EXAM 1 (GI) Flashcards
(103 cards)
1
Q
WHAT ARE THE FOUR LAYERS OF THE GI WALL
A
The layers are the mucosa, the submucosa, the muscularis, and the serosa, which is also called the adventitia.
2
Q
What does the upper esophageal sphincter do
A
keeps air from entering the esophagus when we breathe
3
Q
What does the lower esophageal sphincter do
A
prevents regurgitation of stomach content into the esophagus
4
Q
T/F: Most nutritional absorption happens in the stomach
A
False, its just used to digest. Some things that are lipid soluble may be absorbed (alcohol and aspirin)
5
Q
what are the 3 areas of the stomach
A
fundus (top), body (middle), and antrum (bottom)
6
Q
wheres the pyloric sphincter
A
at end of stomach (antrum). relaxes when food is propelled through the pylorus (gastroduodenal junction)
7
Q
names the stomach’s 3 layers of smooth muscle
A
The stomach has three layers of smooth muscle, an outer longitudinal layer, a middle circular layer, and an inner oblique layer, which is the most prominent.
These layers become progressively thicker in the body and antrum of the stomach where food is mixed and then moved into the duodenum.
8
Q
whats gastrin
A
hormone that causes gastric glands to secrete hydrochloric acid, pepsinogen, and histamine
9
Q
what is intrinsic factor
A
needed to absorb B12, can result in anemia (low RBC, HGB, HCT)
10
Q
what is gastroferrin
A
attaches to iron so it can be absorbed through the small intestine.
11
Q
what is pepsin
A
chief cells of stomach secrete pepsinogen that is converted to pepsin (enzyme used to break proteins in food down) by the acidity of hydrochloric acid
Once chyme enters the duodenum the pepsin becomes inactive d/t alkaline environment of duodenum
11
Q
what protects the mucosal layer by stimulating the secretion of mucus and bicarbonate.
A
Prostaglandins
11
Q
what is the order of the small intestine
A
duodenum, jejunum, ileum
12
Q
what is the peritoneum
A
It’s the serous membrane that surrounds the organs of the abdomen and the pelvic cavity
The visceral peritoneum lies on the surface of the organs, and the parietal peritoneum lines the wall of the body cavity.
The space between these two layers is called the peritoneal cavity.
12
Q
whats considered the door from the small intestine to the large intestine
A
ileocecal valve
13
Q
What does the small intestine do
A
Pancreatic and intestinal enzymes, as well as bile salts work to break down carbohydrates and proteins. Fats are also emulsified.
Nutrients are absorbed by active transport, diffusion, and facilitated diffusion. This includes fat and water soluble vitamins, amino acids from protein digestion. Minerals such as sodium, potassium, calcium, magnesium, and iron are absorbed here.
85 to 90% of the water that enters the GI tract is absorbed in the small intestine.
14
Q
What does the large intestine do
A
absorbes na, k, acids, and bases
15
Q
what are the 5 parts of the large intestine
A
It consists of the cecum, the appendix, the colon, the rectum, and the anal canal.
16
Q
how does the intestinal microbiome affect our bodies
A
play a role in the metabolism of bile salts, estrogens, androgens, lipids, carbohydrates, and medications.
The intestinal bacteria produce antimicrobial peptides, hormones, neurotransmitters, anti-inflammatory metabolites, and vitamins. For example, it’s thought that a significant amount of vitamin K is produced by gut bacteria.
17
Q
what part of the brain regulates vomiting
A
medulla oblongata
18
Q
What are two ways the CTZ (chemoreceptor trigger zone) is stimulated to begin vomiting
A
- signals from stomach/small intestine
- direct action of emetogenic compounds (cancer tx)
19
Q
name receptors included in the emetic response
A
Serotonin, glucocorticoids, substance P, neurokinin1, dopamine, acetylcholine, histamine
20
Q
why use an ssri antagonist
A
odanestron/zofran emesis control
Block serotonin receptors on vagal afferents and in the chemoreceptor trigger zone (CTZ)
21
Q
the difference between primary and secondary constipation
A
Primary condition
Normal transit (functional) – normal rate of stool passage but there is difficulty with stool evacuation
Secondary condition
Caused by many different factors such as diet, medications, various disorders, aging
22
What meds can CAUSE constipation
Furosemide
anti-epileptic drugs such as Phenytoin or Dilantin.
antacids and proton pump inhibitors
the biggest medication that contributes to constipation are OPIOD ANALGESICS
23
Difference between Dx adult and ped constipation
ADULTS: 2 or more sx over 3 months
PEDS: 2 or more sx over 1 month
24
T/F: You can give any pt experiencing abdominal pain a laxative
F: figure out what it is first or you could cause a perforated bowel. can induce labor in pregnant people
25
What are the parameters of an acute diarrheas' dx
more than three loose bowel movements within a 24 hour period
26
what is the most common cause of diarrheas'
viruses/infectious agents
27
difference between persistent and chronic diarrheas' Dx
persisitant: longer than 14, up to 30
chronic: longer than 4 weeks
28
what are the 3 major mechanisms of diarrheas'
osmotic, secretory, and motility
29
Osmotic diarrhea
A nonabsorbable substance in the intestine draws in excess water. This increases stool weight and volume, resulting in large-volume diarrhea.
tube feedings, lactase deficiency
30
Secretory diarrhea
Excessive mucosal secretion of fluid and electrolytes produces large-volume diarrhea.
from viral GI infections (rota, e-coli
31
Motility diarrhea
Excessive motility decreases transit time and the opportunity for fluid absorption, resulting in diarrhea.
IBS, laxatives' abuse
32
T/F: Peroneal skin irritation generally only happens w/ incontinent diarrhea pts
f. both
33
bloody stool is indicative of the presence of
inflammatory bowel disease, such as Ulcerative colitis and crones, as well as certain infections.
34
what are the two types of antidiarrheal
Specific antidiarrheal drugs (medications to treat the underlying cause) Ex: antibiotics, enzymes for insufficiency
Nonspecific antidiarrheal drugs. Ned to be temporary. Ex: opioids
35
Nonspecific antidiarrheal drugs
Diphenoxylate plus Atropine [Lomotil] (feels like morphine w/ out the addiction so they add atropine to ruin the high)
Loperamide [Imodium] (not addictive but can cause your colon to get HUGE)
Bismuth Subsalicylate [Pepto-Bismol] (CAUSES BLACK TONGUE)
Bismuth has antimicrobial and anti-inflammatory action
Subsalicylate has an antisecretory effect
Bulk-Forming Agents
Methylcellulose [Citrucel]
36
MALDIGESTION VS MALABSORBTION
DIGEST: deficiencies of enzymes needed for digestion or inadequate secretion of bile salts and increased reabsorption of bile in the ileum
ABSORB: The result of mucosal disruption caused by gastric or intestinal resection, vascular disorders, or intestinal disease.
