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2 PATHOPHARM > EXAM 1 (GI) > Flashcards

EXAM 1 (GI) Flashcards

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.

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2
Q

What does the upper esophageal sphincter do

A

keeps air from entering the esophagus when we breathe

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3
Q

What does the lower esophageal sphincter do

A

prevents regurgitation of stomach content into the esophagus

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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)

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5
Q

what are the 3 areas of the stomach

A

fundus (top), body (middle), and antrum (bottom)

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6
Q

wheres the pyloric sphincter

A

at end of stomach (antrum). relaxes when food is propelled through the pylorus (gastroduodenal junction)

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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.

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8
Q

whats gastrin

A

hormone that causes gastric glands to secrete hydrochloric acid, pepsinogen, and histamine

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9
Q

what is intrinsic factor

A

needed to absorb B12, can result in anemia (low RBC, HGB, HCT)

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10
Q

what is gastroferrin

A

attaches to iron so it can be absorbed through the small intestine.

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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

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11
Q

what protects the mucosal layer by stimulating the secretion of mucus and bicarbonate.

A

Prostaglandins

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11
Q

what is the order of the small intestine

A

duodenum, jejunum, ileum

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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.

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12
Q

whats considered the door from the small intestine to the large intestine

A

ileocecal valve

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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.

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14
Q

What does the large intestine do

A

absorbes na, k, acids, and bases

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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.

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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.

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17
Q

what part of the brain regulates vomiting

A

medulla oblongata

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18
Q

What are two ways the CTZ (chemoreceptor trigger zone) is stimulated to begin vomiting

A
  1. signals from stomach/small intestine
  2. direct action of emetogenic compounds (cancer tx)
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19
Q

name receptors included in the emetic response

A

Serotonin, glucocorticoids, substance P, neurokinin1, dopamine, acetylcholine, histamine

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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)

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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

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22
Q

What meds can CAUSE constipation

A

Furosemide

anti-epileptic drugs such as Phenytoin or Dilantin.

antacids and proton pump inhibitors

the biggest medication that contributes to constipation are OPIOD ANALGESICS

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23
Q

Difference between Dx adult and ped constipation

A

ADULTS: 2 or more sx over 3 months

PEDS: 2 or more sx over 1 month

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24
Q

T/F: You can give any pt experiencing abdominal pain a laxative

A

F: figure out what it is first or you could cause a perforated bowel. can induce labor in pregnant people

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25
Q

What are the parameters of an acute diarrheas’ dx

A

more than three loose bowel movements within a 24 hour period

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26
Q

what is the most common cause of diarrheas’

A

viruses/infectious agents

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27
Q

difference between persistent and chronic diarrheas’ Dx

A

persisitant: longer than 14, up to 30

chronic: longer than 4 weeks

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28
Q

what are the 3 major mechanisms of diarrheas’

A

osmotic, secretory, and motility

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29
Q

Osmotic diarrhea

A

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

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30
Q

Secretory diarrhea

A

Excessive mucosal secretion of fluid and electrolytes produces large-volume diarrhea.

from viral GI infections (rota, e-coli

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31
Q

Motility diarrhea

A

Excessive motility decreases transit time and the opportunity for fluid absorption, resulting in diarrhea.

IBS, laxatives’ abuse

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32
Q

T/F: Peroneal skin irritation generally only happens w/ incontinent diarrhea pts

A

f. both

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33
Q

bloody stool is indicative of the presence of

A

inflammatory bowel disease, such as Ulcerative colitis and crones, as well as certain infections.

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34
Q

what are the two types of antidiarrheal

A

Specific antidiarrheal drugs (medications to treat the underlying cause) Ex: antibiotics, enzymes for insufficiency

Nonspecific antidiarrheal drugs. Ned to be temporary. Ex: opioids

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35
Q

Nonspecific antidiarrheal drugs

A

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]

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36
Q

MALDIGESTION VS MALABSORBTION

A

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.

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37
Q

Describe the effects of Insufficient pancreatic enzyme production

A

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]

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38
Q

Describe the effects of Bile salt deficiency

A

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)

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39
Q

How do you increase consumption of medium-chain triglycerides in the diet

A

consume cow’s milk, goat’s milk, coconut oil, palm kernel oil, and the coconut meat or dried coconut

40
Q

Vitamin A deficiencies can cause

A

Night blindness

41
Q

Vitamin D deficiencies can cause

A

Decreased calcium absorption
Bone pain
Osteoporosis
Fractures

42
Q

Vitamin K deficiencies can cause

A

Prolonged prothrombin time
Purpura
Petechiae

43
Q

Vitamin E deficiencies can cause

A

Uncertain but may cause testicular atrophy and neurologic deficits in children

44
Q

WHAT ARE CLINICAL MANIFESTATIONS OF DYSPHAGIA

A

Stabbing pain at the level of obstruction
Discomfort after swallowing
Regurgitation of undigested food
Unpleasant taste sensation
Vomiting
Aspiration
Weight loss

45
Q

How do you manage dysphagia

A

Eating small meals slowly
Taking fluid with meals
Sleeping with the head elevated

46
Q

What causes Gastroesophageal reflux disease (GERD)

A

Conditions that increase abdominal pressure or delay gastric emptying can contribute to the development of reflux esophagitis

