Pathophys > GI System > Flashcards

GI System Flashcards

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1
Q

Basic organization of the GI tract

A

mouth -> pharynx -> esophagus -> stomach -> small intestine -> large intestine -> rectum -> anus

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2
Q

purpose of GI

A

-ingestion of food
-propulsion of food and wastes
-secretion of mucus, water, and enzymes
-mechanical & chemical digestion
-absorption of nutrients
-immune and microbial protection against infection
-elimination of waste products

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3
Q

core functions

A

-motility: peristalsis propels, segmentation mixes
-secretion: salivary glands, liver/gallbladder, pancreas
-digestion and absorption: predominantly in the small intestine
-defense: mucosal barrier and microbiome
-elimination: large intestine and rectum

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4
Q

nervous system control of digestion

A

-enteric NS integrates activity
-PSNS increases motility and secretions
-SNS decreases motility/secretions and increases sphincter tone

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5
Q

voluntary vs. involuntary control of digestion

A

-voluntary: chewing, swallow, external anal sphincter
-involuntary: pharyngeal and esophageal phases of swallow; recto-anal inhibitory/defecation reflex

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6
Q

gastric secretions

A

Gastric hydrochloric acid
Gastric lipase
Mucus
Intrinsic factor

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7
Q

Gastric hydrochloric acid location and purpose

A

parietal cells
acidifies stomach to unfold proteins and convert pepsinogen into pepsin for digestion, helps kill ingested microbes & improves iron solubility for absorption

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8
Q

Gastric lipase location and purpose

A

chief cells
initiates lipid digestion

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9
Q

intrinsic factor location and purpose

A

parietal cells
required for vitamin B12 absorption in the terminal ileum

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10
Q

mucus + bicarbonate

A

surface mucus cells, forms mucosal barrier w/ prostaglandins support; NSAIDs impair -> increase ulcer risk

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11
Q

what is the functional unit of the small intestine and how does it aid in digestion and absorption?

A

villus w microvilli (brush border) maximizes surface area; villus core has capillaries (sugars/amino acids) and a lacteal (fats)

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12
Q

parts of small intestine

A

duodenum, jejunum, ileum

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13
Q

how are carbs digested?

A

salivary amylase -> pancreatic amylase -> brush border disaccharidases -> monosaccharides

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14
Q

how are proteins digested?

A

pepsin -> pancreatic proteases (trypsin/chymotrypsin) -> brush-border peptidases -> amino acids/peptides

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15
Q

how are fats digested?

A

bile salt emulsification -> pancreatic lipase -> micelles -> enterocyte re-esterification (fatty acids are absorbed into intestinal cells and are re-assembled into triglycerides for storage or secretion) -> chylomicrons (lipoproteins that transport dietary lipids) -> lacteals (lymphatic vessels of small intestine)

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16
Q

absorption of nutrients

A

water absorbed mostly in small intestine
carbs absorbed mostly in proximal small intestine
protein absorbed mostly in jejunum
fats absorbed mostly in epithelial cells of small intestine

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17
Q

water soluble vs. fat soluble vitamins

A

fat: A, D, E, K - bile-dependent micelles; stored in liver/adipose; deficiency develops slowly
water: B-complex, C - limited stores, require regular intake (B12 is exception with large hepatic stores)

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18
Q

How is bile formed and what is its flow?

A

hepatocytes synthesize bile acids from cholesterol -> conjugate to bile salts when added with amino acids -> stored in gallbladder -> released with meals -> ~95% reabsorbed in terminal ileum -> portal vein back to liver, ~5% lost in stool

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19
Q

function of the gallbladder and what causes it to contract

A

-stores and concentrates bile between meals
-cholecystokinin from duodenum triggers gallbladder contraction and sphincter of Oddi relaxation when fats enter
-vagal stimulation assists, secretin increases hepatic bile production

