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Pathophysiology Exam IV
Terms in this set (171)
yellow discoloraton of the skin and sclera from accumulation of billiruben in tissues and body fluids
yellow skin in babies
Why does jaundice occur in infants?
liver function is not able to conjugate billiruben until two weeks of age
What is neonatal jaundice known as, medically?
transient and mild unconjugated hyperbillirubinemia
What causes jaundice?
due to the red cell breakdown and the inability of the immature liver to conjugate blliruben for excretion
bilirubin staining of the basal nuclei of the brain
What are the three causes of accumulaton of jaundice?
3.) post hepatic
before portal vein
increased breakdown of red blood cels at a rate in excess of the liver's ability to remove biliruben from the blood
-the live is unable to conjugate and excrete excssive bile pigment
-unconjugated biliruben accumulates
within the liver
liver injury impairing conjugation of bilirubin so it cannot be excreted as bile or removed from blood
Why does hepatocellular jaundice occur?
due to hepatocellular damage, lack of enzymes needed to conjugate biliruben or decreased biliruben uptake by the liver
after the liver
bile duct obstructed by tumor or stone impairing delivery of bile into duodenum
-reduced bile clearance from liver
-elevation of conjugated biliruben levels
stoppage of flow of bile
liver function test
used to assess injury to liver cells
alanine aminotransferase (ALT)
liver specific enzyme
aspartate aminotransferase (AST)
enzyme that is derived from other organs
What is tested from the liver in terms of its ability to synthesize proteins?
-coagulatin factors and fibrinogen
What is tested from the liver in terms of excratory function?
What else can be used in a liver function test?
-raadiographs, ultrasound, CT scans, MRI to evaluate he liver structure
used to obtain tissue speciments for microscopic examinaton
What are the indications for a liver biopsy?
-to determine the cause of liver disease
-to evaluate the extent of liver cell damage in persons with chronic hepatitis
How does a liver biopsy work?
-a needle is inserted through the abdominal skin directly into the liver
-specimen is biopsied and examined histologically by a pathologist
-provides a specific diagnosis
-provides a basis for treatment
What causes liver injury?
necrosis, fatty accumulations or both
What does the outcome of liver injury depend on?
the severity of the injury
-mild injuries will lead to a full recovery
-severe injuries will lead to death
inflammation of the liver
What is the etiology of hepatitis?
viral, drug, alcohol toxicities or autoimmune
Chronic injury from what can cause diffuse scarring of the liver in hepatitis?
fatty liver, alcoholic liver disease and cirrhosis
inflammation of the liver caused by a virus
inflammation of the liver caused by the hepatitis A virus (HAV), usually transmitted orally through fecal contamination of food or water
inflammation of the liver caused by the hepatitis B virus (HBV), which is transmitted sexually or by exposure to contaminated blood or body fluids
inflammation of the liver caused by the hepatitis C virus (HCV), which is transmitted by exposure to infected blood; this strain is rarely contracted sexually
secondary infection caused by a mutated hepatitis virus; only develops in patients with Hepatitis B
a virus spread via fecal-oral transmission (contaminated water) especially in developing countries
What is the clinical course of viral hepatitis?
-causes liver injury similar to that of other causes of liver disease (direct cellular injury)
-all viruses produce similar histological signs (diffuse inflammation of hepatic lobules, cellular swelling and necrosis of cells)
What are the clinical signs of viral hepatitis?
-elevation in liver enzymes
-some will be asymptomatic
-some will have clinical illness with abnormal live test with or without jaundice
-some will have few symptoms with abnormal liver test results
What is the outcome of viral hepatitis?
-Hepatitis A: full recovery
-Hepatitis B and C: chronic infection; these people can also produce a carrier state in which they are asymptomatic but still transmit the virus
-chronic hepatitis can lead to cirrhosis and neoplasia
-a small percentage of those with Hepatitis B can develop into hepatic failure with rapid progression
What is the treatment of viral hepatitis?
there is a vaccine for Hepatitis A and B, but not C
caused by an excessive amount of iron absorption, which is then taken up by the cells of parenchymal organs such as the liver and pancreas
What organs are involved in hemochromatosis?
What does accumulation of iron in tissues and organs lead to?
organ damage followed by irreversible scarring
What can hemochromatosis be categorized as?
involves mutation of genes resulting in reduced hepcidin synthesis
How does hepcitin function in the body?
