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Principles of drug Action II > ap exam 2 GI > Flashcards

ap exam 2 GI Flashcards

1
Q

Gastroesophageal refluxdisorder

A
  • Commonly known as “GERD”
  • Occurs when there is reflux of gastric /intestinal contents back into the esophagus
  • Repeated exposure causes irritation / damage togastric mucosa
  • Many cases are episodic and related topredisposing factors such as diet
  • If untreated, can progress to a more severecondition known as erosive esophagitis
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2
Q

pathophysiology of reflux

A
  1. Transient Lower Esophageal Relaxation(tLER) seems to be the most common factor inmild/ moderate cases
  • Normally lower esophageal sphincter (aka cardiac sphincter) is kept closed
  • During the swallowing phase, the lower esophageal sphincter opens
  • This opening is called Lower esophageal relaxation (LER)
  • In patients with GERD, tLER occurs with no swallowing
  1. Decreased esophageal sphincter tone is alsoa contributing factor

•More commonly associated with severe refluxesophagitis

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3
Q

other causes of reflux

A
  • Increased intragastric pressure
  • Delayed gastric emptying
  • Hiatal hernia: part of the stomach bulges into the chest;
  • It delays acid clearance
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4
Q

Barrett’s esophagus

A
  1. Repeated gastric reflux causes conversion ofnormal esophageal squamous epithelium intocolumnar epithelium
  • More resistant to acidic damage
  • Is a risk factor for esophagealcancer
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5
Q

GERD clinical presentation mild

A
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6
Q

GERD clinical presentation severe

A

vSevere cases (esophagitis)

  • Bleeding (hematemesis / melena)
  • Hematemesis is the vomiting of blood
  • Melena is black, tarry stools
  • Ulcerations
  • Significant weight loss
  • Morning hoarseness / laryngitis
  • Coughing / wheezing
  • Pulmonary aspiration
  • food, liquids, saliva, or vomit is breathed into the airways.
  • Aspiration pneumonia

Pulmonary fibrosis

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7
Q

Peptic Ulcer Disease

A

vUlcerative disorder of the uppergastrointestinal tract

  • Gastric ulcer (potentially malignant)
  • Duodenal ulcer (rarely malignant)
  • Stress ulcers
  • Zollinger-Ellison syndrome
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8
Q

Peptic ulcer disease causes and complications

A

vEpigastric pain is the most common symptom of both gastric and duodenal ulcers.

  • Common causes may include:
  • Helicobacter pylori
  • NSAIDs
  • Life styles: Smoking, Alcohol? Diet?
  • Psychological factors?
  • Genetic factors
  • Complications include:
  • Bleeding
  • Obstruction
  • Peroration
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9
Q

Duodenal Ulcer characyeristics

A
  • In duodenum
  • Pain relived by meal
  • Occurs 2-3 hrs after meal
  • are 3x more common than gastric ulcers
  • Increased acid secretion
  • Gastric emptying is often increased
  • Malignancy risk low
  • Melena
  • bleeding, perforation, and obstruction
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10
Q

gastric ulcer characteristics

A
  • In stomach
  • Pain increased by meal
  • Occurs 0.5-1 hrs after meal
  • Are less common than duodenal ulcers
  • Normal acid secretion
  • Gastric emptying is often delayed
  • Malignancy risk higher
  • Vomitting
  • bleeding, perforation, and obstruction
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11
Q

Evidences Implicating H. pylori

A
  • Extremely high prevalence of organism in patients with both DU and GU
  • Patients with ulcers who are treated with antisecretory agents may heal, but relapse rates are high in patients who are H. pylori positive
  • Antibiotic regimens that eradicate organism significantly reduce the incidence of relapse rates
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12
Q

Evidences Exonerating H. pylori

A
  • DU are predominant in males, but the organism is not gender-specific
  • Many patients with positive cultures are asymptomatic and will never develop PUD
  • Ulcers can heal with antisecretory treatment despite the presence of the organism
  • Acid hypersecretion can cause duodenal ulcers without presence of organism
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13
Q

Helicobacter pylori conclusion

A

vConclusions

  • H. pylori infections undoubtedly implicated inpeptic ulcer disease, chronic gastritis and gastric cancer
  • Eradication of the organism results in lowrelapse rates
  • However, other factors must be contributing to thedevelopment of the disease
  • Presence of ulcers in culture (-) patients
  • Lack of disease in culture (+) patients
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14
Q

what are stress ulcers and it risk factors

A

vObserved in patients with highphysiological stress

•Estimated 75-100% of patients have stress- relatedmucosal damage within 24 hours of admission toICUs

