Week 5 (ch. 17) Flashcards
1
Q
Gut wall: Mucosa
A
Epithelium, including mucous producing cells
2
Q
Gut wall: submucosa
A
CT - including blood vessels, nerves, lymphatics, secretory glands
3
Q
Gut wall: serosa
A
visceral peritoneum
4
Q
What are the structures of the gut wall
A
mucosa, submucosa, circular smooth muscle layer, longitudinal smooth muscle layer, serosa
5
Q
What are the structures in the upper GI tract and accessory
A
Oral cavity Esophagus Stomach Liver Pancreas
6
Q
salivary amylase
A
starts chemical breakdown of carbohydrates in oral cavity
7
Q
Deglutition
A
swallowing
8
Q
Esophagus
A
Closed except during swallowing, skeletal muscle at superior end - followed by smooth muscle
9
Q
Describe what happens in the upper GI tract during swallowing
A
a. soft palate is pulled upward
b. vocal cords are approximated
c. epiglottis covers the larynx
d. respirations ceases
e. bolus is seized by the constricted pharynx
f. bolus of food moves into esophagus
10
Q
how many muscle layers does stomach have
A
3
11
Q
What are some functions of the stomach
A
a. Mixing and churning food
b. Initial digestion of proteins
c. production of intrinsic factor
d. formation of chyme
e. absorption of smell and lipid-soluble molecules
12
Q
What chemical digests proteins and how is this chemical formed?
A
Pepsin (in the stomach)
– formed by combination of pepsinogen and HCl
13
Q
Why is intrinsic factor important in stomach?
A
essential for absorption of vitamin B12 in ileum
14
Q
Liver receives blood from where
A
hepatic portal vein
- from intestine to liver
15
Q
What stores nutrients in the liver?
A
Hepatocytes
- play role in carbs, proteins, fat metabolism
16
Q
What are some functions of the liver
A
a. production of plasma proteins and clotting factors
b. breakdown of old and damages erythrocytes
c. bile production
17
Q
Pancreas is what
A
Exocrine pancreas arranged in lobules
18
Q
Pancreas secretes digestive enzymes such as?
A
Trypsin Chymotrypsin carboxypeptidase ribonuclease pancreatic amylase bicarbonate ions
19
Q
What does the pancreatic duct join to enter the duodenum
A
bile duct
20
Q
What structures are in the lower GI tract?
A
Small intestine
Large intestine
21
Q
What are the structures of the SI
A
Duodenum, jejunum and ileum
- villi / microvilli
22
Q
villi and microvilli
A
villi = folds of mucosa microvilli = folds of cell membranes
Both increase surface area for absorption
23
Q
SI is major site of what
A
absorption
24
Q
SI is the site of what production?
A
mucus
enterokinase, peptidases, nucleosidases, lipase, sucrase, maltase, lactase, cholecystokinin (hormone)
25
SI is lacteal, meaning what?
lymphatic vessel
26
Large intestine functions
Fluid/electrolyte reabsorption
| formation of solid feces
27
Large intestine has resident flora, which does what?
Breakdown of certain food material
| Vitamin K synthesis by bacteria
28
Large intestine has Peyer patches, which are?
lymphatic tissue
29
PNS: stimulation and effect
Primarily though vagus nerve
- increased motility
- increased secretions
30
SNS stimulation and effects
Stimulated by factors such as fear, anger
- inhibits GI activity
- causes vasoconstriction
- reduced secretions and regeneration of epithelial cells
31
What do facial nerve and glossopharyngeal nerves do
maintain continuous flow of saliva in mouth
32
Effects of distention and stretching of stomach
- PNS activation
| - increase peristalsis and gastric secretions
33
how often does stomach empty
2-6 hours after meal
34
Gastrin: formation
Secreted by mucosal cells (stomach) in response to distention of stomach or partially digested substances
35
gastrin: function
increase gastric motility, relaxes pyloric and ileocecal sphincters - promotes stomach emptying
36
Histamine
increased secretion of HCl acid
37
Secretin
Decreases gastric secretions
38
Cholecystokinin
inhibits gastric emptying; stimulates contraction of gall bladder
39
Digestion and Absorption: carbohydrates
Digestion starts in mouth followed by digestion in small intestine
40
Digestion and Absorption: proteins
digestions starts in stomach, continues in SI
41
Digestion and Absorption: lipids
Emulsified by bile prior to chemical breakdown. Action of enzymes form monoglycerides and free fatty acids.
