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APA Funds 2 > GI Disturbances > Flashcards

GI Disturbances Flashcards

1
Q

What part of the pharynx do each of the nerves innervate?

–Trigeminal nerve

–Glossopharyngeal nerve

–Superior laryngeal nerve

–Recurrent laryngeal nerve

–Branches of Vagus nerve

A

–Trigeminal nerve - nasopharynx

–Glossopharyngeal nerve - posterior third of tongue and oral pharynx

–Superior laryngeal nerve – tongue base and inferior epiglottis to the vocal cords

–Recurrent laryngeal nerve – vocal cords distally

–Branches of Vagus nerve – remaining larynx and trachea

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2
Q

T/F: Local and general anesthesia depress sensation of the upper airway innervation.

A

True

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3
Q

What does the damage or impairment of the oropharynx innervation increase the risk of?

A

Pathology of the oropharynx, such as pharyngeal tumor, CVA and metabolic toxin will increase aspiration of pneumonia.

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4
Q

What is the anatomical location of the esophagus?

A

-originates at the pharynx (~C6, behind the cricoid cartilage) and ends at the cardia of the stomach (~T11)

* consists of :

upper (cervical) esophagus: C6-T1

Thoracic esophagus

Abdominal esophagus: T11-T12

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5
Q

What are the 2 muscle layers of the esophagus and what is the composition of the muscles?

A

Outer: longitudinal layer

Inner: circular muscular layer

  • Striated (skeletal) muscle dominates top 1/3rd of the esophagus.
  • Striated and smooth muscles in the middle 1/3rd
  • Smooth muscle in the distal 1/3rd
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6
Q

What is the space the esophagus pass through to enter the diaphragm?

A

Right crus

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7
Q

What two drainage system is found outside of the esophagus?

A

Regional lymphatics and thoracic duct

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8
Q

Name the different blood vessels that supply blood to the esophagus.

A

Inferior thyroid artery - cervical (upper) esophagus and its sphincter

bronchial arteries from the thoracic aorta - thoracic esophagus

left gastric artery and left inferior phrenic artery - lower part of the esophagus and its sphincter

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9
Q

Describe the two intrinsic plexuses for the esophagus and their locations.

A

*Myenteric (Auerbach) plexus lies between the longitudinal and circular muscles and provides motor innervations mainly by parasympathetic (CN X) and some by sympathetic nervous system.

*Submucosal (Meissner) plexus connects the mucosa to the circular muscle and has only parasympathetic fibers and provides secretomotor innervation to the mucosa nearest the lumen of the gut.

–This system is a continuum that extends from the esophagus to the anus

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10
Q

Describe the extrinsic innervation of the esophagus?

A

-Sympathetic

•Acts on myenteric plexus to

modulate rather than control

motor activity

-Parasympathetic

  • Cranial nerves IX, X, XI
  • Causes esophageal

muscular contraction (peristalsis)

•Causes relaxation of LES

-Somatic

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11
Q

What stimulates the upper esophageal tone?

A
  • inspiration
  • esophageal distention
  • gagging
  • valsalva maneuver
  • acidity of gastric contents
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12
Q

What reduces the upper esophageal tone?

A
  • Distention
  • Belching
  • Vomiting
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13
Q

What studies can be done to diagnose or find the underlying cause of dysphagia?

A

–Barium contrast studies

–Upper endoscopy

•Biopsy and cytology

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14
Q

How is esophagus affected in chronic alcoholism?

A
  • Impaired esophageal peristalsis
  • LES hypotonia
  • Degeneration of the Auerbach plexus
  • Mallory Weis Tear
  • Barrett Esophagus
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15
Q

What is achalasia and what diseases can cause it?

A

•Failure of the Lower esophageal sphincter tone to relax during swallowing accompanied with a lack of peristalsis

–Diabetes

–Stroke

–Amyotrophic lateral sclerosis (Lou Gehrig’s disease)

–Connective tissue diseases

  • Amyloidosis
  • Scleroderma
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16
Q

What are the surgical options for the treatment of achalasia?

A

penumatic dilation

Heller myotomy or endoscopic myotomy

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17
Q

What is Barrett esophagus and what can cause it?

A

•Normal squamous epithelium changes to metaplastic columnar epithelium

–Chronic exposure to acidic gastric contents – GERD (Assume GERD if the patient has Barrett esophagus.)

–Chronic alcohol abuse

–Smoking

•Closely associated with the eventual development of esophageal carcinoma

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18
Q

What is GERD and its management modality?

A

Loss of LES tone and the ensuing reflux of gastric contents

•Current management modality is medical therapy.

–Proton Pump Inhibitors (PPIs)

–Histamine-2 (H2)-blocking agents

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19
Q

What is hiatal hernia?

A

Protrusion of a portion of the stomach into the thoracic cavity through a weak spot in the diaphragm.

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20
Q

What is the medical management and surgical treatment for a hiatal hernia?

A

H2 blockers

Nissen fundoplication

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21
Q

What is esophageal diverticulum and its three classifications?

A

An esophageal diverticulum is a pouch that protrudes outward in a weak portion of the esophageal lining. This pocket-like structure can appear anywhere in the esophageal lining between the throat and stomach and is named according to its location.

  • Zenker (Upper Esophagus): most common
  • Traction (Middle esophagus)
  • Epiphrenic (Lower esophagus)
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22
Q

What are the causes of esophageal carcinoma?

