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patho CH41

Terms in this set (70)

Normal glucose homeostasis regulated by
1) glucose production in the liver
2) glucose uptake and utilization by peripheral tissues(skeletal muscle)
3) actions of hormones
normal glucose levels
70-120mg/dl
function of insulin
to increase the rate of glucose transport into certian cells of the body
why type 2 diabetics can need insulin
if the pancreas keeps churning out insulin over time, it will eventually degrade and stop
only ___ hours of reserve glucose in the liver
10
gluconeogenesis
formation of glucose from excess amino acids, fat, and other noncarbohydrate sources
glycogenesis
formation of glycogen
lipogenesis
formation of fats
glycogenolysis
process that converts glycogen to glucose
glycolysis
hydrolysis of glucose to pyruvate
lipolysis
catabolic degradation of triacylglycerol
pancreas alpha cells
glucagon
pancreas beta cells
proinsulin
pancreas delta cells
somatostatin(supressed insulin and glucagon)
Pancreas F cells
pancreatic polypeptide
pancreas epsilon cells
make ghrelin, which causes hunger
Insulin effect on fat
increased glucose uptake
-increased lipogenesis
-decreased lipolysis
insulin effect on muscle
increased glucose uptake
-increased glycogen synthesis
-increased protein synthesis
insulin effect on liver
decreased gluconeogenesis
-increased glycogen synthesis
-increased lipogenesis
Hormonal regulation of glucose
-glucose-dependent insulinotropic polypeptide(GIP)
-glucagon-like peptide 1(from cells in the gut. stimulate the production of insulin and inhibit glucagon)
effect of insulin
lower glood glucose
effect of glucagon
increase blood glucose
cortisol and adrenal corticosteroids effect
increase blood glucose
epinephrine effect
increase blood glucose
growth hormone effect
increase blood glucose
thyroxine effect
increase blood glucose
somatostatin effect
inhibits insulin and glucagon
GIP effect
stimulates insulin release
fed state
glucose provides primary energy source Amylin acts on area postremia

INSULIN dominates
Fasting state
glucose is produced by glycogenolysis and gluconeogenesis

GLUCAGON dominates
exercise regulation of glucose metabolism
initially insulin levels drop and glucagon and catecholamine levels rise
why polyuria in diabetes
too much concentrated glucose in blood, results in pulling fluid from cells into blood to dilute it. this increase in fluid volume is excreted .