Formation of Chlyomicrons
42
Digestion and Absorption: Fat soluble vitamin
vitamins A, D, E K
| -- absorbed with fats
43
Digestion and Absorption: Water soluble vitamins
B and C
| -- diffuse into blood
44
Digestion and Absorption: electrolytes
absorbed by active transport or diffusion
45
Where are drugs primarily absorbed?
stomach
46
Where is aspirin usually absopbed?
stomach
47
How is water absorbed
primarily osmosis
48
how much water is secreted into digestive tract each day
about 700 mL
49
how much fluid is ingested in good and fluids each day
about 2300 mL
50
how much fluid leaves the body in feces
only 50-200mL
| -- vomiting and diarrhea disrupt this
51
Common manifestations of Digestive Disorders
Anorexia, nausea, vomiting and bulimia
52
where is the vomiting center located in the body
medulla
- coordinates activities involved in vomiting
- protects airway during vomiting
53
What is commonly effected from bulimia? Why?
Oral mucosa, teeth, esophagus
| -- damage is caused by recurrent vomiting
54
Vomiting Center Activation: what is effected?
a. distention / irritation of digestive tract
b. vestibular apparatus of inner ear (motion)
c. increased intracranial pressure
- - sudden projective vomiting without previous nausea
55
Vomiting Reflex Activities
```
Deep inspiration
Closing glottis, raising soft palate
Ceasing respiration
Relaxation of gastroesophageal sphincter
Contracting abdominal muscles
Reversing peristaltic waves
```
56
Characteristics of Vomitus: Presence of blood
Hematemesis
- coffee grounds vomitus; brown glandular material indicates actions of HCl on hemoglobin
- hemorrhage - red blood may be in vomitus
57
Characteristics of Vomitus: yellow or green
bile from duodenum
58
Characteristics of Vomitus: deeper brown color
may indicate content from lower intestine
59
Characteristics of Vomitus: recurrent vomiting of undigested food
problem with gastric emptying or infection
60
Large volume diarrhea (secretory or osmotic)
Watery stool resulting from increased secretions into intestine from the plasma
Often related to infection
Limited reabsorption because of reversal of normal carriers for sodium and/or glucose
61
Small-volume diarrhea
Often caused by inflammatory bowel disease
- stool may contain blood, mucus and pus
- may be accompanied by abdominal cramps and tenesmus
62
Steatorrhea
"fatty diarrhea"
- frequently bulky, greasy, loos stools
- foul order
- characteristics of malabsorption syndromes
- fat usually the first dietary component affects
- abdomen often distended
63
What syndromes may have Steatorrhea
Celiac disease, cystic fibrosis
64
Why is fat usually the first dietary component affected leading to Steatorrhea ?
presence interferes with digestion of other nutrients
65
Blood in stool: Frank blood
Red blood - usually from lesions in rectum or anal canal
66
Blood in stool: Occult blood
Small hidden amounts, detectable with stool tests
| may be caused by small bleeding ulcers
67
Blood in stool: Melena
Dark-colored, tarry stool
| May result from significant bleeding in upper digestive tract
68
Causes of excessive gas
Eructation
Borborygmus
Abdominal distention and pain
Flatus
69
Gas results from
swallowed air (drinking through straw)
Bacterial action on food
foods or alterations in motility
70
Constipations
less frequent bowel movements than normal
- small or hard stools
- acute or chronic issue
71
Chronic constipation may cause what
hemorrhoids, anal fissures, diverticulitis
72
Causes of constipation
```
Weakness of smooth muscle fibers (age/illness)
low fiber intake
low fluid intake
failure to response to defecation reflex
immobility
neurological disorders
drugs
some antacids, iron meds
obstruction caused by tumors or strictures
```
73
Common complications of digestive tract disorders
dehydration and hypovolemia
74
Digestive tract disorders: Metabolic Alkalosis
Results from loss of hydrochloric acid with vomiting
75
Digestive tract disorders: metabolic acidosis
Severe vomiting causes a change to metabolic acidosis because of the loss of bicarbonate of duodenal secretions.
