Gastrointestinal System Flashcards

(181 cards)

1
Q

What does the Gastrointestinal system do?

A

*Consumes food
*digests food to absorb nutrients
*eliminates waste

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2
Q

Organs and area in the body included in the GI system

A

Upper division: Oral cavity
Pharynx
esophagus
stomach

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3
Q

The Upper GI system

A

Begins process of digestion, including mechanical breakdown and starting chemical digestion (especially mouth and stomach)

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4
Q

Lower division consists of?

A

Small intestine
large intestine (colon)
rectum
anus

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5
Q

what does the lower part of the GI tract do

A

Ends digestion
Absorbs nutrients and water
Forms feces for elimination

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6
Q

Hepatobillary system

A

hepato = liver
billiard = bile system
Liver
gallbladder
pancreas

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7
Q

Four layers in the GI system

A

Mucosa
submucosa
muscle
serosa

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8
Q

Mesentery

A

meso= middle
entery = intestine
Double layer peritoneum containing blood vessels and nerves that supplies the intestinal wall

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9
Q

Peritoneum

A

Large serous membrane that lines the abdominal cavity

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10
Q

parietal peritoneum

A

Outer layer

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11
Q

Visceral peritoneum

A

Inner layer

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12
Q

Peritoneal cavity

A

space between the two layers

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13
Q

Hepatobiliary system consists of what type of organs

A

liver
gallbladder
pancreas

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14
Q

what is the meaning of Vomiting

A

Involuntary or voluntary forceful ejection of chyme from the stomach up through esophagus and out the mouth

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15
Q

Causes of vomiting

A

Protection
reverse peristalsis (goes wrong way, waves push it back up)
Increased intracranial pressure (Pressure inside the skull is higher than normal)
severe pain

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16
Q

Recurrent vomiting can be

A

exhausting and lead to fluid, electrolyte, and pH imbalances

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17
Q

Aspiration can cause

A

serious damage and inflammation and can occur when supine, unconscious, or vomiting or cough reflex is suppressed

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18
Q

Variable colors and consistency of stool

A

Decriptions can aid in the cause and interventions
COCA

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19
Q

Hematemisis

A

*Blood in vomit
Looks like coffee grounds
From protein in the blood being broken down/ partialy digested
Occur in upper GI bleeding- like ulcers

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20
Q

Hematemesis characteristics

A

**Color:Bright red
-Actively bleeding (esophageal varices, Mallory- Weiss Tear, or Severe ulcer
Dark Red (coffee grounds)
-Blood digested/ stomach acid
-Slower/ older bleed
Apperarance:
-Liquid blood
-Clots present
-Coffee ground look
Symptoms:
-Dizziness
-Weakness
-Hypotension
-Tachycardia
-Pallor
-Possible melena (black, tarry stools)

Pallor: pale flushed skin from low hemoglobin

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21
Q

GERD (Gastroesophageal Reflux Disease)

A

Acidic contents of stomach reflux into the esophagus

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22
Q

Gastric secretions can

A

irritate the esophageal mucosa and over time metaplasia occurs as a results

Metaplasia: normal cells get annoyed –> body swaps out for tougher type

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23
Q

causes of GERD

A

certain food
alcohol consumption
nicotine
hernia
obesity
pregnancy
certain meds
delayed gastric emptying

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24
Q

cues of GERD

A

heartburn
epigastric pain
dysphasia (Difficulty swallowing)
dry cough
laryngitis (Inflammation of voice box)
pharyngitis (Inflammation of throat)
regurgitation of food
feeling like lump in throat