kidneys can only reabsorb so much, so some glucose is excreted
why polydipsia in diabetes
because the cells are dehydrated due to their water going into the blood, therefore the body increases thirst to make up for it
why polyphagia in diabetes
because the body isint taking up the glucose, brain thinks body is hungry because the cells are not getting nutrients
stress regulation of glucose metabolism
production of stress hormones(corticosteroids and catecholamines) increase production of glucose
-increased production of FFA
-lead to hyperglycemia
who has diabetes mellitus
16 million in the USA
-1 million/year
-50k people die of it per year in the USA
How do you diagnose DM
-more than one fasting glucose level(>126)
-elevated plasma glucose in response to an oral glucose tolerance test(>200)
-polydipsia, polyphagia, polyuria
some signs and symptoms of diabetes
always tired
crave extra liquids
frequnt urination
numbness and tingling of feet(damage to small blood vessels
-always hungry(cant uptake nutrients)
-unexplained weight loss(cant uptake nutrients)
-blurred vision(lens of eye can uptake ecess glucoe, causing swelling and blurry vision, also increased glucose can damage the small blood vessels of the eye)
-sexual dysfunction(damage to small blood vessels)
Type 1 diabetes
genetic
autoimmune
childhood(juvenile) onset
-antibodies to beta cells, unsulitis
-beta cell depletion from antibodies
-NON OBESE patients
type 2 diabetes
genetic, but different from type 1
-NOT autoimmune
-adult or maturity onset
-insulin may be low, BUT, peripheral resistance to insulin is the main factor
-OBESE patients
gestational diabetes
-onset
-cause
-treatment
pregnancy(peak at fifth or sith month gestation)
-insulin resistance during pregnancy as a result of too much hormone production in the body(for the placenta); inability to make the additional insulin that is needed during pregnancy
HLAs
expression of certain HLAs is associated with increased susceptibility to type I diabetes
Viruses
are considered initiating factors in autoimmune cause of type I diabetes
Insulin resistant
can be due to malfunction in insulin receptor, but the cause is not known
antibodies to insulin receptor
in type II diabetes
glucose transport
low levels of glucose transporters in type I and II diabetes
Type 2 DM
resistant to the action of insulin
-very common: many undiagnosed cases
interactions of metabolic, genetic & environment
-obese patients
type 2 DM risk factors
high BMI(intra-abdominal obesity), family history of DM2, ethnic minority, female gender
ketones in blood because
glucose cant get into cells, body needs energy so it breaks down fat, a byproduct of which is production of ketones. ketoacidosis can lead to a ketoacidosis coma
MODY
maturity onset diabetes of the young
-multiple types
-2-5% of diabetics
-primary beta cell defects
-multiple genetic mechanisms, especially GLUCOKINASE mutations
complications of diabetes mellitus
retinopathy, neuropathy, anginopathy, nephropathy, infection(bacteria like sugar, prone to infection), hyperlipidemia and atherosclerosis(damage to blood vessel wall leads to this), HYPOGLYCEMIA(insulin shock/too much insulin)
-diabetic ketoacidosis(too little insulin)
-protein glycation
microvascular disease complication of DM
capillary basement membrane thickening-ischemia
-retinopathy
-diabetic nephropathy
macrovascular disease complication of DM
unrelated to the severity of disease-causes much morbidity & mortality; glycosylated end products & high serum lipids cause atherosclerosis-ischemia
-coronoary artery disease
-stroke
-peripheral artery disease
diabetic neuropathies complication of DM
most common complication in western countries, nerve cell damage- more sensory than motor
infection complication of DM
sensory impairment, hypoxia(glycosylated RBCs), increased pathogens like glucose, decreased blood supply, abnormal WBCs
protein glycation
nonenzymatic inding of free amino groups of proteins to glucose and other sugars
-protein glycation commonly occurs in RBCs, glumeruli, nerve cells, and other tissues
-extent of protein glycation is proportional to extracellular glucose concentration
-excessive glycation causes alterations in protein's physical and biochemical properties
-new research suggests that many diabetes complications are caused by glycation of specific proteins
protein glycation is measured by
excess glucose adds glucose to sugars. measured by A1C. want low A1C
Functional test in diabetes
postprandial plasma glucose
-oral glucose tolerance test
other tests in diabetes
-glucose
-glycated hemoglobin
-albumin(protein)
-insulin
-keto acids
-hydrogen ion
-electrolytes
-osmolality
-blood fluid volume
-anion gap
-BUN
-lipids
hyperosmolar nonketotic coma
TYPE 2 coma. blood sugar too high, pulling fluid from cells into vascular space.

volume eventually falls too low(polyuria), pressure falls too low, results in coma
postprandial plasma glucose
a high in carbohydrate meal is used(75g glucose drink is preferred) as carbohydrate load
-plasma glucose is measured 2 hours after carbohydrate ingestion
-two postprandial tests with glucose levels >200mg/dl are suggestive of diabetes
Oral glucose tolerance test
-carb intake is controlled 3 days before test
-glucose load is 40g glucose/m^2 body area
-blood glucose is measured 2 hours after glucose load
-glucose level >200mg/dl is suggestive of diabetes
fasting plasma glucose
repeated elvels>126mg/dl...strongly suggests diabetes
-100-126-impaired fasting glucose
-increase in fasting plasma glucose is directly proportional to severity of diabetes mellitus
urinary glucose
renal threshold for glucose is 180g/dl, in diabetics it is increased to 300mg/dl
insulin level Type 1 diabetics
fasting plasma insulin is low
know epected values
.
Type II diabetics
fasting plasma insulin is normal, it is high if plasma glucose >250mg/dl
How to treat it
-exercise, dont eat as much, metformin(type 2, targets liver and makes sure liver doesnt undergo gluconeogenesis)
-increase pancreas' secretion of insulin
-tzd-causes cells to be more sensitive to insulin
keto acids
measured in both blood and urine
-plasma keto acids may be normal even though urinary keto acids are high, this is due to increase urinary excretion of keto acids from renal compensation to low pH
-controlled diabetics should have both normal plasma and urinary keto acid levels.
albumin
urinary protein that is one of the earliest signs of glomerular nephropathy
-albumin/creatinine>20-30mg/day suggest microalbuminuria
-without intervention>macroalbuminuria(>300mg/day)
-leading cause of end stage renal disease in the US
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