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Peptic ulceration > Microanatomy of the GI tract 2 > Flashcards

Microanatomy of the GI tract 2 Flashcards

1
Q

epithelium type of oesophagus

A

Stratified squamous because its protective epithelium

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2
Q

What’s the muscular layer like of the oesophagus (how does it change)

A

1st third: skeletal (voluntary)
Middle third: mixed
Last third: smooth (involuntary)

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3
Q

Outer layer of oesophagus in thorax vs abdomen

A

Adventitia in thorax

Becomes serosa in last part beyond diaphragm (which allows it to secrete water to reduce friction)

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4
Q

What is Barrats oesophagus and why does it occur

A

Metaplasia. Change from stratified to columnar in oesophagus due to repeated damage from gastric reflux

–> Happens because columnar epithelium is more likely to protect against acid in oesophagus

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5
Q

What are rugae

A

Folds which increase the surface area and enable max contact between stomach contents and gastric mucosa

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6
Q

What is the luminal surface of the stomach composed entirely of

A

Columnar epithelial mucous cells for protection

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7
Q

What do gastric pits contain

A

Epithelial cell types which break down food

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8
Q

What is the oblique muscle layer of the stomach used for

A

Facilitates the churning of the food in all directions

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9
Q

What cells are there in gastric pits

A

Mucous cells
Parietal cells
chief cells
Enteroendocrine cells

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10
Q

Where are and What do mucous cells produce

A

At the surface

-Produce mucus and bicarbonate (protect surface from acid and digestion)

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11
Q

What are parietal cells

A

Produce HCl and intrinsic factor

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12
Q

What are chief cells

A

Produce enzymes e.g. pepsinogen

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13
Q

What are enteroendocrine cells

A

Produce hormones e.g. gastrin, serotonin, somatostatin, and VIP

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14
Q

HOW do parietal cells produce HCl

A

By active transport of H+ and passive transport of Cl into the lumen. Stimulated by gastrin, Ach and histamine

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15
Q

Why don’t antihistamines prevent the secretion of stomach acid production

A

Antihistamines target H2 receptors bu histamines in stomach are H2

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16
Q

What bacteria cause gastric ulcers

A

H. Pylori

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17
Q

How does H. Pylori cause gastric ulcers

A

Breaks down protective mucus layer. so not producing mucus so there is no protection from stomach acid. Acid eats down layers of stomach. Initiates acute inflammatory response and becomes chronic (damage and repair happening at the same time) and so a gastric ulcer forms

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18
Q

How can you fix a gastric ulcer caused by H. Pylori

A

1) Get rid of the infection

2) give PPI to enable the mucus cells to grow back over the surface

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19
Q

Why can H. pylori survive acidic conditions

A

Has an alkaline surface

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20
Q

What are the distinguishing features of the duodenum

A
  • Have Brunners glands in the submucosa

- Receives secretions from the liver and pancreas via pancreatic and bile ducts

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21
Q

What are Brunners glands and why does the duodenum have them

A

Because pyloric sphincter allows control of release of chyme so with that comes a lot of HCl. You don’t want acidic attack in duodenum. Brunners glands release alkaline secretions which neutralise chyme when sphincter opens

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22
Q

Distinguishing features of jejunum and why

A

Has lots of plicae and vili because lots of absorption takes place

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23
Q

Distinguishing features of lieum and why

A

Peyers patches (prominent lymphoid tissue clusters that help do lymphoid surveillance) and shorter, sparser plicae and vili

24
Q

Folds in the small intestine in descending size and where they are found

A

Plicae (mucosa and submucosa)

Villi (mucosa)

Microvilli (on the surface of columnar epithelium) (enterocytes)

25
Q

What are villi lined with

A

Simple columnar epithelium

26
Q

what is the impact of the small intestine epithelium having a high cell turnover

A

If you damage small intestine, it will easily repopulate itself

27
Q

Function of enterocytes in the small intestine epithelium

A

Columnar cells with microvilli
ABSORPTION
Brush border enzymes aid digestion

28
Q

Function of goblet cells in small intestine epithelium

A

Secrete mucus (more numerous distally)

29
Q

Function of panted cells

A

Large cytoplasmic granules
DEFENSINS
Protect against infection

30
Q

Function of enteroendocrine cells in the small intestine

A

Triangular cells with small haloed granules. Secrete locally acting hormones regulating secretion and motility

