Pathology Flashcards
1
Q
What supplies blood to the small intestine
A
Superior mesenteric artery
2
Q
What can cause Ischaemia of small bowel
A
Mesenteric artery atherosclerosis, thromboembolism from heart, shock, drugs, hyperviscosity, drugs (cocaine)
3
Q
Hypoxia affects what part of the gut wall the greatest
A
Mucosa, most metabolically active
4
Q
How is degree of small bowel ischaemia classified
A
By the degree of infarction caused. from mucosal (lamina propriae is preserved) to mural (penetrates lamina propriae but can be regenerated, fibrosis occurs) to transmural infarction (gangrene, needs to be resected)
5
Q
What is Meckels diverticlum
A
A congenital diverticulum, a slight bulge in the small intestine present a birth, a vestigial remnant of the vitello-intestinal duct. Most are asymptomatic
6
Q
Which tumours are more common in small intestine, primary or secondary
A
Secondary tumours are more common, metastases from ovary, colon and stomach
7
Q
What type of Lymphomas of small bowel
A
Non-Hodgkin type - No Reed-Sternberg cell (crippled germinal centres mainly of B cells)
8
Q
How can MALTomas of small bowel be treated
A
Surgery and chemotherapy
9
Q
Identify - Small, yellow, slow growing tumour. Locally invasive and can cause intussusception and obstruction. Produce hormone like substances, cause diarrhoea and flushing if metastasize to liver.
A
Carcinoid tumour of small bowel
10
Q
What is Intussusception
A
Folding of the intestine into the section next to it
11
Q
What predisposes to rare tumours of small bowel
A
Crohns and coeliac disease
12
Q
Most common cause of Appendicitis
A
Idiopathic
13
Q
Pathology of acute appendicitis
A
Acute inflammation, mucosal ulceration, serosal congestion, exudate and pus in lumen
14
Q
Complications of appendicitis
A
Peritonitis, rupture, abscess, fistula, sepsis, liver abscess
15
Q
What are Coeliac diseases
A
Autoimmune disorder of the small intestine due to an abnormal immune response to Gluten. This leads to production of various antibodies and inflammation. This reduces absorptive capacity and leads to anaemia.
16
Q
What serology is associated with coeliac disease
A
Human Leukocyte Antigen (HLA) - B8. This is part of the HLA family and codes for Major Histocompatibility Complex (MHC) which distinguishes different antigen
17
Q
What is Dermatitis Herpetiformis associated with
A
It is an itchy, burning skin rash indicating gluten intolerance and sometimes coeliac disease
18
Q
Suspected toxic agent causing coeliac disease
A
Gliadin, component of Gluten
19
Q
What can coeliac disease cause
A
Loss of villi, flat duodenal mucosa, loss of surface area. Thus reduces absorption and anaemia. Steatorrhea occurs due to inabsorption of fats. Reduced intestinal hormone production leads to reduced pancreatic secretion and bile flow causing gallstones
20
Q
There is an increase in intraepithelial lymphocytes and inflammation in lamina propria
A
True
21
Q
Diagnosing coeliac disease
A
Endoscopy - Mucosa maybe normal or attenuated, Serology - For anti-Tissue Transglutinamase, anti-endomesial and anti-gliadin
22
Q
Which oesophagitis is more common, acute or chronic
A
Chronic due to gastric acid reflux causing metaplastic change. Acute oesophagitis is more common in immunocompromised patients such as candiasis, herpes
23
Q
What is reflux oesophagitis
A
Inflammation of oesophagus due to reflux gastric acid
24
Q
Cause of reflux oesophagitis
A
Hiatus hernia (stomach moves into chest cavity), defective sphincter, increased abdominal pressure (pregnancy), abnormal oesophageal motility
25
How is increased desquamation due to reflux oesophagitis compensated for
By basal zone hyperplasia and elongation of connective tissue papillae
26
Complications of reflux oesophageal
Ulceration, bleeding, stricture, Barrett's oesophagus
27
What is Barrette's oesophagus
Metaplastic change of oesophageal stratified squamous epithelium to gastric golumnar goblet cells.
