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Essentials of Pathology > Gastrointestinal and Liver > Flashcards

Gastrointestinal and Liver Flashcards

1
Q

GIT Arrangement (Layers)

A
  1. Mucosa (ELMM) 2. Submuscosa 3. Muscularis externa 4. Adventitia/serosa
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2
Q

Oesophagus

A 
Muscular Tube
Sphincters at top and bottom
- Close between swallows
- Prevent entry of gastric acid
- Impairment can corrode oesphagus
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3
Q

Stomach

A
  • Storage
  • Digestion: mixing
  • First fine of defence against infectious agents
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4
Q

Duodenum

A 
First part of small intestine
Receives:
- Partially digested chyme from stomach
- Bile from liver
- Pancreatic juices
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5
Q

Stomach Secretions

A

2.5 - 3L per day
Pepsinogens: produced by chief cells
Acid (HCl): produced by parietal cells
Intrinsic factor: Produced by parietal cells - required for absorption of Vit D

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6
Q

Stomach/Duodenum Defences Against Acid

A
  1. Mucus production
  2. Bicarbonate production
  3. Prostaglandin production
  4. Tight junctions
  5. Rapid gastric epithelial regeneration
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7
Q

Peptic Ulcers

A

Breach in the mucosa of the stomach or duodenum (usually distal stomach or proximal duodenum) that is produced by the action of gastric secretions

  • Imbalance between gastroduodenal mucosal defence mechanisms and the damaging agents (acid and pepsin)
  • Gastric acid and pepsin are prerequisites
  • Acute and chronic inflammation
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8
Q

Layers of Peptic Ulcer

A
  1. Necrotic slough
  2. Acute inflammatory exudate
  3. Vascular and fibrovascular granulation tissue
  4. Fibrous scar
    - Heal from bottom to the top (opposite to usual healing)
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9
Q

H Pylori: why can survive in stomach

A
  • Small gram neg rods with flagella
    Can survive in stomach because:
  • Able to bore into protective mucus layer (cork screw motion)
  • Motile (swim through viscous mucus)
  • Produces substances that buffers gastric acid
  • Can adhere to gastric epithelial cells (prevent being washed away by constant contractions of stomach)
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10
Q

Action of H. Pylori

A
  • Enhances gastric acid secretion and impairs production of bicarbonate buffer -> reduction in pH
  • Secretes substances which damage surface epithelial cells and weaken the junction between cells
  • Promotes an inflammatory response, recruits inflammatory cells that release mediators -> collateral damage
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11
Q

Chronic use of NSAIDs

A
  • Damages mucus layer of GIT (decreased prostaglandins -> decreased bicarbonate, mucus, blood flow)
  • Allows acid/pepsin to come into contact with mucosa
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12
Q

Symptoms of Chronic Peptic Ulcers

A 
Epigastric pain
Burning
Anaemia
Vomiting 
Nausea 
Bloating
Weight loss
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13
Q

Treatment of Peptic Ulcers

A

Eradicate the cause: treat H.pylori infections, discontinue NSAIDs and reduce acid secretion

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14
Q

Outcomes of Peptic Ulcers

A
  1. Healing: overcome damaging stimulus and defect fills with fibrous scar
  2. Bleeding: penetrate into blood vessels
  3. Perforation: gastric acid -> extensive damage and ulcer extends transmurally -> can lead to pancreatitis or peritonitis -> septicaemia
  4. Obstruction: scarring can lead eventually lead to constriction, especially in pylorus
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15
Q

GERD

A

Failure of lower oesophageal sphincter

If other defence mechanisms of oesophagus (gravity, swallowing, saliva) are overwhelmed -> mucosal damage

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16
Q

GERD Pathogenesis

A

Oesophageal mucosal damage from either:

  1. decreased salivation
  2. impaired oesophageal clearance
  3. decreased LES resting tone
  4. delayed gastric emptying
17
Q

GERD Complications

A

Mucosal damage -> oesophagitis
- If persists -> erosion of luminal surface - ulceration
Oesophageal strictures (abnormal narrowing or tightening)
- Due to fibrosis and healing
Barrett’s Oesophagus: normal squamous epithelium is replaced by columnar epithelium -> associated with increased risk of oesophageal cancer

18
Q

Small Intestine Function

A
  • Digestion

- Nutrient and water absorption

19
Q

Large Intestine Function

A
  • Mainly water absorption
  • Absorption of remaining nutrients and vitamins
  • Compacts bolus and stores fecal matter in rectum
20
Q

Inflammatory Bowel Disease

A
  • Main types: Crohn’s and Ulcerative Colitis
  • Chronic but relapsing diseases
  • Aetiology: combination of genetic, environmental and immunological factors
  • Onset usually in young adults
21
Q

