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351 Cards in this Set
- Front
- Back
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what does the exocrine portion of the pancreas produce and what is its primary cell type?
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mostly acinar cells- produces enzymes and proenzymes. makes up 85% of pancreas
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what does the endocrine portion of the pancreas produce and what type of cells are found in it?
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the islets of langerhans have two cell types:
Alpha cells- glucagon beta cells- insulin makes up 15% of pancreas |
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what is annular pancreas?
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the ventral bud fails to rotate properly and it encircles the duodenum, and can cause constriction. It predisposes the patient to pancreatitis and is often associated with down's syndrome
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what is pancreas divisum
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most common congenital anomaly. Lack of fusion of the ventral and dorsal buds of the pancreas during development.
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why does pancreas divisum predispose patients to pancreatitis?
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dorsal bud drains through the duct of santorini which results in disturbed flow.
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what is the heterotopic pancreas?
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an islnad of pancreas where it is not supposed to be. It can protrude into the lumen of the GI tract and can cause obstruction. It is most commonly seen in the stomach. It can also be seen only in the lining and the enzymes will be eating away at the tissue.
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how can cystic fibrosis affect the pancreas?
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the pancreas is basically replaced with fat, causing pancreatic insufficiency. Enzymes aren't produced anymore. It can affect more organs than just the pancreas.
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what is important to know about cystic fibrosis when it comes to the genetics?
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CFTR- functions as a chloride channel blocker, blocks water, makes the enzymes thicker.
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does Cystic fibrosis cause pancreatitis?
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no, it causes atrophy and fatty replacement. Causes malabsorption in infants and can lead to pulmonary problems later in life.
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what is acute pancreatitis?
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the enzymes are being released already active and it is basically digesting the pancreas itself. It can be caused by ischemia, infection and drugs
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what is inappropriate transport?
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the enzymes are delivered to the lysosomes, the lysosomes attack them. The enzymes damage the lysosomes and it begins to digest in the wrong area. It can be caused by alcohol.
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what 3 things can the activated enzymes do once activated in the pancreas?
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proteolysis
fat necrosis hemorrhage- can lead to thrombosis due to the hageman factor. Can lead to DIC |
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what are the clinical findings of a patient with acute pancreatitis?
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abdominal pain that can be referred to the back that increases with food.
nausea, fever, tachycardia, DIC, adult respiratory distress syndrome, and peripheral vascular collapse with shock. |
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what are the signs associated with acute pancreatitis?
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Cullen's sign- blue bellybutton.
Grey/turner's sign- blue around the flanks of your ribs. Quick rise in amylase followed by a fallout within 3 day Lipase elevated for 7-10 days. Hyperglycemia Hypertriglyceridemia Hypocalcemia |
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what are the two main causes of acute pancreatitis?
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gall stones and alcohol
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decribe what is seen first with acute pancreatitis?
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major edema and pale.
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describe what is seen later with acute pancreatitis?
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hemorrhage and necrosis, and eventually leads to fat necrosis, with massive infltrate by neutrophils. Abcesses can be found.
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what is the prognosis for mild acute pancreatitis?
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good with supportive care.
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what is the prognosis with severe acute pancreatitis?
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not good, 10-20% mortalitiy rate. Causes multisystem organ failure.
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describe the conditions seen with chronic pancreatitis?
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it can have intermittent acute attacks
it is a permanent and progressive impairment of function. |
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who is at risk for chronic pancreatitis? How is that different than acute?
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males and smokers. In acute it was females and gall stones were much more important. With chronic Gall stones are muh less symptomatic.
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what are the signs and symptoms of chronic pancreatitis?
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weight loss, steatorrhea, diabetes, intermettent or low grade chronic abdominal pain. Hard to diagnose because the symptoms are so general. Involved areas of the pancreas are hard and large amounts of fibrosis. It can also have dysplasia.
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what is the key to distinguishing chronic pancreatitis from adenocarcinoma
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the normal lobular architecture with chronic pancreatitis is still preserved.
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what are the common outcomes of chronic pancreatitis?
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ascites, pleural effusions, ulcerations, chronic malabsorption, diabetes
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whatis important to know about auto-immune pancreatitis?
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the patients can spontaneously get better.
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what is hereditary pancreatitis?
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autosomal dominant disorder, onset before 10 years old. Starts severs and gets better. Can be an increased risk for adenocarcinoma
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what is the most common parasitic infection of the pancreas?
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ascaris lumbricoides- enters through the pancreatic duct.
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what is the most common cystic lesion of the pancreas?
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pseudocyst- no epithelial lining. Rarely seen with neoplasms. Can be caused by trauma and pancreatitis. they can resolve spontaneously or can continue to get bigger. They require draining.
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What are the complications of pseudocysts?
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infection, hemorrhage, and rupture.
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where is the most common site for the pseudocyst and what is the most common gross pathology of them?
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in the tail of the pancreas, and they are unilocular and have a thick fibrotic wall.
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what are lymphoepitheial cysts in the pancreas?
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benign, with an epithelial lining stratified squamous). Can be multi and unilocular. Contain a weird cheesy material. You have an abundance of lymphocytes seen within the wall.
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most neoplastic pancreatic tumors are what type?
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ductal (90%)
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decribe ductal adenocarinoma severity?
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1 of the top 5 cancer killers in the civilized world. <5% survival rate for 5 years. Usually not diagnosed until it is in the late stage. It frequently metastatizes to many sites becuase it has no capsule.
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what are the symptoms of pancreatic adenocarcinoma?
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jaundice
rapid weight loss pain usually in the head of the pancreas |
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what are the risk factors for pancreatic adenocarcinoma?
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smoking and high fat intke
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describe the appearance of the pancreatic adenocarcinoma?
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usually in the head, solid, firm, infiltrative,
Very difficult to distinguish from fibrosing chronic pancreatitis because it is not very defined. |
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what are the other possible ductal carcinomas?
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mucin/colloid
adenosquamous medullary undifferentiated |
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what is the most common cystic tumor?
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serous tumors- a tumor with tiny little cysts all throughout it, looks like a sponge. They are lined by cuboidal epithelium. Usually is benign. Does not communicate with the ductal system.
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Describe the appeaance of mucinous cystic neoplasm.
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macrocystic. usually in tail. looks like it is ovarian stromas. No communication with the ductal system
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what is the main diffeence between mucinous cystic neoplasm and intraductal papillary mucinous neoplasm?
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doesn't look like ovarian stroma, found more commonly in males and older, usually occurs in the head and is seen within the duct system. The mucinous cystic neoplasm does not involve duct system, more common in younger females, and is usually seen in the tail.
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what is the most common pediatric pancreatic neoplasm?
