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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
Q

Describe primary aldosteronism and Cushing’s as they relate to saliva production

A

Increased Na+ reabsorption leads to decreased levels of NaCl and increased K+ levels in saliva

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26
Q

Describe digoxin therapy’s effect on salivary production

A

Increased Ca++ and K+ in saliva

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27
Q

Describe GERD

A

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
Q

Describe Barrett’s esophagus

A

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
Q

What is dysphagia?

A

Difficulty swallowing, commonly seen in elderly pts

Caused by various abnormalities

Increased risk for aspiration, choking, malnutrition

30
Q

What are some structural causes of dysphagia?

A

Tongue can’t propel food bolus into esophagus

Diverticula in pharyngeal or esophageal wall

31
Q

What are some functional causes of dysphagia?

A

Neurological defects

Defects in muscle layers

32
Q

What disease states can cause dysphagia?

A

Neurologic disorders

Stroke

Parkinson’s

Myasthenia gravis

Xerostomia

33
Q

Describe achalasia

A

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
Q

How does achalasia appear on barium esophagram?

A

Esophageal dilation with “bird’s beak” appearance of LES

35
Q

Discuss the incompetent LES

A

Most common cause of reflux

Caused by various factors, i.e. drugs, hormones, neuro-humoral agents

36
Q

Describe diffuse esophageal spasms

A

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
Q

Describe a hiatal hernia

A

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
Q

What do mucus neck cells secrete?

A

Mucus

Bicarbonate

39
Q

What do parietal cells secrete?

A

HCl

Intrinsic factor

40
Q

What do chief cells secrete?

A

Pepsinogen

Renin

41
Q

What do enterochromaffin-like (ECL) cells secrete?

A

Histamine

42
Q

What do G cells secrete?

A

Gastrin

43
Q

What do D cells secrete?

A

Somatostatin

44
Q

Where are the oxyntic glands located? What types of cells are contained within these glands?

A

Located in fundus and body/corpus of stomach

Contain parietal, chief, and mucus cells

45
Q

Where are the pyloric glands located? What types of cells do they contain?

A

Located in antrum and pyloric regions of stomach

Contain mostly G cells and mucus cells

46
Q

What stimulus is required for gastric mucus secretion?

A

None, mucus secretion is tonic

Increased secretion with irritation of mucosa

47
Q

What stimulus is required for bicarbonate secretion from gastric mucosa?

A

None, secreted with mucus

48
Q

What stimulate parietal cells to release HCl/IF?

A

ACh, gastrin, histamine

49
Q

What stimulates ECL cells to secrete histamine?

A

ACh, gastrin

50
Q

What stimulates chief cells to secrete pepsinogen and/or gastric lipase?

A

ACh, acid, secretin

51
Q

What stimulates D cells to secrete somatostatin?

A

Acid in the stomach

52
Q

What stimulates G cells to secrete gastrin?

A

ACh, peptides/amino acids in stomach

53
Q

What receptors are present on parietal cells? 5

A

CCKB

M3

H2

Somatostatin

Prostaglandin

54
Q

What agonists act on parietal cells? Where do they bind? What does binding result in?

A

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
Q

What antagonists act on parietal cells? Where do they bind? What does binding result in?

A

Somatostatin - binds to SST receptors

Prostaglandins - bind to PG receptors

Binding results in inhibition of histamine pathway stimulation

56
Q

Describe the alkaline tide

A
  • Production of HCl in parietal cells results in increased HCO3- as a byproduct
  • This HCO3- is secreted into bloodstream, thus raising pH
57
Q

What are the three phases of gastric acid secretion?

A

Cephalic

Gastric

Intestinal

58
Q

Describe the cephalic phase of gastric acid secretion

A

30% of total acid secretion

Governed by conditioned reflexes, leading to increased vagal stimulation (↑ parasympathetic outflow)

59
Q

Describe the gastric phase of gastric acid secretion

A
  • 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
Q

Describe the intestinal phase of gastric acid secretion

A
  • Peptides in duodenum stim gastrin release in stomach
  • Chyme from stomach inhibits brainstem reflexes, decreasing vagal tone
  • Hormones released to inhibit acid secretion
61
Q

What three duodenal hormones inhibit gastric acid secretion?

A

Secretin

GIP

CCK

62
Q

What protects the stomach lining from the effects of acidic gastric juice?

A

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
Q

What are some causes of peptic ulcer formation? (6)

A

H. pylori

Zollinger-Ellison syndrome

NSAIDs

EtOH

Bile acids

Stress

64
Q

Describe the steps of ulcer formation

A
  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
Q
A

GI-II, Exam 1 (8 decks)

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