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Pathology Flashcards

1
Q

Name some inflammatory disorders of oesophagus

A
  • acute oesophagitis

- chronic oesophagitis

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2
Q

Describe acute oesophagitis

A
  • rare
  • corrosive following chemical ingestion
  • infective in immunocompromised pts eg. candidiasis, herpes, CMV
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3
Q

Describe chronic oesophagitis

A
  • common
  • reflux disease ‘ reflux oesophagitis’
  • rare causes include crohns disease
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4
Q

Define reflux oesophagitis

A
  • inflammation of oesophagus due to refluxed low pH gastric gastric content
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5
Q

Describe causes of reflux oesophagitis

A
  • may be due to defective sphincter mechanisms +/- hiatus hernia
  • abnormal oesophageal motility
  • increased intra-abdominal pressure (pregnancy)
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6
Q

Describe the microscopic of reflux oesophagitis

A
  • basal zone epithelial expansion

- intraepithelial neutrophils, lymphocytes and eosinophils

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7
Q

Describe the complications of reflux

A
  • ulceration (bleeding)
  • stricture
  • barrets oesophagus
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8
Q

What is barrets oesophagus?

A

Replacement of stratified squamous epithelium by columnar epithelium

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9
Q

Describe metaplasia in relation to barrets oesophagus

A
  • due to persistent reflux of acid or bile
  • may be due to expansion of columnar epithelium from gastric glands or from submucosal glands
  • may be due to differentiation from oesophageal stem cells
  • protective response, faster regeneration
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10
Q

Describe the macroscopic changes of barrets oesophagus

A

Red velvety mucosa in lower oesophagus

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11
Q

Describe the microscopic changes in barrets oesophagus

A

Columnar lined mucosa with intestinal metaplasia

  • unstable mucosa
  • increased risk of developing dysplasia and carcinoma of the oesophagus
  • requires surveillance
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12
Q

Describe allergic oesophagitis

A
  • eosinophilic oesophagitis
  • personal / family history of allergy
  • asthma
  • young
  • males
  • pH probes negative for reflux
  • increased eosinophils in blood
  • corrugated (feline) or spotty oesophagus
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13
Q

Name the treatments of allergic oesophagitis

A

Treatment may include steroids / chromoglycate / Montelukast

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14
Q

Name the benign tumours of the oesophagus

A

squamous papilloma

  • Rare
  • papillary
  • asymptomatic
  • HPV related

Very rare;

  • leiomyomas
  • lipomas
  • fibrovascular polyps
  • granular cell tumours
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15
Q

Name malignant tumours of the oesophagus

A
  • squamous cell carcinoma

- adenocarcinoma

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16
Q

Describe the epidemiology of squamous cell carcinoma

A
  • commoner in males

- high risk areas NW france, N Italy

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17
Q

Describe the aetiology of squamous cell carcinoma

A
  • vitamin A, zinc deficiency
  • tannic acid / strong tea
  • smoking
  • alcohol
  • HPV
  • oesophagitis
  • genetic
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18
Q

Describe the aetiology of adenocarcinoma of the oesophagus

A
  • commoner in Caucasians
  • incidence increasing in Europe and USA
  • commoner in males / obesity
  • commonest in lower 1/3 of oesophagus
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19
Q

Describe the pathogenesis of adenocarcinoma of oesophagus

A
  • genetic factors, reflux disease, others

> > >

  • chronic reflux oesophagitis

> > >

  • barrets oesophagus (intestinal metaplasia)

> > >

  • low grade dysplasia

> > >

  • high grade dysplasia

> > >

  • adenocarcinoma
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20
Q

Describe the mechanism of metastases of carcinoma of the oesophagus

A
  • direct invasion
  • lymphatic permeation
  • vascular invasion
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21
Q

How may carcinoma of the oesophagus present?

