Exam 2 | GI Pharmacology & Functions Flashcards
1
Q
Gastric secretion pathway | Cephalic Phase
A
- Cephalic phase: neural phase that’s stimulated by thought, smell, taste of food
- Acetylcholine released by vagus nerve → stimulates certain cells in stomach…
- Parietal cells: increases stomach’s gastric acid
- Chief cells: secretes pepsinogen converted → to pepsin that breaks down proteins/polypeptides in stomach
- G-cells: secretes gastrin
- Acetylcholine released by vagus nerve → stimulates certain cells in stomach…
2
Q
Gastric secretion pathway | Gastric Phase
A
- Gastric phase: humoral phase that’s stimulated by distention of stomach
- Increases gastric acid bc you’re starting to eat but still also happens when you don’t eat and thinking of food → peristalsis and stomach rumbling
- Stimulates/Releases…
- G-cells → releases more gastrin
- Parietal cells → increases gastric acid by secreting HCl
- Histamines → increases gastric acid
- Prostaglandins → inflammatory response → increases stomach lining protection
3
Q
Gastric secretion pathway | Intestinal Phase
A
- Intestinal phase: triggered by chyme & counteracts gastric acid secretion by slowing down gastric emptying to give small intestine time to absorb and is stimulated by histamine and digested protein
- Releases…
- Secretin: decreases gastric acid secretion → more time for gastric emptying
- Gastric inhibitory peptide (GIP): decreases gastric acid production → more time for gastric emptying
- Cholecystokinin (CCK): released in response to chyme
- Slows gastric motility ⇒ slows gastric emptying
- Stimulates gallbladder to secrete bile for fat breakdown
- Stimulates pancreas to produce digestive enzymes that break down fats, carbs, proteins in small intestine
- Releases…
4
Q
IS and Gastric Acid Secretion
A
- 1st lvl of defense: prostaglandins + histamines (can also cause gastric acid secretion)
- Mucosal secretions: produces antibodies IgA
- B-cells produce IgA antibodies to protect against pathogens
- Paneth cells: produce defensins and other antibiotic peptides and lysozymes important to mucosal immunity
- Peyer patches: collections of lymphocytes, plasma cells, macrophages
- Produces IgA as a component of gut-associated lymph tissue in small intestine
- Attacks and eats IgA that have marked foreign pathogens (seek and destroy)
5
Q
Hepatic encephalopathy
A
- Liver dysfunction → liver can’t break down toxins, specifically impaired ammonia metabolism → liver can’t break down ammonia to urea that’s filtered in kidneys like usual → circulates to brain → causes confused, agitated, other behavioral disturbances on patient
- If pts have kidney failure, they can’t filter urea → have increased blood, urea, nitrogen (BUN) lvls
- Causes: liver dysfunction, neurologic syndrome of impaired behavioral, cognitive, motor functions
6
Q
Types of viral Hepatitis
A
- Hepatitis Type A: acute infections from contaminated food and water
- Hepatitis Type B: blood-borne infections
- Hepatitis Type C: chronic infections
- Hepatitis Type D: depends on exposure to type B
- Hepatitis Type E: enteric (ingested/passes thru GI system) infections from contaminated food and water
7
Q
Hepatic Portal HTN | What is Hepatic Portal Vein + Causes of Hepatic Portal HTN
A
- Hepatic Portal HTN: blood going thru through liver obstructed due to fibrotic tissue or obstruction → disrupts lymph fluid drainage → accumulation of lymph fluid → increased pressure of lymph fluid and blood pressure in hepatic portal vein → fluid accumulates elsewhere like abdomen or other nearby tissues
- Hepatic portal vein: important for carrying blood from digestive organs (including the spleen, stomach, intestines) to be sent to liver to be filtered before being brought up to heart for distribution to rest of body
- “Pressure of lymph fluid” refers to wtv your body is draining in lymphatic system to get filtered
- Causes include:
- Alcohol (especially chronic): alcohol is toxin that destroys liver cells → makes liver cells fibrotic → no liver filtering → backs up hepatic portal vein → backs up into other veins that are connected to the portal venous system like esophagus which has thin vasculature → so increased pressure ruptures it → pt has hemoptysis
- Fibrosis: tissue thickens or scars due to excessive buildup of fibrous connective tissue
- Cirrhosis: severe liver scarring → increases resistance to blood flow in liver
8
Q
Effects of Hepatic Portal HTN
A
- Liver functions/break down decreases → everything accumulates, esp toxins → hepatic encephalopathy
