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Y4 > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

if someone has an autoimmune condition, what are they more likely to have?

A

another autoimmune condition e.g.
T1DM and coeliac’s disease, thyroid disease, autoimmune hepatitis

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2
Q

pathophysiology of coeliac disease

A

autoantibodies created in response to gluten that target the epithelial cells of the small intestine, leading to inflammation

particularly of the jejunum, leading to villus atrophy = malabsorption of nutrients & symptoms of disease

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3
Q

investigations for coeliac disease

A

need to be eating gluten for at least 6 weeks

anti-TTG and anti-EMA (endomysial) both IgA
** need to check for IgA deficiency beforehand

endoscopic intestinal biopsy (gold standard - duodenal)
-villous atrophy
-crypt hyperplasia

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4
Q

presentation of coeliac disease

A

failure to thrive in children
diarrhoea
abdominal pain/bloating
weight loss
fatigue
anaemia
mouth ulcers
dermatitis herpetiformis (itchy blistering skin rash typically on the abdomen)

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5
Q

complications of coeliac disease

A

hyposplenism
anaemia: iron, folate, B12 (folate more common than b12)
osteoporosis
lactose intolerance
enteropathy-associated T-cell lymphoma of small intestine
subfertility
non-hodgkin lymphoma
oesophageal cancer

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6
Q

what are all new cases of T1DM tested for

A

coeliac disease

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7
Q

what is haemochromatosis

A

an autosomal recessive condition
iron storage disorder that results in excessive total body iron and deposition in tissues

mutation in HFE gene on chromosome 6

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8
Q

presentation of haemochromatosis

A

early symptoms: fatigue, arthralgia, erectile dysfunction
bronze skin pigmentation
diabetes mellitus
liver: chronic liver disease, hepatomegaly, cirrhosis
cardiac failure
amenorrhoea, infertility, reduced libido

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9
Q

reversible vs irreversible complications of haemochromatosis

A

reversible: cardiomyopathy, skin pigmentation
irreversible: diabetes, cirrhosis, arthropathy, hypogonadotrophic hypogonadism

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10
Q

significance of HBsAg in interpreting hepatitis B serology

A

if positive, ongoing infection
1-6 months = acute
>6 months = chronic

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11
Q

significance of anti-HBs and anti-HBc in interpreting hepatitis B serology

A

anti-HBs = implies immunity (either exposure/vaccination), negative in chronic disease

anti-HBc = negative if immunised
IgM anti-HBc appears during acute/recent HB infection and lasts for around 6 months
IgG persists

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12
Q

symptoms of scurvy

A

follicular hyperkeratosis & perifollicular haemorrhages
easy bruising
poor wound healing
Gingivitis with bleeding and receding gums
Sjogren’s syndrome
generalised symptoms = weakness, malaise, anorexia, depression

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13
Q

what is pseudomembranous colitis

A

inflammation of the colon due to overgrowth of c.diff bacteria
develops when the normal gut flora are suppressed
due to broad spectrum antibiotics

risk factors: PPIs, clindamycin, 2nd and 3rd generation cephalosporins

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14
Q

side effects of PPIs

A

hyponatremia, hypomagnasaemia
increased risk of osteoporosis
microscopic colitis
increased risk of c.diff infections

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15
Q

causes of vitamin b12 deficiency

A

pernicious anaemia
Diphyllobothrium latum infection
Crohn’s disease
atrophic gastritis (Secondary to h.pylori infection)
gastrectomy
malnutrition e.g. alcoholism

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16
Q

Ulcerative colitis - CLOSE UP

A

continuous inflammation
limited to colon & rectum
only superficial mucosa affected
smoking is protective
excrete blood & mucus
use aminosalicylates
primary sclerosing cholangitis

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17
Q

different types of autoimmune hepatitis

A

type 1 = affects women in lates 40s/50s, fatigue & features of liver disease, less acute

type 2 = affects teenagers/early twenties, more acute picture of raised transaminases & jaundice

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18
Q

autoantibodies involved in autoimmune hepatitis

A

type 1 - ANA, SMA

type 2 - Anti-liver/kidney microsomal type 1 antibodies (LKM1)

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19
Q

features of autoimmune hepatitis

A

may present with signs of chronic liver disease
acute hepatitis: fever, jaundice
amenorrhoea
ANA/SMA/LKM1 antibodies, raised IgG levels

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20
Q

management of autoimmune hepatitis

A

steroids e.g. prednisolone, azathioprine
liver transplantation

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21
Q

scoring systems used for liver cirrhosis

A

Child-Pugh classification: albumin, bilirubin, prothrombin time, encephalopathy, ascites

Model for End-Stage Liver Disease (MELD): bilirubin, creatinine, INR

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22
Q

pathophysiology of pernicious anaemia

A

antibodies against intrinsic factor/parietal cells
parietal cells release intrinsic factor, essential for the absorption of vitamin b12 in the ileum

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23
Q

role of vitamin b12

A

production of blood cells & myelination of nerve cells

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24
Q

features of pernicious anaemia

A

anaemia features: fatigue, pallor, dyspnoea
peripheral neuropathy
glossitis
neuropsychiatric: depression, memory loss, confusion, poor concentration, irritability

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25
Q

management of pernicious anaemia

A

no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections (1mg of intramuscular hydroxycobalamin)

more frequent doses are given for patients with neurological features

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26
Q

complications of pernicious anaemia

A

subacute combined degeneration of the spinal cord
gastric malignancy

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27
Q

symptoms that should suggest IBS

A

functional bowel disorder, symptoms present for 6 months
not common after 60yrs

abdominal pain/discomfort:
relieved on opening bowels
associated with a change in bowel habit

and 2 of the following:
abnormal stool passage (urgency, incomplete stool evacuation, straining)
bloating
worse after eating
mucus

lethargy, nausea, backache and bladder symptoms may also support the diagnosis

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28
Q

symptoms that should suggest IBS

A

abdominal pain/discomfort:
relieved on opening bowels
associated with a change in bowel habit

and 2 of the following:
abnormal stool passage
bloating
worse after eating
mucus

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29
Q

pathology to rule out with IBS

A

faecal calprotectin (IBD)
coeliac disease
malignancy

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30
Q

management of IBS

A

first line:
loperamide for diarrhoea
laxatives for constipation (avoid lactulose, linaclotide is used 2nd line)
Antispasmodics for cramps e.g. hyoscine butylbromide (Buscopan)

2nd line:
tricyclic antidepressants (better for diarrhoea)
psychological interventions e.g. CBT, psychologically manage condition & reduce distress

regular small meals
adequate fluid intake
avoid caffeine & alcohol
low FODMAP diet (FODMAPs are short-chain carbohydrates that are poorly absorbed in the small intestine, they then encourage the intake of water into the small intestine causing diarrhoea or when reaching the large bowel they are prone to fermentation by bacteria causing bloating)

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31
Q

what causes flares of UC

A

stress
NSAIDs, antibiotics
stopping smoking

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32
Q

flare severity criteria for UC

A

mild:
<4 stools a day, with or without blood
no systemic upset

moderate:
4-6 stools a day, with blood, minimal systemic upset

severe:
>6 bloody stools, systemic upset (fever, tachycardia, abdominal tenderness)

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33
Q

urgent referral for endoscopy criteria

A

dysphagia

upper abdominal mass consistent with stomach cancer

> 55, weight loss AND:
upper abdominal pain
dyspepsia
reflux

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34
Q

non-urgent referral for endoscopy criteria

A

patients with haematemesis

Patients aged >= 55 years who’ve got:
treatment-resistant dyspepsia or

upper abdominal pain with low haemoglobin levels or

raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain

nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain

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35
Q

pathophysiology of h.pylori

A

gram negative aerobic bacteria
forces its way into gastric mucosa, the break it makes exposes gastric epithelium to acidic environment
produces ammonia to neutralise acid, which also directly damages epithelial cells

results in gastritis, ulcers, malignancy

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35
Q

what is essential before a h.pylori test (urea breath test)