A
  • dysphagia; due to tumour obstruction
  • anaemia
  • weight loss, loss of energy
  • due to effects of metastases
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22
Q

Describe oral squamous cell carcinoma

A
  • variable presentations; white, red, speckled, ulcer, lump
  • high risk sites include floor of mouth, lateral border of and ventral tongue, soft palate, retromolar pad / tonsillar pillars
  • rare on hard palate, dorsum of tongue
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23
Q

Describe the aetiology of oral squamous cell carcinoma

A
  • tobacco
  • alcohol
  • betel quid
  • nutritional deficiencies
  • post transplant
  • pt with history of primary orsl SCC, increased risk of developing new second primary

? genetics, chronic infection, viral, HPV

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24
Q

Describe the histopathology of oral squamous cell carcinoma

A
  • considerable variation in appearances, however cytologically malignant squamous epithelium and ALL show invasion and destruction of local tissues
  • variants include verrucous and acantholytic
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25
Q

Describe the histopathological features relating to prognosis of SCC

A
  • tumour diameter
  • depth of invasion
  • pattern of invasion, cohesive versus non-cohesive front
  • lymphovascular invasion
  • neural invasion by tumour
  • involvement of surgical margins
  • metastatic disease
  • extracapsular spread of lymph node metastases
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26
Q

Name some inflammatory disorders of the stomach

A
  • acute gastritis
  • chronic gastritis

Rare;

  • lymphocytic
  • eosinophilic
  • granulomatous
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27
Q

Chronic gastritis can be due to what?

A
  • autoimmune
  • bacterial (H. pylori)
  • chemical
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28
Q

Describe autoimmune chronic gastritis

A
  • rarest
  • anti-parietal and anti-intrinsic factor antibodies
  • atrophy and intestinal metaplasia in body of stomach
  • pernicious anaemia, macrocytic, due to B12 deficiency
  • increased risk of malignancy
  • SACDC
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29
Q

Describe h.pylori associated chronic gastritis

A
  • most common type
  • bacteria inhabits a niche between the epithelial cell surface and mucous barrier
  • gram negative curvilli near rod
  • excites early acute inflammatory response
  • if not cleared then a chronic active inflammation ensues
  • IL8 is critical
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30
Q

H. pylori gastritis increases risk of what?

A
  • lamina propria plasma cells produce anti H.pylori antibodies
  • increases risk of;
  • duodenal ulcer
  • gastric ulcer
  • gastric carcinoma
  • gastric lymphoma
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31
Q

Describe chemical gastritis

A
  • due to NSAIDs, alcohol, bile reflux
  • direct injury to mucus layer by fat solvents
  • marked epithelial regeneration, hyperplasia, congestion and little inflammation
  • may produce erosions or ulcers
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32
Q

Describe peptic ulceration

A

A breach in the gastrointestinal mucosa as a result of acid and pepsin attack

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33
Q

Describe chronic peptic ulcers

A
  • ulceration is longstanding and often deep

Sites;

  • duodenum (1st part)
  • stomach (junction of body and antrum)
  • oesophago-gastric junction
  • stomal ulcers
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34
Q

Describe chronic duodenal ulcers

A
  • pathogenesis; increased attack and failure of defence
  • 50% of patients with duodenal ulceration have increased acid secretion
  • many have inappropriately sustained secretion of acid
  • excess acid in duodenum produces gastric metaplasia and leads to H.pylori infection, inflammation, epithelial damage and ulceration
  • synergism
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35
Q

Describe the pathogenesis of chronic peptic ulcers

A
  • not just due to increased acid production

- failure of mucosal defence is also important

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36
Q

Describe the morphology of peptic ulcers

A
  • 2-10cm across

- edges are clear cut, punched out

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37
Q

Describe the microscopic appearance of peptic ulcers

A
  • layered appearance
  • floor of necrotic fibrinopurulent debris
  • base of inflamed granulation tissue
  • deepest layer is fibrotic scar tissue
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38
Q

Describe complications of peptic ulcers

A
  • perforation
  • penetration
  • haemorrhage
  • stenosis
  • intractable pain
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39
Q

Name benign (polyps) gastric tumours

A
  • hyperplastic polyps

- cystic fundic gland polyps

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40
Q

Name malignant gastric tumours

A
  • carcinomas (adenocarcinomas)
  • lymphomas
  • GI stromal tumours (GISTs)
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41
Q

