GI Disorders Flashcards
1
Q
Initial phase of mechanical breakdown of food, happens in the
A
Oral Cavity
2
Q
Mastication by teeth
A
Initial phase of the mechanical breakdown of food
3
Q
– Initial chemical digestion (enzyme)
A
• Salivary amylase
– starts chemical breakdown of carbohydrates
4
Q
Pharynx is involved in
A
Swallowing (deglutition)
5
Q
Esophagus
A
Closed except during swallowing, skeletal muscle
at superior end – followed by smooth muscle
6
Q
Can effect airway mgmt
A
Disorders of oral cavity, pharynx or esophagus
7
Q
Stomach
A
Expansible muscular sac – acts as reservoir for food and
fluid
8
Q
The stomach and layers
A
Three smooth muscle layers
9
Q
What do the parietal cells secrete?
A
HCL
IF
10
Q
What do the CHIEF cells secrete?
A
PEPSIN
11
Q
What do the G Cells cells secrete?
A
GASTRIN
12
Q
Role of the Production of intrinsic factor –
A
Essential for the absorption of vitamin B12 in ileum
13
Q
Initial digestion of proteins is accomplished by?
A
By pepsin (formed by pepsinogen + HCl)
14
Q
What is the role of the liver?
A
“Metabolic factory” of the body
15
Q
The liver receives blood from the
A
Receives blood from hepatic portal vein –
16
Q
Transport of nutrients form intestine to liver
A
Hepatic portal vein
17
Q
Hepatocytes store nutrients and what is other role
A
play role in carbohydrate, protein, fat metabolism
18
Q
Other roles of the liver
A
• Production of plasma proteins and clotting
factors
• Breakdown of old/damaged erythrocytes
• Bile production
19
Q
Pancreas: Exocrine
A
• Exocrine pancreas arranged in lobules
20
Q
Pancreas Secretes digestive enzymes, electrolytes –
TCC RPB
A
Trypsin Chymotrypsin Carobodxypeptidase Ribonuclease Pancreatic amylase Bicarbonate ions
21
Q
Pancreatic duct joins
A
bile duct to enter duodenum.
22
Q
Lower Gastrointestinal Tract: Small intestine (DJI)
A
Duodenum, jejunum, ileum
23
Q
Villi and microvill role in the small intestine:
A
Villi (folds of the mucosa) and
microvilli (folds of cell membranes)
24
Q
2 substance that increase surface area for absorption
A
Villi and microvilli
25
Major site for absorption of nutrients
Small intestines
26
Lacteal –What are they?
lymphatic vessels of the small intestine which absorb digested fats.
27
Immune surveillance of materials within your digestive system
Peyer's patches
28
Small intestine production of
• Mucus
• Enterokinase, peptidases, nucleosidases, lipase, sucrase,
maltase, lactase; cholecystokinin (hormone)
29
Lower Gastrointestinal Tract: Large intestine
* Resident normal flora
| * Vitamin K synthesis by bacteria
30
Large intestine responsible for
Fluid and electrolyte reabsorption
| Formation and elimination of solid waste
31
Neural and Hormonal Controls
| Parasympathetic nervous system: Stimulatory or inhibitory
Stimulatory
32
Parasympathetic nervous system: Stimulatory -> Primarily through
vagus cranial nerve
33
Role of Parasympathetic nervous system: Stimulatory through vagus CN
Increase motility
| Increase secretions
34
Sympathetic nervous system Stimulatory or inhibitory
Inhibitory
35
Sympathetic nervous system stimulated by
Fear and anger
36
SNS on GI
Inhibits gastrointestinal activity
37
SNS on GI Vasoconstriction/Vasodilation
Causes vasoconstriction
38
SNS on cells
Reduced secretions & regeneration epithelial cells
39
Neural Controls 2 CN –
• C.N. VII & IX
40
Role of CN VII and IX
Maintain continuous flow of saliva in mouth
41
Distention and stretching of stomach: What happens?
PNS activation – ↑ Peristalsis and gastric secretions
42
When does the stomach empties after a meal?
Stomach empties within 2 to 6 hours after meal.
43
Food in intestine stimulates?
Stimulates intestinal activity
44
What is the role of the Enterogastric reflex ?
Inhibits gastric emptying
45
Hormonal controls: Gastrin
| When is it secreted and what does it increase and promote?
- Secreted by stomach in response to distention
- Increases gastric secretions & motility, relaxes pyloric and ileocecal sphincters –
- Promotes stomach emptying
46
Hormonal controls: Histamine(H2 receptor) role
Increased secretion of hydrochloric acid
47
What is the role of Secretin?
Decreases gastric secretions
48
What is the role of Cholecystokinin (CCK)?
Inhibits gastric emptying; stimulates contraction of gallbladder
49
Digestion and Absorption: Carbohydrates
– Digestion starts in mouth.
| – Followed by digestion in the small intestine
50
Digestion and Absorption: Proteins
Digestion starts in stomach; continues in small intestine
51
Digestion and Absorption: Lipids
| FEA
– Formation of chylomicrons
– Emulsified by bile prior to chemical breakdown
– Action of enzymes forms monoglycerides and free
fatty acids
52
Digestion and Absorption: Fat-soluble vitamins are? Meaning
– Vitamins A, D, E, K ; Absorbed with fats
53
What are the Water-soluble vitamins?
| Meaning
– Vitamins B and C – diffuse into blood
54
Digestion and Absorption: Electrolytes
Absorbed by active transport or diffusion
55
Digestion and Absorption: Drugs are primarily absorbed where? and how about transport mechanism
In the intestine.
