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Patho 2 > GI SYSTEM > Flashcards

GI SYSTEM Flashcards

1
Q

Abdominal pain

A

Most common symptom of GI disorders

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2
Q

Anorexia

A

-Lack of appetite
-Common symptom of GI disorder
-May be due to non-intestinal conditions (psychological, widespread cancer, kidney failure, med side effect

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3
Q

Common manifestations of GI Disorders

A

-abdominal pain
-anorexia
-nausea and vomiting
-changes in bowel habits (diarrhea, constipation)
-dysphagia

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4
Q

Nausea and vomiting may indicate…

A

Stomach or duodenal disorder

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5
Q

Stimuli for nausea and vomiting

A

-GI irritation (common)
-Stomach distension (common)
-Unpleasant sights or smells
-General anesthesia
-Dizziness
-Certain drugs

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6
Q

Nausea

A

-Unpleasant sensation with an urge to vomit

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7
Q

Vomiting

A

-forcible expulsion of stomach and sometimes duodenal contents through the mouth

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8
Q

Neuro system and vomiting

A

-Protective reflex regulated by chemoreceptor trigger zone and vomiting centre located in medulla oblongata

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9
Q

How vomiting happens

A

-Involves squeezing the stomach between the diaphragm and abdominal muscles and expelling the contents though open esophageal sphincters

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10
Q

Vomitus containing undigested food

A

-May be an obstruction near pyloric sphincter

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11
Q

Yellow or green vomitus

A

Indicates presence of duodenal bile

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12
Q

Brown colitis

A

May indicate intestinal obstruction

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13
Q

Bloody vomitus

A

-hematemesis
-may indicate damage to GI wall

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14
Q

Consequences of Vomiting

A

Water loss = dehydration
Electrolyte imbalance = hyponatremia, hypokalemia, hypochloremia = metabolic alkalosis

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15
Q

Hypochloremic Metabolic Alkalosis

A

-Characterized by low chloride and potassium levels in the blood and high bicarbonate levels

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16
Q

Mallory-Weiss Syndrome

A

-Frequent and violent episodes of vomiting may tear the esophagus and cause bleeding
-More common in individuals who misuse alcohol

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17
Q

Electrolyte imbalance and vomiting: hyponatremia

A

-Gastric juice contains Na, loss of Na without replacement leads to hyponatremia

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18
Q

Electrolyte imbalance and vomiting: Hypokalemia

A

-Secondary to hyponatremia
-Low Na stimulates Na reabsorption and K excretion in the kidneys

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19
Q

Electrolyte imbalance and vomiting: Alkalosis

A

-Gastric juice contains H, loss of H leads to high bicarbonate levels in the blood and metabolic alkalosis

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20
Q

Definition of Diarrhea

A

-Passage of loose watery stools 3+ times per day

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21
Q

Diarrhea pathophysiology

A

-infection
-inflammation
-food intolerances
-allergies
-certain drugs

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22
Q

Diarrhea mechanisms

A

-increased water secretion
-decreased water reabsorption
-normally small intestine absorbs most of the water and electrolytes in the intestinal tract and large intestine absorb the remainder leaving formed stool

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23
Q

3 types of diarrhea

A

Osmotic, secretory, motility

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24
Q

Osmotic diarrhea

A

-Occurs when solute concentrations in intestinal lumen is higher than in body fluids
-causes influx of water into intestines leading to diarrhea
-undigested or unabsorbed material draws water into lumen

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25
Q

Common causes of osmotic diarrhea

A

-lactose intolerance
-over use of bulk forming or osmotic laxatives (psyllium fibre, polyethylene glycol)

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26
Q

Secretory diarrhea

A

-due to increased water and electrolyte secretion into the intestinal lumen

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27
Q

Causes is secretory diarrhea

A

-Usually caused by infection or inflammation of intestinal mucosa
-Ecoli infection
-food allergies
-inflammatory bowel disease

