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Pathology Term 2 > Week 5 - UPPER GIT > Flashcards

Week 5 - UPPER GIT Flashcards

Oesophagitis, GORD, PUD, Gastric Cancer, Acute Abdo. + Other

1
Q

What is the most common clinical disorder of the oesophagus?

A

Dysphagia –> difficulty swallowing

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2
Q

What term is used to describe painful swallowing?

A

Odynophagia

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3
Q

What are the 3 sites of normal oesophageal narrowing?

A
  1. Oropharyngeal (UOS)
  2. Oesophageal (oesophageal body)
  3. Oesophagogastric (LOS)
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4
Q

What is achalasia?

A

Increased tone (narrowing) of the lower oesophageal sphincter –> due to lack of dilatation

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5
Q

What are oesophageal varices and what is the pathogenesis?

A
  • dilated veins in distal portion of oesophagus
  • portal HTN (from liver cirrhosis) –> dilatation of porta-systemic shunts –> rupture –> massive bleeding (hematemesis)
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6
Q

What is mallory-weiss tears (syndrome)?

A
  • longitudinal mucosal tear at gastro-oesophageal juntion
  • severe/forced vomiting can cause it (i.e. from binge drinking/overeating)
  • hiatus hernia in 75% of pts.
  • spontaneous healing
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7
Q

What is boerhaave syndrome?

A
  • complete oesophageal rupture with contents entering into mediastinum –> mediastinitis
  • common in pacific islands
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8
Q

What is congenital atresia and fistula?

A

*congenital oesophageal disorders

Atresia: - total oesophageal obstruction with just a fibrous thread

Fistula: - one of the ends of the oesophagus forms a connection with the trachea

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9
Q

What is a sliding hernia and a rolling hernia?

A 
Sliding Hernia (95%)
-portion of stomach is pulled up into the oesophagus following strictures/congenital causes --> heartburn

Rolling hernia (5%)
-herniation of stomach wall
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10
Q

Compare causes of acute and chronic oesophagitis

A

Acute
-errosive, alcohol, infection (i.e. candida in IC)

Chronic
-acid reflux (GORD), chemical, alcohol, smoking, candida, radiation, idiopathic (eosinophilic)

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11
Q

What is microscopy of oesophagitis?

A
  • acute inflammation

- eosinophils

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12
Q

What is the pH of gastric acid?

A

1 (million times > than blood)

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13
Q

What is the cause of GORD?

A
  • due to escape of acid into oesophagus –> sudden severe burning pain in epigastrium (heartburn)
  • decreased LOS tone/increased abdominal pressure
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14
Q

What are the risk factors for GORD?

A
  • alcohol
  • smoking
  • obesity
  • CNS depressants
  • pregnancy
  • hiatal hernia
  • delayed gastric emptying
  • increased gastric volume
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15
Q

What are the 6 clinical stages of GORD?

A
  1. functional heartburn
  2. NERD (non-erosive reflux disease)
  3. MERD (minimal ERD)
  4. GORD (erosion + inflammation)
  5. Barret’s (metaplasia)
  6. adenocarcinoma (rare)
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16
Q

Why do you get epithelial hyperplasia in GORD pathogenesis?

A
  • due to increased cell dequamation
  • acid damages epithelial cells
  • therefore increased compensatory epithelial hyperplasia
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17
Q

What is the pathogenesis/stages of GORD?

A
  1. acid reflux (normal pathology)
  2. inflammation
  3. regeneration (epithelial hyperplasia)
  4. metaplasia (barrett’s oesophagus)
  5. mild dysplasia
  6. high grafe dysplasia
  7. adenocarcinoma
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18
Q

What is the epithelial change in Barrett’s oesophagus?

A

METAPLASIA

-stratified squamous (normal) –> columnar (barrett’s)

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19
Q

Compare the 2 types of oesophageal cancers.

A

Squamous cell carcinoma

  • upper/middle 1/3
  • asian countries increased
  • tobacco, diet, toxins
  • keratin pearls
  • hard tumour

Adenocarcinoma

  • lower/distal end
  • western countries increased
  • reflux disease
  • glands –> mucous
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20
Q

What are the mucosal folds of the stomach called?

A

ruggae

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21
Q

What are the 3 types of acute peptic ulcers?

A
  1. stress ulcers: - sepsis, shock, trauma
  2. curling ulcers: - burns (in proximal duodenum)
  3. cushing ulcers: - gastric; duodenal + oesophageal ulcers in intracranial disease
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22
Q

What are the complications of acute peptic ulcers?

A
  • bleeding (20%)
  • perforation (5%)

BUT –> heal within days

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23
Q

What are the causes and symptoms of acute gastritis?

