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Pathophysiology Exam 3 > Lecture 22 > Flashcards

Lecture 22 Flashcards

1
Q

Serous Glands (Parotid)

A

Primarily composed of serous cells, secrete a non viscous saliva containing water, electrolytes, and enzymes

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2
Q

Mixed Glands

A

(Submandibular, sublingual); composed of serous and mucous cells, secrete a viscous saliva rick in mucin glycoproteins

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3
Q

How is salivation regulated?

A

Salivation stimulated by the autonomic nervous system (both branches); parasympathetic does so much more strongly than the sympathetic nervous system

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4
Q

Mumps

A
  • Acute viral illness caused by the mumps virus
  • Symptoms: fever, headache, muscle aches, tiredness, loss of appetite
  • Swelling of salivary glands (Parotid salivary glands)
  • Cause inflammation of brain and/or tissue covering the brain and spinal cord (encephalitis/ meningitis) and inflammation of the testes (orchitis)
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5
Q

Warthin Tumor

A

Papillary cystadenoma lymphomatosum or adenolymphoma is a benign tumor of the salivary glands with a strong association with cigarette smoking

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6
Q

Sjogren’s Syndrome

A
  • Autoimmune disorder characterized by lymphocytic infiltration of exocrine glands (salivary and lacrimal glands)
  • Older than 40 (more women affected)
  • Dry mouth (xerostomia) and dry eyes (keratoconjunctivitis sicca)
  • May also impact digestive organs, lungs, kidneys, joints, blood vessels, nerves
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7
Q

What are the inhibitors of gastric secretion?

A

Secretin, CCK (also inhibits gastric emptying), Somatostatin, GIP

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8
Q

Peptide YY

A

Inhibits emptying

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9
Q

Histamine

A

Stimulating acid secretion as it potentiates the response to Ach and gastrin

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10
Q

What influences gastric secretion?

A

Vagus nerve: directly or through its connectors stimulates parietal cells to secrete HCl

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11
Q

What initiates the vagovagal reflex?

A

Dilation of the stomach

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12
Q

What does the vagovagal reflex promote?

A

The release of acetylcholine (ACh) from the terminal branches of the vagus nerve and the parasympathetic autonomic nerves in the stomach

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13
Q

What does the vagus nerve stimulate?

A
  • Gastric secretion
  • Enterochromaffin-like cells (ECLs) to secrete histamine (H)
  • Enteroendocrine G cells to secrete gastrin (G)
  • Delta (D) cells to secrete somatostatin (S)
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14
Q

What does gastrin stimulate?

A

Parietal cells to produce HCl which stimulates the chief cells to secrete pepsin via pepsinogen

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15
Q

What is the role of pepsin?

A

Cleaves proteins to amino acids (tryptophan and phenylalanine) -> stimulates G cells to release gastrin (promotes HCl production further)

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16
Q

What happens when the gastric pH drops to < 3?

A

Secretion of gastrin stops

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17
Q

What happens when the pH drops to < 2?

A

Inhibitory effect on the parietal cells -> HCL production drops entirely

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18
Q

What is the role of somatostatin?

A

Inhibits the secretion of gastrin and inhibits the secretion of HCl from parietal cells

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19
Q

When food enters the duodenum, what happens?

A

Release of inhibitor of gastric secretion (secretin, cholecystokinin (CCK), somatostatin, and gastric inhibitory peptide (GIP))

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20
Q

What happens when chyme enters the ileum?

A

Release of peptide YY (inhibits gastric emptying along with CCK)

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21
Q

Atrophic Gastritis

A
  • Many glands containing acid-secreting parietal cells are destroyed -> limits the extent of gastric acidification (achlorhydria)
  • Lack of acid production causes a loss of feedback inhibition of gastrin secretion
  • Results in hypergastrinemia and ECL hyperplasia
  • Protein digestion and iron absorption are impaired in patients with achlorhydria
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22
Q

What causes H2 receptor stimulation?

A

Histamine released from ECL cells stimulates gastric acid secretion from parietal cells

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23
Q

Bicarbonate and HCl Secretion

A
  1. Bicarbonate enters into fenestrated capillary with the blood flowing toward the surface epithelium (some diffuses into the mucus blanket to increase pH)
  2. HCO3- diffuses from parietal cells into plasma in exchange for chloride
  3. Release of H+ ions and Cl- by the parietal cell involves the membrane fusion of the tubulovesicular system with apical membrane of canaliculus
  4. H/K-ATPases in the luminal membrane pump H+ ions into lumen (primary active transporter); pumps K+ into cell (then leaks back into the lumen through K channels
24
Q

What can happen as a result of excessive vomitting?

A
  • K depletion (leak)
  • Metabolic alkalosis (loss of hydrogen ions)
25
Q

Explain how parietal cells secrete acid?

