Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BDS2; FHHD > SP1: Gastrointestinal Disease > Flashcards

SP1: Gastrointestinal Disease Flashcards

1
Q

Where is the oesophagus and what is its role

A

In the thoracic cavity; it carries food into the stomach and prevents backflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Outline the structure of the oesophagus and the role of each part

A

Mucosa is made of thee parts

  1. Epithelium = stratified squamous cells; protects from rough food particles
  2. Lamina propria
  3. Muscularis mucosa

Submucosa contains secretory glands releasing mucus to lubricate and protect from stomach acid

Muscularis propria consists of upper 1/3 skeletal and 2/3 smooth muscle; lower 1/3 is responsible for peristaltic action

Adventita gives covering and support

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is zenker’s diverticulum

A

Weakness in the skeletal muscle wall

  • pseudo-diverticulum where the herniation doesn’t include the adventita
  • barium contrast will show collection
  • food will collect here and rot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the symptoms of zenker’s diverticulum

A
  1. Halitosis; uneven tongue surface trapping bacteria causing bad breath
  2. Dysphagia; hard to swallow
  3. Regurgitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is achalasia

A

This is a motility disorder where the lower oesophageal sphincter is unable to relax - this results in functional obstruction because there is failure of the peristaltic mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What cellular differences are present in achalasia and what does this clinically present as

A

There is a reduction in ganglionic cells in the myenteric plexus (these provide motor innervation)

This presents as dysphagia in young children = difficulty swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is oesophagitis

A

Inflammation of the oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 3 types of oesophagitis

A
  1. Infective oesphagitis = bacterial, viral, fungal - incidence is higher with chemotherapy and immunosuppressed patients
  2. Drug induced = aspirin, ibuprofen, doxycycline (need to sit straight otherwise the pill can cause erosive damage)
  3. GORD reflux oesophagitis = this is where the stomach acid destroys the stratified squamous epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What can occur in GORD (gastric oesophageal reflux disease) reflux oesophagitis

A
  • sliding hiatus hernia = protrusion of stomach into thoracic cavity causing back flow
  • delayed gastric emptying
  • dysphagia, heartburn, regurgitation of stomach conents
  • stricture or Barretts oesophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Barretts oesophagus and how does it present

A

Condition where cells in the oesophagus grow abnormally - the distal squamous epithelium is replaced by metastatic columnar epithelium in response to the acidic environment; there is now a band of red, velvety mucosa at GEJ

These are precancerous changes (metaplasia can progress to dysplasia) and there is an increased risk of adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is adenocarcinoma

A

Cancer forming in mucus-secreting glands - this typically occurs in the lower 1/3 of oesophagus and is associated with GERD and Barrett’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why does Barretts oesophagus occur

A

Due to long standing GORD with ulceration and inflammation of squamous epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where does squamous carcinoma occur in the oesophagus

A

In the upper 2/3 of oesophagus

- associated with smoking and alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is gastritis

A

Inflammation of the stomach lining

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What can gastritis be caused by

A
  • NSAIDS (acute) because it blocks prostaglandin synthesis which is normally protective
  • Stress (acute) causes decreased blood flow to mucosa and so there is no regeneration because blood is rediverted from the stomach
  • Zollinger-Ellison syndrome
  • H-pylori associated gastritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Zollinger-Ellison syndrome

A

This is where tumors form in the pancreas or duodenum called gastrinomas

Gastrinomas secrete lots of the hormone gastrin which causes parietal cells to produce stomach acid causing gastritis

17
Q

What is peptic ulcer disease

A

An ulcer is a breach of the mucosa extending through the muscularis mucosa into the deeper layers (can cause hole in stomach)

This is a result of long standing gastritis and occurs more in the duodenum than the stomach; it is associated with H-pylori infections

18
Q

Outline how gastric cancer can arise

A
  1. Low vit C + E
  2. High salt diet
  3. H. Pylori infection

These cause chronic superficial gastritis

Progresses to atrophic gastritis

There is then intestinal metaplasia

Dysplasia

Mutations occur for carcinoma formation

Gastric cancer

19
Q

Intestinal gastric carcinoma

A
  • M > F
  • 55 yr
  • gland forming columnar epithelium
  • polypoid growth
20
Q