A

–Advanced age

–Cachectic (general ill health with malnourishment)

–Suffering from age related disease process

–Suffering from metastasis disease process

–May have associated history of alcohol and tobacco use/abuse

–History of preoperative radiation

  • Bone marrow suppression
  • Intrathoracic and pulmonary fibrosis
  • Increased friability of tissues

–History of chemotherapy

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23
Q

What are some chemotherapy complications for Daunorubicin, Doxorubicin/Adriamycin and Bleomycin?

A

•Daunorubicin and Doxorubicin/Adriamycin:

–Chemotherapy-induced cardiomyopathy

•Bleomycin

–Pulmonary fibrosis (most serious complication)

–Increases sensitivity for oxygen toxicity. This can cause post-op pulmonary fibrosis following supplemental oxygen therapy during general anesthesia.

–Restrictive defect

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24
Q

What are the two section of the stomach and their functions?

A

–Fundus

  • Thin-walled and distensible
  • Upper abdomen
  • Primary function is storage (4 hours); hence no peristalsis

–Distal Stomach

  • Thick-walled
  • Mixing of food
  • Slow release of chyme through pyloric sphincter into the duodenum (peristalsis)
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25
Q

Where is the duodenum located?

A

The duodenum extends from the pylorus to the ligament of treitz, in a sharp curve that almost completes a circle. It is so named because it is about equal in length to the breadth of 12 fingers, or about 25 cm. It is largely retroperitoneal and the position is relatively fixed. The stomach and duodenum are closely related in function and in pathogenesis and manifestation of disease.

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26
Q

Describe the anatomy of the gastric wall.

A
  • Serosa - External layer (connective tissue)
  • Muscularis externa

–Outer: longitudinal

–Middle: circular

–Inner: oblique

  • Submucosa
  • Muscularis mucosae (thin smooth muscle)
  • Mucosa
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27
Q

What are the cells that occupy the surface of gastric mucosa?

A

mucous cells

parietal cells

G cells

ECL cells

Chief cells

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28
Q

What do the G cells produce in the gastric mucosa?

A

-G cells produce gastrin hormone in response to gastric distension. The hormone stimulates histamine release from the enterochromaffin-like cells (ECLs). Histamine release acts as a powerful stimulant of acid production from the parietal cells.

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29
Q

H2 antagonists block histamine release from the ECLs.

True / False

A

False.

H2 antagonists block the H2 receptors at the parietal cells and prevent histamine from binding to the receptors.

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30
Q

What is the effect of a vagotomy?

A

diminshes parietal cell response to gastrin and histamine.

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31
Q

Describe the innervation of the stomach.

A

•Major innervation is Autonomic

–Two branches of the vagus nerve

  • Right vagus becomes right posterior (celiac) branch
  • Left vagus becomes left anterior (hepatic) branch
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32
Q

List the common stomach disorders/diseases.

A
  • Peptic ulcer Disease
  • Gastric ulcer Disease
  • Gastric neoplastic disease
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33
Q

Describe Peptic Ulcer Disease (PUD).

A

•Caused by the erosion of protective mucous layer of the stomach and duodenum

–Chronic oversupply of gastric hydrochloric acid and pepsin

–Subsequent ulceration over time with lesions of varying depth

  • Beyond mucosal layer into submucosa and muscularis epithelial layer into the serosal layer
  • If the LES is incompetent, ulcerative involvement of the esophagus may also occur
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34
Q

Describe Therapeutic Pharmacology for Peptic Ulcer Disease.

A

•H2-receptor Antagonists

–Blocks secretion of hydrochloric acid

–Promotes healing of duodenal ulcers

–Reduces cytochrome P-450 enzyme activity in the liver (prolonged drug metabolism)

*Famotidine is the least likely H2 antagonist offender

•Proton pump inhibitors

–Most effective antisecretory agent

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35
Q

In addition to the H2 blockers and PPI, what are othe pharmacology therapy of peptic ulcer disease?

A
  • Sucralfate
  • Antibiotics
  • Misoprostol
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36
Q

How does sucralfate help manage PUD?

A

•Sucralfate

–Aluminum salt of sulfated sucrose

–Binds to ulcer and Increases (coats) the gastric mucous layer

–Promotes the healing process

–Devoid of side effects

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37
Q

How does misoprostol help manage PUD?

A

–Synthetic prostaglandin: acts on parietal cells in the stomach wall to inhibit acid secretion

–Secondary therapy to prevent ulcers in patients requiring NSAIDs

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38
Q

How does gastritis associated with gastric mucosal acidosis affect peri-operative morbidity and mortality?

A

Peri-operative morbidity and mortality are increased

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39
Q

What are the exocrine functions of the pancreas?

A

External digestive function:

  • Secretes 1500-3000ml of pancreatic juice daily
  • Clear, colorless liquid with a pH of 8.3
  • Ionic composition is Na+, K+, bicarb, chloride
  • Principle function is to adjust duodenal pH
  • Promotes optimal function of pancreatic enzymes
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40
Q

What is the e__ndocrine function of the pancreas?

A

Internal hormonal function:

-Direct (non-ductal) production of insulin and glucagon to meet the physiologic need.

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41
Q

What are the S/S of acute pancreatitis?

A

severe abdominal pain

fever

N/V

jaundice

hypotension

ileus

external distortion of stomach on radiographs

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42
Q

What are the common causes pancreatitis?