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28
Q

Motility diarrhea

A

-Occurs when intestinal motility is disrupted and stool moves too quickly through intestines = decreased water absorption

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29
Q

Causes of motility diarrhea

A

-intestinal surgery
-irritable bowel syndrome
-over use of peristalsis stimulating laxatives (bisacodyl)

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30
Q

Consequences of diarrhea

A

Water loss = dehydration
Electrolyte imbalance = hyponatremia, hypokalemia, acidosis
-hypernatremia is a rare consequence of osmotic diarrhea where only water not sodium is secreted into the intestinal lumen

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31
Q

Diarrhea and acidosis

A

-due to loss on anions (organic acids and HCO3)

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32
Q

Osmotic diarrhea and electrolyte imbalance

A

-osmotic diarrhea represents the loss of electrolyte free water
-large volume osmotic diarrhea can generate hypernatremia

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33
Q

Definition of constipation

A

Difficult or infrequent defecation

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34
Q

Primary constipation

A

Caused by colonic or pelvic floor dysfunction

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35
Q

Categories of primary constipation

A

-normal transit (functional)
-slow transit
-outlet (dyssynergia)

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36
Q

Secondary constipation

A

-due to other disease processes or medications

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37
Q

Categories of secondary constipation

A

-neurological disorders
-myogenic disorders
-endocrine disorders
-medication side effects

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38
Q

Secondary constipation: Neurological disorders

A

-affect nerves and muscles of digestive system
-Parkinson’s disease, multiple sclerosis, spinal cord injuries
-disrupt normal functioning of the colon

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39
Q

Secondary constipation: medications

A

-Opioids, anticholinergics, and calcium channel blockers
-Cause constipation by slowing down colonic transit or reducing the strength of colonic contractions

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40
Q

Normal transit (functional) constipation

A

-most common
-involves normal rate of stool passage but difficulty with stool evacuation
-rate is normal, movement from point a to b is normal

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41
Q

Risk factors for normal transit/functional constipation

A

-Low fibre diet
-Low fluid intake
-Sedentary lifestyle

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42
Q

Slow transit constipation

A

Involves impaired smooth muscle activity in the colon
-more time for water reabsorption

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43
Q

Slow transit constipation cause

A

-decreased colonic motility may be due to enteric nerve plexus dysfunction

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44
Q

Slow transit constipation results in

A

Increased water absorption and hardened stool

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45
Q

Outlet constipation (dyssynergia)

A

-involves skeletal muscle activity of the pelvic floor during bowel evacuation

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46
Q

Outlet constipation (dyssynergia) cause

A

-normally pelvic floor relaxes during defecation but with dyssynergia the pelvic floor contracts during defecation making it difficult to empty the rectum

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47
Q

Potential complications of constipation

A

-Fecal impaction
-Hemorrhoids
-Anal fissures
-Rectal prolapse
-Alkalosis

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48
Q

Chronic constipation and metabolic alkalosis

A

-Chronic constipation sometimes causes alkalosis due to increased HCO3 absorption

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49
Q

Submucosa

A

-contains glands for secretions

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50
Q

Muscularis

A

-smooth muscle
-helps with mechanical digestion and moving food forward to anus
-under control of ANS

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51
Q

Proximal meaning

A

In front of

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52
Q

Dysphagia

A

-Difficulty swallowing
-Can be caused by structural or functional obstruction of the esophagus

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53
Q

Causes of esophageal dysphagia

A

-GERD
-Achalasia
-Diffuse esophageal spasm
-Esophageal cancer
-Scleroderma
-Esophageal stricture

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54
Q

Structural Dysphagia

A

-Caused by a physical obstruction of the esophagus
-eg. esophageal tumor and esophageal stricture

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55
Q

Functional Dysphagia

A

-Impairment of esophageal motility due to neural or muscular disorder
-Eg. stroke, Parkinson’s disease, MS, muscular dystrophy, achalasia

