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Y2 Clinical Pathology > GI > Flashcards

GI Flashcards

1
Q

What is the normal oesophagus like

A

25cm long muscular tube mostly lined with squamous epithelium
Sphincter at upper end (cricopharyngeal) and lower end (gastro-oesophageal junction)
Distal 1.5-2 cm are situated below the diaphragm and lined by glandular columnar mucosa
The squamo-columnar junction is usually located at 40cm from the incisor teeth

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2
Q

What is oesophagitis

A

Inflammation of the oesophagus

Classified:

  • acute
  • chronic

Aetiology:

  • Infectious (bacterial, viral (HSV1, CMV), fungal (candida))
  • Chemical (ingestion of corrosive substances, reflux of gastric contents)
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3
Q

What are the risk factors for reflux oesophagitis

A

Defective lower oesophageal sphincter
Hiatus hernia
Increased intra-abdominal pressure
Increased gastric fluid volume due to gastric outflow stenosis

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4
Q

What is a hiatus hernia

A

Abnormal bulging of a portion of the stomach through the diaphragm

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5
Q

What are the complications of reflux oesophagitis

A 
Ulceeration
Haemorrhage
Perforation
Benign stricture (segmental narrowing)
Barrett's oesophagus
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6
Q

What is Barretts oesophagus

A

Cause:
Longstanding gastro-oesophageal reflux

Risk factors:
Same as for reflux (male, Caucasian, overweight)

Macroscopy:
Proximal extension of the squamo-columnar junction

Histology:
Squamous mucosa replaced by columnar mucosa > “glandular metaplasia”

Premalignant condition with an increased risk of developing adenocarcinoma

Regular endoscopic surveillance is recommended for early detection of neoplasia

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7
Q

What are the two histological types of oesophageal carcinoma

A

Squamous cell carcinoma

Adenocarcinoma

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8
Q

What are the risk factors for squamous cell carcinoma of the oesophagus

A 
Tobacco and alcohol
Nutrition (potential sources of nitrosamines)
Thermal injury (hot beverages)
Human Papilloma Virus
Male
Ethnicity (black)
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9
Q

What usually causes acute gastritis

A

Chemical injury:

  • drugs (NSAIDs)
  • Alcohol
  • Initial response to Helicobacter pylori infection
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10
Q

What are the causes of chronic gastritis

A

Autoimmune:
-anti-parietal and anti-intrinsic factor antibodies

Bacterial infection (Helicobacter pylori)

Chemical injury

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11
Q

What is Helicobacter pylori

A

Gram negative spiral shaped bacterium:

  • 2.5-5.0 micrometres long
  • 4 to 6 flagellae
  • Lives on the epithelial surface protected by the overlying mucus barrier

Damages the epithelium leading to chronic inflammation of the mucosa

More common in antrum than body

Results in glandular atrophy, replacement fibrosis and intestinal metaplasia

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12
Q

What is peptic ulcer disease

A

Localised defect extending at least into submucosa

Major sites:

  • First part of duodenum
  • Junction of antral and body mucosa
  • Distal oesophagus (GOJ)

Main aetiological factors:

  • Hyperacidity
  • H. pylori infection
  • Duodeno-gastric reflux
  • Drugs (NSAIDs)
  • Smoking
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13
Q

What is the histology of an acute gastric ulcer

A
  • Full-thickness coagulative necrosis of mucosa (or deeper layers)
  • Covered with ulcer slough (necrotic debris + fibrin + neutrophils)
  • Granulation tissue at ulcer floor
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14
Q

What is the histology of a chronic gastric ulcer

A
  • Clear-cut edges overhanging the base
  • Extensive granulation and scar tissue at ulcer floor
  • Scarring often throughout the entire gastric wall with breaching of the muscularis propria
  • Bleeding
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15
Q

What are the potential complications of peptic ulcers

A

Haemorrhage
Perforation -> peritonitis
Penetration into an adjacent organ (liver, pancreas)
Stricturing -> hour-glass deformity

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16
Q

What are the types of gastric cancer

A

Most frequently:
Adenocarcinoma

Less frequently:
Endocrine tumours
MALT lymphomas
Stromal tumours (GIST)