A
  • Alcohol abuse
  • Direct or indirect trauma
  • Ulcerative penetration from adjacent structures
  • Infectious processes
  • Biliary tract disease
  • Metabolic disorders
  • Drug side effect
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43
Q

What is the management of acute pancreatitis?

A
  • Nasogastric suction
  • Maintenance of intravascular volume (NPO)
  • Anticipation of respiratory insufficiency
  • Analgesia
  • Nutritional support
  • Common bile duct exploration
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44
Q

What are the S/S of chronic pancreatitis?

A

–Incapacitating upper abdominal pain radiating to the back (Continuous or intermittent in nature)

–Pancreatic calcification

–Steatorrhea

–40% have diabetes from loss of pancreatic function

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45
Q

What are the common causes of chronic pancreatitis?

A
  • Chronic alcoholism
  • Chronic, significant biliary tract disease
  • Long term effects of pancreatic injury
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46
Q

What are the surgical procedures of pancreatitis?

A
  • Drainage of pseudocyst
  • Pancreatojejunostomy
  • Puestow procedure: It involves a side-to-side anastomosis of the pancreatic duct and the jejunum
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47
Q

What is biliary tract (tree) and what comprise it?

A
  • Excretory conduit for the liver
  • Composed of:

–Intrahepatic ducts

–Coalescence of the intrahepatic ducts and the right and left hepatic ducts

–The common hepatic duct

–The gallbladder

–The cystic duct

–The common bile duct

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48
Q

What causes the sphincter of Oddi to dilate?

A

Glucagon

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49
Q

How much bile does the gallbladder store?

A

30ml - 50ml

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50
Q

What causes the gallbladder to contract and release bile?

A

Regulation of gallbladder contraction is primarily hormonal through the action of cholecystokinin which is released from duodenum and mediated by presence of intraluminal amino acids and fats

•Vagal stimulation also plays a role – secondary to cholecystokinin.

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51
Q

What are the three main functions of bile?

A

–Emulsify and enhance absorption of ingested fats and fat-soluble vitamins.

–Provide an excretory pathway for bilirubin, drugs, toxins, and immunoglobulin A (IgA)

–Maintain duodenal alkalization

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52
Q

What is Murphy’s sign?

A

Inspiratory effort accentuates the pain in cholecystitis

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53
Q

What is cholecystitis and what is the clinical presentation?

A

•Acute obstruction of the cystic duct.

  • Patients present with acute, severe, midepigastric pain that often radiates to right abdomen.
  • Jaundice suggests complete obstruction of the cystic duct.
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54
Q

What is choledocholithias?

A

-an obstruction of common bile duct

symptoms are similar to cholecystitis

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55
Q

What are the signs of Charcot Triagle and what does it indicate?

A

Fever (Chills)

Jaundice

upper quadrant pain

–Indicative of acute ductal obstruction r/t cholelithiasis

–Patients also have weight loss, anorexia, and fatigue

•Diagnostic studies demonstrate a dilated biliary tree.

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56
Q

What type of pain will be most seen with post op laparascopic cholecystectomy ?

A

right shoulder pain

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57
Q

What are the anesthesia considerations for a cholecystectomy?

A

–Post-op pain

–Nausea and vomiting

–Peritoneal irritation from CO2

–Intravascular volume restoration

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58
Q

What are the anesthesia considerations for a laparoscopic surgery?

A
  • Abnormal gastroesophageal junction competence from high intra-abdominal pressure/aspiration risk
  • Altered ventilatory dynamic caused by large volume of intra-abdominal carbon dioxide/hypercapnia
  • Decreased venous return from increased intra-abdominal pressure/patient position
  • Manipulation of abdominal viscera may cause bradycardia and hypotension
  • Bleeding at trocar insertion site/inadvertent breech of large vessel ~ hemorrhage
  • Venous CO2 embolism
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59
Q

Name the structures of the small intestine, beginning with the proximal structure to the stomach.

A

–Duodenum ~ 20cm

–Jejunum ~ 100cm

–Ileum ~150cm

(tethered by the mesentery)

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60
Q

What are the three major classes of nutrients that enter the digestion in the small intestine?

A
  • Proteins
  • lipids (fats)
  • carbohydrates
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61
Q

What is absorption and by what mechanism does it occur?

A

*It is the passing of food from the small intestine into the blood vessels.

*Diffusion.

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62
Q

What epithelial cells line the inner wall of the small intestine?

A

simple columnar epithelial tissues

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63
Q

What are the three functional zones of the esophagus?

A

–Upper esophageal sphincter (UES)

–Esophageal body

–Lower esophageal sphincter (LES)

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64
Q

Differentiate rugae and plicae circulares

A

Rugae Plicae circularis

Folds in the stomach folds in the small intestine

Temporary permanent

For distension and contraction for absorption

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65
Q

What are some of the diseases of the small intestine.

A

•Malabsorption Syndromes

–Celiac sprue/Gluten-sensitive enteropathy

–Fat malabsorption

–Protein malabsorption

•Maldigestion Syndromes

–Deficient pancreatic secretion

  • Upper GI bleeding
  • Small bowel obstruction
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66
Q

How long is the large intestine?

A

3-5 feet

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67
Q

Describe the wall of the large intestine.