A

-inflammation of stomach lining with or without ulcers.

causes: - NSAIDS, toxins, alcohol, infections
Sx.: - discomfort, nausea, vomiting, hematemesis

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24
Q

What is chronic gastritis and its causes?

A
  • chronic inflammation with loss of folds
  • increased atrophy and healing
  • mucosa becomes so thin that BVs appear more prominently
  • H. pylori –> 90% of cases (commonest cause)
    also: - autoimmune (pernicious anemia/atrophic gastritis - 10%), radiation, bile reflux, systemis diseases (Crohn’s, amyloidosis)
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25
What are the gross and microscopic features of chronic gastritis?
Gross: - atrophy of mucosal folds - loss of rugae Micro: - plenty of inflammatory cells - gland atrophy with decreased function (NOT malignant)
26
What is the etiology and risk factors for PUD?
Etiology -H. pylori Risk Factors - hyperacidity, NSAIDs, steroids - smoking/alcohol - rapid gastric emptying - duodenal reflux - personality, stress, genetics
27
What is Zollinger-Ellison syndrome?
- hyperacidity causing multiple ulcers due to a gastrinoma of the pancrease - adenoma of pancreas producing increased gastrin which causes INCREASED acid production - MEN 1 syndrome type
28
True or False? | H. pylori is a gram neg. spirochaete that invades gastric tissue
True/False -H. pylori IS a gram neg. spirochaete BUT -it does NOT invade gastric tissue, it colonises the mucous layer of acidic gastric mucosa only
29
What is the pathogenesis of H. pylori infection and its consequences?
- colonises acidic gastric mucosa (NO INVASION) - has 2 enzymes (protease + urease) - protease --> breaks down mucous barrier to release urea from mucous proteins - urease --> breaks down urea to form ammonia which neutralises the acid - reflex hyperacidity results via vagal neural reflexes - reflex hyperacidity inhibits gastrin due to increased acid THEREFORE: - antral gastritis (H. pylori increased in antrum) - hyperacidity - hypogastrinemia
30
What disorders does H. pylori cause and which is the commonest?
- chronic gastritis* --> commonest - PUD - gastric carcinoma - lymphoma
31
How is H. pylori diagnosed?
- fecal Ag test - C13 Urea breath test - H. pylori serology for IgG
32
Why are duodenal ulcers > stomach ulcers (4:1) when H. pylori is mainly located in the antrum?
- hyperacidity from H. pylori infection is well-handled by stomach but more damaging to the duodenum - therefore increased duodenal ulcers (80% DU, 20% GU)
33
What is the typical appearance of peptic ulcers?
- round, small, punched out ulcers (<2cm) - >80% = single ulcer with radiating folds (due to continuous scarring and healing causing contraction at the base of the ulcer)
34
Compare onset of pain between gastric and duodenal ulcers with regards to food
GU: -pain with food as ulcer is in the stomach DU: - ulcer beyond the stomach - therefore contraction during eating prevents the acid going to the ulcer in the duodenum - pain RELIEVED by food as stomach contracts/mixes - therefore increased food intake
35
What is the microscopy of peptic ulcers?
- necrotic layer - inflammatory cells - granulation tissue - collagenous scar
36
What are complications of PUD and mark the commonest?
- chronic bleeding* --> commonest --> anemia (IDA) - acute bleeding (massive/shock) - perforation, peritonitis, pancreatitis - stricture (pyloric stenosis) - gastric carcinoma (NOT duodenal ca.)
37
What are the 2 types of adenocarcinomas in gastric tumours?
1. Intestinal type - common, better prognosis - associated with chronic gastritis and H. pylori - glands - APC mutation 2. Diffuse type - rare, poorer prognosis - genetics (E-cadherin mutation) - NO H. pylori - NO glands - signet ring cells!
38
What are the gross and microscopic features of gastric adenocarcinoma (intestinal type)?
Gross: - large - projectile/exophytic - central ulcerations - haemorrhage Micro: - pleomorphic cells forming irregular glands - hyperchromatic (dark blue) cells
39
What are the gross and microscopic features of gastric adenocarcinoma (diffuse type)?
Gross: - diffuse, thickened wall - "linitis plastica" --> leather-bottle stomach - atrophic mucosa (no folds) - flat or depressed Micro: - no glands - signet ring cells
40
What type of tumour is Gastro-Intestinal Stromal Tumour (GIST)?
Sarcoma
41
What are the gross and microscopic features of appendicitis?
Gross: -acute inflammation Micro: - acute inflammation - plenty of neutrophils
42
What is the etiology of acquired diverticulosis?
constipation (decreased motility)/decreased fibre diet --> hard stools --> increased pressure --> herniation of mucosa through muscle layer
43
What is the commonest type of hernia?