– Various transport mechanisms
– Some (i.e., aspirin) absorbed in the stomach
56
Digestion and Absorption
• Water Absorbed primarily by
– Severe vomiting or diarrhea interrupts recycling
mechanism.
• Affects fluid and electrolyte balance of body
osmosis
57
How much water is secreted into the digestive
| tract each day?
700 mL
58
Amount of water ingested in food and fluids?
2300 mL
59
Amount of water leaves the body in feces.
Only 50 to 200 mL
60
What can interrupt recycling mechanism?
Severe vomiting or diarrhea
61
Affects fluid and electrolyte balance of body
Severe vomiting or diarrhea
62
Neuroendocrine cells of G.I. tract type of cells
Enterochromaffin Cells
63
What does the enterochromaffin cells do?
Use tryptophan hydroxylase-1 to synthesize Serotonin (5-HT)
64
Serotonin does what?
Stimulates secretory, peristaltic and vagal reflexes
| via 5-HT3 receptor
65
Role of 5HT3 receptor ?
Important in generating nausea/vomiting
66
What is the mechanism of Ondansetron (Zofran) ? What other herbal is considered like zofran
5-HT 3 receptor antagonist
| • (Ginger)
67
Neuroendocrine cells of G.I. tract
| Just like the Enterochromaffin cells
Enterochromaffin-like cells (ECL)
68
Where are the ECL found?
Only in the stomach wall
69
Does ECL contain 5-HT?
NO
70
ECL responds to
Respond to Gastrin from G-cells
• Release Histamine --> stimulates parietal cells-->
via H2 receptors --> Increase HCl production
71
Action of H2 blockers?
H2 blockers inhibit HCl pathway leading to decrease gastric secretions
72
May be signs of digestive disorders or other
| conditions elsewhere in the body (PUSMEPO)
```
– Pain
– Uremia
– Systemic infection
– Motion sickness
– Emotional responses
– Pressure in the brain
– Overindulgence of food, drugs
```
73
Common manifestations of Digestive System Disorders
Anorexia, Nausea, Vomiting
74
Anorexia and vomiting
| – Can cause serious complications such as (MAD)
• Dehydration, acidosis, malnutrition
75
Anorexia
| – Often precedes
nausea and vomiting
76
– Unpleasant subjective feeling
– Also stimulated by smells, visual images, pain, and
chemical toxins and/or drug
Nausea
77
Nausea is Stimulated by IDI
irritation,distention, inflammation of digestive tract
78
Vomiting :Vomiting center located in the______
medulla
79
Role of vomiting center in the medulla?
* Coordinates activities involved in vomiting
| * Protects airway during vomiting
80
Vomiting Forceful expulsion from stomach
| • Sometimes includes ____
bile from intestine
81
Vomiting Center Activation DSRPV
Distention or irritation in digestive tract
Stimuli from various parts of the brain
Response to unpleasant sights or smells, ischemia
Pain or stress
Vestibular apparatus of inner ear (motion)
82
Vomiting Center activation and Increased ICP
Increased intracranial pressure
| – Sudden projectile vomiting without previous nausea
83
Stimulation of chemoreceptor trigger zone By
drugs, toxins, chemicals
84
Vomiting Reflex Activities : Deep inspiration
* Deep inspiration
* Closing glottis, raising the soft palate
* Ceasing respiration: Minimizes risk of aspiration of vomitus into lungs
85
Vomiting Reflex Activities : Relaxes
• Relaxing the gastroesophageal sphincter
• Contracting the abdominal muscles
– Forces gastric contents upward
• Reverse peristaltic waves
– Promotes expulsion of stomach contents
86
Characteristics of Vomitus
| • Hematemesis
“Coffee grounds” – brown granular material indicates action of HCl on hemoglobin
87
Characteristics of Vomitus– Frank blood –
acute esophageal or gastric Hemorrhage
88
Characteristics of Vomitus– Yellow or green vomitus
– Bile from the duodenum
89
Characteristics of Vomitus: Deeper brown color
| – May indicate
content from lower intestine
90
Recurrent vomiting of undigested food
– Problem with gastric emptying or infection
91
Diarrhea
Excessive frequency of stools – loose or watery consistency
92
Diarrhea May be accompanied by
cramping pain
93
• Prolonged diarrhea may lead to DEMAW
dehydration, electrolyte imbalance,malnutrition, acidosis, weight loss
94
Common Types of Diarrhea
• Large-volume diarrhea (secretory or osmotic)
LOW
– Limited reabsorption due to reversal of normal carriers for sodium and/or glucose
– Often related to infection
– Watery stool resulting from increased secretions into
intestine from the plasma
95
Small-volume diarrhea (DSM)
– Due to inflammatory bowel disease
– Stool may contain blood, mucus, pus
– May be accompanied by abdominal cramps and tenesmus (recurrent inclination to evacuate the bowel)
96
Common Types of Diarrhea: Steatorrhea
“fatty diarrhea”Frequent bulky, greasy, loose stools
| Foul odor
97
Steatorrhea, Characteristic of malabsorption syndromes
• i.e., celiac disease or cystic fibrosis
98
Cystic and celiac first affected
Fat usually the first dietary component affected
• Presence interferes with digestion of other
nutrients. Abdomen often distended
99
GI bleeding – Upper GI bleeding
• Esophagus, stomach, or duodenum
100
Lower GI bleeding is______ and involves bleeding from the
Below the ligament of Treitz: bleeding from the
| jejunum, ileum, colon, or rectum
101
4 signs of UPPER/LOWER GIB
– Hematemesis
– Hematochezia
– Occult bleeding
– Melena
102
Hematochezia; What is it?