Diffuse gastric carcinoma

A
  • M = F
  • 48 yr
  • poorly differentiated; single signet ring
  • infiltrative growth
21
Q

Peritoneal dissemination

A

Most common cause of metastasis in gastric cancer; this has an ovarian involvement

22
Q

What is celiac disease

A

This is gluten sensitive enteropathy (T-cell mediated inflammatory disorder)

  • There is gliadin protein sensitivity
  • Causing inflammation of the small intestine (diffuse enteritis), malnutrition and diarrhoea
  • Impaired absorption of nutrients
23
Q

What is acute appendicitis

A

Obstruction of appendiceal lumen by fecalith, calculus, tumour or worms

  • increases intraluminal pressure, oedema and exudate due to bacterial invasion
  • leads to ischaemia (which is necrotic)
24
Q

Describe a benign appendix tumour

A

Filled with mucin

25
Q

Describe a malignant appendix tumour

A

There is distention which bursts thus allowing mucin into the cavity

26
Q

What diseases can arise in the colon

A
  1. diverticulosis
  2. idiopathic inflammatory bowel disease
  3. polyps form
  4. familial colorectal cancer syndromes
  5. colorectal cancers
27
Q

What is diverticular disease

A
  • Occurs in distal colon typically LHS
  • Chronic constipation so there is increased intraluminal pressure
  • Caused by a low fibre diet so there is slow transit
  • There are outpouchings of the colon in all layers
  • These pouches mean that contents collect causing diverticulitis
  • This can perforate causing peritonitis
28
Q

What is ulcerative colitis (Inflammatory bowel disease )

A

Ulcerative colitis is inflammation of the lower end of large bowel and rectum; these lesions are continuous

  • granular, ulcerated mucose, no fissuring
  • often intensely vascular
  • normal serosa
  • malignant changes are well recognised
29
Q

What is Crohn’s disease (Inflammatory bowel disease )

A

Crohn’s disease is a long-term condition where the gut becomes inflamed

  • it skips lesions so is transmural
  • rectum is normal
  • discretely ulcerated mucosa, cobblestone appearance, fissuring
  • serositis is common
  • malignant changes are less common
30
Q

What are the extra-intestinal manifestations in inflammatory bowel disease

A
  • Eyes : conjunctivitis and uveitis
  • Joints : polyarthropathies
  • Liver : sclerosing cholangitis and cholangiocarcinoma
  • Skin : erythema nodosum + pyoderma gangrenosum
31
Q

What are polyps

A

Tumourous masses that protrude into the gut lumen

  • Sessile polyp = flat
  • Pedunculated Polyps = mushroom appearance
32
Q

What are the types of non-neoplastic polyps

A

These don’t become cancerous

  1. Hyperplastic polyp : <5mm
  2. Juvenille polyp : focal and sporadic, 1-3mm rounded, pedunculated with cystically dilated glands (associated with adenoma and adenocarcinoma)
  3. Peutz-Jeghers polyp : large pedunculated and loulated with arborising smooth muscle around the glands
33
Q

What are the types of neoplastic polpys

A

Adenomatous polyps arise from dysplastic epithelium

  • Tubular = small and pedunculated
  • Villous = large and remain sessile
  • Tubolovillous

These are all predisposed to becoming cancerous

34
Q

What hereditary syndromes are associated with polys

A
  1. Familial adenomatous polyps (precancerous)
  2. Altered APC gene
  3. Autosomal dominant
  4. Gardner syndrome
35
Q

What is the carcinogenesis if sporadic colorectal cancer

A

It has a specific succession of mutations starting with adenoma formation and ending in carcinoma state

  1. Mutation in APC gene (tumour supressor gene) triggering formation of non-malignant adenomas = polyps
  2. Mutations in KRAS, TP53 and DDC
  3. Adenomas change to carcinomas within 10 years when they breach the basement membrane and become malignant

BDS2; FHHD (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions