Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
102 Cards in this Set
- Front
- Back
|
what are the congenital pancreatic anomalies?
|
heterotopias- not in normal place
pancrease divisum- main duct is goes to minor sphincter instead of major papilla like its suppose to. annular pancreas-pancreas surround duodenum |
|
|
what is a common problem associated with pancreas divisum?
|
major cause of pancreatitis
|
|
|
what is a common marker of acute pancreatitis?
|
increased amylase level
|
|
|
what is the most common cause of auct pancreatitis in north america?
|
alcohol abuse main
biliary tract stones second drugs idiopathic |
|
|
what are the direct metabolite causes of acute pancreatitis?
|
alcohol/drug damage
hyperlipoproteinemia hypercalcemia uremia pregnancy diabetes mellitus |
|
|
what are the drugs most commonly associated with causeing acute pancreatitis?
|
antibiotics-didanosidine
pentamidine, sulfonamides, tetracycline chemotherapy- asparaginase, cytarabine, 6-mercaptopurine diuretics-furosemide immunosuppressant-azathioprine opiates steroids estrogen |
|
|
what are the physcial/vascular causes of acute pancreatitis?
|
cholelithiasis/gallstones
trauma-most common cause of AP in children iatrogenic: endoscopy/surgery ischemic/vascular: vasculitis, thrombosis, shock |
|
|
what are the infectious causes of acute pancreatitis?
|
viral-mumps, entervirus, CMV
mycoplasma, mycobacteria parasites-ascaris, clonorchis |
|
|
what is the pathologic sequence of events in acute pancreatitis?
|
inciting injury-alcohol/drug/obstuction etc
activations/release of enzymes acinar injury increased activation/release of enzymes more acinar injury eventually proteolysis then blood vessel damage-hemorrhage leads to fat necrosis and release of lipase that causes acute inflammation and edema. |
|
|
what are the three ways alcohol can cause pancreatic injury?
|
direct acinar cell injury
can cause defective intracellular transport can cause ductal constriction that leads to duct obstructions. |
|
|
what are the two enzymes released in the active from acinar cell damage?
|
amylase and lipase
|
|
|
what enzyme activates the non active enzymes released from acinar cell injury?
|
trypsin
|
|
|
what is the clinical presentation of acute pancreatitis?
|
rapid onset severe constant epigastric pain radiating to the back
nausea and vomiting due to ileus/duodenal obstuctions,sentinel loop 2/3 have fever and most have shock due to fluid shifting to inflamed area |
|
|
what is the cause of acute hemmorhaic pancreatitis?
|
release of protyolytic enzymes from the pancreas during pancreatitis leads to blood vessel daamage
|
|
|
what are the two signs of hemorrhagic pancreatitis?
|
cullens sign-discoloration around umbilicus
grey turner sign- discolorations around the flank |
|
|
what are the immediate complications that arise in acute pancreatitis?
|
shock
ARDS acute renal failure DIC, pleural effusion jaudince hypcalcemia/hypomagnesemia acidosis(lactic and diabetic ketoacidiosis) |
|
|
what are the long term complications of acute pancreatitis?
|
pancreatic abscess
pancreatic pseudocyst duodenal obstruction hyperglycemia, hyperlipidemia chonic pancreatitis 75% progress if reccurrent. |
|
|
what are lab findings in acute pancreatitis?
|
serum and urine amylase elavated early(55-60kD)
serum lipase elvated later 72-96 hours nor in urine only serum hypcalcemia elvated WBC neutrophils radiogrphic left sided pleural effusion, sentinel loop |
|
|
what is the triad of sypmtoms for chonic pancreatitis?
|
pseudocyst/calcifications, steatorrhea and diabetes mellitus
|
|
|
what are the causes of chronic pancreatitis?
|
recurrent acute pancreatitis usually causesd by alcohol abuse or duct obstuction
|
|
|
what is the differentail of causes of chronic pancreatitis?
|
trauma
autoimmune(sjogrens syndrome) cystic fiborsis idiopathic pancreas divisum hypercalcemia/hyperlipidemia drugs tropical pancreatitis hereditary(AD) |
|
|
what is seen on histo with chronic pancreatitis?
|
sparing of islets
dilated ducts fibrosis and atrophy inspissated concretions within dilated ducts |
|
|
what is the presentation of chonic pancreatitis?