37
Describe the effects of Insufficient pancreatic enzyme production
Insufficient pancreatic enzyme production
NONE OF THE FOLLOWING ENZYMES PRODUCED:
Lipase (fat)
Amylase (carbohydrates)
Trypsin (protein)
Chymotrypsin (protein)
Deficit of fat-soluble vitamins
A, D, E, and K
Treated with supplemental pancreatic enzymes with meals
PANCRELIPASE [Creon]
38
Describe the effects of Bile salt deficiency
Conjugated bile salts are needed to emulsify (break down) and absorb fats. Bile salts are conjugated (made water soluble) in the bile that is secreted from the liver
Causes
Advanced liver disease
Obstruction of the common bile duct, resulting in cholestasis
Intestinal stasis (lack of motility)
Diseases of the ileum
Poor intestinal absorption of lipids causes fatty stools (steatorrhea), diarrhea, and loss of fat-soluble vitamins (A, D, E, K)
39
How do you increase consumption of medium-chain triglycerides in the diet
consume cow's milk, goat's milk, coconut oil, palm kernel oil, and the coconut meat or dried coconut
40
Vitamin A deficiencies can cause
Night blindness
41
Vitamin D deficiencies can cause
Decreased calcium absorption
Bone pain
Osteoporosis
Fractures
42
Vitamin K deficiencies can cause
Prolonged prothrombin time
Purpura
Petechiae
43
Vitamin E deficiencies can cause
Uncertain but may cause testicular atrophy and neurologic deficits in children
44
WHAT ARE CLINICAL MANIFESTATIONS OF DYSPHAGIA
Stabbing pain at the level of obstruction
Discomfort after swallowing
Regurgitation of undigested food
Unpleasant taste sensation
Vomiting
Aspiration
Weight loss
45
How do you manage dysphagia
Eating small meals slowly
Taking fluid with meals
Sleeping with the head elevated
46
What causes Gastroesophageal reflux disease (GERD)
Conditions that increase abdominal pressure or delay gastric emptying can contribute to the development of reflux esophagitis
47
Tx of choice for GERD
PPIs
Omeprazole
Dexlansoprazole
Esomeprazole
Lansoprazole
Pantoprazole
Rabeprazole
Irreversibly inhibits enzyme (ATPase) that generates gastric acid
Metabolized by the liver, excreted by the kidneys
Hypomagnesemia, don't have HIV/fungus
48
What are the two types of stomach hernias
Sliding hiatal hernia – most common; stomach slides or moves into the thoracic cavity through the esophageal hiatus
Paraesophageal hiatal hernia – greater curvature of the stomach herniates through a secondary opening in the diaphragm and lies alongside the esophagus; strangulation of the hernia is a major complication
49
What is Gastroparesis
Delayed gastric emptying in the absence of mechanical gastric outlet obstruction
Associated with diabetes mellitus B/C OF NERVE DAMAGE
TREATED W/ METOCLOPRAMIDE [Reglan]
Suppresses emesis (by blocking receptors for dopamine and serotonin in the CTZ)
Increases upper GI motility (by enhancing the actions of acetylcholine)
Adverse effects
Sedation and diarrhea (with high doses).
Tardive dyskinesia (with long-term, high-dose therapy)
50
wHAT ARE THE CLINICAL MINFESTATIOSN OF Pyloric obstruction
PAIN AFTER EATING AND FULLNESS
Succussion splash – sloshing sound caused by rolling or jarring of the abdomen
51
most common type of intestinal obstruction
Simple obstruction
Mechanical blockage of the lumen by a lesion
52
wHAT IS THE Failure of intestinal motility
Often occurs after intestinal or abdominal surgery, pancreatitis, or hypokalemia CALLED
Functional obstruction (paralytic ileus)
53
What is the most likely reason for a small bowel obstruction
adhesions secondary to abdominal surgery
54
What is the most likely reason for a large bowel obstruction
colon/rectal cancer
55
acute vs chronic gastritis
Acute gastritis
Caused by injury of the protective mucosal barrier by drugs, chemicals, or H pylori infection
Chronic gastritis
Causes chronic inflammation, mucosal atrophy, and epithelial metaplasia. Theres type a-c
56
sx of gastritis
Anorexia, fullness, nausea, vomiting, & epigastric pain
57
where does peptic ulcer disease happen in the body
the lower esophagus, stomach, or duodenum
58
What are the 3 levels of peptic ulcer disease
Superficial
Erosions that erode the mucosa
Deep
True ulcers that extend through the muscularis mucosae
Zollinger-Ellison syndrome
Rare syndrome associated with peptic ulcers caused by gastrin-secreting neuroendocrine tumor or multiple tumors of the pancreas or duodenum
59
What 4 things are necessary to protect gi lining
Mucus
Secreted cells of the GI mucosa
Forms a barrier to protect underlying cells from acid and pepsin
Bicarbonate
Secreted by epithelial cells of stomach and duodenum
Most remains trapped in mucus layer to neutralize hydrogen ions that penetrate the mucus
Blood flow
Poor blood flow can lead to ischemia, cell injury, and vulnerability to attack
Prostaglandins
Stimulate the secretion of mucus and bicarbonate
60
What is the most common type of ulceration in Peptic Ulcer Disease
Duodenal ulcers
Causes
Helicobacter pylori infection
Use of NSAIDs
RELIEVED BY EATING FOOD OR TAKING ANTACIDS
61
Where do Gastric ulcers tend to develop
in the antral region of the stomach, adjacent to the acid-secreting mucosa of the body
FOOD CAUSES PAIN
62
The primary clinical manifestation of stress-related mucosal disease is
bleeding
63
nAME 3 TYPES OF Stress-Related Mucosal Disease
Ischemic ulcers
Within hours of trauma, burns, hemorrhage, heart failure, or sepsis
Curling ulcers
Ulcers that develop as a result of burn injury
Cushing ulcers
Ulcers that develop as a result of a brain injury or brain surgery
64
Ulcerative colitis (UC) is
a chronic inflammatory disease that causes ulceration of the colonic mucosa.
