Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Adv Patho > Exam 4- GI/Liver > Flashcards

Exam 4- GI/Liver Flashcards

1
Q

OSMOTIC DIARRHEA

A

ETIOLOGY: bacterial infection (e. coli), parasites, viral infection, drugs, celiac disease or UC, genetic d/o like congenital chloride diarrhea

  • due to unabsorbed nutrients in the stool
  • osmotic load causes fluid retention in the bowel
  • seen with lactose intolerance and Zollinger Ellison syndrome and celiac disease

CLINICAL MANIFESTATION: stomach pain, bloating, nausea, watery bowel movement;

PATHOLOGY:occurs when too many solutes — the components of the food you eat — stay in your intestine and water can’t be absorbed properly. This excess water causes your bowel movements to be loose or more liquid than solid. Eating food that can’t be that can be absorbed and instead draw water into your intestine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

SECRETORY DIARRHEA

A

ETIOLOGY:
large volume: caused be excessive mucosal secretion of chloride- or bicarbonate rich fluid or inhibition of net sodium absorption. Usually caused by enterotoxins (E.coli), viruses (rotavirus), or exotoxins from overgrowth cdiff.
-increased water and electrolytes secretion by toxin or VIP in the intestinal lumen

Small volume: caused by IBD, UC, Crohns, colitis, fecal impaction

CLINICAL MANIFESTATIONS: stomach pain, bloating, nausea, watery bowel movement;

PATHOLOGY: large volume of feces caused by excessive amounts of water secretion. Occurs when your body secretes electrolytes into your intestine. This causes water to build up.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

MOTILITY DIARRHEA

A

ETIOLOGY: diarrhea caused by resection of small intestine, surgical bypass of an area of the intestine, fistula formation between loops of intestine, irritable bowel syndrome, diabetic neuropathy, hyperthyroidism, and laxative abuse

CLINICAL MANIFESTATION: dehydration, electrolyte imbalance (hyponatremia, hypokalemia), metabolic acidosis, and weight loss, fever, cramping pain, and bloody stools, bloating, anal and perianal skin irritation.

PATHOLOGY: large volume of feces caused by excessive amounts of water secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

DYSPHAGIA

A

Difficulty swallowing or perception of obstruction during swallowing

PATHOLOGY: mechanical obstruction of the esophagus or functional d/o that impairs esophageal motility.

  • Functional dysphagia-caused by neural or muscular d/o that interfere with voluntary swallowing or peristalisis
  • Mechanical dysphagia- can be intrinsic or extrinsic. Intrinsic is obstruction in wall of esophageal lumen. Extrinsic obstruction originate outside the esophageal lumen and narrow the esophagus by pressing inward on esophageal wall

EVALUATION: barium xray, swallow study, endoscopy, imaging scans, esophageal muscle test, fiber optic endoscopic evaluation of swallowing

TREATMENT:Medication, Swallowing retraining, Botulinum toxin, Dilation, Enteral feeding, Esophageal stent placement, Surgery, Treatment for specific swallowing disorders.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ACHALASIA

A

ETIOLOGY: It may be caused by an abnormal immune system response.
May be related to cell mediated and antibody mediated immune response against unknown antigen in myenteric neurons
-A motility d/or of esophagus d/t nerves fro swallowing being damanaged

CLINICAL MANIFESTATION: a backflow of food in the throat (regurgitation), chest pain, and weight loss, discomfort after swallowing, unpleasant taste, vomiting.
*discomfort 2-4 sec after eating=upper esophageal obstruction; discomfort 10-15 sec= lower obstruction

PATHOLOGY: Achalasia results from damage to nerves in the food tube (esophagus), preventing the esophagus from squeezing food into the stomach.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

GERD

A

ETIOLOGY: reflux of acid and pepsin or bile salts from the stomach to the esophagus that causes esophagitis.

RISK FACTORS: vomiting, coughing, lifting, bending, obesity, or pregnancy

CLINICAL MANIFESTATION: heartburn chronic cough, asthma attacks, laryngitis, sinusitis, and upper abdominal pain within 1 hr of eating. Symptoms worsen when person lays down

PATHOLOGY: abnormalities in lower esophageal sphincter function, esophageal motility, and gastric motility or emptying can cause GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

UPPER GI BLEED

A

ETIOLOGY: bleeding from the esophagus, stomach, or duodenum

RISK FACTORS: helicobacter pylori infection, NSAIDs, aspirin, selective serotonin reuptake inhibitors, and other antiplatelet and anticoagulant medications