Describe the epidemiology of gastric adenocarcinomas

A
  • incidence varies widely
  • high incidence in japan, china, Columbia and Finland
  • in UK proximal tumours of cardia / GOJ increasing and distal tumours deceasing
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42
Q

Describe the aetiology of gastric adenocarcinomas

A
  • H.pylori infection prevalence runs parallel to incidence of gastric cancer in same populations
  • pts with anti-h.pylori antibodies have higher risk of cancer
  • h.pylori is the major cause of chronic gastritis
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43
Q

Describe the pathology of gastric adenocarcinoma

A
  • h.pylori infection

> > >

  • chronic gastritis

> > >

  • intestinal metaplasia / atrophy

> > >

  • dysplasia

> > >

  • carcinoma
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44
Q

Describe the aetiology of gastric adenocarcinoma

A
  • other pre malignant conditions
  • pernicious anaemia
  • partial gastrectomy
  • HNPCC / lynch syndrome
  • menetriers disease
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45
Q

Describe the subtypes of gastric adenocarcinoma

A
  • intestinal type; exophytic / polypoid mass

- diffuse type; expands / infiltrates stomach wall

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46
Q

Describe a benign peptic ulcer

A

Mimics cancer but is more punched out and lacks a raised rolled edge

  • all gastric ulcers must be regarded as potentially malignant
47
Q

Describe the spread of gastric adenocarcinoma

A
  • local; into other organs and into peritoneal cavity and ovaries (kruckenberg)
  • lymph nodes
  • haematogenous (to the liver)
48
Q

Describe gastric lymphoma (MALToma)

A
  • derived from mucosa associated lymphoid issue (MALT)
  • associated with h.pylori infection
  • continuous inflammation induces an evolution into a clonal B cell proliferation, low grade lymphoma
  • if unchecked evolves into a high grade b-cell lymphoma
49
Q

Describe the aetiology of ischaemia of the small bowel

A
  • mesenteric arterial occlusion;
    1. mesenteric artery atherosclerosis
    2. thromboembolism from heart (eg. A.fib)
  • non occlusive perfusion insufficiency;
    1. shock
    2. strangulation obstructing venous return (eg. hernia, adhesion)
    3. drugs eg. cocaine
    4. hyperviscosity
50
Q

Describe the pathogenesis of ischaemia of the small bowel

A
  • the mucosa is the most metabolically active part of the bowel wall and therefore the most sensitive to the effects of hypoxia
  • the longer the period of hypoxia the greater the depth of the damage to the bowel wall and the greater the likelihood of complications
  • in non occlusive ischaemia much of the tissue damage occurs after reperfusion
51
Q

What is the outcome of mucosal infarct?

A

Regeneration; mucosal integrity restored

52
Q

What is the outcome of mural infarct?

A

Repair and regeneration; fibrous stricture

53
Q

What is the outcome of transmural infarct?

A

Gangrene; death if not resected

54
Q

Describe complications of ischaemia of the small bowel

A
  • resolution
  • fibrosis, stricture, chronic ischaemia, mesenteric angina and obstruction
  • gangrene, perforation, peritonitis, sepsis and death
55
Q

Describe meckels diverticulum

A
  • result of incomplete regression of vitello-intestinal duct
  • tubular structure, 2 inches long, 2 foot above IC value for 2% of people
  • may contain heterotopic gastric mucosa
  • may cause bleeding, perforation or diverticulitis which mimics appendicitis
  • commonly asymptomatic, incidental finding
56
Q

Name secondary tumours of the small bowel

A
  • much more common
  • ovary
  • colon
  • stomach
57
Q

Name primary tumours of the small bowel

A
  • much rarer
  • lymphomas
  • carcinoid tumours
  • carcinomas
58
Q

Describe lymphomas of the small bowel

A
  • rare all non hodkins in type
  • maltomas (B cell) derived
  • enteropathy associated T cell lymphomas (associated with coeliac disease)
  • treated by surgery and chemotherapy
59
Q