starts in the rectum and moves in a continual fashion toward the cecum
Bloody diarrhea is common
65
Crohn disease (CD) is
an idiopathic inflammatory disorder that affects any part of the GI tract from the mouth to the anus.
Inflammation involves all layers of the bowel wall.
66
LIVER COVERED BY GLISSON CAPSULE THAT, WHEN DISTENDED, CAUSES PAIN BECAUSE IT IS INNERVATED
t
67
T/F: HEPATIC PORTAL VEIN CARRIES AROUND 70% OF NUTRIENT FILLED BLOOD away FROM LIVER (BLOOD PROCESSED BY LIVER)
T. It carries blood to the liver from the gi that collected nutrition
68
What does the liver need to do in order to create clotting factors
it needs vit k to make clotting factors but vit k can only be absorbed through fat. Vitamin K absorption depends on adequate bile production in the liver
69
Metabolic detoxification (biotransformation) is
the process by which the liver alters exogenous and endogenous chemicals (e.g., drugs), foreign molecules, and hormones to make them less toxic or less biologically active.
Although metabolic detoxification is usually protective, the end products of metabolic detoxification sometimes become toxins
Example: The end products of alcohol metabolism (e.g., acetaldehyde and hydrogen) can damage the liver.
70
what minerals and vitamins does the liver store
Iron is stored as ferritin
Copper
stores vitamins B12 and D for several months and vitamin A for several years
also stores vitamins E and K
The liver also synthesizes phospholipids and cholesterol
71
The endocrine pancreas secretes
hormones
Insulin: Stimulates protein and fat synthesis and decreases the blood glucose level
Amylin: Delays gastric emptying and suppresses glucagon secretion after meals
Glucagon: Increases the blood glucose concentration by stimulating glycogenolysis and gluconeogenesis in muscle and lipolysis in adipose tissue
Somatostatin: Inhibits secretion of insulin, glucagon, and pancreatic polypeptide
Pancreatic polypeptide: Inhibits gallbladder contraction and exocrine pancreas secretion
72
The exocrine pancreas secretes
enzymes and networks of ducts that secrete alkaline fluids to assist in digestion
Proteins (proteases)
Enzymes include trypsin, chymotrypsin, carboxypeptidase, and elastase
Carbohydrates (amylases): Breaks down starches to disaccharides
Fats (lipases)
Secreted in inactive forms and activated in the duodenum by Enterokinase
73
What are the 5 complications of liver disorders
Portal hypertension
Ascites
Hepatic encephalopathy
Jaundice
Hepatorenal syndrome
74
pathphys of portal hypertension
Liver inflammation leads to liver necrosis
Liver necrosis leads to liver fibrosis and scarring
The fibrosis and scarring causes resistance to blood flow
To reduce pressure, the body develops alternate circulatory pathways, (collateral circulation)
This leads to the development of esophageal and gastric varices and hemorrhoids
Confirmed by upper GI endoscopy at the time of bleeding
Evaluation of portal venous pressure (rarely performed)
75
Clinical Manifestations portal hypertension w/ varices
Vomiting of blood (hematemesis) from bleeding esophageal varices (most common)
Hemorrhoidal varices and copious rectal bleeding
76
pathophys of ascites (Portal hypertension)
Portal hypertension causes increased resistance of blood flow through liver
This leads to an increased capillary filtration pressure
This causes proteins to shift from the blood vessels into the lymph space
When the lymphatic system is unable to carry off the excess proteins and water, they leak into the peritoneal cavity
