Pathology Flashcards
(114 cards)
1
Q
Name some inflammatory disorders of oesophagus
A
- acute oesophagitis
- chronic oesophagitis
2
Q
Describe acute oesophagitis
A
- rare
- corrosive following chemical ingestion
- infective in immunocompromised pts eg. candidiasis, herpes, CMV
3
Q
Describe chronic oesophagitis
A
- common
- reflux disease ‘ reflux oesophagitis’
- rare causes include crohns disease
4
Q
Define reflux oesophagitis
A
- inflammation of oesophagus due to refluxed low pH gastric gastric content
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)
6
Q
Describe the microscopic of reflux oesophagitis
A
- basal zone epithelial expansion
- intraepithelial neutrophils, lymphocytes and eosinophils
7
Q
Describe the complications of reflux
A
- ulceration (bleeding)
- stricture
- barrets oesophagus
8
Q
What is barrets oesophagus?
A
Replacement of stratified squamous epithelium by columnar epithelium
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
10
Q
Describe the macroscopic changes of barrets oesophagus
A
Red velvety mucosa in lower oesophagus
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
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
13
Q
Name the treatments of allergic oesophagitis
A
Treatment may include steroids / chromoglycate / Montelukast
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
15
Q
Name malignant tumours of the oesophagus
A
- squamous cell carcinoma
- adenocarcinoma
16
Q
Describe the epidemiology of squamous cell carcinoma
A
- commoner in males
- high risk areas NW france, N Italy
17
Q
Describe the aetiology of squamous cell carcinoma
A
- vitamin A, zinc deficiency
- tannic acid / strong tea
- smoking
- alcohol
- HPV
- oesophagitis
- genetic
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
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
20
Q
Describe the mechanism of metastases of carcinoma of the oesophagus
A
- direct invasion
- lymphatic permeation
- vascular invasion
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
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
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
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
25
Describe the histopathological features relating to prognosis of SCC
- 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
26
Name some inflammatory disorders of the stomach
- acute gastritis
- chronic gastritis
Rare;
- lymphocytic
- eosinophilic
- granulomatous
27
Chronic gastritis can be due to what?
- autoimmune
- bacterial (H. pylori)
- chemical
28
Describe autoimmune chronic gastritis
- 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
29
Describe h.pylori associated chronic gastritis
- 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
30
H. pylori gastritis increases risk of what?
- lamina propria plasma cells produce anti H.pylori antibodies
- increases risk of;
- duodenal ulcer
- gastric ulcer
- gastric carcinoma
- gastric lymphoma
31
Describe chemical gastritis
- 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
32
Describe peptic ulceration
A breach in the gastrointestinal mucosa as a result of acid and pepsin attack
33
Describe chronic peptic ulcers
- ulceration is longstanding and often deep
Sites;
- duodenum (1st part)
- stomach (junction of body and antrum)
- oesophago-gastric junction
- stomal ulcers
34
Describe chronic duodenal ulcers
- 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
35
Describe the pathogenesis of chronic peptic ulcers
- not just due to increased acid production
| - failure of mucosal defence is also important
36
Describe the morphology of peptic ulcers
- 2-10cm across
| - edges are clear cut, punched out
37
Describe the microscopic appearance of peptic ulcers
- layered appearance
- floor of necrotic fibrinopurulent debris
- base of inflamed granulation tissue
- deepest layer is fibrotic scar tissue
38
Describe complications of peptic ulcers
- perforation
- penetration
- haemorrhage
- stenosis
- intractable pain
39
Name benign (polyps) gastric tumours
- hyperplastic polyps
| - cystic fundic gland polyps
40
Name malignant gastric tumours
- carcinomas (adenocarcinomas)
- lymphomas
- GI stromal tumours (GISTs)
41
Describe the epidemiology of gastric adenocarcinomas
- incidence varies widely
- high incidence in japan, china, Columbia and Finland
- in UK proximal tumours of cardia / GOJ increasing and distal tumours deceasing
42
Describe the aetiology of gastric adenocarcinomas
- 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
43
Describe the pathology of gastric adenocarcinoma
- h.pylori infection
>>>
- chronic gastritis
>>>
- intestinal metaplasia / atrophy
>>>
- dysplasia
>>>
- carcinoma
44
Describe the aetiology of gastric adenocarcinoma
- other pre malignant conditions
- pernicious anaemia
- partial gastrectomy
- HNPCC / lynch syndrome
- menetriers disease
45
Describe the subtypes of gastric adenocarcinoma
- intestinal type; exophytic / polypoid mass
| - diffuse type; expands / infiltrates stomach wall
46
Describe a benign peptic ulcer
Mimics cancer but is more punched out and lacks a raised rolled edge
- all gastric ulcers must be regarded as potentially malignant
47
Describe the spread of gastric adenocarcinoma
- local; into other organs and into peritoneal cavity and ovaries (kruckenberg)
- lymph nodes
- haematogenous (to the liver)
48
Describe gastric lymphoma (MALToma)
- 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
Describe the aetiology of ischaemia of the small bowel
- 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
Describe the pathogenesis of ischaemia of the small bowel
- 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
What is the outcome of mucosal infarct?
