GI P1 Flashcards
What are the major function of the GI system?
Major fxns:
ingestion (take nutrients in)
Digestion (eliminate solid waste)
Absorption
Of nutrients, vitamins, mineral, electrolytes, water= supply energy to fuel body.
- collection and elimination of solid wastes
The gi tract is an..
Extension of the external environmnt
For something to be considered par of your body,
It had to cross intestinal wall, enter your blood, r your lymph nodes
What are the 4 divisions/sections of the gi tract
- Upper (mouth, esophagus, stomach) **intake valve
- Middle (small intestine:consists of duodenum, jejunum, & ileum) **majority of digestion and absorption
- Lower (cecum, colon, rectum, anal canal & appendix) **mostly storage & waste
- Accessory organs (salivary glans, liver, exocrine pancreas) *food doesn’t actually pass through=produce enzymes and digestive secretions that help food digestion
What is your normal flora?
Bacteria in intestines
Appendix = safe house for normal flora
Probs that could affect different divisions ofGI tract:
Upper: weak or incompetent esophageal sphincter (end of the esophagus that joins the stomach)
Job of esophageal sphincter?
Prevent reflux: you don’t want food in stomach refluxing into esophagus= complaints of heartburn, hoarse voice, dry cough de to acid reflux (inflammation)
If the reflux is CHRONIC…
It is referred to as GERD (Gastrointestinal reflux dz)
Caused by: weak/incompetent esophageal sphincter
Due to chronic inflammation what will we see?
More serious than a heart attack = scar tissue formation in esophagus.
Prob w scar tissue? Narrowing or stricture, which would cause pt to complain of difficulty swallowing.
What is the medical term for difficulty swallowing?
Dysphagia (feeling like food is stuck in your throat/esophagus) ex: taking vitamins, feeling like its stuck)
Probs that could affect different divisions of GI tact:
Lower: Appendicitis (inflammation of appendix)
Why is obstructions in the appendix a problem?
Obstruction is a problem bc secretions can’t get out= increased accumulation and pressure that will compress on the blood vessels in wall of appendix
What will result if pressure compresses on blood vessels in the appendix?
Results in appendix becoming ischemic(impaired blood flow/oxygen)
If appendix is ischemic= death of tissue
If appendix is ischemic=death of tissue
What is the medical term for death or tissue?
Gangrenous or necrotic meaning it could rupture or perforate
Upper GI:
When cells are exposed to chronic irritation /inflammation=
Undergo metaplasia in esophagus(changing from one cell type o another that is better able to withstand irritation)
If this happens this could result in……?
Dysplasia!(term used to describe presence of abnormal cells within a tissue or organ) which is a RF for cancer
What are the 5 layers/ structure of the GI Wall?
- Mucosa (very inside layer made up of epithelial cells that produce mucus)
Purpose=lubricate and protect inner lining of GI tract - Submucosa (made of CT, has all blood vessels, nerves, and glands that make DIGESTIVE ENZYMES)
- Circular smooth muscle (mixing action of GI tract)
- Longitudinal smooth muscle (facilitates movement of contents of GI tract)
- Serous a (very outside double-layered membrane called the peritoneum
One layer of the peritoneum is attached to_______ and the other layer is attached to ________
- Outside of GI tract
- Abdominal wall
Between the two peritoneum layers (GI tract & abdominal wall) is the…
Peritoneal space/cavity: has small amount of fluid to decrease friction
PROBS that affects GI wall:
I there is a large amount of fluid in peritoneal space, this is called..
Ascites
PROBS that affect GI wall:
If injured by trauma or disease, like any other tissue, this might cause
GI bleed
Look for pts who have blood in stool or in vomit
Red or black/ tarry stool indicates..
Blood in stool: occult (hidden/cant always be seen w eyes)
If hidden do chemical tests like Guaiac or hemoccult
Black/ tarry stool: Melina (exposure to digestive enzymes)
GI bleeds: vomit also called ______ in medical terminology
Hematemesis (hema: blood, -emesis: vomit)
Hematemesis could be bright red (anal, rectal, or esophageal bleeding) or have a dark/chunky coffee ground look (comes from stomach or small intestine)
What makes vomit look dark/chunky coffee grounds?
Exposure to all acids in digestive enzymes
Sterile questions:
Peritoneum is___
GI tract is _____
STERILE
NOT STERLE
Since GI Tract is not sterile, if the contents were to leak in the peritoneal space, what happens?
Appendix ruptures, stomach ulcer proliferating through stomach wall, or GI surgery/stab or gunshot wound
If content leaks in peritoneal space this means?
We are contaminating a sterile space so we should expect inflammation and infection to occur, fever, high WBC ct., pain (aggravated by movement,etc..)