Describe carcinoid tumours of the small bowel

A
  • rare, commonest site is the appendix
  • small, yellow, slow growing tumours
  • locally invasive
  • can cause intussusception, obstruction
  • produce hormone like substances
  • if metastases to liver occur a carcinoid syndrome occurs producing flushing and diarrhoea
60
Q

Describe carcinoma of the small bowel

A
  • rare, associated with crohns disease and coeliac disease
  • identical to colorectal carcinoma in appearance
  • presents late
  • metastases to lymph nodes and liver occur
61
Q

Describe appendicitis

A
  • common cause of an acute abdomen
  • commoner in children but occurs in adults
  • vomiting, abdominal pain, RIF tenderness and increased WCC
62
Q

Describe the aetiology of acute appendicitis

A
  • unknown
  • faecoliths (dehydration)
  • lymphoid hyperplasia
  • parasites
  • tumours (rare)
63
Q

Describe the pathology of acute appendicitis

A
  • acute inflammation (neutrophils)
  • mucosal ulceration
  • serosal congestions, exudate
  • pus in lumen

Acute inflammation must involve the muscle coat

64
Q

Describe the complications of appendicitis

A
  • peritonitis
  • rupture
  • abscess
  • fistula
  • sepsis and liver abscess
65
Q

Describe the aetiology of coeliac disease

A
  • gliadin a component of gluten is the suspected toxic agent
  • but tissue injury may be a bystander effect of abnormal immune reaction to gliadin
  • mediated by T cell lymphocytes which exist within the small intestinal epithelium ‘intraepithelial lymphocytes’ (IELS)
66
Q

What is the normal lifespan of an enterocyte?

A

72 hours

67
Q

Name the three zones of the liver

A
  • periportal zone
  • mid acinar
  • pericentral
68
Q

Describe the liver and injury

A
  • very resistant to injury
  • the liver has a large functional reserve
  • some liver insults can produce severe parenchymal necrosis but heal entirely by restitution
  • some types of injury leave permanent damage
  • some types of injury produce predictable pathological patterns
69
Q

Describe the pathogenesis of liver disease

A
  • insult to hepatocytes, viral drug toxin, antibody
  • grading, degree of inflammation
  • staging, degree of fibrosis
  • cirrhosis
70
Q

Name causes of acute onset of jaundice

A
  • viruses
  • alcohol
  • drugs
  • bile duct obstruction
71
Q

Name consequences of acute liver failure

A
  • complete recovery
  • chronic liver disease
  • death from liver failure
72
Q

Describe jaundice classification by site and type

A
  • site; pre-hepatic, hepatic, post-hepatic

- type; conjugated and unconjugated

73
Q

Describe pre-hepatic jaundice

A
  • too much haem to break down
  • haemolysis of all causes
  • haemolytic anaemias
  • unconjugated bilirubin
74
Q

Describe hepatic jaundice

A
  • liver cells injured or dead
  • acute liver failure (virus, drugs, alcohol)
  • alcoholic hepatitis
  • cirrhosis (compensated)
  • bile duct loss (atresia, PBC, PSC)
  • pregnancy
75
Q

describe post-hepatic jaundice

A
  • bile cannot escape into the bowel
  • congenital biliary atresia
  • gallstones block CB duct
  • strictures of CB duct
  • tumours (Ca head of pancreas)
76
Q

Describe cirrhosis of liver

A
  • final common endpoint for liver disease
  • irreversible
  • defined by bands of fibrosis separating regenerative nodules of hepatocytes
  • macronodular or micronodular (alcoholic)
  • alteration of hepatic microvasculature
  • loss of hepatic function
77
Q

Describe complications of cirrhosis

A
  • portal hypertension (porto-caval anastomoses)
  • oesophageal varices
  • caput medusa
  • haemorrhoids
  • ascites
  • liver failure
78
Q

Describe alcoholic liver disease

A
  • common pathology
  • indication for biopsy; usually to rule out another condition
  • pathology depends largely on the extent of alcohol abuse
  • pathology also depends upon individual factors
79
Q

Describe the outcome of alcoholic liver disease

A
  • cirrhosis
  • portal hypertension, varices and ascites
  • malnutrition
  • hepatocellular carcinoma
  • social disintegration
80
Q

Describe non-alcoholic steatohepatitis (NASH)

A
  • non-drinkers
  • pathologically identical to alcoholic liver disease
  • occurs in patients with diabetes, obesity, hyperlipidaemia
  • on the increase
  • may lead to fibrosis and cirrhosis
81
Q

Describe primary biliary cirrhosis

A
  • rare autoimmune disease, unknown aetiology
  • associated with autoantibodies to mitochondria
  • females (90%)
  • indication for biopsy; stage the disease
  • may see granulomas and bile duct loss
  • outcome: unpredictable
82
Q

Describe autoimmune hepatitis

A
  • commoner in females
  • associated with other AI diseases
  • chronic hepatitis pattern
  • numerous plasma cells
  • autoantibodies to smooth muscle, nuclear or LKM, raised IgG
  • may have triggers, including some drugs
83
Q

Describe chronic drug-induced hepatitis

A
  • similar features to all other types of chronic hepatitis
  • may trigger an autoimmune hepatitis
  • chronic active process
  • causes are too many to list
84
Q

Describe drugs and the liver

A
  • innumerable drugs can damage the liver
  • may be dose related or idiosyncratic
  • can cause hepatitis, granulomas, fibrosis, necrosis, failure, cholestasis or cirrhosis
  • can mimic any liver disease
85
Q

Describe primary sclerosing cholangitis

A
  • chronic inflammatory process affecting intra and extra hepatic bile ducts
  • leads to periductal fibrosis, duct destruction, jaundice and fibrosis
  • associated with ulcerative colitis
  • males
  • increased risk of malignancy in bile ducts and colon
86
Q

Name some storage diseases

A
  • haemochromatosis
  • wilsons disease
  • alpha 1 antitrypsin deficiency
87
Q

Describe iron and the liver

A
  • haemochromatosis is excess iron within the liver
  • primary; genetic condition, increased absorption of iron
  • secondary; iron overload from diet, transfusions, iron therapy
88
Q

Describe primary haemochromatosis

A
  • an iron handling / storage disorder
  • inherited autosomal recessive condition
  • gene defect v.complex
  • excess absorption of iron from intestine, abnormal iron metabolism, worse in homozygotes, men
  • iron deposited in liver, asymptomatic for years
  • eventually deposited in portal connective tissue and stimulates fibrosis
  • cirrhosis if not treated
  • predisposes to carcinoma
  • also causes diabetes, cardiac failure and impotence
89
Q

Describe the outcome of haemochromatosis

A
  • outcome depends on genetics, therapy (venesection) and cofactors such as alcohol
  • cirrhosis
  • hepatocellular carcinoma
90
Q

Describe wilsons disease

A
  • inherited autosomal recessive disorder of copper metabolism
  • copper accumulated in liver and brain (basal ganglia)
  • Kayser-Fleischer rings at corneal limbus
  • low serum caeruloplasmin
  • causes chronic hepatitis and neurological deterioration
91
Q

Describe alpha 1 antitrypsin deficiency

A
  • inherited autosomal recessive disorder of production of an enzyme inhibitor
  • causes emphysema and cirrhosis
  • cytoplasmis globules of unsecreted globule of protein in liver cells
92
Q

Name tumours of the liver

A
  • hepatocellular adenoma
  • hepatocellular carcinoma (hepatoma)
  • multiple secondary
  • metastases from colon, pancreas, stomach, breast, lung, others
93
Q

Describe cholelithiasis (gallstones)

A
  • defined as hard stone-like or gravel-like material formed within the biliary system most commonly the gallbladder
94
Q

Describe normal bile

A
  • micelles of cholesterol, phospholipid, bile salts and bilirubin
  • stored and concentrated in GB, released by CCK into 2nd part of duodenum through common bile duct and ampulla of vater
95
Q

