albumin gradient (SAAG) <11g/L

Serum-ascites albumin gradient (SAAG) >11g/L

152
Q

SAAG >11g

Exudate

A

Indicates portal HTN:

Cirrhosis
Hepatitis
Cardiac ascites
Budd-chiari etc.

153
Q

SAAG <11g

Transudate

A

Peritoneal carcinomatosis
TB peritonitis
Pancreatic ascites
Bowel obstruction

154
Q

Management of ascites

A

Reduce dietary sodium
Fluid restrict
Aldosterone antagonists: (e.g. spironolactone)
Drainage if tense ascites (therapeutic abdominal paracentesis)
Prophylactic abx for spontaneous bacterial peritonitis

155
Q

Spontaneous bacterial peritonitis

A

Form of peritonitis

Usually seen in patients with ascites secondary to liver cirrhosis

156
Q

Features of SBP

A

Ascites
Abdo pain
Fever

157
Q

SBP investigations

A

Paracentesis: neutrophil count > 250 cells

E. coli often found on ascitic fluid culture

158
Q

Treatment of SBP

A

IV cefotaxime

159
Q

Budd-Chiari syndrome

A 
Hepatic vein thrombosis caused by:
Haematological disease such as PRV
Thrombophilia
Pregnancy
COCP
160
Q

Triad in Budd-Chiari

A

Abdominal pain (sudden, severe)
Ascites
Tender hepatomegaly

161
Q

Ix in Budd-Chiari

A

Doppler US

162
Q

Treatment of Budd-Chiari

A

Surgical shunts (e.g. TIPS)

163
Q

Alpha-1 antitrypsin deficiency (A1AT)

A

Common inherited condition (autosomal recessive)causing lack of protease inhibitor (Pi), which is normally produced by the liver and usually protects cells from enzymes such as neutrophil elastase

164
Q

Features of alpha-1 antitrypsin deficiency

A

COPD (if young, non-smoker, often affects lower lobes most) - by causing emphysema
Liver cirrhosis
Hepatocellular carcinoma
Cholestasis in children

165
Q

Ix in A1AT

A

A1AT concentrations

Spirometry - obstructive picture

166
Q

Management in A1AT

A

No smoking
Supportive
IV A1AT protein concentrates
Surgery - lung transplant

167
Q

C difficile gram

A

Gram positive rod

168
Q

Clostridium difficile

A

Develops in response to broad-spectrum abx (C abx). PPIs a risk factor as well

Causes pseudomembranous colitis

169
Q

Features of C diff infection

A

Diarrhoea
Abdominal pain
Raised WCC (characteristic)
Toxic megacolon can develop

170
Q

Diagnosis of C diff

A

C diff toxin in stool (CDT)

171
Q

Management of C diff

A 
Oral metronidazole (10-14 days)
Vancomycin
172
Q

Achalasia features

A

Dysphagia of both solids and liquids at the same time
Heartburn
Regurgitation of food - may lead to cough, aspiration pneumonia etc

173
Q

Achalasia

A

Failure of oesophageal peristalsis and failure of relaxation of lower oesophageal sphincter (LOS)
Due to degenerative loss of ganglia from Auerbach’s plexus

174
Q

Achalasia Ix

A

Oesophageal manometry - excessive LOS tone which doesn’t relax on swallowing
Barium swallow - grossly expanded oesphagus
CXR - wide mediastinum, fluid level

175
Q

Treatment of achalasia

A

Intra-sphincteric injection of botulinum toxin
Heller cardiomyotomy
Pneumatic (balloon) dilation

176
Q

What is the cardiac sphincter

A

A sphincter between the oesophagus and stomach

177
Q

Peptic stricture

A

Longer history of dysphagia
Usually has symptoms of GORD
Lack of systemic features seen with malignancy
Usually non-progressive

Often caused by GORD

178
Q

Peptic strictures pathophysiology

A

GORD
Causes inflammation (oesophagitis)
Causes peptic strictures

179
Q

Oesophageal carcinoma pathology

A

Two types:
SCC (middle 1/3rd)
Adenocarcinoma (lower 1/3rd)

180
Q

Management of oesophageal carcinoma

A

Surgical resection
Ivor-Lewis type oesophagectomy
Adjuvant chemotherapy/radiotherapy

181
Q

Peptic stricture management

A

Surgical

Treat underlying cause:
H2 antagonists (ranitidine)
PPIs

182
Q

Hiatus hernia

A

This is where the stomach pushes up into the lower chest through a weakness in the diaghram. Two types:

Sliding:
95% of hiatus hernias
Gastroesophageal junction moves above the diaghram

Rolling (paraoesophageal):
Top of the stomach does not pass through, a different part of the stomach does

183
Q

Features of hiatus hernia

A

No symptoms itself

Can cause problems with sphincter and thus cause reflux

184
Q

Management of hiatus hernia

A

Lifestyle (lose weight, stop drinking, stop smoking etc.)
PPIs/ranitidine/antacids
Surgery

185
Q

How do we diagnose hiatus hernia

A

Barium swallow

Endoscopy

Pass Medicine (24 decks)

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