Lesson 9 Gastrointestinal Systems Flashcards
1
Q
A major disorder of upper GI tract, is diagnosed if a person has esophagitis more than a few times a week. most commonly in infants and in persons older than age 40 years.
A
gastroesophageal reflux disease (GERD)
2
Q
This disease is associated with esophogitis and GERD, and if left untreated there is the possibility of acute GI bleeding.
A
peptic ulcer disease (PUD)
3
Q
How is the lower esophageal sphincter (LES) affected in GERD patients?
A
a functional or mechanical problem that decreases muscular tone: Relaxation of the LES allows for regurgitation of stomach contents into the esophagus
4
Q
This is the delayed emptying of gastric contents into the duodenum
A
Gastroparesis
5
Q
Why is gastroparesis problematic for GERD patients?
A
causes increased gastric distention that leads to increased pressure within the stomach against the LES. (lower esophageal sphincter)
6
Q
How can GERD progress to a serious illness?
A
esophageal epithelial cells are not able to withstand the acidity of the refluxed stomach contents. The gastric acid can quickly erode the protective mucosal epithelial layer and lead to ulceration of the esophagus. Repeated injury to the epithelial layer commonly causes metaplasia, the change of esophageal epithelial cells into stomachlike columnar epithelium.
7
Q
What is the metaplastic cellular change at the gastroesophageal junction called?
A
Barrett’s esophagus, is a precancerous change of cells
8
Q
Which factor determines the seriousness of an upper GI bleed?
A
(can’t find a distinct answer in the book)
An acute UGIB can quickly develop into hypovolemic shock.
a large blood loss causes sudden hypotension and hypovolemia.
Hematemesis is vomitus with bright-red, bloody streaks or a dark, coffee-ground appearance. The presence of bright-red blood indicates a current bleed.
9
Q
This is the presence of blood in the stool that is not visible
A
occult blood
10
Q
PUD, esophageal varices, Mallory–Weiss syndrome, Boerhaave syndrome, esophageal cancer, and hemorrhagic gastritis, can cause what?
A
upper GI bleed
11
Q
This is is associated with a rupture, tear, or perforation in the esophageal or gastric lining, resulting in blood loss. large blood loss causes sudden hypotension and hypovolemia. rapid onset of anxiety, dizziness, weakness, shortness of breath, or change in mental status. Tachycardia and tachypnea will occur because of decreased cardiac output. The skin will be pale and clammy as a result of the body’s effort to shut down peripheral blood flow.
A
Acute Upper GI bleed
12
Q
This is the result of a small tear or opening in the GI tract that causes a gradual, small amount of blood loss. causes complaints of fatigue, low hemoglobin, and low iron levels
A
Chronic upper GI bleed
13
Q
This is treated primarily with PPIs such as omeprazole (PrilosecR) for 4 to 8 weeks.
A
chronic upper GI bleed
14
Q
This is treated with rapid fluid replacement, insertion of a nasogastric tube to prevent abdominal distention from accumulation of blood, and administration of blood transfusions. might need endoscopy, coagulation, or surgical repair
A
Acute Upper GI bleed
15
Q
What are the two major causes of peptic ulcer disease (PUD)?
A
the bacterium H. pylori and the use of NSAIDs or aspirin.
16
Q
This is inflammatory erosion in the stomach or duodenal lining. The incidence of this disease is equal in males and females.
A
Peptic ulcer disease (PUD)
17
Q
What is the most significant risk factor for developing PUD?
A
the presence of H. pylori
18
Q
Why do NSAIDs and aspirin cause PUD?
A
They counteract prostaglandin E secretion, the major stimulant of gastric mucus production, and diminish the stomach’s protective layer.
19
Q
Hydrochloric acid (HCl) is normally found in the stomach. How can HCl disorder
contribute to PUD?
A
Hypersecretion of HCl can lead to erosion of the mucus membrane in the stomach or duodenum, which permits the diffusion of HCl into the stomach wall and blood vessels=inflammatory response=release of protaglandins and histamine=stomach cells triggered to release more mucus and bicarbonate to neutralize, but the parietal cells keep releasing histamine and HCl=continued damage
20
Q
What are complications of PUD?
A
bleeding and perforation
21
Q
this occurs when part of the stomach pushes up through the opening in the diaphragm and protrudes into the thoracic cavity. This allows acid from the stomach to reflux back up into the esophagus.