A

–Composed of longitudinal muscle and numerous outpouchings (haustrations) throughout its length

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68
Q

What is the arterial supply of the large intestine?

A

–Superior mesenteric artery

–Inferior mesenteric artery

–Internal iliac artery

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69
Q

Describe the diseases of the large intestine.

A

•Inflammatory Bowel Disease

–Chrohn’s Disease

–Ulcerative colitis

  • Diverticulitis (inflammation) /Diverticulosis (pouches)
  • Abdominal Compartment Syndrome
  • Colonic polyps
  • Colon Cancer
  • Colon volvulus
  • Ischemic Bowel
  • Appendicitis
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70
Q

What are the anesthesia considerations for intestinal surgery?

A
  • Aspiration Risk
  • Fluid and electrolyte status
  • History of steroid use ~ perioperative coverage
  • Avoid Nitrous Oxide
  • TPN (we do not stop since it’s calculated based on 24hr)
  • Bowel prep (dehydration)
  • Malnutrition and anemia
  • Thermoregulation – SCIP 36*C
  • Post op ileus (do not give Reglan)
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71
Q

What is a spleen?

A
  • The spleen is a non-vital organ located in the left upper quadrant of the abdominopelvic region.
  • It is the largest lymphatic organ, acting as a site of lymphocyte proliferation and in immune surveillance and response.
  • In the fetus, it is a hematopoietic organ.
  • Organs and structures that border the spleen are the diaphragm, stomach, left kidney, pancreas and left colic flexure.
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72
Q

Describe the tissues that make up the esophageal mucosal lining.

A

Squamous epithelium

Columnar epithelium: distal 1-2 cm that connects to the stomach (same tissue as the stomach)

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73
Q

What separates the two layers of the esophageal muscles and what is its function?

A

The myenteric plexus of Auerbach (A): a tangled network of nerve fibers involved in the secretion of mucus and in peristalsis of the smooth muscle of the esophagus.

This is mainly a parasympathetic (vagus nerve) plexus along with some postganglionic sympathetic nerves.

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74
Q

Which nervous system is primarily responsible for the digestive system?

A

Parasympathetic nervous system (Rest and Digest)

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75
Q

Describe the esophageal innervation.

A

•Extrinsic -

–Sympathetic

•Act on myenteric plexus to

modulate rather than control

motor activity

–Parasympathetic

  • Cranial nerves IX, X, XI
  • Causes esophageal

muscular contraction

•Causes relaxation of LES

–Somatic

76
Q

Are the upper and lower esophageal opened or closed at rest?

A

closed

77
Q

Which nervous system stimulates peristaltic activity?

A

parasympathetic nervous system

78
Q

What is the predominant nerve in the esophagus?

A

Vagus nerve (CN X)

79
Q

What action initiates the peristalsis of the esophagus?

A

swallowing

80
Q

How does the peristalsis of the esophagus affect the LES?

A

peristalsis initiated by swallowing decreses LES tone for the duration of the peristaltic wave.

Once ingested and/or the abdominal pressure rises, the LES tone is increased via Vagal afferent pathways.

81
Q

What is the pressure of the LES tone?

A

•Normal LES tone is 20 mmHg

–Mediated by intrinsic myogenic and excitatory neural mechanisms

–Vagal innervation is predominant

82
Q

What is the consideration for performing a barium contrast in a patient with dysphagia?

A

Barium can just sit in their esophagus d/t decreased motility and cause aspiration

83
Q

What is Mallory-Weiss Tear and what disease state does it indicate?

A

A tear in the mucosal layer at the junction of the esophagus and stomach

Indicates chronic alcoholism

84
Q

What are the primary symptoms of hiatal hernia?

A

–Retrosternal pain of a burning quality that commonly occurs after meals (heartburn)

–Ulceration and may result in GERD (H1, H2 blockers)

–Assumed predisposed to developing peptic esophagitis

–Shortness of breath

–Anemia (from ulceration)

–Treated surgically, with the primary goal to reestablish gastroesophageal competence.

–Aspiration and necrosis from constriction are some of the concerns.

85
Q

What are the types of hiatal hernia?

A

–Sliding / Type I

–Paraesophageal / Type II

–Mixed / Type III

–Type IV

86
Q

What is type I hiatal hernia?

A

Type I: sliding - Part of the stomach moves up through the hiatus and into the chest cavity. This pushes the lower esophageal sphincter (LES) / Gastroesophageal (GE) junction up into the chest cavity away from the hiatus. Away from the hiatus, the LES loses the support that it needs from the diaphragm to stay closed. This raises the risk for symptoms of heartburn and gastroesophageal reflux disease.

Most common: 95%

87
Q

What is type II hiatal hernia?

A

Paraesophageal hernia:

Less common, but is more cause for concern. The esophagus and gastroesophageal (GE) junction stay in their normal locations, but part of the stomach (fundus) squeezes through the hiatus, landing it next to the esophagus. Although you can have this type of hernia without any symptoms, the danger is that the stomach can become “strangled,” or have its blood supply shut off.

Anemia results from damage and ulceration to the lining of the stomach due to compression of the stomach at the level of esophageal hiatus

88
Q

What is type III hiatal hernia?

A

Type III hiatal hernias are combined hernias in which the gastroesophageal (GE) junction is herniated above the diaphragm and the stomach is herniated alongside the esophagus. The majority of paraesophageal hernias are type III

89
Q

What is type IV hiatal hernia?

