Clinical Correlations from Dr. Choudhury's saliva lecture Flashcards

1
Q

Xerostomia

A

dry mouth due to absence of saliva production (drugs, radiation treatment, autoimmune disease).
buccal infections/dental caries
very common symptoms

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2
Q

Sjorgen’s syndrome

A

autoimmune process-targets salivary and lacrimal glands
glandular atrophy and decreased saliva production (xerostomia), dry eyes (keratoconjuctivitis sicca)
difficulty in chewing, swallowing and speech.
dry oral mucosa, superficial ulceration, buccal infections/dental caries

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3
Q

Drooling/ Ptyalism

A

excessive salivation due to increase nervous stimulation

treatment: anticholinergics and surgical removal of sublingual glands

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4
Q

Parkinson’s, tumors of mouth/esophagus

A

increased saliva production due to unusual local reflexes and increase neurological stimulation

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5
Q

cystic fibrosis

A

elevated Na+, Cl- and protein in saliva, sweat, pancreatic fluid & bronchial secretion
CF patients lacks CFTR or chloride transporter

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6
Q

Addison’s

A

increase Na+ in saliva (↓ Na+ reabsorbed)

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7
Q

Primary aldosteronism & Cushing’s Syndrome

A

decrease Na+ in saliva (↑ Na+ reabsorbed), salivary NaCl is zero, increase K+ levels

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8
Q

digoxin therapy

A

increase Ca2+ & K+ in saliva

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9
Q

vagotomy

A

(cutting of vagus nerve):

- inhibits gastric acid secretion 
- used to treat peptic ulcers
- side effects: delay in gastric emptying, diarrhea

Selective vagotomy:
-cutting vagal nerves supplying parietal cells only

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10
Q

Peptic ulcer disease and aspirin

A
Aspirin (a weak acid) is easily
      absorbed in low pH of the stomach
Once absorbed it acts by acid 
      stimulating histamine release and
      disruption of local mucosa
Aspirin suppresses protective
      mucosal barrier production
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11
Q

Peptic ulcer disease

A

Referred due to pathogenesis related to injurious
effects of gastric acid and pepsin
Common locations: esophagus, stomach, and duodenum
Both gastric ulcer disease and duodenal ulcer disease
Ratio of gastric ulcer to duodenal ulcer is 1:4

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12
Q

gastric ulcer disease

A

Occurs in the gastric mucosa
Increased acid secretion (H. pylori increases gastrin secretion,
Pepsin remains active for too long
Failure in mucosal defense mechanisms (NSAIDS, H. pylori-70%)

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13
Q

duodenal ulcer disease

A

Occurs in the duodenum
Increase acid secretion in the gastric region (H.pylori-100%)
Pepsin remains active for too long
Decrease bicarbonate secretion from pancreas (pancreatitis)

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14
Q

Comparison of gastric, peptic and duodenal ulcers

A

Gastric ulcers: increased H+, pepsin; less mucosal protection
Peptic ulcers: increased H+, pepsin; less mucosal protection
Duodenal ulcers: increased H+ and pepsin, 2-3 X more parietal cells than normal

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15
Q

ZES

A

Rare condition, one or more tumors form in pancreatic islet cells or duodenum.
These tumors are called gastrinomas that secrete large amounts of hormone gastrin.
gastrin secretion gastrin directly stimulates parietal cells HCl secretion.
gastrin secretion gastrin releases histamine from ECL, histamine HCl secretion.
gastric acid secretion both at rest and after meal.
Results in gastric and/or duodenal ulceration (common) due to acid and pepsin activity.

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16
Q

Atrophic Gastritis: lack parietal cells

A

Chronic inflammation of gastric mucosa due to H.pylori gastric acid. Secretion of HCl, pepsin and intrinsic factor is impaired, leading to Vit B12 deficiency and anemia.

17
Q

pernicious anemia

A

autuimmune condition, antibodies against parietal cells and/or IF H+ and
somatostatin inhibition of gastrin, therefore gastrin but no H+
IF, therefore no Vit B12 absorbtion manifests as pernicious anemia-leads to neurological disorders

18
Q

proton pump inhibitors

A

Histamine potentiates effects of gastrin & ACh on parietal cells via H2 to release acid
Inhibiting H2 will decrease H+ release in the stomach
PPIs inhibits proton pump and decreases H+ release, increases gastric pH
Long term side effects of PPIs usage are:
Pneumonia
Clostridium difficle growth in gut
Osteoporosis