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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
Q

What are the gross and microscopic features of chronic gastritis?

A

Gross:

  • atrophy of mucosal folds
  • loss of rugae

Micro:

  • plenty of inflammatory cells
  • gland atrophy with decreased function (NOT malignant)
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26
Q

What is the etiology and risk factors for PUD?

A

Etiology
-H. pylori

Risk Factors

  • hyperacidity, NSAIDs, steroids
  • smoking/alcohol
  • rapid gastric emptying
  • duodenal reflux
  • personality, stress, genetics
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27
Q

What is Zollinger-Ellison syndrome?

A
  • 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
Q

True or False?

H. pylori is a gram neg. spirochaete that invades gastric tissue

A

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
Q

What is the pathogenesis of H. pylori infection and its consequences?

A
  • 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
Q

What disorders does H. pylori cause and which is the commonest?

A
  • chronic gastritis* –> commonest
  • PUD
  • gastric carcinoma
  • lymphoma
31
Q

How is H. pylori diagnosed?

A
  • fecal Ag test
  • C13 Urea breath test
  • H. pylori serology for IgG
32
Q

Why are duodenal ulcers > stomach ulcers (4:1) when H. pylori is mainly located in the antrum?

A
  • 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
Q

What is the typical appearance of peptic ulcers?

A
  • 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
Q

Compare onset of pain between gastric and duodenal ulcers with regards to food

A

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
Q

What is the microscopy of peptic ulcers?

A
  • necrotic layer
  • inflammatory cells
  • granulation tissue
  • collagenous scar
36
Q

What are complications of PUD and mark the commonest?

A
  • chronic bleeding* –> commonest –> anemia (IDA)
  • acute bleeding (massive/shock)
  • perforation, peritonitis, pancreatitis
  • stricture (pyloric stenosis)
  • gastric carcinoma (NOT duodenal ca.)
37
Q

What are the 2 types of adenocarcinomas in gastric tumours?

A
  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
Q

What are the gross and microscopic features of gastric adenocarcinoma (intestinal type)?

A

Gross:

  • large
  • projectile/exophytic
  • central ulcerations
  • haemorrhage

Micro:

  • pleomorphic cells forming irregular glands
  • hyperchromatic (dark blue) cells
39
Q

What are the gross and microscopic features of gastric adenocarcinoma (diffuse type)?

A

Gross:

  • diffuse, thickened wall
  • “linitis plastica” –> leather-bottle stomach
  • atrophic mucosa (no folds)
  • flat or depressed

Micro:

  • no glands
  • signet ring cells
40
Q

What type of tumour is Gastro-Intestinal Stromal Tumour (GIST)?

A

Sarcoma

41
Q

What are the gross and microscopic features of appendicitis?

A

Gross:
-acute inflammation

Micro:

  • acute inflammation
  • plenty of neutrophils
42
Q

What is the etiology of acquired diverticulosis?

A

constipation (decreased motility)/decreased fibre diet –> hard stools –> increased pressure –> herniation of mucosa through muscle layer

43
Q

What is the commonest type of hernia?

A

Inguinal

-indirect + direct

44
Q

What are the 2 types of ischaemic bowel disease?

A
  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
Q

What is the etiology of ischaemic bowel disease? and mark the commonest.

A
  • atherosclerosis* –> commonest (mesenteric artery)
  • aortic aneurysm; cocaine abuse
  • hypercoagulable states, OCD use
  • cardiac failure, shock, dehydration
  • vasculitis –> PAN, Wegner’s…
46
Q

What is acquired megacolon?

A

loss of ganglions due to inflammation, strictures, toxic in UC (ganglia normal)

47
Q

What is the pathogenesis and Sx. of appendicitis?

A

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
Q

What are the complications of acute appendicitis?

A
  • rupture
  • abscess
  • peritonitis
49
Q

What are the complications of diverticulosis?

A
  • peritonitis
  • bleeding
  • diverticulitis (secondary infection - i.e. from stool)
  • abscess (pus)
50
Q

What is intususception?

A

when one part of the tube gets into the distal portion resulting in obstruction/retention of intestinal content + telescoping of intestinal loop

51
Q

What is the pathogenesis of ischaemic bowel disease?

A

Reperfusion injury

  • initial obstruction
  • death of tissue
  • reperfusion –> release of bacterial products, inflammatory mediators –> systemic shock/organ failure
52
Q

What is meckel’s diverticulum + its features?

A
  • 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
Q

What is chaga’s disease?

A
  • acquired megacolon

- trypanosoma cruzi ( protozoa damages the ganglia –> loss of ganglia)

54
Q

What are the DDx. for acure appendicitis?

A
  • mesenteric lymphadenitis
  • diverticultitis (typically LLQ pain)
  • salpingitis/ovulation pain/ectopic pregnancy –> F
55
Q

What are the 2 parts of telescoping of the intestinal loop in intususception?

A

internal portion

  • intussusceptum: - narrow
  • causes obstruction/ischaemia

proximal portion

  • intussuscipens
  • causes dilatation/retention
56
Q

What are the clinical Sx. of intestinal obstructions? What is the commonest type?

A

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
Q

What are the gross features of ischaemic bowel disease?

A
  • dark
  • inflamed
  • oedematous
  • BLACK
58
Q

What are diverticula? Where are they typically found?

A
  • blind pouches (multiple)

- usually in sigmoid colon

59
Q

What are the 2 types of diverticula?

A
  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
Q

What is Hirschprung/congenital megacolon?

A
  • 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
Q

What is the key difference in appearance between oesophagitis + barret’s and why?

A

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
Q

What is multiple peptic ulcers suggestive of?

A

multiple etiologies

  • maybe zollinger-ellison syndrome
  • H. pylori
63
Q

What is the type of epithelium in the oesophagus vs. the stomach?

A

oesophagus: - stratified squamous
stomach: - columnar (mucous glands)

64
Q

What is the Dx. if there are columnar mucosa with glands present in oesophagus?

A

Barret’s oesophagus

-due to intestinal metaplasia

65
Q

What is the precursor lesion of Barret’s oesophagus?

A

chronic oesophagitis

66
Q

What is the microscopy of H. pylori gastritis?

A
  • bacteria within gland lumen (H. pylori) –> wavy spiral bacilli
  • chronic infalmmation in the stroma (between glands)
  • plasma cells + lymphocytes
67
Q

What are the gross and microscopic features of oesophagus adenocarcinoma?

A

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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