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25
Complications of GERD
**higher risk of cancer Esophagitis (Inflammation of Esophagus) Strictures (Abnormal narrowing of tube in body) Ulcerations (Open sores/ eroded away) Esophageal cancer chronic pulmonary disease
26
Dysphagia
*difficulty swallowing Infections or inflammation changes in the oral cavity Esophageal Atresia (A= w/o & tresia = opening) (Defect of the esophagus ends in a pouch instead of stomach) Esophageal stenosis (steno= narrow) (Narrowing of the esophagus) or structure. Esophageal diverticulosis (Pouch like outpouching forms in the wall of the esophagus) tumors stroke cerebral damage (brain damage)
27
Causes of dysphagia
Infections or inflammation changes in the oral cavity Congenital Esophageal Atresia, Esophageal stenosis or structure. Esophageal diverticula tumors stroke cerebral damage achalasia (lower esophageal sphincter fails to relax) Parkinsons disease Alzheimers disease muscular dystrophy (progressive muscle weakness & muscle wasting) Huntingtons disease (Neurodegenerative disorder that affects movement, cognition, behavior) cerebral palsy (permanent movement and posture disorders caused by nonprogressive brain injury or abnormal brain development that occurs before, during, or shortly after birth) multiple sclerosis (chronic autoimmune disease where the immune system attacks the myelin sheath in the central nervous system (brain and spinal cord). amyotrophic lateral sclerosis ( progressive neurodegenerative disease that destroys motor neurons in the brain and spinal cord.) Guillian-Barre syndrome (acute autoimmune disorder where the immune system attacks the peripheral nerves, causing rapid muscle weakness and paralysis)
28
Cues of dysphagia
a sensation of food being stuck in the front of the throat choking coughing pocketing food in cheeks difficulty forming a food bolus delayed swallowing odynophagia
29
Odnophagia
Painful swallowing causes and cues: can be similar to dysphagia
30
Gastritis
Inflammation of the stomach mucosal lining (the stomach or a region)
31
What are acute gastritis symptoms?
Can be mild transient irration or severe ulceration with hemmorhage Develops sudden nausea abdominal pain vomiting hiccups hematemesis
32
Chronic gastritis
Develops gradually Erosive or nonerosive May be asymptomatic but usually accompanied by a dyspepsia (dull epigastric pain with nausea and heartburn) A sensation of fullness after minimal intake Nausea or vomiting Increase risk for peptic ulcers gastric cancer anemia Hemorrhage
33
Helicobacter pylori
(H. Pylori) Most common cause of chronic gastritis Embeds in the mucous layer Activating toxins and enzymes that cause inflammation Genetic vulnerability and lifestyle behaviors may increase the susceptibility
34
Indication of ulceration and bleeding
Hematemesis and dark tarry stool
35
Peptic ulcer disease
Lesions affecting the lining of the stomach (gastric) or duodenum (duodenal)
36
Gastric ulcer
uncommon, but more serious with NSAID use and malignancy pain is **Worse with eating**
37
Duodenum ulcer
associated with excessive acid or helicobacter pylori infections. Epigastric pain that is relieved in the presence of food
38
Stress ulcer
major physiological stressor on the body (large burns, trauma, sepsis, surgery, or head injury)
39
Cues of Peptic ulcer disease
Epigastric or abd. pain Abd. cramping Heartburn indigestion nausea vomiting hematemesis melena unexplained weight loss fatigue
40
Cholelithiasis (Gallstones)
Common condition that affects both genders and all ethnic groups relatively equally
41
Risk factors of Gallstones
Age obesity Diet rapid weight loss pregnancy hormone replacement long term parental nutrition
42
Calculi
May very in size and shape
43
Cholecysitis
Inflammation or infection in the biliary system cause by calculi Varies in severity depending on the size and shape
44
If cholecystitis obstructs the bile flow
can cause gallbladder rupture fistula formation gangrene hepatitis pancreatitis carcinoma
45
Cue of Gallstones
Biliary colic abd. distention nausea vomiting jaundice fever leukocytosis
46
Disorders of liver
Hepatitis Cirrhois Portal hypertension Ascites Hepatic encephalopathy Esophageal varices
47
Function of Liver
Bile secretion Bilirubin metabolism Blood storage clotting factor synthesis Nutrient metabolism metabolic detoxification mineral and vitamin storage