Regeneration; mucosal integrity restored
52
What is the outcome of mural infarct?
Repair and regeneration; fibrous stricture
53
What is the outcome of transmural infarct?
Gangrene; death if not resected
54
Describe complications of ischaemia of the small bowel
- resolution
- fibrosis, stricture, chronic ischaemia, mesenteric angina and obstruction
- gangrene, perforation, peritonitis, sepsis and death
55
Describe meckels diverticulum
- 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
Name secondary tumours of the small bowel
- much more common
- ovary
- colon
- stomach
57
Name primary tumours of the small bowel
- much rarer
- lymphomas
- carcinoid tumours
- carcinomas
58
Describe lymphomas of the small bowel
- 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
Describe carcinoid tumours of the small bowel
- 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
Describe carcinoma of the small bowel
- rare, associated with crohns disease and coeliac disease
- identical to colorectal carcinoma in appearance
- presents late
- metastases to lymph nodes and liver occur
61
Describe appendicitis
- common cause of an acute abdomen
- commoner in children but occurs in adults
- vomiting, abdominal pain, RIF tenderness and increased WCC
62
Describe the aetiology of acute appendicitis
- unknown
- faecoliths (dehydration)
- lymphoid hyperplasia
- parasites
- tumours (rare)
63
Describe the pathology of acute appendicitis
- acute inflammation (neutrophils)
- mucosal ulceration
- serosal congestions, exudate
- pus in lumen
Acute inflammation must involve the muscle coat
64
Describe the complications of appendicitis
- peritonitis
- rupture
- abscess
- fistula
- sepsis and liver abscess
65
Describe the aetiology of coeliac disease
- 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
What is the normal lifespan of an enterocyte?
72 hours
67
Name the three zones of the liver
- periportal zone
- mid acinar
- pericentral
68
Describe the liver and injury
- 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
Describe the pathogenesis of liver disease
- insult to hepatocytes, viral drug toxin, antibody
- grading, degree of inflammation
- staging, degree of fibrosis
- cirrhosis
70
Name causes of acute onset of jaundice
- viruses
- alcohol
- drugs
- bile duct obstruction
71
Name consequences of acute liver failure
- complete recovery
- chronic liver disease
- death from liver failure
72
Describe jaundice classification by site and type
- site; pre-hepatic, hepatic, post-hepatic
| - type; conjugated and unconjugated
73
Describe pre-hepatic jaundice
- too much haem to break down
- haemolysis of all causes
- haemolytic anaemias
- unconjugated bilirubin
74
Describe hepatic jaundice
- liver cells injured or dead
- acute liver failure (virus, drugs, alcohol)
- alcoholic hepatitis
- cirrhosis (compensated)
- bile duct loss (atresia, PBC, PSC)
- pregnancy
75
describe post-hepatic jaundice
- bile cannot escape into the bowel
- congenital biliary atresia
- gallstones block CB duct
- strictures of CB duct
- tumours (Ca head of pancreas)
76
Describe cirrhosis of liver
- 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
Describe complications of cirrhosis
- portal hypertension (porto-caval anastomoses)
- oesophageal varices
- caput medusa
- haemorrhoids
- ascites
- liver failure
78
Describe alcoholic liver disease
- 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
Describe the outcome of alcoholic liver disease
- cirrhosis
- portal hypertension, varices and ascites
- malnutrition
- hepatocellular carcinoma
- social disintegration
80
Describe non-alcoholic steatohepatitis (NASH)
- 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
Describe primary biliary cirrhosis
- 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
Describe autoimmune hepatitis
- 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
Describe chronic drug-induced hepatitis
- similar features to all other types of chronic hepatitis
- may trigger an autoimmune hepatitis
- chronic active process
- causes are too many to list
84
Describe drugs and the liver