• Red blood – usually from lesions in rectum or anal canal
103
Occult blood
* Small hidden amounts, detectable with stool test
| * May be caused by small bleeding ulcers
104
Melena
* Dark-colored, tarry stool
| * from significant bleeding in upper GI tract
105
Constipation may be due to
May be due to decreased peristalsis – Increases time for reabsorption of fluids
106
Effects of Chronic constipation (HAD)
may cause hemorrhoids, anal fissures, or diverticulitis.
107
Main Cause of Constipation
• Weakness of smooth muscle due to age or
| illness
108
Other Causes of constipation
| FINDOS
* ↓ dietary fiber
* ↓ fluid intake
* Failure to respond to defecation reflex
* Immobility
* Neurologic disorders
* Drugs (i.e., opiates)
* Some antacids, iron supplements
* Obstructions caused by tumors or strictures
109
Constipation Fiber and water
* ↓ dietary fiber
| * ↓ fluid intake
110
Common complications of GI tract disorders.
Dehydration and hypovolemia
111
• Electrolytes and N/V/D
Lost in vomiting and diarrhea
112
Acid-base imbalances
| – Metabolic alkalosis
loss of HCl w/ vomiting
113
Severe vomiting causes a change to_____
Metabolic acidosis
114
Why do you have metabolic acidosis?
Severe vomiting causes a change to metabolic acidosis due to the loss of bicarbonate of duodenal secretions.
• Diarrhea causes loss of bicarbonate.
115
3 types of Abdominal Pain
* Visceral
* Somatic
* Referred
116
Visceral Pain are
Burning Sensation
Dull, aching pain
Cramping or diffuse pain
Colicky often severe pain
117
Visceral Pain : Burning sensation associated with
Inflammation and ulceration in upper GI tract
118
Visceral Pain: Dull, aching pain is
Typical result of stretching of liver capsule
119
Visceral Pain: Cramping or diffuse pain
– Inflammation, distention, stretching of intestines
120
Visceral Pain: Colicky, often severe pain –
Recurrent sooth muscle spasms or contraction
| • Response to severe inflammation or obstruction
121
Somatic pain receptors directly linked to
spinal nerves
122
Somatic pain may cause
May cause reflex spasm of overlying abdominal
| muscles
123
Somatic pain characteristics
Steady, intense, often well-localized pain
124
What is rebound tenderness?
“Rebound tenderness” – over area of involvement / inflammation of peritoneum
125
What is referred pain?
• Pain perceived at a site different from origin.
126
Referred pain results when
when visceral and somatic nerves converge at one spinal cord level.
127
Types of Malnutrition
Malnutrition
| • May be limited to a specific nutrient or general limited
128
Limited malnutrition
Vitamin B12 deficiency = pernicious anemia
| – Iron deficiency = iron deficient anemia
129
Generalized malnutrition
Chronic anorexia, vomiting, diarrhea
130
Malnutrition: Other systemic causes
* IBS
* Cancer tx
* Cachexia
* Limited availability of food
131
Basic Diagnostic Tests
| •
Radiographs: With or w/o Contrast
• Ultrasound: May show unusual masses
• CT scans
• MRI
• CT and MRI may use radioactive tracers.
– Can be used for liver and pancreatic abnormalities
132
Use for liver and pancreatic abnormalities
CT and MRI
133
Diagnostic tests using
Radioactive tracers
134
Basic Diagnostic Tests UPPER GI
• Endoscopy for upper GI
| – Biopsy may be done
135
Sigmoid & colonoscopy can do
– Biopsy and removal removal of polyps
136
Laboratory analysis of stool specimens
Check for infection, parasites / ova, bleeding, tumors,
| malabsorption
137
Blood tests for GI
– LFT, pancreatic function, cancer markers
138
Common Therapies
| • Dietary modifications (GFR)
– e.g., gluten-free diet (celiac disease)
– Reduced intake of alcohol and coffee
– ↑ fiber and fluid intake
139
GI disorders; Stress reduction why?
– Stress impairs immune function and tissue healing
140
Drugs For GI disorders
```
Antacids
Antiemetics
Laxatives or enemas
Antidiarrheals
Sulfasalazine
ABX
Sulcrafate
Anticholinergics
H2 Blockers
PPIs
```
141
Role of antacids?
– To relieve pyrosis
142
Role of Antiemetics
– To relieve vomiting
143
Role of Laxatives or enemas
– Treatment of acute constipation
144
Role of Antidiarrheals
– Reduction of peristalsis
| – Relieve cramps
145
Sulfasalazine action
– Anti-inflammatory and antibacterial
| – For acute episodes of inflammatory bowel disease
146
ABX action
| - Clarithromycin or azithromycin
– Effective against Heliobacter pylori infection
| • Usually combined with a proton pump inhibitor
147
Sucralfate action
– Coating agent
– Enhance gastric mucosal barrier against irritants
such as NSAIDs
148
Anticholinergic drugs action
– Reduce secretions &motility
149
H-2 blockers action
– Useful in gastric reflux
150
PPIs action
– Reduce gastric secretion
151
Congenital abnormalities: Cleft lip and cleft palate
High risk of aspirating fluid into respiratory passages
152
Cleft lip and palate implications
May require intubation with RAE endotracheal tube for
| surgical repair
153
Disorders of the Oral Cavity Inflammatory lesions: aphthous ulcers USS
– Streptococcus sanguies may be involved
– Small, painful lesions
– Usually heal spontaneously
154
Candidiasis
– May appear as red, swollen areas
– May be irregular patches of a white curdlike material
– Oral candidiasis (thrush)
155
People at risk of developing oral candidiasis (3)
| PID
* People receiving broad-spectrum antibiotics
* Immunocompromised individuals or persons with diabetes
* During and after cancer therapy
156
May appears as red, swollen areas
Oral Candidiasis
157
– May be irregular patches of a white curdlike material
Oral Candidiasis
158
Herpes simplex type 1 infection
– Herpes simplex virus type 1 (HSV-1)
– Transmitted by
close contact
159
HSV-1 Virus
remains dormant in sensory ganglion
160
HSV-1 Virus
– Activated by stress, trauma, other infection
161
HSV-1 virus results in the Formation of
blister, ulcers, clear fluid release – contains virus. Acute stage may be alleviated by antiviral medication.
