Exam 4: Ch. 21-23, 25-27 Flashcards
largest organ in the body
liver
4 functions of liver
- metabolism (carbohydrates, protein, and fat)
- synthesis (proteins, clotting factors)
- storage (vitamin b12)
- detoxification and excretion
the liver has a double blood supply. what does this mean?
there is a portal vein and a hepatic artery that supply the liver
portal vein
supplies liver with 75% of its blood, is rich in nutrients, low in oxygen
hepatic artery
supplies liver with 25% of its blood, is high in oxygen and low in nutrients
bile
aqueous solution with various dissolved substances (conjugated bilirubin, bile salts, cholesterol, minerals)
where does bile come from?
RBC break down, iron is reused, and iron-free heme pigment or bilirubin is excreted in the bile
is bile always present?
yes, small quantities are always present
lecithin
lipid that also functions as a detergent, is also present in bile
where is bile stored?
gallbladder, it is released into the duodenum to help with digestion
3 manifestations of liver injury
cell necrosis, fatty change, and mixed necrosis and fatty change
4 common types of liver injury
viral hepatitis, fatty liver, alcoholic liver disease (hepatitis), cirrhosis
does hepatitis A contain DNA or RNA?
RNA
incubation period of hepatitis A
2-6 weeks
transmission methods of hepatitis A
person to person contact, and fecal contamination of food or water
is there prevention for hepatitis A?
vaccine, and immune globulin given after exposure to the virus
does hepatitis B contain DNA or RNA?
DNA
incubation period of hepatitis B
6 weeks to 4 months
transmission of hepatitis B
blood or bodily fluids
how is hepatitis B diagnosed?
with an antigen-antibody test
- infected people are HBsAg positive and lack anti-HBs
- immune people have anti-HBs
can hepatitis B be carried?
yes, 10% of those infected become carriers
is there prevention for hepatitis B?
vaccine, and immune globulin given after exposure to the virus
which type of hepatitis is seen the most in the US?
hepatitis C
does hepatitis C contain DNA or RNA?
RNA
transmission of hepatitis C
blood and bodily fluid
how is hepatitis C diagnosed?
with an antigen-antibody test
- infected people have the virus present and an active infection
- if anti HCVs are detected it does not confer immunity
can hepatitis C be carried?
yes, 75% of those infected become carriers
is there prevention for hepatitis C?
no
who is at risk for hepatitis C?
IV drug users, people that received transfusions before 1992, healthcare workers exposed to blood or bodily fluids
does hepatitis D contain DNA or RNA?
RNA
what makes hepatitis D different from other types?
it is a small and defective virus that can’t produce its own virus coat, so it can only infect people that have hepatitis B
what are most of the cases of hepatitis D in the US from?
sharing used needles
does hepatitis E contain DNA or RNA?
RNA
transmission of hepatitis E
oral-fecal contact, and contaminated water
is there prevention for hepatitis E?
no
fatty liver
fat accumulates as a result of liver injury, common in heavy drinkers and alcoholics, and damage is reversible
alcoholic liver disease
group of structural and functional changes in the liver resulting from excessive alcohol consumption
severity of alcoholic liver disease depends on what?
amount and duration of alcohol consumption
3 stages of progression of alcoholic liver disease
- alcoholic fatty liver-mild
- alcoholic hepatitis-degenerative changes and necrosis of liver cells
- alcoholic cirrhosis-diffuse scarring, disturbed liver function
cirrhosis
scarring of the liver from any cause with derangement of liver function and regeneration
-can result from any liver injury
manifestations of cirrhosis
liver failure, portal hypertension, ascites
ascites
accumulation of fluid in peritoneal cavity
portal-systemic anastomoses
procedure where portal vein is connected to systemic vein in the liver to control varices
varices
dilated veins as a result of portal hypertension
transjugular intrahepatic portosystemic shunt
a shunt is placed between hepatic and portal vein branches so the blood can bypass the cirrhotic liver
hepatic encephalopathy
deterioration of brain function characterized by confusion, disorientation, and eventually coma
what causes hepatic encephalopathy?
