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BIOL 135 > 3+4 - GASTROINTESTINAL TRACT DISORDERS AND DIAGNOSIS > Flashcards

3+4 - GASTROINTESTINAL TRACT DISORDERS AND DIAGNOSIS Flashcards

1
Q

What makes up gastrointestinal tract?

A 
mouth
pharynx
oesophagus 
stomach 
pancreas
small intestine
large intestine
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2
Q

Structure of the stomach

A 
fundus cardia 
body
rugae (folds) 
pylorus
duodenum
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3
Q

Structure of the stomach wall

A

mucosa
submucosa
muscularis
serosa

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4
Q

MUCOSA

A

consists of simple columnar epithelial cells called surface mucous cells, which secrete mucus

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5
Q

SUBMUCOSA

A

areolar connective tissue

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6
Q

MUSCULARIS

A

3 layers of smooth muscle

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7
Q

SEROSA

A

simple squamous epithelium and areolar connective tissue

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8
Q

GASTRIC PIT

A

gastric glands are the columns of various secretory cells (e.g. parietal cell, chief cell) lining the gastric pit.
To form a gastric pit, the surface epithelial cells extend into the lamina propria. (The lamina propria consists of areolar connective tissue.)

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9
Q

Chief cells

A

these produce PEPSINOGEN (protease) which gets converted to the active PEPSIN at low pH, and gastric lipase.

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10
Q

G cells

A
  • within the gastric gland
  • enteroendocrine cells -they secrete the hormone gastrin into the blood. (This facilitates production of gastric juice when there is food in the stomach.)
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11
Q

chyme

A

gastric juices mixed with food, secreted into duodenum

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12
Q

SECRETION OF HYDROCHLORIC ACID BY GASTRIC PARIETAL CELLS

A
  1. ATP powers PROTON PUMPS in the parietal cell membrane, which enables H+ to be secreted into the gastric pit.
  2. Cl- diffuses into the stomach via the Cl- channels in the cell.
  3. Parietal cells contain the enzyme CARBONIC ANHYDRASE which converts carbon dioxide and water to carbonic acid.
  4. This dissociates into H+ (actively transported out of cell into chyme by exchange with K+) and bicarbonate ions.
  5. The bicarbonate ions leave the cell into the bloodstream in exchange for chloride ions.
  6. H+ and Cl- combine in chyme
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13
Q

The small intestine

A

Most digestion and absorption of nutrients occurs in the small intestine (by virtue of its long length, and large surface area.

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14
Q

What does the small intestine consist of ?

A

duodenum, jejunum and ileum.

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15
Q

Layers of the small intestine wall

A

mucosa, submucosa, muscularis and serosa

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16
Q

mucosa in small intestine

A

contains crevices called INTESTINAL GLANDS (CRYPTS OF LIBERKUHN) – these secrete INTESTINAL JUICE
Within the intestinal glands there are also enteroendocrine cells which secrete hormones such as secretin and cholecystokinin and paneth cells which secrete lysozyme – (this kills bacteria)

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17
Q

submucosa in duodenum

A

duodenal glands secrete alkaline mucus.

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18
Q

MICROVILLI

A

projections of the apical surface of the epithelial cells.

These form a ‘BRUSH BORDER’.

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19
Q

enzymes in brush border

A

for final digestion

- lactase, sucrase, peptidase, nuclease, phosphatase

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20
Q

pancreas

A

secrete main digestive enzymes for larger molecules (lipase).
Secreted as zymogens, activated when mixed with chyme

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21
Q

haematoxylin

A

basic dye, stains acidic structure blue

- nuclei as DNA content (- charge)

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22
Q

eosin

A

acidic dye, stains basic structures pink

- cytoplasmic proteins (+ charged amino acids)

23
Q

Eosin Y

A

acidic and binds to basic components of the cell to produce a red colouration

24
Q

What is helicobacter pylori?

A

gram-negative, motile bacteria that grows in the digestive tract and has a tendency to attack the stomach lining.

25
Q

What does Helicobacter pylori cause?

A

GASTRITIS (stomach inflammation)

STOMACH ULCERATION (gastric ulcer)

DUODENAL ULCERATION

26
Q

What is an ulcer?

A
  • Break in the lining of the gut which fails to heal

* Often inflamed which causes more acid secretion

27
Q

What percent of stomach ulcers (gastric and duodenal) are caused by H. pylori?