CLINICAL MANIFESTATION: frank red blood in emesis or coffee ground color stool

PATHOLOGY:cause by esophageal or gastric varices, tear eso-gastric junction, cancer, andiodysplasias, peptic ulcers, severe retching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

LOWER GI BLEED

A

ETIOLOGY: bleeding from the small intestine, colon, or rectum

RISK FACTORS: age, overuse of NSAIDs, chronic constipation leading to hemmorhoids, family hx like IBD, bleeding d/o of family hx of bleeding d/o

CLINICAL MANIFESTATION: bright red blood in stool, abd cramps or pain, faintness/dizziness, paleness, SOB

PATHOLOGY: caused by polyps, inflammatory bowel disease, diverticulosis, cancer, vascular extasias, or hemorrhoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

PYOLRIC OBSTRUCTION

A

ETIOLOGY: is a result of any disease process that causes a mechanical impediment to gastric emptying. Can be due to a mechanical cause or motility d/o

RISK FACTORS: PUD, gastrointestinal tumors, pancreatitis

CLINICAL MANIFESTATION: nausea, nonbilious vomiting, epigastric pain, early satiety, abdominal distention, and weight loss

PATHOLOGY:
can be congenital or acquired. Acquired caused by peptic ulcer disease or tumor near the pylorus. Duodenal ulcers are more likely than gastric ulcers to obstruct the pylorus. Ulceration causes obstruction resulting from inflammation edema, spasm, fibrosis or scarring. Tumor caused obstruction by growing into the pylorus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

INTESTINAL OBSTRUCTION

A

ETIOLOGY: is a blockage that keeps food or liquid from passing through your small intestine or large intestine (colon). Can be SBO or LBO

RISK FACTORS: hernias, crohns, abd/joint/or spine surgery, swallowing a foreign body, decrease blood supply to small bowel, abnormal growth of tissue in or next to small intestine, tumors, cancer

CLINICAL MANIFESTATION:constipation, vomiting, inability to have a BM or pas gas, swelling of abd.

PATHOLOGY: Ingested fluid and food, digestive secretions, and gas accumulate above the obstruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ILEUS

A

ETIOLOGY:the motor activity of the bowel is impaired, usually without the presence of a physical obstruction.

RISK FACTORS: electrolyte imbalance involving potassium and calcium, hx of intestinal injury or trauma, hx of crohns or diverticulitis, sepsis, PAD, exposure to radiation near abd

CLINICAL MANIFESTATION: distended abd, fullness, gas, abd spasms, constipation, diarrhea, n/v

PATHOLOGY:Caused by Bacteria or viruses that cause intestinal infections (gastroenteritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

3 ULCERATIVE DISEASE

A
  1. gastric ulcers
  2. duodenal ulcers
  3. stress r/t mucosal ulceration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

DUODENAL ULCERS

A

ETIOLOGY:a peptic ulcer that develops in the first part of the small intestine (duodenum)

RISK FACTORS: alcohol abuse, H pylori infection (90%), hx radiation therapy, NSAIDs (ibuprofen, naproxen, or asprin), stress, severe illness, tobacco use

CLINICAL MANIFESTATION: belching, burning stomach or upper abd pain that may be severe, fullness, loss of appetite, n/v

PATHOLOGY:stomach acid damages the lining of the digestive tract: H pylori decrease mucosal protection and increases gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

STRESS RELATED MUCOSAL ULCERATION

A

ETIOLOGY: acute form of erosive, inflammatory peptic ulcer that tends to accompany the physiologic stress of severe illness; multisystem organ failure, or major trauma, including severe burns or head injury.

RISK FACTORS: immense physical stress like those pts in ICU; stress-related ulcer, H, pylori infection, NSAIDs

CLINICAL MANIFESTATION: upper abd pain/n/v, anemia, bloated, pain that varies with food intake

PATHOLOGY: COME ON SUDDENLY, USUALLY AS RESULT OF PHYSIOLOGICAL STRESS; changes in body’s pH; caused by mucosal ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

2 INTESTINAL DISEASES

A
  1. ulcerative colitis

2. crohn’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CROHN’S DISEASE

A

ETIOLOGY: an idiopathic inflammatory d/o that is distinguished from UC in that it affects any part of the GI track from the mouth the anus and involves “skip lesions” with inflamed areas mixed with un-inflamed areas, non-caseating granulomas, fistulas, and deep penetrating ulcers

RISK FACTORS: family hx, cigarette smoking, Jewish ethnicity, urban residency, age less than 40 years, slight predominance in women, and altered gut microbiome

CLINICAL MANIFESTATION: irritable bowel; diarrhea, sometimes rectal bleeding if colon is involved; abd pain, diarrhea, weight loss, anemia, and fatigue