accumulation of toxic substances (ammonia, bacterial decomposition products) in blood that are usually detoxified and excreted by the liver
primary biliary cirrhosis
autoimmune disease that attacks the intrahepatic bile duct, this can lead to liver failure and require a liver transplant
secondary biliary cirrhosis
obstruction of large extra hepatic bile ducts (from gallstone, carcinoma), treated by reliving or bypassing the obstruction
Reye syndrome
virus that causes liver and brain damage, and aspirin is thought to increase the effects of this
characteristics of Reye syndrome
affects mainly infants and children, manifests with fatty liver and dysfunction, cerebral edema
cholelithiasis
gallstone formation in the bladder
cholelithiasis is highest in:
women, especially those who have had several children, use oral contraceptives, and that are obese
complications of cholelithiasis
biliary colic (pain) if the stone gets into ducts (common and cystic obstruction)
common duct obstruction
gallstone obstructs the common bile duct, causes obstructive jaundice
cystic duct obstruction
gallstone obstructs the cystic duct, doesn’t cause jaundice but acute cholecystitis may occur
cholecystectomy
surgical removal of gallbladder, used to treat cholelithiasis
cholecystitis
inflammation of the gallbladder, gallstone obstructing the cystic duct or the neck of the gallbladder can cause this
benign adenoma
uncommon liver tumor, occur in women that take contraceptive pills
primary carcinoma of the liver
uncommon in US and Canada but common in Asia and Africa because of high incidence of hepatitis B carriers
metastatic liver carcinoma
common in developed countries, spreads from primary sites such as the GI tract, lung, and breast
jaundice
yellow discoloration of skin and sclera (whites of eyes) from accumulation of bile pigment in tissues
cause of hemolytic jaundice
increased breakdown of red blood cells, bilirubin released
cause of hepatocellular jaundice
liver injury impairs the conjugation of bilirubin, it builds up
cause of obstructive jaundice
bile duct obstructed by tumor or gallstone, impairing delivery of bile into duodenum
liver biopsy
needle inserted through abdominal skin directly into the liver to determine the cause of liver disease or evaluate extent of liver cell damage
individuals at risk for developing hepatitis C include the following except:
a. intranasal cocaine users
b. healthcare personnel exposed to blood and body fluids
c. intravenous drug users
d. children born to mothers who test HCV positive
e. children’s daycare personnel
a. intranasal cocaine users
hepatitis C is transmitted through blood and bodily fluids, options b-e all involve blood and bodily fluids
what does it mean to say the pancreas is both an endocrine and exocrine gland?
it secretes pancreatic juice into the duodenum (exocrine) and secretes insulin discharge directly into the bloodstream (endocrine)
Islets of Langerhans
small clusters of cells scattered throughout the endocrine tissue of the pancreas, responsible for secreting glucagon, insulin, and somatostatin
alpha cells
make up some pancreatic islets, secrete glucagon which raises blood glucose
beta cells
make up some pancreatic islets, secrete insulin which lowers blood glucose
delta cells
make up some pancreatic islets, secrete somatostatin which inhibits secretion of glucagon and insulin both
acute pancreatitis
pancreatic juices escape from the ducts into the pancreatic tissues, causing destruction and hemorrhaging. this happens because pancreatic juices continue to be secreted despite an obstruction, building up pressure causing the ducts to rupture
predisposing factors to acute pancreatitis
gallbladder disease/stones–gallstones can obstruct the pancreatic duct, causing rupture
excessive alcohol consumption–stimulates pancreatic secretions, and induces spasms in the pancreatic sphincter that results in high pressure
clinical manifestations of acute pancreatitis
severe abdominal pain, seriously ill, and high mortality rate
chronic pancreatitis
repeated episodes of mild inflammation of the pancreas, and each episode destroys some tissue which is replaced by scar tissue
manifestations of chronic pancreatitis
difficulty digesting and absorbing nutrients, not enough pancreatic tissue to produce enzymes, destroyed pancreatic islets can lead to diabetes