-it is normally released by the liver in response to increase in iron in the liver and inhibits iron absorption into the blood from enterocytes
-regulation of intestional absorption of dietary iron is abnromal leading to iron accumulation
may result from chronic hemolytic disorders and/or multiple transfusions
-chronic liver disease -> decease in hepcidin
What are the clinical manifestations of hemochromatosis?
-abnormal skin pigmentation
-secondary diabetes mellitus from detsruction of pancratic islets
-death, resulting from cirrhosis or cardiac diseases
How is hemochromatosis diagnosed?
-can be diagnosed before irreversible damage occurs
-screen test involves detection of increase amount of iron in serum
How is hemochromatosis treated?
-regular phlebodamy to deplete iron tissue stores
-with treatment, life expectancy is nomal
fat accumulates in liver secondary to injury
What are the causes of fatty liver?
-drugs, chemicals and solvents
-diabetes and obesity
What is the etiology of fatty liver?
-diabetes mellitus: condition induces mobilization of more fat than the hepatocytes can handle; decrease uptake of fat by adipocytes ad it accumulates in the liver
-obesity: excess dietary intake
-alcoholism: chemical injury to hepatocytes, causing the liver to increase in size
-acute starvation: depletion of proteins needed to synthesize lipoproteins
alcoholic liver disease
a group of structural and functional changes in the liver resulting from excessive alcohol consumption
What are the three stages of alcoholic liver disease?
-alcoholic fatty liver
alcoholic fatty liver
mildest form of alcoholic liver disease; reversible
causes degenerative changes and necrosis of liver cells
What accumulates in the liver with alcoholic hepatitis?
-mallory bodies, which are irregular, pink deposits in the cytoplasm
What happens to the liver in alcoholic hepatitis?
a disease involving scarring and deterioration of liver cells as a result of chronic alcohol abuse
What is alcoholic cirrhosis associated with?
a history of repeated bouts of alcoholic hepatitis
diffuse scarring of the liver from any cause with derangement of liver function and regeneration
In which conditions is cirrhosis seen?
-alcoholic liver disease
-hepatitis B or C
-severe liver necrosis
-repeated liver injury due to drugs and chemicals
-longstanding bile duct obstruction
How does cirrhosis manifest?
-ascitis, esophogeal varicies and splenomegaly
-liver is converted into a mass of scare tissue containing nodules of normal and degenerating cells along with inflammatory cells
-disorganization of the liver
-intrahepatic branches of the hepatic artery and portal vein are constricted by scar tissue
-dcerease in liver cell function by scarring
-impared bile synthesis
-reduced plamsa proteins
What are the clinical manifestation of cirrhosis?
-hepatomegally initally, then increase in size
How does cirrhosis manifest in men?
-estrogen elimination is reduced because of the liver's inability to inactivate it
-leads to increase in estrogen levels
-testictular atrophy, decreasd sex drive and mammory gland hypertrophy
Why does portal hypertension occur in cirrhosis?
-scar tissue obstructs the portal vein leading to a incerase in pressure
-this increase in pressure affects the capillaries and leads to a leakage of fluid from the capilaries
Why is there low albumin levels in cirrhosis?
an inability to produce it
-this leads to a decrease colloid osmotic pressure and fluid leaks from the portal capillary beds causing ascties
Why do portal systemic shunts develop from cirrhosis?
-they bypass routes connecting systemic portal veins
-anastomoses develop between branches of portal and system veins
-blood shunted away from high pressure portal system into low pressure veins of systemic circulation
-anastomoses between veins around spleen and stomach
-leads to an increase in blood flow to the esophogeal vein
-develops betwen portal vein and veins draining the abdomial wall -> superor mesentaric and IVC
neurologic abnormalities associated with failing liver
How does hepatic encephalopathy present?
deterioration of brain function, characterized by impaired consciousness, confusion disorientation and eventually coma
formation of stones in the gallbladder, composed of cholesterol
What is included in normal bile composition?
-cholesterol is insolube in aqueous solution
-bile salts and lecithin increase its solubility in solution
-anything that disrupts the relative ratio between cholesterol and bile salts and lecithin can lead to precipitation of cholesterol, causing crystals to form
What are the factors that influence the solublity of cholesterol in bile?
-increase in cholesterol
-decrease in salts/lecithin
What is the incidence of cholelithasis?
-higher in woman than men
-especially women who have borne children, take contraceptive pills and are obese
-infection can lad to gallstones
What is the manifestation of cholelithasis?