A
  1. Gastrin (+), Histamine (+), ACh (+), Somatostatin (-) bind to receptors on parietal cell
  2. Second messengers -> H+/K+-ATPase
  3. CO2 is generated within the parietal cells or diffuses into them where it reacts with water to form HCO3- and H+ ions
  4. Insertion of the pump into the plasma membrane
  5. Acid secretion
26
Q

Alkaline tide

A

Occurs after a meal due to bicarbonate entry into circulation; not precipitated into metabolic alkalosis as pancreas secretes HCO3- into the gut lumen to counteract gastric secretions following a large meal

27
Q

What stimulates mucus production?

A

Prostaglandins; mucosal blood flow is highly dependent on the local production of prostaglandins

28
Q

What is the effect of anti-inflammatory drugs on mucosal blood flow?

A

Impairs mucosal blood flow by inhibiting prostaglandin synthesis -> compromises protective abilities of the mucosa (secretion of mucus and HCO3-) and can cause irritation of the mucosa (gastritis) or even ulceration (peptic ulcer disease, PUD)

29
Q

Gastro- Esophageal Reflux Disease (GERD)

A
  • Progesterone (the pill), fatty foods, caffeine, ethanol, smoking affects LES closure strength -> reflux -> ulcerations mediated by pepsin and HCl
  • Symptoms: heartburn and esophagitis
  • Treatment: surgical repair, gastric acid inhibitors
30
Q

What is the normal function of the Lower Esophageal Sphincter (LES)?

A

Prevents the reflux of gastric juice into esophagus

31
Q

Hiatal Hernia

A
  • Defect in the diaphragm that allows a portion of the stomach to pass through hiatus (diaphragmatic opening) into thorax
  • Predisposing factors: increased intra-abdominal pressure (pregnancy, obesity, ascites, chronic straining or coughing)
  • Symptoms and treatment similar to GERD
32
Q

Why do cardiac and esophageal causes of chest pain share similar symptoms?

A

-Two structures have the same nerve supply:
1. Afferent visceral sensory pain fibers from the esophagus end without synapses in the first four segments of the thoracic spinal cord (sympathetic and vagal pathways)
2. Pathways also occupied by afferent visceral sensory fibers from heart

33
Q

Explain the treatment of GERD and the pharmacologic regulation of parietal cell activity.

A
  1. Vagus -> ACh -> (Inhibitor: Atropine) -> M3 receptor
  2. G cells -> Gastrin -> CCKB receptor
    1 and 2 pathways -> Gq -> IP3/Ca2+ -> H+/K+-ATPase -> (Inhibitor: Omeprazole (Prilosec)) -> H+ secretion
  3. ECL cells -> Histamine -> (Inhibitor: Cimetidine (Tagamet)) -> H2 receptor -> Gs -> cAMP -> H+/K+- ATPase -> (Inhibitor: Omeprazole (Prilosec)) -> H+ secretion
  4. Somatostatin and Prostaglandins -> Gi inhibits cAMP
34
Q

What inhibits parietal cell activity?

A

Antihistamines (H2-blockers (ex: cimetidine)) and anticholinergics (ex: atropine)

35
Q

What inhibits H+/K+- ATPase pump (and thus reduces gastric secretion)?

A
  • Proton pump inhibitors (PPIs): (ex: Omeprazole)
  • H2-receptor blockers: blacks insertion of proton pump (ex: Cimetidine)
36
Q

Barrett’s Esophagus

A
  • Gastroesophageal reflux disease: mucosal epithelium of the esophagus takes on the appearance of gastric mucosal epithelium (differentiates from stratified squamous epithelium into a columnar epithelium (metaplasia))
  • Increases the risk for development of esophageal adenocarcinoma (distal third of the esophagus)
  • Columnar metaplasia in the lower esophagus
  • Can be detected by endoscopy
37
Q

Carcinoma of the Esophagus

A
  • Squamous cell carcinoma begins as an it situ lesion (squamous dysplasia: carcinoma in situ at other sites)
  • Half of the squamous cell carcinomas occurs in the middle third of the esophagus
  • Absence of the serosa from much of the esophagus may contribute to the tendency for esophageal cancers to spread locally before detection
38
Q

Peptic Ulcer Disease (PUD)

A
  • Erosion in the lining of the stomach or the first part of the small intestine (duodenum)
  • Duodenal ulcers (DU) and gastric ulcers (GU)
  • Caused by action of HCl and pepsin
  • Epithelial barrier and slightly alkaline mucus are broken down (Aspirin, NSAIDs, alcohol, bile acids)
39
Q

Why does Helicobacter pylori infections impact ulcers?