A
hiatal hernia
22
Q
How can gastroenteritis pathogens cause watery diarrhea?
A
These microorganisms cause diarrhea by adherence to the mucosa, invasion into the mucosal layer, or toxin production. The end result of most microbial infections is increased fluid to shift into the lumen of the intestine, to a point where the excessive fluid cannot be adequately reabsorbed. This fluid shift results in watery, small intestinal contents that pass into the large intestine and are then excreted as diarrhea.
23
Q
This is a protrusion of a section of the small intestine through a weakened abdominal wall muscle
A
Hernia
24
Q
This occurs from an irritation to the lining of the stomach, small intestine, or large intestine by a pathogen or toxin. The disease can occur from a virus, bacteria, parasite, or chemical toxin. It is transmitted from person to person or can be a waterborne or foodborne illness.
A
Gastroenteritis
25
This type of diarrhea occurs because of an increase in the osmotic load presented to the intestinal lumen because of diminished absorption.
osmotic diarrhea
26
This type of diarrhea occurs when the mucosal lining of the intestine is inflamed, edematous, and unable to reabsorb fluid or nutrients.
inflammatory diarrhea
27
This type of diarrhea occurs when an organism stimulates the intestine to secrete fluid and mucus.
Secretory diarrhea
28
This type of diarrhea is caused by intestinal neuromuscular disorders.
motility diarrhea
29
Which individuals are most at risk for viral or bacterial gastroenteritis?
individuals who are in close contact with others, such as those in nursing homes, day-care centers, cruise ships, and dormitories
30
What is the primary clinical presentation of gastroenteritis?
nausea, vomiting, abdominal cramping, and diarrhea.
31
What are the clinical signs or red flags that may indicate a need for hospitalization in patients with acute gastroenteritis?
* Severe volume depletion/dehydration
* Abnormal electrolytes or renal function
* Bloody stool/rectal bleeding
* Weight loss
* Severe abdominal pain
* Prolonged symptoms (more than 1 week)
* Hospitalization or antibiotic use in the past 3 to 6 months
* Age 65 or older
* Comorbidities (e.g., diabetes mellitus, immunocompromised)
* Pregnancy
32
What specifically named diet is recommended for someone with gastroenteritis?
The BRAT diet (bananas, rice, applesauce, and toast)
33
This is also known as sprue and gluten-sensitive enteropathy, is a condition that occurs from a hypersensitivity reaction to gluten, a by-product of wheat, barley, and rye. The cause is unknown, but it is considered an autoimmune disease.
Celiac Disease
34
What is the etiology of Celiac disease?
a gluten-derived peptide called gliadin damages the intestinal mucosa in persons with genetic predisposition to this disease. The exact etiology is unknown, but T cells predominate in an autoimmune inflammatory reaction against intestinal villi.
35
In celiac disease, what does the inability to digest carbs lead to?
a buildup of gases within the intestinal system, causing abdominal bloating and diarrhea
36
This is the name for the loss of fat in stool, which causes it to be light colored and soft.
Steatorrhea
37
What are the initial symptoms of celiac disease? what is seen as the disease progresses?
fatigue, abdominal pain, bloating, and steatorrhea. As the disease progresses, symptoms associated with vitamin deficiencies will present, including anemia, high incident of fractures or bone pain, abnormal growth, bruising, poor skin turgor, and dehydration.
38
How is celiac disease treated?
aimed at making dietary changes, identify and eliminate gluten products in the diet. The patient frequently needs vitamin replacement. If the immune response is extreme, corticosteroids may be prescribed.
39
What is inflammation of a vestigial part of the intestine-can lead to perforation if not diagnosed promptly?
appendicitis
40
what are segmental mixing or kneading movements that shuffle the contents back and forth among the haustra in the large intestine? and what is its purpose?
Haustrations: increases the contact time with the mucosa to facilitate the absorption of water and electrolytes and allow time for bacteria to accumulate. The circular muscles contract and relax at different sites, creating a shuffling effect.
41
what are the movements that generally occur after meals? A large segment of the colon (longer than 20 cm) contracts as one unit, moving fecal contents forward. A series of these movements lasts approximately 10 to 30 minutes and occurs several times per day.
Propulsions
42
What increases the membrane permeability to sodium, and it increases both the diffusion of sodium into cells and its active transport into interstitial fluid in the large intestine?