-biliary collic if store is extruded into ducts
-pain in URQ
-associatd with eating a fatty meal
-pain results from sapam of thee smooth muscle in the ducts combined with forceful cntracuon of the gallbladder to propel the store throughout the duct
occurs when the common bile duct is obstructed
What is characteristic of obstructive jaundice?
-no bile enters into the duodenum
-reduced bile clearance from the liver causes biliruben and bile salts to accumulate in the liver then the blood
-biliruben in the blood causes jaundice
-bile salts in blood are carried to peripheral tissue and produce pruritus
cyctic duct obstruction
no jaundice; acute cholecysttis may occur with preexisting infection in gallbladder
How are gallstones treated?
-cholecystectomy - laproscopic surgery
-chenodeoxycholic acid dissolves gallstones
inflammation of the gallbladder
What is characteristic of cholecystitis?
-chronic infection is common
-gallstones may predispose to cholecystitis
-impaction of a stone in the neck of the gallbladder may cause acute cholecystitis
What do pancreatic secretions include?
-contain protolytic enzymes that break down dietary proteins
-secretes pancreatic lipase
-secretes pancreatic amylase
-pancreatic enzymes are secreted in the inactive form and become activated in the intestine
inflammation of the pancreas
What is the etiology of pancreatitis?
-alcohol abuse: alcohol stimulates pancreatic secretions and induces spasms of the pancreatic sphincter
-abdominal and surgical trauma
-drugs such as steroids and thazide diuretics
What is the pathogenesis of pancreatitis?
-escape of pancreatic juice from the ducts of the pancreatic tissue, which leads to destruction of the pacreatic tissue by the activatd ezymes in the fluid leading to acute inflammatory reaction of the affected tissue
-involves autodigeston of pancreaatic tissue by inappropriate activation of pancretic enzymes
How does pancreatitis present?
-acute abdominal pain in the LUQ
-elevated serum pancreatic enzymes (lipase and amylase)
How does mild from pancreatitis present?
abdominal pain with elevated pancreatic enzymes
How does severe acute pancreatitis present?
severe abdominal pain and severe illness
-enzymes destroy pancreatic tissue along with pancreatic blood vessels, leading to hemmorhage
What are the major endocrine glands?
-adrenal cortex and medulla
-ovaries and testies
chemical messengers that are manufactured by the endocrine glands, travel through the bloodstream, and affect other tissues
How are hormones transported?
through the blood
under activity of a gland
What are the two situations that lead to hypoactive glands?
-gland fails to secrete its hormone or secretes an inadequate amount
-there is a loss of target tissue sensitivity
overactivity of a gland
What are the two instances that would lead to hyperactivity of a gland?
-gland secrets an excessive amount of its hormone caused by a hypertrophied glad or a glandular tissue
-gland is overstimulted by tropic hormones
total pituitary impairment that brings about a progressive and general loss of hormone activity
What causes panhypopituitarism?
a tumor or disturbance of its blood supply
How is panhypopituitarism treated?
-identify underlying cause
tumor on the pituitary gland
What are many pituitary tumors caused by?
anterior lobe pituitary tumors
produce tumors that cause clinical manifestations
does not produce hormones but exert other effects
How are pituitary tumors treated?
-determines by type, size and hormone produced by tumor
-drugs to suppress tumor growth
-surgical recession: usual surgical approach is through the nasal cavity
What do pituitay adenomas cause?
-gigantism in children
before epiphyseal closure, increase height with proportionaley large body
enlargement of the extremities
-enlargement of growth hormone after epiphyseal closure
How is acromegaly treated?
surgical removal/radiation of tumor
What is the function of the thyroid gland?
synthesizes, stores and releases thyroid hormones, which contain iodine
What are two impprtant thyroid hormones?
thyroxine (T3) and triiodothyronine (T4)
What are the effects of T3 and T4?
regulate growth and development
-stimulates protein anabolism by increasing its rate
secretion of thyroid hormone is chronically reduced
What are the clinical manifestations of hypothyroidism?
-decreased heart rate
-slow, dull reflexes
-feeling of being cold
-dry skin, alopecia
-constipation: the digestive system works sluggishley
-althersclerosis: lack of thyroxin increases the amount of circulating lipids
What is the etiology of hypothyroidism?
-thyroid gland dysfunction
-secondary to pituitary disease
What will a lab test for hypothyroidism display?
elevated TSH and low T3 and T4 levels
an autoimmune disease in which the body's own antibodies attack and destroy the cells of the thyroid gland
How is Hashimoto's thyroiditis treated?
