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Digestive > Organ Pathology > Flashcards

Organ Pathology Flashcards

1
Q

Transaminase tests

A

AST and ALT

Elevation = hepatic inflammation and hepatocellular injury

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2
Q

GGT and ALP tests

A

Elevation = cholestasis

Bile stasis/obstruction

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3
Q

Bilirubin test

A

Elevation = jaundice

Due to biliary obstruction or hepatocellular injury

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4
Q

Albumin and clotting factor tests

A

Abnormal = impaired synthesis by liver

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5
Q

Risk factors for Hepatitis C

A 
Injecting drug use
Unscreened blood and donated organs
Sexual transmission
Mother to baby
Occupational
Tattoos
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6
Q

Hepatitis C treatment

A

Used to be interferon based. Suboptimal cure rates, problematic side effects, long duration
Now, direct acting antivirals taken as short course of tablets with better cure rates

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7
Q

Portal hypertension

A

High pressure in portal vein
Difficult for blood in portal circulation to return to right heart so porto-systemic collaterals can form to try and divert blood from portal circulation back to right heart - varices formation

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8
Q

3 causes of portal hypertension

A

Pre-hepatic: portal vein thrombosis
Intra-hepatic: cirrhosis
Post-hepatic: hepatic vein thrombosis or right sided heart failure

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9
Q

Hepatic encephalopathy

A 
Result of chronic liver failure
Liver can't detoxify substances produced by bacterial metabolism causing ammonia build up which can pass blood brain barrier
Mood and personality change
Inverted sleep patterns
Confusion
Bizarre behaviour
Drowsiness
Coma
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10
Q

HE treatment

A

Lactulose
Type of laxative which seems to decrease ammonia generation by bacteria and convert it to a non-absorbable molecule
Not curative

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11
Q

Ascites

A

Fluid in peritoneum causing abdominal distension
Caused by portal hypertension among other things
Increased hydrostatic pressure, decreased oncotic pressure

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12
Q

Budd-Chiari syndrome

A

Acute thrombosis of hepatic veins
Outflow of blood from liver is obstructed
Liver becomes acutely congested causing hepatocellular damage
Portal hypertension occurs, ascites develops

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13
Q

Budd-Chiari causes

A

75% no obvious cause

25% tumour, pregnancy, oral contraceptive, clotting disorders

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14
Q

Budd-Chiari management

A

Portocaval shunting to divert blood flow
Anticoagulation
Diuretics

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15
Q

5 general responses of hepatic injury

A 
Intracellular accumulation
Cell death
Inflammation
Regeneration
Fibrosis
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16
Q

Hepatic failure

A

Sudden massive destruction or endpoint of chronic damage

Have to lose over 80% capacity for functional loss

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17
Q

Signs of hepatic failure

A

Jaundice
Hypoalbuminaemia
Increased ammonia = HE

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18
Q

Cirrhosis mechanism

A

Activated stellate cells cause myofibroblast proliferation and fibrogenesis
Activated Kupffer cells release cytokines
Cytokines induce inflammation causing hepatocyte dysfunction and death

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19
Q

Fibrosis mechanism

A

Proliferating hepatocytes encircled by fibrosis = parenchymal nodules
Formation of these nodules disrupts architecture of liver
Shunts formed, PV and HA blood bypasses functional liver cells causing progressive fibrosis

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20
Q

4 consequences of portal hypertension

A

Ascites
Portosystemic shunts
Congestive splenomegaly
Hepatic encephalopathy

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21
Q

Hepatitis A

A

Benign, acute, mostly asymptomatic
Faecal-oral transmission
Can cause mild illness and jaundice

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22
Q

Hepatitis B

A

Chronic or acute
Blood and body fluid borne
Immune response to viral antigens on infected hepatocytes leads to liver cell damage

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23
Q

Drug and toxin induced liver injury

A

Either predictable or unpredictable hepatotoxins
Cholestasis, hepatocellular necrosis, fatty liver, fibrosis, granulomas, vascular lesions, neoplasms
Acute = likely to be paracetamol
Chronic = likely to be alcohol