Aldosterone
43
How much of the bulk of solid feces is bacteria?
1/3
44
Commonly used drugs, particularly those with which kind of side effects can interfere with intestinal motility?
anticholinergic
45
What can chronic use of laxatives lead to?
lack of natural colonic motility. Excessive laxative use is defined as more than three times per week for at least 1 year.
-also: serious medical consequences, such as fluid and electrolyte imbalance, steatorrhea, protein-losing gastroenteropathy, osteomalacia, and vitamin and mineral deficiencies.
46
This is the anatomical and physiological change in the colon that occurs with chronic use of stimulant laxatives.
Cathartic colon
47
This occurs when hard stool that cannot be passed is lodged in the sigmoid colon and rectum.
fecal impaction
48
This is the urge to defecate but there is no passage of stool, liquid, or gas from the colon.
Obstipation
49
What is the difference between IBS (irritable bowel syndrome) and IBD (inflammatory bowel disease)?
IBS= frequent episodes of abdominal pain, bloating, and abdominal distention. no pathological change within the interior of the bowel, and etiology is unclear.
IBD= caused by pathological changes in the wall of the colon. UC and Crohn’s disease, both types of IBD, cause severe abdominal pain, diarrhea, bloody stools, and weight loss. The bowel mucosa is friable, edematous, ulcerated, scarred, and bleeding.
50
This is an inflammatory disorder of the colon, caused by weak areas that form pouches off the wall of the large intestine. Commonly, these pouches become filled with stagnant intestinal contents, leading to obstruction and inflammation of the bowel wall.
Diverticulitis
51
Right lower quadrant (RLQ) tenderness is commonly caused by what?
Appendicitis
52
LLQ tenderness is commonly associated with what?
Diverticulitis
53
Upper right quadrant (URQ) tenderness elicited by palpation is called what? What does this indicate?
Murphy's sign
Cholecystitis: gallbladder inflammation
54
What additional examination do women need with abdominal pain and why?
pelvic examination and pregnancy test to rule out ectopic pregnancy.
55
This is a surgical procedure in which the healthy end of the intestine is brought out of the abdomen through an incision in the anterior abdominal wall.
Ileostomy: small intestine
colostomy: large intestine
56
This is a chronic, transmural, inflammatory process of the bowel that often leads to fibrosis and obstructive symptoms; it can affect any part of the GI tract from the mouth to the anus. The most common location is the terminal ileum and ascending right colon.
Crohn's disease
57
What is the cause of Crohn's disease?
No known cause
theories= genetic, immunological, infectious, and environmental influences that contribute to an overactive inflammatory response to unknown triggers.
58
What are the risk factors for Crohn's disease?
genetic predisposition, ethnicity, and cigarette smoking. (caucasians more likely, urban living, mutations of genes, consuming refined sugars and saturated fats, stress factors)
59
What are the complications of Crohn's disease?
small bowel obstruction due to chronic inflammation, stricture or spasm in the intestine=narrowed lumen, impactions, adhesions after surgery, microperforations, localized peritonitis or abscess, high risk for venous thrombo and PE.
60
This disease affects the entire thickness of the bowel wall and all layers of the submucosa. The mucosa is chronically inflamed and contains a high number of immunoglobulins, T cells, and macrophages. T cells attract nonspecific inflammatory cells, especially neutrophils, which play a major role in tissue damage. This response produces cytokines, growth factors, antibodies, and proteases, which all contribute to continual tissue destruction.
Crohn's disease
61
The lesions are visible as edematous, reddish-purple areas in a segmental pattern. There are areas of disease separated by healthy areas, referred to as what?
skip lesions
62
In crohn's disease the bowel mucosa develops granulomas; this is exhibited as an effect called what?
cobblestoning
63
This is the extreme dilation of a segment of the diseased colon, commonly the transverse colon. It causes complete obstruction and impaired absorption of fluids and electrolytes. Life-threatening perforation and peritonitis can result. Occurs in Crohn's disease
Toxic megacolon
63
What are the intestinal symptoms of Crohn's disease?
abdominal tenderness, increased bowel sounds, steady progressive weight loss, anorexia, nausea, vomiting, diarrhea, pallor, and, in acute exacerbations, fever. Severe bouts can cause intestinal obstruction with accompanying signs of borborygmi (hyperactive bowel sounds), abdominal distention, and tympany on percussion.