48
Acute hepatitis
Proceds though three phases Prodromal Icteric recovery phase
49
Prodromal
Period of fatigue (something doesn't feel right) anorexia malaise headache low grade fever Lasts 2 weeks
50
lcteric
2 weeks after exposure to the virus and lasts up to 6 weeks
51
Cues of Icteric phase
Onset of jaundice bilirubinuria or clay color stools Hepatomegaly right upper quad. pain
52
recovery phase
resolution of jaundice 8 weeks after exposure liver may still be enlarged for another 1-4 weeks
53
Chronic hepatitis
Continued hepatic disease lasting longer than 6 months Symptom severity and disease progression may vary depending on degree of liver damage Deteriorate with widespread hepatocyte necrosis Fibrosis Diffuse scarring Cirrhosis Increased risk for hepatocellular carcinoma
54
Hepatitis
Inflammation of the liver
55
causes hepatitis
infection (usually viral) contagious Usually recover with time and no damage Age and comorbidities increase risk of liver failure cancer or cirrhosis
56
Non-infectious Hepatitis
alcohol meds (Tylenol, antiseizure meds, and antibiotics) or autoimmune disease (SLE, RA) Usually recover, may develop liver failure cancer or cirrhosis Not contagious can be acute or chronic, active or non active
57
Hep A
Fecal- oral from another infected person: contaminated food and water supplies 1-2 months No carrier state No chronic Yes vaccine DX: Blood detection of anti-HAV
58
Hep B
contact from blood or body fluids from woman to fetus Antigen forms - been there before 2-3 months Yes carrier state Yes chronic Yes vaccine DX: blood detection of Hep B surface antigen (HBsAg)
59
Hep C
excessive tattoos, needle use Contact with infected blood 2-3 months Yes carrier state Yes chronic No vaccine DX: blood detection of anti-HCV
60
Hep D
infected blood and bodily fluids woman to fetus must have surface antigen B present (HBsAg) to be infected 2-3 months Yes carrier Yes chronic No vaccine DX: Blood detection of anti-HDV
61
Hep E
Fecal-Oral from another infected person 1-2 months No carrier No chronic No vaccine DX: Blood detection of anti-HEV
62
Cirrhosis
Chronic, progressive, irreversible, diffuse damage to hepatocytes resulting in Cellular death of the liver and damage Can develop still after the removal of the underlying cause
63
Causes of Cirrhosis
Hepatitis All the factors that lead to hepatitis
64
Most frequent diseases from cirrhosis
can develop hep c and chronic alcohol abuse | most frequent causes of cirrhosis in the U.S.
65
Cues of cirrhois
* Portal hypertension * varicosities of the abdomen and esophagus * enlargement of nearby organs * Bleeding, slow or severe, in the esophagus * Ascites * Jaundice Intolerence to fat and fat soluble vitamin deficiency Clay-colored stools Bilirubinuria (dark urine) Intense itching
66
Ascites
Most common in cirrhosis fluid accumulates within the paratineal cavity Portal Hypertension Elevated pressure in the liver Leads to increase in hydrostatic and osmotic pressure Increased capillary permeability and fluid movement into the interstitial space
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Pancreatisis
Inflammation of the pancreas acute or chronic
68
Pancreatic injury
causes pancreatic enzymes to leak into the pancreatic tissue and initiate auto digestion resulting in edema vascular damage hemorrhage necrosis
69
Pancreatic tissue is replaced by
Fibrosis causing exocrine and endocrine changes and dysfunction of the islets of Langerhans
70
Acute pancreatitis
Considered a medical emergency mortality increases with age and comorbidity
71
Common cause acute pancreatisis
Obstructing cholelithiasis (gallstone)
72
Cues of acute pancreatisis
Sudden and severe Sudden upper abdominal pain that radiates to the back nausea vomiting anorexia diarrhea Mild jaundice Elevated amylase and lipase
73
Chronic pancreatitis
Leads to irreversible cellular and tissue changes Impact exocrine and endocrine function of the pancreas Most common cause is chronic alcohol abuse
74
Cues of Chronic pancreatitis
Severe intermittent episodes of upper abd. pain radiating to back diarrhea steatorrhea (fatty stool) weight loss
75
Diarrhea
Change in bowel pattern characterized by an increased frequency, amount, and water content of the stool
76
results from diarrhea
Increased fluid secretion decreased fluid absorption alteration in GI peristalsis
