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T Year > GI Pathology > Flashcards

GI Pathology Flashcards

1
Q

What are the types of mucosa along the GI tract?

A

Oesophagus - stratified squamous (white)
Stomach - thick glandular (red brown)
Small intestine - glandular with villi
Colon and rectum - glandular with crypts

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2
Q

What is GORD

A

regurgitation of the acidic gastric contents into the lower oesophagus. the acid injury the squamous epithelium lining the oesophagus and results in inflammation

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3
Q

what are risk factors for GORD?

A

obesity
pregnancy
smoking, alcohol, coffee
hiatus hernia

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4
Q

What are complications and presentation of GORD?

A

regurgitation of acid contents into the mouth - water brash

oesophgitis - heart burn

barretts oesophagus

stricture - progressive dysphagia

bleeding - peptic ulcer may bleed. large bleeds may present with haematemesis or meleana. multiple smaller bleeds over time may present as anaemia.

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5
Q

What is Barrett’s oesophagus?

A

occurs in approx 10% of patients with long standing GORD.

metastatic process in the lower oesophageal mucosa.

it is an adaptive response to prolonged injury caused by GORD.

it is ASYMPTOMATIC and most cases are identified when patients undergo GI endoscopy for evaluation of upper GI symptoms such as GORD or dyspepsia.

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6
Q

How many Barrett’s Oesophagus patients progress to invasive adenocarcinoma?

A

2%

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7
Q

Oesophageal cancer epidemiology

A

most common in the 50-70y age group

M>F

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8
Q

Oesophageal cancer presentation

A

presents as progressive dysphagia from solids to liquids

non specific B symptoms

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9
Q

Investigation of oesophageal cancer

A

endoscopy and biopsy

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10
Q

what are the most common types of oesophageal cancer?

A
  1. adenocarcinoma

2. squamous cell carcinoma

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11
Q

how is oesophageal cancer staged?

A

TNM system

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12
Q

how is oesophageal cancer managed?

A

discussed at MDT meeting

curative intent - surgery with or without neoadjuvant therapy

palliative therapy - dilatation, stenting, radiotherapy etc

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13
Q

what is the prognosis of oesophageal cancer?

A

very poor
5-10% 5y survival

usually presents late

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14
Q

what is gastritis?

A

inflammation in the stomach

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15
Q

causes of gastritis

A

NNSAIDs

H.Pylori infection

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16
Q

what is H Pylori

A

gram negative bacteria that colonises the stomach
read by oral-oral or fecal-oral
lives in thick mucus layer on the mucosal surface
synthesises urease which catalyses the conversion of urea to ammonia, which neutralises the gastric acid and thus improves survival of the bacteria

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17
Q

what are the consequences associated with h.pylori infection?

A

more than 80% have an asymptomatic mild chronic gastritis
minority develop symptomatic gastritis
minority develop a peptic ulcer
small minority develop gastric carcinoma
very small minority develop gastric lymphoma

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18
Q

what is a peptic ulcer

A

a breach in the mucosa of the lower oesophagus, stomach and duodenum which fails to heal over a reasonable period of time

most commonly located in the gastric antrum or proximal duodenum

by definition, the breach extends through the full thickness of the mucosa. it MAY extend into the submucosa or deeper layers of the wall

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19
Q

what are the commonest causes of gastric and duodenal peptic ulcers?

A

h pylori
NSAIDs

other contributory factors:
alcohol, smoking, stress

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20
Q

what is a stress (curling) ulcer?

A

seen in patients with massive trauma, extensive burns, sepsis, raised ICP or shock.

thought to arise as a consequence of mucosal ischaemia leading to increased susceptibility to acid pepsin injury

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21
Q

what is the MOST common cause of oesophageal peptic ulcers?