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20
Q

GERD - mechanism, triggers, complications

A

transient LES relaxations -> reflux
triggers: nicotine, high-fat foods, chocolate, mint, caffeine, risks increase w obesity/pregnancy
complications: erosive esophagitis -> Barrett’s esophagus (metaplasia - increased adenocarcinoma risk)
management: lifestyle + PPI; barrett’s -> endoscopic surveillance, treat dysplasia

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21
Q

Sliding hiatal hernia

A

part of the stomach moves above the diaphragm into chest cavity thru hiatus; common; reflux-prone

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22
Q

paraesophageal hiatal hernia

A

part of stomach pushes thru diaphragm and lies next to esophagus instead of below it ; risk of incarceration/strangulation -> surgical evaluation if symptomatic

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23
Q

mechanical motility obstruction

A

adhesions, hernia, tumors, strictures, volvulus (physical blockage)

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24
Q

functional motility obstruction

A

impaired peristalsis without physical blockage - post op, peritonitis, severe illness, paralytic ileus (most common) medications/electrolytes

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25
proximal obstruction
early/persistent vomiting -> loss of HCl -> metabolic alkalosis w volume depletion
26
distal obstruction
greater distension/dehydration; lactic acidosis from hypoperfusion can occur (insufficient O2 in tissues -> cells use anaerobic met.)
27
gastritis common causes
H. pylori, NSAIDs, alcohol; chronic forms may progress to atrophy and reduced acid alarming: GI bleed, iron-deficiency anemia, progressive dysphagia, weight loss, persistent vomiting
28
PUD H. pylori mechanism
inflammation -> decreased somatostatin/increased gastrin -> increased acid and impaired defense
29
PUD NSAIDs mechanism
decreased COX-1 prostaglandins -> decreased mucus/bicarbonate and mucosal blood flow
30
Zollinger-Ellison pathophys
overproduction of gastrin leading to severe stomach ulcers Gastrinoma -> marked acid hypersecretion -> refractory/multiple/distal ulcers; diarrhea/steatorrhea from lipase inactivation and bile salt precipitation; consider MEN1
31
Duodenal vs gastric ulcers
Duodenal: -NSAIDs or H pylori -chronic intermittent pain in epigastric area -pain-food-relief pattern -nocturnal pain common Gastric: -NSAIDs, H pylori or duodenal reflux -duodenal reflux of bile-alkaline reflux gastritis -pain-food-relief pattern less than duodenal ulcers -tend to be chronic
32
ulcerative colitis
IBD; continuous **colonic** disease; watery diarrhea, mucus/blood; impaired water absorption
33
crohn's disease
IBD; transmural, skip lesions **anywhere** mouth to anus; granulomas/fistulas; weight loss, diarrhea; macrocytic anemia if ileum involved (B12/folate malabsorption)
34
diverticulosis
herniations in mucosa of colon wall, little pouches form in the inside lining of the colon, caused by increased pressure in colon bc of low dietary fiber, usually no problems but rarely can cause bleeding or develop an infection (precursor to diverticulitis)
35
diverticulitis
inflammation of diverticulum in the colon LLQ pain, low-grade fever, leukocytosis, complications include obstruction, fistula, perforation/abscess; CT to confirm; many uncomplicated cases managed outpatient with selective antibiotics and close follow up
36
appendicitis
inflammation of vermiform appendix obstruction and inflammation can cause appendix to by hypoxic begins as generalized abdominal pain that locates in RLQ, low grade fever
37
IBS
functional disorder of bowel motility, classified as diarrhea or constipation dominant recurrent abdominal pain > 1 day/week in last 3 months plus >2: related to defecation, change in stool frequency, change in stool form, subtype by stool pattern
38
prehepatic portal hypertension
block before the liver, thrombosis, narrowing of hepatic portal vein
39
intrahepatic portal hypertension
block within the liver, vascular remodeling, thrombosis, fibrosis, inflammation
40
posthepatic portal hypertension
block after the liver, hepatic vein thrombosis, cardiac disorders
41
hemolytic jaundice