PATHOLOGY: inflammatory lesions begin in the intestinal submucosa and spread with discontinuous transmural involvement (skip lesions), mutations in Toll-like receptor, gene name CARD15/NOD2. overreact to normal flora of bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

5 TYPES OF LIVER INJURY/FAILURE

A
  1. Hepatitis A
  2. Hepatitis B
  3. Hepatits C
  4. Hepatitis D
  5. Hepatitis E
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

HEPTITIS A

A

ROUTE: fecal oral route; 4-6 week incubation period

RISK FACTORS: poor sanitation, lack of safe water, sexual contact with infected person

CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice

PATHOLOGY: acute infection; is caused by a picornavirus usually transmitted by the fecal-oral route

IMMUNITY: antibodies to HAV (anti-HA) develop within 4 weeks after incubation
**IgM increases&raquo_space; IgG increases for several years which leads to immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

HEPATITIS B

A

ROUTE: sexual intercourse, blood, perinatal (mother to baby); 6-8 week incubation period

RISK FACTORS: unprotected sex, IV drug uses, men with men, mother to infant, job that exposes you to blood

CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice

PATHOLOGY: can be acute or chronic (>6 months)the interaction of the virus and the host immune system, which leads to liver injury and, potentially, cirrhosis and hepatocellular carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

HEPATISIS C

A

ETIOLOGY:Serum, sexual contact; 6-8 week incubation

RISK FACTORS: IV drug use; HIV; Hep B infection

CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice

PATHOLOGY: can develop into cirrhosis and then hepatocellular carcinoma.

Antibody: anti HCV IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

HEPATITIS D

A

ETIOLOGY: occurs in people who are also infected with the hepatitis B virus.

RISK FACTORS: IVDU

CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice

PATHOLOGY: Hepatitis D virus is hepatotropic. Replication within hepatocytes results in cytotoxicity and direct liver damage. The virus depends on the viral coat of HBsAg molecules on HBV for replication

Antibody used for dx: anti-HD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

HEPATITIS E

A

ETIOLOGY: co-infection with HBV, HIV; transmitted fecal oral route; MOST COMMON IN ASIAN AND AFRICAN COUNTRIES

RISK FACTORS: contaminated water supplies, poor sanitation, ingestion of undercooked meat and shellfish

CLINICAL MANIFESTATION: usually asymptomatic and resemble Hep A or it can progress to liver failure or chronic hepatitis

PATHOLOGY:

ANTIBODY: anti-HEV IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

CHOLELITHIASIS

A

ETIOLOGY: hardened deposit within the fluid in the gallbladder aka gallstones that are hardened deposits of digestive fluid (cholesterol, excess bilirubin) with impaired contractility

RISK FACTORS: female, obese, pregnant, sedentary, high fat diet

CLINICAL MANIFESTATION: RUQ pain, indegestion, n/v, abd cramping–may have no signs

PATHOLOGY:

  • *Cholesterol gallstones due to over secretion of cholesterol by liver cells and hypomotility.
  • *Pigmented gallstones, high heme turnover, bilirubin higher concentration which crystallize and become stones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CHOLECYSTITIS

A

ETIOLOGY: inflammation of gallbladder

RISK FACTORS: obese, pregnancy, hormone therapy, older age, diabetes, Native American or Hispanic

CLINICAL MANIFESTATION: severe pain in RUQ, pain that spreads to your right shoulder or back, tender abd, nausea

PATHOLOGY: gallstones that block the gallbladder preventing biliary outflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

CIRRHOSIS

A

ETIOLOGY: fibrosis of liver

RISK FACTORS: hepatitis, alcohol abuse

CLINICAL MANIFESTATION: jaundice, itchy skin, easy bruising, ascites, hepatic encephalopathy, weight, BLE edema, fatigue,

PATHOLOGY: a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

COMPLICATIONS OF CIRRHOSIS

A
  1. portal htn
  2. ascites
  3. hepatic encephalopathy
  4. jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

ACUTE PANCREATITIS

A

ETIOLOGY: a condition where the pancreas becomes inflamed (swollen) over a short period of time due to obstruction to the outflow of pancreatic digestive enzymes caused by bile duct or pancreatic duct obstruction. Enzymes become activated while still in the pancreas, irritating the cells of the pancreas causing inflammation

RISK FACTORS/CAUSES: alcohol abuse; gallstones; steroids; mumps virus, autoimmune, idiopathic, hypertriglyceridemia and hypercalcemia, drugs

CLINICAL MANIFESTATION: EPIGASTRIC PAIN, CULLEN SIGN (GREY AREA AROUND UMBILICAL AREA) , GREY TURNER SIGN (GREY SIGN ON FLANKS)abd pain, n/v, fever, bad pain may radiate to back, abd distention, jaundice

PATHOLOGY: is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes.