28
How does Barrette's mucosa look macroscopically
Red velvety mucosa in oesophagus
29
Allergic oesophagitis is more common in what gender
Male > females, increased eosinophils in blood
30
What is spotty/feline/corrugated oesophagus known as
Allergic oesophagus
31
How is allergic oesophagitis seen microscopic
Increased intraepithelial eosinophils
32
Treatment of allergic oesophagitis
Steroids, chromoglycate, montelukast (leukotriene receptor antagonist)
33
What is a papilloma
Small wart like growth on the skin or mucous membrane, derived from epidermis and usually benign
34
Common causes of small cell carcinoma
Vitamin A or Zinc deficiency, tannic acid, smoking, alcohol, HPV, genetic, gastric reflux
35
What cancer of oesophagus is more common in caucasians
Adenocarcinoma of oesophagus, more common in obese males
36
Pathogenesis of adenocarcinoma of oesophagus
Chronic reflux oesophagitis - Barrett's oesophagus - Low grade dysplasia - High grade dysplasia - Adenocarcinoma
37
Adenocarcinoma can cause?
Dysphagia and obstruction
38
General symptoms of metastases
Anaemia, weight loss, loss of energy
39
How can oral squamous cell carcinoma present
Variable, usually - red, white, speckled, ulcer lump
40
What is verrucous carcinoma
Uncommon variant of squamous cell carcinoma often seen in those who chew tobacco or use snuff orally.
41
What can cause gastrooesophageal reflux disease
Incompetent lower oesophagus sphincter, poor oesophageal clearance, barrier function/visceral sensitivity
42
What is water brash
Sour taste in the mouth due to stomach contents rising up the oesophagus.
43
What is odynophasia
Painful swallowing
44
Investigations for GORD
Endoscopy, barium swallow (ancient, not used anymore), oesophageal manometry & pH studies, nuclear studies
45
Common cause of dyspepsia
Indigestion is commonly caused by GORD
46
What is pernicious anaemia
Anaemia in which the body has lost stomach cells that are involved in the synthesis of intrinsic factor. This intrinsic factor helps absorb vitamin B12.
47
LIfestyle modifications for GORD
Stop smoking, lose weight, avoid provoking, prop up bed head
48
Are antacids useful for GORD
Symptomatic relief, however it does not heal oesophagitis nor prevent further complications
49
Histamine (H2) receptor antagonists that can be used for GORD
Cimetidine - Rapid symptomatic relief, less effective at healing than placebo
Ranitidine - Poor in preventing relapse and complications, tolerance after 4/52 week therapy
50
Proton pump inhibitors vs H2 receptor antagonist in treatment of GORD
Proton pump inhibitors such as Omeprazole are more effective at symptom relief and healing than H2 antagonists (ranitidine, cimetidine)
51
Treatment of GORD or hiatus hernia in young patients
Nissen fundoplication, heals oesophagitis with good control of symptoms
52
Is Barrett's oesophagus reversible
No but recent findings point otherwise
53
Type of hiatus hernia
Sliding where the stomach slides into the oesophagus increasing risk of GORD. Second type is paraoesophageal hiatus hernia where the stomach pushes through beside the oesophagus
54
What is gastroparesis
Disease of the muscles of stomach or nerves controlling these muscles that causes it to stop working. It results in inadequate grinding and poor emptying of food from stomach.
55
Symptoms of gastroparesis
Feeling of fullness, nausea, vomiting, weight loss, upper abdominal pain
56
Causes of gastroparesis
Idiopathic, diabetes mellitus, cannabis, medication (opiates, anticholinergics), systemic disease (systemic sclerosis)
57
Management of gastroparesis
Remove precipitating factors (drugs), liquid diet, eat little and often, promotility agents, gastric pacemaker
58
What is achalasia
Disease of muscles of lower oesophagus that prevents relaxation of sphincter and absence of contractions and hence peristalsis of oesophagus.