47
Q

Tx of choice for GERD

A

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
Q

What are the two types of stomach hernias

A

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
Q

What is Gastroparesis

A

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
Q

wHAT ARE THE CLINICAL MINFESTATIOSN OF Pyloric obstruction

A

PAIN AFTER EATING AND FULLNESS

Succussion splash – sloshing sound caused by rolling or jarring of the abdomen

51
Q

most common type of intestinal obstruction

A

Simple obstruction
Mechanical blockage of the lumen by a lesion

52
Q

wHAT IS THE Failure of intestinal motility
Often occurs after intestinal or abdominal surgery, pancreatitis, or hypokalemia CALLED

A

Functional obstruction (paralytic ileus)

53
Q

What is the most likely reason for a small bowel obstruction

A

adhesions secondary to abdominal surgery

54
Q

What is the most likely reason for a large bowel obstruction

A

colon/rectal cancer

55
Q

acute vs chronic gastritis

A

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
Q

sx of gastritis

A

Anorexia, fullness, nausea, vomiting, & epigastric pain

57
Q

where does peptic ulcer disease happen in the body

A

the lower esophagus, stomach, or duodenum

58
Q

What are the 3 levels of peptic ulcer disease

A

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
Q

What 4 things are necessary to protect gi lining

A

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
Q

What is the most common type of ulceration in Peptic Ulcer Disease

A

Duodenal ulcers

Causes
Helicobacter pylori infection
Use of NSAIDs

RELIEVED BY EATING FOOD OR TAKING ANTACIDS

61
Q

Where do Gastric ulcers tend to develop

A

in the antral region of the stomach, adjacent to the acid-secreting mucosa of the body

FOOD CAUSES PAIN

62
Q

The primary clinical manifestation of stress-related mucosal disease is

A

bleeding

63
Q

nAME 3 TYPES OF Stress-Related Mucosal Disease

A

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
Q

Ulcerative colitis (UC) is

A

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
Q

Crohn disease (CD) is

A

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
Q

LIVER COVERED BY GLISSON CAPSULE THAT, WHEN DISTENDED, CAUSES PAIN BECAUSE IT IS INNERVATED

A

t

67
Q

T/F: HEPATIC PORTAL VEIN CARRIES AROUND 70% OF NUTRIENT FILLED BLOOD away FROM LIVER (BLOOD PROCESSED BY LIVER)

A

T. It carries blood to the liver from the gi that collected nutrition

68
Q

What does the liver need to do in order to create clotting factors

A

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
Q

Metabolic detoxification (biotransformation) is

A

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
Q

what minerals and vitamins does the liver store

A

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
Q

The endocrine pancreas secretes

A

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
Q

The exocrine pancreas secretes

A

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
Q

What are the 5 complications of liver disorders

A

Portal hypertension
Ascites
Hepatic encephalopathy
Jaundice
Hepatorenal syndrome

74
Q

pathphys of portal hypertension

A

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
Q

Clinical Manifestations portal hypertension w/ varices

A

Vomiting of blood (hematemesis) from bleeding esophageal varices (most common)

Hemorrhoidal varices and copious rectal bleeding

76
Q

pathophys of ascites (Portal hypertension)

A

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
Q

3 ways ascites happens

A

Portal hypertension
Hypoalbuminemia
Hyperaldosteronism

78
Q

pathophys of ascites (Hypoalbuminemia)

A

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
Q

pathophys of ascites (Hyperaldosteronism)

A

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
Q

Pathophysiology of hepatic encephalopathy

A

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
Q

what causes Jaundice (icterus)

A

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
Q

what are the 2 types of Hepatorenal syndrome

A

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
Q

Clinical Manifestations of Hepatorenal syndrome

A

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
Q

liver Laboratory Data

A

Elevated liver function tests (AST, ALT)
Elevated direct (conjugated) and indirect (unconjugated) serum bilirubin
Elevated blood ammonia
Prothrombin time is prolonged

85
Q

Causes of liver cirrhosis

A

hep b/c, alcohol, obesity. diabetes, autoimmune

86
Q

labs positive for liver cirrhosis

A

Liver function tests (elevated)
Serum albumin (decreased)
Serum electrolytes (hypokalemia, hyponatremia)
Prothrombin (PT) time (prolonged)
Complete blood count (anemia, thrombocytopenia, leukopenia)

87
Q

tx of liver cirrhosis

A

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
Q

Hepatocytes are targeted by the virus in what two possible ways

A

Through direct action of the virus
Cell-mediated immune responses

89
Q

Viral Hepatitis clinical manifestations 3 phases

A

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
Q

Chronic active hepatitis

A

Liver function tests remain abnormal for longer than 6 months
Chronic active hepatitis constitutes a carrier state

91
Q

Cholelithiasis is also known as

A

Gallstones

Cholecystitis: Inflammation of the gallbladder or cystic duct

92
Q

describe indv that would likely get gall stones

A

middle aged obese female taking birth control that is on an extreme weight loss diet

93
Q

what is the Most common type of gall stone

A

Cholesterol stones (70% cholesterol)

94
Q

Other types of gallstones

A

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
Q

Difference between acute and chronic cholecystitis

A

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
Q

Sx of Cholelithiasis

A

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
Q

cause of Acute pancreatitis

A

Obstruction to the outflow of pancreatic digestive enzymes caused by bile or pancreatic duct obstruction.

Chronic alcohol use is second most common cause

98
Q

Clinical Manifestations Acute pancreatitis

A

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
Q

lab results Acute pancreatitis

A

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
Q

Name the Digestive Congenital Impairments

A

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))

2 PATHOPHARM (9 decks)

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