64
What systemic symptoms can Crohn's disease cause?
arthritis, uveitis, cheilitis, and dermatological problems
Cheilitis= inflam lesion of lips
uveitis=inflam of middle layer of eye--> retinal detatchment
hepatic or bile duct inflam can occur
65
Why are colonoscopy and biopsy the best diagnostic tools to distinguish Crohn’s
from ulcerative colitis?
Crohn's= any part of GI tract from mouth to anus
UC= only large intestine
Crohn's= affects GI with skip lesions=healthy tissue interrupted by areas of dieased
UC= affects from rectum to continually upward into colon
Crohn's= affects whole thickness of intestinal wall
UC=only upper layers (mucosa and submucosa)
Crohn's= cobblestoning
UC=pseudopolyps
Crohn's= anal fistula and anal fissures
UC=No fistuals or fissures
Crohns= does not predispose to cancer
UC= predisposes to colon cancer
66
This is thought to be an autoimmune disease of the colon. It affects the mucosal layer of the large intestine, is more likely to present with blood in the stool and a colonoscopy will show pseudopolyps. It is also more likely to lead to cancer.
Ulcerative colitis
67
LBO (large bowel obstruction) has a high mortality rate if diagnosis and treatment are not commenced within the first how many hours?
24 hours
68
This type of large bowel obstruction physically blocks the movement of material through the intestines. may be caused by scar tissue from prior surgery (adhesions), benign or malignant tumors, abdominal hernia, a swallowed foreign body, a gallstone that migrated into the intestine, bolus of undigested food, intussusception, volvulus, stricture, fecal impaction, or diverticula.
mechanical obstruction
69
This type of large bowel obstruction stem from certain intestinal conditions, such as a disruption of the peristalsis caused by weakness of muscles of the intestinal wall (dysmotility syndrome or pseudo-obstruction) or paralysis of the bowel wall (paralytic ileus).
Nonmechanical
70
What is the pathophysiology of a mechanical large bowel obstruction?
an obstruction that causes the bowel to become dilated proximal to the obstruction. This distention of the bowel results in an increase in peristalsis in an effort to excrete intestinal contents through the obstruction. As the distention progresses and pressure rises within the bowel, the bowel’s ability to absorb fluids is impaired, and blood flow to the bowel is decreased, causing ischemia.
if not resolved= perforation=spilling of fecal material into the peritoneal cavity, causing peritonitis.
71
What is the pathophysiology of nonmechanical LBO?
motility through the intestine is impaired. This can be caused by weakness of intestinal peristalsis, also known as paralytic ileus. Ileus can result from neurological disease, acute colonic pseudo-obstruction, metabolic disturbances, ischemia of the bowel, or infection of an abdominal organ.
72
This is an inflammation of a blind-ended, pouchlike area that protrudes from the cecum, where the small intestine meets the large intestine.
Appendicitis
73
What is the cause of appendicitis?
It is hypothesized that appendicitis results from a nearby blockage, commonly caused by stool or fecalith (calcified feces). Blockage of the appendix often occurs when neighboring mesenteric lymph nodes become inflamed in response to a viral or bacterial infection and compress the appendix. the protective mucosa layer of the appendix becomes compromised as luminal bacteria multiply and attack the wall of the appendix, causing inflammation. This inflammation, in combination with tissue ischemia, leads to necrosis and perforation of the appendix.
74
Typical manifestations of appendicitis include abdominal pain that originates in the umbilical region radiating to the RLQ, also known as
McBurney's point
(rebound tenderness is also apparent)
75
The examiner deeply palpates the abdomen; upon release of the hand, the patient feels intense pain.
Rebound tenderness
76
Examiner asks the supine patient to actively flex the right thigh at the hip. If abdominal pain results, this is positive for?
Psoas sign
77
The examiner palpates the LLQ of the abdomen. If pain in the patients RLQ develops, this is positive for ?
Rovsing's sign
78
Internal and external rotation of the patient’s flexed right hip causes pain in the RLQ.
obturator sign
79
What are the treatments for appendicitis?
surgical removal and ABX (in acute)
Some pts with non-perforated can be treated with ABX alone
80
This is a GI disorder characterized by abdominal pain and altered bowel activity in the absence of specific pathology. No specific motility or structural disorders of the intestine or bowel are seen. Lay terms for it are colitis, irritable colon, or spastic colon
IBS (irritable bowel syndrome)
81
These causes of acute abdominal pain will show pain in which quadrant?