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pancreatoblastoma
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what does the endocrine neoplasms involve?
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islets of langerhan
usually the tumors is still functional. Commonly seen in MEN 1 syndrome insulinopmas are usually benign. |
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how does a patient with insulinoma usually present?
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confused
sweating hypoglycemia (nervous) high insulin levels almost always benign usually associated with MEN 1 |
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describe gastrinomas?
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can be found in pancreas, duodenum or peripancreatic tissue.
Increased gastric secretion more malignant than insulinoma associated with zollinger-ellison sydrome (severe peptic ulcers) and MEN 1 |
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what are the 4 phases of infection with acute hepatitis?
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incubation- asymptomatic, most infectious to others in the last days of incubation.
preicteric- nonspecific symptoms icteric- jaundice, not always present. Tender enlarged liver. convalescent- resolution |
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with viral hepatitis, what causes the jaundice?
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the increased conjugated bilirubin
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what is fulminant hepatitis
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liver failure within 2-3 weeks due to ischemia, toxins or acute hepatitis. subacute is within 3 months. Very high mortalitiy rate. Transplant is needed.
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is acute hepatitis usually a lobular or a portal injury?
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lobular
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what is chronic hepatitis?
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some kind of evidence of hepatitis for over 6 months. With a variety of outcomes to resolution, carcinoma, cirrhosis, hepatic failure
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what is the number one cause of chronic hepatitis?
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viral hepatitis B and C
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what complications are seen with chronic hepatitis?
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elevated LFT's
Jaundice hepatocellular carcinoma cirrhosis liver failure vasculitis glomerulonephritis |
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what kind of inflammation is usually present in chronic hepatitis?
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portal inflammation/damage, not lobular.
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what is the grade and stage of hepatitis?
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grade determines the level of inflammation
stage determines the level of fibrosis |
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which type of hepatitis is only an acute infection?
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A
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what types of hepatitis can cause chronic infections?
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BCD
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How is HAV transmitted?
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by close personal contact, usually the fecal oral route. Contaminated water/shellfish, or blood contact (rare)
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who is most at risk?
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kids and older adults
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what is used to diagnose an acute HAV infection
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IgM antibody present in the blood.
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how is HBV transmitted?
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usually sexual, or mom to baby. High levels are found in blood and wounds, moderately found in sex fluids and saliva
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what is typically the only marker used to diagnose HBV during the window stage?
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IgM anti-HBc
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what is the numer one cause of iver transplant in the US?
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HCV
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what is the main problem associated with HCV?
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chronic infection (over 80%) that can lead to cirrhosis, hepatocellular carcinoma, and chronic mortality.
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What is required for HDV to replicate?
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HBV- either acquired simultaneously (coinfection), or introduced into a patient that already has HBV (superinfection).
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what type of HDV causes severe acute disease? Which type causes chronic disease?
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acute- coinfection
chronic- superinfection |
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how is HDV transmitted?
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just like B and C
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how is HEV transmitted?
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just like A
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describe E
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pregnant women are at risk. Causes acute only.
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what other viruses can causes hepatitis?
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herpes viruses
adenovirus (enteric) viral hemorrhagic fevers. |
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what is the most important pathogen in transplant patients?
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CMV
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what is biliary atresia?
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absence or destruction of the extrahepatic biliary tree, and is the #1 cause of death in liver disease in kids.
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what is cholelithiasis?
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gall stones
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what are the two types of gall stones?
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cholesterol (80%) and pigment stones (20%)
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what are the risk factors for choleterol stones?
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forty
fat female fertile |
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what are the risk factors for pigment stones?
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hemolytic syndromes
severe ileal dysfunction bacterial contamination of the bilairy tree |
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what are the most common complications involved with gall stones?
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cholecystitis
empyema (pus in gall bladder) pancreatitis get stuck at the iliocecal valve- gallsotne ileus |
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what does calculous mean?
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caused by gall stones
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what type of patients are usually affected by acute acalculous cholecystitis?
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severely ill patients- postop, severe trauma, MSOF, severe burns
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describe the gallbladder carcinoma
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usually have an insidious onset, symptoms are usually indistinguishable from cholecystitis. 90% are adenocarcinomas, and they normally spread locally and to the liver.
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what toxin is associated with more mortality and morbidity than any other toxin on a personal, environmental, and occupational level.
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Tobacco
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what is a co-carcinogen?
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a toxin that can mix with other tosxins in the environment to make them even more toxic than just by themselves. (ex tobacco)
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other than the lungs, what other organs can tobacco cause cancer in?
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lips, oral cavity, larynx, esophagus, bladder, pancreas, kidney
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what risk factors and how many cigarettes a day can cause it?
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low, birth weight, born premature, and increased risk of spontaneous abortions, fetal hypoxia
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what factorsare taken into account when determining the cigarette smoking risk of cancer?
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#/per day
# of years age started occupational exposure genetic factors |
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what are the three methods of entry for cigarette smoke?
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directly through mucous membranes
swallowed through alveolar capillary beds |
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when you stop smoking what risk factors decrease?
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MI is very soon, lung and larynx after 1-2 years, excess mortality baseline after 20 years.
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what can second-hand smoke cause?
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SIDS
asthma respiratory and ear infections |
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what are pneumoconioses?
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diseases due to the exposure of an aerosol
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what are the pathologic principles of pneumoconioses?
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dust retained in the lungs
size, shape, & bouyancy of particles solubility and physiochemical reactions additional effects of other irritants |
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what is anthracosis
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the asymptomatic and more mild form of coal worker's pneumoconicosis. It causes the black pigmentation of the lungs. you get accumulation of the carbon in the lungs lymoh nodes
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what is the difference between anthracosis and simple coalworker's pneumoconicosis?
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the accumulation of macrophages, but there still isn't much if any pulmonary disfunction. Coal macules 1-2 mm in size, closer to the alveolar ducts and respiratory bronchioles.
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what is the difference between simple and complicated coalworker's pneumoconicosis?
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fibrosis of the lungs with loss of function. blackened scars 2-10 cm in size.
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what is progressive massive fibrosis?
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generic term for fibrosing of the lungs that can be a complication of any of the pneumoconicoses
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what is the cause of the lung fibrosis in the mines?
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carbon dust and maybe silica
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what is Caplan's syndrome?
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RA + pneumoconicosis = distinct pulmonary lesions similar to RA nodules.
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in the few cases of simple and complicated coalworker's pneumoconicosis where PMF develops, what can be the complications involved?
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pulmonary dysfunction
pulmonary hypertension Cor pulmonale |
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what is currently the most common prevelant chronic occupational disease in the world and what causes it?