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24
Q

Alcoholic liver disease

A

Changes in lipid metabolism, decreased export of lipoproteins and cell injury caused by ROS and cytokines leads to hepatic steatosis, alcoholic hepatitis and cirrhosis

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25
Q

Metabolic liver disease

A

Also known as non-alcoholic fatty liver disease
Associated with obesity and related illnesses
Initially only hepatic steatosis, then steatosis and inflammation, then cirrhosis

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26
Q

Haemochromatosis

A

Excessive accumulation of body iron deposited in liver and pancreas
Autosomal recessive

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27
Q

Cholestasis of sepsis

A

Infection, ischaemia or circulating microbial products can cause widespread inflammation stopping bile from flowing out of liver

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28
Q

Autoimmune cholangiopathies

A

Primary biliary cirrhosis (destruction of bile canaliculi) and primary sclerosing cholangitis (destruction of bile ducts)

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29
Q

2 types of benign liver tumour

A

Cavernous haemangioma

Hepatocellular adenoma

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30
Q

4 types of malignant liver tumour

A

Hepatocellular carcinoma
Hepatoblastoma
Cholangiocarcinoma
Hepatic metastases

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31
Q

5 causes of jaundice

A

Haemolysis
Gilberts syndrome
Cholestasis
Liver obstruction (internal or external)

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32
Q

ALP

A

Alkaline phosphatase
Hydrolyses phosphate groups
Found in liver, bone, intestine, placenta and some tumours
>600 units per litre considered pathological
High in gallstones and tumours

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33
Q

GGT

A 
Gamma-glutamyl transferase
Mostly biliary (liver)
Elevated in inflammation/obstruction of biliary system, also drugs and alcohol
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34
Q

ALT

A 
Alanine aminotransferase
Normal concentration <45 units per litre
Found mostly in hepatocyte cytosol
Key for gluconeogenesis
Elevated in hepatitis
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35
Q

AST

A

Aspartate transaminase
Key for gluconeogenesis
Found in hepatocyte cytosol and mitochondria
Less liver specific and shorter half life than ALT
Elevated in hepatitis

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36
Q

Albumin

A

Normal concentration 35 - 47 g/L
Found in liver
Decreases due to cirrhosis, over excretion by kidneys, illness and redistribution

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37
Q

Globulins

A

Reflect inflammation

Elevated in chronic hepatitis and cirrhosis

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38
Q

Prothrombin

A

Reflects clotting factor synthesis

Elevation due to vitamin K deficiency or liver failure

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39
Q

Glucose

A

Liver maintains fasting blood glucose

Inability to maintain glucose indicates serious disease

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40
Q

Enzymatic signs of scarring and declining function

A

Increased GGT and ALP
Increased AST/ALT ratio
Increased globulins, bilirubin, ammonia and prothrombin
Decreased albumin and glucose

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41
Q

CEA

A

Carcinoembryonic antigen
Indicates cancer or cirrhosis, hepatitis, ulcerative colitis, smoking
>20 ng/mL indicates malignant cancer

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42
Q

Gilberts syndrome

A

Bilirubin levels high, other tests normal
Worsens after illness, fasting or alcohol
Persistent mild jaundice
Normally diagnosed by making patient fast for 48 hours. If bilirubin rises to more than double normal, Gilberts assumed

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43
Q

Most common causes of liver failure test abnormalities

A

Fatty liver
Viral hepatitis
Alcohol
Haemochromatosis

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44
Q

Acute pancreatitis

A

Inflammation of the pancreas associated with acinar cell injury
Autodigestion by pancreatic enzymes
Cell injury response mediated by inflammatory cytokines
Caused by obstruction or direct injury to acinar cells

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45
Q

Main categories of acute pancreatitis and their most common causes

A

Metabolic - alcohol
Mechanical - gallstones and trauma
Vascular - shock and vasculitis
Infection - mumps