162
When HSV-1 may spread to
– May spread to eyes
| • Conjunctivitis and keratitis
163
Syphilis: when is it contagious
– Highly contagious during first and second
| stages
164
Syphillis; Primary stage
* Chancre, a painless ulcer on tongue, lip, palate
| * Heals spontaneously (1 or 2 weeks)
165
Syphillis: Secondary stage
Red macules or papules on palate – highly infectious
• Heals spontaneously
– Both stages treated with long-acting penicillin
166
Syphillis: Tertiary stage
• Infects CNS
167
Caries : what is the initiating microbe? and what follows
– Streptococcus mutans – – Lactobacillus follows in large numbers
168
With CARIES
– Bacteria break down sugars and produce large
| quantities of lactic acid -->Lactic acid dissolves mineral in tooth enamel--> Tooth erosion and caries formation
169
What is Caries promoted by?
frequent intake of sugars and acids
170
Anti-caries treatment
– Fluoride –
171
Gingivitis: Changes in the gingivae may be a______and what is it ?
• Creates extensive grooving on tooth surface
• Increase plaque retention and damage to gingivae
local or systemic problem
| – Inflammation of the gingiva
172
In gingivitis, Tissue becomes becomes
red, soft, swollen, bleeds easily
173
Gingivitis, May be a result from
– accumulated plaque
– Toothbrush trauma
– Inadequate oral hygiene
174
• Results from improper or excessive brushing
Gingivitis
175
Periodontal disease is a
– Infection and damage to the periodontal ligament
| and bone
176
Peridontal disease Predisposing condition is
gingivitis.
177
Peridontal disease caused by _________as a result of __________causing ________
– Caused by microorganisms as a result of poor
dental hygiene
– Subsequent loss of teeth possible
178
Peridontal have several________ what is it aggravated by?
– Several categories depending on degree of disease
– May be aggravated by systemic disease and
medications that reduce salivary secretions
179
Periodontitis occurs when_________and as a result
| •
organisms enter the gingival blood vessels and travel to the connective tissues and bone of the dental
arch.• Resorption of bone and loss of ligament fibers
result in weakened attachment of teeth.
180
May result in total loss of tooth from socket
Peridontitis
181
Treatment of Peridontitis (ALI)
• Treated by
Antimicrobials
local surgery of gingiva, and
Improved dental hygiene
182
Disorders of the Oral Cavity: Hyperkeratosis – ex. Leukoplakia – What is it?
Whitish plaque or epidermal thickening of mucosa
183
Hyperkeratosis : is related to :
– related to smoking /chronic irritation
– Epithelial dysplasia beneath plaque may develop
into squamous cell carcinoma.
184
Can also occur on vocal cords
Hyperkeratosis
185
Squamous cell carcinoma
| • Often develops when (age)
after 40
186
Squamous cell carcinoma causes
– Smokers, preexisting leukoplakia, alcohol abuse
| – Multiple lesions possible
187
Squamous cell carcinoma affect the
– Floor of the mouth, lateral lateral borders of the borders of the tongue
188
• Kaposi sarcoma in patients with
AIDS
189
Has better prognosis.
• Lip cancer
190
Lip cancer is common
– Common in smokers, particularly pipe smokers
191
Sialadenitis
| •
– Inflammation of the salivary glands
– May be infectious or noninfectious
– Most commonly affected is parotid gland
192
What is Mumps? It is a ______infection
infectious parotitis; – Viral infection
193
Noninfectious parotitis, occurs in
– Often in older adults who lack adequate fluid
| intake and mouth care
194
DysphaSia
Inability to speak
195
DysphaGIA
Difficulty swallowing
196
Causes of DysphaGIA
Causes:
– Neurologic deficit
– Muscular disorder
– Mechanical obstruction
197
Presentation of DYSPHAGIA
Results/presentation
– Pain with swallowing
– Inability to swallow larger pieces of solid material
– Difficulty swallowing liquids
198
Dysphagia -->Neurologic deficit from: – SIBA
– Stroke
– Infection
– Brain damage
– Achalasia
199
DysphaGIA is a failure of the
Failure of the lower esophageal sphincter to relax
| due to lack of innervation
200
DYSPHAGIA- Muscular disorder –
Impairment from muscular dystrophy
201
Dysphagia
| • Mechanical obstruction: Congenital Atresia
Congenital atresia
• Developmental anomaly
• Upper and lower esophageal segments are separated –
202
What is Stenosis?
May be ____or _____
May be secondary to CUFR
• Narrowing of the esophagus
• May be developmental or acquired
• May be secondary to chronic inflammation,
ulceration, radiation therapy, fibrosis,
203
• Stenosis or stricture may also result from ? and may requ9ired
- from scar tissue.
• May require treatment with repeated mechanical
dilation
204
Dysphagia
• Mechanical obstruction (Cont’d) – Esophageal diverticula
What is it?
It is ______or _________ following ______
What does it cause?