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56
Q

Achalasia is caused by

A

Loss of esophageal innervation

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57
Q

GI Disorders 3 Broad Categories

A
  1. Altered GI tract motility disorders
  2. Altered GI tract integrity disorders
  3. Maldigestion and malabsorption disorders
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58
Q

Altered motility disorders patho physiological characteristics

A

-Due to obstruction or peristaltic dysfunction

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59
Q

Examples of altered motility disorders

A

-GERD
-Mechanical obstruction
-Functional obstruction

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60
Q

Altered integrity disorders pathophysiological characteristics

A

-Damage to GI tract wall due to infection, inflammation, or structural change

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61
Q

Example of altered integrity disorders

A

-Gastritis
-PUD
-IBD
-Diverticular disease

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62
Q

Maldigestion and Malabsorption disorder pathophysiological characteristics

A

-Poor digestion and absorption of intestinal contents; often secondary to altered motility or integrity

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63
Q

Maldigestion and Malabsorption Disorder examples

A

-Digestive enzyme deficiency
-Bile salt deficiency
-Celiac disease

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64
Q

Motility and GI system

A

-coordinated smooth muscle contractions of the muscularis propel food and secretions through the digestive tract
-The GI tracts capability to mix and move material along its length is called motility

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65
Q

Altered GI motility refers to

A

-abnormal speed or
-abnormal direction material moves though GI tract

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66
Q

Abnormal Speed

A

-If motility is too fast, the GI tract does not have enough time to digest and absorb nutrients or reabsorb water = often associated with diarrhea
-If motility is too slow then GI tract may reabsorb too much water which causes constipation
-No movement at all can be caused by an obstruction like a tumour

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67
Q

Abnormal direction

A

-If GI motility is reversed, material in GI tract moves forward towards the mouth instead of the anus (acid reflux and vomiting)

68
Q

Examples of motility issues

A

-Hiatal hernia
-GERD
-Pyloric obstruction
-Intestinal obstruction

69
Q

Hiatal Hernia

A

-Occurs when a section of the stomach protrudes upward into the thoracic cavity through the diaphragms esophageal hiatus

70
Q

Risk factors for hiatal hernia

A

-Any condition that weakens the diaphragm
-Aging (muscles/diaphragm weaken)
-Increased intrabdominal pressure (obesity, pregnancy, coughing, straining during BM) can weaken diaphragm
-Increased intrathoracic pressure (COPD, asthma, mechanical ventilation) can weaken diaphragm
-Nicotine weakens muscle and diaphragm

71
Q

Potential symptoms of hiatal hernia

A

-often asymptomatic on its own, clinical manifestations reflect damage and inflammation of the esophagus and stomach due to acid reflux
-heartburn
-regurgitation
-dysphagia
-chronic cough

72
Q

Two types of hiatal hernia

A
  1. Sliding hiatal hernia
  2. Paraesophageal hiatal hernia
73
Q

Sliding hiatal hernia

A

-most common type
-gastroesophageal junction and portion of the stomach slide up into the chest through the esophageal hiatus
-gastroesophageal junction moves up and down within the chest with respiration and swallowing

74
Q

Paraesophageal hiatal hernia

A

-Less common, more severe
-portion of stomach pushes though the esophageal hiatus next to the esophagus and stays in the chest cavity
-in severe cases the herniated stomach can twist upon itself and cut off its blood supply leading to a medical emergency =gastric Volvulus

75
Q

Gastric volvulus

A

When the stomach twists upon itself and cuts off blood supply

76
Q

Gastroesophageal Reflux Disease (GERD)

A

-chronic regurgitation of stomach contents through the lower esophageal sphincter (LES) into the esophagus

77
Q

GERD and reflux esophagitis

A

-Repeated exposure to acid and enzymes irritates the esophageal mucosa and causes reflux esophagitis