A

•80% gastric and 95% duodenal ulcers caused by H. pylori

28
Q

H.pylori symptoms (ulcers)

A

upper abdominal pain, nausea

29
Q

H.pylori treatment (ulcers)

A

antibiotics and proton-pump inhibitors (pump in parietal cells stops HCl production in stomach)

30
Q

H.pylori form ulcers

A

•Motile – swim into the mucus layer
•H. pylori produces enzyme UREASE
Urease catalyses the breakdown of urea into ammonia and CO2 ~ These further react to form NH3 and HCO3- which both neutralise stomach acid

31
Q

Urea breath test

A

Give 13C labelled urea to patient orally (14C produced naturally). Bacteria in stomach contains urease that convert urea to ammonia and 13CO2.
Diffuses into blood and can be exhaled.
Breath sample ran on mass spec, peak at 45.

32
Q

COELIAC DISEASE

A

Sensitivity to GLIADIN –
component of GLUTEN in wheat, barley, rye
Autoimmune disease
Reversible

33
Q

Symptoms of coeliac disease

A

Diarrhoea, weight loss

34
Q

Diagnosis of coeliac

A

by biopsy of small intestine mucosa and ELISA

35
Q

coeliac treatment

A

gluten-free diet

36
Q

Coeliac histology

A
  • flattening of the surface of the jejunum, expansion of the lamina propria and lymphocytic infiltration of the mucosa.
    This lymphocytic infiltration occurs as part of the inflammatory response.
37
Q

Coeliac cause

A
  • Tissue Transglutaminase (TTGA) attaches to gliadin peptides followed by phagocytosis
  • Activation of T and B cells
  • AutoAntibodies produced against TTGA
  • Immune destruction of intestinal mucosa
38
Q

Coeliac ELISA

A 
• Identify anti-TTGA in patient’s serum. 
Antigen = TTGA. 
Add serum. 
Add anti-human labelled antibody. 
Detect by fluorescent label on antibody
39
Q

CROHN’S DISEASE

A

• Chronic inflammatory disease affecting small intestine (sometimes large
intestine).
• Submucosa thickened – oedema and inflammation
• Patchy distribution – normal GI tract wall in between (skip lesions)

40
Q

Chron’s disease cause

A

unknown

41
Q

Chron’s disease symptoms

A

•diarrhoea (may contain blood), abdominal pain, tiredness, weight loss.

42
Q

Chron’s disease diagnosis

A

intestinal biopsy, fecal tests, barium meal, CT/MRI scan.

43
Q

Chron’s disease treatment

A

surgery, corticosteroids, antibiotics, but no cure.

44
Q

What causes cystic fibrosis?

A

Mutation in Cystic Fibrosis Transmembrane Conductance Regulator gene (CFTR)

45
Q

Chloride ion channel

A
  • Important in sweat production

* Important in intestinal chloride ion secretion

46
Q

How does the Mutation in Cystic Fibrosis Transmembrane Conductance Regulator gene (CFTR) affect the cells

A

Less Cl- released

Less H2O release

THICK mucus

47
Q

CFTR PROTEIN ACTION

A 
cAMP increase in cell
Protein kinase A activated
CFTR phosphorylated – channel opens
Secretion of chloride, sodium and water follow
Mucus liquefied = normal
48
Q

effects of cystic fibrosis on lungs

A

Viscous mucus accumulates - chest infections, inflammation, structural change.

49
Q

effects of CF on GI tract

A

Viscous mucus accumulates -exocrine ducts in pancreas blocked.
malabsorption

50
Q

SWEAT GLANDS IN CYSTIC FIBROSIS

A
  • Sodium and chloride content of sweat is increased in Cystic Fibrosis
  • In normal sweat glands, CFTR facilitates movement of Cl- FROM the sweat to the cytoplasm of the cell.
  • CFTR not working in cystic fibrosis, so Cl- stays on surface of skin, combines with Na+ to give NaCl
51
Q

PILOCARPINE IONTOPHORESIS SWEAT TEST

A

Pilocarpine stimulates localised sweating
Iontophoresis = electric charge used for drug delivery via skin
Collection of sweat using filter paper or microtubing
High chloride/sodium indicates positive for Cystic Fibrosis

52
Q

Detection of Cystic Fibrosis gene mutations

A

Over 1300 CF mutations known, Commonest DF508 (phenylalanine deletion position 508).
So
Amplify the section of the patient’s genome by PCR with specific primers to detect mutation.
Or
When voltage applied small DNA molecules move faster than large ones
Stain gel to visualise DNA

53
Q

Lactose intolerance (Lactase deficiency)

A

Insufficient lactase made in small intestine

Undigested lactose causes fluid retention in faeces (symptom: diarrhoea)

54
Q

Lactose intolerance (Lactase deficiency) detection

A

Bacterial fermentation of lactose produces H2 in breath (detect via mass spec)

Lactose meal diagnostic test – 50g lactose given then determine blood glucose levels over 3 hours. <1mmol/l over 3h = lactose intolerant

BIOL 135 (10 decks)

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