59
Common cause of chronic gastritis
ABC - Autoimmune, bacterial and chemical
60
Cause of autoimmune chronic gastritis
Anti-parietal and auto-intrinsic factor antibodies leads to atrophy and intestinal metaplasia in body of stomach
61
What can autoimmune gastritis lead to
Pernicious anaemia causing B12 vitamin deficiency. This can lead to subacute combined degeneration of spinal cord (SACDC)
62
What is subacute combined degeneration of spinal cord (SACDC)
Degeneration of spinal cord at posterior and lateral columns due to vitamin B12 deficiency. Usually associated with pernicious anaemia
63
Most common cause of chronic gastritis
Helicobacter pylori infection. Lives between epithelial cell surface and mucous barrier.
64
What are peptic ulcerations
Breach in the gastrointestinal mucosal lining as a result of acid and pepsin attack
65
Pathogenesis of peptic ulcers
Excess acid in duodenum produces gastric metaplasia and leads to H.pylori infection, inflammation, epithelial damage and ulceration. The GALT is also unable to cope with this increased acid and H.pylori infection
66
Morphology of peptic ulcers
2-10 cm across, edges are clear cut and punched out
67
What are gastrointestional stromal tumours (GIST)
Most common in stomach but can be found in small intestine. Begin in interstitial cells of Cajal (ICC)
68
Other causes of gastric adenocarcinoma
Pernicious anaemia, partial gastrectomy, HNPCC, Menetrier's disease
69
What is hereditary nonpolyposis colorectal cancer (HNPCC)
Lynch syndrome is an autosomal dominant genetic condition that predisposes to high risk of colon cancer.
70
What is Menetrier's disease
Premalignant disease of stomach characterized by massive gastric folds, excessive mucous production with resultant protein loss and little or no acid production
71
Types of gastric adenocarcinoma
Intestinal - Polypoid mass
| Diffuse - Expands/infiltrates stomach
72
Are all gastric ulcers malignant
No, however all gastric ulcers must be regarded as potentially malignant.
73
Benign peptic ulcer vs malignant
Benign peptic ulcer mimics caner however is more punched out and lacks a raised rolled edge
74
What is linitis plastica
Leather bottom stomach which is a morphological variant of diffuse stomach cancer.
75
What is signet ring cell gastric adenocarcinoma
Rare form of malignant adenocarcinoma of stomach. Presence of signet ring cells (cells with a large vacuole)
76
Some types of diffuse gastric adenocarcinoma
Linitis plastica, signet ring type, sclerosis
77
Intestinal vs diffuse gastric adenocarcinoma, which has better prognosis
Intestinal as it spreads relatively less
78
What is a Krukenberg tumour
A tumour that has metastasized into the ovary from a primary site, classically the GI tract. It's most common site is from gastric adenocarcinomas
79
Gastric lymphoma is also known as
MALToma
80
Low grade vs high grade tumour
Low grade - Grow slowly and less likely to spread
| High grade - Grow faster and more likely to spread
81
How can dyspepsia be divided
According to Rome III criteria -
Epigastric pain syndrome - Epigastric pain or burning
Postprandial distress syndrome - Postpradial fullness and early satiety
82
Cause of dyspepsia
Peptic ulcer disease, drugs (NSAID, Cox2 inhibitors), gastric cancer, idiopathic, GORD, irritable bowel syndrome
83
Alarm symptoms of dyspepsia which constitutes referral to hospital
Dysphagia, evidence of GI blood loss, persistent vomiting, unexplained weight loss, upper abdominal mass. This is complicated dyspepsia
84
Test and treat strategy of dyspepsia
Check H.pylori status and eradicate if infected. Continue acid inhibition if still symptomatic
85
Causes of peptic ulcer disease
H.pylori is the main cause for gastric and duodenal. NSAIDs can also cause the same
86
B cell gastric lymphoma is also called
MALToma
87
How can H.pylori infection be identified
Gastric biopsy urease breath test, faecal antigen test, IgA serology (less accurate with increasing age)
88
What is the urease breath test
Diagnostic procedure to test for H.pylori infection. Based on the ability of the bacteria to convert urea to ammonia and CO2
89
What are stool antigen tests
Non-invasive diagnostics for H.pylori. Less expensive than urea breath test
90
How can peptic ulcer disease be tested
Proton pump inhibitor, presence of H.pylori, withdraw NSAIDs, change lifestyle
91
Treatment for non-H.pylori/non-NSAID ulcer
Nutrition and optimise comorbidities
92
Anti-secretory therapy for peptic ulcer disease
PPI (Omeprazole 20-40mg/day) heals duodenal ulcers more rapidly than histamine H2 receptor (Ranitidine) antagonists for the first four weeks of therapy.