excessive RBC destruction cause: membrane defect of erythrocytes, anemias, immune rxn, infection, toxins, transfusion rxn
42
obstructive/cholestatic jaundice
obstruction in passage of conjugated bilirubin from liver to intestine: impaired bile flow cause: gallstones/tumor, drugs
43
hepatocellular jaundice
failure of liver cells to conjugate bilirubin and of bilirubin to pass from liver to intestine cause: genetic defect, hepatitis or biliary cirrhosis
44
hepatitis A
incubation 15-50 days, fecal-oral transmission, acute onset with fever, tends to be mild, does not cause chronic hepatitis, affects children and young adults, prevention w vaccine, hygiene, immune serum globulin
45
hepatitis B
incubation 60-180 days, parenteral - sexual transmission, insidious onset, severe - may be prolonged or chronic, can cause chronic hepatitis, affects all ages, prevention w vaccine and hygiene
46
hepatitis C
incubation 35-72, parenteral, insidious onset, mild to severe, can cause chronic hepatitis, affects all ages, hygiene, screening blood, interferon or ribavirin
47
hepatitis sequence
prodromal icteric recovery chronic
48
prodromal phase of hepatitis
2 weeks after exposure, lasts 3-4 days, malaise, fatigue, mild fever, GI symptoms (anorexia, nausea, vomiting, altered smell or taste)
49
icteric phase of hepatitis
1-2 weeks after prodromal, 2-6 weeks, constitutional symptoms improve, pruritis develops
50
recovery phase of hepatitis
resolution of jaundice about 6-8 weeks after exposure
51
chronic phase of hepatitis
years, persistent clinical manifestations, liver inflammation
52
cirrhosis
inflammation, irreversible fibrosis/nodules (thickening) -> portal hypertension and liver dysfunction causes: alcohol, non-alcoholic fatty liver disease, autoimmune cholestatic diseases, low albumin and elevated INR reflect impaired synthetic function
53
Gallbladder disease
gallstones form from bile and cholesterol, gallbladder becomes inflamed, distended or stones can block bile, presents with epigastric and right sided pain and heartburn, pancreatitis is complication
54
cholelithiasis
gallstones from cholesterol
55
cholecystitis
inflammation of the gallbladder, from cholelithiasis
56
choledocholithiasis
presence of gallstones in the common bile duct; jaundice occurs with bile duct obstruction; risk increased in obese middle-aged females, high dietary cholesterol, pancreatitis is a potential complication
57
pancreatitis
damage to pancreas due to leak of enzymes causing autodigestion of pancreatic tissue, vascular permeability and potential hypovolemia, characterized by severe pain causes: alcohol and gallstones severe epigastric pain radiating to back; smoking increases risk, chronic pancreatitis often alc-related
58
GI cancer
esophageal cancer: adenocarcinoma (barrett's) vs squamous cell (tobacco/alc) gastric cancer: H. pylori risk link (distal)
59
adenomatous polyp
projection arising from intestinal mucosal epithelium, most polyps benign, can be detected early colorectal: adenoma-carcinoma sequence, screening age 45
60
pyloric stenosis
affects first born males, could be caused by hypersecretion of gastrin, olive shaped mass can be palpated on infants belly, projectile vomiting and weight loss; hypertrophied pyloric sphincter -> gastric outlet obstruction
61
intussesception
telescoping of bowel, most common cause of bowel obstruction in children, colicky abdominal pain, irritability, knees to chest, vomiting, currant-jelly stools
62
GERD in newborns and infants
reflux common due to immature lower esophageal sphincter, characterized by regurgitation and vomiting, when reflux symptoms become troublesome or complications develop risk factors: prematurity, neurologic, impairment, esophageal atresia, obesity, hernia, achalasia
63
neonatal jaundice
physiologic: transient bilirubin increase with normal adaptation pathologic: first 24 hours, total bilirubin > 20 mg/dL or indirect > 15 -> evaluate for hemolysis (ABO incompatibility), treat to prevent kernicterus (phototherapy/exchange)
64
hirschsprung's disease
congenital condition where nerve cells are missing in a section of the large intestine symptoms: constipation, diarrhea, vomiting abd. distension & bloating
Pathophys
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