Diarrhea causes loss of bicarbonate.
76
Visceral pain digestive tract: Burning sensation
inflammation and ulceration in upper digestive tract
77
Visceral pain digestive tract: dull, aching pain
typical result of stretching of liver capsule
78
Visceral pain digestive tract: cramping or diffuse pain
inflammation, distention, stretching of intestines
79
Visceral pain digestive tract: Colicky, often severe pain
Recurrent smooth muscle spasms or contraction
| - response to severe inflammation or obstruction
80
Somatic pain receptors are directly linked to what
spinal nerves
81
rebound tenderness
Identified over area of inflammation when pressure is released
82
Somatic pain digestive tract:
Steady, intense, often localized
- may cause reflex spasms of overlying abdominal muscles
- involvement or inflammation of parietal peritoneum
83
referred pain
Pain is perceived at a site different from origin
84
referred pain results from what
when visceral and somatic nerves converse at one spinal cord level
- source of visceral pain is perceived as the same as that of the somatic nerve
85
Causes if limited malnutrition - specific problem
Vitamin B12 deficiency
| Iron deficiency
86
Causes of generalized malnutrition
```
Chronic anorexia, vomiting, diarrhea
Other systemic causes
- chronic inflammatory bowel disorders
- cancer treatment
- wasting syndrome
- lack of available nutrients
```
87
Sigmoidoscopy and colonoscopy
Diagnostic test
| - biopsy and removal of polyps may be done
88
Laboratory analysis of stool specimens
check for infections, parasites and ova, blooding, tumors, malabsorption
89
Disorders of Oral cavity: Cleft lip / palate
Congenital abnormality
- arise 6-7 week of gestation
- multifactorial origin
- high risk of aspiration
- speech impaired (speech therapy)
- feeding problems in infant
- surgical repair asap
90
Disorders of Oral cavity: Herpes Simplex 1 infection
HSV-1
- kissing/close contact
- dormant virus on sensory ganglion
- cause: stress, trauma, infection
- antiviral medication
- can spread to eyes (conjunctivitis and keratitis)
91
Disorders of Oral cavity: Syphilis
Cause: Treponema pallidum
- oral lesions
- highly contagious during 1st and 2nd stages
- treated with long-acting penicillin
92
Primary Stage Syphilis
Chancre, a painless ulcer on tongue lip or palate
93
Secondary syphilis
Red macules or papules on palate - highly infections
heals spontaneously
94
Disorders of Oral cavity: Aphthous ulcers
Steptococcus sanguis may be involved
- part of oral resident flora
Small painful lesions on
- movable mucosa
- buccal mucosa
- floor or mouth
- soft palate
- lateral borders of tongue
usually heals spontaneously
95
Disorders of Oral cavity: Dental caries
Streptococcus mutans - initiating microbe
Lactobacillus follows in large numbers
--> bacteria break down sugards and produce large amount of lactic acid which dissolves mineral in tooth enamel which can lead to tooth erosion and formation of caries
96
anti-caries treatment
fluoride
97
what promotes the growth of dental caries
sugars and acids
98
Disorders of Oral cavity: Gingivities
Changes in Gingivae may lead to a local or systemic problems.
- inflammation of the gingiva --> tissue become red, soft, swollen, bleed easily. This may result from too much plaque, bad hygiene or toothbrush trauma
99
Disorders of Oral cavity: Periodontal disease
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.
