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Cases > Case 3 - GI > Flashcards

Case 3 - GI Flashcards

0
Q

Why does alcohol over consumption develop at first?

A

Positive Reinforcement, a feeling a euphoria that brings psychological rewards; negative reinforcement follows, that is using alcohol to lessen stress and anxiety.

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1
Q

Describe the zones of a hepatocyte

A

Zone 1 is the periportal zone, Zone 2 is the Intermediate Zone and Zone 3 is the Centrilobular zone. Hepatocyte acinus is split into 3 concentric elliptical zones and in a hepatitis infection, Zone 1 is affected first as the cells in tho zone receive sinusoidal blood transport contents first, such as O2 and nutrients, so that these cells will receive the viral infection first.

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2
Q

What two types of cells are found in the salivary glands and what are their functions?

A

Acinar cells - active transport of electrolytes and passive transport of water follows (saliva is isotonic to plasma here, in acinus) Duct cells - reabsorption of sodium and Chloride ions

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3
Q

Describe the content of saliva at low and high rates of secretion

A

Low rate - Low Na+, HCO3-, Cl- K+ concentration higher here High rate - High Na+, HCO3- Cl-

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4
Q

What are the stages of swallowing? What occurs during these phases? Mention control and whether phase is voluntary or involuntary

A

See notes for the 11 steps of these stages; 1) Oral - voluntary - initiates involuntary 2) Pharyngeal - involuntary - controlled by medulla and lower pons Swallowing centre inhibits respiratory centre 3) Oesophageal - involuntary - controlled by medulla and lower pons Starts with relaxation of lower oesophageal sphincter

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5
Q

What do parietal cells secrete and How?

A

See diagram.. These secrete HCl and INTRINSIC FACTOR (IMPORTANT FOR Vitamin B12)

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6
Q

What do chief cells secrete and how?

A

See diagram.. They secrete pepsinogen

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7
Q

Why do chief cells stain darker than parietal cells?

A

Dye stains rough endoplasmic reticulum.Chief cells have more endoplasmic reticulum than parietal cells so chief cells appear darker than parietal cells

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8
Q

What is the function of the HCl produced by parietal cells

A

Remember: A kitten does kill Activates pepsinogen to pepsin secreted by chief cells Kills microbes with lysozymes Denatures protein Breaks down

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9
Q

What cells are found in the oxyntic mucosa?

A

Surface mucous cells Neck mucous cells Stem cells Parietal cells Chief cells

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10
Q

What cells are found in the pyloric mucosa?

A

G cells D cells

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11
Q

What is the difference between surface mucous cells and parietal cells?

A

Surface mucous cells - secrete viscous mucus forming a protective layer against acidic contents Neck mucous cells - secrete watery mucus, allowing mixing with chyme for lubrication

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12
Q

What triggers the cephalic phase to begin producing gastric secretion before food even enters the stomach?

A

1) seeing, thinking, smelling and chewing food 2) stimulates vagal nerves of the myenteric plexus 3) stimulates chief cells and parietal cells DIRECTLY 4) Stimulates G cells, thus stimulating chief and parietal cells INDIRECTLY

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13
Q

What is the major stimulation for gastric secretion in the gastric phase?

A

Protein present in the stomach

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14
Q

What stimulates the intestinal phase of digestion (gastric secretion) ? Remember this phase is inhibitory.

A

Intestinal phase starts when food enters duodenum 1) gastric secretion inhibits as major stimulus : protein in stomach not there anymore 2) high gastric acidity, low pH (usually buffered by proteins but nit there anymore) 3) acid, lipid ( ** these cause release of enterogastrones)

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15
Q

What are enterogastrones?

A
  • Gastric inhibitory peptide (GIP) responds to fatty acids - Secretin, responds to acid - Cholecystekinin (CcK) responds to fatty acids - Somatostatin ,responds to fats and glucose They inhibit gastric secretion and motility
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16
Q

How does acetylcholine stimulate parietal cells to secrete HCl?

A

Acetylcholine bind to its G coupled receptor Gq activates phospholipase C See schematic diagram in case 3 notes on Jeff’s lecture

17
Q

Within the Antrum of the stomach, what hormone is released? Why is there a decrease of this hormone in the intestinal phase?

A

Gastrin secreted from antrum of the stomach As protein leaves stomach and enters duodenum, there is less vagal stimulation as well as intrinsic.. So G cells are not stimulated as much, therefore a decrease in gastrin secretion

18
Q

What hormone is produced in the antrum and duodenum that responds to acidic gastric juice?

A

Somatostatin produced by D cells This decreases vagal stimulation thus decreasing stimulation of parietal cells, G cells, ECL cells

19
Q

What hormones associated with the intestinal phase of gastric secretion are produced in the duodenum?

A

The enterogastrones ; CCK - from I cells Secretin - from S cells

20
Q

In pancreatic secretion, what does secretin do?

A

Stimulates duct cells to secrete water and bicorbornate. It initiates the cAMP, Gs pathway, protein kinase A phophorylates CFTR channel so Cl- can leave to maintain a high Cl- gradient. See diagram under graph in case 3 notes of Jeff’s lecture

21
Q

Where does the majority of the pancreatic juice stimulation take place?

A

In the intestinal phase

22
Q

What controls HCO3- secretion from duct cells?