Dx: lipase and amylase levels, leukocytosis, c-reactive protein and lactate, enlarged pancreas, decreased ionized calcium levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

CHRONIC PANCREATITIS

A

ETIOLOGY: is a painful disease of the pancreas in which inflammation has resolved, but with resultant damage to the gland characterized by fibrosis, calcification and ductal inflammation.

RISK FACTORS/CAUSES: alcohol abuse, cigarette smoking, obesity, diabetes, family hx; gallstones, autoimmune d/o, hypertryglycerides, tumor, cystic fibrosis

CLINICAL MANIFESTATION: usually asymptomatic for awhile, epigastric pain that radiates to back, exocrine and endocrine insuffciency, steatorrhea

PATHOLOGY: relapsing episodes of pancreatitis which leads to pancreatic injury

Dx. : elevated bilirubin; 72 hour stool collection to dx fat malabsorption, CT scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

5 GI TRACK CANCERS

A
  1. Gastric cancer
  2. esophageal cancer
  3. colorectal cancer
  4. pancreatic cancer
  5. liver cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

PYLORIC STENOSIS (babies)

A

ETIOLOGY: an uncommon condition in infants that blocks food from entering the small intestine

RISK FACTORS: boys, premature birth, smoking during pregnancy, family hx, early abx use

CLINICAL MANIFESTATIONS: vomiting after feeding; dehydration

PATHO: hallmark of pyloric stenosis is marked hypertrophy and hyperplasia of both the circular and longitudinal muscular layers of the pylorus.[3] This thickening leads to the narrowing of the lumen of the gastric antrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

CLEFT LIP/PALATE (babies)

A

ETIOLOGY: A cleft lip is an opening in the upper lip; a cleft palate is an opening in the roof of the mouth.

RISK FACTORS: smoking during pregnancy, diabetes, use of certain meds during first trimester

CLINICAL MANIFESTATIONS: difficult speaking and feeding

PATHO:
cleft lip- incomplete fusion of the nasomedial and intermaxillary process
cleft palate- failure of the primary palatal shelves, or processes, to fuse in the 3rd trimester; can occur with or without cleft lip

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

NEWBORN JAUNDICE (babies)

A

CAN BE CAUSED BY: infection, viral or bacterial infection, internal bleeding, enzyme deficiency, liver malfunciont

ETIOLOGY: excess bilirubin in blood

CLINICAL MANIFESTATIONS: yellow skin,

PATHO: baby’s liver isn’t mature enough to get rid of bilirubin in the bloodstream
Newborns produce more bilirubin than adults do because of greater production and faster breakdown of red blood cells in the first few days of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

MECONIUM ILEUS (babies)

A

ETIOLOGY: lack of contraction in muscles of intestines due to meconium

RISK FACTORS: cystic fibrosis

CLINICAL MANIFESTATIONS: abd distention, hyperactive peristalsis, but rectal ampulla empty; distended abd will show patterns of dilated intestinal loops

PATHO: intestinal obstruction in the neonatal period caused by meconium formed in utero that is abnormally sticky and accumulates and obstructs ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

NECROTIZING ENTERCOLITIS

A

ETIOLOGY: necrotic bowel

RISK FACTORS: premature babies

CLINICAL MANIFESTATIONS: vomiting, diarrhea, feeding intolerance, and high gastric residuals after feeding

PATHO:
too little oxygen or blood flow to the intestine at birth or later. injury to the intestinal lining. heavy growth of bacteria in the intestine that erodes the intestinal wall. viral or bacterial infection of the intestine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Cause of large volume diarrhea

A

excessive amounts of water or secretions, or both, in the intestines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Cause of small volume diarrhea

A

volume of feces is not increase, usually results from extensive intestinal motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Evaluation and treatment of GERD

A

EVALUATION: upper endoscopy, ambulatory acid probe test, esophageal manometry, xray of upper GI

TREATMENT: meds (antacids, proton pump inhibitor, antidiarrheal), lose weight, stay up after eating, avoid large meals, avoid foods that increase acid (caffeine), decrease fatty foods and alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is digestion

A

Digestion is the breakdown of large insoluble food molecules into small water-soluble food molecules so that they can be absorbed into the watery blood plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Absorption

A

is the process of transferring small absorbable units with water, electrolytes, vitamins from GI lumen into the blood and lymph.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Motility