May result in total loss of tooth from socket
100
Periodontal disease treatment
Treated by antimicrobials, local surgery of gingiva, and improved dental hygiene
101
Disorders of Oral cavity: Hyperkeratosis
Whitish plaque or epidermal thickening of mucosa
102
Where does Hyperkeratosis occur
buccal mucosa, palate, lower lip
103
Hyperkeratosis may be related to what
smoking or chronic irritation
104
Why do Hyperkeratosis lesions require monitoring
Epithelial dysplasia beneath plaque may develop into squamous cell carcinoma
105
Hyperkeratosis example
Leukoplakia
106
common types of cancer of oral cavity
```
Squamous cell carcinoma
Kaposi sarcoma (AIDs patients)
```
107
Oral cancer predisposing factors
smoking, alcohol abuse, preexisting leukoplakia
108
Sialadenitis
Inflammation of salivary glands
- infectious and non-infectious
- parotid gland most affected
109
Salivary gland disorders: Mumps
Infectious parotitis
- viral infection
- vaccine available
110
Salivary gland disorders: noninfectious parotitis
often seen in older adults who lack adequate fluid intake and mouth care
111
What are most malignant tumors of salivary glands?
mucoepidermoid carcinoma.
112
Caused of dysphagia
```
neuro deficit
- infection, stoke, brain damage, achalasia
muscular disorder
- impairment from muscular dystrophy)
mechanical obstruction
```
113
achalasia
failure of the lower esophageal sphincter to relax because of lack of innervation
114
left off on slide 46
g
115
Dysphagia: congenital atresia
developmental anomaly
| upper and lower esophageal segments are separated
116
Dysphagia: stenosis
narrowing of esophagus
117
Dysphagia: esophageal diverticula
out-pouchings of esophageal wall
| - congenital or acquired following inflammation
118
Dysphagia: tumors
may be internal or external
119
esophageal cancer: what kind of cells
primarily squamous cell carcinoma
120
esophageal cancer: location
usually distal esophagus
121
esophageal cancer is associated with chronic inflammation because?
- chronic esophagitis
- achalasia
- hiatal hernia
- alcohol abuse, smoking
122
hiatal hernia
part of stomach protrudes into thoracic cavity
123
sliding hernia
most common
| - portions of the stomach and gastroesophageal junction slide up above the diaphragm
124
rolling or paraesophageal hernia
part of the fundus of the stomach moves up through the enlarged or weak hiatus in the diaphragm and may become trapped
125
what happens when food lodges and becomes trapped in hernia
inflammation of mucosa
reflux of food up esophagus
chronic esophagaitis
126
signs of hernia
heartburn pr pyrosis
belching
discomfort when lying down
substernal pain that radiates to should or jaw
127
gastroesophageal reflux disease (GERD)
Periodic reflux of gastric contents into distal esophagus causes erosion and inflammation
128
GERD often seen with with other disease
hiatal hernia
129
what may be a factor of GERD
delayed gastric emptying
130
GERD: avoid what
Caffeine, fatty and spicy foods, alcohol, smoking, certain drugs
131
Acute Gastritis: what
gastric mucosa is inflammed
| - may be ulcerated and bleeding
132
Acute gastritis may result from?
```
Infection by microorganisms
Allergies to foods
Spicy or irritating foods
Excessive alcohol intake
Ingestion of aspirin or other NSAIDs
Ingestion of corrosive or toxic substances
Radiation or chemotherapy
```
133
Basic signs of gastrointestinal irritation
- Anorexia, nausea, vomiting may develop
- Hematemesis caused by bleeding
- Epigastric pain, cramps or general - discomfort
- With infection, diarrhea may develop.
134
Acute gastritis is usually self-limiting, meaning
Complete regeneration of gastric mucosa
Supportive treatment with prolonged vomiting
May require treatment with antimicrobial drugs
135
Chronic gastritis: what
Characterized by atrophy of stomach mucosa
- loss of secretory glands
- reduced production of intrinsic factor
136
What is often present in Chronic gastritis
Helicobacter pylori
137
sings of Chronic gastritis
may be vague
| - Mild epigastric discomfort, anorexia, intolerance for certain foods
138
increased risk of what with Chronic gastritis
peptic ulcers and gastric carcinoma
139
gastroenteritis
inflammation of stomach and intestines
| - usually caused by infection or allergic reactions to food or drugs
140
gastroenteritis: describe the effect that microbes have as they are transmitted by fecally contaminated food, soil or water
a. most infections self limiting
b. serious illness may result in compromised house or virulent organisms
c. may cause epidemic outbreaks in refugee or disaster settings
d. safe sanitation essential for prevention
141
Peptic ulcer (gastric and duodenal): cause
most caused by H. pylori infection
142
Where do peptic ulcers usually occur
proximal duodenum and antrum of stomach
143
Describe how the development of gastric ulcers begin
1. breakdown of mucosal barrier
2. decreased mucosal defense
- more common in gastric ulcer development
144
What is a predominant factor in duodenal ulcers
increased acid secretion
145
damage to mucosal barrier predisposes someone to the development of ulcers and is associated with what?