* Outpouchings of the esophageal wall
* Congenital or acquired following inflammation
* Causes irritation, inflammation, scar tissue
205
Dysphagia ESOPHAGEAL DIVERTICULA Signs include
| DFCCH
dysphagia, foul breath, chronic cough, hoarseness –
206
Dysphagia: Mechanical Obstruction : Tumors
• May be internal or external
207
Scar tissue contract associated with
Fibrosis
208
Tumor associated with
Compression
209
What happens with Diverticulum?
Undigested food in pouch obstructs esophagus
210
Fistula can
complicates airway
211
Fistula is a developmental
Defect connection between esophagus and trachea
212
Congenigal Tracheoesophagus FISTULA
Dilation may cause airway impingement
213
What happens in TEF
Loss of peristalsis in lower esophagus
| Food collection in lower esophagus
214
Esophageal Cancer: What is it? and where does it commonly occur?
* Primarily squamous cell carcinoma
| * Most commonly in distal esophagus
215
• Significant dysphagia in later stages in this cancer
Esophageal CA
216
Esophageal CA prognosis
• Poor prognosis due to late manifestations
217
Esophageal CA: Associated with chronic irritation due to
| CAHA
– Chronic esophagitis
– Achalasia
– Hiatal hernia
– Alcohol abuse, smoking
218
Hiatal Hernia: What is it?
Part of the stomach protrudes into the thoracic cavity.
219
What is a Sliding hernia?
– More common type
– Portion and part of stomach and gastroesophageal
junction slide up above the diaphragm
220
• Rolling or paraesophageal hernia –
Part of the fundus of the stomach moves up through an enlarged or weak hiatus in the diaphragm and may become trapped.
221
Which hernia is the most common type
Sliding hernia
222
Paraesophageal hernia is associated with
Sac and peritoneum in mediastinum
223
Sliding hiatal hernia
Part of the fundus above diaphragm
224
Hiatal Hernia- Food may_________ causes __________
| reflux of ___________may cause ?
may lodge in pouch of the hernia – Causes inflammation of the mucosa – Reflux of food up the esophagus from hernia – May cause chronic esophagitis
225
What are the Signs of Hiatal hernia?
| SIFH
– Substernal pain that may radiate to shoulder and jaw
– Increased discomfort when laying down
– Frequent belching
– Heartburn or pyrosis
226
GERD: What occurs with GERD?
• reflux of gastric contents into esophagus causing erosion and inflammation
227
Where is GERD Seen and what does the severity depends on?
* Often seen in conjunction with hiatal hernia
| * Severity depends on competence of the LES
228
Causes of GERD : What may be a factor and how does medication help?
* Delayed gastric emptying may be a factor.
| * Use of medication may reduce reflux and inflammation.
229
GERD
| • Anesthesia concerns:
Aspiration
230
Possible related respiratory concerns with GERD:
• Laryngitis
• Asthma (50% of pt.s have endoscopic evidence of
esophagitis)
• Recurrent pneumonia
231
Gastritis – Acute
* Gastric mucosa is inflamed.
| * May be ulcerated and bleeding
232
Gastritis is Caused by:
| ISIA RIE
```
– Infection by microorganisms
– Spicy or irritating foods
– Ingestion of corrosive or toxic substances
– Allergies to foods
– Radiation or chemotherapy
– Ingestion of aspirin or other NSAIDs
– Excessive alcohol intake
```
233
Gastritis – Acute
| • Basic signs (AIHE)
–Anorexia, nausea, vomiting may develop
– Infection, diarrhea may develop.
– Hematemesis due to bleeding
– Epigastric pain, cramps or general discomfort
234
Gastritis is usually UCS
Usually self-limiting:
– Complete regeneration of gastric mucosa 1-2 days
– Supportive treatment with prolonged vomiting – (May require treatment with antimicrobial drugs)
235
```
Gastritis – Chronic
Characterized by _____
loss of _______
Reduced production of ________
Often present is
```
• Characterized by atrophy of stomach mucosa
– Loss of secretory glands
– Reduced production of intrinsic factor
– H. pylori infection is often present.
236
Gastritis – Chronic signs
Signs may be vague.
– Mild epigastric discomfort, anorexia, intolerance
for certain foods
237
Risk associated with Gastritis - Chronic
Increased risk of peptic ulcers and gastric
carcinoma
• (Certain autoimmune disorders are associated
with one type of chronic gastric atrophy.)
238
Gastroenteritis MIU
• Inflammation of stomach and intestine
• Usually caused by infection
• May also be caused by allergic reactions to food or
drugs
239
Gastroenteritis microbes
• Microbes can be transmitted by fecally contaminated
| food, soil, and/or water
240
Gastroenteritis most infections are
Self limiting
241
Essential for prevention of gastroenteritis
– Safe sanitation essential for prevention.
242
Peptic Ulcers – Gastric & Duodenal
| Most are due to
• Most are due to H. pylori infection.
243
Peptic ulcers - Occur most commonly
| Found in
Occur most commonly in the proximal duodenum
| • Also found in the antrum of the stomach
244
Peptic Ulcers- GASTRIC and DUODENAL: development
Development begins with breakdown of mucosal barrier. –
245
What is the predominant factor in duodenal ulcers?
Increased acid secretion
246
What is More common in gastric ulcer development?
Decreased mucosal defense
247
Peptic Ulcers – Gastric & Duodenal PATHO
Damage to __________Predisposes to___________ and is associated with
IEUA
• Damage to mucosal barrier predisposes to
development of ulcers and is associated with – Inadequate blood supply
Excessive Glucocorticoids(secretion or medication)
Ulcerogenic substances break down mucus layer (ASA, NSAIDS, alcohol)
Atrophy of gastric mucosa (chronic gastritis)
248
Damage to mucosal barrier predisposes to development of ulcers is associated with Inadequate blood supply, how?