|
abdominal pain
nausea vomiting weight loss/malabsorption hyperglycemia jaundice fever and elvated amylase steatoreahea |
|
|
what is the calceum condition in chonic compared to acute pancreatitis?
|
chonic is hypercalcemia-
acute is hypocalcemia-because of suponification of lipids that release free FA that bind calcium and magnesium |
|
|
what are the cysts of the pancreas?
|
psuedocysts
congenital cysts(polycystsic kidney disease) cystic neoplasm(<5%) |
|
|
what are the cystic neoplasms?
|
serious cystadeoma-benign
muscinous cysademona muscinous cystadenomcarcioma solid-pseudoppallillary neoplasm(young female, benign) |
|
|
what it the most common cause of chronic pancriatitis in children?
|
cystic fibrosis
|
|
|
what is cystic fibrosis?
|
inhertied epithelial transport disorder
abnormal fluid secretion in exocrine glands, sweat, pancreatic respriatory tract, GI, and reproductive extremely thick secretions abnomral clearance and obstuctions |
|
|
what is the presentation of cystic fibrosis?
|
recurrent pulmonary infections
bronchiectasiss pancreatic insufficiency steatorrhea/malnutrition hepatic cirrhosis, intestinal obsturction male infertility |
|
|
what is the prognsosis of CF?
|
most common lethal genetics disease affecting the caucasion populations
|
|
|
what is the genetics behind CF?
|
AR
chromosome 7 CFTR gene-cholorid channel 500 to 600 different mutations clinical testing for most common 70 most common mutation is F508 |
|
|
what are some deficiencies found in CF patients?
|
vit. a, d e, and K
|
|
|
what is the main cause of death in CF?
|
recurrent respiratory infection
treated with lung/liver/pancreas transplantation |
|
|
what is found in adenocarcinoma of the pancreas?
|
obstructive jaundice
pain weight loss anorexia, acholic stools courvoisiers sign-dialated GB palpable in RUQ mirgratory thrhombophlebitis all these symptoms are seen late |
|
|
what is the prognosis of adenocarinoma?
|
4th more common lethal cancer
|
|
|
what r the mutations associate with carcinoma of the pancreas?
|
codon 12 K-ras
inactivation of p16 and p53 |
|
|
where do most carcinoma of pancreas arise?
|
60% found in head
|
|
|
what are the three most common organs of metastatiss for cacinoma of pancreas?
|
liver lung and bone
|
|
|
what is a marker of very poor prognosis in carcinoma of the pancreas?
|
invasion of the celiac axis
|
|
|
what are the biomarkers of pancreatic cancer early?
|
CA19-9-elevated in many types of GI cancer and 10% of caucasions lack the lewis antigen and do not produce CA19-9
CEA-also elavated in GI cancers as well as lung and breast, elvated in smokers, pancreatitis, cirrhosis and COPD |
|
|
what are the three types of islet cell tumors?
|
insulinoma
glucagonoma somatostatinoma |
|
|
what is presenation of insulinoma?
|
usually benign, hypoglycemia, elevated C-peptide and insulin distinguishes from injected insulin
|
|
|
what is the presenation of glucogonoma?
|
usually malignant, hyperglycemia, DM rash(migratory necrolytic erythema)
|
|
|
what is the presentation of somatostatinoma?
|
DM steatorrhea, gallstones, achlorhydria
|
|
|
what is the definition of diabetes mellitus?
|
chronic disorder of carbohydrate, fat, and protein metabolism, accompanied in most cases by a deficient or defective insulin secretory response to a carbohydrate load, with resultant hyperglycemia.
|
|
|
what is proinsulin
|
insulin and C-peptide
|
|
|
what is the 4 different ways to dx criteria for Diabetes millitus?
|
fasting plasma glucose greater than 126mg/dL on more than one occasion
random PG greater than 200mg/dL plus classic signs/symptoms of DM(polyuria/polydipsia/polyphagia) PG greater than 200mg/dL 2 hours after glucose load(normal 75-100) Hb A1c> 6.5% |
|
|
what are the three tissues affected by insulin?
|
adipose
striated muscle liver |
|
|
what is the effect of insulin on the fat?
|
increase glucose uptake
increase lipogenesis decrease lipolysis |
|
|
what is the effect of insulin on liver
|
decrease gluconeogenesis
increase glycogen synthesis increase lipogenesis |
|
|
what is the effect of insulin on strieted muscle?
|
increase glucose uptake
increase glycogen synthesis increase protein synthesis |
|
|
contrast the effects of insulin and glucagon?