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17
Q

What is the aetiology of gastric adenocarcinoma

A 
Diet (smoked/cured meat or fish, pickled veg)
H. pylori infection
Bile reflux
Hypochlorhydia (allows bacterial growth)
~1% hereditary
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18
Q

What is coeliac disease

A

AKA coeliac sprue or gluten sensitive enteropathy
Immune mediated enteropathy (a disease of the intestine, especially the small intestine)
Reaction to ingestion of gluten containing cereals
~ 0.5% to 1% of population
Commonly those 30 to 60yo

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19
Q

What are gluten containing cereals

A

Wheat
Rye
Barley

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20
Q

Why is coeliac disease difficult to be diagnosed

A
  • Atypical presentations / non specific symptoms
  • Silentdisease: Positive serology / villous atrophy but no symptoms
  • Latentdisease: Positive serology but no villous atrophy
  • Symptomatic patients: Anaemia, chronic diarrhoea, bloating, or chronic fatigue
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21
Q

How is coeliac disease diagnosed

A

Non-invasive serologic tests usually performed before biopsy

The most sensitive tests:

  • IgA antibodies to tissue transglutaminase (TTG)
  • IgA or IgG antibodies to deamidated gliadin
  • Anti-endomysial antibodies - highly specific but less sensitive

Tissue biopsy is diagnostic (2nd biopsy after Gluten free diet)

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22
Q

What is the treatment of coeliac disease

A

Gluten free diet results in symptomatic improvement for majority of patients
Reduces risk of long-term complications including anaemia, female infertility, osteoporosis and cancer

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23
Q

What is the morphology in coeliac disease

A

Villous atrophy
Crypt elongation
Increased IELs
Increased lamina proprietary inflammation

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24
Q

What is diverticulosis of the colon

A

Protrusions of mucosa and submucosa through the bowel wall
Commonly sigmoid colon
Located between mesenteric and anti-mesenteric Tania coli
Less commonly extensors into proximal colon

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25
Q

What is the pathogenesis of diverticulosis of the colon

A

Increased intra-luminal pressure:

  • irregular, uncoordinated peristalsis
  • overlapping (valve like) semicircular arcs of bowel wall

Points of relative weakness in the bowel wall:

  • penetration by nutrient arteries between mesenteric and anti mesenteric Tania coli
  • age related changes in the connective tissue
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26
Q

What are the clinical features of diverticular disease

A

Asymptomatic 90-99%
Cramping abdominal pain
Alternating constipation and diarrhoea
Acute and chronic complications (10-30%)

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27
Q

What are the potential complications of diverticular disease

A

Acute:

  • Diverticulitis/ peridiverticular abscess (20-25 % )
  • Perforation
  • Haemorrhage (5%)

Chronic:
-Intestinal obstruction (strictures: 5-10 % )
-Fistula (urinary bladder, vagina)
-Diverticular colitis (segmental and granulomatous)
Polypoid prolapsing mucosal folds

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28
Q

What is colitis

A

Inflammation of the colon
Acute (days to a few weeks)
Chronic (months to years)

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29
Q

What are the types of acute colitis

A
  • Acute infective colitis eg. campylobacter, shigella, salmonella, CMV
  • Antibiotic associated colitis (including PMC)
  • Drug induced colitis
  • Acute ischaemic colitis (transient or gangrenous)
  • Acute radiation colitis
  • Neutropenic colitis
  • Phlegmonous colitis
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30
Q

What are the types of chronic colitis

A
  • Chronic idiopathic inflammatory bowel disease
  • Ischaemic colitis
  • Diverticular colitis
  • Microscopic colitis (collagenous & lymphocytic)
  • Chronic infective colitis eg. amoebic colitis & TB
  • Diversion colitis
  • Eosinophilic colitis
  • Chronic radiation colitis
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31
Q

What are the idiopathic inflammatory bowel diseases

A

Ulcerative colitis
Crohn’c disease
Unclassified and indeterminate colitis (10-15%)