Caused by vasoconstriction (by stress, smoking, shock;
| circulatory impairment in older adults; scar tissue; anemia)
249
Peptic Ulcers – Gastric & Duodenal
| • Also caused by increases in: VAG - SIR
– *acid-pepsin secretion (alcohol, caffeine)
– *gastrin secretion
– *vagal stimulation
– sensitivity to vagal stimuli
– Increased number of acid-pepsin secretory
cells in the stomach (genetic anomaly)
– Rapid gastric emptying
250
Peptic Ulcers – Gastric & Duodenal
| • Complications: Hemorrhage (MCD)
* Due to erosion of blood vessels
* Common complication
* May be the first sign of a peptic ulcer
251
Peptic Ulcers – Gastric & Duodenal
| • Complications: Perforation (CUR)
* Chyme can enter the peritoneal cavity
* Ulcer erodes completely through the wall.
* Results in chemical peritonitis
252
Peptic Ulcers – Gastric & Duodenal
| • Complications: Obstruction
• May result later due to the formation of scar tissue
253
Peptic Ulcers – Gastric & Duodenal
| Signs and symptoms:
Epigastric burning or localized pain usually following
| stomach emptying
254
Peptic Ulcers – Gastric & Duodenal-> Diagnostic tests:
– Fiberoptic endoscopy
– Barium x-ray
– biopsy
255
Peptic Ulcers – Gastric & Duodenal; TREATMENT
– Combination of antimicrobial & PPI to eliminate H. pylori
256
Stress Ulcers
| • Associated with (SBH)
– Severe trauma or systemic problems
– Burns, head injury
– Hemorrhage or sepsis
257
Stress ulcer associated with (RMF)
– Rapid onset
– Multiple ulcers (usually gastric) may form within hours of precipitating event
– First indicator – hemorrhage and severe pain
258
Gastric Cancer: Arises primarily in________
| • Mostly in_________
mucous glands
| antrum or pyloric area
259
Gastric Cancer: Early carcinoma –
Confined to mucosa & submucosa
260
Gastric Cancer• Later stages –
Involves muscularis – Eventually invades serosa and spreads to lymph nodes
261
Gastric Cancer : Early stages and prognosis
Asymptomatic in the early stages – prognosis often poor
262
Gastric Cancer Key contributing factors
• Diet seems to be a key factor particularly
smoked foods, nitrites, and nitrates.
• Genetic influences play a role, too.
263
Gastric Cancer : Symptoms
Symptoms vague until cancer is cancer is advanced which IS THE REASON for late diagnosis
264
GASTRIC cancer Tx or therapy and survival
Surgery together with chemotherapy and
| radiation may relieve symptoms. – Survival rate < 20%
265
What is Dumping syndrome and when does it develop?
* Can develop after gastric surgery.
| * Control of emptying lost and gastric contents are “dumped” into the duodenum without complete digestion.
266
Pathophysiology of Dumping Syndrome
Hyperosmolar chyme draws fluid from vascular compartment into intestine.
– Intestinal distention
– Increased intestinal motility
267
Signs and symptoms of Dumping Syndrome
– Hypotension, Tachycardia, Diaphoresis, Pallor
268
Dumping Syndrome when does it occur? Other symptoms
• Occurs during or shortly after meals
| – Abdominal cramps, nausea, diarrhea
269
Dumping and glucose and how it may be resolved
• Hypoglycemia 2 to 3 hours after meal:
– High glucose levels in chyme stimulate
increased insulin secretion → hypoglycemia
• May be resolved by dietary changes
270
How to prevent Dumping syndrome? and when does it resolve.?
– Frequent small meals – high in protein, low in simple carbohydrates
• Often resolves over time
271
Pyloric Stenosis: what is it?
•
• Surgery often required.
• May be acquired later in life – Persistent feeling of fullness – Increased incidence of vomiting
Narrowing and obstruction of pyloric sphincter
| • developmental anomaly
272
Pyloric Stenosis Signs appear within –
several weeks after birth.
273
Primary signs of Pyloric Stenosis (PIF)
– Projectile vomiting immediately after feeding
– Infant fails to gain weight ,dehydration, persistent hunger
– Firm mass can be palpated at pylorus.
274
Acute Pancreatitis
• Inflammation of the pancreas
– Results in auto-digestion of the tissue
• May be acute or chronic
275
Pancreatitis emergent?
Acute form is considered a medical emergency
276
Pancreatitis Pathophysiology
– Pancreas lacks a fibrous capsule
– Destruction may progress into tissue surrounding the
pancreas
– Substances released by necrotic tissue lead to
widespread inflammation
277
Acute Pancreatitis untreated can lead to
– Hypovolemia and circulatory collapse may follow
278
Acute Pancreatitis complications
| CAGS
• Chemical peritonitis results in bacterial peritonitis
– Septicemia may result
**– Adult respiratory distress syndrome and acute renal
failure occur in 25% of patients
**– GI hemorrhage & DIC may also occur
279
Etiology of Pancreatitis is (GAS)
– Gallstones
– Alcohol abuse
– Sudden onset may follow intake of a large meal or a
large amount of alcohol
280
Acute Pancreatitis – PRIMARY Signs and Symptoms
* Severe epigastric or abdominal pain radiating to the back – primary symptoms
* Signs of shock due to hypovolemia
281
Acute pancreatitis and fever
• Low-grade fever until infection develops
| – Then body temperature may rise significantly
282
Abdominal assessment with Acute pancreatitis
• Abdominal distention and decreased bowel sounds
| – Decreased peristalsis and paralytic ileus
283
Acute Pancreatitis SSHL
| • Diagnostic tests
– Serum amylase: first rise, then fall after 48 hours
– Serum lipid levels elevated
– Hypocalcemia (pancreatic lipase chelates Ca++)
– Leukocytosis
284
Treatment of Acute Pancreatitis (OTA)
– Oral intake is stopped.