- 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
Describe primary sclerosing cholangitis
- 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
Name some storage diseases
- haemochromatosis
- wilsons disease
- alpha 1 antitrypsin deficiency
87
Describe iron and the liver
- haemochromatosis is excess iron within the liver
- primary; genetic condition, increased absorption of iron
- secondary; iron overload from diet, transfusions, iron therapy
88
Describe primary haemochromatosis
- 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
Describe the outcome of haemochromatosis
- outcome depends on genetics, therapy (venesection) and cofactors such as alcohol
- cirrhosis
- hepatocellular carcinoma
90
Describe wilsons disease
- 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
Describe alpha 1 antitrypsin deficiency
- 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
Name tumours of the liver
- hepatocellular adenoma
- hepatocellular carcinoma (hepatoma)
- multiple secondary
- metastases from colon, pancreas, stomach, breast, lung, others
93
Describe cholelithiasis (gallstones)
- defined as hard stone-like or gravel-like material formed within the biliary system most commonly the gallbladder
94
Describe normal bile
- 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
Describe the pathogenesis of cholesterol gallstones
- 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
Describe risk factors and appearance of cholesterol stones
- cholesterol excess in bile
| - female, obesity, diabetes, genetics
97
Describe pathogenesis of pigment stones
- excess bilirubin cannot be solubilised in bile salts
98
Describe risk factors for and appearance of pigment stones
- excess bilirubin (pigment stones)
| - due to excess haemolysis ie haemolytic anaemias
99
Describe pathogenesis of gallstones
- 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
Describe the pathology of gallstones
- acute cholecystitis
- chronic cholecystitis
- mucocoele
- empyema
- carcinoma
- ascending cholangitis
- obstructive jaundice
- gallstone ileus
- acute pancreatitis
- chronic pancreatitis
101
Describe cholecystitis
- inflammation of gallbladder
- usually associated with gallstones
- acute or chronic
- common
102
Describe acute cholecystitis
- gallstones obstructing outflow of bile
- initially sterile, then becomes infected
- may cause empyema, rupture, peritonitis
- causes intense adhesions within 2-3 days
103
Describe chronic cholecystitis
- associated with gallstones
- may develop insidiously or after bouts of acute cholecystitis
- gallbladder wall is thickened but not distended
104
Describe carcinoma of gallbladder
- rare
- adenocarcinoma
- associated with gallstones
- local invasion of liver
- poor prognosis
105
Carcinoma of bile ducts (cholangiocarcinoma)
- rare
- associated with ulcerative colitis and primary sclerosing cholangitis
- presents with obstructive jaundice
- adenocarcinoma
106
Describe pancreatitis
- inflammation of the pancreas may be acute or chronic
| - overlap exists between acute and chronic
107
Describe acute pancreatitis
- adults
- sudden onset, severe abdominal pain
- patients may be severely shocked
- elevated serum amylase
108
Describe aetiology of acute pancreatitis
- alcohol
- cholelithiasis
- shock
- mumps
- hyperparathyroidism
- hypothermia
- trauma
- iatrogenic
109
Describe pathogenesis of acute pancreatitis
- 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
Describe complications of acute pancreatitis
- death
- shock
- pseudocyst formation
- abscess formation
- hypocalcaemia
- hyperglycaemia
111
Describe chronic pancreatitis
- relapsing disorder may develop insidiously or following bout of acute pancreatitis
112
Describe the aetiology of acute pancreatitis
- alcohol
- cholelithiasis
- cystic fibrosis
- hyperparathyroidism
- familial
113
Describe pathology of chronic pancreatitis
- replacement of pancreas by chronic inflammation and scar tissue
- destruction of exocrine acini and islets
114
Describe carcinoma of pancreas
- adenocarcinoma
- aetiology unknown
- associated with smoking, diabetes, familial pancreatitis
- poor prognosis