A

Secretin hormone is released in response to ACID in the duodenum during intestinal phase

23
Q

How does secretin cause more carbonate secretion?

A

Through the cAMP pathway, Gs coupled receptor Activates protein kinase A which phosphorylates CfTR channel to allow CL- to leave cell.. Allowing for the HcO3- antiporter with Cl- to continue to pump out carbonate

24
Q

To what stimulus does CCK get secreted from I cells in terms of pancreatic stimulation?

A

Presence of fats Also presence of proteins

25
Q

What are choleretics and what are the most potent choleretics?

A

Substances that increase bile secretion in the liver Most potent are bile salts themselves

26
Q

What are cholagogues? Name one.

A

Substances that increase the flow of bile by emptying the gall bladder CCK****

27
Q

Name the two mechanisms of bile secretion

A

Bile acid dependent 1 Depends on rate of bile acid return Bile acid independent 2 Secretion of electrolytes and water from hepatocytes and duct cells

28
Q

What is secretin’s role in bile formation?

A

Secretin causes increased bile independent bile secretion - increases bile flow - increases cell sensitivity to CCK - increases volume of bile by secreting bicarbonate and water

29
Q

Is secretin a choleretic?

A

No. Secretin is a hydrocholeretic as it only increases electrolytes and water in the bile

30
Q

Sarah has just started eating her lunch. What hormones have been released to initiate her appetite, what hormone would make her stop eating? Talking about short term hormones here, mention where these hormones would be released,

A

In response to no nutrients, ghrelin is secreted from duodenum Ghrelin promotes pathway for secretion of Orexins from lateral hypothalamus, promoting appetite **ghrelin is the hunger hormone

It is the hormone PYY secreted from the ilium of the GI tract that inhibits hypothalamus neurones from stimulated orexins by NPY

31
Q

Sarah has now finishing eating her lunch, which was at her favourite vintage cafe. What hormones will be released and where from, to stop Sarah eating?

A

1) PYY, secreted from ilium, inhibits pathway to promote orexins from promoting appetite. PYY is therefore anorexogenic 2) In response to digestive products from Sarah’s lunch i.e. Increased fats, nutrients,, CCK is released from I cells. This stimulates satiety centre in brain stem.. Making Sarah feel full

32
Q

What is the role of leptin in terms of food intake, and where is it secreted from?

A

See the diagram I photocopied from Sherwood Human Physiology. Leptin is secreted from adipocytes. The more fat, the more leptin. Leptin inhibits pathway for promoting appetite by orexins, and stimulates pathway for appetite suppression.

33
Q

A 37 year old patient comes is complaining of long term epigastric pain. He mentions he has lost weight in the last couple of months, “it just hurts when I eat.”. What tests would you order? What is the differential diagnosis?

A

Could have gastric ulceration. Biggest cause is usually H. Pylori, (NSAIDs, carcinoma possible as well)

Tests;

1) Urea breath test
2) Stool antigen test
3) immunoassay to detect H Pylori antigen
3) IgG antibodies

34
Q

What is H. Pylori and what is its prevelance?

A

1) Gram-negative urease producing bacterium.
2) In greatest numbers under mucous layer of gastric pits, as ammonia is produced it neutralises stomach acid and is able to survive
3) Higher in developing countries

35
Q

What is the pathogenesis of H. Pylori?

A

1) Infects stomach mucosa (highly adapted urease producing bacterium)
2) Inflammatory response - Gastritis
3) G cells release gastrin
4) Gastric metaplasia
5) Damage to mucosa
6) Damage to mucosa

36
Q

Treament for H. Pylori?

A

Remember 3,2,1.

3 drugs: proton pump inhibitor, 2 antibiotics

2: times a day
1: week

STOP NSAIDs

Gastrectomy in severe cases

37
Q

Mechanism of action of proton pump inhibitors ? Side effects?

** Omeprazole / Lansoprazole

A

1) inhibit H+/K+ ATPase (LAST STEP in HCl secreion in parietal cell)
2) decreases H+, and acid secretion
3) Weak base accuulates in cannliculi in acid environment
4) Nausea, dizziness, diarrhoea

*Careful with liver disease patients, pegnant, breastfeeding patients

**more effective than antacids

38
Q

Mechanism of action of H2 antagonists?

**Ranitidine / Cimetidine

A

** Remember histamine stimulate parietal cell to secrete HCL

1) Inhibits histamine2 receptors at mainly gastric acid secretions
2) decreases activation of pepsinogen as less HCL released (their stimulant for release)
3) also promote duodenal and gastric ulcer healing

39
Q

When would you as a doctor, request endoscopy for your patient?

A

Remember GUIDE Poly and Angel

G- GI bleeding

U- Unitintention weigth loss

I- Iron defeciency anaemia

D- Dysphagia

E- Epigastric mass

P- Persistent vomiting

A- Age (Over 55) and acute onset dysphagia

40
Q

A patient comes to see you with occasional indigestion. He says he gets it once or twice a week and is worried. What woul you prescribe is anything? 3 weeeks later the same patient comes back saying he now gets indigestion constantly. Would would you do differently now?

A

Occasional - tell him avoid acidic spicy food, encourage lifestyle changes

Suggest antacids

Persisitent symptoms - Proton Pump Inhibitor Inhibitor therapy given once or twice daily

Cases (15 decks)

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