Gastric ulcer, ruptured spleen, aortic aneurysm, pancreatitis
LUQ
82
These causes of acute abdominal pain will show pain in which quadrant?
Hepatitis, duodenal ulcer, acute cholecystitis
RUQ
83
These causes of acute abdominal pain will show pain in which quadrant?
Hernia, appendicitis, ovarian cyst, kidney stone, pyelonephritis, ectopic pregnancy, salpingitis, mesenteric adenitis, Meckel's diverticulitis, bowel obstruction/perforation/ischemia, inflamm bowel disease
RLQ
84
These causes of acute abdominal pain will show pain in which quadrant?
hernia, diverticulitis, ovarian cyst, kidney stone, pyelonephritis, ectopic pregnancy, bowel obstruction/perforation/ischemia, inflamm bowel disease
LLQ
85
These causes of acute abdominal pain will show pain where in the body?
esophagitis, pancreatitis, perforated ulcer, acute cholecystitis, myocardial infarction
Epigastric
86
What appears to be the causative factor in irritable bowel syndrome?
The patient commonly reports a stressor in his or her life.
87
How do complications and variations of gastrointestinal disorders
and injuries affect the body?
(my general thought based on review of the text): it affects absorption of vitamins, minerals, proteins, carbs, fats, etc, the building blocks our bodies need. When disturbances happen in the GI system it will affect the rest of our body.
88
These are the functional cells of the liver that are capable of regeneration, excrete metabolic substances into small channels called canaliculi.
Hepatocytes
89
These are specific macrophages of the liver, line the sinusoids and protect the body by detoxifying the bloodstream.
Kupffer cells
90
How does the liver aid in digestion?
manufactures bile and secretes it into the hepatic duct, which enters the common bile duct and, in turn, empties into the intestine for digestion of fats.
91
The liver manufactures most of the body’s ___________. Proteins are broken down (referred to as deamination) into ammonia, which is then absorbed into the bloodstream and excreted in urine.
Albumin
92
How is the liver involved in carb metabolism?
Glucose builds up in the liver, which is stored in the form of glycogen (glycogenesis). There is also breakdown of glycogen by the liver when the body needs it (glycogenolysis).
93
What does the liver synthesize using vitamin K?
coagulation factors ( fibrinogen and coagulation factors I, II, VI, IX, and X for clotting. With the exception of factor VIII, all of the elements of clotting are made by the hepatocytes. Prothrombin is produced by the liver with the assistance of vitamin K and bile. )
94
How is the liver involved in detoxification?
The portal vein brings all substances absorbed by the GI system into the liver, which then detoxifies substances through biotransformation and first-pass effects.
95
This vital organ in the body stores vitamin A, D, B12, iron, and copper, produces B lymphocytes, synthesizes angiotensinogen, synthesizes thrombopoietin, which stimulates platelet production in bone marrow.
Liver
96
How is the liver involved with the recycling of worn out RBCs?
conjugates bilirubin into bile (bilirubin is a yellow-colored compound, is derived from the breakdown of aged red blood cells (RBCs). Hemoglobin in the RBCs breaks down into heme and globin)
97
This is yellowing of the skin and sclera, is the key symptom of liver disease
jaundice
98
What three specific etiologies can cause Hyperbilirubinemia?
* Excessive RBC hemolysis
* Hepatocellular injury
* Bile duct obstruction
99
What type of jaundice happens when there is a large amount of hemolysis, bilirubin levels can overwhelm the liver, and some bilirubin can go into the bloodstream without being conjugated, which is why prolonged hemolysis increases both conjugated and unconjugated bilirubin concentrations?
Prehepatic jaundice
100
What type of jaundice happens when the liver is having problems conjugating the bilirubin, resulting in only a portion becoming conjugated?
intrahepatic jaundice
101
What type of jaundice happens in bile duct obstruction, the liver can conjugate the bilirubin, but the bile duct does not allow its excretion, resulting in increased levels of conjugated bilirubin circulating in the bloodstream?
