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GI-II, Exam 1 > Phys Review - Choudhury - KK > Flashcards

Phys Review - Choudhury - KK Flashcards

1
Q

What is role do water and mucus play in saliva?

A
  • Facilitate speech
  • Dissolve particles
  • Allow for tasting of food
  • Provide lubrication for swallowing
    • Assist in forming food into bolus
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2
Q

What is the function of salivary α-amylase?

A

Carbohydrate digestion (cleaves α-1,4 glycosidic bonds)

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3
Q

What is the function of salivary lingual lipase?

A

Initiates fat digestion

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4
Q

What is the function of salivary ribonuclease?

A

Hydrolysis of RNA

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5
Q

What are the antibacterial components of saliva?

A
  • Lysozyme (esp. against Bacillus and Strep)
  • Lactoperoxidase (esp against bacteria in milk and mucosal lining)
  • IgA glycoprotein (against viruses and bacteria)
  • Lactoferrin (chelates iron, thus inhibiting microbial growth)
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6
Q

What is the role of bicarbonate in saliva?

A
  • Neutralizes acid produced by bacteria, thus inhibiting tooth decay
  • Neutralizes gastric acid refluxed from stomach into esophagus
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7
Q

Why is saliva hypotonic?

A

Allows for the ability to taste carbs and fats

-can’t taste protein (i.e. tofu)

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8
Q

What is the initial site of saliva synthesis?

A

Acinus of salivary gland

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9
Q

What cells modify the ionic profile of saliva?

A

Ductal cells

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10
Q

What is secreted into the acinus?

A

H2O, K+, Na+, Cl-, HCO3-, zymogens of salivary enzymes

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11
Q

Describe the movement of salivary components in the ducts

A
  • Ductal cells are impermeable to water
  • Na+ and Cl- reabsorbed
  • K+ and HCO3- secreted
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12
Q

What happens to the concentration of saliva at high flow rates?

A

Less time for ductal cells to modify constituents, so concentrations more closely resemble plasma

(higher Na+ and Cl-, lower K+ than at baseline)

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13
Q

What happens to the concentration of saliva at low flow rates?

A

More time for ductal cells to modify constituents, so less resemblance to plasma

(Low Na+ and Cl-, high K+)

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14
Q

What are the ionic transporters found on the luminal surface of ductal cells?

A

Na+/H+ exchanger

Cl-/HCO3- exchanger

K+/H+ exchanger

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15
Q

What part of the nervous system controls most of salivary production/concentration?

A

ANS, specifically parasympathetic division

-more profound stimulation/inhibition from parasympathetic as opposed to sympathetic

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16
Q

What factors stimulate salivary production?

A

Conditioned responses (smell, sight, taste, sound)

Chewing

Spicy/sour foods

Smoking

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17
Q

What factors inhibit production of saliva?

A

Sleep

Fear

Anti-cholinergics, anti-nicotinics, anti-depressants

Dehydration

Fatigue

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18
Q

What factors modulate production of saliva?

A

Blood secretion

Myoepithelial cell contraction

Hormonal secretion

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19
Q

Describe xerostomia

A

Dry mouth due to absent saliva production

Caused by: drugs, radiation tx, autoimmune disease

Leads to: buccal infections, dental caries

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20
Q

Describe Sjögren’s syndrome

A

Autoimmune disease involving salivary and lacrimal glands

Glandular atrophy leads to xerostomia and dry eyes

Results in difficulty chewing, swallowing, and speaking

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21
Q

Describe drooling in the instance of abnormal saliva production

A

Excessive salivation due to increased nervous stimulation

Tx: anticholinergics, removal of sublingual salivary glands

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22
Q

What are conditions in which unusual local reflexes and or increased neurological stimulation lead to excessive salivation?