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Silicosis- inhalation of crystalline silicon dioxide from sand blasters and mine workers. It usually takes decades of exposure.
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what is the pathophisiology of silicosis?
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particles interact with pulmonary macrophages and epithelial cells causing injury and fibrosis. Macrophages release mediators (IL-1, TNF, fibronectin, etc.)
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describe the morphology of silicosis?
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early- small nodules at the top of the lungs.
late- small nodules become hard collagenous scars and undergo cavitation, eggshell like on radiographs. |
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how is silicosis usually discovered?
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chest radiograph in an asymptomatic worker.Shortness of breath is not noted until PMF in late stages of teh disease.
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is silicosis associated with lung cancer?
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no
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what is exposure to asbestos associated with?
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fibrotic pleural plaques
pleural effusions parenchymal interstitial fibrosis bronchogenic carcinoma mesotheliomas larynx and extrspulmonary cancers |
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with asbestos what determines if it causes disease?
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concentration, size, shape and solubility
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what are the two different forms of asbestos?
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serpentine- curly and flexible
amphibole- straight, stiff, more brittle, and more pathogenic |
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what disease is specifically associated with amphiboles?
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mesothelioma
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what is the morphology of asbestosis?
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starts at the bifurcation of small ducts and airways at alveolar ducts and respiratory bronchioles, damages macrophages and they send out the chemical mediators.Then you get diffuse interstitial fibrosis with asbestos bodies (golden brown fusiform or beaded rods with a transulcent center).
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what is a ferruginous body
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an asbestos body covered with iron to make it hard to distinguish as an asbestos body.
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what are pleural plaques?
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plaques of dense collagen that rarely are seen outside of asbestos exposure.
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what is malignant mesothelioma?
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in either the visceral or the parietal pleura, increased with people with heavy exposure to asbestos. It has a long latent period betweeen the exposure to the asbestos and the manifestation of the tumor.
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what types of cells are found in malignant mesothelioma?
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mesenchymal stromal cells resembles sarcoma, epithelial like cells resembles adenocarcinoma.
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what is usually the first manifestation of asbestosis?
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dyspnea (10-20 yrs post exposure)
productive cough. can remain static or progress to cor pulmonale, CHF, and death. |
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what are the adverse effects of acetaminophen toxicity?
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15-25 grams toxic level
hepatic centilobular necrosis begins with nausea and vomiting and shock, after a few days jaundice can develop. |
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what are the adverse effects of aspirin toxicity?
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2-4 grams in kids, 10-30 grams in adults.
respiratory alkalosis -> metabolic acidosis can also occur in those that take 3 gms/day |
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what does alcohol affect?
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CNS depressant
inhibitory neurons first then cortical and medullary. |
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what are the impairment levels of alcohol?
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20-30 ml = impaired
80-100= leaglly intoxicated 200-250= narcosis 300-400= coma and respirator arrest. |
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describe the absorption of lead?
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higher in children, usually insidious, enhanced by calcium, iron, and zinc deficiency
1/2 life of 30 years absorbed in blood and bones absorbs through lungs and GI tract. |
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what are the effects of lead toxicity?
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retardation
Anemia (elevated blood levels of protoporphyrin) behavoir abnormalites learning diabilities |
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what is abrasion?
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tearing away of teh superficial layers of teh skin by a blunt trauma caused by friction between skin and blunt surface
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what is a contusion?
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hemorrhage and edema of the skin caused by blunt trauma, but does not disrupt the surface of the skin.
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what is a laceration?
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rough edged split or tear in the skin caused by blunt trauma
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what is an incised wound
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smooth edged cut in the skin caused by a sharp trauma
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what are the two different ways that hypothermia causes damage?
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direct- water in cell freezes and the remaining fluid in the cell has a higher salt concentration.
indirect- caused by circulatory changes. |
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what is trench foot?
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slow chilling induces vasoconstriction and paralysis and increased permiability and edema
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what is frostbite?
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sudden acute change in temperature
vasoconstriction and increased viscosity ischemia can cause infarction edema upon heating. |
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with which form of hyperthermia does sweating stop?
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heat stroke
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what rectal tempurature is considered dangerous and has a mortalitiy rate of over 50%?
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106 degrees
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what influences the severity of electrical injuries?
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magnitude, duration, path, and tissue resistence.
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what is a roentgen?
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unit of charge produced by x-rays or gamma rays that ionize a specific volume of air.
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What is a Rad?
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dose of radiation that will produce the absorption of 100 ergs of energy per gram of tissue
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what is a Gray?
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amount of energy that will produce the absorption of i joule of energy/kilogram of tissue (100Rads)
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what is more leathal a single dose of radiation to the whole body, or a regional dose?
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whole body.
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what are the effects of radiation injury?
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overt necrosis - no effect, depends on the dose,
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what are the effects of radiation exposure to the skin?
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desquamanation and atrophy
hyper and hypopigmentation damage to blood vessels impaired healing, ulceration and increased susecpatability to infection. |
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what are the effects of radiation exposure on bones?
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decreased cellularity
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blood vessles?
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initial inflammatory reaction, followed by subintimal fibrosis, muscle wall fibrosis, and narrowing of teh lumen and degeneration of teh elastic lamina
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gonads?
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sterility
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what is the cause of primary diabetes?
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hyperglycemia
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what are the two types of primary diabetes?
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type 1- insulin dependent
type 2- non insulin dependent (majority, 80-90%) |
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where does diabetes fit amongst the most common causes of death?
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7th
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what is the most important stimulus to release and synthesize insulin
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oral glucose
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what does insulin do?
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transmembrane transport of glucose and aminoacids
glycogen formation glucose conversion into triglycerides Nucleic acid synthesis protein synthesis inhibition of lipolysis |
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what cell types do not require an insulin receptor for transmembrane transport of glucose?
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Neurons
RBC renal tubular cells the rest require an insulin receptor |
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what causes a type one diabetes
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severe or absolute lack of insulin due to a decreased Beta cell mass in the islate of langerhans.
it can be due to heredity, autoimmune, or an enviromental insult. |
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what genes are associated with type one diabetes?
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HLA-DR3 and 4 ( but it is still found prevelently in the general population)
genetic susecpability only accounts for 10% of the risk |
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what percentage of the B cells are destroyed before the disease starts to show its symptoms?
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90%
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what eveidence shows that you have AI caused diabetes?
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over expression of MHC1 and under expression of MHC2 on the beta cells, and lymphocytic infiltrate
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what can a patient with AI diabetes have AI against?
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insulin
GAD |
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what is the pathogenesis of type 2 diabetes?
|
enigmatic
no AI genetic factors have more important role than in type 1 Lifestyle |
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what are the two metabolic defects associated with type 2 diabetes?