– Treatment of shock and electrolyte imbalances
– Analgesics for pain relief
285
Pancreatic Cancer
| • Risk factors
– Smoking
| – Pancreatitis and dietary factors
286
Pancreatic CA: Adenocarcinoma
– most common form
| – Arises from the epithelial cells in the ducts
287
Pancreatic Cancer : Signs and symptoms
Early manifestations?
What occur early?
* Weight loss and jaundice early manifestations
* Frequently asymptomatic until well advanced
* Metastases occur early.
288
Pancreatic Cancer mortality
– Mortality is close to 95%.
289
Gastrinoma: What it it and what does it cause?
* Gastrin secreting tumor in Pancreas or Duodenum
| * Causes gastric hypersecretion.
290
Gastrinoma and Anesthesia considerations.
– Large volumes of gastric fluid usually present at
time of anesthesia induction = ↑risk of reflux /aspiration.
– Profuse watery diarrhea = hypokalemia & metabolic
alkalosis.
291
Useful medication for preventing acid hypersecretion
```
IV ranitidine (H2 blocker) useful for preventing acid
hypersecretion intra-op.
```
292
Celiac Disease: what is it? What is it primarily?
Malabsorption syndrome
• Primarily a childhood disorder
– May occur in middle age adults
293
Celiac disease Pathophysiology DPCM
```
• genetic link
• Defect in intestinal enzyme
– Prevents digestion of gluten
– Causes atrophy of villi
• Malabsorption and malnutrition result.
```
294
Celiac Disease
| • First signs appear
about 4 - 6 months of age (with
| addition of cereals to newborn’s diet)
295
Celiac disease: Manifestation –
Steatorrhea , muscle wasting wasting, failure to gain weight
| – Irritability and malaise common
296
Celiac disease:
| Dx and Tx
* Diagnosed by a series of blood tests
| * Treatment: Gluten-free diet – Intestinal mucosa returns to normal after a few weeks without gluten intake.
297
IBD - Inflammatory Bowel Disease: what are they ? what is the _________.
• Crohn disease & Ulcerative Colitis
| Exact cause unknown.• Genetic factors involved
298
• Crohn disease vs UC age of manifestation
often during adolescence
| • Ulcerative colitis – 20s to 30s
299
Crohn Disease area affected
| •
• May affect any area of the digestive tract – Most frequently the small intestine
300
Cronh's disease Inflammation occurs in
in characteristic distribution. – “Skip lesions lesions” – affected areas separated by areas of normal tissue
301
Croh's disease with progressive PDI
– Progressive inflammation and fibrosis may cause obstructed areas.
– Damaged walls impair processing and absorption of food.
– Inflammation stimulates intestinal motility
302
Crohn Disease there is interference with: HAMP
```
Digestion and absorption leading to
Hypoproteinemia,
Avitaminosis
Malnutrition
Possibly steatorrhea
```
303
Crohn' s: Other complications, Children and treatment
Adhesions between loops may form and fistulas may develop.
• Children – Delayed growth
• Treatment: Glucocorticoids
304
Ulcerative Colitis: inflammation
• Inflammation starts in the rectum
• Progresses through the colon
• Mucosa and submucosa are inflamed.
– Tissue destruction destruction interferes interferes with absorption of fluid and electrolytes in the colon.
305
UC and diarrhea
Severe acute episodes – toxic megacolon may develop
• Diarrhea marked with up to 12 stools per day.
– Contains blood and mucus
– Accompanied by cramping pain
306
Treatment of IBD
Anti-inflammatory medications
– Sulfasalazine or glucocorticoids
• Antimotility agents: Nutritional supplements
• Antimicrobials: Immunotherapeutic agents
307
IBD surgical resection
Surgical resection
| – Usually ileostomy or colostomy
308
What is appendicitis? Pathophysiology OFIA
Obstruction by fecalith, gallstone, or foreign material
Fluid builds up inside the appendix – Microorganisms proliferate
Ischemia and necrosis of the wall – Results in increased permeability
Appendix wall becomes inflamed – Purulent exudate forms – Appendix is swollen.
309
Appendicitis and peritonitis
Bacteria and toxins escape into surroundings. – Leads to abscess formation or localized bacterial peritonitis
310
Appendicitis when does it Abscess develop?
may develop when inflamed area is walled off. – Inflammation and pain may temporarily subside.
• Localized infection or peritonitis develops
around the appendix. – May spread along the peritoneal membranes
311
Appendicitis
| Pathophysiology
* Increased necrosis and gangrene in the wall – Due to increasing pressure within the appendix
* Appendix ruptures or perforates – Release of contents into peritoneal cavity – Generalized peritonitis
* May be life-threatening
312
Treatment of Appendicits
Treatment – Surgical removal of appendix and
| antimicrobial drugs
313
Appendicitis – Signs and Symptoms
• General periumbilical pain
• Nausea and vomiting common
• Pain becomes severe and localized in LRQ.
• LRQ rebound tenderness develops.
– Involvement of parietal peritoneum over
appendix
314
Appendicitis – Signs and Symptoms
| • After rupture
– Pain subsides temporarily.