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46
Q

Enzyme release in acute pancreatitis and the consequences

A

Protesases - proteolytic destruction of acini, ducts and islets
Lipases - fat necrosis
Elastases - blood vessel destruction leading to interstitial haemorrhage
Cell injury response - inflammation, oedema, impaired blood flow, ischaemia

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47
Q

Pancreatic obstruction in acute pancreatitis

A

Mainly by gallstones and ductal concretions in alcoholics
Increased intrapancreatic ductal pressure
Accumulation of enzyme rich interstitial fluid
Fat necrosis
Oedema and inflammation leading to compromised blood flow

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48
Q

Primary acinar cell injury in acute pancreatitis

A

Secondary to viruses, drugs, trauma and ischaemia

Releases enzymes

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49
Q

Clinical features of acute pancreatitis

A

Epigastric pain
Nausea and vomiting
Fever and tachycardia
Abdominal tenderness - in rare cases ileus and shock

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50
Q

Diagnosis of acute pancreatitis

A

High white cell count
Elevated serum amylase (lipase)
CT to look for oedema, necrosis and pseudocysts
Laparotomy (rare)

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51
Q

Management of acute pancreatitis

A

Rest the pancreas and close monitoring
IV fluids
Analgesia

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52
Q

Complications of acute pancreatitis

A 
Hypotension
Shock
Renal and respiratory failure
Low calcium, hyperglycaemia and jaundice
Pseuodocysts
53
Q

Chronic pancreatitis

A

Repeated bouts of inflammation with loss of parenchyma and replacement by fibrous tissue
Often due to heavy alcohol intake causing intraductal plugs of protein and cell debris
Also previous acute pancreatitis, severe malnutrition and CFTR mutations
Atrophy of exocrine compartment but islets relatively unaffected

54
Q

Clinical features of chronic pancreatitis

A 
Repeated attacks of abdominal pain often brought on by alcohol - can be more persistent
If ongoing, loss of exocrine function causing malabsoprtion, pseudocysts
Diabetes mellitus (rare)
55
Q

Diagnosis of chronic pancreatitis

A 
CT
Serum amylase (not entirely accurate)
56
Q

Pancreatic carcinoma

A

Poor prognosis. Whipples procedure performed in 15-20% cases
Common in smokers, alcohol and coffee suggested but not confirmed
If in the head, invades ampulla causing biliary obstruction
If in the tail, neck or body, silent and metastatic

57
Q

Clinical features of pancreatic carcinoma

A 
Obstructive jaundice
Pain
Weight loss
Pancreatitis
Thrombophlebitis
58
Q

Cholelithiasis

A

Gallstones
Mostly silent
Most are cholesterol based (yellow/green)
Remainder are bilirubin/calcium salts (brown/black)

59
Q

Cholesterol stones

A

Bile supersaturated with cholesterol. Conditions favour crystal formation. Cholesterol crystals remain in gallbladder long enough for stones to form (cholestasis)

60
Q

Risk factors for cholelithiasis

A

Increased age and female
Oral contraceptives, pregnancy, obesity, rapid weight loss
Gallbladder stasis
Family history

61
Q

Risk factors for pigment stones

A

Chronic haemolytic syndromes

Bacterial infection of biliary tree

62
Q

Clinical consequences of gallstones

A

Mostly asymptomatic
Cholecystitis
Biliary colic

63
Q

Clinical features of cholecystitis

A

Right upper quadrant abdominal pain and tenderness with fever
Neutrophil leukocytosis
Elevated bilirubin, ALP and GGT
DIagnosed by ultrasound

64
Q

Acute cholecystitis

A

Most causes precipitated by gallstones
Obstruction of neck of gallbladder or cystic duct
Chemical irritation followed by bacterial infection

65
Q

Chronic cholecystitis

A

Long term association of gallstones and low grade inflammation
Gallbladder often contracted with thickened wall

66
Q

Management of cholecystitis

A

Initially - can settle with conservative therapy such as IV fluids and analgesia but can require acute surgical intervention
Long term - laparoscopic cholecystectomy