The osmotic pressure of the proteins then draws more fluid into the peritoneal cavity
77
3 ways ascites happens
Portal hypertension
Hypoalbuminemia
Hyperaldosteronism
78
pathophys of ascites (Hypoalbuminemia)
Hepatocyte failure leads to decreased albumin synthesis
This decreases the capillary oncotic pressure
This leads to the leakage of plasma out of the vascular space into the peritoneal cavity, leading to ascites
79
pathophys of ascites (Hyperaldosteronism)
Hepatocytes are damaged, leading to decreased liver catabolism (breakdown) of circulating aldosterone
This leads to activation of the RAAS system (end product is more aldosterone) and ADH secretion
This leads increased renal reabsorption of sodium and water, causing ascites
80
Pathophysiology of hepatic encephalopathy
Liver dysfunction and the development of collateral vessels that shunt blood around the liver to the systemic circulation permit toxins absorbed from the GI tract and normally removed by the liver, to accumulate and circulate freely to the brain.
The accumulated toxins alter cerebral energy metabolism, interfere with neurotransmission, and cause edema.
81
what causes Jaundice (icterus)
Extrahepatic (posthepatic) obstruction to bile flow
Conjugated (water-soluble) bilirubin is unable to flow to the duodenum
It accumulates in the liver and enters the bloodstream
82
what are the 2 types of Hepatorenal syndrome
Type 1
Occurs with a sudden decrease in blood volume and hypotension
The decrease in blood volume and hypotension result in decreased renal perfusion
Type 2
Develops slowly and is related to ascites.
Ineffective circulating blood volume due to pooling of blood in the splanchnic circulation
The splanchnic (visceral) blood flow provides blood to the esophagus, stomach, small and large intestines, liver, gallbladder, pancreas, and spleen
Intrarenal vasoconstriction due to vasoactive substances that accumulate in the blood in liver failure (i.e., RAAS activation)
83
Clinical Manifestations of Hepatorenal syndrome
Oliguria
Sodium and water retention (usually with ascites and peripheral edema)
Hypotension
Peripheral vasodilation
Systolic blood pressure is usually below 100 mm Hg.
Nonspecific symptoms include anorexia, weakness, and fatigue
Urine is concentrated
Urine sodium concentrations are below normal
84
liver Laboratory Data
Elevated liver function tests (AST, ALT)
Elevated direct (conjugated) and indirect (unconjugated) serum bilirubin
Elevated blood ammonia
Prothrombin time is prolonged
85
Causes of liver cirrhosis
hep b/c, alcohol, obesity. diabetes, autoimmune
86
labs positive for liver cirrhosis
Liver function tests (elevated)
Serum albumin (decreased)
Serum electrolytes (hypokalemia, hyponatremia)
Prothrombin (PT) time (prolonged)
Complete blood count (anemia, thrombocytopenia, leukopenia)
87
tx of liver cirrhosis
Conservative Therapy
Rest
B-complex vitamins
Avoiding alcohol
Minimizing or avoiding aspirin, acetaminophen, and NSAIDs
Treatment of complications (portal hypertension, ascites, etc.)
Liver transplantation
88
Hepatocytes are targeted by the virus in what two possible ways
Through direct action of the virus
Cell-mediated immune responses
89
Viral Hepatitis clinical manifestations 3 phases
Prodromal (preicteric) phase
Begins about 2 weeks after exposure and ends with the appearance of jaundice
Fatigue, anorexia, malaise, nausea, vomiting, headache, hyperalgia, cough, and low-grade fever
Infection is highly transmissible during this phase.