•Risk factors

  • Shock
  • Burns
  • Sepsis

Severe trauma

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15
Q

stres ulcer pathophysiology and mechanism

A

Pathophysiology

•Gastric acid is involved, but hypersecretion istypically not seen

2 main accepted mechanisms

  • Mucosal ischemia
  • Decreased oxygen delivery
  • Decreased bicarbonate delivery to site
  • Reduced removal of gastric acid
  • Enhanced back diffusion of hydrogen ions
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16
Q

Zollinger -Ellison Syndrome

A
  • Gastrin-secreting Tumors (Gastrinoma)
  • Often in duodenum(50–90%), less frequently in pancreas (10–40%) or gastric wall (up to 10%)
  • Pathophysiology
  • Excessive acid production
  • Serous and aggressive peptic ulcers
  • Symptoms: abdominal pain; chronic diarrhea, dyspepsia; weight loss; bleeding
  • Complications: hemorrhage, perforation, and obstruction
  • Treatment: surgery; H2 antagonists; and anticholinergics; antacids
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17
Q

Inflammatory Bowel Disease(IBD)

A
  • IBD is a group of chronic inflammatorydisorders
  • 2 major classifications
  • Ulcerative colitis: continous colonic involvement
  • Crohn’s disease: skip lesion

True etiology unknown

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18
Q

Ulcerative colitis

A
  1. The inflammation causes ulcerations of the mucosa in the colon.
  2. Symptoms

•may include abdominal pain, malnutrition, and exudative, bloody diarrhea.

3.Etiology may be related to:

  • Environmental exposure
  • Environmental factors may trigger a breakdown inmucosal immune response to enteric bacteria
  • Cigarette smoking retains a protective effect
  • Genetic disposition
  • High frequency in Jewish population
  • First degree relatives have a 10-fold risk of the disease
19
Q

Ulcerative colitis disease characteristics

A
  • Primarily involves the colonic mucosa /submucosa
  • The rectum is usually involved
  • Colon appears ulcerous, hyperemic andhemorrhagic
  • Inflammation is uniform and continuous
  • Deeper layers of the bowel usually not involved
20
Q

Ulcerative colitis complications

A
  • Toxic megacolon (16%)
  • Hemorrhage (bleeding) (6-10%)
  • Perforation (2-3%)
  • Colon cancer
21
Q

Crohn’s Disease

A

•May be present from mouth to the anus

  • •Ileum and ascending colon (most common)
  • •Other regions possible
  • In small bowel is known as regional enteritis
  • Chronic inflammation extending through all layersof intestinal wall
  • Inflammation is often discontinuous (skip lesions)
  • Crohn’s disease is most prevalent in adults ages 20 to 40
  • Presence of granulomas,
22
Q

chrons disease symptoms and possile causes

A
  • Symptoms
  • Chronic diarrhea with abdominal pain, fever, anorexia, and weight loss
  • The abdomen is tender, and a mass or fullness may be palpable.

Possible causes

  • genetic factors
  • infection
  • allergies
  • immune disorders
  • lymphatic obstruction
23
Q

Crohn’s Disease

Pathophysiology

A
  • Pathophysiology of disease: progressive inflammation
  • Crohn disease begins with crypt inflammation leading to ulcers. Fibrosis occurs, thickening the bowel wall (due to hypertrophy of the muscularis mucosae) and causing stenosis, or narrowing of the lumen. (cobblestoned appearance to the bowel, see pic.)
24
Q

chrons disease complications

A
  • Complications
  • fistula, aka abnormal tunnel
  • intestinal obstruction
  • nutrient deficiencies caused by malabsorption of bile salts and vitamin B12 and poor digestion
  • fluid imbalances
25
Q

Crohn Disease and UC Comparison

A

vCrohn Disease

  • Terminal ileum
  • Skip lesions
  • Transmural lesions
  • Crampy abdominal pain
  • Slight risk for cancer
  • Complications include fistulas, abscess, obstruction

vUlcerative colitis

  • Rectum
  • Contiguous lesions
  • Lesions in submucosa or mucosa
  • Bloody (exudative) diarrhea
  • Marked risk for cancer
  • Perforation, hemorrhage, toxic megacolon
26
Q

IBS

A

IBS is chronic or recurrent diarrhea, constipation, and/or abdominal pain and bloating. Spastic contractions of the colon.