67
Q

Choledocholiathis

A

Presence of stones in the biliary tree
Can lead to biliary obstruction with colicky abdominal pain and obstructive jaundice
Cna also lead to pancreatitis and cholangitis

68
Q

Carcinoma of the gallbladder

A

Late presentation, poor prognosis
Older, female patients
Increased with gallstoned and chronic infections
Most are adenocarcinomas, rarely squamous or mixed
Most have invaded liver by time of diagnosis

69
Q

Carcinoma of extrahepatic bile duct

A

Uncommon adenocarcinomas that may involve the ampullary region
Often present with slowly progressive obstruction of bile duct causing jaundice, pale stools, weight loss and nausea

70
Q

Polyp

A

Circumscribed growth or tuour which projects above surrounding mucosa
Can be neoplastic or non-neoplastic
Majority occur sporadically in the colon and increase in frequency with increasing age
Some people prone to developing large numbers of polyps due to polyposis syndromes

71
Q

Non-neoplastic polyps

A

Result of abnormal mucosal maturation, inflammation or hyperplasia

72
Q

Neoplastic polyps

A

Result of proliferation and dysplasia
Called adenomatous polyps
Precursors of carcinoma

73
Q

Sessile

A

Unbranched, immobile

74
Q

Pedunculated

A

Branched, somewhat mobile

75
Q

Hyperplastic polyps

A

Non-neoplastic

Benign, asymptomatic, small and sessile

76
Q

Juvenile polyps

A

Non-neoplastic
Common in children
Usually occur in rectum and present with rectal bleeding
Composed of abundant inflamed lamina propria containing cystically dilated glands

77
Q

Inflammatory polyps

A

Non-neoplastic
Often seen in IBD and Crohns
Benign pseudopolyps

78
Q

Adenomas

A

Neoplastic
Familial
Can be sessile or pedunculated
Classified as tubular, villous or tubulovillous

79
Q

Malignant risk factors of polyps

A

Polyp size - the bigger the polyp, the more cells vulnerable to changes
Architecture - villous
Severity of dysplasia

80
Q

FAP

A

Familial adenomatous polyposis syndrome
Hundreds of adenomas, first appearing in teens/early twenties
Normally develop into cancer within 10-15 years
Genetic defect in APC gene on chromosome 5

81
Q

Adenoma-carcinoma sequence

A

Normal epithelium
—–> Loss/mutation of APC locus on chromosome 5
Hyperproliferative epithelium
—–> Loss of DNA methylation
Early adenoma
—–> Mutation of ras gene on chromosome 12
Intermediate adenoma
—–> Loss of tumour suppressor on chromosome 18
Late adenoma
—–> Loss of p53 gene on chromosome 17
Carcinoma

82
Q

Colorectal carcinoma

A

Most are sporadic, some have underlying genetic component (hereditary non-polyposis carcinoma of the colon, HNPCC)
Younger patients tend to have FAP or ulcerative colitis
High red meat and carb intake, low vegetable intake
Can occur anywhere in colon but rare in small intestine
Can be well, moderately or poorly differentiated

83
Q

Dukes staging system of colorectal carcinoma

A 
A = tumour protrudes submucosa or muscularis externa
B = tumour protrudes into serosa
C = tumour protrudes through serosa into body caivty and infects nodes
84
Q

TNM staging system of colorectal carcinoma

A 
T = Extent of invasion through bowel wall
N = number of lymph nodes involved
M = metastatic presence
85
Q

4 rare tumours of the colon

A

Carcinoid - endocrine cell tumours
Lymphoma - primary blood cancer causes secondary bowel cancer
Anorectal - dominated by squamous cell carcinomas
Mesenchymal - gastrointestinal stromal tumours and lipomas

86
Q

Courvoisiers sign

A

Palpable gallbladder

Often present in cases of prolonged biliary obstruction

87
Q

Cystic fibrosis in pancreatic disease

A

Decreased function of CFTR gene prevents Cl- secretion. To neutralise, Na+ and H2O stay inside cell
Secretions are sticky and clog passages causing decreased lung function and increased susceptibility to lung infection
Cl- accumulates in ductal cells in the pancreas. Same thing happens here causing sticky mucus, blocked passages and blocked enzymes