- Inadequate blood supply (vasoconstriction)
- excessive glucocorticoid secretion / meds
- ulcerogenic substances break down mucous layer (aspirin, NSAID, alcohol)
- atrophy of gastric mucosa
146
increase acid pepsin related to gastric ulcers may also lead to what?
- Increased gastrin secretion
- Increased vagal stimulation
- Increased sensitivity to vagal stimuli
- Increased number of acid pepsin secretory cells in the stomach (genetic anomaly)
- Increased stimulation of acid pepsin secretion d/t Alcohol, caffeine, certain foods
- Interference with normal feedback mechanisms
- Rapid gastric emptying
147
Complications of peptic ulcer: hemorrage
Caused by erosion of blood vessels
May be the first sign of a peptic ulcer
148
Complications of peptic ulcer: perforation
Ulcer erodes completely through the wall.
Chyme can enter the peritoneal cavity.
Results in chemical peritonitis
149
Complications of peptic ulcer: obstruction
may result later because the formation of scar tissue
150
peptic ulcer s/s
epigastric burning or localized pain, usually following stomach emptying
151
peptic ulcer diagnostic test
Fiberoptic endoscopy
Barium x-ray
Endoscopic biopsy
152
peptic ulcer treatment
Combination of antimicrobial and proton pump inhibitor to eliminate H. pylori
Reduction of exacerbating factors
153
Stress ulcers associated with
severe trauma or systemic problems
- burns, head injuries
- hemorrhage or sepsis
154
stress ulcers: rapid onset
multiple ulcer (usually gastric) may form within hours of precipitating event
155
first indicator of stress ulcer
hemorrhage and severe pain
156
Gastric cancer: where
mucous glands mostly in antrum or pyloric area
157
Gastric cancer: early carcinoma
confirmed to mucosa and submucosa
158
gastric cancer: later stages
involves muscularis
| eventually invades serosa and spreads to lymph node
159
gastric cancer: prognosis
poor bc asymptomatic in early stages
160
key factor of gastric cancer
diet
| - smoked foods, nitrates, nitrites
161
survival rate of gastric cancer
less than 20%
162
gastric cancer treatment
surgery and chemo
163
Dumping syndrome
Control gastric emptying is lost and gastric contents are "dumped" into duodenum without complete digestion
164
Dumping syndrome may follow
gastric resection
165
Dumping syndrome: Hyperosmolar chyme draws fluid from vascular compartment into intestine, which can cause
Intestinal distention
Increased intestinal motility
Decreased blood pressure → anxiety and syncope
166
Dumping syndrome occurs when
during or shortly after meals
167
Dumping syndrome s/s
adb. cramps, nausea, diarrhea
168
Dumping syndrome: hypoglycemia 2-3 hours after meals, why
High blood glucose levels in chyme stimulate increased insulin secretion → drop in blood glucose levels.
169
Dumping syndrome: treatment
dietary changes (frequent small meals high in protein, low in simple carbs)
often resolves over time
170
pyloric stenosis
Narrowing and obstruction of pyloric sphincter
171
pyloric stenosis signs / symptoms
Signs appear within several weeks after birth
- Projectile vomiting immediately after feeding
- Firm mass can be palpated at pylorus.