A

In type IV hiatal hernias, other organs in addition to the stomach (colon, small intestine, spleen) also herniate into the chest

90
Q

What risk does esophageal diverticula cause?

A

Places the patient at risk for pulmonary aspiration of regurgitated food and also from food/fluids ingested but sequestered within the pouch.

91
Q

How is the staging of esophageal cancer done?

A

I am not memorizing this. I’ll just get this question wrong.

92
Q

What are some anesthesia considerations in patients with esophageal disorder?

A
  • A history of GERD with active reflux symptoms warrants a plan for aspiration prophylaxis during induction and emergence from general anesthesia. (Actually, just treat for GERD regardless.)
  • Mandates the use of an endotracheal tube to create a sealed airway to prevent the risk from passive regurgitation and aspiration. (No LMA)
  • A rapid sequence induction (RSI) with cricoid pressure should be used. (Rapid means hurry. No time to tape the eyes. Don’t mask ventilate - risk of gastric distension = reflux & aspiration)
  • The patient must be fully awake and have demonstrated conscious control of the airway prior to extubation. (No deep extubation)
93
Q

What are the surgical management for esophageal diseases?

A
  • Upper Endoscopy and related procedures
  • Surgical management of GERD:

–Nissen Fundoplication

•Laparoscopic technique:

–DaVinci robotic assistance

–“Esophyx” (not seen as much)

–NOTES “natural orifice transluminal endoscopic surgery”

  • Open – left posterior thoracotomy
  • Open – abdominal approach
94
Q

Name the surgical managements for an esophageal cancer.

A
  • Ivor-Lewis repair
  • McKeown repair
  • thoracoscopic port placement for minimally invasive esophagectomy
  • transthoracic esophagectomy with a left thoracoabdominal approach
95
Q

What are the physical characteristics of patients with obstructing esophageal diseases?

A

elderly, debilitated, and malnourished.

96
Q

What is the pre-op goal of patients with obstructing esophageal diseases?

A

Mitigate malnourishment, anemia, dehydration, and electrolyte abnormalities by means of intravenous support and appropriate laboratory monitoring.

*NGT, JT, TPN, PEG (not really preferred) for liquid nutrition consisting of 2,000Kcal, high-protein diet for at least 10 days prior to surgery.

*Cardiovascular, renal, hepatic, and respiratory function should be documented and optimized.

*If the patient is aspirating, the esophagus should be evacuated and the patient should be given nothing by mouth until after the operation. Aspiration pneumonia should always be corrected preoperatively.

97
Q

Describe Ivor-Lewis repair.

A

aka transthoracic esophagectomy

A combination of two separate surgical procedures – a laparotomy (abdominal) incision to allow for mobilization of the stomach, and a right-sided thoracotomy for excision and resection of the esophagus.

The esophageal tumor is removed through an abdominal incision and a right thoracotomy. The esophagogastric anastomosis (reconnection between the stomach and remaining esophagus) is located in the upper chest.

98
Q

Describe McKeown repair.

A

A right neck incision for excision of the diseased esophagus. The distal remnant of the esophagus is anastomosed to the cervical esophagus.

Complication: RLN injury when the surgical hand is inserted through the neck incision

99
Q

Illustrate thoracoscopic port placement for minimally invasive esophagectomy

A
100
Q

Illustrate transthoracic esophagectomy with a left thoracoabdominal approach.

A
101
Q

What are the intraoperative complications for esophagectomy?

A

arrhythmias and hypotension

hemorrhage

injury to the recurrent laryngeal nerve

injury to the tracheobronchial tree.

102
Q

Why is RLN injury a risk in esophagectomy?

A

Drawing illustrates the anatomic location of the recurrent laryngeal nerves (arrowheads) and their relationship to adjacent structures. Arrows indicate the vagus nerves. Note the lymph nodes along the recurrent laryngeal nerves. Accurate dissection of the recurrent laryngeal nerve lymph nodes and preservation of these nerves are important surgical issues.

103
Q

What are the most serious postoperative complications for esophagectomy?

A

Anastomotic leak

mediastinitis

sepsis

respiratory failure

104
Q

What purpose do the mucous cells of the gastric mucosa serve?

A

Secrete mucous that provides a protective barrier to the acid outflow of parietal cells.

105
Q

What exchange pump do parietal cells require in order to secrete acid into the stomach?

A

Acid secretion of parietal cells requires a hydrogen/potassium (H+/K+) exchange pump powered by ATP

106
Q

What three factors induce the acid release from the parietal cells in the stomach?

A

–Vagal stimulation (acetylcholine) of the parasympathetic (rest and digest) system

–Gastrin release by the G cells in the antrum of the stomach in response to gastric distention

–Histamine (H2) which is a powerful stimulant of the acid secretion from the enterochromaffin-like cells (ECLs).

107
Q

What do enterochromaffin-like cells (ECLs) of the stomach release?

A

Enterochromaffin-like cells (ECLs) release histamine (H2), which also is a powerful stimulant of the acid secretion

108
Q

What do G cells of the stomach release?

A

G cells release gastrin hormone in response to gastric distension and stimulates acid production from the parietal cells.

109
Q

What type of acid is produced by the parietal cells of the stomach?

A

Hydrochloric acid (HCl)

110
Q

What two external factors stimulate acid and pepsinogen production in the stomach?