77
Acute diarrhea
Often caused by viral or bacterial infections ( C. diff) or certain meds (antibiotics, antacids, laxatives) Self limiting Infectious most likely viral Cramps Fever chills nausea vomiting blood/ pus/ mucous hyperactive bowel sounds fluid and electrolyte imbalances
78
Chronic diarrhea
Last longer then 4 weeks
79
Causes of chronic diarrhea
Inflammatory bowel diseases malabsorption syndromes endocrine disorders chemotherapy and radiation
80
Diarrhea originating in the small intestine
Stools are large, loose, and provoked by eating Usually accompanied by pain in the right lower quad.
81
Diarrhea in the large intestine
Stools are small and frequent Freq. accompanied by pain and cramping in the left lower quad.
82
Constipation
Change in the bowel pattern characterized by infrequent passage of stool in reference to the individuals typical bowel pattern
83
Stool remains in the _____ while constipated
Large intestine longer then usual Increasing the amount of water removed
84
Causes of constipation
Low-fiber diet Not a lot of physical activity insufficient fluid intake delaying the urge to defecate laxative abuse stress travel bowel diseases certain medications mental health problems neurologic diseases colon cancer
85
Common constipation
Children who are toilet training Lead to functional fecal incont. Repetitive voluntary or involuntary passage of stool in inappropriate places in children 4 or older
86
Cues of constipation
Pain during the passage of bowel movement inability to pass stool after straining or pushing for more than 10 min no bowel movement for more then 3 days hypoactive bowel sounds
87
Complications of constipation
anal bleeding anal fissure pH disturbances Hemorrhoids diverticulitis impaction intestinal obstruction fistula
88
Intestinal obstruction
Blockage of intestinal contents in the small intestine or large intestine
89
Mechanical obstructions of Intestinal obstruction
Foreign bodies tumors adhesions hernias intussusception volvulus strictures Crohns disease diverticulitis fecal impaction
90
Functional obstructions of Intestinal obstruction
Neurologic impairment intra-abdominal surgery complications chemical, electrolyte, and mineral disturbances intra-abdominal infections abd. blood supply impairment renal and lung disease Use certain meds.
91
Intestinal blood flow for obstruction
Become impaired, leading to ischemia and necrosis
92
Intestinal contents of obstruction
can seep into the abd. as the pressure increases
93
Complications of obstruction
Perforation pH imbalances Fluid disturbances shock death
94
Cues of obstruction
abd. distention abd. cramping colicky pain nausea vomiting constipation diarrhea steatorrhea decreased or absent bowel sounds restlessness diaphoresis tachycardia progressing to weakness confusion shock
95
Appendicitis
Inflammation of the appendix Caused by infection from trapped fecal material
96
Appendicitis triggers
local tissue edema obstructing the appendix
97
Fluid builds from appendicitis
Inside the appendix microorganisms proliferate (multiply)
98
The appendix fills with
Purulent exudate Area blood vessels become compressed Ischemia and necrosis develop
99
Pressure inside the appendix
Escalates, forcing bacteria and toxins out to surrounding structures
100
Complications of appendicitis
Abscesses Peritonitis gangrene death
101
Cues of appendicitis
Sharp right lower abd. pain towards the umbilicus gradually intensifies (12-24 hours) Rebound tenderness Pain may occur anywhere in abd. Pain will temporarily subside if the appendix ruptures, then pain will return and escalate Nausea vomiting abd. distention occasional diarrhea
102
Peritonitis
Inflammation of the peritoneum (lining of the abd.)
103
Causes of Peritonitis
Chemical irritation (ruptured gallbladder) direct organism invasion (appendicitis) Bacteria escape into the peritoneal cavity, triggering inflammation, infection and septic shock
104
Peritonitis cues
Sudden and severe Large volumes of fluid leak into the peritoneal cavity Nausea and vomiting Decreased peristalsis Intestinal obstruction Indicators of infection (fever, malaise, leukocytosis) Indications of sepsis and shock (tachycardia, hypotension, restlessness, and diaphoresis)
105
Classical manifestation
Abd. rigidity/ pain Due to inflammation and abd. muscle spasms
106
Celiac disease