88
Q

Diarrhoea

A

> 200 g/day

Loose consistency, frequent

89
Q

Acute diarrhoea

A

Up to 14 days
Infection (viruses most common)
Can cause inflammatory, omsotic or secretory diarrhoea

90
Q

Chronic diarrhoea

A

More than 14 days

Inflammatory, osmotic, secretory or fatty

91
Q

Campylobacter diarrhoea

A

Inflammatory
Acute
Caused mucosal inflammation causing increased exudate

92
Q

Giardia diarrhoea

A

Osmotic
Acute
Mild villous atrophy leads to carbohydrate malabsoprtion
Undigested sugars are osmotically active which draws fluid in

93
Q

Enterotoxigenic E. coli diarrhoea

A

Secretory
Acute
Toxins stimulate excessive fluid secretion

94
Q

Chronic inflammatory diarrhoea causes

A

IBD
Diverticulitis
Small intestinal bacterial overgrowth causing direct inflammation of enterocytes

95
Q

Chronic osmotic diarrhoea causes

A

Carbohydrate malabsoprtion
Coeliac
Small intestinal bacterial overgrowth causing malabsorption of osmotically active by-products of bacteria metabolism
Laxative abuse

96
Q

Chronic secretory diarrhoea causes

A

Terminal ileal resection causing bile acid malabsorption
Chloecystectomy causing continuous bile flow into the small intestine
IBD
Diverticulitis
Small intestinal bacterial overgrowth causing unabsorbed food products and bile acids to stimulate secretory colon cells
Disordered motility
Laxative abuse

97
Q

Chronic fatty diarrhoea causes

A

Pancreatic exocrine insufficiency
Bile acid malabsorption
Small intestinal bacterial overgrowth causing deconjugation of bile acids leading to impaired micelle formation and impaired fat digestion and absorption
Coeliac
Short bowel syndrome (not enough mucosal surface)

98
Q

SIBO

A

Small intestinal bacterial overgrowth
Excess colonic bacteria in small intestine casuing bloating, flatulence, discomfort, malabsoprtion and steatorrhoea
Predisposed by impaired motility, anatomic disorders, metabolic and immune diseases

99
Q

Diarrhoea in SIBO

A

Inflammatory: bacteria inflames enterocytes
Osmotic: Malabsorption of osmotically active byproducts of bacteria metabolism
Secferotry: Unabsorbed food and bile stimulates secertory cells
Fatty: Deconjugated bile acids causes impaired micelle formation therefore impaired fat digestion and absoprtion

100
Q

Functional gut disorders

A 
No structural or tissue abnormality
Disturbed motility
Visceral hypersensivity
Brain-gut dysfunction
Psychosocial factors
Can affect any part of the gut
101
Q

Oesophageal functional gut disorders

A

Globus

Functional heartburn

102
Q

Stomach functional gut disorders

A

Functional dyspepsia

Fucntional vomiting

103
Q

Bowel functional gut disorders

A

Irritable bowel

Functional abdominal pain

104
Q

IBS

A

Swinging bowel
Abdominal pain relieved with bowel movement
May occur after gastroenteritis
Symptoms include urgency, bloating, flatulence, fatigue, poor sleep

105
Q

Alarm symptoms

A 
If present, serious pathology should be considered
Nocturnal diarrhoea or pain
Rectal bleeding
Anaemia and iron deficiency
Weight loss
Vomiting
Being over 50
Family history of colon cancer
106
Q

Altered gut motility in in IBS

A

Can increase and decrease

Exaggerated response = diarrhoea, reduced response = constipation

107
Q

Visceral hypersensitivity in IBS

A

Sufferers tend to perceive distension more than normal and describe it as painful or unpleasant rather than just uncomfortable

108
Q

Peripheral sensitisation in visceral hypersensitivity

A

Symptoms sometimes start after an episode of gastroenteritis. Previous tissue inflammation or injury may upregulate sensitivity and excitability of nociceptors leading to hyperalgesia and allodynia

