GI System Flashcards
GI Tract
GI TUBE: anything passing through is external, once absorbed it is internal mouth esophogus stomach small intestine large intestine recturm anus
zymogens
enzymes that are inactive “ogen” = inactive, immature
fxns of GI tract
- INGESTION of food
- MOTILITY: peristalsis and segmenta - propulsion of food and wastes from mouth to anus
- SECRETION of mucus, water, and enzymes
- MASTICATION mechanical digestions of food particles
- chemical digestion of food particles
- absorption of digested food - small intestines
- elimination of waste products by defecation
GI Enzymes
- carbs: amylase (saliva, pancrease)
- protein: prolease (stomach pepsin) (pancrease trypsin, chymotrpson)
- lipids/fats: lipase (after emulsification by bile)
- nucleic acid/DNA/RNA: nuclease
GI tract Layers
- mucosa: inner layer, absorption
- submucosa: secretions, blood supply
- muscularis: 2 layers of smooth muscle - circular (pinch and constrict) & longitudinal (propel food forward)
- serosa: visceral layer - peritoneum
Mouth
- chewing and mixing food with saliva: mastication, and start of chemical digestion
- taste buds (CN VII, IX): salty, sour, sweet, bitter, umami
- olfactory nerves (CN I) smell involved in taste
- teeth - 32 premanent teeth, mastication
salivary glands
- paried glands: submandibular, sublingual, parotid
- saliva: water with mucous, sodium, bicarbonate, chloride, potassium, and amylase (carb digestion)
- bollus = matter that we swallow
deglutination
swallowing - then involuntary movement begins
- esophogus: peristalsis & segmentation
- upper esophogeal sphincter: stenotic sphincter, oral cavity to eshophogus, Choking, gerd
- lower esophageal sphincter: cardiac sphincter = entrance to stomach, vomiting, heart burn
stomach
- holds food 2-6 hours
- hollow, muscular organ that stores food, secretes digestive juices, mixes food with juices, and propels partially digested food (Chyme = bollus once mixed with gastric juices in stomach)
- 3 layers: longitudinal, circular, oblique
Stomach Gastric Juices
JUICES
- mucus
- HCL acid: converts pepsinogen to pepsin
- enzymes: pepsin (breaks down protein)
- hormones: gastrin and grelin (hunger hormones), regulates gastric juices
- intrinsic factor: vitamin B12 absorption, pernicuious anemia
GLANDS/PITS
- parietal cells: hydrochloric acid (breaks down) and intrinsic factor (b12)
- chief cells: pepsinogen (protein digestion)
- G Cells: gastrin and grelin (hunger cells)
- hydrochloric acid: denatures proteins, antimicrobal, converts pepsinogen to pepsin
vagus nerve –> gastrin –> hisamine –> parietal cells –> HCL
Gastric Secretion
gastric secretion/acid secretion/ saliva secretions
- cephalic phase: congitive - thinking about food makes you salivate and secrete gastric juices
- gastric phase: stomach - chemicle signal (exposure to tongue) and chemoreceptors (smell and taste)
- intestinal phase: food enters into duodenum (through pyloric sphincter), decreased saliva and gastric juices, inhibition phase
small intestines
- 5-6 cm long
- absorption - doesn’t secrete anything
- three segements: dueoden –> jejunum –> ilium (iliosecal valve from small to large intestine)
- peritoneum - mesentaries, hold intestines in place in body
- villi: lactile (drains fats in middle of villi), has hairs to increase surface area, burshborder epithelium
intestinal digestion
pancreatic enzymes: amylase (carbs), trypsinogen and chymotripsinogen (protein), lipase (fats), nuclease (DNA, RNA)
- Bile salts: made in liver, stored in gallbladder
intestinal absorption
carbs, proteins, fats, water, electrolytes
where are diff nutrients absorbed?