A
  • Thrives in acidic conditions
  • Antibiotics: Metronidazole
  • Inhibitors of acid secretion
40
Q

G-Cell Neoplasia (Gastrinoma)

A

Increase in basal activity of vagus nerve stimulates release of excessive gastrin -> hyperplasia of ECL cells -> excess histamine secretion -> chronically stimulated parietal cells -> excess HCl -> peptic ulcers

41
Q

What is a common factor between PUD and Zoellinger-Ellison Syndrome?

A

GI bleeding (needs to be ruled out by endoscopy, evaluations of bleeding patterns, and biopsy)

42
Q

What does a duodenal ulcer indicate?

A

High probability of H. pylori and a low probability of malignancy

43
Q

Zoellinger-Ellison Syndrome

A
  • Malignant (gastrinoma)
  • Symptoms of PUD occur in association with hypersecretion of gastric acid and the presence of gastrinoma (gastrin secreting malignant tumor of non-beta islet cells of pancreas or other organs)
  • Triad
  • 20-30% of Multiple Endocrine Neoplasia-1 cases exhibit ZES
44
Q

Achalasia of Esophagus

A
  • Achalasia: degenerative esophageal disease culminating in aperistalsis of the esophageal body and abnormal relaxation of the lower esophageal sphincter
  • T-cell mediated destruction and fibrous replacement of the esophageal myenteric neural plexus
  • Commonly idiopathic (can be seen in Chagas’ disease)
45
Q

Chagas’ Disease

A
  • Achalasia
  • Infection with the protozoan Trypanosoma cruzi (Kissing bug: South America) -> requires brief exposure to the acidic phagolysosome -> stimulate development of the intracellular stage of the parasite -> parasites reproduce in the cytoplasm of the host cells and then develop flagella, lyse host cells, enter the bloodstream, and penetrate smooth, skeletal, and heart muscle
  • Parasitization of scattered myofibers by trypanosomes accompanied by an inflammatory infiltrate of neutrophils, lymphocytes, macrophages, and occasional eosinophils renders distinctive myocarditis (Chronic Chagas cardiomyopathy: treated by cardiac transplantation)
  • Manifests as Megasophagus
  • Loss of ganglia
  • May also destroy the myenteric plexus of the colon (toxic megacolon)
46
Q

What does destruction of the myenteric plexus cause?

A

Dysregulation of esophageal smooth muscle activity (Achalasia)

47
Q

What does decreased or absent peristaltic activity in the distal esophagus, impaired LES relaxation, and increased LES pressure cause?

A
  • Result is the food cannot pass easily into the stomach -> difficulty swallowing (dysphagia), chest pain from esophageal distention, frequent bouts of pneumonia from aspiration of esophageal content
  • Neural function cannot be restored
  • Treatments: palliative and directed toward symptom control and preservation of the esophagus (passive conduit) -> reduction of lower esophageal sphincter pressure and minimizing gastroesophageal reflux
  • Effected laparoscopically by modified Heller myotomy and Dor (partial anterior) fundoplication
48
Q

Megacolon

A
  1. Congenital (Hirschsprung disease)
  2. Acquired: occur at any age as a result of Chagas disease, obstruction by a neoplasm of inflammatory structure, toxic megacolon complicating ulcerative colitis, visceral myopathy, or in association with functional psychosomatic disorders
    - Cause: prolonged constipation
49
Q

Hirschsprung Disease

A
  • Congenital disorder of the large intestine in which autonomic ganglia in the smooth muscle are absent or reduce (both myenteric and submucosal plexus are involved)
  • Also called congenital aganglionic megacolon
  • Cause: normal migration of neural crest cells from cecum to rectum is arrested prematurely or when the ganglion cells undergo premature death (genetic component)
  • Coordinated peristaltic contractions are absent and functional obstruction occurs -> dilation proximal to the affected segment
  • Coexists with other anomalies (Down syndrome)
50
Q

Where do the cells of the myenteric and submucosal plexuses originate from?

A

Vagal segment (plexuses form during 12-16 week)

51
Q

What is the cause for the majority of Hirschsprung familial cases?

A

Heterozygous loss-of-function mutations in the proto-oncogene RET (encodes tyrosine kinase receptor)

52
Q

What are some of the genetic factors that impact Hirschsprung’s Disease?

A

Mutations in genes encoding proteins involved in enteric neurodevelopment: RET ligand glial-derived neurotrophic factor, endothelin, endothelin receptor

53
Q

Chronic Chagas Disease

A
  • 20% of people 5-15 years after initial infection
  • Mechanism of cardiac and digestive tract damage is controversial
  • Probably results from an immune response induced by T. cruzi parasites
54
Q

What does damage to the myenteric plexus cause?

A

Dilation of the colon (megacolon) and esophagus

55
Q

What does damage to myocardial cells and to conductance pathways cause?

A

Dilated cardiomyopathy and cardiac arrhythmias

Pathophysiology Exam 3 (10 decks)

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