• Pain recurs – severe generalized abdominal pain and guarding
• Low grade fever and leukocytosis
– Development of inflammation
315
Appendicitis: Peritonitis “______”
Boardlike; abdomen, tachycardia, hypotension
– As peritonitis develops, abdominal wall muscles
spasm.
– Toxins lead to reduced blood pressure.
316
Diverticulum
– Outpouching (herniation) of the mucosa
| through the muscular layer of the colon
317
• Diverticulosis
– Asymptomatic
318
• Diverticulitis
– Inflammation
319
Diverticular Disease
Form
Congenital
weaker areas
• Form at gaps between muscle layers
• Congenital weakness of wall may be a factor.
Weaker areas bulge when pressure increases.
• Many cases are asymptomatic.
320
Diverticula disease symptoms
– Cramping, tenderness, nausea, vomiting
| – Slight fever and elevated white blood cell count
321
In diverticula stasis
• stasis of material in diverticula leads to inflammation and
infection.
322
• Treatment of diverticulitis
– ABX
| – Dietary modifications to prevent stasis
323
Initial signs of Colorectal Cancer depend
largely on the location of the growth.
324
Colorectal Cancer Treatment
– Surgical removal with radiation and/or chemotherapy
325
General signs of Colorectal Cancer
– Fatigue, weight loss, anemia
– Change in bowel habits
• Alternating diarrhea and constipation
– Bleeding
326
What is intestinal Obstruction? Where is more common?
• Lack of movement of intestinal contents
| – More common in small intestine
327
What are the Mechanical obstructions?
– tumors, adhesions, hernias, other tangible obstructions
328
Functional obstructions
– impaired peristalsis
329
Disease associated with Functional obstructions
* Spinal cord injury
| * Paralytic ileus due to toxins or electrolyte imbalance
330
Intestinal Obstruction
| •
• Gases and fluids accumulate proximal to blockage, distending the intestine.
• Increasingly strong contractions of proximal
intestine – Effort to move contents along
331
When Pressure increases in lumen.
– More secretions enter the intestine.
– Compression of veins in wall
• Intestinal wall becomes edematous.
• Prevention of absorption
332
Intestinal Obstruction leads to
• Intestinal distention leads to persistent vomiting.
– Additional loss of fluid and electrolytes
– Hypovolemia can result.
333
During intestinal Obstruction, Intestinal wall becomes
ischemic wall becomes ischemic and necrotic
334
During intestinal Obstruction If obstruction is not removed,
gangrene follows.
• Ischemia and necrosis → decreased innervation
and cessation of peristalsis
• Paralytic ileus occurs if it is not a cause to begin
with
335
Intestinal Obstruction promotes
• Obstruction promotes rapid reproduction of
intestinal bacteria.
– Some produce endotoxins.
– Affected wall becomes necrotic and more
permeable.
336
During intestinal obstruction– Bacteria and toxins
leak into peritoneal cavity (peritonitis) or into blood (bacteremia and septicemia).
• Perforation of the necrotic segment may occur.
– Generalized peritonitis and septic shock
337
Intestinal Obstruction
• Functional obstructions (paralytic ileus) from:
MAS PITSH
– ***Mesenteric thrombosis (Dehydration in HHS)
– abdominal surgery
– Pancreatitis, peritonitis, infection in the abdominal
cavity
– Inflammation related to severe ischemia
– Toxemia
– spinal cord injury
– Hypokalemia
338
Mechanical obstruction from:
| MAH SIV HP
```
– Masses – tumors or foreign bodies
– Adhesions that twist or constrict intestine
– Hernias
– Strictures from scar tissue
– Intussusception
– Volvulus
– Hirschsprung disease
– persimmons
```
339
• Mechanical obstruction - small intestine signs and symptoms.
– Severe colicky abdominal pain
| – Intermittent bowel sounds can be heard.
340
Paralytic ileus Signs and symptoms
– Pain is steady.
| – Bowel sounds decreased or absent
341
Intestinal obstruction: Vomiting and abdominal distention
– Occurs quickly with obstruction of S.I.
– Vomiting is recurrent – eventually with bile-stained
content
342
• Obstruction of the small intestine is
a medical emergency!
343
Large Intestine Obstruction
| – Develops slowly with mild signs such as:
– Constipation
– Mild abdominal pain, followed by abdominal distention
– Anorexia, vomiting, more severe pain
344
• Treatment of Large Intestinal Obstruction
– Treatment of underlying cause
– Fluid and electrolyte replacement
– Surgery and antimicrobial therapy
345
What is Peritonitis?
• Inflammation of the peritoneal membranes
346
Chemical peritonitis may result from (CUBBE)
```
– Chyme spilled from perforated ulcer
– Urine leaking from ruptured bladder
– Bile from ruptured gallbladder
– Blood – Any other foreign material in cavity
– Enzymes released with pancreatitis
```
347
Peritonitis
| • Bacterial peritonitis Develop by
– By direct trauma to intestine
– Ruptured appendix
– Intestinal obstruction and gangrene
– Any abdominal surgery – If foreign material is left or infection develops
348
Peritonitis and women
Pelvic inflammatory disease in women
| – When infection reaches the cavity through fallopian tubes
349
Peritonitis Signs and symptoms
– Sudden, severe, generalized abdominal pain
– Localized tenderness at site of underlying problem
– Vomiting is common; abdominal distention
– Dehydration, hypovolemia, hypotension – Tachycardia, fever, and leukocytosis
350
Treatment of Peritonitis (DAS)
– Depends on primary cause
– Aggressive ABX treatment – specific to causative organism
– Surgery may be required