A

means muscular contractions. When we eat, the food need to be broken down to small pieces and mixed, stored and moved forward, the food we eat can be digested and absorbed. Motility refers to the muscular contractions that mix and move forward of the contents in the GI tract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Secretion

A

secretes water mucus, electrolytes (such as HCl), enzymes, and bile salts which are all important for digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

4 primary functions of GI

A
  1. digestion
  2. absorption
  3. motility
  4. secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Mouth and salivary gland

A

Motility: chewing
Secretion: amylase, mucus, lysozyme mucus
Digestion: carbohydrate digestion begins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Pharynx and esophagus

A

Motility: swallowing

SECRETION: mucus

DIGESTION: none

ABSORPTION: none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Exocrine Pancrease

A

MOTILITY: not applicable

SECRETION:
-pancreatic digestive enzymes: trypsin, chymotrypsin, amylase, lipase
-Pancreatic aqueous
-NaHCO3 secretion
DIGESTION: These pancreatic enzymes accomplish digestion in duodenal lumen

ABSORPTION: not applicable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Liver

A

MOTILITY: Not applicable

SECRETION: Bile: bile salts, alkaline secretion bilirubin

DIGESTION: bile does not digest anything, but bile salts facilitate fat digestion and absorption in duodenal lumen

ABSORPTION: not applicable

47
Q

Small Intestine

A

MOTILITY: segmentation, migrating motility complex

SECRETION: Succus entericus (aka intestinal fluid): mucus and salt (small intestine enzymes are not secreted but function intracellularly in the brush border-disaccharidases and amniopeptidases

DIGESTION: in lumen under influence of pancreatic enzymes and bile, carbs and protein digestion continue and fat digestion is completely accomplished; in brush border, carb and protein digestion completed

ABSORPTION: all nutrients, most electrolytes, and water

48
Q

Large Intestine

A

MOTILITY: mass movements

SECRETION: mucus

DIGESTION: none

ABSORPTION: salt and water converting contents to feces

49
Q

What makes up the digestive tube?

A

mucosa, submucosa, and the muscularis externa, and the serosa

50
Q

What do exocrine cells in the mucous membrane do?

A

secretion of digestive juice
-secrete mucus to facilitate the movement of particles along the body’s various tubes, such as the throat and the intestines.

51
Q

Endocrine cells in the mucous membrane secrete what

A

gastrointestinal hormones, and cells specialized for absorbing digestive nutrients

52
Q

What are the 2 intrinsic nerve plexuses in the GI tract

A
  1. the submucous plexus located in the submucosa

2. myenteric plexus located between the smooth muscle layers

53
Q

Portan vein

A

carries blood from one capillary network to another

54
Q

Hepatic portal vein

A
  • formation by union of splenic and superior mesenteric veins
  • receives blood from digestive organ capillaries and delivers it to the liver capillaries
55
Q

The hepatic portal vein receives _____________ blood from the inferior, superior, and splenic veins

A

deoxygenated

56
Q

The hepatic portal vein delivers 70% of the blood supply to the liver which is rich in nutrients from where

A

the digestive tract

57
Q

Splenic vein gets blood from where

A

portions o the stomach, pancreas and portions of large intestine

58
Q

Superior mesenteric vein gets blood from where?

A

small intestines and portions of large intestine, stomach and pancreas

59
Q

Effects of aging on the GI system

A
  1. starts <50 years old
  2. taste buds decline in number, salivary secretion decreases
  3. decreases in the stomach volume and the lining’s capacity to resist damage decrease
  4. in small intestine, decreased in lactase levels and excessive growth of certain bacteria–lactose intolerance, pain and/or bloating, decreased absorption of certain nutrients, such as vitamin B12, iron, and calcium
  5. decrease motility in large intestines and rectum-constipation
  6. rate of liver regeneration decreases
  7. decrease secretion of HCl-, intrinsic factor
  8. altered mucous barrier, intestinal flora
60
Q

Three mechanisms of diarrhea

A
  1. osmotic diarrhea
  2. secretory diarrhea
  3. motility diarrhea
61
Q

Acute bleeding includes:

A
  1. hematemesis-throwing up blood
  2. melena-dark stool; partly digest blood
  3. hematochezia-blood in stool
62
Q

Intestinal obstruction can be caused by what?

A

Herniation, adhesions; volvulus (torsion), intussusception

63
Q

What is gastritis

A

inflammation or break in gastric mucosa

64
Q

peptic ulcer is

A

a break or ulceration in the mucosal lining of the lower esophagus, stomach or duodenum caused by excessive secretion of gastric acid, disruption of the protective mucosal barrier or both.