- stomach: water, alcohol, caffein, nasals (aspirin)
- duodeunum: iron, calcium, fats, sugars, water, proteins, vitamins, magnesium, sodium
- jejunum: sugars, proteins
- ilium: bile salts, vit b12, chloride
- colon: water, electrolytes
large intestine
- cecum: next to appendix, iliocecual valve
- appendix: stores microbial flora of gut
- colon: ascending, transverse, descending, sigmoid
- recturm
- anus
- colorectal cancer is most common in rectum and sigmoid. most fatal. highest site of pathogens, compactions, constipation
liver
LOBES: separated and attached to the anterior abdominal wall by falciform ligament
- right lobe - caudate lobe, quadrate lobe & left lobe
- Hepatic portal vein & system
- vein enters into liver to be detoxified then puts it into systemic circulation: blood from GI tract, filtrations from spleen, other bad stuff absorbed
- if liver fails then you get hepatic portal hypertension = ascites, splenomegaly, verses
LIVER LOBULES
- hepatocytes
- sinusoids (specialized capillaries)
- kupffer cels (Macrophages)
- common bile duct
liver secretion of bile
- cholesterol produces bile
- bile is alkaline, yellow/green, contains bile salts, cholesterol, bilirubin, electrolytes and water
- bile is formed by hepatocytes and secreted into bile canaliculi
functions of liver
- blood storage
- bacterial/foreign particle removal
- synthesizes plasma proteins/ clotting factors
- produces bile
- metabolizes fats, proteins, carbs
- detoxes metabolic products and wastes
- storage of minerals, vitamins
gallbladder
stores and concentrates bile between meals
- lies inferior to liver
pancrease
- secrete enzymes and alkaline fluids to assist in digestions
- exocrine: amylase, lipase, trysin, chymotrypsin, nuclease
- endocrine: insulin, glucagon (NOT GI, blood sugar)
SECRETIONS: bicarb, symogens, pancreatic amylase, pancreatic lipase, nuclease
symptoms of GI dysfunction
- anorexia: lack of desire to eat
- vomiting: emptying of stomach and intestinal contents, hyper salivation, tachycardia
- nausea: most common symptom
- retching: dry heaving, nonproductive vomiting, can induce vomiting of bile
- abdominal pain: referred pain, dull, achy, decrease in number of nociceptors
- constipation: sigmoid or recturm, infrequent or difficult defecation
- diarrhea: frequency or volume increases, fluidity, weight of feces
> mechanisms of diarrhea - osmotic diarrhea: electrolyte change draws fluid into intestine instead of out
- secretory diarrhea: bacterial toxins in instestin, food poisoning, increase in H2O, increased motility
- motility diarrhea: increased motility decreases digestion increases diarrhea, smooth muscle or nerve issue (anxiety), caffeine
- GI bleed: hematemesis (vom blood), hematochezia (Bloody stools)
dysphagia
- difficulty swallowing
- achalasia: loss of nervous control, decreases swallowing ease
Gastroesophageal reflux (GERD)
reflux of chyme from stomach to esophagus
- insufficiency of cardiac sphincter
- inflamm of esophoagus = reflux esophagitis
- any condition that increases abdominal pressure can contribute to gerd
hiatal hernia
- movement of intestine into an area it shouldn’t be
- through diaphragm
- protrusion of upper portion of stomach through diaphragmatic hiatus into thorax
- sliding or paraesophageal
pyloric obstruction
stenosis, bottom of stomach
- blocking or narrowing of opening between the stomach and duodenum
- vomiting soon after eating
dumping syndrome
rapid emptying of chyme from a surgically created residual stomach into the small intestine
- pyloric unsufficiency: bypasses pyloric sphincter, violet diarrhea
- bariatric surgeries
- clinical complication of partial gastrectomy or pyloroplasty surgery
intestinal obstruction
any condition that prevents flow of chyme through intestinal lumen or failure of normal intestinal motility - mechanical blockage
- ileus: an obstruction of intestines from folding, pinching, lack of peristalsis = decreases peristalsis, physiological response = ischemia/necrosis
peptic ulcer disease
break or ulceration in protective mucosal lining of lower esophagus, stomach, duodenum
- acute and chronic ulcers
- upper GI ulceration in esophogus, stomach or duodenum
Duodenal Ulcers
Duodenal ulcers:
- small intestine
- most common
- H pylori infection
- hyper secretion of stomach acid and pepsin (use of nasals, cigarette smoking produces acid)
1st. H pylori
2nd. nsaids
gastric ulcers
stomach
- tend to develop in astral region of stomach
- 1st over use of nasals
- 2nd. H pylori
stress ulcers
peptic ulcer that is related to severe illness, neural injury, systemic stress/trauma
maldigestion
- failure of chemical processes of digestions
leads to…
malabsorption: failure of intestinal mucosa to absorb digested nurients - frequently occur together
pancreatic insufficiency
insufficient pancreatic enzyme production: lipase, amylase, trypsin, chymotrypsin
- causes: pancreatitis, pancreatic carcinoma, pancreatic resection, cystic fibrosis
- fat maldigestions is a major problem, so patient will exhibit fatty stools and weight loss
lactase defficiency
issue breaking down dairy cow milk
- can’t break down lactose into monosaccharides and therefore prevents lactose digestion and monosaccharide absorption
- isn’t broken down in small intestine then moves to large intestine where there is increased flatulance and diarrhea