Posthepatic jaundice
102
What are the most common viruses that infect the liver?
hepatitis virus A, B, C, D, and E. Other viruses include cytomegalovirus and Epstein–Barr virus (EBV)
103
This occurs when the liver is affected by drugs or toxic substances. What is the most common cause?
toxic hepatitis, Acetaminophen
104
A patient with this often reports extreme fatigue, abdominal pain, weakness, anorexia, nausea, vomiting, abdominal bloating, changes in bowel habits, and weight loss. Interestingly, smokers often lose their taste for tobacco.
liver disfunction
105
These are fine capillaries that fan out from a central point on the skin’s surface that can indicate liver disfunction
spider angioma
106
This is a common cause of long-term, chronic liver disease. With chronic inflammation, stellate cells within the liver are stimulated to synthesize collagen and fibrotic tissue. Other classic histological features of the disease include bile duct damage, lymphoid follicles or aggregates, and macrovesicular steatosis. Steatosis is the infiltration of fat in the liver. Fatty liver is a characteristic change.
Alcohol abuse
107
How are viruses that affect the liver diagnosed?
A hepatitis serology panel is done that includes specific laboratory data regarding hepatitis A, B, C, D, or E
108
How is Hep A transmitted?
caused by ingestion of contaminated food or water or contracted from person to person by the fecal–oral route. The virus is able to live on surfaces at room temperature, but is killed by cooking food thoroughly.
109
Which liver virus is the only DNA virus?
Hep B
110
What are two different characteristics that distinguish HBV and HCV?
HBV=DNA virus
HCV=RNA virus
HBV=Major mode of transmission is sexual contact
HCV= Transmission is via blood, as in IV drug use
HBV=infected people carry it for life
HCV= can be considered cured with agressive treatment
111
Fatty liver develops in every individual who consumes more than how much alcohol per day?
60 grams of alcohol per day
112
What does chronic ingestion of alcohol inhibit in the liver?
oxidation of fatty acids
Fat accumulates in and around hepatocytes as constant alcohol use occurs, and this fat accumulation within the hepatocyte disrupts the integrity of the organelles. Nuclear disruption causes death of the hepatocytes. Disrupting the mitochondria leads to free radical release and inflammation.
113
When the liver demonstrates fibrosis and scar tissue, the disorder is referred to as what?(often is a silent and gradual disease; most patients remain asymptomatic until a late stage of liver impairment marked by ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, or variceal bleeding from portal hypertension. )
cirrhosis
114
Patients with acute alcoholic hepatitis typically present with what symptoms?
mild, nonspecific symptoms of RUQ pain, nausea, malaise, and low-grade fever. Jaundice and darkened urine may be present because of liver dysfunction and bilirubin accumulation in the bloodstream. The liver is usually enlarged, often with mild hepatic tenderness.
115
individuals with severe alcoholic hepatitis are at high risk of?
death
116
What are symptoms of alcohol withdrawl?
restlessness, mood disturbance, tremors called delirium tremens, and, possibly, seizures.
117
What are increased risks for patients with alcohol abuse and why?
risk of bleeding esophageal varices and subdural hematoma in head injury due to Decreased synthesis of coagulation factors
118
This is an elevated pressure within the portal vein, is a key pathophysiological change associated with cirrhosis. (cirrhosis is causing restricted blood flow of the portal vein through the liver, which causes back up of pressure to GI system)
Portal hypertension
119
What are the consequences of portal hypertension?
Increased venous pressure builds within the vascular beds of the GI system, producing splenomegaly, esophageal varices, rectal varices, and eventually ascites. The esophageal veins and rectal veins are fragile submucosal veins that are prone to rupture; ruptured esophageal veins can cause vomiting of blood (hematemesis), whereas ruptured rectal veins can cause rectal bleeding.
120
Dilated, superficial veins become visible around the umbilicus, a sign referred to as what?
caput medusa
121
what is the purpose of bile?
emulsifies fats and facilitates absorption of fat-soluble vitamins. It also carries waste products for elimination (such as bilirubin)
122
The purpose of this organ is to produce the digestive enzymes lipase, which digests fats, and amylase, which digests carbohydrates. Trypsin and chymotrypsin, other enzymes also manufactured by it, digest proteins. It also produces bicarbonate, which is a natural antacid.
Pancreas
123
These are the most common stones formed in the gallbladder
Cholesterol stones
124
These are small, hard gallstones composed of calcium bilirubinate and inorganic calcium salts. it's related to alcoholic liver disease, chronic hemolysis and aging
Black pigment stones
125
These are composed of calcium salts of unconjugated bilirubin, with small amounts of cholesterol and protein. They are often located in the bile ducts and cause obstruction and inflammation.
