what is diabetes?
a group of metabolic disorders that affect the eye, kidney, nervous system and micro/macro vascular system
any cell that uses ____ will be affected by diabetes
type I diabetes affects who more commonly? what else can it be called? what HLA types are associated?
young caucasians are more at risk, (skips generations), in total 5-10% of diabetics. HLA DR3-4 are involved
what is the most commonly diagnosed diabetes type?
type II, insulin resistant
what are gestational diabetics in danger of?
becoming type II diabetic within 10 years
what are the symptoms of diabetes?
blurred vision, frequent urination, thirst
why does dr. allen theorize dark skinned people get diabetes more often?
cell membranes in warmer climates use more saturated fats/cholesterols b/c it holds up better under oxidizing sun rays, but these saturated fats also disrupt the actions of the insulin receptors
what does type I diabetes result from? can viruses or toxins be involved?
autoimmune destruction of pancreatic beta cells. rubella can cause type I diabetes, when body is responding to viral protiens, (some of which have homology with the pancreatic proteins, resulting in destruction of islet cells). people with certain HLA types in conjunction with certain toxins have a higher risk of type I diabetes
type 2 diabetes ultimately leads to 1 or more of what effects on the pancreatic beta cells?
underexpression of GLUT2
reduced glucokinase synthesis
“desensitization” of the beta cell, reduced pool of inositol, (2nd messenger), precursor
what is one way that pregnant women can become diabetic?
a protein called lactogen is produced by the placenta, which uses the same signaling pathway, the increased demand causes a lag in the cellular response to insulin
where are the 3 places insulin resistance can manifest?
preceptor, receptor, post-receptor
what are pre-receptor defects in terms of type II diabetes?
neutralizing antibodies floating around in the pts system before it even has a chance to bind to the receptor
what are receptor defects in terms of type II diabetes?
ligand-hormone binding problems, including membrane fluidity problems and more rarely: antibody to the receptor, defective receptors due to protease action, and low receptor numner
what are post-receptor defects in terms of type II diabetes?
improper membrane fluidity, defective signal transduction, (area of a lot of current rx focus)
what is the purpose of doing a c-peptide test?
to determine how much insulin the pt is making, independent of cellular response. sometimes due to insulin resistance, the pt is already putting out a lot of insulin with little to no response. giving them drugs to increase this output is not going to help
what is “essential HTN”?
when high insulin in the blood due to unresponsive receptors or drug action starts binding to alpha adrenergic receptors
what are the causes of hyperglycemia in type II diabetes?
increased glucose resistance, increased glucose secretion, impaired insulin secretion and decreased glucose disposal, (resulting in hyperuinsulinemia)
what are the 3 diabetes diagnostic criteria?
>2 fasting, (no oral intake for at least 8 hours), plasma glucose >126 mg/dl
>symptoms of diabetes+causal plasma glucose conc >200mg/dl
>2 hr PG >200mg/dl during an OGTT using 75g of glucose
what is another good diagnostic tool for diabetes testing?
the lyseine residue in hemoglobin A1 binds to glucose in an irreversible rxn, and this can be tested for
what are the criteria for pre-diabetes?
FBG 100-125 mg/dL
PBG 141-199 mg/dL
what are serious complicatios of type 2 diabetes?
retinopathy, abnormal ECG, absent foot pulse/ischemic feet, impaired reflexes/decreased vibration sense, MI/angina/claudication,stroke/transient ischemic attack
how does diabetes affect the vasculature?
its not just LDLs at fault, its what is in them that can worsen problems with plaque formation, b/c if oxidized fats are consumed, they will be recognized and attacked by the immune system, causing inflammation @ branching of arteries. the hard plaque can stimulate the formation of blood clots that can go other places + cause strokes etc.
is there a possible link between HSV and related oxidative stress and inreased inflammation around oxidized atherosclerosis
what is C-reactive protein?
a protein made in the liver in response to inflammation, can be used to test whether the pt has a higher possibility of becoming a diabetic down the road
is there a possible link between gingivitis and other chronic inflammatory problems leading to insulin resistance?
why might diabetics show high levels of TNF, (tumor necrosis factor -> inflammatory cytokine)?
it has the same method of transduction as insulin, similar problem with resistance
what are the 2 kinds of retinopathy?
simple and proliferative
what are some characteristics of proliferative retinopathy?
increased capillary permeability, (things leak out). pts see color, but little detail. microaneurysms, dialated veins, hard exudates
what is the sequence of diabetic retinopathy?
mild nonproliferative diabetic retinopathy, (NPDR)->moderate NPDR->severe NPDR->very severe NPDR ->proliferative diabetic retinopathy(PDR)
how does diabetes cause blindness?
endothelial cells in the blood vessels secrete VEGF, (vascular endothelial growth factor), in response to hypoxia, (due to glucose-bound Hb in diabetics). Vit C is excreted through the kidneys along with glucose due to high levels, and lack of Vit C causes problems with vessel integrity so the new vessels formed in the eye leak blood. when the scabs form, they tighten and can detach the retina
why does hypoxia occur in diabetes pts?