A

no antibiotics for 4 weeks
no PPIs for 2 weeks

used as test of eradication after therapy

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36
Q

stages of non-alcoholic fatty liver disease

A

steatosis
steatohepatitis
Fibrosis
Cirrhosis

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37
Q

associated features of non-alcoholic fatty liver disease

A

T2DM
obesity
hyperlipidaemia
low activity levels
high cholesterol
jejunoileal bypass
sudden weight loss/starvation

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38
Q

differentials for abnormal liver function tests

A

USS (non-alcoholic fatty liver disease)
Hepatitis B & C serology
Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis)
caeruloplasmin (Wilson’s)
Alpha 1 Anti-trypsin levels
transferrin & ferritin (haemochromatosis)

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39
Q

presentation of NAFLD

A

asymptomatic
hepatomegaly
ALT is typically greater than AST
increased echogenicity on ultrasound

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40
Q

investigation in NAFLD

A

enhanced liver fibrosis blood test

41
Q

management of NAFLD

A

Weight loss
Exercise
Stop smoking
Control of diabetes, blood pressure and cholesterol
Avoid alcohol

42
Q

what drugs tend to cause cholestasis

A

COCP
antibiotics e.g. flucloxacillin, co-amoxiclav, erythromycin
sulfonylureas
anabolic steroids, testosterones

raised ALP, GGT

43
Q

what should happen to males drinking >50 units a week & females >35 with normal LFTs

A

should be referred for ELF test or fibroscan, even if liver function tests are normal

44
Q

investigations for haemochromatosis

A

general population: transferrin saturation
family members: HFE mutation

**ferritin is an acute phase reactant, transferrin will indicate if ferritin is high due to inflammation/NAFLD or iron overload

Liver biopsy with Perl’s stain can be used to establish the iron concentration in the parenchymal cells

45
Q

management of haemochromatosis

A

venesection - transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
desferrioxamine may be used second-line

46
Q

complications of haemochromatosis

A

chronic liver disease/carcinoma
cardiomyopathy
T1DM
hypothyroidism
Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis
Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility)

47
Q

features of c.diff infection

A

diarrhoea
abdominal pain
raised WCC
if severe, toxic megacolon can develop

48
Q

criteria for varying severities of c.diff infection

A

mild:
normal WCC

moderate:
raised WCC
3-5 loose stools a day

severe:
raised WCC
temp >38.5, evidence of severe colitis (abdominal/radiological signs)

life-threatening:
hypotension
partial/complete ileus
toxic megacolon

49
Q

diagnosis of c.diff infection

A

Clostridium difficile toxin (CDT) in the stool

50
Q

management of c.diff infection

A

first-line therapy is oral vancomycin for 10 days

second-line therapy: oral fidaxomicin

third-line therapy: oral vancomycin +/- IV metronidazole

recurrent episode:
within 12 weeks of symptom resolution: oral fidaxomicin
after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin

Life-threatening Clostridium difficile infection:
oral vancomycin AND IV metronidazole
specialist advice - surgery may be considered

51
Q

criteria for same day admission for someone presenting with jaundice

A

acutely unwell
fever
encephalopathy (confusion, ataxia)
cholangitis
dehydrated
bilirubin >100
abnormal coagulation
abnormal kidney function
suspected paracetamol overdose
frail/significant co-morbidities

52
Q

differentials for dysphagia

A

oesophageal cancer
oesphagitis
oesophageal candidiasis
achalasia
pharyngeal pouch
systemic sclerosis
myasthenia gravis
globus hystericus

53
Q

what is primary sclerosing cholangitis

A

biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts

54
Q

associations of primary sclerosing cholangitis

A

UC
crohn’s
HIV

55
Q

presentation of PSC

A

cholestasis: jaundice, raised ALP, bilirubin, pruritus
RUQ pain
fatigue

56
Q

investigation for PSC

A

ERCP/MRCP - beaded appearance

57
Q

complications of PSC

A

cholangiocarcinoma
increased risk of colorectal cancer

58
Q

what is Peutz Jeghers syndrome

A

autosomal dominant condition characterised by numerous hamartomatous polyps in the GI tract (mainly small bowel) & pigmentation of lips, face, palms & soles