78
Q

GERD causes

A

-reflux esophagitis
-relatively common, 1 in 6 Canadians

79
Q

GERD caused by

A

Weakening of LES

80
Q

GERD risk factors

A

-Hiatal hernia (protrusion of stomach through diaphragm) weaker LES
-Obesity increased pressure on stomach, weakens LES
-Pregnancy, hormonal changes during pregnancy relax LES
-Smoking (nicotine) weakens LES and increases stomach acid production
-Alcohol and caffeine consumption relaxes LED and increased stomach acid production

81
Q

General Pathogenesis and Complications of GERD

A

-Some condition weakens LES —> Stomach contents reflux into esophagus —> refluxuate irritates and erodes esophageal mucosa —> esophageal inflammation (reflux esophagitis)—> esophageal fibrosis = esophageal obstruction AND esophageal mucosal dysplasia —> Barrett esophagus = esophageal cancer

82
Q

Barret Esophagus

A

Esophageal mucosal dysplasia which can lead to precancerous Barrett esophagus
-approx 15% of Canadians with GERD develop Barrett esophagus
-primary risk factor for esophageal cancer

83
Q

Clinical Manifestations of GERD

A

-heartburn (most common)
-regurgitation
-dysphagia
-n/v
-chronic cough d/t refluxate damage to the larynx

84
Q

Heart burn

A

-burning sensation in chest that often occurs after eating or lying down
-pain can be severe and be mistaken for heart attack

85
Q

Pyloric obstruction

A

-Condition in which the opening between the stomach and small intestine (pylorus) becomes narrowed or blocked
-Can be congenital (infantile hypertrophic pyloric stenosis) more cases are acquired
-Thickened pyloric muscle narrows the pyloric canal making it difficult for food to pass through from the stomach to small intestine

86
Q

Causes of Pyloric Obstruction

A

-Congenital
-Duodenal ulcers
-Gastric ulcers
-Tumors

87
Q

Gastric ulcers/ duodenal ulcers and pyloric obstruction

A

-main cause of acquired pyloric obstruction are peptic ulcers (both)
-Tissue damage and chronic inflammation leads to scarring and thickening of the pylorus
-duodenal ulcers more likely to cause obstruction than gastric ulcers

88
Q

Potential symptoms of pyloric obstruction

A

-Nausea and vomiting (stomach becomes distended with food)
-sometimes projectile vomiting
-dehydration
-hypochloremic alkalosis (d/t prolonged vomiting) and prolonged obstruction causing stomach to secrete more acid further exacerbating metabolic alkalosis (also increased risk for gastric ulcers d/t this)
-Weight loss

89
Q

Intestinal Obstruction

A

-Occurs when intestinal blockage partially or completely interrupts flow of intestinal contents
-Small bowel more common than large bowel obstruction because of its narrower lumen

90
Q

2 types of intestinal obstruction

A

Mechanical, functional

91
Q

Mechanical Intestinal Obstruction

A

-Occurs when there is a physical blockage of the intestines
-More common

92
Q

Functional Intestinal obstruction

A

-Occurs when intestinal muscles are unable to move contents through the digestive tract
-Eg. paralytic ileus caused by decreased or complete absence of intestinal motility

93
Q

Causes of Mechanical Obstruction (SBO)

A

-Adhesions
-Hernia
-Intussusception
-Crohn Disease

94
Q

Main Causes of Mechanical Obstruction (LBO)

A

-Tumour
-Volvulus
-Diverticular Disease
-Ulcerative Colitis

95
Q

Adhesions

A

-SBO
-bands of scar tissue that form between intestinal loops often because of prior abdominal surgery
-leading cause of small bowel obstruction

96
Q

Hernia

A

-SBO
-protrusion of small intestine through a weak spot in the abdominal wall or inguinal ring

97
Q

Tumour

A

-LBO
-eg. Colorectal cancer
-Leading cause of large bowel obstruction

98
Q

Intussusception

A

-SBO
-When one part of the small intestine telescopes into another part causing a blockage