- Infant fails to gain weight, dehydration, persistent hunger
172
pyloric stenosis treatment
surgery
173
signs of pyloric stenosis if acquired lated in life
Persistent feeling of fullness
Increased incidence of vomiting
174
pyloric stenosis cause
developmental anomaly
175
Cholelithiasis
formation of gallstones
176
cholecystitis
inflammation of gall bladder and cystic duct
177
cholangitis
inflammation usually related to infection of bile ducts
178
Choledocholithiasis
Obstruction of the biliary tract by gallstones
179
gallstones may consist of
Cholesterol or bile pigment
| Mixed content with calcium salts
180
small vs large gallstones
small: may be silent and excreted in bile
larger: obstruct flow of bile through gallbladder
181
possible locations of gallstones
Biliary Ducts & Pancreas
182
Gallstone risk factors / causes
```
Women
High cholesterol in bile
High cholesterol intake
Obesity
Multiparity
Oral contraceptives or estrogen supplements
Hemolytic anemia
Alcoholic cirrhosis
Biliary tract infection
```
183
Gallstones can cause obstruction of a duct by large calculi, which causes what
sudden, severe waves of radiating pain
184
gallstone treatment
laparoscopic surgery
| low fat diet
185
why might jaundice develop from gallstones
bile backs up into liver and blood
186
pain related to gallstones decreases if gallstones move where
duodenum
187
Prehapatic jaundice
results of excessive destruction of RBC
188
What diseased might you see prehepatic jaundice
hemolytic anemias or transfusion reactions
189
intra-hepatic jaundice
occurs with disease or damage to hepatocytes
190
what disease might you see intra-hepatic jaundice
hepatitis or cirrhosis
191
Posthepatic jaundice
caused by obstruction of bile into gallbladder or duodenum
192
what disease might you see posthepatic jaunduce
tumor or cholelithiasis
193
bilirubin measurements: direct or conjugated bilirubin
cause be measured in blood
194
bilirubin measurements: total bilirubin
measured in blood
195
bilirubin measurements: how do you get indirect or unconjugated bilirubin
Total bilirubin - direct bilirubin
196
Type of jaundice indicated how ?
by increase in serum bilirubin level and changes in stools
197
bilirubin measurement for prehepatic jaundice?
Unconjugated bilirubin level elevated
198
bilirubin measurement for Intrahepatic jaundice
Both unconjugated and conjugated bilirubin levels may be elevated.
199
bilirubin measurement for posthepatic jaundice
increase conguated bilirubin level
| - light colored stool caused by absense of bile
200
hepatitis
inflammation of liver
201
viral hepatitis
cell injury results in inflammation and necrosis in liver
| - liver is edematous and tender
202
viral hepatitis: causative agents
```
Hepatitis A virus (HAV)
Hepatitis B virus (HBV)
Hepatitis C virus (HCV)
Hepatitis D virus (HDV)
Hepatitis E virus (HEV)
```
203
Hepatitis A virus (HAV): type is virus
small RNA virus
| - acute but self-limiting infection
204
Hepatitis A virus (HAV): transmission
Fecal-oral route
- areas of bad sanitation / hygiene
- often from contaminated water or shellfish
- sexually transmitted (anal)
205
Hepatitis A virus (HAV): carrer or chronic state?
no
206
Hepatitis A virus (HAV): what happens before onset of signs
fecal shedding of virus
207
Hepatitis A virus (HAV): vaccine
available for travelers, food care workers, and health care workers
208
Hepatitis C virus (HCV): type of virus
single-stranded RNA virus
209
Hepatitis C virus (HCV): transmission
most common type transmitted by blood transfusion
210
Hepatitis C virus (HCV): carrier / chronic state
May exist in carrier state
| about 50% of pt. enter chronic state
211
Hepatitis C virus (HCV): increased risk of what
hepatocellular carcinoma
212
Hepatitis C virus (HCV): treatment
interferon injections
213
Hepatitis D virus (HDV): virus type
incomplete RNA virus
214
Hepatitis D virus (HDV): requires what
HBV to replicate and produce active infection
215
Hepatitis D virus (HDV): effect on HBV
increases severity of HBV
216
Hepatitis D virus (HDV): transmission
blood
217
Hepatitis E virus (HEV): virus type
single-stranded RNA virus
218
Hepatitis E virus (HEV): transmission
oral-fecal
219
Hepatitis E virus (HEV): chronic or carrer state
no
220
Hepatitis: Preicteric stage s/s
Fatigue and malaise
Anorexia and nausea
General muscle aching
221
Hepatitis: Icteric stage s/s
Onset of jaundice
Stools light in color, urine becomes darker
Liver tender and enlarged, mild aching pain
222
Hepatitis: Posticteric stage - recovery stage s/s
Reductions in signs
| Weakness persists for weeks
223
Viral hepatitis: bodies defense
only body defense is formation of antibodies via vaccination
224
Viral hepatitis: supportive measures
Rest, diet high in protein, carbohydrate, and vitamins
225
Chronic hepatitis can be treated with interferon: what does this do?