A

Parkinson’s

Tumors of mouth or esophagus

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23
Q

Describe cystic fibrosis as it relates to saliva production

A

Pts lack CFTR or chloride channel

Results in elevated Na+, Ca++, and protein in saliva

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24
Q

Describe Addison’s disease as it relates to saliva production

A

Decreased Na+ reabsorption leads to increased Na+ in saliva

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25
Describe primary aldosteronism and Cushing's as they relate to saliva production
Increased Na+ reabsorption leads to decreased levels of NaCl and increased K+ levels in saliva
26
Describe digoxin therapy's effect on salivary production
Increased Ca++ and K+ in saliva
27
Describe GERD
Disease characterized by stomach fluid refluxing into esophagus, causing "heartburn" Results from weak LES or decreased salivary bicarb Can lead to irritation or ulceration of esophageal lining
28
Describe Barrett's esophagus
Pre-cancerous change in terminal esophagus Due to chronic acid exposure Squamous epithelium replaced by columnar epithelium Considered a complication of GERD Can evolve into esophageal cancer
29
What is dysphagia?
Difficulty swallowing, commonly seen in elderly pts Caused by various abnormalities Increased risk for aspiration, choking, malnutrition
30
What are some structural causes of dysphagia?
Tongue can't propel food bolus into esophagus Diverticula in pharyngeal or esophageal wall
31
What are some functional causes of dysphagia?
Neurological defects Defects in muscle layers
32
What disease states can cause dysphagia?
Neurologic disorders Stroke Parkinson's Myasthenia gravis Xerostomia
33
Describe achalasia
Special form of dysphagia **Characterized by:** increased LES pressure with failure of LES to relax, along with absence of peristalsis within esophagus **Caused by:** Nerve degeneration (esp. enteric NS), lack of NO/VIP, Chagas disease (*Trypanosoma cruzi*)
34
How does achalasia appear on barium esophagram?
Esophageal dilation with "bird's beak" appearance of LES
35
Discuss the incompetent LES
Most common cause of reflux Caused by various factors, i.e. drugs, hormones, neuro-humoral agents
36
Describe diffuse esophageal spasms
Irregular, uncoordinated, sometimes powerful contractions of the esophagus Can cause dysphagia, regurgitation, and chest pain Cause is unknown May result from disruption of nerve activity
37
Describe a hiatal hernia
Herniation of part of the stomach into the thorax through a tear or area of weakness in the diaphragm Results in sx similar to GERD
38
What do mucus neck cells secrete?
Mucus Bicarbonate
39
What do parietal cells secrete?
HCl Intrinsic factor
40
What do chief cells secrete?
Pepsinogen Renin
41
What do enterochromaffin-like (ECL) cells secrete?
Histamine
42
What do G cells secrete?
Gastrin
43
What do D cells secrete?
Somatostatin
44
Where are the oxyntic glands located? What types of cells are contained within these glands?
Located in fundus and body/corpus of stomach Contain parietal, chief, and mucus cells
45
Where are the pyloric glands located? What types of cells do they contain?
Located in antrum and pyloric regions of stomach Contain mostly G cells and mucus cells
46
What stimulus is required for gastric mucus secretion?
None, mucus secretion is tonic Increased secretion with irritation of mucosa
47
What stimulus is required for bicarbonate secretion from gastric mucosa?
None, secreted with mucus
48
What stimulate parietal cells to release HCl/IF?
ACh, gastrin, histamine
49
What stimulates ECL cells to secrete histamine?
ACh, gastrin
50
What stimulates chief cells to secrete pepsinogen and/or gastric lipase?
ACh, acid, secretin
51
What stimulates D cells to secrete somatostatin?
Acid in the stomach
52
What stimulates G cells to secrete gastrin?
ACh, peptides/amino acids in stomach
53
What receptors are present on parietal cells? 5
CCKB M3 H2 Somatostatin Prostaglandin
54
What agonists act on parietal cells? Where do they bind? What does binding result in?
ACh - binds to M3 receptors Gastrin - binds to CCKB receptors Histamine - binds to H2 receptors All increase acid secretion **NOTE:** these can directly bind receptors on parietal cells. ACh can also act indirectly, binding to ECL cells and stimulating histamine release
55
What antagonists act on parietal cells? Where do they bind? What does binding result in?
Somatostatin - binds to SST receptors Prostaglandins - bind to PG receptors Binding results in inhibition of histamine pathway stimulation
56
Describe the alkaline tide
* Production of HCl in parietal cells results in increased HCO3- as a byproduct * This HCO3- is secreted into bloodstream, thus raising pH
57
What are the three phases of gastric acid secretion?
Cephalic Gastric Intestinal
58
Describe the cephalic phase of gastric acid secretion
30% of total acid secretion Governed by conditioned reflexes, leading to increased vagal stimulation (↑ parasympathetic outflow)
59
Describe the gastric phase of gastric acid secretion
* 50-60% of total acid secretion * Distension of gastric mucosa by food activates local vagal and ENS reflexes * stims release of acid and pepsinogen * Presence of peptides/amino acids stimulates gastrin release
60
Describe the intestinal phase of gastric acid secretion
* Peptides in duodenum stim gastrin release in stomach * Chyme from stomach inhibits brainstem reflexes, decreasing vagal tone * Hormones released to inhibit acid secretion
61
What three duodenal hormones inhibit gastric acid secretion?
Secretin GIP CCK
62
What protects the stomach lining from the effects of acidic gastric juice?
Gastric mucosal cells * Secrete HCO3--rich mucus that neutralizes acid * Membranes are impermeable to HCl * Connected by tight junctions so HCl can't pass between
63
What are some causes of peptic ulcer formation? (6)
*H. pylori* Zollinger-Ellison syndrome NSAIDs EtOH Bile acids Stress
64
Describe the steps of ulcer formation
1. Acid and pepsin break though mucosal barrier 2. Acid stims histamine release 3. Histamine stims parietal cells to release acid 4. Acid diffuses through broken barrier 5. Cycle continues
65

GI-II, Exam 1 (8 decks)

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