65
Q

Risk factors for Peptic ulcer

A
  • genetic predisposition, H.pylori infection, habitual use of NSAIDs.Alcohol, smoking, acute pancreatitis, chronic obstructive pulmonary disease, obesity, cirrhosis, age >65y, stress…
  • Can be acute or chronic.
  • Chronic use of NSAIDs suppresses mucosal prostaglandin synthesis, resulting in decreased bicarbonate secretion and mucin production, increased secretion of hydrochloric acid
66
Q

Curling’s ulcer

A

A stress‐induced ulcer of the stomach or duodenum that occurs in relation to extreme physical stress.

Stress‐related mucosal disease can cause mucosal erosions and superficial hemorrhages in patients who are critically ill or in those who are under extreme physiologic stress, resulting in minimal‐to‐severe gastrointestinal blood loss and leading to blood transfusion if not addressed in time.

67
Q

Zollinger‐Ellison Syndrome

A

Rare digestive disorder that results in too much gastric acid neuroendocrine tumor or multiple tumors (gastrinoma) of the pancreas or duodenum that can cause the formation of ulcers

Causes: abd pain, acid reflux, and diarrhea, weight loss

68
Q

Key characteristics of UC

A
  • increased risk of obstruction and colon cancer
  • intermittent periods of remission and exacerbation
  • loss off absorptive mucosal surface, bleeding, cramping pain, and urge to defecate, frequent bloody diarrhea with passage of purulent mucus, frequent diarrhea (more than 6 a day), anemia, weight loss
    complications: anal fissures, hemorrhoids, and perirectal abscess
69
Q

Irritable bowel disease

A

is a group of symptoms that occur together, including repeated pain in your abdomen and changes in your bowel movements, which may be diarrhea, constipation, or both.

  • functional disorder-no specific altered structures or biochemical processes
  • several hypotheses - visceral hypersensitivity, abnormal GI motility and/or secretion, food allergy/intolerance, psychosocial

Ex: UC and Crohn’s

70
Q

What is a common cause of acute liver failure

A

acetaminophen overdose

71
Q

Chronic liver failure is associated with

A

liver metabolism and extra liver abnormalities

72
Q

What is diarrhea?

A
  • > or =3 loose or liquid stools/day
  • osmotic (water drawn into the intestine)
  • secretory (Increase Cl- or HCO3- secretion or low Na+ absorption)
  • infection
  • endotoxin (c diff)
  • inflammatory bowel disease
  • motility
  • intestine shortened, neuropathy, hyperthyroidism
  • negative effects on fluid, electrolyte, acid-base balance
73
Q

Phases of hepatitis infection: **

A

Incubation-HAV 30 days: HBV up to 6 mo.; HCV 1-2 mo

Prodromal-2 wks after exposure to jaundice; likelikhood infectious very high

Icteric- may or may not be jaundiced (HBV, HCV); symptoms of specific illness; increased bilirubin, increased PT

Recovery - posticteric; livery enzymes within norms; chronic active hepatitis (carrier)

74
Q

What happens in cholelithiasis?

A

-“supersaturated” cholesterol form crystals&raquo_space; aggregate&raquo_space; + mucin&raquo_space; matrix within the gallbladder that lodge in the cyst or common duct

75
Q

What is cirrhosis

A

inflammatory, fibrotic disease related to alcohol or hepatitis

76
Q

How does ethanol effect liver dysfunction?

A

Alcohol changes the chemicals that break down and remove scar tissue. This means that scar tissue builds up in the liver. Scar tissue replaces normal healthy cells. This means that the liver can’t work properly and can fail, leading to death.How does ethanol effect liver dysfunction?

ethanol metabolizes to acetaldehyde via 3 enzymes&raquo_space; alcohol dehydrogenases, cytochrome P-450, catalase - forms NADH

77
Q

What are toxic effects of alcohol

A

GI bacteria endotoxins translocate&raquo_space; injury, inflammation&raquo_space; necrosis&raquo_space; collagen formation&raquo_space; fibrosis, scarring

78
Q

Complications of cirrhosis

A
  1. portal htn
  2. ascites
  3. hepatic encephalopathy
  4. jaundice
79
Q

Cirrhosis portal hypertension

A

Your body carries blood to your liver through a large blood vessel called the portal vein. Cirrhosis slows your blood flow and puts stress on the portal vein. This causes high blood pressure known as portal hypertension.