93
Antacids in ulcer therapy
Antacids and sucralfate are superior to placebo in healing duodenal ulcers but not other types.
94
Treatment of H.pylori infection
Triple therapy for one week -
PPI + Amoxicillin 1 g bd + Clarithromycin 500mg BD
PPI+Metronidazole 400mg bd+Clarithromycin 250mg bd
95
Are 2 week regimes for H.pylori infection better?
Yes, higher eradication rate however low compliance
96
Is dual therapy of PPI + 1 antibiotic recommended
No
97
What is patient is still symptomatic despite H.pylori eradication therapy
Re-test
98
Complications of peptic ulcer disease
Anaemia, bleeding, perforation, gastric outlet/duodenal obstruction - fibrotic scar
99
Follow up for ulcers
Duodenal ulcers -
No follow up required unless there's ongoing symptoms
Gastric ulcers -
Endoscopy at 6-8 weeks to ensure healing and no malignancy
100
What is achlorhydria
Absent HCl in gastric secretions. Up risk gastric cancer
101
Correa's hypothesis of gastric cancer
H.pylori infection - chronic gastritis - atrophy - intestinal metaplasia - dysplasia - neoplasia
102
How does H.pylori inhibit gastric secretions
Direct effect of bacterial product - ammonia, methyl histamine, cave's factor
Effect of body inflammation induced by H.pylori -
IL-1B in H.pylori gastritis, powerful inhibition of gastric secretion
103
How does host genetic affect H.pylori infection outcome
Presence of IL-1B pro-inflammatory host genotype -
Acid hyposecretion leading to body predominant gastritis, atrophic gastritis and cancer
Absence of IL-1B pro-inflammatory host genotype
Normal or high acid secretion, antral predominant gastritis and duodenal ulcer or no disease
104
Is a GI bleed an medical emergency
Yes
105
Major cause of upper GI tract bleeding
Duodenal ulcer, gastric erosions and gastric ulcers
106
What is a Mallory-Weiss syndrome/tear
Tear in mucous membrane of the lining where oesophagus meets the stomach. Often haematemesis
107
First step management for upper GI bleeding
Resuscitation (A,B,C) -
Airway protection, oxygen, IV access, fluids
After resuscitation, endoscopy
108
Poor prognostic group for upper GI bleed
```
The 100 rule
Systolic BP < 100mmHg
Pulse > 100/min
Hb < 100 g/l
Age > 60, comorbid disease, postural drop in BP
```
109
What is OGD also known as
Oesophageal-gastroduodenoscopy or endoscopy
110
What can be used to quantify GI bleeding risk after successful resuscitation
Blatchford score in NHS Tayside
111
Signs of recent haemorrhage
Active bleeding/oozing, overlying clot/ visible vessel
112
How does Haemospray work
Absorbs water, then acts as a cohesive and adhesive, forming a mechanical barrier over bleeding site
113
Peptic ulcer found on endoscopy, bleeding or stigmata of recent haemorrhage
Adrenaline injection/heater probe thermo-coagulation/clips
114
Treatment course for peptic ulcer on endoscopy after bleeding stops
Omeprazole 80mg IV + 8mg/hr for 72 hours
| H.pylori eradication and course of oral PPI
115
Re-bleed after initial haemostasis
Omperazole 80mg IV + 8mg/hr for 72 hours
Further attempt at endoscopic therapy
Surgery if bleed continues
116
Risk factors for variceal bleeding
Portal pressure > 12 mmHg
Varices > 25% oesophageal lumen
Presence of red signs
Degree of liver failure (Child's A
117
Aims of management of varicose veins
Resuscitation, haemostasis , prevent complications of bleeding, prevent deterioration of liver function, prevent early re-bleeding
118
Common cause of variceal bleeding
Liver cirrhosis
119
What are your initial considerations for variceal bleeding
Coagulopathy (excessive bleeding), parenteral nutrition, replace electrolytes, antibiotics, hypoglycaemia, central venous vs portal pressure monitoring
120
How can haemostasis after variceal bleed be achieved
Terlipressin, endoscopic variceal lighting, sclerotherapy, sengstaken-blakemore balloon, TIPS
121
What is Terlipressin
A vasopressin prodrug used in variceal bleed haemostasis. Splanchnic vasoconstrictor with beneficial effect on renal perfusion
122
What is endoscopic variceal ligation
Banding of bleeding varices via endoscopy
123
What is sclerotherapy
Chemical called sclerosant is injected into a vein. This causes it to shrink and then dissolve over a period of weeks.