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dearangement of B cell secretion of insulin
insulin resistence in the peripheral tissues |
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who is at risk for type 2 diabetes involving deranged Beta cell secretion
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people with modest hyperinsulinemia and Beta cell hyperresponsiveness
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what can cause the insulin resistance in type 2 diabetes?
|
decresed number of insulin receptors
impairment of the post-receptor signaling these result in inability of circulating insuin to work proplerly, more persistent hyperglycemia, and more prolonged stimulation of the beta cells |
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what percentage of patients with type 2 diabetes are obese?
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80%
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what is amylin?
|
37 AA peptide produced by Beta cells, copackaged and secreted with insulin, in type 2, more amylin is produced and accumulates outside the islets of langerhans and has staining appearance of amyloid.
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what type of diabetes has an insulin secretory defect, but does not have beta cell loss?
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MODY
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what complications can occur with diabetes?
|
microangiopathy
retinopathy neuropathy nephropathy |
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what are the complications mostly caused by
|
hyperglycemia
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what are the metabolic events that occur in the genesis of complications?
|
nonenzymatic glycosination- glucose attches to amino acid portion of protein without help, correlates to the level of glucose in blood and form advanced glycosylation end products (AGE), or they can bind to receptors.
intracellular hyperglycemia- causing hyperglycemia in cells that don't require an insulin receptor that is metaboized to form sorbitol- causing cataracts and impairs iron pumps which damages schwann cells and pericytes of the retinal capillaries activation of protein kinase C- causing production of VEGF which is implicated in retinal neovascularization, you lose the effects of nitrous oxide, increased vasoconstrictor factors, and increased TGF-1 that causes an increase in ECM and basement membrane material, reduces fibrinolysis by producing PAI-1, and the production of pro-inflammatory cytokines by vascular epithelium |
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what can AGE's cause?
|
cross-linkage of polypeptides of the same protein
trap nonglycosinated protein confer resistence to proteolytic digestion binding to receptors induce lipid oxidation inactivate nitric oxide |
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what can AGE binding to receptors cause?
|
release of cytokines and growth fctors
monocyte emigration increased vascular permiabilitiy increased procoagulent permiability enhanced proliferation and synthesis of ECM |
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what happens to the pancreas in both type one and type two diabetes?
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1- reduction in size and number of islets, leukocyte infiltration of islets
2- sublt decrease in islets mass, amyloid replacement of islets |
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what happens to the vascularity in both type os diabetes?
|
both have accelerated atherosclerosis in large and medium sized vessels, causes MI
gangrene Hyaline arteriosclerosis, which can be seen without HTN. microangiopathy- diffuse thickening of the basement membrane, basal lamina, involved with retinopathy, neuropathy, and nephropathy. It involves type 4 collagen |
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what is the second most COD wit diabetes?
|
renal failure- especially in type 1
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what DM complication is often seen with glomerular lesions
|
nodular glomerularsclerosis
afferent and efferent arteriolar sclerosis diffuse glomerularsclerosis exudative lesions |
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what eye problems are associated with diabetes?
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cataracts
glaucoma retinopathy |
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what is background retinopathy
|
nonproliferative (no new blood vessels)
microangiopathy, hemorrhages, and aneurysms edema exudate venous dilitation |
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what is proliferative retinopathy?
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neovascularization
fibroplasia |
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what nerve problems can DM cause?
|
peripheral neuropathy- primarily sensory (stocking and glove), but can be motor too
loss of proprioception autonomic neuropathy |
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what dermatologic complications can be seen with DM?
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shin spots on extensor surface
necrobiosis lipoidica- ulcerating |
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clinical course of type one diabetes?
|
abrupt
polyuria, dipsia, phagia, and ketosis weight loss muscle weakness usually by age 20 ketoacidosis- insidious or acute |
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what are the signs and symptoms of ketoacidosis?
|
polyuria, polyphagia, polydipsia
weakness orthostatic hypotension GI symptoms rapid deep respiration |
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what lab signs indicate ketoacidosis?
|
ketones
hyperglycemia metabolic acidosis potassium high initially, eventually stores are depleted depleted phosphates elevated BUN |
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what is seen with hypoglycemia unawareness?
|
normal insulin levels
glucagon respone is diminished loose epinephrine response, and the threshold for release is lowered. |
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how is the hypothalamus affected when hypoglycemic?
|
adaptive response which allows the breain to continue taking up normal levels of glucose even when hypoglycemic
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what is usually the first sign of hypoglycemia?
|
neurohypoglycemia (visual disturbances, CNS symptoms)
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what is the usualy clinical course for type 2 DM?
|
polyuria, polydipsia
obese diagnosis made after blood testing hyperosmolar nonketotic coma |
|
|
describe the hyperosmolar nonketotic coma
|
type 2
30-50% mortality dehydrated sunken eyes steady pulse cool skin can be brought on by illnesses level of unconsiousness is directly proportionte to the serum osmolarity. |
|
|
what lab test indicate a hyperosmolar nonketotic coma
|
hyperglycemia
body stores of potassim depleted lack of significant metabolic acidosis usually negative ketones |
|
|
how do you diagnose diabetes?
|
symptoms + random plasma glucose levels higher than 200, or fasting higher than 126, or 2 hour glucose higher than 200.
|
|
|
what is a normal fasting glucose?
|
<100
|
|
|
what is intermediate fasting glucose?
|
100-125
|
|
|
what is an intermediate reading with the glucose tolerance test?
|
140-199
|
|
|
what is considered essential tight control of glucose levels?
|
home glucose monitoring
|
|
|
what does hemoglobin A1C measure?
|
average blood glucose levess over previous weeks
|
|
|
what is Microalbuminuria used to measure
|
detectes early glomerulr disease
marker for cardiovascular disease >300mg of albumin per day |
|
|
what is dawn phenomena?
|
fasting hyperglycemia due to AM cortisol secretion, treat by giving insulin dose
|
|
|
what is rebound phenomena?
|
hyperglycemia followed by hypoglycemia, treat by decreasing insulin, or excersize, or increase food
|
|
|
desribe type 1 hypersensitivity
|
(anaphlactic)IgE mediated from mast cells and basophils in response to an antigen
it involves both the release of preformed primary mediators (5-30 min)and the de novo synthesis of secondary mediators (2-8 hours, can cause severe inflammation). It can be caused by other things too. |
|
|
what things cause a type 1 primary hypersensitivity?
|
histamines
chemotactic factors enzymes proteoglycans |
|
|
what are the things that cause a type 1 secondary hypersensetivity?
|
lipid mediators (leukotrienes, prostaglandins)
cytokines |
|
|
what can cause a systemic anaphlaxys?