- Hepatic portal HTN gunked up → no drainage of fluid → fluid goes to peritoneal cavity → ascites
- Blood that comes from spleen encounters blockage due to portal vein HTN → blood backs up to spleen → splenomegaly
- Esophagus (other veins that are connected to the portal venous system) has thin vasculature → so increased pressure ruptures it → pt has hemoptysis
- Hepatic portal vein also goes to intestines → so back up in vein causes fluid to accumulate in intestine varices → ruptures → pt has hematochezia
- Hepatic portal vein also innervates stomach → so back up in vein causes fluid to accumulate in stomach varices → ruptures → stomach bleeding
9
Q
Ascites management | Diet restrictions
A
- Ascites: accumulation of fluid in peritoneal cavity bc hepatic portal HTN gunked up → no drainage → liver can’t break down albumin to maintain fluid in vasculature bc albumin helps pull water to bloodstream/interstitial vessel
- Management:
- Restrict sodium-high foods bc ascites is associated w/ renal sodium and water retention and eating more sodium ⇒ pulling more water in bc water goes w/ sodium ⇒ exacerbates fluid accumulation in peritoneal cavity
- Give patient more albumin/protein because it helps water to bloodstream/interstitial vessel and out of the peritoneal 3rd space cavity
- Tell pt not to drink alcohol bc alcohol damages it damages liver that produces albumin that’s needed to help pull water to bloodstream and not peritoneal cavity
- Tx: Paracentesis: blunt needle that taps peritoneal cavity to drain fluid (not blood bc it’s lymph interstitial fluid that’s unable to be filtered by liver)
- Drained via gravity
- Causes huge fluid shifts in system bc changes in hydrostatic pressure ⇒ drop in BP ⇒ monitor pt’s BP
10
Q
Rebound tenderness and guarding is indicative of?
A
Cholecystitis: gallstones stuck in bile duct → hardened deposits of fats and other types of lipids get stuck in bile duct that’s important for draining and sending bile → gallbladder backs up → inflamed sack → gallbladder pain/“colic pain” that can present as rebound tenderness and abdominal guarding/tensing
11
Q
Metabolism of bilirubin
A
- RBC destroyed → results in hemoglobin → hemoglobin splits to heme and globin → heme turns to biliverdin → unconjugated bilirubin (lipid soluble)
- In plasma/blood, unconjugated bilirubin + albumin = albumin allows/pulls unconjugated bilirubin →
- In liver hepatocytes, unconjugated bilirubin + glucuronic acid joins to make = conjugated bilirubin in bile channels that’s now water soluble and can be excreted w/ bile →
- If hepatocytes in liver were deceased/dysfunctioning → no albumin → unconjugated bilirubin can’t be pulled into blood → build up unconjugated bilirubin ⇒ jaundice
- In intestine, conjugated bilirubin excreted w/ stools → turns to urobilinogen in liver → so that urobilinogen can be excreted as feces or urine in kidneys
12
Q
Causes of jaundice | Obstructive & Hemolytic
A
- Obstructive jaundice: something blocks gallbladder’s bile ducts (ie. stones) → obstructs bile flow → bile duct can’t drain bile to intestine like usual → bile backs up in liver → liver that processes bilirubin and excretes it to bile as usual can’t → bilirubin stuck → builds up in bloodstream
- Hemolytic jaundice: RBCs breaking down too fast → increased production of unconjugated bilirubin bc liver can’t produce enough albumin to start conjugation process of it fast enough → discoloration of sclera, skin, dermis, etc.
13
Q
Where do PUDs mostly occur
A
- Duodenum
- Stomach
- Esophagus
14
Q
Goals of Antibiotics + PPI/H2 Regimen Together
A
- Treat infection (H. pylori that causes PUDs)
- Reduce gastric acid
- Mitigate pain
15
Q
PPI Goals, MOA, Nursing Consideration
A
- Goals: reduce gastric acid and give PUDs time to heal
- MOA: reduces acid secretion in stomach by binding irreversibly to enzymes that acts on potassium/hydrogen pump mediated by ATPase → prevents H+ from leaving cell and binding to chloride ions bc they make gastric acid combined → decreases gastric acid secretion
- Nursing Considerations:
- Best to administer before breakfast on empty stomach bc stomach produces lots of stomach while eating so give it before eating to let med marinate
- Can be given w/ antacids bc they form synergistic effect by further neutralizing stomach environment pH
- Monitor LFTs bc this med is metabolized by liver so if pt has liver failure ⇒ med can’t be processed ⇒ stays in system ⇒ toxicity