Decrease viral replication
- effective 30-40% ind.
- drug combination (slow-acting interferon plus antiviral drugs) more effective
226
Toxic or nonviral Hepatitis
Variety of hepatotoxins can cause inflammation and necrosis of the liver.
May result from sudden exposure to large amounts or from lower dose and long-term exposure
227
drugs and chemicals that can cause Toxic or nonviral Hepatitis
Drugs include:
Acetaminophen, halothane, phenothiazines, tetracycline
```
Chemicals include:
Carbon tetrachloride (not used currently), toluene, ethanol
```
228
Cirrhosis
Progressive destruction of liver
229
Cirrhosis causes
alcoholism
biliary cirrhosis
postnectrotic cirrhosis
metabolic abnormalities
230
biliary cirrhosis associated with
associated with immune disorders
231
Postnectrotic cirrhosis
Linked with chronic hepatitis or long-term exposure to toxic materials
232
Cirrhosis leads to
Extensive diffuse fibrosis
- Interferes with blood supply
- Bile may back up.
Loss of lobular organization
Degenerative changes may be asymptomatic until disease is well advanced.
233
Cirrhosis diagnosis
Liver biopsy and serologic test to determine cause and extent of damage
234
Cirrhosis (Alcoholic Liver Disease): initial stage
Fatty liver
- enlargement of liver
- Asymptomatic and reversible with reduced alcohol intake
235
Cirrhosis (Alcoholic Liver Disease): second stage
Alcoholic Hepatitis
a. inflammation / cell necrosis
b. fibrous tissue formation (irreversible)
236
Cirrhosis (Alcoholic Liver Disease): third stage
End stage cirrhosis
a. fibrotic tissue replaces normal tissue
b. little normal function remains
237
slide 80: functional loss with cirrhosis
go look
238
Cirrhosis: initial manifestations
Mild and vague
- chronic infection s/s
- dull aching pain may be present in upper right abdominal quadrant
239
Advanced cirrhosis s/s
```
Ascites and peripheral edema
increased bruising
esophageal varies
jaundice
encephalopathy
```
240
Cirrhosis treatment
```
Avoidance of alcohol
Supportive or symptomatic treatment
Dietary restriction
Balancing serum electrolytes
Paracentesis
Antibiotics
Liver transplant
```
241
Hepatocelluar carcinoma
most common primary tumor of liver
| - more common in cirrhotic livers
242
Liver cancer: secondary or metastatic cancer
Arises from areas served by the hepatic vein or spread along the peritoneal membranes
243
liver cancer: initial signs and diagnosis
signs: mild and general
Diagnosis: usually occurs with advanced stages
244
liver cancer treatment
possible lobectomy, radio-frequency ablation (RFA) procedure
245
Acute pancreatitis
Inflammation of pancreas; results in auto-digestion of tissue
246
causes of acute pancreatitis
- gallstones
- alc abuse
- sudden onset may follow large meal or large amount of alcohol
247
pancreatitis can be acute or chronic, what is acute consider?
medical emergency
248
describe patho of pancreatitis
Pancreas lacks capsule
- substances released by necrotic tissue lead to widespread inflammation
- destruction may progress into tissue surrounding pancreas
249
Acute pancreatitis
Severe epigastric/abdominal pain radiating to back
signs of shock
low grade fever until infection develops
abdominal distention (decreased peristalsis and paralytic ileus)
250
Acute pancreatitis Diagnostic tests
Serum amylase levels—first rise, then fall after 48 hours
Serum lipid levels are elevated.