|
oral or parental administration of an allergen. causes puritis, erythema, and urticaria within minutes of being exposed. can cause bronchoconstriction, laryngeal edema, obstruction, shock and death within minutes to hours.
|
|
|
what causes a type 2 hypersensitivity?
|
antibodies directed against antigens present on the surface of cells and tissue components.
|
|
|
what are the 3 different ways a type 2 hypersensetivity can be caused?
|
antibody reacts to cell curface antigen and leads to fication of complement. phagocitized
cells are coated with IgG and are killed by cells with Fc receptors. Not phagositized antibodies against cekll surface receptors that impair cell function. |
|
|
what causes type 3 hypersensetivity?
|
antigen-antibody complexes that produce tissue damage because it can activate the complement system. can be both systemic (acute serum sickness) and local (arthus reaction).
|
|
|
what is an arthus reaction?
|
localized area of tissue necrosis, usually involving the skin.
|
|
|
what causes a type 4 hypersensitivity?
|
initiated by T-cells (delayed)
also involved with TB, fungi, protozoa, skin graft rejection. |
|
|
in transplant rejection what causes the Tcell mediated direct pathway rejection?
|
recipient T-cells reject donor cells becuase of foreign MHC
|
|
|
what about the indirect pathway
|
T-cells reject it after they are presented by the recipient's own antigen presenting cells.
|
|
|
what causes a hyperacute transplant rejection?
|
when the recipient has preformed antibodies already in circulation
|
|
|
what is the initial target in the rejected transplant organ when the recipient did not have a preformed antiboy in circulation?
|
donors blood vessels
|
|
|
what are the different scenarios that can be seen in acute transplant rejection?
|
days after if not treated
months to years later after immunosuppression is terminated |
|
|
what is X-linked Agammaglobulinemia of Bruton?
|
Failure of precursor-B-cells to differentiate into B cells. No light chains found, lots of heavy chains in cytoplasm. Due to mutations in tyrosine kinase. Almost entirely in males. becomes apparent at 6months when babies lose mom's IgG. Babies get sick a lot (pyogenic, viral and giardia).
no plasma cells increased incidence of AI diseases. |
|
|
what is common variable immunodeficiency?
|
heterogenous group of disorders.
sporadic and inheritied (variable forms). normal levels of B cells, but can't differntiate to plasma cells hypogammaglobulinemia seen in all platients, usually IgG. increased risk for lymphoid malignancy and GI carcinoma |
|
|
what is DiGeorge's syndrome?
|
thymic hypoplasia- T cell deficiency due to failure of the 3 and 4th pharyngeal pouches in gestation
variable absence of cell-mediated immune response, tetany, congenital defects, and abnormal facial appearance. poor defense against viral and fungal infections. 22q11 deletion |
|
|
what is different with partial Digeorge syndrome?
|
have a small thymus, and the T-cell function will improve with age.
|
|
|
What do all SCIDs have in common?
|
defects in both humoral and cellular immunity.
treated with bone marrow transplant. most are x-linked, rest are AR. |
|
|
what two systems does HIV target?
|
immune system (CD4)
CNS |
|
|
what is the pathogenesis of HIV?
|
inversion of CD4/CD8 ratio
quantity and quality is infected hypergammaglobulinemia when ico-infected with EBV or CMV. But can't fight off anything new. |
|
|
what acts as a reservoir for HIV
|
monocytes
macrophages- carries it to the brain. HIV has neurotoxic effects. dendritic cells |
|
|
what happens in the early acute phase of HIV infection
|
transient viremia
seeding of lymphoid tissue temporary dcrease in CD4 T-cells seroconversion appears as a self-limited acute illness follicular hyperplasia in lymph nodes |
|
|
what happens in the middle or chronic phase?
|
asymptomatic
latent low grade viral replication at the end- increased viremia, rash, and fatigue lymph nodes become atrophic |
|
|
what happens in the final phase?
|
rapid decline in host defense
low CD4 t-cell count weight loss diarrhea secondary neoplasms (karposi's sarcoma and lymphoid tumors, non-hodgkins lymphoma) opportunistic infections |
|
|
what is amyloidosis?
|
pathologic proteinaceous material deposited between cells in various tissues and organs.
It is not a single chemical entity (2 major and several minor proteins). deposited by several mechanisms. |
|
|
what does an amyloidosis appear like under a microscope, x-ray crystallography?
|
non-branching fibrils
cross B pleated sheet conformation, the B pleated sheets are what are responsible for allowing us to stain it with Congo red. |
|
|
what are the three classes seen in amyloidosis?
|
AL- amyloid light chains
AA- amyloid associated (nonimmunoglobulin sythesized in the liver) Ab-amyloid- found in Alzheimers |
|
|
tell me more about AA
|
derived from a larger precursor serum AA, which behaves as an acute phase reactant
it is a major component of amyloid deposited secondary to chronic inflammatory diseases. An enzyme defect prevents SAA degradation to end products may be responsible for it in some individuals |
|
|
what is primary amyloidosis?
|
immune dyscrasisi- b cell proliferation
|
|
|
what is secondary amyloidosis?
|
complication of a chronic inflammatory process or tissue destructive process.
also called reactive systemic amyloidosis, the common feature is the protracted breakdown of cells |
|
|
where does the deposition begin?
|
between cells
|
|
|
is the presence of an autoimmune anitbody enough to diagnose someone with an autoimmune disease?
|
no, you need evidence of an autoimmune reaction, judgement that the immunologic findingsd are not merely secondary, and that there is a lack of another secondart cause.
|
|
|
what are the 3 systems involved in peripheral tolerance?
|
1. clonal deletion by activation induced cell death- controlled by the Fas-Fas ligand system.
2. clonal anergy - prolonged or irreversible functional inactivation of lymphocytes 3. peripheral suppression by Tcells- suppressor T cells that regulate other T cells |
|
|
with autoimmune disease, if you have the predisposing gene, does it indicate that you hae the disease?
|
no
|
|
|
are most autoimmune diseases usually a single gene disorder?
|
no, most of them have complex multingenic patterns of susceptability
|
|
|
what is RF and autoantibody against?
|
Fc portion of the autologous IgG
|
|
|
what type of antibody is most RF?
|
IgM
|
|
|
why do some people with RA test negative for RF?
|
because the RF test only checks for the IgM type of RF. It could also be IgA, IgE, or IgG
|
|
|
what are anti-nuclear antibodies?
|
antibodies directed against non-organ specific nuclear antigens. DNA, RNA and associated proteins, histones, etc. It is present in a low titer in about 5-15% of individuals When it has a high titer it usualy indicates connective tissue disease.
|
|
|
with lupus, what organ affected usually is the one that causes death?