In the case of peritonitis, third spacing can happen..
By fluid shifting either in the peritoneal space or the GI tract
Why is there fluid shift?
Part of the inflammatory response=blood vessels get “leaky”
Third spacing (fluid leaving blood vessels) →
Hypovolemia (low blood vol.) → hypotension (low BP) → tachycardia (body’s attempt to bring BP back up)
Mobility in the GI tract →
Motility(move from one end to another)
→smooth muscle happens automatically (don’t have to think ab it, it just happens)
2 places that have voluntary skeletal muscle instead of smooth muscle
- Pharynx (upper part of the esophagus) top of gi tract- voluntary control over what you swallow
- External anal sphincter (voluntary control of bowel movement)
PROBS that can affect GI motility (move from one end to another)
- infection/ inflammation in intestines: peristalsis becomes fast = diarrhea
- vomiting (reverse peristalsis) → things are moving through GI tract in wrong direction
Vomiting center in the medulla:
GI tract → vomiting center (vomit to relive dissension) → cerebral cortex (see/smell something horrid) → ‘vesti’bular center (inner ear=balance/carsick,sea sick, air sick) →chemoreceptor trigger zone( job: monitor blood for presence of anything poison/toxic// protective purpose)
If there is a lot of diarrhea what kind of problem happens?
FLUID IMBALANCE, ELECTROLYTE IMBALANCES, & MALNUTRITION/MALABSORPTION
What is the useful purpose of vomiting ?
-tells you something is wrong (dz process)
-gets rid of poisons/toxins
If there’s too much vomiting for a prolonged time, what problems will it cause?
Acid-base imbalances, fluid imbalance, electrolyte imbalance
How GI fxn is regulated: 3 control mechanisms
1.Enteric nervous system (intrinsic)
2. Autonomic NS
3. GI Hormones that regulate digestion
- Enteric Nervous system or intrinsic
Network of nerves that are located on the wall of the G.I. tract and they are responsible for a lot of local reflexes that occur there. Example, if you eat a lot, the stomach/duodenum gets distended = reflex increase motility/peristalsis in the intestines(relief of distention)
→also mediates input from the 2nd control mechanism
- Autonomic NS
- Sympathetic= decreased G.I. motility and production of secretions(mouth goes dry) part of the fight or flight/stress crisis response=not important to digest in crisis
Vs 2. Parasympathetic= increase G.I. motility and secretions. Promotes digestion and motility.
What happens if the parasympathetic nerves get damaged?
Problems with G.I. motility and impaired digestion (impaired gastric emptying=bloating, getting full fast= impaired G.I. motility)
When there is problems with G.I. motility and impaired digestion, this is called (medical terminology)
Gastroparesis (Gastro: stomach, -paresis: “weakness”)
The parasympathetic nerves being damaged is a common sign in patients with
Diabetes mellitus (high sugar in the blood, when not controlled it damages the blood vessels that supply blood to the parasympathetic nerves →atrophy(body part or tissue shrinks or wastes away due to lack of use or stimulation) → secretions suffer
3.GI hormones that regulate digestion (3)
Gastrin, Secretin, CCK (cholecystokinin): these 3 hormones are produced by GI tract & are involved in regulating the GI fxn
Digestion begins in the …
Mouth w/ saliva from salivary grands
→ breaking food down into basic parts
Proteins → amino acids
Starches → monosaccharides
Saliva contains
Mucus (lubrication) and antibacterial properties (food we eat that is not necessarily sterile).
Two digestive enzymes in saliva: (start the digestion of starches)
- Tyelin
- Amylase
Stomach enzymes: (4)
1.Gastrin,
2.Pepsinogen (enzyme that starts digestion of protein),
3.hydrochloric acid (acidity lowers ph of stomach & activates pepsinogen & dissolves fibers in the food we eat & bactericidal:pathogens that got in through saliva, die in stomach cuz of HCL) and Intrinsic factor (to absorb vitamin B12//prob if cant absorb b12= pernicious anemia)
4. Mucus (protection)= acid, enzymes, & friction
digestion begins in
Mouth and ends in stomach (small intestine)
Stomach enzyme: Pepsinogen
Pepsin: enzyme that starts digestion of protein (from chief cells)
Stomach enzyme: HCL
- Acidity lowers stomach pH
- Activates pepsinogen & dissolves the fibers in the food we eat
- bectericidal pathogens that enter through saliva, die in stomach due to HCL
Stomach enzyme: Intrinsic factor
- absorbs vitamin b12
- if there’s a problem w absorbing vitamin b12=pernicious anemia
Stomach enzyme: mucus:
- protects stomach from what’s inside: HCL (acid), pepsin (enzymes), & friction from food.