A

The sight and smell of food stimulates acid and pepsinogen production

111
Q

What suppresses gastrin release?

A

•Luminal acid suppresses gastrin feedback through negative feedback.

112
Q

What structure in the stomach allows for the distension?

A

Rugae: It is a series of ridges produced by folding of the wall of an organ. The purpose of the gastric rugae is to allow for expansion of the stomach after the consumption of foods and liquids. As the stomach expands, rugae disappears; hence, the rugae is temporary.

113
Q

What does the chief cells of the stomach secrete?

A

Pesinogen, which is a precursor of Pepsin, which is activated by the parietal cells.

Pepsin is an enzyme that breaks down proteins into smaller peptides.

(Peptides will be broken down into amino acids and amino acids will be broken down into individual amino acid in the small intestine to facilitate absorption.)

114
Q

What do parietal cells of the stomach secrete?

A

*Hydrochloric acid (HCl)

*Intrinsic factor which allows the ileum to asbsorb vitamin B12.

115
Q

Define H2 antagonists.

A

They block the action of histamine at the histamine H2 receptors of the parietal cells in the stomach, thereby decreasing the production of HCl.

Histamine released by enerochromaffin-like cells (ECLs) signal the parietal cells to produce acid.

Ex. Ranitidine, Cimetidine

116
Q

Define proton pump inhibitors.

A

Proton pump inhibitors act by irreversibly blocking the hydrogen/potassium ATP system (the H+/K+ ATPase, or, more commonly, the gastric proton pump) of the gastric parietal cells.

Ex.:

  • Omeprazole
  • Prostaglandins
117
Q

Anticholinergic agents are useful in managing oversecretion of gastric acid.

True/False

A

False

Anticholinergic agents have a minor (not therapeutic) effect on parietal-cell secretion.

*more useful as an antisialogogue

118
Q

In addition to the aid in digestion, what are other gastric functions?

A

•Barrier against ingested pathogens

–Acidic environment

–Immunosurveillance

•Thermoregulation

–Heats or cools ingested substances

119
Q

What are the four major arteries that supply blood to the stomach?

A

–Right and Left gastric arteries

–Right and Left gastroepiploic arteries

120
Q

What are the associated causes of PUD?

A

+•Helicobacter pylori bacterium is the major etiologic factor

  • Overuse of medications such as aspirin and nonsteroidal anti-inflammatory drugs (NSAIDS), and corticosteroids
  • Excessive alcohol consumption, tobacco use, stress, and receiving radiation therapy can increase one’s risk for peptic ulcers
121
Q

What is the treatement plan for PUD with S/S of bleeding?

A
122
Q

What complications may result from the use of oral antacids?

A

–May produce an acid rebound in which gastric acid secretion may increase after existing acids are neutralized by calcium containing antacids.

–Milk-alkali syndrome: manifest as skeletal muscle weakness and polyuria

  • Hypercalcemia
  • Alkalosis
  • Elevated BUN

–Acute hypophosphatemia – secondary to large amounts of aluminum-containing antacids.

  • Manifest as skeletal muscle weakness and fatigue
  • Pathologic fractures
  • Osteoporosis
123
Q

What are some common doses of PPI?

A

20-40mg once a day

124
Q

How do antibiotics help manage PUD?

A

–Combination therapy with a variety of antibiotics to treat H.pylori

125
Q

What are the recommended treatment strategies for H. pylori?

A
126
Q

When is surgical intervention indicated in PUD?

A

•Surgical treatment is no longer considered primary therapy, but is reserved for patients who do not respond to medical therapy or for treatment of complications such as:

–Gastrointestinal hemorrhage

–Ulcerative perforation

–Obstruction

127
Q

What surgical treatments are there for PUD?

A
  • Antrectomy with pyloroplasty and vagotomy
  • Parietal-cell vagotomy (disables parasympathetic nerve stimulation in the production of acid)

–Selective sectioning of vagal fibers of the gastric fundus and parietal cells.

128
Q

What epithelial cells are in the stomach?

A

simple columnar epithelium. This type of epithelium provides the greatest surface area for absorption or secretion.

(vs. Squamous epithelium in the esophagus)

129
Q

List the different types of gastric neoplasm.

A

•Majority of gastric neoplasms are malignant

–95% - adenocarcinoma

–4% - lymphoma

–1% - leiomyosarcoma

130
Q

What are the S/S of gastric neoplasm?

A

Early: heartburn, upper abdominal pain, nausea

Late: weight loss, anorexia, jaundice, vomiting, dysphagia, occult stool

131
Q

What are the surgical treatments for gastric neoplasm?

A

•Surgical treatment of gastric carcinoma

–Total or subtotal gastrectomy

–Billroth II -gastrojejunostomy

–Omentectomy, lymph node dissection, and spleenectomy based on extent of disease

132
Q

Describe billroth 2 gastrojejunostomy and its indication.

A

*The greater curvature of the stomach is connected to the first part of the jejunum in end-to-side anastomosis. This often follows resection of the lower part of the stomach (antrum).

*The Billroth II is often indicated in refractory peptic ulcer disease and gastric adenocarcinoma.

133
Q

Increased gastric mucosal acidosis is common among which types of patients?

A

–Critically ill patients

–Pt. undergoing prolonged, complex surgical procedure

–Pt. undergoing cardiopulmonary bypass

134
Q

What can gastritis associated with gastric mucosal acidosis progress to?