|
kidneys
|
|
|
who is most likely to get lupus?
|
young black females (20-30 years)
|
|
|
what are the four thins that people with lupus have antibodies against?
|
DNA
histones nonhistone proteins bound to DNA nuclear antigens |
|
|
what are the diagnostic antibodies for lupus?
|
double stranded DNA
SM antigen |
|
|
what other things can people with lupus have antibodies against besides the main organs?
|
platelets
red cells phospholipids - procoagulative |
|
|
what type of cell is usually affected in lupus?
|
T- helper cell
|
|
|
most of the visceral lesion seen in lupus is due to the deposition of what?
|
immune complex
hypersensitivity III |
|
|
ANA to the red cells, platelets and WBC are usually due to what?
|
type II hypersensitivity
|
|
|
what is the appearance of the skin in lupus?
|
liquifactive degeneration at the dermal/epidermal junction. The immunoglobulin is found at both involved and uninvolved skin.
|
|
|
what are the 5 different kind of renal problems seen with lupus?
|
1. no change - rare
2. mesangial GN- mildest, milde hematuria 3. focal proliferate GN - half of glomeruli, only portions of glomeruli. presents with hematuria and proteinuria. 4. difuse proliferative GN - crescents and sub endotheilal deposits. most or all glomeruli with all parts og it involved. 5. membranous GN - wide spread thickening of capillary walls. severe proteinuria and nephrotic syndrome. |
|
|
what is a wire loop lesion?
|
when extensive subendothelial deposits create a peculiar thickening of the capillary wall seen with light microscope. Usually in class 4, but can also be seen in types 3 and 5. Not a good prognosis.
|
|
|
what happens to the joints when they are affected by lupus?
|
nonerosive synovitis with little or no deformity.
|
|
|
what can happen to the CNS with lupus?
|
ascribed to acute vasculitis causing periocarditis or along with valvular involvement of the heart.
|
|
|
what heart syndrome can be caused by lupus?
|
libman-sacks endocarditis- non-bacterial verruceal endocarditis
|
|
|
how many of the 11 symptoms must a patient have to be diagnosed lupus?
|
4
|
|
|
what is your typical presentation with lupus?
|
young women with butterfly rash, fever, pain, but no deformity in one or more joints, and pleuritic chest pain, and photosensitivity.
|
|
|
what do the lupus variants typically involve?
|
skin, with mild if any systemic involvement.
|
|
|
what is seen with chronic discoid lupus?
|
scaly erythmatous plaques
atrophic scars on face and scalp. May have ANA, but not to double stranded DNA. |
|
|
what is seen with subacute cutaneous lupus?
|
skin involved
widespread but superficial nonscarring lesions SS-A and HLA-DR3 autoantibodies |
|
|
what is seen with drug induced lupus?
|
antihistone antibodies
associated with HLA-DR4 caused by hydrazaline, procainamide, isoniazide, and D-penecillamine |
|
|
what are the charcteristics of sjogrens syndrome?
|
dry eyes and dry mouth from immunological destruction of the lacrimal and salivary glands. Can be primary or in association with other diseases. Mostly in women 35-40 yrs old. HLA class II association. problems with oral hygeine, trouble swallowing, enlarged lymph nodes
|
|
|
what abnormalities are seen with sjogrens?
|
ANA, RF and antibodies directed against Ribonucleoprotein are common.
|
|
|
what does a person with sjogren syndroome have a 40 fold increased risk of developing?
|
non-hodgkins lymphoma
|
|
|
what are the characteristic seen with systemic sclerosis, or scleroderma?
|
excessive fibrosis throughout the body. usually involves skin but can also affect the GI, kidneys, heart, lungs, and muscles. Can be diffuse or local. Usually seen in black women age 50-60.
|
|
|
describe the common course seen with scleroderma?
|
diffuse sclerotic atrophy of skin beginning in the fingers. Early sign is edema with perivascular infiltrate of T cell. Later sign is increased dermal collagen with loss of adenexia, capillaires with thickened walls
|
|
|
other than the skin, whereelse can you see problems with scleroderma?
|
GI problems especially in esophogus
inflammation of synovium renal problems- malignantn hypertension, HTN, lungs- pulmonary HTN heart pericarditis, with effusion, myocardial fibrosis |
|
|
what ANAs are usually specific for scleroderma?
|
antibodies against DNA topoisomerase I, and anticentromere antibody
|
|
|
what are the clinical stymtopms sometimes associated with scleroderma?
|
raynauds
dysphagia abdominal pain intestinal obstruction respitory distress malignant hypertension mild proteinuria |
|
|
what are the 3 usual COD seen with scleroderma?
|
HF
pulmonary insufficiency Renal failure |
|
|
what dies CREST mean associated with systemic scleroderma?
|
C- calcinosis
R - raynauds E- esophageal dysphagia S- sclerodactyly T - telangectasia usually seen late in the disease. |
|
|
what are the cahracterisitcs of MCTD
|
has symptoms similar to those seen with scleroderma, lupus, and polymyositis
|
|
|
what is dermatomyocytis?
|
in kids and adults
lilac discoloration of the upper eyelids with periorbital edema. Can also have scaly dusky red lesions or patched over the knuckles, elbows, and knees (grotton lesions). |
|
|
describe the muscle weakness seen with dermatomyocytis?
|
proximal muscles affected first, fine movements affected late. bilateral symetric
|
|
|
what do patients with dermatomyocytis have an increased risk of developing?
|
visceral cancers
|
|
|
what is the primary target that causes the problems with the muscles in dermatomyocytis?
|
capillaries attacked my complement and immunoglobulin
|
|
|
what is polymyocytis?
|
only involves the proximal muscles and there is no cutaneous involvement.usually in adults and stil has a slight increased risk of developing visceral cancer.
|
|
|
what is the difference between primary and secondary Oa?
|
primary- insidious associated with aging
secondary- trauma or congenital malformation |
|
|
what joints tend to be more genetically related to OA than others?
|
hands and hips
|
|
|
what are the main two changes seen in the cartilage
|
alterations to the proteoglycans and the collagen
|
|
|
how do chondrocytes play a role in the development of OA?
|
they produce IL-1 and TNF-alpha that stimulate the production of metalloproteinases and inhibits the synthesis of type 2 collagen.
|
|
|
what does eburnated mean?
|
no bone on top of it
|
|
|
what 5 complications can be seen with OA?
|
cartilage degradation
cartilage loss bone eburnation cysts non-specific synovitis |
|
|
what are the radiographic changes seen with OA?
|
joint space narrowing
subchondral bone sclerosis subchondral cysts osteophytes |
|
|
what are the clinical sgins and symptoms seen with OA?