A

GORD

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22
Q

the three factors of chronic inflammation

A

persistent tissue injury
ongoing inflammatory response
attempts to heal by fibrosis/scar formation

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23
Q

complications of peptic ulcers

A

bleeding
perforation
stricture formation
malignant change

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24
Q

epidemiology of gastric cancer

A

peak incidence in the over 50y age group

M>F

incidence has fallen in the west over the last 50 years - falling prevalence of h pylori and improved diet

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25
Q

risk factors for gastric cancer

A 
h pylori infection
cigarette smoking
alcohol
diet - food with nitrates/nitrite components, salt based preservatives (fresh fruit and vegetables protective!)
autoimmune gastritis
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26
Q

presentation fo gastric cancer

A 
history of new onset dyspepsia
unintended weight loss
progressive dysphagia
vomiting
virchow's node
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27
Q

main type of gastric cancer

A

adenocarcinoma

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28
Q

the two main types of gastric adenocarcinoma

A

intestinal-type adenocarcinomas - show gland formation, lined by mucus-secreting cells. better prognosis than diffuse type. tend to occur in older individuals

diffuse-type adenocarcinomas - consist of signet ring cells, with a diffuse pattern infiltration. very aggressive, very bad prognosis. tend to occur in younger age group.

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29
Q

key investigations of gastric cancer

A

endoscopy and biopsy

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30
Q

staging of gastric cancer

A

TNM

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31
Q

prognosis of gastric cancer

A

around 5% at 5y

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32
Q

gallstones epidemiology

A

10-15% of adult western world develop gallstones

2-4% of people with gallstones develop symptoms each year

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33
Q

types of gallstones

A

mixed stones (75%) - ca salts, bile pigment, cholesterol

cholesterol stones (20%) - large sized, yellow

bilirubinate stones (5%) - small sized, pigmented

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34
Q

pathogenesis of gallstones

A

normally cholesterol is solubilised in ice as a micelle with bile salts

an imbalance between the proportions of cholesterol and bile salts leads to precipitation of the excess component as gallstones

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35
Q

risk factors for cholesterol stones

A 
female sex
obesity
middle age
family history
crohns disease

increased levels of cholesterol!

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36
Q

risk factors for billirubinate stones

A

haemolytic anaemias

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37
Q

investigations of gallstones

A

USS of gallbladder will identify 90% of gallstones

LFTs performed to assess liver function

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38
Q

acute cholescystitis

A

impacted stone occludes the cystic duct for a prolonged period of time, it will rub and damage the mucosal lining and thereby incite an acute inflammatory response in the gallbladder wall - development of acute cholecystitis

the presence of fever usually indicated acute cholecystitis

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39
Q

what is acute acalculus cholecystitis

A

thought to result from ischaemia - cystic after is an end artery

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40
Q

chronic cholecystitis

A

repeated episodes of biliary colic and acute cholecystitis result in chronic inflammation with healing by fibrosis.

as a consequence, the gallbladder wall becomes thickened and the gallbladder shrinks size

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41
Q

ascending cholangitis

A

if a gallstone impacts and obstructs the common bile duct it will cause obstructive jaundice

the jaundice develops because bile is unable to drain into the duodenum for excretion

this can develop into ascending cholangitis which is inflammation of the bile duct - biliary obstruction causes stasis which predisposes to superimposed infection: gut bacteria gain entry to the biliary tree via the ampulla of vater

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42
Q

what is charcot’s triad?

A

jaundice
fever (usually with rigors)
RUQ pain

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43
Q

relationship between gallstones and acute pancreatitis

A

if a gallstone passes down the CBD and obstructs the ampulla of water it will result in acute pancreatitis

reflux of pancreatic secretions back up the pancreatic duct which causes pancreatic auto digestion and results in pancreatitis

44
Q

what is gallstone ileus

A

gallstone larger enough to cause small bowel obstruction enters the small bowel via a fistula which forms between the inflamed wall of the gallbladder and a loop of small bowel.

colicky abdominal pain, vomiting, distension, absolute constipation

45
Q

courvoisier’s law

A

in a jaundiced patient, the presence of a palpable gallbladder means that the jaundice is unlikely to be due to gallstones impacted in the biliary system

This is because a patient with jaundice due to a gallstone in the common bile duct is likely to have a fibrotic shrunken gallbladder because of repeated episodes of biliary colic and acute cholecystitis As a consequence, the gallbladder is impalpable.

46
Q

what are the functions of the pancreas

A

exocrine - secreting digestive enzymes into the pancreatic duct system

endocrine - secreting hormones such as insulin and glucagon directly into the blood

47
Q

what is the most common type of pancreatic cancer

A

adenocarcinoma arising from the glandular duct cells that line the ducts of the exocrine system

48
Q

what are the risk factors fro pancreatic cancer?