27
Q

IBS symptoms: Typical Features

A
  • Loose/frequent stools
  • Constipation
  • Bloating
  • Abdominal cramping, discomfort, or pain
  • Symptom brought on by food intake/specific food sensitivities
  • Symptoms dynamic over time (change in pain location, change in stool pattern)
28
Q

Irritable bowel syndrome

A
  • not a single disease but rather a symptom cluster
  • associated with altered brain-gut communications
  • Disturbed brain functions
  • High sensitivity to visceral stimuli
  • Disturbed gut physiology
  • Gut microbiota
  • Gut immune function and inflammation
  • Increased intestinal permeability, sensitivity and motility
29
Q

Pathophysiology - diarrhea

A

-There are 4 main mechanisms by which diarrheadevelops:

  • Decreased absorption –Osmotic (ex, lactose or sorbitol)
  • Increased secretion –Secretory or watery (non-invasive infections, ex, Cholera toxin, rotavirus)
  • Excessive exudation –Exudative, bloody (IBD, or invasive infection)
  • Increased GI motility –Motility-related (IBS)
30
Q

Treatment – non-pharmacologic of diarrhea

A

vFluid and electrolyte replacement

  • In all patients with diarrhea, fluid and electrolytelosses are the most important focus of therapy
  • In infants with a large percentage of total body water, dehydration can be quickly fatal
  • Rehydration should not be accomplished withhypotonic solutions, or hyponatremia may result
  • In addition to fluids, electrolytes must also bereplaced
31
Q

Osmotic diarrhea

A
  • Poorly absorbed solutes pull water to lumen via osmosis
  • Malabsorption of food: lactose, with lactase insufficiency

•Ingestion of antacids

•Sorbitol (sugar alcohol, Laxative)

  • Interferes with water absorption
  • Three factors
  • Amount of non-absorbed solutes
  • Volume of water needed to dilute the solutes to isotonicity
  • Volume of water accompanying the Na, Cl that equilibrate across the gut epithelia
32
Q

Secretory (watery, non-invasive) diarrhea

A
  • Increased active secretion or decreased absorption of water
  • Infections exemplified by Vibrio cholera (Cholera toxin)
  • Cholera toxin Rx with Gs system to increase cAMP
  • Phosphorylation of CFTR (chloride channel) stimulates secretion of Cl-
  • Decreased absorption of Na+ and increased water secretion
  • Diarrhea continues without food intake

-Other infections: Some E. coli; S. aureus; rotavirus, norovirus

33
Q

Exudative (invasive, bloody) diarrhea

A

-Definition of exudation:

•Leaking of the blood from blood vessels to interstitial tissue

-Intestinal or colonic mucosa inflamed/damaged

  • IBD (Crohn’s disease and ulcerative colitis)
  • Infectious: C. diff, salmonella, shigella, Yersinia, some other E. coli all damage the mucosa and cause exudation of blood cells

-Outpouring of plasma, mucus and blood into the stool

34
Q

Motility related diarrhea

A
  • Rapid movement of food through the intestines (hypermotility)
  • Limited contact time between luminal content and mucosa
  • Anxiety
  • Diabetic neuropathy
  • Vagotomy
  • Hyperthyrodism
  • IBS

-Treatment: Anti-motility drugs such as loperamide

35
Q

Constipation causes

A
  • Low fiber diet
  • Medical problems
  • GI obstructions
  • Diabetes,
  • Pregnancy
  • Drug-induced: eg, opioid
  • Insufficient biles
  • Defecation defects
  • Psychological factors
36
Q

nausea

A

NTS: Nucleus Tractus Solitarius;

Located near VC in medulla;

Pass info from GIT to VC

37
Q

definitions of vomiting and nausea

A
  • Nausea = the imminent need to vomit
  • Vomiting = emesis = the forceful expulsion of gastric contents due to GI retroperistalsis
  • Retching = the labored movement of the abdominaland thoracic muscles prior to vomiting
38
Q

vComplications of severe vomiting include:

A
  • Dehydration
  • Electrolyte disturbances
  • Hypokalemia (Low potassium)
  • Hypochloremic metabolic alkalosis
  • (loss of acid from stomach)

•Significant weight loss / malnutrition

39
Q

Pathophysiology - vomiting

A

The act of vomiting requires coordinated efforts of different systems

  • deep breath
  • closure of the glottis and opening of upper esophageal sphincter
  • contraction (lowering) of the diaphragm
  • closure of the pyloric sphincter
  • opening of lower esophageal sphincter (LES), and
  • contraction of the abdominal muscles will increase intraabdominal pressure
40
Q

Pathophysiology - vomiting

Input to the Vomitting Center

A
  • Chemoreceptor trigger zone (CTZ)
  • Cortical structures such as vision and smell centers
  • Afferent impulses from periphery including GI
  • Vestibular apparatus
41
Q

Pathophysiology - vomiting

Chemoreceptor trigger zone CTZ

A
  • Located in medulla near the 4th ventricle of thebrain: area postrema
  • Associated with chemical-induced or pregnancy related vomiting (drugs)
  • Triggered by:
  • Drugs
  • Ketoacidosis
  • Uremia
  • Metabolic disorders
42
Q

Several neurotransmitters are involved in thevomiting response

A
  • Acetylcholine
  • Dopamine
  • Histamine
  • (Opioid peptides)
  • Serotonin
  • Substance P (mediated by neurokinin)

vDrug therapy is used to antagonize the response tothese neurotransmitters

43
Q
A

Principles of drug Action II (10 decks)

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