109
Q

Central sensitisation in visceral hypersensitivity

A

Peripheral sensitisation may lead to surrounding uninjured tissue to become hypersensitive as well leading to global sensitisation throughout the body

110
Q

Gate control theory

A

Spinal cord has a method of controlling pain signals. Hypervigilance of gate control can lead to brain focusing on processing unpleasant stimuli
Tends to increase with stress

111
Q

Treatment of IBS

A 
Multidisciplinary approach
Conventional treatments (laxatives, fibre supplements, TCAs and anti-motility drugs) with dietary exclusions, probiotics and psychological therapies
112
Q

Ulcerative colitis pathology

A

Continuous in the colon, begins in the rectum and spreads proximally
Diffuse and granular mucosal inflammation but doesn’t involve other gut layers
Rarely macroscopic ulceration

113
Q

Ulcerative colitis histology

A 
Mucosal inflammation
Crypt branching and atrophy
Crypt abscess
Loss of goblet cells
Paneth cell metaplasia
114
Q

Ulcerative colitis clinical signs

A

Bloody diarrhoea
Frequent and urgent bowel movements
Abdominal discomfort
Fever, malaise, weight loss

115
Q

Toxic megacolon

A

Progressive dilation causing muscular paralysis which decreases peristalsis - can lead to perforation

116
Q

Crohns pathology

A

Can be in any part of the GI tract but most commonly the colon and ileum
Discontinuous skip lesions
Transmural inflammation

117
Q

Transmural inflammation

A

Common in Crohns
Starts as small ulcers on mucosa and progresses to deep penetrating ulcers with fissuring, showing a cobblestone appearance

118
Q

Crohns histology

A

Transmural inflammation across the entire depth of the intestine wall
Non-caseating and non-necrotising granulomas

119
Q

Granuloma

A

Activated macrophages fuse together to make a giant cell which can group together in an area of inflammation

120
Q

4 clinical subtypes of Crohns

A

Inflammatory
Structuring
Fistulising
Perianal

121
Q

Inflammatory Crohns

A

Colitis - bloody diarrhoea
Ileitis - abdominal pain, malabsorption leading to watery or fatty diarrhoea
Gastritis and duodenitis - dyspepsia

122
Q

Stricturing Crohns

A

Initially inflammatory due to oedema but becomes fibrotic due to scarring
Causes abdominal pain and distension, vomiting and decreased bowel movements

123
Q

Fistulising Crohns

A

Inflammation penetrates gut wall and goes through adventitia or serosa. Becomes sticky and moves into wall of neighbouring tissue
Can be enterocutaneous, enteroenteric, enterocolic or rectovaginal

124
Q

Perianal Crohns

A

Perianal fistulas occur which can get infected and become perianal abscesses
Anal fissures

125
Q

General treatment of IBD

A

5-ASAs
Steroids
Immunosuppression
Monoclonal antibodies

126
Q

Surgery in IBD

A

Colectomy can cure ulcerative colitis and help Crohns but no definitive treatment for Crohns
Can treat complications such as bowl obstruction, perforation, fistula, abscess

127
Q

Genetics of Coeliac disease

A

Incomplete dominance
Two susceptibility genes: HLA-DQ2 and HLA-DQ8
HLA-DQ2.5 carriers will get coeliac
HLA-DQ2.2 carriers might get coeliac
HLA-DQ8 carriers generally need another allele to get coeliac
Populations without HLA-DQ2 (e.g. Asian populations) don’t get coeliac disease

128
Q

Pathology of Coeliac disease

A

Gluten exposure required
Villous atrophy and crypt hypertrophy
Loss of brush border enzymes and loss of stimulus for pancreatic and bile secretion

129
Q

Coeliac antibodies

A

Anti-TTG IgA mucosal antibodies for treatment
Some sufferers have IgA deficiency therefore IgG form of antibodies needed instead
Diagnosed with a combination of blood test for tissue transglutaminase antibody and biopsy to check for villous atrophy

Digestive (9 decks)

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