cystic fibrosis
hereditary disease that mainly manifests in infancy and childhood that involves mutation of CF gene on chromosome 7
mortality rate of cystic fibrosis
over 50% die before age 32
pathogenesis (how it develops) of cystic fibrosis
defective transport of chloride, sodium, and water across the cell membrane, and deficient electrolytes and water in mucus. mucus gets too think and obstructs pancreatic ducts, bronchi, bronchioles, and bile ducts
obstruction of pancreatic ducts causes:
atrophy and fibrosis
obstruction of bronchi causes:
lung injury
obstruction of biliary ducts causes:
liver scarring, nothing can get to liver so tissue dies and is replaced by scar tissue
treatment of cystic fibrosis
pills with pancreatic enzymes to compensate for lack of, treatment of pulmonary bacterial infections to preserve lung function, and eventual lung transplant
diabetes mellitus
two types, very common, and manifests as hyperglycemia (increased blood glucose)
type 1 diabetes
insulin deficiency, occurs primarily in children and young adults
type 2 diabetes
body doesn’t respond to insulin, most common type, mostly adult onset but increasing in obese children
what causes type 1 diabetes
damage to pancreatic islets leading to reduction or absence of insulin secretion
diabetic ketosis (ketoacidosis)
complication of type 1 diabetes, overproduction of ketone bodies
what causes type 2 diabetes
insulin secretion is normal or increased, but the tissues don’t respond correctly, and pancreas can’t increase insulin output to compensate
hyperosmolar nonketotic coma
complication of type 2 diabetes, blood sugar increases 10-20x normal value, and there is no ketosis. coma due to hyperosmolarity (water moves out of cells, cells dehydrated)
prediabetes
number of insulin-producing beta cells is beginning to decline, and provides an indication that weight loss, exercise, and healthy eating habits are needed or diabetes will occur
pharmacologic treatment for prediabetes
a-glucosidase inhibitors: improve glucose tolerance
pregnancy-associated diabetes
high level of placental hormones cause pregnant woman to be less responsive to insulin, and those that can’t secrete more develop gestational diabetes. usually relents after birth
metabolic syndrome
group of conditions identified in person with impaired glucose tolerance that can progress to diabetes
complications of metabolic syndrome
obesity, insulin resistance (diabetes), blood-lipid abnormalities, hypertension
insulin
influences carbohydrate, protein, and fat metabolism; its main stimulus for release is high blood glucose (it lowers blood sugar)
insulin promotes:
- glucose entry into cells
- utilization of glucose as energy
- storage of glucose as glycogen
- conversion of glucose into triglycerides
- storage of triglycerides as fat
ketone bodies
created when glucose is absorbed but not used, body uses fat as energy which is broken down into fatty acid and glycerol. fatty acid broken into acetyl-CoA, which are converted into ketone bodies
ketosis
accumulation of ketone bodies in blood and excreted in urine with water and electrolytes
hyperglycemia
elevated blood glucose, can come from other conditions that impair glucose usage such as chronic pancreatic disease, endocrine diseases, certain drugs
treatment of type 1 diabetes
diet, insulin injections with custom dosage to keep blood glucose controlled
treatment of type 2 diabetes
weight reduction and diet usually helps alone, if not then oral hypoglycemic drugs are used
how diabetes is monitored
frequent periodic measurements of blood glucose, urine tests to detect glucose in urine, and measuring glycosylated hemoglobin
too much insulin causes what?
large drop in glucose leading to insulin shock
why is vigorous exercise bad for a diabetic patient taking insulin?
with high physical activity there is high glucose utilization, this means there will be more insulin in the blood, and too much insulin leads to insulin shock
glycosylated hemoglobin
excess glucose molecules attach permanently to RBC, that circulate in the body. concentration of these is proportional to glucose levels for past 6-12 weeks
in normal people, what percent of hemoglobin is glycosylated?
6%
in people with well and poorly controlled diabetes, what percent of hemoglobin is glycosylated?
