Lecture 11: GI Sys Flashcards
1
Q
2 divisions of the GI sys
A
- GI tract
- major function of this is digestion + elim of waste - accessory glands
- secrete fluid and enzymes to aid in digestion
2
Q
4 basic processes of the GI sys
A
- digestion
- absorption
- secretion
- motility
3
Q
describe the stomach
A
food storage, digestion, and emptying. HCl secretions and intrinsic factors (B12 absorption), pepsinogen (protein breakdown) and gastrin (releases gastric acid) and stomach mucus
4
Q
describe the small intestine
A
Absorption (20% in first section of SI)
5
Q
describe the large intestine
A
Reabsorption of fluids and electrolytes
Movement of feces out for excretion
6
Q
is absorption regulated
A
everything is absorbed whether or not we need them
Malabsorption can be affected by any changes to the normal eating and digestion process - inability to eat properly, swallowing problems, short gut, etc..
7
Q
1/3 cardiac output goes to GI from
A
spleen (?) - mucosa can be damaged from decreased perfusion
Mucosa breakdown can result in bleeding
8
Q
what breakdowns food and kills bacteria
A
acid in stomach
9
Q
what are the 4 layers of the GI tract
A
- mucosa
- submucosa
- muscularis externa
- serosa
10
Q
describe the mucosa
A
- innermost layer of epithelia cells
- forms a continuous barrier separating lumen from external environment
- absorption (transport lumen to blood stream)
- secretes mucous for protection and coats the lining, muscle contraction to promote contact w mucosal surface, rich in bicarbonate to protect, has parietal cells for HCL and cells to release pepsin and gastrin
11
Q
describe the submucosa
A
- thick layer of connective tissue - contains large blood and lymphatic vessels
- gives GI tract dispensability and elasticity
- at risk for bleeding if layer is exposed
12
Q
describe the muscularis externa
A
- primarily smooth muscle fibers - largely responsible for motility
13
Q
describe serosa
A
- outer layer - continuous w peritoneum - a membrane lining the inside of the abdo cavity
14
Q
describe epithelial cells of gastric mucosa
A
- packed close together
- surface cells produce alkaline mucus, secrete bicarbonate-laden
- alkaline helps protect against acidic environment. constantly peeling away and replaced as a protective lining
15
Q
why is the stomach needed w acid
A
for protection against acid environment
16
Q
describe gastric mucosal cells
A
- mucus (lubricant) with bicarb neutralizes acid
- the gastric mucosa also can increase blood flow = additional buffer for acid neutralization
- mucosal cells synthesize prostaglandins
- prostaglandins increase blood supply and flow and enhance mucous and blood flow secretion and inhibit acid by inhibiting histamine in parietal cells
- lipid-soluble substances like alcohol, NSAIDS, and aspirin can break through the barrier and damage these cells, causing edema and bleeding
17
Q
3 main causes of GI hemorrhage
A
- peptic ulcer disease (mostly in duodenum)
- stress-related mucosal disease (SRMD)
- esophagogastric varices
18
Q
what’s included in an upper GI bleed
A
esophagus, stomach, or duodenum
19
Q
what’s included in a lower GI bleed
A
jejunum, ileum, colon, rectum
20
Q
whats classified as a GI bleed
A
- venous, capillary, or arterial bleeding
- “massive” more than 1.5L or 25% of vascular volume
- lower are less common, often from diverticulitis, ischemia, inflammation, or cancer
21
Q
describe peptic ulcer disease (GI bleed)
A
- protective mechanisms cease to function = mucosal breakdown
- break down extends through the entire mucosa and into the muscle layers damaging blood vessels and causing hemorrhage
- after mucosal lining is penetrated, gastric secretions auto digest the layers of the stomach or duodenum
Erosion of mucosa from HCl digestive action
Mucosa prevents HCl autodigestion - damage prevents this
Ulcers from stomach acid
Stomach is protected from gastric-mucosal barrier preventing this
Mucous secretion entraps hydrogen to prevent entrance through the barrier
Bicarb neutralizes the acid
High turnover rate = mucosa repairs itself mostly
Breakdown can turn into a bleed
Compensatory increase in blood flow
Prostaglandin, histamine, and other increases cap blood flow
Increase nutrition to the area to promote healing
Breakdown can go all the way into the muscle layer
22
Q
2 main cause of peptic ulcers
A
- bacterial action of Helicobacter pylori (H. Pylori)
- spiral bacterium infecting superficial gastric mucosa and disrupting the mucous layer - drugs
- NSAIDS, ASA, ibuprofen, naproxen (inhibit prostaglandin synthesis, direct injury to mucosal layer)
- corticosteroids (decrease rate of mucosal cell renewal and thereby decrease its protective effects
23
Q
describe stress related mucosal disease
A
- same mech as peptic ulcer disease, main cause of disruption of gastric mucosal resistance is caused:
- increased acid production
- decreased mucosal blood flow, resulting in ischemia and degeneration of the mucosal lining
24
Q
describe esophageal varices
A
- engorged and distended blood vessels of the esophagus and proximal stomach
- develop as a result of portal HTN caused by hepatic cirrhosis