99
Q

Volvulus

A

-LBO
-occurs when a portion of the small or large intestine twists around itself causing a blockage

100
Q

Diverticular Disease

A

LBO
-inflammation or infection of small pouches called diverticula in large intestine wall can cause blockage

101
Q

Crohn’a disease/ulcerative colitis

A

-aka Inflammatory bowel disease
-crohns = SBO, ulcerative colitis = LBO
-can cause inflammation and narrowing of the intestine

102
Q

Pathogenesis of mechanical obstruction

A

Intestinal obstruction —> air and gas —> intestinal distension proximal to obstruction —> intestinal perforation/peritoneal transudation—> bacterial migration —> peritonitis and sepsis ALSO intestinal distension proximal to obstruction —> loss of intestinal absorption —> intestinal fluid sequestration —> fluid and electrolyte imbalance

103
Q

General Pathogenesis and complications other format

A
  1. Intestinal lumen becomes obstructed
  2. Proximal (above) the obstruction the intestinal contents accumulate, distal to the blockage the intestine compresses as its contents pass towards the anus
  3. Swallowed air and gas from bacteria fermentation can accumulate adding to bowel distension
  4. As the bowel distends, normal absorptive function is lost and fluid is sequestered into the bowel lumen which can cause fluid and electrolyte imbalance
  5. There may also be transudative loss of fluid from the intestinal lumen into the peritoneal cavity
  6. Gut bacteria may also pass into the into the peritoneal cavity during the transudative process which can lead to peritonitis and sepsis
  7. Obstruction eventually may lead to strangulation, gangrene and perforation of bowel, peritonitis and sepsis
104
Q

Potential symptoms of mechanical obstruction

A

-Severe colicky pain
-Absolute constipation
-Abdominal distension
-Nausea and vomiting (SBO)

105
Q

Potential consequences of mechanical obstruction

A

-Fluid and electrolyte losses
-Hypovolemic shock
-Alkalosis (SBO)/ Acidosis (LBO)
-Intestinal necrosis and perforation
-Peritonitis and sepsis

106
Q

Metabolic alkalosis more like associated with..

A

Small bowel obstruction d/t copious vomiting

107
Q

Metabolic acidosis more likely associated with …

A

-large bowel obstruction d/t failure to reabsorb HCO3

108
Q

Integrity disorders

A

-Any breakdown in the guts wall structure may lead to altered GI tract integrity
-Infectious, inflammatory and erosive disorders are the root of most examples of altered GI tract integrity

109
Q

Examples of altered GI tract integrity and one outlier

A
  1. Gastritis
  2. Peptic ulcer disease
  3. inflammatory bowel disease
  4. Inflammatory bowel syndrome (not actually integrity, but is motility disorder and not associated with inflammation)
  5. Diverticular disease
  6. Appendicitis
110
Q

Integrity disorders: Gastritis

A

-Inflammation of the stomachs lining due to breakdown of the mucosal barrier
-mucosal barrier protects the stomach from injury by hydrochloric acid (HCL) and digestive enzymes found in gastric juice = d/t thick layer of mucus secreted onto its surface

111
Q

Causes of Gastritis

A

-H.pylori infection
-NSAID overuse (irritate gastric mucosa and reduce mucus secretion by inhibiting prostaglandin synthesis)
-Alcohol, smoking, drugs (such as cocaine damage mucosa)
-Acute stress (causes release of certain hormones such as cortisol which can reduce blood flow to stomach and increase acid production)
-Immune dysfunction (immune system may attack and damage gastric mucosa eg. Gastritis more common in people with hashimoto disease and type 1 diabetes)

112
Q

Gastritis complications

A

-Regardless of cause, mucosal damage to stomach leads to inflammation which results in
-abdominal pain
-anorexia
- nausea and vomiting

113
Q

Gastritis complications

A

-If left untreated
-gastric ulcers
-GI bleeding
-stomach cancer

114
Q

Helicobacter Pylori Infection

A

-Infection of the stomach and is most common cause of gastritis
-In Canada 8 to 10 million people are infected, people with Type O blood @ greater risk
-Bacteria secretes enzymes and toxins that break down stomachs mucus barrier allowing HCL to damage the gastric mucosa

115
Q

Type O blood and H pylori

A

-May be at further risk because they exhibit enhanced mucosal binding of the bacteria and increased inflammatory response both of which cause more mucosal damage

116
Q

Diseases associated with h pylori

A

Gastritis
Peptic ulcers
Stomach cancer (WHO considers it a carcinogen d/t increased risk of gastric cancer)

117
Q

Integrity Disorders: Peptic Ulcers

A

-Circumscribed area of mucosal inflammation and ulceration of the esophagus, stomach, or duodenum
-Like gastritis, develops when the mucosal barrier is eroded
-can be single or multiple, acute or chronic, deep or superficial

118
Q

Causes/Etiology of Peptic ulcers

A

-Similar etiology as gastritis
-H. Pylori (usual cause)
-NSAID overuse (usual cause)
-alcohol use, smoking, certain drugs
-stress
-advanced age
-chronic disease

119
Q

Peptic Ulcers: Erosions

A

Superficial ulcers of the gastric mucosa that do not extend into the submucosa

120
Q

Peptic Ulcers: True ulcers

A

-Extend into the submucosa, damage blood vessels, cause bleeding and may even perforate the GI wall leading to peritonitis and sepsis

121
Q

Gastric vs Duodenal Ulcers: Location

A

Gastric: Stomach
Duodenal: Duodenum

122
Q

Gastric Vs Duodenal Ulcers: Prevalence

A

Gastric: less common
Duodenal: More common (because does not have mucus barrier = easy for h. Pylori and acid erosion

123
Q

Gastric vs Duodenal Ulcers : Cause

A

Gastric: more likely d/t NSAID overuse
Duodenal: more likely d/t h. Pylori infection (duodenum doesn’t have mucus barrier, straight shot for h. Pylori)

124
Q

Gastric vs Duodenal Ulcers: Mechanism

A

Gastric: Gastritis
Duodenal: Mucosal damage from stomach acid (duodenal damage is result of increased acid secretion and emptying of stomach but gastric damage not usually associated with increased acid secretion)

125
Q

Gastric vs Duodenal Ulcers: Pain

A

Gastric: Higher in abdomen
Duodenal: Lower in abdomen

126
Q

Gastric vs Duodenal Ulcers: Timing of pain

A

Gastric: tends to occur when stomach is full/after eating
Duodenal: Tends to occur when stomach is empty typically between meals and at night (when stomach full gastric juices not entering duodenum, busy with food in stomach) = may be relieved by eating or drinking which dilutes or buffers acid in duodenum

127
Q

Gastric Vs Duodenal Ulcers: Progression

A

Gastric: Usually heal slowly and are chronic
Duodenal: Tend to heal spontaneously and exhibit a pattern of exacerbation-remission

128
Q

Gastric vs Duodenal Ulcers: Complications

A

-both can lead to bleeding or perforation
-Gastric: more likely to bleed and are associated with a higher risk of developing stomach cancer than duodenal
-Duodenal: More likely to cause obstruction and intestinal perforation

129
Q

Stress Ulcers

A

-An acute form of peptic ulcer associated with severe illness or trauma (NOT caused by stress)

130
Q

Types of Stress Ulcers

A

-Ischemic ulcers
-Curling Ulcers
-Cushing ulcers

131
Q

Stress Ulcers: Ischemic

A

-Can be caused by any disorder that significantly reduces GI tract blood supply

132
Q

Stress ulcers: Curling ulcers

A

-Develops because of burn injuries, reduced plasma volume leads to ischemia and necrosis of gastric mucosa