|
insidious
morning stiffness less than one hour deep achy pain that worsens with use crepitus limited range of motion pannus proliferative synovitis ankylosis vasculitis nodules |
|
|
what are heberden's nodes?
|
osteophytes in the dips
|
|
|
where is the genetic disotition for RA found?
|
HLA-DRB1
|
|
|
how long does the morining stiffness last with RA?
|
more than one hour
|
|
|
what complications are seen with systemic RA?
|
decreased life expectancy
systemic amyloidosis felty's syndrome- decreased WBC. splenomegaly, proteinuria, and leg ulcers |
|
|
what are the different characteristics seen between adult and juvenile RA?
|
juvenile - usually oligoarthritis,
usually systemic bigger joints involved usually no nodules usually no RF ANA positive |
|
|
what are the common characterisitics of the seronegative spondyloarthropathies?
|
typically begin in ligaments
sacroiliac joints no RFassociated with HLA B27 |
|
|
what is ankylosing spondylitis?
|
chronic inflammatory disease of axial joints, 90% have HLA B27. Chronic synovitis, destruction of articular cartilage, bony ankylosis, and can involve the peripheral joints
|
|
|
what is reiter's syndrome?
|
triad of arthritis, non gonococcal urethritis, and conjunctivitis
|
|
|
what is reactive arthritis?
|
non-infectious arthritis of appendicular skeleton within one month of a primary infection somewhere else in the body.
|
|
|
Psoriatic arthritis?
|
rare with epeople that have psoriasis. Asymmetric inflammatory arthritis usually.
papillary hyperplasia and inflamation in the synovium. Pencil in cup appearance on radiographs |
|
|
what is tuberculous arthritis?
|
severe joint destruction due to complication of TB OM or spread in blood. Usually affects the weight bearing joints
|
|
|
what is Potts disease?
|
TB arthritis in the spine
|
|
|
what is the difference between primary and secondary gout?
|
1- insidious
2- overproducer or undersecretor or inborn errors of metabolism |
|
|
what are the primary predisposing factors for gout?
|
age
obesity alcohol genetic medications |
|
|
what is pigmented villinodular synovitis
|
clonal proliferation of cells with consistent chromosomal abnormalities, typically affects one joint diffusely. Red brown to mottled orange/yellow color. convoluted synovium (finger like projections, the appearance of a tangled mat). Tumor cells are bland mononuclear cells and giant cells. Typically a monoarticular arthrtitis and it can erode into adjacent bone.
|
|
|
what is a giant cell tumor of tendon sheath?
|
painless mass involving tendon sheaths along the fingers. Similar to PVDS
|
|
|
what is a synovial cyst?
|
herneation of the synovium through the joint capsule, or a massive enlargement of a bursa
|
|
|
what is a baker's cyst?
|
synovial cyst in the popliteal space in RA
|
|
|
what is ganglion cyst?
|
arises in collagenous connective tissue. No lining. no communication with the joint space. It arises from cystic or mucoid degeneration of the connective tissue.
|
|
|
what is parakeratosis?
|
preservation of nuclei in the stratum corneum with a decreased granular layer. A sign of increased cell turnover, that they don't have enough time to shed off their nucleus.
|
|
|
what is epidermal hyperplasia, or acanthosis?
|
increased proliferation of the spinous layer.
|
|
|
what is acanthaloyis?
|
discohesion of individual keratocytes within the stratum corneum
|
|
|
what is papillomatosis
|
the papillae of the dermis proliferate to the outside above the skin surface
|
|
|
what is vitiligo?
|
hypopigmentation macules, associated with autoimmune diseases
|
|
|
what is melasma?
|
a mask like zone of hyperpigmentation on cheeks and nose. often associated with pregnancy or birth control. due to an increase in pigment in the melanocytes.
|
|
|
what are ephilis?
|
freckles. fade and reappear with sun exposure. Not an increase in melanocytes, just in the pigmentation inside the melanocyte
|
|
|
what is a lentigo simplex?
|
like a freckle but does not involve sun exposure. Does have an increased number of melanocytes.
|
|
|
what are solar lentigo?
|
multiple, dark brown black macules with increased basal melanocytes on sun exposed skin too long in the elderly.
|
|
|
what are nevi?
|
most common melanocytic tumor in humans. Increased melanocytic proliferation in the dermal and epidermal layers. uniform round, well defined edges.
|
|
|
what are the 3 stages of a nevus?
|
1- Junctional: melanocytes are disbersed in multiple descrete nests along the junction.
2- Compound nevus: junctional + intradermal, present as dome shaped or elevated lesions. 3- Intradermal: melanocytes are confined only to the demis. |
|
|
what are the three different types of melanocytes seen in an intradermal nevus?
|
superficial- type A - large round and pigment producing
deep- type B - smaller, less pigment, lymphocyte like, often in cords type c- spindled wavy type cells present at the base. |
|
|
how are dysplastic nevi related to melanoma?
|
are a marker for increased ris for the patient to have melanoma elsewhere, but are not precursors to become melanomas themselves.
|
|
|
what are the distinguishing ABCD's of malignant melanoma?
|
A- asymmetric
B- border is irregular C- color variation D- diameter is increasing |
|
|
what are the common risk factors for developing malignant melanoma?
|
fair skinned
sun exposure family history dysplastic nevus |
|
|
what are the two growth phases of melanoma?
|
radial - grows along the junction layer.
vertical- invades into the dermis and has bad metastatiic potential. |
|
|
how are malignant melanomas categorized?
|
clarks levels
1: all within epidermis 2: into the papillary dermis 3:reach level of superficial plexus 4:reach level of reticular dermis 5:reach level of subcutaneous adipose tissue. |
|
|
what are seborrheic keratosis?
|
most common epidermal tumor in the elderly. Stuck on greasy waxy papules and plaques.
|
|
|
what does it mean if you get several sebhorreic keratoses all at the same time?
|
sign of leser-trelat, it is associated with internal malignancy
|
|
|
what is prurigo nodularis?
|
pruritic nodules on the neck, extremities, and genitalia
|
|
|
what is acanthosis nigracans?
|
hyperpigmentation zones of the skin usually in skin folds like the axilla. benign in kids, can be malignant in adults
|
|
|
what are fibroepithelial polyps?
|
flesh colored bag-like tumors.
|
|
|
what are epidermal inclusion cysts?
|
cystic expansion of epidermis formed along hair lines. filled with keratin. inside it has a layer of keratinocytes with the keratin inside it. It hurts if the cyst ruptures because the body will attack it.
|
|
|
what is keratoacanthoma/
|
rapidly developing solitary neoplasm. Grow for a few weeks and usually inolude on their own. Often ulcerate or have a keratin filled plug and crater.