7% in well controlled, 8% in poorly controlled
carcinoma of the pancreas
usually develops in the head of the pancreas, blocking the common bile duct and causing obstructive jaundice
islet cell tumors
usually benign, produce hyperinsulinism (too much insulin) and hypoglycemia (too little blood glucose)
insulin performs all of the following functions except:
a. promotes entry of amino acids into the cells
b. promotes storage of glucose in muscle and liver cells
c. promotes entry and absorption of glucose into cells for energy use
d. promotes breakdown of fat
e. lowers blood glucose
d. promotes breakdown of fat
insulin does promote amino acid entry, glucose usage and storage, and lowers blood sugar.
function of gastrointestinal tract
digestion and absorption of food
components of gastrointestinal tract
oral cavity, esophagus, stomach, small/large intestines, anus
how does cleft lip/palate develop?
when the two tissues that fuse at the midline experience maldevelopment
what kind of inheritance pattern does cleft lip/palate have?
multifactorial inheritance
when can cleft lip be surgically corrected?
soon after birth
when can cleft palate be surgically corrected?
when the child is 1-2 years old, followed by speech therapy to correct nasal speech
what is surgical correction of cleft lip and cleft palate called?
cheiloplasty
two types of teeth
temporary/deciduous (20) and permanent (32)
dental plaque
sticky film on teeth that forms with bacteria in the oral cavity mix with saliva
caries
tooth decay that forms as a result of plaque mixed with the action of bacteria
dental cavity
loss of tooth structure from bacterial action
gingivitis
inflammation of the gums due to masses of bacteria/debris accumulating around base of teeth
periodontal disease
inflammation of the gums extends to the tissues that support teeth, and form small pockets of infection between teeth and gums
stomatitis
inflammation of the oral cavity
causes of stomatitis
irritants such as alcohol, tobacco, and hot/spicy foods
infectious agents such as herpes virus, fungus, and bacteria
carcinoma of the oral cavity
develops in the squamous epithelium, and can be in the lips, cheek, tongue, palate, and back of throat
esophagus
muscular tube that extends from pharynx to stomach, with sphincters at both ends
upper esophageal sphincter
sphincter at the top of the esophagus that opens to allow passage of swallowed food
lower gastroesophageal/cardiac sphincter
sphincter between esophagus and stomach that opens to allow passage of food into the stomach
what causes esophageal diseases?
failure of cardiac sphincter to function properly (GERD), tears in esophageal lining, esophageal obstruction
symptoms of esophageal disease
dysphagia (difficulty swallowing), substernal discomfort, inability to swallow, regurgitation of food into trachea, choking
two major disturbances of cardiac sphincter
cardiospasm and incompetent cardiac sphincter
cardiospasm
cardiac sphincter fails to open properly, esophagus becomes dilated proximal to sphincter, treated by period stretching of sphincter or surgery
incompetent cardiac sphincter
sphincter doesn’t close properly, allowing gastric juices to leak into the esophagus
complications of incompetent cardiac sphincter
reflux esophagitis, ulceration and scarring, and Barrett’s esophagus
what can obstruct the esophagus?
carcinoma, tumor that narrows lumen and infiltrates tissues and trachea, food impaction, and stricture (scar tissue)
acute gastritis
inflammation of the gastric lining
how do NSAIDS cause acute gastritis?
they inhibit the COX enzyme. COX protects gastric mucosa and mediates inflammation. if COX is inhibited then inflammation is not controlled
how can alcohol cause acute gastritis?
it is a gastric irritant because it stimulates gastric acid secretion
H. pylori
small, curved gram negative organisms that colonize the surface of gastric mucosa, and they produce a substance that decomposes urea into ammonia which allows these organisms to flourish
H. pylori gastritis
when these organisms flourish they produce enzymes that break down mucus layer. it is common and increases with age, and spreads via person to person contact and fecal-oral route
H. pylori gastritis carries an increased risk of what?
gastric carcinoma and malignant lymphoma
peptic ulcer
develops when increased acid secretions and digestive enzymes causes mucus digestion and injury, commonly found in distal stomach or proximal duodenum
complications of peptic ulcers
hemorrhage, perforation, peritonitis, obstruction from scarring
treatment of peptic ulcers
antacids-block acid secretion
antibiotics-destroy H. pylori that cause mucus injury
surgery if needed
manifestations of stomach carcinoma
vague upper abdominal discomfort and iron-deficiency anemia (chronic blood loss)
diagnosis of stomach carcinoma
biopsy by means of gastroscopy
treatment of stomach carcinoma
surgical resection of affected part, surrounding tissue, and lymph nodes
prognosis of stomach carcinoma
relatively poor, often far advanced when diagnosed
acute enteritis
common intestinal infection that is short in duration. causes nausea, vomiting, abdominal discomfort, loose stools