IBD: Pathogenesis

A

Defective host interactions with intestinal microfloral
->
Epithelial dysfunction
->
Aberrant mucosal inflammatory responses (chronic inflam)
- Persistent activation of the immune system
- Destructive local immune response (T cell activation)

22
Q

IBD: extra-intestinal complications

A

Mainly related to malnutritions and ongoing joint inflammation

  • Join pain (arthritis)
  • Skin conditions
  • Eye inflam
  • Liver disorders
  • Osteoporosis
23
Q

Crohn’s Disease

A
  • Affects any part of the GIT (Mainly SI)
  • Usually diagnosed 15-30 yrs old
  • Can be familial
  • 2-4 times more common in smokers
  • F > M
  • TNF-alpha thought to be a major factor
24
Q

Crohn’s Disease: Symptoms

A
  • Intermittent attacks
  • Weight loss
  • Perianal fissures
  • Malabsorption -> malnutrition
  • Aching joints, skin rashes, eye inflam
25
Q

Crohn’s Pathology” Macroscopic

A
  • Transmural inflammation - granulomatous (non-caseating necrosis)
  • Skip lesions - mucosal ulcers
  • Bowl and adjacent mesentery: thickened and oedematous, mesenteric lymph nodes enlarged, firm and mattered together
  • Creeping fat: extension of mesenteric fat
  • Cobblestone appearance: nodular swelling and fibrosis, focal mucosal ulcers
26
Q

Crohn’s Disease: Complications

A
  • Bowel obstruction
  • Ulcers
  • Malabsorption of specific nutrients/vitamins if involves small bowel
  • Fistulas to other organs, including bladder and vagina, peri-anal (common) -> septicaemia
  • Anaemia
27
Q

Crohn’s Disease: Treatment

A
  • No cure
  • Medications: corticosteroids
  • Surgical resection
  • Drainage of abscesses
28
Q

Ulcerative Colitis

A
  • LARGE INTESTINE only
  • Chronic inflam disease of the colon
  • Affects rectum and extends proximally
  • Predominantly mucosa involvement (superficial ulceration!)
  • Diagnosis 15-30 and 50-70 years
    Colon - ALWAYS involved
    Rectum - usually involved
    Anus - seldom involved
29
Q

UC: Symptoms

A
  • Abdominal pain
  • Blood or pus in stool
  • Diarrhoea
  • Proctitis (inflammation of rectum)
  • GI bleeding
30
Q

UC: Macroscopic

A
  • Superficial erosions or ulcers
  • Mucosal surface = red, raw and granular
  • Mucosal folds are lost (atrophy)
  • Inflammatory polpys
31
Q

UC: Treatments

A
  • Diet
  • Mild/moderation: anti-inflammatories or immunosuppressive drugs
  • Severe: surgical resection of inflamed/dysfunction region
32
Q

Coeliac Disease

A
  • Autoimmune disease
  • Genetic predisposition
  • Hypersensitivity reaction to gluten
  • Triggers immune system to damage mucosa
  • Generalised malabsorption
  • SI mucosal lesions
33
Q

CRC: Risk Factors

A
  • Age
  • Prior CRC
  • IBD
  • Lifestyle: smoking, alcohol, obesity
  • Genetic factors
  • Diet: fibre, fat, meat
34
Q

Polyps

A
  • BENIGN
  • Lesion that protrudes into the lumen
  • Non neoplastic or neoplastic
35
Q

Adenomatous Polyps

A
  • Neoplastic
  • Direct precursor of adenocarcinoma
  • Can be pedunculated or sessile (flat)
  • Generally asymptomatic
  • Adenomas divided into 3 subtypes based on histology: tubular, tubulovillous or villous
36
Q

Familial Adenomatous Polyposis (FAP)

A
  • An inherited disorder characterised by 100-1000s of adenomas along mucosa (genetic defect is mutation of APC gene on Chr 5)
  • Polyps develop by late teens
  • CRC occurs in all patients if untreated
  • Total colectomy (removal of entire colon) before onset of cancer is curative
37
Q

CRC: Pathology

A
  • Polypoid, ulcerating, infiltrative, annular (ring shaped) and constrictive
  • Majority are adenocarcinomas
  • Commonly metastasis to lived
38
Q

CRC: Clinical Features

A
  • Can be asymptomatic for years
  • Most common clinical sign: occult faecal blood
  • Left CRC: smaller lumen and solid faeces, produces obstructive symptoms, change in bowel habits, abdominal pain
  • Right CRC: wider lumen and liquid faeces, chronic asymptomatic bleeding, anaemia

Essentials of Pathology (10 decks)

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