Hb A1 binds to glucose irreversibly in conditions of hyperglycemia
what is the first stage of kidney disease?
hyperinsulinemia provokes IGF1 action, (insulin like growth factor), tells the kidney to dump excess glucose. this extra exertion by the kidney causes it to grow larger
what is the second stage of kidney disease?
the glomeruli begin to show damage and microalbuminurea occurs, (albumin in the urine), due to glycosylated collagen in the basement membrane of the kidney capillaries
what is the third stage of kidney disease?
the albumin excretion exceeds 200 micrograms/minute and blood levels of creatinine and urea-nitrogen rise. increased creatinine means a lot of nephron cells are dead
nephropathy can be either diffuse or ______?
nodular, which refers to the widening of the glomerular basement membrane and mesangial thickening
what is ascites? what is the tx?
albumin contributes to oncotic blood pressure, when it is lost, (as is the case in diabetic kidney damage), blood pressure drops and fluid traves from intravascular to extravascular space ->”thirdspacing” in the peritoneal wall. treatment is with albumin if CV is ok, parasenthesis, (needle drain), if not
what causes “moon face”?
nephrotic syndrome
what does peripheral neuropathy affect?
it is numbness to touch, but gives the sensation of pain. it happens bilaterally in the arms and legs
what does autonomic neuropathy affect?
it affects the trunk, GI, CV, bladder dysfunction, ED/impotence
how does autonomic neuropathy affect the GI tract?
in the GI tract, nerve conduction/peristalsis is slowed=gas, and diarrhea from SCFAs and constipation is more likely
how does autonomic neuropathy affect the CV?
orthostatic hypotension, (pts get dizzy when they stand up from dropped BP). syncope. diabetics can also have an MI and never know due to reduced sensation.
what are some general nerve problems experienced by 60-70% of diabetics?
impaired sensation/pain in feet & hands. slowed digestion in stomach, carpal tunnel syndrome
what is a problem related to peripheral neuropathy in diabetes pts?
if they injure themselves, they may not feel it and it can become more infected. they heal slower b/c of microvascular perfusion.
risk factors for diabetes include:
glucose control
duration of diabetes
damage to blood vessels
mech. injury to nerves
autoimmune factors
genetic susceptibility
lifestyle factors
what is the main metabolic factor in terms of diabetic neuropathy? what are 2 others?
hyperglycemia. advanced glycosylation end products, (AGE) may be a trigger for the immune system to go after nerve fibers. ischemia, lack of oxygen to the nerve and nerve fiber repair mechanisms are slowed, (transcription of repair protiens may not occur)
how do foot ulcers occur on diabetic pt’s feet?
a callus develops, skin cracks, bacteria enter. lack of blood and defense at the area, low O2 tension -> ulcer
what needs to be measured in diabetic pts before they are put on insulin?
their own endogenous production of insulin as well as antibodies
what is the first step in treating diabetics?
non invasive tx, diet/exercise etc
what do thiazolidinediones and biguanides do? do they have side effects?
they activate the PPAR, (proxisomal proliferative activating receptor), molecules that increase the transcription of glucose transporters. one of them, (resalin), has caused hepatic carcinomas, and edema/cardiac complications are also an issue.
what do sulfonylureas and meglitinides do?
they provoke pancreatic cells to release proinsulin hormone which increases secretion, not production of insulin
what do alpha-glucosidase inhibitors?
these slow the absorption of starches, can be uncomfortable for pt, (gas)
what is byetta?
mimics incretin hormone which curbs appetite, somehow related to leptin, not as many side effects as TZDs
what is januvia?
depeptiyle peptidase IV inhibitor
what is amylin?
for type I diabetics
what is IFG2?
humolog, fast actin insulin which reduces blood sugar if taken right before a meal. has been proven to speed up complications with retinopathy/nephropathy
what is the sequence of therapy for diabetes type II pts?
diagnosis->therapeutic lifestyle change->monotherapy->combination therapy(oral rxs)->combination therapy(oral rxs w/insulin)
what does the combination of metformin and TZDs address in terms of the liver?
they work to reduce the glucose production in the liver, (metformin/glucophage improves hyperglycemia primarily through its suppression of hepatic glucose production).
what do the sulfonylureas address, (glucatrol and amaryl)
they work to increase insulin secretion when it is impaired in the pancreas, (when c-peptide level is low, insulin is low)
what do alpha glucosidase inhibitors do?
decrease postpranial glucose by inhibiting breaking off the glucose molecule from the polysaccarides entering the bowel
what is used when you have increased free FAs? why would diabetics have this?
TZDs. diabetics have an increase in free fatty acids due to unregulated hormone sensitive lipase that cleaves them trying to bring up the blood sugar level, (stimulated by epinephrine)
what does the combination of metformin and TZDs address in terms of the muscle?
they work against decreased glucose uptake/utilization in the muscle. Cr imitates metformin, unsure why
what should be ruled out when treating pts?
rule out the possibility of other hormones causing the insulin resistance, (like growth hormone, cortisol, and gluconeogenic hormones)
what state should be attempted to be preserved in tx of diabetics?
main goal is to keep euglycemic state normal
what should be controlled in terms of diabetic tx?
the blood lipid profile needs to be controlled, (hyperlipidemia contributes to insulin resistance)
how can the oxidative load be reduced?
diabetics should not be eating fried foods or be exposed to chronic inflammation, (also increases oxidative index, increasing blood glucose level)
what is a drug that can improve blood rheology, (correct tissue O2 levels)
trental: anti-TNF and improves proteinurea
why are supplements important to explore?
food today has less nutrients in it than in the past
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