**can present with small bowel obstruction often due to intussusception
GI bleeding

59
Q

management of Peutz Jeghers syndrome

A

conservative unless complications develop

60
Q

what to think with T2DM and abnormal LFTs

A

non alcoholic fatty liver disease

61
Q

symptoms of oesphageal cancer

A

dysphagia
weight loss
anorexia
vomiting
odynophagia, hoarse voice, cough, melaena

62
Q

features of cyclical vomiting syndrome

A

severe nausea and vomiting lasting hours to days
Prodromal intense sweating and nausea
Well in between episodes

might have:
weight loss
reduced appetite
abdominal pain
diarrhoea
photophobia
headache

63
Q

what is cyclical vomiting syndrome

A

rare
seen in children more than adults
seen in females more than males

associated with migraines

64
Q

investigations of cyclical vomiting syndrome

A

clinical diagnosis
pregnancy test to exclude in women
routine blood tests to identify any underlying condition

65
Q

management of cyclical vomiting syndrome

A

avoidance of triggers
Prophylactic treatments include amitriptyline, propranolol and topiramate.
Ondansetron, prochlorperazine and triptans in acute episodes

66
Q

management of GORD

A

endoscopically negative:
full dose PPI for one month
if response = offer low dose treatment
no response = offer H2RA e.g. ranitidine

endoscopically proven oesphagitis:
full dose PPI 1-2 months
if response: lower dose
no response: double dose PPI for 1 month

lifestyle:
weight loss
smaller, lighter meals
avoid heavy meals before bed
sit upright after eating
stop smoking
reduce tea, coffee, caffeine

67
Q

complications of GORD

A

oesphagitis
ulcers
anaemia
benign strictures
Barrett’s oesphagus
carcinoma

68
Q

what can often be used to test for H.pylori

A

stool test

69
Q

management of patients with a raised ALT

A

all patients should be investigated with a raised ALT with a liver screen including USS

70
Q

presentation of UC

A

bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the LLQ

71
Q

investigations for UC

A

colonoscopy + biopsy
** if severe colitis use flexible sigmoidoscopy to prevent perforation

findings:
red, raw mucosa that bleeds easily
no inflammation beyond submucosa
pseudopolyps

barium enema:
loss of haustrations
narrowing of colon if long standing disease

71
Q

investigations for UC

A

colonoscopy + biopsy
** if severe colitis use flexible sigmoidoscopy to prevent perforation

findings:
red, raw mucosa that bleeds easily
no inflammation beyond submucosa
pseudopolyps

barium enema:
loss of haustrations
narrowing of colon if long standing disease

72
Q

what is melanosis coli

A

disorder of pigmentation of the bowel wall
histology shows pigment laden macrophages

associated with laxative abuse

72
Q

what is melanosis coli

A

disorder of pigmentation of the bowel wall
histology shows pigment laden macrophages

associated with laxative abuse

73
Q

presentation of crohn’s

A

non-specific e.g. fatigue, weight loss
diarrhoea
abdominal pain
perianal disease e.g skin tags, ulcers

74
Q

Is small bowel or large bowel obstruction more common

A

Small bowel

75
Q

Pathophysiology of bowel obstruction

A

Obstruction of food, fluids and gas results in a build up proximal to the obstruction, resulting in back pressure which causes vomiting & dilatation of intestines proximal to the obstruction

GI tract secretes fluid later absorbed in the colon, when there is an obstruction & fluid can’t be absorbed, fluid loss from intravascular space leads to hypovolaemia and shock = third spacing

The higher up the intestine the obstruction, the greater the fluid loss as there is less bowel for fluid to be reabsorbed

76
Q

Causes of bowel obstruction

A

Adhesions and hernias (small bowel)
Malignancy (large bowel)

Other causes: intussusception, strictures, diverticular disease, volvulus

77
Q

What causes adhesions

A

Abdominal or pelvic surgery
Peritonitis
Endometriosis
Abdominal or pelvic infections e.g. PID

Can be congenital or secondary to radiotherapy

78
Q

What is closed loop obstruction

A

Two points of obstruction along the bowel, middle section sandwiched between 2 points of obstruction

E.g. adhesions
Hernias
Volvulus
Single point of obstruction with competent ileocaecal valve (does not allow any movement back into ileum)