Describe the pathogenesis of cholesterol gallstones

A
  • gallstones form when there is an imbalance between the ratio of cholesterol to bile salts disrupting micelle formation
  • free crystallisation of cholesterol on micelle surface
96
Q

Describe risk factors and appearance of cholesterol stones

A
  • cholesterol excess in bile

- female, obesity, diabetes, genetics

97
Q

Describe pathogenesis of pigment stones

A
  • excess bilirubin cannot be solubilised in bile salts
98
Q

Describe risk factors for and appearance of pigment stones

A
  • excess bilirubin (pigment stones)

- due to excess haemolysis ie haemolytic anaemias

99
Q

Describe pathogenesis of gallstones

A
  • gallbladder pH and mucosal glycoproteins may be contributory factors
  • infection and inflammation of biliary lining
  • most gallstones are a mixture (mixed stones)
  • pure cholesterol an pure pigment stones do occur
  • calcium carbonate stones do occur
100
Q

Describe the pathology of gallstones

A
  • acute cholecystitis
  • chronic cholecystitis
  • mucocoele
  • empyema
  • carcinoma
  • ascending cholangitis
  • obstructive jaundice
  • gallstone ileus
  • acute pancreatitis
  • chronic pancreatitis
101
Q

Describe cholecystitis

A
  • inflammation of gallbladder
  • usually associated with gallstones
  • acute or chronic
  • common
102
Q

Describe acute cholecystitis

A
  • gallstones obstructing outflow of bile
  • initially sterile, then becomes infected
  • may cause empyema, rupture, peritonitis
  • causes intense adhesions within 2-3 days
103
Q

Describe chronic cholecystitis

A
  • associated with gallstones
  • may develop insidiously or after bouts of acute cholecystitis
  • gallbladder wall is thickened but not distended
104
Q

Describe carcinoma of gallbladder

A
  • rare
  • adenocarcinoma
  • associated with gallstones
  • local invasion of liver
  • poor prognosis
105
Q

Carcinoma of bile ducts (cholangiocarcinoma)

A
  • rare
  • associated with ulcerative colitis and primary sclerosing cholangitis
  • presents with obstructive jaundice
  • adenocarcinoma
106
Q

Describe pancreatitis

A
  • inflammation of the pancreas may be acute or chronic

- overlap exists between acute and chronic

107
Q

Describe acute pancreatitis

A
  • adults
  • sudden onset, severe abdominal pain
  • patients may be severely shocked
  • elevated serum amylase
108
Q

Describe aetiology of acute pancreatitis

A
  • alcohol
  • cholelithiasis
  • shock
  • mumps
  • hyperparathyroidism
  • hypothermia
  • trauma
  • iatrogenic
109
Q

Describe pathogenesis of acute pancreatitis

A
  • bile reflux, duct obstruction due to stone damage to sphincter of oddi all cause pancreatic duct epithelial injury
  • loss of protective barrier allows autodigestion of pancreatic acini
  • release of lytic pancreatic enzymes proteases and lipases
  • intra and peripancreatic fat necrosis (lipases)
  • tissue destruction and haemorrhage (proteases)
110
Q

Describe complications of acute pancreatitis

A
  • death
  • shock
  • pseudocyst formation
  • abscess formation
  • hypocalcaemia
  • hyperglycaemia
111
Q

Describe chronic pancreatitis

A
  • relapsing disorder may develop insidiously or following bout of acute pancreatitis
112
Q

Describe the aetiology of acute pancreatitis

A
  • alcohol
  • cholelithiasis
  • cystic fibrosis
  • hyperparathyroidism
  • familial
113
Q

Describe pathology of chronic pancreatitis

A
  • replacement of pancreas by chronic inflammation and scar tissue
  • destruction of exocrine acini and islets
114
Q

Describe carcinoma of pancreas

A
  • adenocarcinoma
  • aetiology unknown
  • associated with smoking, diabetes, familial pancreatitis
  • poor prognosis

GI (11 decks)

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