133
Q

Stress Ulcers: Cushing

A

-associated with brain trauma, caused by increased gastric acid secretion resulting from brain stem compression and vagal nerve overstimulation

134
Q

Inflammatory Bowel Disease (IBD)

A

-Designates two related inflammatory intestinal disorders: ulcerative colitis (UC), Crohn’s disease (CD)
-Canadians have highest incidence in the world (Manitoba the worst)

135
Q

IBD etiology

A

-probably multifactoral
-environmental
-infectious agent
-autoimmune predisposition
-environmental factors and infection agents may damage the mucosal barrier and illicit an autoimmune response against an individuals own intestinal mucosa

136
Q

IBD: UC and CD common/shared Pathogenesis

A

-Produce bowel inflammation
-Involve abnormal immune response to intestinal cells
-Are characterized by remissions and exacerbations of diarrhea, fecal urgency, and weight loss
-Are associated with increased risk for intestinal obstruction and colon cancer

137
Q

Ulcerative Colitis

A

-A chronic relapsing bowel disease characterized by inflammation and ulceration of the colonic mucosa

138
Q

Ulcerative colitis etiology/cause

A

-complex and multifactoral
-Genetics
-Environmental (diet, infection, NSAIDs)
-altered immune response to intestinal microflora may play a role in the development of UC

139
Q

Ulcerative Colitis: Pathogenesis

A

-Immune “confusion” —> inflammation —> ulceration
-UC centres on an inappropriate immune response against gut microbes in genetically susceptible pts
-intestinal immune system becomes overly active causing immune cells to attack harmless gut bacteria and mucosal cells = results in release of inflammatory cytokines and recruitment of immune cells to the colonic mucosa leading to chronic inflammation
-over time inflammation leads to the characteristic features of UC including mucosal ulcerations, drivability and crypt abscesses

140
Q

Ulcerative colitis: manifestations

A

-Depend on severity
-Mild UC involves less muscosa do frequency of BM, bleeding and pain is minimal
-Severe UC involves more mucosa and is characterized by pain, fever, elevated pulse, frequent diarrhea, and bloody stools
-dehydration, weight loss and anemia may occur

141
Q

Ulcerative Colitis: Complications

A

-related to chronic nature of inflammatory disease
-scarring can causes narrowing of colon (stricture) and obstruction of
-severe inflammation can extent deeper into colonic wall leading to perforations, abscesses, fistulas
-long term inflammation also increases risk for colorectal cancer
-chronic inflammation and immune system direction can also result in systemic effects affecting joints skin and eyes

142
Q

Crohns Disease

A

-Chronic relapsing bowel disease characterized by submucosa inflammation and granuloma formation (beginning in colons submucosa)

143
Q

Crohn’s disease: etiology/cause

A

-same as UC
-genetic predisposition, environmental factors, and altered immune response

144
Q

Crohn’s disease: Pathogenesis

A

-Like UC
-abnormal immune response in gut
-immune system mistakenly identifies harmless gut bacteria triggers an immune response that breads to chronic inflammation
-unlike UC inflammation begins in the submucosa and spreads with discontinuous transmural involvement (skip lesioning)
-over time inflammation leads to characterized features of UC includinging submucosa granulomas and cobble stone appearance of mucosa

145
Q

Crohn’s disease manifestations

A

-depends on severity and location
-often no symptoms early in disease
-abdominal pain, fever, diarrhea common
-occasionally bloody diarrhea
-reduced nutrient absorption occurs if the ileum is affected which can lead to weight loss, malnutrition, and vitamin deficiency
-nutritional diarrhea is most common symptom

146
Q

Crohn’s disease complications

A

-like UC
-strictures, obstructions, fistulas, and increased risk for colorectal cancer
-given transmural nature of CD, perforations are more common
-may also be associated with extra intestinal complications of joints skin and eyes