|
insulin- anabolic hormone, causes transmembrane transport of glucose and amino acids, and fromation of glycogen in liver and skeletal muscle
glucose conversion to triglycerides decreases plasma glucose glucagon-catabolic hormone, glycogenolysis, gluconeogenesis, ketogenesis, increases plasma glucose |
|
|
what a lab finding in type 1 diabetes mellitus not found in type 2?
|
ketonuria
|
|
|
what is the pathologic process of type 1 diabetes mellitus?
|
autoimmune destruction of beta cells in the pancreatic islets (insulitis) by T lymphocytes resulting in deficiency of insulin production.
|
|
|
what gene is type 1 diabetes linked to?
|
HLA-D linked
|
|
|
what is a dangerous complication of type 1 DM?
|
ketoacidosis
|
|
|
what are the three islet cell autoantibodies that cause damage in type 1 DM?
|
anti-islet auto antigen
anti-insulin anti-GAD(glutamic acid decarboxylase) |
|
|
when are islet cel autoantibodies seen?
|
appear years before onset of DM due to failure of self tolerance in T cells
|
|
|
what is the 5 risk of developing DM type 1 if all 3 islet cell autoantibodies are present?
|
almost 50%
risk is less if you don't have all three present |
|
|
what are the three theories of viral cause of DM type 1?
|
bystander-direcet beta cell injury releasing antigens by the virus
molecular mimicry- viral proteins mimic beta cell antigens viral deja vu- early viral infection that persists in tissue with subsequent infection by a related virus that shares teh antigenci epitopes and leads to inmmune response to the infected islet cells |
|
|
what is the genetic predisposition for DM type 1
|
HLA DR3 DR4
|
|
|
what is the DM1 classic triad?
|
polyuria, polydipsia, polyphagia
|
|
|
what is the onset age for DM1?
|
less than 20. presence of anti islet autoantibodies can be at 10 with continuous loss of insulin production till no insulin is produced but actual DM is not clinical till usually around 20
|
|
|
what is diabetic ketoacidosis?
|
hyperglycemia greater than 250mg/dL with acidosis (pH<7.3) and ketosis
|
|
|
what is required for Diabetic ketoacidosis to occurs?
|
lack of insulin and Increased glucagon
|
|
|
what is the pathologic process of ketoacidosis?
|
glucogneogeneiss and glycogenolysis lead to marked hyperglycemia
peripheral lipolysis, dramaticallly increased free fatty acids and glycerol FFA is converted to ketoacids in the liver leads to high amounts of ketone bodies |
|
|
what are the ketone bodies?
|
acetoacetic acid, beta hydroxybuteric acid and acetone
|
|
|
what is usually the trigger of dibabetic ketoacidosis?
|
infection or other stress may trigger DKA
|
|
|
what is the most important ketone body in DKA?
|
beta hydroxybuteric acid
|
|
|
what is the histologic hallmark of type 2 DM?
|
amylin deposition in the pancreatic eyelets
|
|
|
which type of DM is more influenced by gentics?
|
Type 2
|
|
|
what is the pathologic process of type 2 DM?
|
deranged beta cell function leads to insulin ressitance
|
|
|
what is the connection between obesity and type 2 DM?
|
adipose is hormone producing tissue those hormones lead to decreased sensitivity to insulin
|
|
|
where is the initial abnormality in type 2 DM?
|
the glucose transporters are defective which means insulin is unable to bind them and direct the disposition of glucose into the cells.
|
|
|
what is the chain of event in DM type 2?
|
genetic defects and obesity lead to peripheral tissue insulin resistance of the GLUT(glucose transporters) which leads to inadequate glucse utilization.
this causes increased insulin secretion due to hyperglycemia(increased insulin often from genetic defect as well) persistant hyperglycemia leads to beta-cell exhaustion which is the cause of type 2 diabetes. |
|
|
what is the normal presentation of type 2 DM?
|
polyuria, polydipsia, seldom polyphagia
occurs mainly in older people obese no ketoacidosis instead they can present with hyperosmolar nonketotic coma |
|
|
why is there seldom ketosis in type 2 DM?
|
because there is usually still some insulin produced
|
|
|
what is the cause of hyperosmolar nonketotic coma?
|
dehydration caused by osmotic fluid loss due to peeing off glucose.
|
|
|
contrast type1 and type2 DM?