bile salt defficiency
can’t emulsify fat
- conjugated bile salts are synthesized from cholesterol in the liver needed to emulsify and absorb fat
- can results from liver disease and bile obstructions
- poor intestinal absorption of lipids causes fatty stools, diarrhea, loss of fat-soluable vitamins (A, K, D, E)
fat soluble vitamin deficiencies
- vit A: retina vitamin, lack of clack and white vision, night vision
- vit D: decreased calcium absorption, bone pain, osteoporosis, fractures
- vit K: prolonged prothrombin time, pupura, petachiae, lack of clotting
- vit E: regulates cell processes
inflammatory disorders
chronic, relapsin inflammatory bowel disorders or unknown origin
- genetics, allegations of epithelia barrier functions, immune reactions to intestinal flora, abnormal t cell responses
- idiopathic
gastritis
inflammation of stomach lining
- inflame of gastric mucosa
- acute - over consumption
- chronic - infection, h pylori, nsaids, alcohol
ulcerative colitis
large intestine
- chronic inflamm causes ulceration of colonic mucosa - sigmoid colon and rectum
- may lead to increased risk of colon cancer
H pylori
normal in large intestine
- not normal in stomach or small intestine
hematochysia
bleeding from colon
chrohn’s disease
anywhere from mouth to anus
- idopathic inflamm disorder that affects any part of digestive tract
- difficult to differentiate ulcerative colitis with crohn’s
- causes skip lesions (spots of necrosis) and cobblestone effect (deep ulcerations)
diverticular disease of the colon
diverticula = out pouching
- herniations of mucosa through the muscle layers of the colon wall, especially the sigmoid colon
diverticulosis = one of more pouches
- asymptomatic diverticular disease
- weakening of intestinal wall
diverticulitis = inflammatory stage of diverticulosis
- food traps in diverticula
- tomato and chile seeds lodge in diverticula
appendicitis
houses flora (bacteria)
- inflamm of the vermiform appendix
- possible causes are obstruction, ischemia, increased intraluminal pressure, infecton, ulceration
- RLQ pain with rebound tenderness
- rupture releases tons of bacteria
irritable bowl syndrome
idiopathic
- 20% worldwide
- more common in women
- youth and middle age
- associated with anxiety and depression
obesity
genetics, hormones, increase in body fat
- BMI greater than 30
- cause of morbidity, death, increased health care costs
risk factor for many diseases and conditions
- associated with hormone imbalances and hypothalamus dysfunction
starvation
short term: glycogenolysis, gluconeogenesis (normal weight loss)
long term: marasmus (emaciated), kwashiorkor (protruding belly)
portal hypertension
liver disorder
- high BP in portal venous system caused by resistance to portal blood flow
- varices: back up of venous blood that can lead to vein rupture and blend in the GI tract
- splenogmegaly
- ascites
- hepatic encephalopathy
hepatic encephalopathy
neurologic syndrome of impaired cognitive function
- develops rapidly during fulminant hepatitis or slowly during chronic liver disease
jaundice
lack of bilirubin metabolism in liver leading to yellowing
- obstructive jaundice - post hepatic and intrahepatic
- hemolytic jaundice - perhepatic, excessive hemolysis of RBSs or absortion of a hematoma
viral hepatitis
systemic viral disease of acute or chronic inflammation that primarily affects the liver
- HEP A: infections hepatitis
- HEP B: serume hepatitis
- HEP C, D, E, G
Hep A
transmitted by fecal-oral route
- found in feces, bile, sera
- risk factors - crowded, unsanitary conditions, food and water contamination
HEP B
transmitted through contact with infected blood, body fluids, contaminated needles
- maternal transmission can occur if the mother is infected during the 3rd trimester
- can cause chronic hepatitis
- hep B vaccine
HEP C
responsible for most cases of post-transfusion hepatitis
- also implicated in infectious related IV drug use
- 50%-80% of hepatitis C cases result in chronic hepatitis
HEP D
depends on HEP B for replication
HEP E
fecal-oral transmission
- developing countries
HEP G
recently discovered
- parentally and sexually transmitted
Cirrhosis
irreversible inflammatory disease that disrupts liver function and even structure
- slow development to chronic disease
- decreased hepatic function caused by nodular and fibrotic tissue synthesis
- biliary channels become obstructed and cause portal hypertension
- blood shunted away from liver and hypoxic necrosis develops
- alcoholic: oxidation of alcohol damages hepatocytes
- bilary: cirrhosis begins in the bile canaliculi and ducts
- fatty liver disease: fat build up causes fibrosis and scarring, NASH
disorders of gallbladder
obstruction or inflammation (Cholecystitis) is most common cause of gallbladder problems
- cholelithiasis - gallstone formation
- cholesterol, most common
- pigmented, cirrhosis
disorders of pancreatitis
- inflamm of pancreas
- caused by injury or damage to pancreatic cells and ducts, causing leakage of pancreatic enzymes into pancreatic tissue
- activated zymogens cause autodigestions of pancreatic tissue and leak into bloodstream to cause injury to blood vessels and other organs
- chronic pancreatitis - related to alcohol abuse