A

Sepsis

•The abdominal viscera is particularly at risk to diminished blood flow (ischemia) and break down of the intestinal barrier may occur. This leads to translocation of bacteria and endotoxins into the bloodstream.

135
Q

Which pacreatic cells release glucagon, insulin, and pancreatic enzymes?

A

Alpha cells - glucagon

Beta cells (Islets of Langerhans) - insulin

Duct cells - NaHCO3

Acinar cells - pancreatic enzymes

136
Q

Describe the stimulation and response of the ductal cells.

A

HCO3- is produced by the ductal cells in response to secretin released by the duodenum. HCO3- helps neutralize the acidity of the stomach chyme entering duodenum through the pylorus.

137
Q

What cells release secretin and how does secretin aid digestion?

A

Secretin (released by duodenum in response to acid chyme entering from the stomach) helps regulate the pH of the duodenum by:

(1) inhibiting the secretion of gastric acid from the parietal cells of the stomach
(2) stimulating the production of bicarbonate from the ducts of the pancreas to be released into the duodenum
(3) It also stimulates bile production by the liver

138
Q

What is cholecystokinin (CCK)?

A

A hormone released by the duodenum stimulated by the presence of fat.

It causes the release of digestive enzymes and bile from the pancreas and gallbladder and is responsible for stimulating the digestion of fat and protein

139
Q

What factors stimulate the release of pancreatic enzymes?

A

CCK (cholecystokinin)

Vagal stimulation

Secretin causes HCO3- to be released

140
Q

What are the major pancreatic enzymes?

A

Amylase: catalyses the hydrolysis of starch into sugars

Lipase: catalyzes the hydrolysis of fats (lipids)

Trypsin: catalyzes the hydrolysis of peptide bonds, breaking down proteins into smaller peptides

141
Q

Where is duodenum located?

A

In the proximal intestine. Connects from the stomach.

142
Q

What is the cure rate for pancreatic cancer?

A
  • Cure rate 5% or less
  • Vague and general symptoms prior to onset of jaundice
  • By the time a diagnosis is made, lesion may be unresectable
  • Considerable number of these patients will undergo laparotomy
  • Procedures are palliative or aimed at a cure
143
Q

What are the complications of post-op pancreatic cancer?

A

hemorrhage

coagulopathy

hepatic, renal, pulmonary, and cardiovascular failure.

144
Q

What is a Whipple procedure?

A

a major surgical operation involving the removal of the head of the pancreas, the duodenum, the proximal jejunum, gallbladder, and part of the stomach.

145
Q

What is a biliary tract disease?

A

a symptomatic expression of the presence of gallstones or inflammatory process attributable to infection or ischemia.

146
Q

How is gallstone formed and what is its composition?

A
  • Gallstone formation is caused by physicochemical derangements in the formation of bile.
  • 90% of gallstones will appear as radiolucent structures on x-ray.
  • Composition

–Hydrophobic cholesterol crystals

–Calcium bilirubinate

147
Q

Describe the gallbladder.

A
  • Pear shaped organ capable of holding 30-50cc of bile.
  • After food is ingested, the gallbladder contracts, emptying bile into the duodenum to assist in digestion.
148
Q

What is Endoscopic retrograde cholangiopancreatography (ERCP)?

A

Endoscopic retrograde cholangiopancreatography (ERCP) is a technique that combines the use of endoscopy and fluoroscopy to diagnose and treat certain problems of the biliary or pancreatic ductal systems.

149
Q

What labs are done for cholecystitis?

A

•Labs may demonstrate increase in plasma bilirubin, alkaline phosphatase, amylase, and WBCs.

150
Q

What should be ruled out with a patient presenting with midepigastric pain?

A
  • Patients with cholecystitis present with symptoms that are often confused with myocardial infarction.
  • R/O cardiac event with serial enzymes and EKGs.
151
Q

What are the complications of cholecystitis?

A

volume depletion/dehydration

gallbladder perforation leading to peritonitis

ileus

152
Q

A patient complaining of severe midepigastric pain, nausea, vomiting, fever, and pain radiating to the back has KUB done which reveals free abdominal air. What can be suspected from the KUB result and what should be done?

A

Perforated gallbladder

–Requires emergency exploratory laparotomy

153
Q

Name the two pathologies in the illustration:

gallstones in the cystc duct

gallstones in the commonn bile duct

A

gallstones in the cystic duct: cholecystitis

gallstones in the common bile duct: choledocholithiasis

154
Q

What is cholelithiasis?

A

presence of stones in the gallbladder or the diseases caused by gallstones.

155
Q

A patient who has undergone a laparascopic cholecystectomy complains of right shoulder pain that is unrelieved with pain meds. What may this be an indication of?

A. Myocardia infarction

B. Complication from the procedure

C. CO2 insufflation during surgery

D. Peritonitis from an accidental intraoperative gallbladder perforation

A

C.

Absorption of CO2 during insufflation can cause right shoulder pain and is difficult to treat even with pain meds.

156
Q

What are the two major functions of the small intestine?

A

chemical digestion

absorption

157
Q

What two hormones are released by the small intestine (duodenum), what triggers the release, and what is the target response?

A
  1. secretin in response to the food entering into the duodenum from the stomach. The hormone inhibits the secretion of gastric acid from the parietal cells of the stomach and stimulates the production of bicarbonate from the ductal cells of the pancreas.
  2. cholecystokinin aka pancreozymin released in response to lipids, carbohydrates and protein entering the duodenum.