|
type 1-
insulin dependent, onset less than 20 normal or decreased weight antiislet antibodies ketoacidosis 50%twin link HLA-D linked autoimmunity severe insulin deficiency insulitis, cell depleteion type 2 may or may not need insulin onset greater than 20 obese no anti islet Ab ketoacidosis is rare hyperosmolar nonketotic coma 90-100% twin concordance no HLA-D linkage insulin resistance relative insulin deficiency islet amyloid protien(amylin) no insulitis and atrophy |
|
|
what is MODY?
|
genetic defect in beta cell function
no beta cell loss defect in insulin secretion/production in response to elevations of plasma glucose AD inheritance onset usualy before 25 absence of obesity and autoantibodies |
|
|
what are the complications of DM?
|
cardiovascular
-atherosclerosis -microangiopathy ocular -cataracts -retinopathy renal -proteinuria -glomerular injury -renal failure neuropathy infectious disease |
|
|
what are the three key metabolic pathways that create complications from diabetes ?
|
non-enzymatic glycation-advanced glycation end products(AGEs)
activation of protein kinase C polyol pathways |
|
|
what are the products of nonenzymatic glycation?(AGE)
|
changes in:
hemoglobin collagen, connective tissue protiens, LDL, receptors, nucleic acids |
|
|
what is the mechanism of non enzymatic glycation?
|
glucose binds protein to create schiff base that turns into amadori product which turns into protein cross linked product
|
|
|
what is an implication of build up of AGE products?
|
all the age products increase cholesterol and free radical damage to endothelial cells this means the AGE products play a role in increased atherosclerosis in diabetes patients
|
|
|
How can we monitor AGE products?
|
Hb A1c 4-6% is normal any greater than 7% in diabetics is uncontrolled
|
|
|
What is the process of the protien kinase C pathway in diabetics?
|
hyperglycemia leads to diacylglycerol which increased PKC
PKC increases: proangiogenci molecules(VEGF) profibrogenic moelcules(TGF-beta) procoagluant molecules(PAI-1) pro-inflammoatory cytokines this creates an inflammed state that leads to free radical damage in tissue and increase deposition within vessel walls |
|
|
what is the cause of diabetic neuropathies?
|
polyol pathways
|
|
|
what is the polyol pathway?
|
hyperglycemia is turned to sorbital by aldose reductase
sorbital somehow reduces the amount of NADH in the cell which leads to inabitly to keep glutathione in a reduced form which makes it harder for cells to handle oxidative damage obviously this is most important in nerves that can't be regenerated. |
|
|
what occurs in the islets of infants of diabetic mothers?
|
increased islet mass
|
|
|
which type of diabetes is associated with reduced islet mass?
|
type 1
|
|
|
what are the cardiovascular complication of DM
|
accelerated atherosclerosis
ischemic heart disease vascular insufficiency in extremeities(this is why they lose finger and toes) abnomral clotting hyaline arteriolosclerosis microangiopahty, thickening of the basement membranes |
|
|
what are the renal complications of DM?
|
glomeruloar lesions
-capillary basement memberane thickening -diffuse glomerulosclerosis (increased glomerular caplillary permability) -nodular glomerulosclerosis (kimmelstiel-wilson disease) renal vascular lesions-due to atherosclerosis pyelonephirtis- due to decreased immune function |
|
|
why is there decreased immune function in DM?
|
damage to immune cells
neutrophils? |
|
|
what is the tipoff of kidney damage in DM?
|
microalbuminuria- 30-300mg in urine
usually seen around 10 year mark of disease |
|
|
why could somone in severe DKA have negative ketone bodies?
|
during DKA beta hydroxybutarate is the main form of the ketone bodies and our tests dont pick that up.
|
|
|
what is potassium level in acidosis? magnesium as well
|
elevated in serum bc body dumping it out of the cells
|
|
|
what is the most frequent cause of death in diabetes mellitus?
|
MI
|
|
|
why is MI high cause of death in diabetes?
|
DM causes accelerated atherosclerosis due to creation of a proinflammatory state.
|
|
|
what causes the atheroslcerosis in DM
|
glycation end products (AGES) and activation of protein kinase C
|
|
|
what is the cause of nerve issues like vision and loss of sensation in DM? also kidney
|
polyol pathway.
|
|
|
what cells do not need insulin to take up glucose and what is the implication of this with DM?
|
kidney,eye, nerves
in DM no insulin so high glucose enters these ares to much and causes damage |