Small intestine: (2) JOBS
23 ft long and skinny loops of villi (increase surface area)
- (1)makes lots of secretions and (2)receives lots of secretions from accessory organs → GI Tract
Exocrine vs endocrine
Exocrine: secrete substances to the ductal system
ENdocrine: secretes products directly IN to bloodstream
Exocrine pancreas makes _____ that help digest food.
Pancreatic enzymes (work better in a slightly alkaline environment.) Bicarbonate → neutralize acid → enzymes work more effectively.
Pancreatic enzymes (3)
PANCREATIC
Amylase (digestion of carbs)
Proteolytic enzymes like trypsin (breakdown proteins)
Lipase (break down fats)
Pancreatic
Lipase →
Amylase →
Protease →
Pancreatic
Lipase → fats
Amylase → startch
Protease → protein
Stomach contents are:
Thick and concentrated: HCL → water to help neutralize acid to protect the mucosa of small intestine
The small intestine mixed bile from:
The liver and lots of serious fluid that gets released to the G.I. tract (dilute what comes from stomach = nutrients get absorbed better in watery environment)
Role of bile:
To emulsify fats (break down into small enough pieces)
Digestive enzymes that are produced in the small intestine are called
Brush border enzymes(hang out on the border of the villi)
Large intestine ONLY secretes
Mucus and maybe water
Large intestine fxn:
Store solid waste until time to get rid of it
Absorbs water
ONLY SECRETES mucus
Interference of both small and large intestine?
Not enough digestive enzyme= problem could be inflammation or autoimmune attack on organs
What are the two problems if there is not enough digestive enzymes?
- Most obvious, trouble digesting nutrients(nutritional deficiencies, not absorbing vitamins and protein)
- Diarrhea.(nutrients don’t get absorbed, and it stays in the colon.)
What is the reason why we don’t all have peptic ulcers?
Because of the gastric mucosal barrier: digestive enzymes are meant to break down protein, and mechanical friction from the food we eat
Gastric mucosal barrier protects our stomach- the barriers are:
- Mucus (in the name): produces bicarbonate
- Really tight junctions btwn epithelial cells (prevents acids leaking in and causing damage)
- Lipid layer: protects stomach lining from damage caused by water soluble substances.water and fat don’t mix=fatty lipid layer protect cells underneath from harmful water-soluble substances
Epithelial cells: also make bicarb which is held at a surface of the stomach by the mucus that’s produced. Acid →go through bicarbonate →before contact with cells
What happens if gastric mucosal layer gets broken? (2)
- Gastritis which is inflammation of the stomach lining.
- Peptic ulcer disease, which is a chronic health problem, ulcers, heal, and tend to recover.
There are often episodes of remissions and exacerbations(healed, scar tissue, not as strong as sturdy as undamaged tissue)
And peptic ulcer disease when ulcers recur in episodes of remissions and exacerbations what does this mean?
It becomes chronic, ulcers, recur in the same spot over and over
PF for PUD:
What happens when a patient takes lots of NSAIDs?
They are at higher risk for ulcers because they are not making as much protective G.I. Prostaglandins
Primary symptom of PUD
Epigastric pain (between meals or @ night due to stomach being empty)
S/s of gastric ulcer:(3)
Opposite of duodenal ulcers
- Eating triggers pain (food → stomach → makes more acid → aggravates ulcer pain)
- Lasts a few hours (until food leaves stomach) = pain lessens
- Less likely to wake up w ulcer pain (food not in stomach anymore)
S/s of duodenal ulcers:
Opposite of gastric ulcer
- Eating relieves pain. (People put food in their stomach, pyloric sphincter tightens, less leakage of gastric acid into duodenum where the ulcer is)
- Pain occurs 2 to 5 hours after eating, when food leaves the stomach, enters the duodenum where the ulcer is.
- Ulcer pain at night= still food in the small intestine
Patient to have ulcer pain at night, monitor for serious complications like injure tissue, which could result to bleeding
Stress ulcers are common in
ICU/pts on ventilators
Stress ulcers r/t
- Sympathetic NS effects (under stress = f/f response)
- Decreased blood in GI tract = f/f response: blood shunted away from skin & GI tract—>goes to brain and skeletal muscle—> under crisis= NEED brain and skeletal muscles to do F/F—> ischemia(blood shunted away)
Anti ulcer med: prevents stress ulcers
inflammatory bowel dz: accompanied by recurrent diarrhea—> urgency to go now
SEPARATED INTO 2 DZS:
1. Affect diff sections of GI tract
2. Affects diff layers of GI wall
3. Different tissue response to inflammation
Crohn’s Dz aka Regional Enteritis
Ulcerative colitis
*look at notes & quizlet
Irritable bowel dz vs. irritable bowel syndrome
Syndrome :not autoimmune(IBS)
Dz:autoimmune (IBD)
Loos at notes and quizlet for differences
If you have a patient with IBD, you can’t just focus on assessing the G.I. system. Why is that?