-condition responds well to treatment and the symptoms disappear
condition present at birth that results in lack of thyroid hormones; results in poor physical and mental development; formerly called cretinism
What is the etiology of congenital hypothyroidism?
-error in fetal development if the thyroid gland fails to form
-the gland is nonfunctional due to genetic disease that results in deficiency of enzymes needed for thyroid hormone synthesis
How does the infant appear at birth if they have congenital hypothyroidism?
they will appear normal because the mother has supplied thyroid hormone to the fetus
What are the clinicial manifestations of congenital hypothyroidism?
-mental retardtaion, hypothyroidism and varyg degress of other growth and development abnormalities
How is congenital hypothyroidism treated?
-lifelong hormonal therapy
enlargement of the thyroid gland
exceess secretion of thyroid hormone
decrease of hormone secreted due to
-hyposecretion of thyroid hormone, causing the removal of the inhibitation TSH
How is a nontoxic goiter treated?
-administration of thyroid hormone, which suppresses TSH output by the negative feedback mechanism
-enlarged gland shrinks because of the lack of overstimulation of TSH
-a large nodular goiter may need to be surgically removed if it compresses the trachea or obstructs the neck veins
hyperthyroidism (Grave's Disease)
abnormally high secretion of thyroid hormones
What are the levels within the body of a patient with Grave's Disease?
high levels of T3 and T4, and low levels of TSH
What are the clinical manifestations of hyperthyroidism?
-the person has a tremendous appetite but loses weight, appearing emanciated
-thyroxine speeds up the passage of food through the digestive tract; there is n time for normal reabsorption of water from the large intestine, so diarrhea occurs
-tachycardia, rapid pulse rate and palpation
-the person is extremley nervous, excitable and is always tired, but has difficulty sleeping because of hyperactivity of the body
-the high metabolic rate causes excessive heat production, which results in profuse perspeation; the skin is always moist and an insatiable thirst follows h loss of water
protrusion of the eyes out of the eye socket
What causes exopthalmus?
infiltration of T lymphocytes in the fat, connective tissues and muscles of eye movement, leading to inflammaton and edema, pushing the eyes forward
How is hyperthyroidism treated?
-large doses f radioactive iodine -> irritation destroys part of the gland
What are the hormones secreted from the adrenal cortex?
-gonadocorticoids: androgens and estrogen
Addison's disease (hypoadienocortism)
an adrenal cortical hypo-function
What is the etiology of Addison's disease?
destruction or damage to the adrenal glands by infections, autoimmune or idiopathic
What are the clinical manifestations of Addison's disease?
-weakness, fatigue, decreased appetite, weight loss
-cortisol deficiency leads to low blood glucose, impaired protein and carbohydrate metabolism and generalized weakness
-aldosteone deficiency leads to hyponatremia, hyperkalemia, dehydration and hypotension
bronzed or sun tan apperance
Why does hyperpigmentation occur in Addison's disease?
-pituitary gland produces more adrenocortocotropic hormone (ACTH) in response to a deficiency of cortocsteroids
-precursors of ACTH stimulate melanocytes to produce melanin, especially in areas that are exposed to sunlight
precipitated by physical or emotional stress, sudden withdrawal of hormone
What are the characteristics of an Addisonian crisis?
acute presentation of abdominal pain, nausea, vomiting, diarrhea, hyonatremia, hyperkalemia, hypotension, dehydration and unconsciousness
How is Addison's disease treated?
lifelong hormone replacement
Cushing's syndrome (hyperadrenocortism)
excss glucocorticoid production
What are the causes of Cushing's syndrome?
-hormone-producing pituitary microadenoma
-hormone-producing adrenal cortex tumor
-administration of large amounts of corticosteroid
-other tumors (nonpituitary ACTH secreting tumor)
What are the clinical manifestations of Cushing's syndrome?
-excess glucocorticord hormones
-hyperglycemia (adrenal diabetes)
-polydipsia and polyuria
-altered fat metabolism
-mobilization of lipids: trunk obesity, buffalo hump, moon shaped face
-skin becomes thin resulting in bruises, striae on abdomen, buttocks and breasts
-poor wound healing
-bones are likley to fracture
-cortisol inhibits immune and inflammatory response
-cortisol stimules gastric acid secreation
How is Cushing's syndrome treated?