31
Q

Where are brush border enzymes produced

A

Vili

32
Q

What is luminal digestion done by

A

chyme and pancreatic secretions mix to break down food into component parts

33
Q

What is membrane digestion done by

A

Brush border enzymes

34
Q

How are proteins digested

A

By stomach and in duodenum by pancreatic enzymes. Enterocytes have membrane peptide hydrolyses to finally break down proteins to amino acids

35
Q

How are carbohydrates digested

A

Salivary and pancreatic amylase converts starch to glucose and maltose. Membrane sacharridases form monosaccharides

36
Q

How are lipids digested

A

Broken down by bile to a fine emulsion of triglycerides then pancreatic lipases to monoglyceride and free fatty acids. In the enterocytes they are reconstituted to triglycerides and coated with phospholipid and protein for transport (as chylomicrons)

37
Q

How do amino acids and monosaccharides enter the blood

A

Enter the intestinal capillaries and are taken to the liver in the portal system

38
Q

Causes of malabsorption in the small intestine

A
  • Insufficient pancreatic enzyme (e.g. CF)
  • Insufficient bile
  • Loss of small intestinal surface area
  • Lack of mucosal brush border enzymes
39
Q

What is celiac disease

A

Intolerance to gluten. Response to that is build up of lymphocytes in epithelial layer in villi. It is a chronic inflammatory response so the villi are damaged. You lose the villi gradually. Very important to exclude gluten from diet

40
Q

Manifestations of malabsorption

A
  • Dairrhoea (water) and steatorrheoea (fat)
  • Haemopoietic (anaemia due to deficiency in iron, folate and B12. Bleeding due to vitamin K deficiency (fat soluble)
  • Skeletal (osteopenia (more porous bones) due to Ca, Mg, vit D and protein deficiency)
  • Endocrine (impotence, infertility, amenorrhea. Hyperparathyroidism due to low Ca and Via D)
  • Skin : oedema and dermatitis (vit A)
  • Nervous system: peripheral neuropathy (vit A and B12)
41
Q

Symptoms of coeliac disease in adults and children

A

Diarrhoea, abdominal distension, malnutrition

-failure to thrive in children

42
Q

What cells do the large intestine contain and what do they do

A

goblet cells for lubrication
Enterocytes: absorption
Enteroendocrine cells and stem cells

43
Q

Why are there more goblet cells in the large intestine

A

More difficult to shift the solid waste so goblet cells lubricate it

44
Q

What is the colon specialised for

A

Water absorption

45
Q

What cells are numerous in the colon

A

Goblet cells

46
Q

What influences transit rate in the GI tract

A

Slower: Constipation due to dehydration/lack of fibre. Consquence can be diverticulosis
Faster rate: IBS and diarrhoea
Blocked: Obstruction

47
Q

What causes diverticulosis

A

Low fibre. Harder to move contents of bowel so puts pressure on bowel

48
Q

How does diverticulosis present

A

Inflammation/perforation of diverticula. Lower left quadrant pain and tenderness. Mild fever and raised WBC

49
Q

How to treat diverticulosis

A

Antibiotics and withhold solid food

50
Q

What is the obstruction of small bowel due to

A

mechanical obstruction or impairment of peristalsis (due to nerve or muscle damage e.g. after abdominal surgery)

51
Q

What does the obstruction of the small bowels result in

A

Distension and loss of fluids and electrolytes
-Interruption of blood flow (strangulation due to increased pressure), necrosis and rapid bacterial growth, gangrene and perforation

52
Q

Symptoms of obstruction of small bowel

A

Pain, absolute constipation, abdominal distension and vomiting, no passing of stool, vomiting if they’re trying to eat

53
Q

Two main inflammatory diseases of colorectal area

A

Crohn’s disease and ulcerative colitis

54
Q

What are the two sphincters in the anal canal and are they involuntary or voluntary

A

Internal anal sphincter: smooth muscle thickening at the end of the rectum (involuntary)

External anal sphincter: skeletal muscle- under voluntary control

55
Q

What epithelium is the rectum

A

Columnar epithelium

56
Q

venous supply of the anal canal

A

Haemorrhoidal plexi which can become distended due to congestion: piles

Peptic ulceration (8 decks)

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