A

smoking is the only well recognised risk factor

occurs more in elderly males

49
Q

head of pancreas presentation

A

obstructive jaundice

B symptoms

50
Q

management of pancreatic cancer

A

majority (80%) present with advanced disease ad treatment is palliative - chemo, stunting CBD, symptom control

minority (20%) are suitable for curative surgery (Whipples Procedure) when tumour appears to be confined to the pancreas and lymph nodes are not involved

51
Q

what is a whiles procedure?

A

In a Whipple’s pancreatico-duodenectomy, the distal stomach, gallbladder, common bile duct, head of pancreas, duodenum, proximal jejunum and regional lymph nodes are resected.
The reconstruction restores intestinal function by re-establishing flow of pancreatic juices, bile and food along the GI tract.

52
Q

pancreatic cancer prognosis

A

After a Whipple’s procedure, the 5 year survival is between 20-40%.
In contrast, the overall survival for pancreatic cancer at 5 years (including the majority of patients who have advanced disease) is about 5%.

53
Q

what is coeliac disease

A

intolerance to gluten (GLIADIN) which is found in wheat, barley and rye

54
Q

pathogenesis of coeliac disease

A

The pathogenesis of coeliac disease is not fully understood: it is thought that gliadin triggers inappropriate
activation of intestinal T cells in genetically susceptible individuals (people with HLA-DQ2 and HLA-DQ8 haplotypes), resulting in damage to intestinal epithelial cells.

Gluten is digested by luminal and brush-border enzymes in the small intestine into amino acids and peptides, including a 33-amino acid gliadin peptide. Gliadin is deamidated (deamidation = removal of an amide group from an organic compound) in the mucosa by *ssue transglutaminases (tTG).
In individuals with the HLA-DQ2 and HLA-DQ8 haplotypes, the deamidated gliadin closely fits the MHC II grooves and is presented to T helper cells by an;gen presenting cells.

This initiates a Th2- predominant immune
response which generates cytotoxic T cells
against gliadin.

The cytotoxic T cells migrate into the intestinal
epithelium which is visible on biopsy as
intraepithelial lymphocytes [intraepithelial = within the epithelium].

The T cells damage and destroy epithelial cells resulting in progressive villous atrophy. As a result, the crypts become hyperplastic to compensate for the cell loss.

55
Q

what antibodies are useful diagnostically in coeliac disease?

A

antigliadin
antiendomysial
antiTTG

56
Q

clinical presentation of coeliac disease

A

malabsorption symtoms (diarrhoea, steatorrhoea, weight loss, lethargy,bloating, abdo pain)

non specific symptoms e.g. anaemia, IBS, abdo pain

failure to thrive and delayed puberty in children

dermatitis herpetiformis over elbows - itchy and blistering

some are symptomatic

57
Q

diagnosis of coeliac disease

A

history and examination
serology: total IgA, IgA tTG, EMA
(must be eating gluten 6 weeks)

gold standard is endoscopy and duodenal biopsy

58
Q

treatment of coeliac disease

A

life long gluten free diet

59
Q

complications of coeliac disease

A

malabsorption
osteopenia/osteoporosis
dermatitis herpetiformis
lymphoma

60
Q

clinical features of peritonitis

A 
tachycardia
pyrexia
tenderness and guarding
rebound tenderness
localised pain during distant palpation
absence of bowel sounds
61
Q

investigations of peritonitis

A 
primarily a clinical diagnosis
FBC (leucocytosis)
serum amylase would show pancreatitis
erect CXR would show perforation
CT may pinpoint the cause
62
Q

management of peritonitis

A 
IV fluids and electrolyte replacement
antibiotic therapy
pain relief
gastric aspiration
surgery may be indicated depending on the cause
63
Q

types of intestinal obstruction

A

mechanical obstruction

paralytic obstruction

64
Q

how can mechanical obstruction be classified

A

speed of onset
anatomical site
simple vs strangulating
open loop vs closed loop

65
Q

causes of small bowel obstruction

A
  1. ADHESIONS
  2. hernias
    interssusception
    volvulus
    crohn’s disease
66
Q

causes of large bowel obstruction

A

colorectal cancer (adenocarcinoma)
diverticular strictures
sigmoid volvulus

67
Q

what is intussusception?

A

when a segment of small bowel prolapses into the immediately adjoining bowel

commonest form is ileocolic

68
Q

what is volvulus

A

abnormal twisting of a segment of the bowel around its site of a mesenteric attachment resulting in a closed loop obstruction

there is also occlusion of the main vessels at the base of the involved mesentery which amy result in strangulation

most commonly occurs in the SIGMOID, but can also occur in the caecum and small intestine

69
Q

what are precipitating factors of volvulus?

A

abnormally mobile loop of intestine e.g. a particularly long sigmoid loop

abnormally loaded loop e.g. chronic constipation

loop fixed at its base by adhesions, around which it rotates

a loop of bowel with a narrow mesenteric attachment

70
Q

management of volvulus

A

Volvulus may be treated by passing a long soft rectal tube through a sigmoidoscope and advancing it into the sigmoid colon. This often untwists an early volvulus and is accompanied by passage of vast amounts of flatus and liquid faeces. If this fails, the volvulus is untwisted at laparotomy and the bowel is decompressed via a rectal tube threaded up from the anus. If infarcMon/gangrene has occurred, the affected segment is resected and the two open ends are brought out as a double-barreled colostomy which is later closed.

71
Q

Colorectal cancer and obstruction

A

• bowel cancer (almost always adenocarcinoma) may present as large bowel obstruction. This is more
common with left-sided tumours because the bowel contents are more solid by the Mme they reach the
left side.
• the obstruction may be chronic with insidious onset and slowly progressive symptoms. A chronic
obstruction may develop acute symptoms as the obstruction suddenly becomes complete (ie. when a
narrowed lumen becomes totally occluded). This is often termed acute-on-chronic obstruction.
• don’t forget that colorectal cancer presents as an emergency (such as bowel obstruction) in around 20%
of cases.

72
Q

common causes of bowel obstruction in neonates

A

congenital atresia and stenosis
volvulus
hirschsprung’s disease
meconium ileus

73
Q

common causes of bowel obstruction in infants

A

intussusception
hirschsprung’s disease
strangulated hernia
mocker’s diverticulum

74
Q

clinical features of mechanical bowel obstruction

A

colicky abdo pain
abdo distension
vomiting
absolute constipation

changed bowel sounds (tinkling eventually)
dehydration
hypotension
tachycardia
empty rectum on PR examination
75
Q

signs of strangulating obstruction

A

toxic appearance with tachycardia and fever
colicky pain becoming continuous as peritonitis develops
tenderness, guarding rebound tenderness
absent bowel sounds

76
Q

management of mechanical bowel obstruction

A 
iv fluid/electrolytes
close monitoring
NG suction
(drip and suck)
iv antibiotics if strangulation is suspected
investigate the cause
77
Q

causes of paralytic ileus

A

postoperative state
generalised peritonitis
drugs e.g. opiates, anticholinergics
electrolyte imbalances

78
Q

pathophysiology of paralytic ileus

A

The effects of paralytic ileus are similar to those of a simple mechanical obstruction:
The lack of coordinated peristalsis results in a functional obstruction. Gas (mainly swallowed air) and fluid/ electrolytes accumulate in the bowel lumen. As the bowel dilates, the blood supply to the bowel is compromised resulting in ischaemia which, if not reversed, may result in infarction (gangrene) and perforation.

79
Q

clinical features of paralytic ileus

A

pain - but NOT colicky
abdo distention
constipation
ileus

80
Q

causes of bowel infarction

A 
strangulating bowel obstruction
embolus causing obstruction of a mesenteric artery
thrombus occlusion
aortic dissection into mesenteric artery
compression of veins in bowel wall
vasculitis
81
Q

clinical features of bowel infarction

A

colicky abdo pain
rectal bleeding
shock
elderly with AF

may produce similar signs to peritonitis

82
Q

management of bowel infarction

A

The management of bowel infarction is beyond the scope of these notes. However, in general the patient should be resuscitated with iv fluids and given broad spectrum antibiotocs. They usually undergo urgent laparotomy where any dead bowel is resected. Revascularisation by embolectomy or bypass may improve doubkully viable bowel and allow primary anastomosis.