124
What's a Sengstaken-Blakemore tube (S-B tube)
Tube passed down into the oesophagus with a gastric balloon in the stomach. This is inflated to apply pressure and reduce blood flow to oesophageal varices and stop bleeding. This is rarely used nowadays
125
How is TIPS used in variceal bleeding
Transjugular intrahepatic portosystemic shunt (TIPS) is used to reduce portal hypertension and its complications such as variceal bleeding. A stent is inserted between the hepatic and portal vein
126
First step management of variceal bleeding
Resuscitation, antibiotics, terlipressin + early OGD with/out endoscopic variceal ligation (EVL)
127
Variceal bleeding stops after first step treatment
Propanolol + banding to follow up
128
Variceal bleed continues after first step management
Endoscopic variceal ligation or S-B tube
| If bleed continues, TIPS. If hepatic function remains poor consider transplant
129
What are polyps
Abnormal growth of tissue projecting from mucous membrane.
130
Pedunculated vs sessile polyps
Pedunculated polyps have a narrow elongated stalk attached to the surface whereas sessile polyps have no stalk
131
Are all polyps cancerous?
No, they can also be due to adenoma inflammation such as in inflammatory bowel disease
132
Which polyps have better prognosis, pedunculated or sessile
Pedunculated as it hangs by a stalk. This stalk can be cut off easily
133
Molecular genetics of adenoma-carcinoma sequene
Normal epithelium - APC mutation - Small adenoma - k-ras mutation - Large adenoma - chromosome deletion, p53 mutation - Invasive carcinoma - nm23 deletion - Metastases
134
Why must all adenomas be removed
As they can become malignant
135
Primary treatment for adenocarcinoma
Surgery
136
Explain duke staging A of colorectal carcinoma
Confined by muscularis propriae, usually day discharge
137
Explain duke staging B of colorectal carcinoma
Through muscularis propriae, may or may not need chemotherapy depending on other features such as age, health
138
Explain duke staging C of colorectal carcinoma
Metastatic and lymph nodes, needs adjuvant chemotherapy
139
Which side is generally presented with colorectal carcinoma problems
Left (75%). Generally present with altered bowel habits, obstruction, blood in rectum
140
Why do caecal carcinoma not usually bleed
Caecum has high capacity to expand. It can easily swell to accommodate the tumour and hence no bleeding is seen.
141
If constipation with sudden diarrhoea and blood is seen, what might this suggest
Colorectal carcinoma on the left side, rectum or sigmoid
142
Typical histopathological appearance of large bowel carcinoma
Adenocarcinoma
143
Which lymph nodes does colorectal cancer affect
Mesenteric nodes
144
Why are metastases from large bowel commonly found on the liver
As the blood supply from the large bowel is to the liver
145
Inherited bowel cancer syndromes
Familial adenomatous polyposis (FAP) > 100 polyps, patient presents early on (16) and develops colorectal cancer by 27
Hereditary non polyposis colorectal cancer (HNPCC) or Lynch syndrome < 100 polyps. Patient has late presentation of colorectal cancer, around 50 - 60
146
Differentiate between inherited colorectal carcinoma between their causes
Familial adenomatous polyposis - Defect in tumour suppression
Hereditary non-polyposis colorectal cancer - Defect in DNA mismatch repair
147
Which of the inherited colorectal carcinoma affects right side more
Lynch syndrome with more mucinous tumours
148
Most common genetic mutation in large bowel cancer
APC gene mutation