Also known as celiac sprue or gluten-sensitive enteropathy Inherited, autoimmune, malabsorption disorder, most common in Caucasian females Primarily a childhood disease, but can develop at any age
107
Celiac disease results from
A combination of the immune response to an environmental factor (gliadin) and genetic predisposition Defect in the intestinal enzymes that prevent digestion of gliadin (product of gluten digestion) Intestinal villi atrophy and flatten, decreased enzyme production, less surface area for absorption
108
Complications of celiac disease
Anemia arthralgia myalgia bone disease dental enamel defects and discoloration intestinal cancers depression growth and development delays in children hair loss hypoglycemia mouth ulcers increased bleeding tendencies neurologic disorders skin disorders vitamin or mineral deficiency endocrine disorders
109
Cues of Celiac disease
Abd. pain Abd. distension bloating gas indigestion constipation diarrhea changes in appetite lactose intolerance nausea vomiting steatorrhea unexplained weight loss irritability lethargy malaise behavioral changes
110
Crohns disease
Chronic inflammation autoimmune condition (genetic and environmental factors)
111
Crohns Disease characterized
Patchy areas of inflammation (skip lesions) involving the full thickness of the intestinal wall and can lead to ulceration, fistula, and abscesses
112
The entire wall of crohns
Becomes thick and rigid, granulomas develop, and the intestinal lumen becomes narrowed and potentially obstructed
113
The damaged intestinal wall of Crohns
Loses the ability to digest and absorb
114
Cues of Crohns
Abd. cramping and pain (RLQ), diarrhea, steatorrhea, constipation, palpable abd. mass, melena, anorexia, weight loss, Indications of inflammation (fever, fatigue, arthralgia, and malaise)
115
Ulcerative colitis
Progressive condition of the large intestinal mucosa
116
What is ulcerative colitis
Chronic autoimmune inflammation triggered by T-cell accumulation in the colon mucosa causes epithelium loss, surface erosion, and ulceration that begins in the rectum and extends to the descending colon
117
The mucosa of Ulcerative colitis
Becomes inflamed, edematous, and friable
118
Necrosis of the epithelial tissue (ulcerative colitis)
can result in abscesses, ulcerations, and hemorrhage
119
Cues of ulcerative colitis
blood diarrhea, watery stool with blood and mucus, abd. pain, nausea, vomiting, weight loss, anemia, fever, and indications of inflammation (fever, fatigue, and malaise)
120
Crohns disease Info compared to ulcerative colitis
Location: small intestine and ascending colon Pattern: Skip lesions Depth: primarily submucosa Diarrhea: watery Abd. Pain: yes Bowel obstruction: common Cancer risk: increased
121
Ulcerative colitis info. compared to Crohns
Location: descending colon Pattern: continuous Depth: primarily mucosa Diarrhea: bloody Abd. Pain: Yes Bowel obstruction: uncommon Cancer risk: Higher risk than with Crohns
122
Diverticular disease (Diverticulosis, Diverticulitis)
Conditions related to the development of diverticula, outwardly bulging pouches of the intestinal wall that occur when mucosa sections of large intestine submucosa layers herniate through a weakened muscular layer
123
Diverticular disease may be
Congenital or acquired
124
Diverticular disease is thought to be caused by
A low-fiber diet and poor bowel habits that result in chronic constipation
125
The muscular wall of Diverticular disease
can become weakened from the prolonged effort of moving hard stools and chronic constipation
126
Manifestations of Diverticular disease
Abd. pain in LLQ, guarding, and rigidity, fever, nausea, vomiting and sudden rectal bleeding
127
Diverticulosis
Asymptomatic diverticular disease, usually with multiple diverticula present
128
Diverticulitis
Diverticula have become inflamed, usually because of retained fecal matter
129
Diverticulitis can results in
Potentially fatal obstructions, infection, abscess, perforation, peritonitis, hemorrhage, and shock Often asymptomatic until the condition becomes serious
130
Info. of Appendicitis
Onset: usually gradual but can be sudden Location: periumbilical early: RLQ late Characteristics: diffuse early, localized late Description: ache Radiation: none Intensity: ++ to +++
131
Info. of Cholecystitis