If there are extra intestinal manifestations: G.I. problems will happen first and then then develop in other body systems or the other way around
In a patient with IBD, if they are not responding to medication treatment, what do we do?
We perform an ostomy (take section of intestine and open it up on abdominal wall= content draining outside of the body)
A pouch is worn so it collects what drains out of the ostomy
When do we preform a temporary ostomy?
Why do pts do this?
In pt’s with ulcerative colitis (trouble clearing inflammation/getting pt into remission)
Temporary ostomy allows colon to rest—>ulcerations have a chance to heal—> surgically reconnect the 2 parts of the GI tract
People do this because they say they hate “spending their life in the bathroom”
Pancreas
Endocrine cells: islet of Langerhans: make insulin and glucagon( both regulate glucose metabolism)
Exocrine cells: acinar cells: lobes around drainage ducts= drain into the main pancreatic duct, will empty through ampulla of vater through the sphincter of oddi into the duodenum
Pancreas creates
Trypsin inhibitor: which prevents trypsin from activating in pancreas
Trypsin activates all digestive enzymes of pancreas
Common disorder of exocrine pancreas:
Acute pancreatitis: inflamed pancreas=pancreatic enzymes activating in pancreas.
“Auto digestion:” digests itself
PF to pancreatitis: (2)
- Biliary tract dz: bile ducts in & out of liver (hepatic, cystic and common bile duct)
Gallstones in pancreas = not enough trypsin inhibitor = starts digesting itself
In the bile ducts in & out of liver there’s 3 ducts:
Hepatic duct: brings bile from LIVER
Cystic duct: brings bile from gall bladder
Common bile duct (hepatic and cystic form this duct=joins w pancreatic duct)
What does it mean to be hyperglycemic?
When the pancreas starts to digest self, it affects the endocrine pancreas, and it can release insulin to control glucose
Part of treating the signs and symptoms is also giving insulin and calcium
in acute pancreatitis, it can cause more damage like spreading to the lungs and eventually leading to death
Once the pancreatic digestive enzymes (pancreatic amylase, trypsin, and pancreatic lipase) are activated inside the pancreas, the enzymes start to break down tissue in the pancreas. If blood vessels in the pancreas are damaged, then some of the digestive enzymes can get into the bloodstream through the damaged areas of the blood vessels, and then get carried to other parts of the body (like the lungs) where they can then start “digesting” (aka attacking its own tissue) leading to inflammation and causing damage (auto digestion)in those other parts of the body. These enzymes are not supposed to be elsewhere in the body bc they are pancreatic enzymes.
What can go wrong in the bile and the gallstones in biliary tract dz?
Sometimes in Biliary tract disease, you have bile coming down the bile duct and instead of draining into the small intestine… it will reflux back up the pancreatic duct into the pancreas
IF YOU HAVE BILE REFLUXING UP INTO PANCREAS, that can activate some of the pancreatic enzymes & pancreas will start digesting itself.
OR Gall stones will start to form and block enzyme from getting out of the pancreas—> since pancreatic enzymes can’t leave pancreas—> the amount of enzymes in pancreas will start to build and eventually there will be not be enough trypsin inhibitor to keep it from activating—> so the enzymes will activate inside the pancreas and the pancreas will start digesting itself
What results when the pancreas starts to digest itself?
Severe pain in the epigastric and abdominal areas
Often the pain will radiate to the back because pancreas is located in the retroperitoneal space which is why pain radiates the back, retro means behind.
Abnormal labs: amylase &lipase
Increase in serum amylase (goes up in the first 3 to 4 days)
Increase in serum lipase (10 to 14 days) these are both digestive enzymes (not found in the blood)
CATS of hypocalcemia
Convulsions(muscles contracts and relax rapidly and repeatedly), Arrhythmias(improper beating of the heart), Tetany (due to low ca levels:muscle cramps/spasms/tremors- tetanus shot, Spasms & Stridor
What is hyperglycemia? (High blood glucose level)
Glucose levels increase, digestive, enzymes, activate, and start digesting. The pancreas, enzymes will not only attack, pancreas cells, but they’ll start digesting the endocrine pancreatic cells. Reduction in insulin production= blood glucose levels increase
How to prevent pancreas from making more enzymes?
The more enzymes that gets made and released= the more pancreatic damage
We quit feeding them, when food hits the stomach, the pancreas gets signal to make more enzymes to digest that food=NPO—> tube—> hooked to suction to make sure stomach stays empty—> Not stimulating digestive enzymes