Hypocalcemia
Leukocytosis
251
Acute pancreatitis treatment
Oral intake is stopped.
Treatment of shock and electrolyte imbalances
Analgesics for pain relief
252
Pancreatic cancer risk factors
smoking
| pancreatitis and dietary factors
253
Adenocarcinoma
most common type of Pancreatic cancer
- arises in ducts
254
Pancreatic cancer early manifestions
weight loss and jaundice
255
Pancreatic cancer mortality rate
metastases occur early
| - mortality 95%
256
celiac disease
Malabsorption syndrome; genetics
257
celiac disease defect is where
intestinal enzyme (gliadin)
- prevents the breakdown of gluten
- atrophy of villi in intestine
258
celiac disease: first signs
usually as children when cereals are first introduced into the diet
259
celiac disease manifestations
Steatorrhea, muscle wasting, failure to gain weight
Irritability and malaise common
260
celiac disease diagnosis
blood tests
261
celiac disease treatment
gluten free diet, intestinal mucosa returns to normal after a few weeks without gluten
262
Chron disease: where?
May affect anywhere in digestive tract, SI most affects
263
Chron disease: describe the inflammatoin
inflammation occurs in characterist distribution
| -"skip" lesions - affected areas are separated by areas of normal tissue
264
Chron disease: what causes obstructed areas?
Progressive inflammation and fibrosis
- damaged walls impair processing and absorption of food
- inflammation stimulates intestinal motililty
265
Chron disease interferes with digestion and absoption, leading to what?
Hypoproteinemia, avitaminosis, malnutrition, possibly steatorrhea
266
complications of Chrons disease
Adhesions between loops may form and fistulas may develop.
267
Chrons disease in children: complications
delayed growth and sexual maturation
268
Chrons disease treatment
Glucocorticoids
269
Ulcerative colitis
inflammation starts in rectum and progresses through colon. mucosa and submucosa are inflammed.
270
Ulcerative colitis: tissue destruction inferes with what
absorption of fluid and electrolytes in colon
271
Ulcerative colitis: when might megacolon develop
severe acute episodes
272
Ulcerative colitis s/s
diarrhea, up to 12 a day
- contains blood and mucus
- cramps
273
IBS manifestions
Lower abdominal pain
Diarrhea
Constipation, alternating with diarrhea
Bloating, nausea
274
IBS diagnosis
signs and symptoms
- Testing for food allergies
- Testing for bacterial or parasitic infections
- No single cure for IBS
275
IBS treatment
```
Team approach
Anti-inflammatory meds
Antimotility agents
Nutritrional supplements
Antimicrobials
Immunotherapeutic agents
Surgical resection
```
276
Appendicitis
Obstruction of lumen; fluid builds inside
| - purulent exudate, swollen
277
Appendicitis treatment
surgical removal and antimicrobial drugs
278
treatment of diverticulitis
antimicrobial drugs
| dietary modifications to prevent stasis
279
Diverticulitis stasis
material trapped in pouch leads to inflammation and infection
280
colorectal cancer: most malignancies develop from what
adenomatous polyps
| - early diagnosis essential
281
colorectal cancer: risk factors
genetics
Long-term ulcerative colitis
environmental factors (low fiber)
282
colorectal cancer. treatment
surgical removal with radiation and or chemo
283
intestinal obstruction: what
lack of movement of intestinal content through intestine - most common in SI
284
intestinal obstruction: mechanical obstruction
Result from tumors, adhesions, hernias, other tangible obstructions
285
intestinal obstruction: functional or adynamic obstructions
result from impairment of peristalsis
| - spinal cord injry
286
Peritonitis
inflammtion of peritoneal membranes
287
Chemical peritonitis may result from
Enzymes released with pancreatitis
Urine leaking form a ruptured bladder
Chyme spilled from a perforated ulcer
Bile escaping from the ruptured gallbladder
Blood
Any other foreign material in the cavity
288
Bacterial peritonitis caused by
Direct trauma affecting the intestine
Ruptured appendix
Intestinal obstruction and gangrene
289
pelvin inflammatory disease in women
when (peritonitis) infection reaches the cavity through fallopian tubes