- tiny, thin-walled vessels of esophagus and proximal stomach that receive this diverted blood lack sturdy mucosal protection
- vessels become engorged/dilated = forming esophagogastric varices
- resistance impedes blood flow into, thru, and out of liver
- varices may develop in esophagus, stomach, duodenum, colon, rectum, or anus
25
3 GI bleed complications
1. hemorrhage
- result of erosion of granulation tissue at base of ulcer during healing or erosion of ulcer thru major blood vessel
2. perforation
- severe upper abdo pain
- bowel sounds absent
- resp shallow and rapid
- fire abdomen, abd bloating
- elevated HR, fever
- +/- nausea
- can lead to peritonitis
3. gastric outlet obstruction
- obstruction at the pylorus, outlet of the stomach
26
what is hematemesis
- condition where person bleeds internally and vomits as a result
- bright red or brown, "coffee grounds" emesis (depends on amount and length of contact w gastric secretions)
27
lab studies for a GI hemorrhage
- Hgb, hematocrit, INR, PTT, Creat, UREA, GFR, lytes, liver function, cardiac enzymes
- H. pylori - blood test, stool sample, urea breath test, occult blood
28
how to determine severity and location of bleeding
nasogastric lavage - can help determine ongoing bleeding, location, and prepare pt for endoscopy
29
2 characteristics of a upper GI bleed
1. hematemesis
2. melena
30
what is melena
black, tarry stools (may take several days to clear after bleeding stops)
usually UGIB
31
characteristic for lower GI bleed
hematochezia
32
hematochezia
bright red stools
33
gastric ulcer GI hemorrhage assessment s/s you would see
- eating - makes pain worse
- pain - dull/aching
- wt loss
- severe - vomiting bright or coffee ground
34
general s/s of GI hemorrhage
indigestion, epigastric pain
35
duodenal ulcer GI hemorrhage assessment s/s
- eating - feels better, pain 3-4 hours after eating
- wakes in night
- pain - gnawing
- normal wt
- severe-tarry, dark stool
36
GI hemorrhage diagnostic procedures
- Xray
- scopes (esophagogastroduodenoscopy, colonoscopy, enteroscopy)
- ultrasound
- upper GI series
- abd ct w contrast
37
esophagogastroduodenoscopy
upper GI tract
38
colonoscopy
lower GI tract
39
enteroscopy
small bowel
40
what is a class 1 GI hemorrhage
< or equal to 15% - 750 mL
- assessment mainly normal - may have orthostatic HTN
41
what is a class 2 GI hemorrhage
15-30% - 750-1500 mL
HR > 100, tachypnea, BP may be normal supine, cap refill sluggish, urine output low (25-30 mL/hr)
42
what is a class 3 GI hemorrhage
30-40% - 1500-2000 mL
- HR 120+, hypotension, skin cool and pale, confused, hyperventilating urine output low (5-15 mL/hr)
43
what is a class 4 GI hemorrhage
>40% - greater or equal to 2000 mL
profoundly hypotensive, HR 140+, confused, lethargic, urine output absent
44
2 GI bleed management
- conservative therapy
- acute GI bleed
45
what is included in conservative therapy
- diet (avoid spicy/acidic foods)
- low fiber, bland diet
- adequate rest
- elim or reduction of stressors
- smoking cessation
- pain resolves in 3-6 days, ulcer healing is slower (may take up to 3-9 wks)
- H. Pylori - treat w antibiotics (clarithromycin, metronidazole, amoxicillin)
- histamine 2 receptor blockers (ranitidine)
- antacids (mag hydroxide, calcium carbonate)
- cytoprotective therapy (sucralfate)
46
how do we manage an acute GI bleed
1. respond to hemodynamic instability
- obtain IV access - 16-18 gauge needle - rapid admin of fluids
- VS, SaO2
- NPO
- resp support
2. administer volume replacement
- crystalloids (NaCl, RL_, colloids (albumin pentaspan), blood products (PRBC) or a combo (type and cross in prep for possible transfusion)
- PRBC - HGB less than 70 and or pt symptomatic
- minimize fluid loss
- accurate ins and outs (u/o at least 30 mL/hr, foley cath)
- respond to abnorm INR, PTT
- identify and stop source of bleeding
- endoscopic procedures
- NG tube
- assess for fluid overload
- follow up assess of lab values
- assess for further bleeding
- reduce gastric acidity and support gastric mucosal defense mechanisms
- octreotide (sandostatin) - upper gastrointestinal bleeding, esophageal varices
- antibiotic therapy - treat H. pyloric infection/peritonitis
47
3 GI surgical options
1. vagotomy
- cut part of vagus nerve to reduce the stim to the gut to produce HCI
2. pyloroplasty
- opening of pylorus that has narrowed due to scarring
3. gastric resection
- removal of diseased part of stomach
- location removed dependent on area of disease - usually pyloric valve or duodenum
- at risk for Dumping Syndrome - stomach is unable to regulate the movement of food into the small intestine
48
follow up care for GI bleeding
- avoid gastric irritants such as alcohol and smoking
- prevent or decrease stress-inducing situations at home or at work
- take only prescribed medications
- if ASA (aspirin), corticosteroids, NSAIDs, are required - provide instruction regarding the potential adverse effects that these drugs may have on the GI mucosa
- dietary mods - avoid or elim foods and beverages that cause irritation
- self identification of further S/S