Icteric phase
Begins 1 to 2 weeks after the prodromal phase and lasts 2 to 6 weeks
Jaundice, dark urine, and clay-colored stools are common
The liver is enlarged, smooth, and tender, and percussion or palpation of the liver causes pain
GI and respiratory symptoms subside, but fatigue and abdominal pain may persist or become more severe.
Individuals who develop chronic HBV, HDV, or HCV infection do not become jaundiced and may not be diagnosed.
Recovery phase
Begins with resolution of jaundice, about 6 to 8 weeks after exposure
Symptoms diminish, but the liver remains enlarged and tender
Liver function returns to normal 2 to 12 weeks after the onset of jaundice.
90
Chronic active hepatitis
Liver function tests remain abnormal for longer than 6 months
Chronic active hepatitis constitutes a carrier state
91
Cholelithiasis is also known as
Gallstones
Cholecystitis: Inflammation of the gallbladder or cystic duct
92
describe indv that would likely get gall stones
middle aged obese female taking birth control that is on an extreme weight loss diet
93
what is the Most common type of gall stone
Cholesterol stones (70% cholesterol)
94
Other types of gallstones
Pigmented brown stones are associated with biliary stasis, bacterial infections, and biliary parasites. These form from calcium bilirubinate and fatty acid soaps that bind with calcium.
Black gallstones are are associated with chronic liver disease and hemolytic disease. They are composed of calcium bilirubinate with mucin glycoproteins.
95
Difference between acute and chronic cholecystitis
Acute cholecystitis: The gallbladder is edematous and hyperemic and may be distended with bile or pus.
Pain is similar to that caused by gallstones.
Fever
Rebound tenderness
Abdominal muscle
lab data: up WBC, Serum bilirubin and alkaline phosphatase levels may be elevated
May indicate blockage of the bile duct
Chronic cholecystitis: The wall of the gallbladder becomes scarred after an acute attack. Decreased functioning occurs if large amounts of tissue become fibrotic.
Fat intolerance
Dyspepsia
Heartburn
Flatulence
96
Sx of Cholelithiasis
Epigastric and RUQ pain, intolerance to fatty foods, heartburn, flatulence
Pain (biliary colic) occurs 30 minutes to several hours after eating a fatty meal
Jaundice
97
cause of Acute pancreatitis
Obstruction to the outflow of pancreatic digestive enzymes caused by bile or pancreatic duct obstruction.
Chronic alcohol use is second most common cause
98
Clinical Manifestations Acute pancreatitis
Abdominal pain due to distention of the pancreas, peritoneal irritation, and biliary tract obstruction.
Eating worsens the pain
Pain commonly starts when the patient is recumbent (lying down)
Low grade fever
GI: N/V, jaundice, abdominal tenderness with muscle guarding, diminished or absent bowel sounds, abdominal distention
CV: Hypotension, tachycardia
Lungs: Crackles
Skin
Areas of cyanosis or greenish to yellow-brown discoloration of the abdominal wall
Grey Turner spots or sign, a bluish flank discoloration
Cullen sign, a bluish periumbilical discoloration
99
lab results Acute pancreatitis
Serum amylase and lipase
Serum amylase level is usually high early and stays high for 24 to 72 hours.
Serum lipase level is high in acute pancreatitis
Elevated liver enzymes (AST, ALT)
Hyperbilirubinemia
Elevated triglycerides
Hyperglycemia
Hypocalcemia
Leukocytosis
100
Name the Digestive Congenital Impairments
Cleft Lip and Palate
Esophageal atresia (EA)(MOST COMMON, esophagus ends in a blind pouch)
Infantile Hypertrophic Pyloric Stenosis (IHPS) )(An acquired narrowing and distal obstruction of the pylorus, Individual muscle fibers of the longitudinal and circular muscles thicken, so the entire pyloric sphincter becomes enlarged and inflexible )
Intestinal malrotation (causes the parts of the intestine to settle in the wrong part of the abdomen, which can cause them to become blocked or to twist)
Hirschsprung disease (Lacking neural stimulation, muscle layers fail to propel feces through the colon, leading to functional obstruction
This causes the proximal colon to become distended (megacolon))