147
Q

UC vs CD: Cause

A

-UC: family history less common, smoking decreases disease severity
-CD: Family history more common, smoking increases disease severity and risk

148
Q

UC vs CD: Location of inflammation

A

UC: rectum and distal colon (descending) usually
CD: ileum and proximal (ascending) colon usually but can affect any part Of GI from mouth to anus

149
Q

UC vs CD: Pattern of inflammation

A

UC: continuous and affects uniform areas typically starting at rectum and extending proximal in a continuous fashion
CD: skip lesions, patchy with healthy tissue between affected areas

150
Q

UC vs CD: Depth of inflammation

A

UC: usually limited to mucosa
CD: usually below mucosa, can be transmural (involve entire thickness of intestinal wall)

151
Q

UC vs CD: Microscopic features

A

UC: mucosal ulcerations, friable appearance of mucosa, diffuse inflammation and ulceration of colonic mucosa with crypt abscesses and crypt distortion
CD: submucosal granulomas, cobblestone appearance to mucosa, skip lesions, transmural inflammation

152
Q

UC vs CD: Manifestations

A

UC: bloody diarrhea more common, malabsorption less common
CD: bloody diarrhea less common, malabsorption more common, weight loss/malnutrition and vitamin deficiency more common

153
Q

Inflammatory bowel syndrome

A

-Functional disorder of colonic smooth muscle (effects colon contractions causing abdominal issues)
-Unlike IBD no structural changes like inflammation or damage to GI mucosal lining ( NOT an integrity disorder)
-more of a motility disorder

154
Q

IBS potential causes

A

-exact cause unknown
-stress, diet, and genetics may place role

155
Q

IBS manifestations

A

-pain
-gas and bloating
-constipation or diarrhea

156
Q

Diverticular Disease

A

-Condition that occurs when small pouches (diverticula) form in the outer wall of the colon
-Pouches vary in size and number

157
Q

Diverticulosis vs Diverticulitis

A

Diverticulosis: Diverticula with no associated manifestations
Diverticulitis: infected or inflamed diverticula
-Diverticula are often found in older adults and are usually asymptomatic (diverticulosis)

158
Q

Diverticulitis manifestations

A

-abdominal pain, bloating, constipation, diarrhea, rectal bleeding

159
Q

Diverticular disease risk factors

A

-older age, obesity, smoking, poor diet, lack of physical activity, medication use (aspirin and nsaids)

160
Q

Diverticula and polys

A

NOT THE SAME
-polyps is an abnormal tissue growth that protrudes from the mucous membrane lining of a hallow organ into its lumen
-polyps are often discovered during colonoscopies of other diagnostic procedures
-most polyps are benign but some can be precancerous or cancerous

161
Q

Appendicitis

A

-most common surgical emergency of the abdomen

162
Q

Appendicitis Pathogenesis

A

-lumen obstruction —> increased lumen pressure —> inflammation —> ischemia —> perforation/peritonitis/sepsis (complications)

163
Q

Pancreatic insufficiency

A

-causes malabsorption associated with insufficient amounts of enzymes that digest protein, carbohydrates, and fats into components that can be absorbed by the intestine

164
Q

Deficient lactase productions

A

In the brush border of the small intestine inhibits breakdown of lactose which prevents lactose absorption and causes osmotic diarrhea

165
Q

Bile salt deficiency

A

Causes fat malabsorption including fat soluble vitamins, steatorrhea
-can result from inadequate secretion of bile, excessive bacterial deconjugation of bile or impaired reabsorption of bile salts caused by ileal disease

166
Q

Upper GI bleed causes

A

-peptic ulcer disease
-erosive gastritis/esophagitis
-esophageal varices

167
Q

Lower GI bleed causes

A

-Diverticulosis
-Ischemic/infectious colitis
-inflammatory bowel disease
-hemorrhoids

Patho 2 (1 decks)

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