83
Q

where sis the most common site of diverticular disease

A

sigmoid

84
Q

what is a diverticulum

A

a pouch of colonic mucosa that has herniated through the muscularis propria and has come to lie in the subserosal (pericolic) fat outside the bowel wall

85
Q

important factors in the development of diverticula

A

areas of weakness in the colonic wall

raised intraluminal pressure due to insufficient dietary fibre

86
Q

diverticulosis

A

diverticula are present but asymptomatic

87
Q

diverticulitis

A

acutely inflamed diverticulum. this is the most common presentation

88
Q

acute diverticulitis

A

initiated when faecal matter impacts and obstructs the neck of a diverticulum

this traps bacteria with consequence bacterial replication in the occluded lumen resulting in infection and mucosal injury

local trauma (rubbing) to the mucosa by the faecolith may also cause mucosal injury

89
Q

complications of diverticular disease

A 
abscess formation
perforation and peritonitis
fistula
stricture
lower GI bleeding
90
Q

management of peptic ulcers

A

triple therapy: 2x ABx and PPI
amoxicillin and clarythromycin
lanzoprazole, omeprazole

91
Q

causes of acute pancreatitis

A

IGETSMASHED

idiopathic
gallstones
ethanol
trauma
steroids
mumps
autoimmune
scorpion venom
hypothermia/hypercalcaemia/hyperlipidaemia
ERCP and emboli
drugs
92
Q

pancreatitis investigations

A 
amylase and LIPASE
ABG
AXR
CT
USS
ERCP
CRP
93
Q

complications of pancreatitis

A 
abscess
shock
renal failure
sepsis
bleeding
thrombosis

fistulae

94
Q

management of pancreatitis

A

severity assessment (glasgow criteria - PANCREAS)
NBM, NJ tube, fluids
analgesia
hourly and daily monitoring
possible ITU, oxygen, ABx
ERCP and gallstone removal is progressive jaundice
repeat imaging to monitor

95
Q

glasgow criteria for severity pancreatitis

A 
PaO2 <8kPa
Age >55y
Neutrphilia >15
Calcium <2
Renal function (urea >16)
Enzyme (LDH <600, AST <200)
Albumin <32
Sugar >10
96
Q

C diff infection signs and symptoms

A

foul odour of stool, green brown
significant diarrhoea
fever
abdominal pain

97
Q

management of acute liver failure

A 
ABCDE
vitamin K if PTT is raised
stop all hepatotoxic drugs
Abx prophylaxis if ascites to stop SBP
daily bloods
lactulose - helps remove ammonia
close monitoring
98
Q

examples of hepatotoxic drugs

A

paracetamol
rifampicin
pyrazinamide

99
Q

common causes of upper GI bleeds

A 
varices 10-20%
reflux oesophagitis 2-5%
mallory-weiss 5-10%
peptic ulcers 50%
haemorrhage gastropathy and erosions 15-20%
drugs
malignancy
100
Q

treatment of bleeding oesophageal varices

A

banding, sclerotherapy, sengstaken-blakemore tube

101
Q

treatment of peptic ulcers

A

endoscopic haemostats with adrenaline injection, coagulation with thermal therapy, IV PPI therapy for 72 hours following endoscopic therapy

102
Q

Acute hepatitis symptoms and stages

A
  1. prodromal stage - non specific flu like symptoms
  2. yellowing of the skin and eyes (up to 4 weeks) - hepatomegaly, abdo pain, ?splenomegaly, weight loss
  3. recovery phase - resolution of symptoms, but still increased LFTs and hepatomegaly
103
Q

Ulcerative Collitis

A

diarrhoea, often with blood
relapses and remits
severe fulminant colitis
LIF pain

only colon, begins in rectum and extends proximally
continuous
red mucosa, bleeds easily
mucosal inflammation
goblet cell depletion and crypt abscesses

104
Q

Crohn’s disease

A 
abdominal pain
weight loss
RIF pain
diarrhoea
bleeding
anal tags, fissures, etc
relapses and remits
all of GIT
oral and perianal
skip lesions
cobblestone appearance
transmural inflammation
granulomas in 50%
105
Q

management of IBD

A 
oral 5-ASA mesalazine
steroids: prednisolone, IV hydrocortisone
liquid internal nutrition
thiopurine drugs
metronidazole
methotrexate

colectomy or panproctocolectomy are surgical options if medication failure or complications

106
Q

extra-gut manifestations of IBD

A

eyes - uveitis, conjunctivitis
joints - arthralgia, arthritis
skin - erythema nodosum, pyoderma gangrenous
hepatobiliary - fatty liver, sclerosing cholangitis, chronic hepatitis, cirrhosis, gallstone
renal calculi - oxalate stones

107
Q

complications of IBD

A 
toxic dilation of colon and perforation
stricture formation
abscess formation (CD)
fistulae and issues (CD)
colon cancer

T Year (18 decks)

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