-surgical removal of enlarged glands or tumors
-hormone therapy is required to replace the hormones normally secreted by the adrenal cortex
What are the cells in the pancreas?
-alpha cells: secrete glucagon; raise blood glucose
-beta cells: secrete insulin; lower blood glucose
-delta cells: secrete somtostatin; inhibit secreteion of glucagon and insulin
What is the action of insulin?
-promotes entry of glucose into cells
-favors utilization of glucose as a source of energy
-promotes storage of glucose as glycogen in muscles cells and hepatocytes
-promotes conversion of glucose into triglycerides
-promotes storage of newly formed triglycerides into fat cells
-promotes entry of amino acids int cells and stimulates protein synthesis
a group of metabolic disorders characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both
type 1 diabetes mellitus
diabetes in which no beta-cell production of insulin occurs and the patient is dependent on insulin for survival
type 2 diabetes mellitus
diabetes in which either the body produces insufficient insulin or insulin resistance (a defective use of the insulin that is produced) occurs; the patient usually is not dependent on insulin for survival
What is the clinical manifestation of both diabetes mellitus type 1 and 2?
What is the etiology of type 1 diabetes mellitus?
-autoimmune destruction of the beta cells
What is the etiology of type 2 diabetes mellitus?
-complex metabolic disease
-insulin secretion is normal or increased
-reduced response of cells to insulin
-incidence high in some populations
refers to metabolic abnormalites that include obesity, insulin resistance, high triglyceride levels and low HDL levels, hypertension, cardiovascular disease and incrased risk of development of diabetes type II
Which diabetes is more common?
What happens in diabetes type II?
pancreatic islets secrete normal or higher amounts of insulin initially, but the cells are insensitive to the action of the insulin and are unable to respond apropriatley
placental hormones cause less responsiveness to insulin, causing resistance
What are the clinical manifestations of type II diabetes mellitus?
-fatigue and weakness
-dry mucous membranes
glucose in the urine
greatly increased urination and dehydration that results when high levels of glucose cannot be reabsorbed into the blood from the kidney tubules and the osmotic pressure of the glucose in the tubules also prevents water reabsorption
What are the complications of type I diabetes mellitus?
-excess ketone bodies accumulate because the body cannot process them effectivley
excessive production of ketones, making the blood acid
Why does ketoacidosis occur?
-buffer systems cannot maintain normal pH
-body turns to fat as a source of energy
-fat is broken down into fatty acid and glycerol
-fatty acid is broken down further into two carbon fragments combined with carrier molecule, acetyl coenzyme A
-some acetyl co-A are converted by the liver to ketone bodies and can be used as a source of energy
-more acetyl co-A molecules are produced than can be oxidized as a source of energy
accumulation of ketone bodies in the blood and excreted in the urine together with water and electrolytes
What are the complications of type II diabetes mellitus?
-absence of ketosis
What happens to the body when it goes into hypoosmolar coma?
-heavy diuresis occurs that drops the plasma volume signifigantly
-low plasma volume and hyperosmolrity caused by the increase glucose levels results in a loss of cerebral fluid
-water moves out of the cells into extracellular fluid
-cells become dehydrated disturbing functions of neurons leading to coma
How is diabetes mellitus diagnosed?
-glycosylated hemoglobin (A1C) provides information of blood glucose levels over several months
-irreversible attachment of glucose to hemoglobin
-test results give you a picture of average blood sugar levels over the past two to three months, the life span of a RBC
How is diabetes mellitus type I treated?
requires insulin; dosage adjusted to control blood glucose levels
How is diabetes mellitus type II treated?
-weight and diet management
-oral hypoglycemic drugs if patient does not respond to diet and exercise
What is the goal in treatment of diabetes mellitus type II?
achieve control of blood glucose as close as possible to normal
What are the three ways in which treatment goals for diabetes type II can be achived?
-frequent periodic measurements of blood glucose
-urine test: detects glucose spilling into the urine when blood glucose is too high
-measurement of glycosylated hemoglobin: serves as an index of longterm control of hyperglycemia
What are the complications of chronic hyperglycemia?
-damage induced in large and medium sized arteries (ex: coronary artery) leads to acceletared atherosclerosis
-damage to capillares of the skin, retina, muscle and renal glomeruli occurs because of a thickening of the basement membrane
-foot ulcers from impaired pain sensation
-increased susceptibility to infection
-hypoglycemia: too much insulin lowers glucose
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