Inguinal | -indirect + direct
44
What are the 2 types of ischaemic bowel disease?
1. chronic mucosal - wall intact - intermittent bloody diarrhoea followed by recovery - only mucosal gangrene 2. acute transmural - sudden cramping - LLQ pain - desire to defecate blood/bloody diarrhoea
45
What is the etiology of ischaemic bowel disease? and mark the commonest.
- atherosclerosis* --> commonest (mesenteric artery) - aortic aneurysm; cocaine abuse - hypercoagulable states, OCD use - cardiac failure, shock, dehydration - vasculitis --> PAN, Wegner's...
46
What is acquired megacolon?
loss of ganglions due to inflammation, strictures, toxic in UC (ganglia normal)
47
What is the pathogenesis and Sx. of appendicitis?
Patho: - increased in young adults - luminal obstruction by stool/fecalith*(commonest)/tumour (carcinoid) --> increased luminal pressure --> infection --> acute inflammation Sx. -periumbilical pain --> RLQ, nausea, vomiting
48
What are the complications of acute appendicitis?
- rupture - abscess - peritonitis
49
What are the complications of diverticulosis?
- peritonitis - bleeding - diverticulitis (secondary infection - i.e. from stool) - abscess (pus)
50
What is intususception?
when one part of the tube gets into the distal portion resulting in obstruction/retention of intestinal content + telescoping of intestinal loop
51
What is the pathogenesis of ischaemic bowel disease?
Reperfusion injury - initial obstruction - death of tissue - reperfusion --> release of bacterial products, inflammatory mediators --> systemic shock/organ failure
52
What is meckel's diverticulum + its features?
- congenital remnant of vitello-intestinal duct (connects terminal ileum --> umbilicus) - TRUE diverticulum (all layers are affected) - 2% population - 2 feet from ileocolic junction - 2cm in size - presents at 2yrs of age * 2222
53
What is chaga's disease?
- acquired megacolon | - trypanosoma cruzi ( protozoa damages the ganglia --> loss of ganglia)
54
What are the DDx. for acure appendicitis?
- mesenteric lymphadenitis - diverticultitis (typically LLQ pain) - salpingitis/ovulation pain/ectopic pregnancy --> F
55
What are the 2 parts of telescoping of the intestinal loop in intususception?
internal portion - intussusceptum: - narrow - causes obstruction/ischaemia proximal portion - intussuscipens - causes dilatation/retention
56
What are the clinical Sx. of intestinal obstructions? What is the commonest type?
Sx. -abdo. pain, distension, constipation, vomiting *HERNIA = commonest due to defect/weak abdo. wall 1. Mechanical - hernia, adhesions, intussesception/volvulus, tumours, strictures 2. Functional - ischaemia/infarction - infalmmation (toxic megacolon in UC)
57
What are the gross features of ischaemic bowel disease?
- dark - inflamed - oedematous - BLACK
58
What are diverticula? Where are they typically found?
- blind pouches (multiple) | - usually in sigmoid colon
59
What are the 2 types of diverticula?
1. Acquired (false) - don't have all the layers (NO muscular layer) - most common 2. Congenital (true) - have ALL the layers - i.e. Meckel's
60
What is Hirschprung/congenital megacolon?
- lack of ganglions in terminal colon (rectum) --> decreased motility/peristalsis - narrowing results terminally, while proximal (normal) colon dilates - males 4:1 - marked intestinal obstruction - constipation, vomiting, diarrhoea * complications - enterocolitis, fluid/electrolyte disturbances
61
What is the key difference in appearance between oesophagitis + barret's and why?
Oesophagitis - diffuse inflammation - unclear border Barrett's - well-demarcated border of inflammation - erythematous *well-demarcated border is due to intestinal metaplasia causing a change in epithelium
62
What is multiple peptic ulcers suggestive of?
multiple etiologies - maybe zollinger-ellison syndrome - H. pylori
63
What is the type of epithelium in the oesophagus vs. the stomach?
oesophagus: - stratified squamous stomach: - columnar (mucous glands)
64
What is the Dx. if there are columnar mucosa with glands present in oesophagus?
Barret's oesophagus | -due to intestinal metaplasia
65
What is the precursor lesion of Barret's oesophagus?
chronic oesophagitis
66
What is the microscopy of H. pylori gastritis?
- bacteria within gland lumen (H. pylori) --> wavy spiral bacilli - chronic infalmmation in the stroma (between glands) - plasma cells + lymphocytes
67
What are the gross and microscopic features of oesophagus adenocarcinoma?
Gross: -tumour with central ulceration in lower oesophagus Micro: -pleomorphic/hyperchromatic cells forming irregular glands *SAME AS GASTRIC ADENOCARCINOMA

Pathology Term 2 (6 decks)

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