Onset: Sudden Location: RUQ or MUQ Characteristics: Localized Description: cramping radiation: back or right shoulder Intensity: ++
132
Info. of acute pancreatitis
Onset: sudden Location: epigastric, upper abd. Character: Localized Description: Blunt Radiation: back Intensity: ++ to +++
133
Metaplasia
The reversible change of one mature cell type into another mature cell type.
134
Why does metaplasia occur
To help cells adapt to a persistent stressor or environmental change.
135
Is metaplasia reversible?
Yes, if the stressor is removed, cells can return to their normal type.
136
What happens if the stressor persists?
Cells may develop pathologic or precancerous changes.
137
Example of metaplasia in GERD
Squamous epithelium of the esophagus changes to glandular epithelium.
138
Cause of esophageal metaplasia in GERD
Chronic exposure to stomach acid.
139
Name of esophageal metaplasia in GERD
Barrett’s esophagus.
140
Example of respiratory metaplasia
Columnar cells in bronchial tubes change to squamous cells.
141
Cause of bronchial metaplasia
Chronic exposure to cigarette smoke or toxins.
142
What is squamous metaplasia?
Replacement of normal columnar cells with squamous cells to withstand stress.
143
Risk of long-term metaplasia
Increased risk of dysplasia and cancer if stress continues.
144
Purpose of metaplasia
A protective survival mechanism against chronic irritation.
145
Metaplasia vs dysplasia
Metaplasia is adaptive and reversible; dysplasia is abnormal growth and potentially precancerous.
146
Gastritis
Inflammation of the stomach lining (gastric mucosa) that impairs gastric function.
147
Types of gastritis
Acute and chronic.
148
What structure is affected in gastritis
Gastric mucosa (stomach lining).
149
Primary effect of gastritis
Impaired stomach function and inflammation.
150
Main functions of the stomach
Protection, digestion, and limited absorption.
151
What substances are primarily absorbed in the stomach
Water and alcohol.
152
Protective role of stomach acid
Destroys microorganisms and harmful substances.
153
Stomach acid as a defense mechanism
Acts as the first line of defense against pathogens.
154
What happens during gastric digestion
Food and liquids mix with gastric secretions.
155
Components of gastric secretions
Mucus, acid, enzymes, hormones, and intrinsic factor.
156
Function of mucus in the stomach
Protects the stomach lining from acid damage.
157
Function of gastric acid (HCl)
Breaks down food and kills microorganisms.
158
Function of gastric enzymes
Aid in chemical digestion of food.
159
Intrinsic factor (IF)
Substance necessary for vitamin B12 absorption.
160
Where gastric secretions are produced
Gastric glands.
161
Cells that produce gastric secretions
Specialized epithelial cells lining gastric glands.
162
Why intrinsic factor is important
Prevents vitamin B12 deficiency and pernicious anemia.
163
What happens when gastric mucosa is inflamed
Digestion and protective functions are impaired.
164
165
Acute gastritis
Short-term inflammation of the gastric mucosa.
166
Common causes of acute gastritis
Ingestion of irritants such as aspirin (NSAIDs), alcohol, and microorganisms.
167
Duration of acute gastritis
Occurs suddenly and lasts for a short period.
168
Is acute gastritis reversible?
Yes, if the causative agent is removed.
169
Role of stomach acid in acute gastritis
The role of acid hypersecretion is unclear.
170
Normal environment of gastric mucosa
Functions best in a highly acidic environment.
171
What happens when irritants affect the stomach
Inhibition of protective mucus production.
172
Result of decreased mucus protection
Gastric mucosa becomes vulnerable to acid damage.
173
Inflammatory response in acute gastritis
Ranges from mild redness (erythema) to erosion and perforation.
174
Erythema
Redness caused by inflammation.
175
Cellular damage in acute gastritis
Epithelial cells become necrotic.
176
What happens to underlying tissue
Gastric tissue becomes eroded.
177
Complication of mucosal erosion
Hemorrhage (bleeding).
178
What occurs when acid escapes damaged mucosa
It corrodes nearby gastric tissue.
179
Severe complication of acute gastritis
Gastric perforation.
180
Why hemorrhage occurs in acute gastritis
Damage and erosion of gastric blood vessels.
181
Overall pathophysiology of acute gastritis
Irritant exposure → decreased mucus → acid injury → inflammation, necrosis, and possible bleeding or perforation.