|
|
|
what are epidermal actinic keratoses?
|
premalignant tumor. irregular erythmatous plaque after prolonged sun exposure. THickened, blue-gray elastic fibers in dermis. "solar dlastosis"
|
|
|
what are epidermal squamous cell carcinomas?
|
2nd most common form of skin cancer. on sun exposed sights. shallow ulcers with keratinatous crustsand elevated inundated periphery.
|
|
|
what are the risk factors for epidermal squamous cell carcinoma?
|
sun exposure
carcinogen exposure chronic ulcers arsenic ionizing radiation immunosuppression |
|
|
what is the first stage of epidermal squamous cell carcinoma/
|
full thickness atypia without invasion into the dermis.
invades through the basement membrane into the dermal layer. |
|
|
what is a verrucous squamous cell carcinoma?
|
wart tumor that tends to grow either on the genitocrurual surface or plantar surface of the foot.
|
|
|
what is the most common type of epidermal cancer?
|
basal cell carcioma
|
|
|
describe the appearance of basal cell carcinoma?
|
pearly nodule with telangectasia, can ulcerate. Very rarely do they metastatize.
|
|
|
what is nevoid basal cell carcinoma syndrome?
|
AD
caused by gene mutation in the PATCH gene get multiple BCC at an early age |
|
|
what is a xanthoma?
|
tumor like collection of foamy like macrophages.Can be associated with high triglyceride and high cholestrol disorders.
|
|
|
what is mycosis fungoides
|
T-cell lymphoproliferative disorder confined to the skin. Scaly red brown patches often confused with eczema or psoriasis. Malignant T-cell lymphocytes that are infiltrating into the epidermis.
|
|
|
what is dyshidrotic eczema?
|
symmetric involvemnt of the palmar hands and feet and lateral aspects of the digits. Recurrent pruritic deap seated vescicles.
|
|
|
what is psoriasis?
|
well demarcated pink plaques
loose silver scales on sites of trauma commonly sen at the elbows, knees, sacrum, and the umbilicus, or on the extensor surfaces. can cause nail changes. |
|
|
what is kebner's phenomenom?
|
when you get psoriasis after trauma.
|
|
|
what causes the plaques with psoriasis?
|
extremity papillary shapes of the dermal epidermal junction, very thin and very thick in a wavelike pattern.
|
|
|
what is lichen planus?
|
purple pruritic polygonal papules that coalesque to form plaques usually on the flexor surfaces. damage is geing done to the epidermal/dermal junction.
|
|
|
what antibodies can be sen with immunoflouresence when looking at lupus?
|
IgG, IgA, And complement C3 can all be seen along the dermal/epidermal junction. (full house)
|
|
|
what is pehphigus vulgaris?
|
very flaccid blisters. only blister that involves the oral mucosa. ANA to the desmosomes of the keratinocytes. Seperation is within the epidermis. Tombstones appearance becuase of the hemidesmosomes still hanging on. Caused by an IgG disposition.
|
|
|
what is bullous pemphigoid?
|
blisters underneath the epidermal layer. Seperating the dermal/epidermal layers. Firm blisters.ANA against the hemidesmosomes filled with eosinophils. Caused also by IgG and C3.
|
|
|
what is dermatitis herpetiformis?
|
blisters so small it looks more like vescicles. Abscess fills with neutrophils. Has IgA as its ANA.
|
|
|
with erythema nodosum, what layer is the inflammed portion?
|
in the adipose tissue.
|
|
|
what are superficial fungal infections?
|
primarily caused by dermatophytes. Erythematous plaques with a raised erythematous border.
|
|
|
where are the following fungal infections located:
T capitis Tbarbae Tcorporis Tcruris T pedis onychomycosis? |
head
beard body inginal areas feet nails |
|
|
what is scabies?
|
contagious pruritic dermatosis. Erythmatous papules and linear defined streaks.caused by the sarcobes female mite.
|
|
|
what are the three M's of herpes?
|
multinucleated
molding of the nucleoli margination of the chromatin |
|
|
what zone of the liver recieves the least amount of perfusion?
|
Zone 3, centilobular
|
|
|
what are the signs of liver degeneration?
|
swelling, with irregular organelles ballooning in the cytoplasm
foamy retained bile in the cells, also called feathery degeneration |
|
|
what can cause an acute hepatitis?
|
Adenovirus
Hep B yellow fever drug toxicity |
|
|
what can cause a chronic hepatitis?
|
Heb B, C
ANA hep Wilson's |
|
|
what are the signs of hepatic regeneration
|
thickened hepatic cords
increased bile duct proliferation increased mitotic activity disorganized appearing parenchyma |
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what does liver fibrosis cause?
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dividing of the liver into nodules of active hepatocyteproliferation, which end stage is cirrhosis
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what is cirrhosis?
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not a specific disease, but the end stage of many diseases. Bridging fibrous septae, reorganized vascularity, regenerative parenchymal nodules, and it must be diffuse. It increases the risk for hepatocellular carcinoma
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what are the causes of cirrhosis?
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alcohol
viruses biliary disease cryptogenic primary hemochromatosis |
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how is cirrhosisformed?
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the Ito cells are changed to myofibroblastic cells after being stimulated by cytokines from inflammatory cells, injured hepatic cells, endothelium, or bile duct epithelium. These activated cells produce collagen that create fibrotic bridges between the portal ductts and the central veins. This causes new vascularization to shunt blood away from the hepatocytes causing less exchange and increasing the resistance, causing portal hypertension and complications
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other than cirrhosis, what else can cause portal hypertension?
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splenomegaly
heart failure fatty liver venous thrombosis TB sarcoidosis shistosomething |
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what other complications can be seen when someone has cirrhosis?
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esophageal varices
caput medusae portosystemic shunting hemorhoids splenomegaly hepatic encephalopathy ascites hepatorenal syndrome hepatopulmonary syndrome encephalopathy |
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what is ascites?
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excess fluid in the peritoneal cavity due to acsess hepatic lymph drainage
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what kind of things can cause massive hepatic necrosis which leads to liver failure?
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mushrooms
MAOI's halothane TB drugs acetaminophen HAV HBV most are unknown causes |
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what are some porblems that can cause severe liver dysfunction without any overt liver necrosis?
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tetracycline toxicity
reye's syndrome acute fatty liver of pregnancy |
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what are the clinical features of liver failure?
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hypoalbuminemia (peripheral edema, ascites)
hyperammoniaemia (encephalopathy, fetor hepaticus) hyperbilirubinemia (jaundice) coagulopathy hyperestrogenism (hypogonadism, gynecomastia, spider angiomata, palmar erythema) |