79
Q

Consequences of a closed loop obstruction

A

Do not have an open end where they can drain and decompress
Will continue to expand, leading to ischaemia and perforation

EMERGENCY SURGERY

80
Q

Presentation of bowel obstruction

A

Vomiting (green bilious vomiting)
Abdominal distension
Diffuse abdominal pain
Constipation and lack of flatulence
Tinkling bowel sounds in early bowel obstruction

81
Q

How to tell the difference between small and large bowel on X-ray

A

Small bowel = valvulae conniventes
Mucosal folds extending full width of the bowel

Large bowel = haustra
Pouches formed by muscles in walls of large bowel, do not extend full width of bowel

82
Q

Investigation for bowel obstruction

A

Abdominal X-RAY = initial
>3cm diameter small bowel
>6cm colon
>9cm caecum
Free intraperitoneal gas might indicate perforation

Erect CXR can demonstrate air under the diaphragm if intra-abdominal perforation
Contrast abdominal CT scan

83
Q

Initial management of bowel obstruction

A

ABCDE approach:
May be haemodynamically unstable if hypovolaemic shock, bowel ischaemia or perforation, or sepsis

Nil by mouth
IV fluids to hydrate and correct any electrolyte abnormalities
NG tube with free drainage (reduce risk of vomiting and aspiration)

84
Q

Key blood findings in bowel obstruction

A

U&Es
Metabolic alkalosis (vomiting)
Bowel ischaemia (raised lactate)

85
Q

Further management of bowel obstruction

A

Conservative management if patient stable and secondary to adhesions/volvulus
If this fails, definitive management anyway is surgery

Exploratory surgery
Adhesiolysis
Hernia repair
Emergency resection of tumour
Stents may be inserted during colonoscopy

86
Q

When will IV ABx be started during bowel obstruction

A

Perforation suspected or surgery planned

87
Q

Role of mesentery

A

Membranous peritoneal tissue that creates a connection between the bowel and posterior abdominal wall

Bowel gets its blood supply via the mesentery through the mesenteric arteries

88
Q

What is a volvulus

A

Condition where the bowel twists around itself and the mesentery it is attached to
Leads to a closed bowel obstruction

Bowel vessels might be involved, leading to ischaemia, necrosis and bowel perforation

89
Q

What are the 2 types of volvulus

A

Sigmoid
Caecal

90
Q

Associations of sigmoid volvulus

A

More common (80%), affects older individuals
Associated with chronic constipation (becomes overloaded with faeces, sinks downwards and causes a twist)

Chagas’ disease
Neurological conditions e.g. Parkinson’s, duchenne muscular dystrophy
Psychiatric e.g. scizhophrenia

91
Q

Associations of caecal volvulus

A

All ages
Pregnancy
Adhesions

92
Q

Presentation of volvulus

A

Same as bowel obstruction

93
Q

Investigations of volvulus

A

Abdominal X-ray - coffee bean sign
Contrast CT to confirm

94
Q

what type of peptic ulcer are more common

A

duodenal > gastric

95
Q

pathophysiology of peptic ulcers

A

stomach mucosa is prone to ulceration from breakdown of the protective layer of the stomach/duodenum or an increase in the production of stomach acid

protective layer can be broken down due to: medications (steroids/NSAIDs) or H.pylori

increase in production of stomach acid: caffeine, stress, alcohol, smoking, spicy foods

96
Q

presentation of peptic ulcers

A

epigastric pain
nausea and vomiting
dyspepsia
haematemesis, coffee ground vomit, melaena
iron deficiency anaemia

*** eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.

97
Q

investigations for peptic ulcers

A

endoscopy
- rapid urease test (CLO) can be performed to check for H.pylori
- biopsy should be considered to check for malignancy

98
Q

management for peptic ulcers

A

high dose PPIs
endoscopy can be used for monitoring

99
Q

complications of peptic ulcers

A

bleeding - most common complication, with the gastroduodenal artery being a source of significant GI bleeding

perforation - epigastric pain that becomes generalised due to peritonitis
can be diagnosed with an erect CXR indicating air under the diaphragm

scarring and strictures of the muscle and mucosa, which can lead to pyloric stenosis

Y4 (16 decks)

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