Brown pigment stones
126
This is a syndrome of spasmodic pain associated with irritation of the gallbladder, commonly secondary to gallstones.
Biliary Colic
127
The pain of cholecystitis commonly radiates to where?
right shoulder or posterior thoracic region at the scapula. called Collin's sign
128
is an invasive procedure that uses an endoscope with a camera to inspect the anatomy of the biliary tract. In addition to visualization, it can be used to remove obstructive gallstones from the common bile duct.
Endoscopic retrograde cholangiopancreatography (ERCP)
129
If the patient has pancreatitis, and the goal is to rest the GI system and pancreas, what should the patient's diet be free from?
fat, caffeine, and alcohol.
130
Pancreatic cancer commonly requires surgery called what?
Whipple procedure.
131
Because epigastric pain with radiation to the shoulder is a common symptom, many patients can mistake an episode of acute cholecystitis for what?
Cardiac chest pain
132
The inflammatory process associated with acute cholecystitis can also occur because of bacterial infection that can progress to a purulent effusion of the gallbladder, called what?
empyema
133
The patient presents with the following symptoms: abdominal pain in the RUQ, anorexia, nausea, vomiting, eructations, heartburn, feeling full after eating, and, perhaps, fever, Murphy’s sign, Collins’s sign. Although the pain may initially be described as spasmodic or colicky, it becomes constant in many cases.
acute cholecystitis
134
What is the treatment of choice for symptomatic cholelithiasis and cholecystitis?
Laparoscopic cholecystectomy
135
When there is concern that stones may have moved into the common bile duct, what may also be performed during surgery?
intraoperative cholangiography and choledochoscopy (This allows full exploration of the common bile duct. )
136
When a patient has acute cholecystitis and the patient has acute pain that is transient and followed by relief of pain, what could this indicate?
Rupture of an acutely inflamed gallbladder as contents are released from the distended, perforated gallbladder into the abdomen. It is critical to report this finding immediately to avoid sepsis.
137
Why is dilauded the pain medication of choice for acute cholecystitis patients?
morphine and codeine are contraindicated because they can cause spasm of the sphincter of Oddi. Dilaudid does not cause spasm of the sphincter of Oddi
138
How can gallstones affect the pancreas?
obstruction of the pancreatic duct by a gallstone or other cause, with release of digestive enzymes that back up into the pancreatic gland parenchyma, followed by autodigestion.
139
The classic symptom associate with this disease is severe abdominal pain, which is dull, penetrating, and steady. pain is sudden in onset and gradually intensifies. Mostly in epigastric region and radiates straight into the back. Nausea, vomiting, and diarrhea with anorexia. Fever, tachycardia, and hypotension commonly accompany the pain. Dyspnea and tachypnea may also occur because of irritation of the diaphragm.
Acute pancreatitis
140
is a dark-blue discoloration around the umbilicus that resembles a bruise resulting from blood in the peritoneal cavity because of hemorrhagic pancreatitis.
Cullen sign
141
is a dark-blue discoloration resembling bruises along the flanks resulting from retroperitoneal blood dissecting along tissue planes
Grey Turner sign
142
how is acute pancreatitis treated?
no proven therapy that directly ameliorates pancreatic inflammation. The main treatment goal for acute pancreatitis is to provide supportive care and minimize pancreatic stimulation.
Pain meds, may need surgical intervention
143
What should be suspected in patients who have moderate-to-severe acute pancreatitis; who have worsening symptoms after initial improvement; and who develop new fever, marked by leukocytosis, positive blood cultures, or other evidence of sepsis.
Infected pancreatic necrosis
144
What are the systemic complications of acute pancreatitis?
cardiovascular, renal, and respiratory failure. Cardiovascular complications include profound hypotension.
145
This is defined as inflammation of the pancreas that does not heal and that leads to permanent damage. it occurs when digestive enzymes attack the pancreas and nearby tissues, causing episodes of pain.
chronic pancreatitis
146
What is the most common cause of chronic pancreatitis?
long-term, heavy alcohol use and can be triggered by one acute attack that damages the pancreatic duct.
147
What is the treatment for chronic pancreatitis?
commonly requires hospitalization for pain management, IV hydration, and nutritional support. Nasogastric feedings may be necessary for several weeks if the person continues to lose weight. When a normal diet is resumed, synthetic pancreatic enzymes may be prescribed if the pancreas does not secrete enough of its own.
148