It causes the release of digestive enzymes and bile from the pancreas and gallbladder, respectively, and also acts as a hunger suppressant.

158
Q

Where does the chemical digestion of food take place?

A

stomach

small intestine

159
Q

Where does the mechanical digestion of food occur?

A

In the mouth during mastication

160
Q

Does the large intestine take part in the digestion process?

A

Yes.

Bacterial digestion

161
Q

Where does most of the chemical digestion take place?

A. Mouth

B. Stomach

C. Small intestine

D. Large intestine

A

Small intestine

162
Q

What are villi and microvilli? What are their roles?

A

The are a finger-like projection of the tissues from the plicae circulares and epithelial cells in the small intestine.

Plicae circulaes, villi, and microvilli increase the surface area to maximize absorption.

163
Q

Parasympathetic activity causes contraction (closure) of the lower esophageal sphincter.

True / False

A

False

•Causes relaxation of LES

164
Q

What distinction can be made in the stomach muscles that is not found in the esophagus or small intestine?

A

The stomach is the only organ in the digestive system to have an oblique muscle in addition to the two muscles commonly found in the esophagus and small intestine.

165
Q

What is the primary site of absorption?

A

The small intestine

166
Q

What enzymes breakdown proteins?

A

Proteins are digested in the small intestine by the proteolytic enzymes to brekdown protein into smaller peptides.

Two notable enzymes are trypsin and chymotrypsin, secreted by the pancreas.

Carboxypeptidase, aminopeptidase and dipeptidase breakdown peptides into amino acids for absorption.

167
Q

Describe the digestive process of lipids.

A
  • Bile salts attach to triglycerides to help emulsify them, which aids access by pancreatic lipase.
  • Pancreatic lipase breaks down triglycerides into free fatty acids and monoglycerides (glycerol).
  • The bile salts are the “middle man” that hold the triglycerides in the watery surroundings until the lipase can break them into smaller components that are able to enter the villi for absorption.
168
Q

Describe the process of carbohydrates breakdown.

A
  • Pancreatic amylase breaks down carbohydrates into oligosaccharides. Brush border enzymes take over from there.
  • The most important brush border enzymes are dextrinase and glucoamylase which further break down oligosaccharides into monosaccharides. Other brush border enzymes are maltase (maltose+glucose), sucrase (fructose+glucose), and lactase (galactose+glucose).

Carbohydrates are ultimately degraded into simple sugars, or monosaccharides (e.g., glucose) for absorption.

169
Q

What is haustrations?

A

small pouches caused by sacculation (sac formation), which give the colon its segmented appearance

170
Q

What are the four functions of the large intestine?

A
  • Peristalsis
  • Bacterial digestion
  • Absorption: Vitamins B, K, and some electrolytes (Na+ and Cl–), and most of the remaining water is absorbed by the large intestine. (1-2 liters per day)
  • Defecation
171
Q

What vitamins are produced by the large intestine?

A

Vitamin K and certain B vitamins are produced by bacterial activity.

172
Q

What are the structural differences in the large intestine between Crohn’s disease and ulcerative colitis?

A

Crohn’s:

fat deposits, cobblestoning, fissure, thickened wall.

UC:

ulceration, loss of haustra, pseduopolyps

173
Q

What are the pathology differences between Crohn’s disease and ulcerative colitis? (part 1/2)

A
174
Q

What are the pathology differences between Crohn’s disease and ulcerative colitis? (part 2/2)

A
175
Q

What is the function of the spleen?

A
  • In the infant and adult, it destroys old red blood cells, recycles iron and globin and stores functional red blood cells, expelling them in response to a hemorrhage.
  • It also stores platelets, lymphocytes and provides immune surveillance.
176
Q

What are some of the indications for splenectomy?

A
  • Idiopathic thrombocytopenic purpura
  • Thrombotic thrombocytic purpura
  • Hodgkin disease
  • Lymphoma
  • Certain leukemias
  • Hereditary hemolytic anemia
  • Hypersplenism
  • Thalassemia
  • Sickle cell disease
  • Blunt or penetrating trauma
177
Q

The esophageal sphincters are closed at rest.

True / False

A

True

178
Q

Sympathetic system speeds up the digestive process.

True / False

A

False.

Sympathetic systems slows down the digestive process.

Parasympathetic systems speeds it up. (Rest and digest)

179
Q

What initiates esophageal peristalsis?

A

Swallowing

180
Q

Swallowing is a voluntary muscles movement.

True / False

A

False

181
Q

The downward movement of ingested food along the esophagus is controlled by voluntary muscle movement.

True / False.

A

False

Peristalsis of any digestive tract is an involuntary muscle movement

182
Q

Swallowing decreases the LES tone.

True / False

A

True

183
Q

What is the complication of Heller myotomy?

A

Reflux.

The surgery is usually combined with a partial fundoplication to reduce the incidence of post-op acid reflux.

184
Q

What is Billroth 2 surgery indicated for?

A

Billroth 2 gastrojejuostomy is indicated for PUD and gastric adenocarcinoma.

185
Q

What is Puestow procedure indicated for?

A

To treat chronic pancreatitis

186
Q

What is the indication for Whipple procedure?

A

pancreatic cancer

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