GI System Flashcards

1
Q

What do accessory glands do?

A

Digestion, absorption, secretion, motility

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2
Q

List the layers of mucosa in order from superficial to deep

A

Serosa (lining of cavity), muscular external (motility), submucosa (BV, dispensability, elasticity), and mucosa (separates lumen from environment, absorption)

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3
Q

How does the stomach remain protected from the acidic environment it creates to digest food?

A

Epithelial cells of gastric mucosa (alkaline mucous), and the gastric mucosal cells which neutralize the acid with bicarb, increase blood flow, and synthesize prostaglandins

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4
Q

List the most common causes of GI hemorrhage?

A

Peptic ulcer disease, stress-related mucosal disease, esophagogastric varicose

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5
Q

Where do we see GI hemorrhage?

A

Upper: esophagus, stomach, duodenum
Lower: Jejunem, ileum, colon, rectum

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6
Q

What leads to peptic ulcer disease?

A

The body’s protective measures stope working which lead to mucosal breakdown. This extends into the muscle layers, leading to damaged blood vessels and bleeding- basically the penetrated lining allows the stomach to eat itself

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7
Q

What are the two main causes of peptic ulcer disease?

A

Bacteria: Helicobacter pylori
Drugs: NSAIDS (ASA, ibuprofen, naproxen), Corticosteriods

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8
Q

Stress-related MD is caused by the same pathogenesis of PUD, but what leads to the disruption in this disease?

A

Increased acid production and decreased mucosal blood flow leading to ischemia and damage to the mucosal lining

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9
Q

What are esophageal varicose?

A

Engorged and distended blood vessels of the esophagus and proximal stomach

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10
Q

What causes esophageal varices?

A

Portal HTN from hepatic cirrhosis (chronic liver disease) the resistance impedes blood from through the liver and develop into varices

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11
Q

Talk about the complication of hemorrhage in a GI bleed ?

A

Result of the erosion of granulation tissue at base of ulcer in healing or erosion of the ulcer through a major blood vessel

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12
Q

Gi-bleed complication of perforation?

A

Severe upper ABD pain, bowel sounds absent, resp shallow/rapid, firm ABD, elevated HR, fever, nausea, peritonitis

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13
Q

What is a gastric outlet obstruction?

A

Obstruction at the pylorus, the “outlet” of the stomach

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14
Q

What are the stages in a GI assessment when taking a client’s Hx?

A

Common GI symptoms, lifestyle, medical Hx, family Hx, current medication use

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15
Q

What meds should we take care to ask about?

A

Laxatives (can cause bleeding), ASA< NSAIDS, corticosteroids, anticoagulants

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16
Q

What labs are ordered in a GI hemorrhage assessment?

A

Hgb, hematocrit, INR, PTT, Creat, UREA, GFR, electrolytes, liver function, cardiac enzymes, H-pyloiri blood test, stool sample, urea breath test, occult blood

17
Q

How can you tell the severity and location of bleeding?

A

Nasogastric lavage

18
Q

What type of bleeding tells us it is an upper GI bleed?

A

Hematemesis (coffee grounds), melon (black, tarry stools)

19
Q

What colour are stools in a lower GI bleed ?

A

Bright red

20
Q

What are some key S&S that tells us the bleed is gastric?

A

eating-makes pain worse
Pain-dull/aching
Weight loss
Severe- vomiting bright red/coffee grounds

21
Q

What are some S&S that tell us the pain is duodenal?

A

Eating- feels better, pain 3-4h after eating
Wakes in night
Pain-gnawing
Normal weight
Severe, tarry dark stool

22
Q

What are we looking for with a colonoscopy?

A

lower GI tract

23
Q

What are we looking for with a enteroscopy?

A

Small bowel

24
Q

How many classes of hemorrhage are there?

25
Which class of hemorrhage is most severe?
4- here, the client is more than 40%, more than 2000ml and they are hypotenuse, HR140+, confused, lethargic, no urine
26
How do we engage in conservative therapy with GI management?
Diet- no spicy food, acidic food, low fibre, bland diet -Rest -no stress -no smoking -pain resolves in 3-6days, ulcer slowly healing
27
Conservative therapy treatment: H- pylori
Antibiotics
28
Conservative therapy treatment: meds?
Histamine 2 receptor blockers (ranitidine), proton pump inhibitors (pantoloc), antacids, cytoprotective therapy
29
When a patient is in an acute state with a GI bleed, how do you manage them?
Respond to hemodynamic instability- IV access, fluids, VS, Resp support Volume replacement (crystalloids, colloids, blood products), PRBC (low Hg), minimize fluid loss
30
What should the ins and outs be in an acute GI bleed? what is our aim for the patient?
Put in a foley and they need at least 30ml an hour
31
Do we put in an Ng tube when client is facing an acute GI bleed?
yes
32
How do we reduce gastric acuity and support the mucosal defence mechanisms?
Proton pump inhibits, H2 receptor antagonist, antacids, gastric mucosal agent (sucralfate) which binds to injured tissue
33
Vagotomy
Cut parts of vagus nerve to reduce stimulation to the gut to make HCL
34
Pyloroplasty
Opening of the pylorus that has narrowed due to scarring
35
Gastric resection
Removal of disease parts of the stomach, location removed dependent on area of disease, at risk for dumping syndrome
36
Dumping syndrome
Stomach cannot regulate movement of food into the small intestine