  • intrahepatic (ex cirrhosis) or extrahepatic (right side heart failure)
  • may result in varices: esophageal&raquo_space; increased risk rupture
80
Q

Cirrhosis ascites

A
  • fluid in peritoneal cavity; complication of portal htn, right side heart failure, nephrotic syndrome, hypoalbuninemia
  • post likely “cause” is splanchnic vasodilation&raquo_space; decrease systemic vascular resistance&raquo_space; Na retention (stimulated by RAAS)&raquo_space; increase ADH&raquo_space; fluid retention and transudation
81
Q

What is peritonitis?

A

Fluid in the peritoneal cavity that is infected

82
Q

Cirrhosis - Hepatic encephalopathy

A
  • neurologic impairment from accumulated “un-detoxified” gi toxins-cytokines, serotonin, tryptophan, ammonia
  • ammonia is especially challenging -metabolizes to glutamine in brain and interferes with neurotransmitters
  • ammonica is broken down in liver to urea and sent kidneys for excretion, but with cirrhosis the liver cann’t break it down and it builds up
  • look for :impaired cognitive function, asterixis, EEG changes
83
Q

Cirrhosis - Jaundice

A
  • due to hyperbilirubinemia
  • portal blood flow is distorted accompanied by a decrease in hepatic clearance of bilirubin.
  • obstruction to outflow-conjugated bilirubin in urine; none in stool
  • obstruction within liver-both conjugated and unconjugated bilirubin increase
84
Q

Nonalcoholic fatty liver disease

A
  • hepatocytes infiltrated with triglycerides (primarily)
  • associated with obesity, metabolic syndrome, DM2
  • risk=cirrhosis, liver failure, cancer
85
Q

Biliary cirrhosis

A

**When bile ducts become damaged, bile can back up into the liver, causing damage to liver cells. This damage can lead to liver failure

  • process begins in bile duct and canaliculi
  • primary-due to antigen antibody mediated destruction; antinuclear, antimitochondrial antibodies present
  • secondary-d/t prolonged obstruction of common bile duct which lead to necrosis
86
Q

Pancreatitis

A
  • acute, chronic, mild to severe
  • alcohol or obstructive (bile or pancreatic ducts); adverse drug reaction less common
  • elevation of pancreatic enzymes-amylase, lipase&raquo_space; proteolytic enzymes cause autodigestion&raquo_space; inflammation&raquo_space; proinflammatory cytokines + vasoactive peptides
87
Q

What systemic effects can pancreatitis have?

A

pleural effusion, acute lung injury, abscess formation, sepsis, systemic inflammatory response syndrome

88
Q

Chronic pancreatitis

A

pancreatic tissue gradually replaced by fibrotic and/or calcified tissue, formation cysts, strictures, obstruction

89
Q

GI disorders in children

A
  1. pyloric stenosis
  2. cleft lip/cleft palate
  3. neonatal jaundice
  4. GI effects cystic fibrosis
90
Q

GI effets of cystic fibrosis

A
  • fibrocystic disease of pancreas-leading to pancreatic enzyme deficiencies
  • pancreatic ducts obstructed by thick mucus&raquo_space; degeneration, fibrotic changes&raquo_space; potentially affetcs beta cells
  • enzyme deficiencies&raquo_space; protein, fat, CHO digestion&raquo_space; failure absorb fat soluble vitamins, growth failure, decreased bone mineral deposits
91
Q

GI disorders in neonates

A
  1. esophageal atresia
  2. meconium ileus
  3. necrotizing enterocolitis
92
Q

Esophageal atresia

A
  • trachea/esophagus fails to differentiate during 4-6 wk fatal development
  • esophagus ends in blind pouch, may occur with esophageal fistula
93
Q

necrotizing enterocolitis

A
  • newborns, especially low birth weight; d/t immature mucosal barrier
  • ischemic, inflammatory process that leads to bowel necrosis, perforation
94
Q

If pt is Hep A IgM neg and IgG pos, what is their status?

***

A

Negative for Hep A and immune due to previous illness or received vaccine

95
Q

if pt is Hep A IgM neg and IgG neg, what is their status?

***

A

Negative for Hep A, but susceptible to Hep A infection (never vaccinated or did not maintain antibody response

96
Q

Diverticulosis

A
  • condition in which there are small pouches or pockets in the wall or lining of any portion of the digestive tract.
  • mucosa herniates through smooth muscle layer colon wall
97
Q

GASTRIC ULCER

A

ETIOLOGY: 70% usually cause by H.Pylori which induces local inflammation

RISK FACTORS: long term use NSAIDs use (arise due to decrease in mucosal protection against gastric acid

CLINICAL MANIFESTATION: epigastric pain that worsens after eating, loss of appetite, and weight loss

PATHOLOGY:are a break in the mucosa of the stomach lining that penetrates through the muscularis mucosa and extends more than 5 mm in diameter. When alterations occur to the defense mechanisms of the stomach, it can cause changes in the gastric mucosa which will eventually result in erosion and then ulceration.