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32
Q

What is the clinical presentation of ulcerative colitis

A 
Diarrhoea (> 66%) with urgency/tenesmus
Constipation (2%)
Rectal bleeding (> 90%)
Abdominal pain (30 – 60%)
Anorexia
Weight loss (15-40%)
Anaemia
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33
Q

What are the potential complications of ulcerative colitis

A

Toxic megacolon and perforation
Haemorrhage
Stricture (rare)
Carcinoma

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34
Q

What is the clinical presentation of Crohn’s disease

A
  • Chronic relapsing disease
  • Affects all levels of GIT from mouth to anus
  • Diarrhoea (may be bloody)
  • Colicky abdominal pain
  • Palpable abdominal mass
  • Weight loss / failure to thrive
  • Anorexia
  • Fever
  • Oral ulcers
  • Peri-anal disease
  • Anaemia
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35
Q

What are the potential complications of Crohn’s disease

A 
Toxic megacolon
Perforation
Fistula
Stricture (common)
Haemorrhage
Carcinoma
Short bowel syndrome (repeated resection)
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36
Q

What is ischaemic colitis

A

Colonic injury secondary to an acute intermittent or chronic reduction in blood flow
May be occlusive or non-occlusive (NOMI)
Usually multifactorial and associated with other vascular diseases

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37
Q

What are colorectal polyps

A 
Mucosal protrusion
Solitary or multiple (polyposis)
Can be pedunculated or sessile or flat
Small or large
Due to mucosal or submucosal pathology or a lesion deeper in the bowel wall
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38
Q

What are the risk factors for colorectal cancer

A 
Diet:
-Dietary fibre (protective)
-Fat
-Red meat
-Folate (protective)
-Calcium
Obesity / Physical Activity
Alcohol
NSAIDs & Aspirin (protective)
HRT and oral contraceptives
Schistosomiasis
Pelvic radiation
Ulcerative colitis and Crohn's disease
Inherited susceptibility
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39
Q

What cancers are patients with Lynch syndrome at increase risk of

A 
Endometrial
Ovarian
Gastric
Small bowel
Urinary tract
Biliary tract
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40
Q

What are the sterile sites in the GI tract

A

Peritoneal space
Pancreas
Gall bladder
Liver

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41
Q

What are the non-sterile sites in the GI tract

A 
Mouth
Oesophagus
Stomach
Small bowel
Large bowel
42
Q

What is angular cheilitis

A

Acute or chronic inflammation of the skin and contiguous labial mucosa located at the lateral commissures of the mouth
Presents with erythema, maceration, scaling and fissuring at the corners of the mouth, with lesions usually bilateral and may be painful
Treated with topical antifungals/antibiotics

43
Q

Which patients may present with hairy leukoplakia and why

A

HIV patients caused by Epstein Barr virus

44
Q

What are peritonsillar abscesses

A

Unilateral swellings of tonsil
Normally streptococcus A
Symptoms: painful swallowing, unilateral sore throat and ear ache
Signs: muffled voice, trismus (lock jaw), unilateral deviation of the uvula towards the unaffected side and soft palate fullness or oedema
Oral airway may be compromised and drooling may occur
Surgical drainage and antibiotic management normally indicated

45
Q

What is parotitis

A

Non mumps:
Occurs in patients with poor oral hygiene and dehydration
Staph aureus
Normally unilateral
Sudden swelling from cheek to angle of jaw and bacteraemia may result
Systemically unwell
Surgical drainage should be considered and antibiotics given

46
Q

What is Ludwig’s angina

A

A bilateral infection of the submandibular space
Aggressive, rapidly spreading cellulitis without lymphadenopathy with potential for airway obstruction
Requires careful monitoring and rapid intervention for prevention of asphyxia and aspiration pneumonia
If abscesses form, surgical drainage is required
Antibiotics given

47
Q

What are the deep neck space infections

A
  • Peritonsillar abscess (quinsy)
  • Acute suppurative parotitis
  • Submandibular space infections (Ludwig’s angina)
  • Pretracheal space infections
  • Prevertebral space infections
  • Parapharyngeal space infections
  • -Carotid sheath involvement
  • -Suppurative jugular thrombophlebitis (also known as Lemierre’s syndrome)
  • Retropharyngeal and danger space infections
48
Q

What is mucositis

A

Inflammation of the mucous membranes of the GI tract
Chemo induced
Lasts about 2 weeks after stopping chemo

49
Q

What is the medical definition of trauma

A

An injury or wound to living tissue caused by an extrinsic agent

50
Q

What is shock

A

Interruption to the supply of substrates to the cell:
oxygen, glucose, water, lipids, amino acids, micronutrients

Interruption to the removal of metabolites from the cell:
CO2, water, free radicals, toxic metabolites

51
Q

What happens in phase 1 after trauma

A 
Shock
Develops within 2-6 hours after injury
Lasts 24-48h
Cytokines, catecholamines and cortisol secreted
IncreasedHeart rate (tachycardia)
Increased respiratory rate
Peripheral vasoconstriction: (selective peripheral shut-down to preserve vital organs)
Hypovolaemia
Primary aims:
-stop bleeding
-prevent infection
52
Q

What happens in phase 2 after trauma

A 
Catabolic state
Develops ~ 2 days after injury
Necessary for survival but is persists/severe, increased mortality
Catecholamines
Glucagon
ACTH ->Cortisol
^  Oxygen consumption
^ metabolic rate
^ Negative nitrogen balance 
^ Glycolysis 
^ Lipolysis 
Primary aims:
-Avoid sepsis
-provide adequate nutrition
53
Q

What happens in phase 3after trauma

A

Occurs approx 3-8 days after uncomplicated surgery
May not occur for several weeks after severe trauma and sepsis
Coincides with beginning of diuresis and request for oral intake
Gradual restoration of:
-Body protein synthesis
-Normal nitrogen balance
-Fat stores
-Muscle strength
Primary aims:
Adequate nutrition supply is critical in this phase
Refeeding syndrome risk
May last a few weeks / a few months
Obesity paradox

54
Q

What is the inflammatory response at a trauma site

A

Bacteria and pathogens enter wound
Platelets release clotting factors
Mast cells secrete factors that mediate vasodilation to increase blood delivery to the injured area
Neutrophils and macrophages recruited to phagocytose pathogens
Macrophages secrete cytokines to attract immune cells and proliferate inflammatory response
Inflammatory response continues until wound is healed

55
Q

What are the catabolic and anabolic hormones

A

Catabolic:
ACTH (so also cortisol)
Glucagon
Catecholamines

Anabolic:
Growth hormone
Insulin

56
Q

What are the five cardinal signs of inflammation

A 
Heat
Redness
Swelling
Pain
Loss of function
57
Q

How is lactate used as a prognostic marker in trauma

A

Failure of blood lactate to return to normal following trauma resuscitation carries a poor prognosis

58
Q

What is primary malnutrition

A

Protein calorie undernutrition (starvation)

Dietary deficiency of specific nutrients (trace elements, water soluble vitamins, fat soluble vitamins)

59
Q

What is secondary malnutrition

A

Nutrients present in adequate amounts but:
-appetite is suppressed
-absorption and utilisation are inadequate
Increased demand for specific nutrients to meet physiological needs

60
Q

What are the consequences of malnutrition

A 
Negative nitrogen balance
Muscle wasting
Widespread cellular dysfunction
Associated with:
-infection
-poor wound healing
-changes in drug metabolism
-prolonged hospitalisation
-increased mortality
61
Q

What is the overall incidence of malnutrition in hospitalised patients

A

~50%

62
Q

How many newborns are affected by cystic fibrosis

A

1 in 2,500 in UK

63
Q

What is the function of cystic fibrosis transmembrane regulator protein

A

Facilitates production of thin, watery, free-flowing mucus to:
-lubricate airways and secretory ducts
-protect lining of airways, digestive system, reproductive system
So that macromolecules can be secreted smoothly out of secretory ducts

64
Q

What are the functions of the pancreas

A

Exocrine:
Secrete digestive enzymes (trypsin, lipase, phospholipase, elastase, amylase) which require activation

Endocrine:
Secrete peptide hormones into blood (insulin and glucagon)

65
Q

What is pancreatitis

A

Inflammation of the pancreas
Associated with injury to the exocrine parenchyma
Acute: gland reverts to normal if underlying cause removed
Chronic: irreversible loss of the pancreatic tissue

66
Q

What are causes of acute pancreatitis

A 
Gallstones (50%)
Alcohol (25%)
Rare causes(<5%):
-vascular insufficiency
-viral infection (mumps, coxsackie B)
-hypercalcaemia
-ERCP
-Inherited causes
Idiopathic (10%)
67
Q

What is hereditary pancreatitis

A

Recurrent attacks of severe pancreatitis
Usually begins in childhood
PRSS1 inherited mutations- autosomal dominant
SPINK 1 gene- autosomal recessive

68
Q

What do PRSS1 inherited mutations do

A

Alter a site on the cationic trypsinogen molecule that is essential for inactivation of trypsin by itself
Mutations result in trypsin being resistant to cleavage by another trypsin molecule
Small amounts of trypsin activation results in activation of other digestive enzymes resulting in pancreatitis

69
Q

What does SPINK 1 gene code for

A

A trypsin inhibitor which helps prevent auto digestion of pancreas by activated trypsin

70
Q

What are the clinical features of acute pancreatitis

A

Presents in emergency state
Sudden onset of severe abdominal pain radiating to back
Nausea and vomiting
May be mild (recovery within 5-7 days) but can be serious with high mortality
Raised serum amylase/lipase (>3x normal)
Persistent hypocalcaemia is a poor prognostic sign

71
Q

What are the potential complications of acute pancreatitis

A

Shock
Intravascular coagulopathy
Haemorrhage
Pseudocysts (collections of pancreatic juice secondary to duct rupture)

72
Q

What is chronic pancreatitis

A

Progressive inflammatory disorder in which parenchyma of pancreas is destroyed and replaced by fibrous tissue
Irreversible destruction of the exocrine tissue, followed by destruction of the endocrine tissue
Leads to malnutrition and diabetes

73
Q

How does chronic pancreatitis present

A

Intermittent abdominal pain
Back pain
Weight loss
Fibrosis of exocrine tissue

74
Q

What are the complications of chronic pancreatitis

A

Malabsorption of fat (lack of lipase):

  • staetorrhoea
  • impairment of var soluble vitamin absorption (A, D, E, and K)
  • Diabetes (late feature)
  • pseudocysts
  • severe chronic pain
  • Mortality rate 50% with 20-25 years of disease onset
75
Q

What is a desmoplastic response

A

Intense non-neoplastic host reaction composed of fibroblasts, lymphocytes and extracellular matrix

76
Q

What are the poor prognostic factors of pancreatic adenocarcinoma

A 
Extension of tumour outside of the pancreas
Metastatic spread to local lymph nodes
Vascular and perineurial invasion
Poor differentiation 
Positive margins on resection
77
Q

What is cholangiocarcinoma

A

Malignant tumour of bile duct cells

78
Q

What is angiosarcoma

A

Aggressive tumour of blood vessels

79
Q

What are the potential complications of gallstones

A 
Obstruction at neck (pain)
Chronic cholecystitis
Perforation
Obstruction at pancreatic level (pancreatitis)
Adenocarcinoma (rare)
80
Q

What is chronic cholecystitis

A

Inflammation of the gallbladder

81
Q

What can cause liver disease

A 
Poisoning
Drugs
Infection
Alcohol
Inadequate perfusion
Fatty liver
Autoimmunity
Metabolic
Tumours and metastases
82
Q

What are the systemic effects of liver disease

A 
Jaundice
Oestrogen (gynaecomastia, spider naevi, liver palms, testicular atrophy)
Bruising 
Pigmentation
Clubbing
Dependent oedema
ascites
encephalopathy 
Osteomalacia/ osteoporosis
83
Q

What are the available liver function tests, testing

A 
Production of metabolites
Clearance of endogenous substances
Clearance of exogenous substances
Hepatocellular damage 
Biliary tract damage
Through Imaging and biopsy
84
Q

What are the routine LFTs

A 
Alkaline phosphatase
ALT (alanine aminotransferase)
Bilirubin
Albumin
Total protein
GGT (gamma glutamyl transferase)
85
Q

What are the three stages of alcoholic liver disease

A

Fatty liver
Alcoholic hepatitis
Cirrhosis

86
Q

What is primary biliary cirrhosis

A

Chronic cholestatic condition with destruction of bile ducts

87
Q

What is primary sclerosing cholangitis

A

Progressive disease characterised by diffuse inflammation and fibrosis of the biliary system

88
Q

What do levels of bilirubin show

A

Excretory capacity of the liver and free flow of bile

89
Q

When should LFTs be measured

A 
Signs and symptoms:
-Pain
-itchy
-jaundice
-TATT
-Bruising
Lifestyle:
-Alcohol
-Obesity
-Diabetes
-recent travel
-drug use
Is liver disease present?:
-hepatitis
-haemochromatosis
-liver cancer
-drugs
How sever?:
-Chronic hepatitis vs acute onset
90
Q

What are the disorders of the pancreas

A 
Acute pancreatitis
Chronic pancreatitis
Pancreatic insufficiency
Cystic fibrosis
Carcinoma of the pancreas
91
Q

What are the medical liver diseases

A 
Jaundice
Acute and chronic hepatitis:
-viral
-alcohol
-obesity
-drugs
-inherited (haemochromatosis, Wilson's, Alpha-t antitrypsin deficiency)
-Autoimmune
Cirrhosis
Hepatic failure
92
Q

What is jaundice

A

Visible when bilirubin >40umol/l
Commonest sign of liver disease

Pre-hepatic:

  • too much bilirubin produced (haemolytic anaemia)
  • unconjugated (bound to albumin, insoluble, not excreted) showing symptoms of yellow eyes/skin only

Hepatic:

  • too few functioning liver cells (acute diffuse liver cell injury, end stage chronic liver disease, inborn errors)
  • mainly conjugated (soluble) patients symptoms of yellow eyes and dark urine

Post-hepatic:

  • bile duct obstruction (stone, stricture, tumour in bile duct or pancreas)
  • Conjugated (soluble, excreted but can’t get into gut) symptoms of yellow eyes, pale stool and darkurine
93
Q

What is unconjugated bilirubin, how does it become conjugated and where does it then go

A

Bilirubin produced by red blood cell breakdown
Metabolised in liver (conjugated)
Excreted in bile with some being re-absorbed from the gut

94
Q

What is hepatitis

A

Inflammation in the liver (any liver disease that is not neoplastic)

95
Q

What is NAFLD

A

Non-alcoholic fatty liver disease

96
Q

What is DILI

A

Drug induced liver injury

97
Q

What is the commonest cause of acute liver failure in the UK

A

Paracetamol as at toxic levels it results in necrosis of a high proportion of hepatocytes in a predictable zonal distribution without any inflammation

98
Q

What is Wilson’s disease

A 
Inborn error of copper metabolism
Copper accumulates in:
-liver causing cirrhosis
-Eyes causing Kayser-Fleischer rings
-Brain causing ataxia etc
Treatment to chelate copper and enhance its excretion
99
Q

What is a potential complication of cirrhosis of the liver

A

Hepatocellular carcinoma

100
Q

What is the definition of cirrhosis

A

Define histologically as a diffuse hepatic process characterised by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules

End stage of all chronic liver disease.

Liver is converted into a mass of regenerating nodules wrapped by fibrous scar tissue

101
Q

What are the causes of cirrhosis

A

Alcohol
Non-alcoholic steatohepatitis (metabolic syndrome)
Chronic viral hepatitis (B orC)
Autoimmune liver disease (autoimmune hepatitis, primary biliary cirrhosis, primary sclerosis cholangitis)
Metabolic (iron, copper, alpha 1 antitrypsin)

102
Q

What is the role of liver biopsy in chronic liver disease

A

Information of:

  • stage of disease
  • cause of disease
  • current activity
  • response to treatment

Y2 Clinical Pathology (11 decks)

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