98
Q

How does NSAID cause ulcers?

A

it blocks cyclooxygenase from making prostaglandins that increase gastric mucous that decrease gastric acid

99
Q

ZOLLINGER-ELLSION SYNDROME

A
  • type of peptic ulcer
  • rare digestive disorder that results in too much gastric acid. This excess gastric acid can cause peptic ulcers in your stomach and intestine.
  • s/s: PAIN THAT IMPROVES WITH EATING AND PRESENT WITH WEIGHT GAIN: diarrhea,
100
Q

Ulcerative cholitis

A
  • effects more of the rectum and large bowel
  • inflammation and ulcer formation that is continuous
  • faulty immune system causing an overdrive, environment, stress, bacteria, viral, NSAIDs, genetic
  • affects more of the inner lining of intestinal wall
S/S: 
Urgent BM
Loss of weight, low RBCs
Cramps abd
Electrolyte imbalance
Rectal bleeding
Severe diarrhea

CURE: is surgery; colectomy and may have ostomy, anastamosis and pouch is created to the ilium so that ostomy is not needed

COMPLICATIONS: rupture of bowel, toxic magacolon (leads to rupture), weight loss, dehydration (inflammation doesn’t allow for water absorption), anemia (bleeding ulcers)l inflammation of joints, eyes, skin, and liver

101
Q

If you have UC or Crohn’s what foods do you want to avoid

A

hard to digest foods (popcorn, nuts), high fiber foods, fatty food, dairy, spicy food

102
Q

Crohns

A
  • scattered patches throughout the GI tract
  • affects entire lining of intestinal wall
  • commonly found in terminal ileum and start of colon

S/S: RLQ pain, ulcers in mouth, anal fissures, weight loss

CURE: none; bowel resection, ileostomy

COMPICATIONS:
Abscessing Fistulas May Form Sepsis; malnutrition, fissures (anal), strictures (obstructions)

103
Q

What happens in pancreatitis

A
  • leads to digestion of the pancreas by its own enzymes and/or irreversible structure damage to the organ
  • enzymes are activated inside pancreas instead of the duodenum
  • CBGs can be elevated because Islet of Langerhans don’t work properly
  • pancreas will swell and leak the digestive enzymes out into surrounding tissues and organs
  • comes on suddenly (acute form)

Complications: ascites, malabsorption, fibrosis, cysts, abscesses, GI pain, internal bleeding, shock

104
Q

What does bicarb do?

A

neutralizes stomach acid

105
Q

What causes ACUTE pancreatitis?

A
  • gallstones and alcohol
  • high amount of amylase and lipase produce by acinar cells of pancreas
  • reversible of treated quickly
106
Q

What causes CHRONIC pancreatitis

A
  • repeated episodes of acute pancreatitis and YEARS OF ALCOHOL ABUSE
  • damage is irreversible
107
Q

How does alcohol effect the pancreas

A

pancreatic acinar cells metabolize alcohol into toxic byproducts that damage pancreatic ducts, and enzymes that are normally released into the digestive tract build up and begin to digest the pancreas itself. The damaged pancreatic tissue promotes inflammation, which leads to further damage of the pancreas.

108
Q

Test for pancreatitis

A

ERCP–procedure to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas

109
Q

Treatment for pancreatitis

A 
NPO
IV fluids
Diet
Minitor I/Os
Meds: PPI, antacids, H2 blockers
110
Q

stomach

A

Motility: receptive relaxation peristalsis

SECRETION: gastric juice: HCL, pepsin, mucus, intrinsic factor

DIGESTION: carb digestion continues in body of stomach; protein digestion begins in antrum of stomach

ABSORPTION:

  1. none
  2. no food stuffs; a few lipid soluble substances, such as alcohol and aspirin
111
Q

Liver gets oxygenated blood from where?

A

the hepatic ARTERY

112
Q

Patient is HBAb core is neg and HBAb surface is positive, what is their status?

A

They are immune protected. Surface antibodies are present due to natural infection. Has recovered from a prior Hep B infection. Cannot infect others.

113
Q

If HBAg surface is neg, HBaB is core neg and HBAb surface is pos, what is their status?

A

immunity d/t vaccine

114
Q

Patient is HBAg surface pos and HBIgG core pos and HBAb surface neg, what is their status?

A

no immunity, chronically infected

Adv Patho (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions