Term
|
Definition
polyuria, pyolydypsia, polyphagia (due to losso f calories in urine), weight loss, blurred vission (sorbitol).
muscle fatiugeg and cramps, parathesias. |
|
|
Term
| cretira for diagnosis of DM |
|
Definition
FPG >126
casual glucose > 200
Glucose tolerance > 200.
(hba1c more than 6.5) |
|
|
Term
| impaired glucose tolerance |
|
Definition
fasting between 1010-126
imparied lucose tolerance between 140 and 200.
hba1c betwen 5.7 and 6.5 |
|
|
Term
| causes fo hyeprglycemia in diabetes |
|
Definition
liver produces glucose inapparopriately. Insulin normally represses liver glucose produciton, impaired insuli secretion prevents this. This also meansi mpaired taking up of glucose after meal
so when fasting= liver is dumping too much glucose
postprandially= impaired idsposal of glucose and uptake. |
|
|
Term
| pancreatic destruciton causes |
|
Definition
pancreatitis, rubella, cytomegalovirus,
cystic fiborsis, hemochromatosis. |
|
|
Term
|
Definition
| absolute insulin defficiency. with acute onset of symptoms |
|
|
Term
| whcih diabetes dtendnecy to young age |
|
Definition
|
|
Term
| which diabetes is ketosis prone |
|
Definition
| type I (fatmeatbolism is impaired a s well) |
|
|
Term
| which diabetes common among caucasian |
|
Definition
|
|
Term
| familial risk of type I DM |
|
Definition
|
|
Term
|
Definition
| insulin atnibodies, apncreatic Islet cells |
|
|
Term
| HLA dr 3 and 4 associated wdith |
|
Definition
|
|
Term
| environemtnal stimuli for TYpe I DM |
|
Definition
|
|
Term
| antibody levels in type I DM |
|
Definition
| may not be elveated if al latnigen is gone |
|
|
Term
| beta-cell / insulin decrease |
|
Definition
| beta cell levers go down slower than insulin levels due to comepnsation by beta cels |
|
|
Term
| ilnesses and insulin levels in tYpe I DM |
|
Definition
| patient may be briefly symptomatic during illness, and then may go back up to normal |
|
|
Term
| Type I diabetes symtpom manifestation |
|
Definition
| only once patient dips below critical insulin levels. |
|
|
Term
| older patinets suffer from which DM |
|
Definition
|
|
Term
| Dm with strong genetic componenet |
|
Definition
|
|
Term
| genetics of type II diabetes |
|
Definition
| insulin esitancei s autosomal dominant. |
|
|
Term
| biggest risk factor for Type II diabetes |
|
Definition
|
|
Term
|
Definition
| benign obesity , normal abdmoinal fat stores with chidlhood onset. , few associated metabolic abnormaliteis |
|
|
Term
|
Definition
| metabolic obesity, increased abdominal fat. Adult weight gain, multipl asosciatedm etabolci abnormalities. |
|
|
Term
| pathogenesis of insulin sydnrome |
|
Definition
abnormal insulin sensitity and secretion leads to hyperinsulinemia which leads to obesity. which leads to insulin resistance syndrome/metbolic syndrome.
Exacerbated by inactvitiy. |
|
|
Term
| Diagnosis of Metabolic syndrome |
|
Definition
look at waist circumference.
also elevated TG, cholesterol, BP, and FPG. |
|
|
Term
| CVD risk rpogresison adn DM |
|
Definition
| happens prior to DM. patietns with emtabolci sydnrome already ahve increased CAD risk |
|
|
Term
| progression to type II DM |
|
Definition
| abnormal insulin sensitivy leads to icnreased insulin production which leads to central obesity leading to insulin resistance syndrome, Eventually **progressive loss of Beta cells** occurs due toh igh gluose and FFA, this leadt o imparied glucose tolerancea nd diabetes mellitus. |
|
|
Term
| Dm is acontinuum, levels keep getting proogressively worst. |
|
Definition
|
|
Term
| hyperglycemia relationship to beta cells and muscles |
|
Definition
gulcose is toic to beta cells leading to insulin deficiency.
Hyperglycemia leads to insulin resistance, by downregulating glucose receptors, more insulin needed to maintain these receptors, since less receptors are required for the same amoutn of glucose to enter muscls |
|
|
Term
DKA VS. NKHC
common age
symptom duration
glucose level
sodium level
bicarb level
Ph level
ketone
Serum Osm
mortality rate |
|
Definition
Diabetic ketoacidosis:
age: less than 40
symptoms: less than 2 days
glucose level: less than 600
sodium level normal or low
bicarb level less than 15
Ph level less than 7.35
ketone present
Serum Osm less than 320
mortality rate 3-10 percent
NKHC:
common age more than 40
symptom duration more than 5 days
glucose level more than 600
sodium level normal or high
bicarb level more htan 15
Ph level more than 7.3
ketone absent
Serum Osm mroe than 320
mortality rate 10-20 percent |
|
|
Term
| signs and symtposm of DKA |
|
Definition
| polyuria, polyphagia, weight loss, abdominal pain nausea vomitting. kussmal respirations (to alleviate acidosis). Fruity odor to breath. dehydration, tachycardia and hypotension and luekocytsosis |
|
|
Term
| hormonal changes in DKA nad. NKHC |
|
Definition
decreased insulin concentration/action, increased glucagon (further stimulating ketone formation)
increased catecholamines (from dehydration and acidosis, icnreased glucose production and lessu tilziation). |
|
|
Term
|
Definition
due to low glucagon/high insulin- insulin is resposnbily for fully metabolziing FFa.
ketons are partially metabolized FFA |
|
|
Term
|
Definition
Dehydration: caused by icnreased glucose levels and nausea/vomitting (vomitting due to acidosis)
increased glucose - due to increased glucagon, reduced insulin and increased catecholamines
Catecholamien activation: due to dehydration.
Acidosis- due to incomplete lipolysis.
and glucagon stimualting further ketone formaiton
lipolysis: due to low insulin levels (decreased glucose utilization) and increased catecholamines. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| high due to unmeasured acids- acetoacetate |
|
|
Term
| corrected sodium calcualtion |
|
Definition
| sodium plsu 1.6 per 100 mg/dl glucose due to fluid suckd out of cels causing dilutiional hyopnatermia |
|
|
Term
|
Definition
2(sodium plus potassium plus (glucose/18))
urea is freely permeable across cell. Omsolalliaty is what is correlated with mental function |
|
|
Term
| rsponsiveness of pathways to insulin |
|
Definition
- increased plasma flux into cells causing hypokalemia
-lipolysis inhibition
-hepatic glucose output
-peirpheal glucose disposal |
|
|
Term
| DKA vs. hyperosmolar with regard to insulin levels and dehydration |
|
Definition
much lessi nsulin si requierd to control fat metabolism than glucose metabolism, in NKHC, fat metabolism is under control, so we do not see symptoms .
DEHydration- rapid onset of hyperosmolarity inhibits lipolysis- another reason why we dont see ketones in NKHC |
|
|
Term
| NKCH more common in which diabetes |
|
Definition
|
|
Term
| DKA more common in which diabetes |
|
Definition
|
|
Term
| Diabetic complications overview |
|
Definition
Microvascular: retinopathy, neuropathy, and nephropathy
macrovascular complications (accelerated atherosclerosis): stroke, heart disease, peripehral vascular disease |
|
|
Term
| complciation of DM occur in tissues that dont require insulin for glucose uptake |
|
Definition
| they readily aborb glucose better without insulin present, insulin dependant tissues cant, so the glucose increases to compensate so they can stil labsorb. |
|
|
Term
| msot common complication of DM |
|
Definition
| cardiovascular complications followed by renal |
|
|
Term
|
Definition
| due to peripheral ascualr disease and neuropathy |
|
|
Term
|
Definition
micoanuerrsysm and hard exudates of protein secondary to capilalry leakage
eventually proliferative retinopathy hapepns with enovascularization- (ischemai causign growth of new blodo vessels) |
|
|
Term
| first manifstation of diabetic nepropathy |
|
Definition
| proteinuria, which wil lthen be follwod by decreased in creatinine clearance. |
|
|
Term
| 3 types of diabetic neuropathy and features |
|
Definition
diffuse sensonry motor:
universal in almost all diabetics, all senses , with a stockign glove distrubtion.
mononeruopathy: crnial nerves (occlusion in microvasculature)
radiculopathy
autonomic neuropathy- heavy mortaltiy asosciated with this.
not on slides but mentioned:
heavily associated with mortality- leads to delayed gastric emptying, gastroparesis, orhotsatic hypoetnsion and prdisposition to cardiac arrythmias |
|
|
Term
| etiology of DM complications |
|
Definition
sorbitol and fructose accumulation
endothelial dysfunction-
nonenzymatic glycosylation |
|
|
Term
| sorbitol mechanism of damage |
|
Definition
| glucose gees itno cells gets converted into sorbitol and fructose- gets trapepd in celsl causing osmotic damge as wel las decreasing uptake of myoinostol- ingeral for cel membranes |
|
|
Term
| nonenzymatic glycolastion |
|
Definition
| glycosaylation alters structure/funciton of peptidesthat have amino groups. |
|
|
Term
|
Definition
| noneznymatic glycolastion of rbcs. |
|
|
Term
| PKC-B has a role in what DM |
|
Definition
| has a role in micorvascular disease |
|
|
Term
| early changes in diabetes |
|
Definition
endothelial dysfunciton, icnreased blood flow
bm thickening
increased permeability of BM |
|
|
Term
| lowering glucose most useful in reducing: |
|
Definition
| microvascular ocmplacaitons not MACROvascular |
|
|
Term
|
Definition
| less tha n7 or less than 6.5 |
|
|
Term
|
Definition
type 2: similar to any health ydiet, main goals are weight control and athersclerotic cardiovascular disease. includes limiting fat and calories and sugar.
type I: match insulin peacks with carb intake, minimize post meal hyperglycemia and carb countin. prvent atherosclertoic vascualr disease |
|
|
Term
| excercise effect on diabetics |
|
Definition
| increases insulin levels and decrases glucose levels |
|
|
Term
|
Definition
| 50 percent basal, 50 eprcent meal related |
|
|
Term
|
Definition
either pumps ,pancreatic trnasplants and islet cell transplant.
both translpatns require immunosupresison |
|
|
Term
| goljan card: diabetes is the most common cause of |
|
Definition
| blindness, below the knee amputation, and peripheral neruopathy. |
|
|
Term
| maturity onset diabetes of the young features |
|
Definition
| AD inheritance <25 and NOT obese, due to imapired glucose induced secretion of insulin. |
|
|
Term
type I and II comparison:
speed of onset
body habitus
genetics
associations
pathogenesis |
|
Definition
pseed of onset of type I is rapid, speed of onset of type II is insidious
body habitus of type I is thin, of type II is obese
genetic association of type I is HLA-DR3 and dr4
association of TYPe I is other autoimmune disease |
|
|
Term
| reactive hypoglycemia can be an early finding of |
|
Definition
|
|
Term
| Goljan: metabolic sydrome physical finding and disease association |
|
Definition
| acanthosis nigricans and alzheimers disease. |
|
|
Term
| goljan effect of obesity on insulin |
|
Definition
| downregulates isnulin receptor causing inuslin resistance and excarbating it |
|
|
Term
| goljan: role non enzymatic glycosylation in diabetes |
|
Definition
| increases vessel permeability to proetins , Hyaline arteriosclerosis, and produciton of hba1c |
|
|
Term
| goljan: enzyme converting glucose to soribtol |
|
Definition
|
|
Term
| Goljan: DM osmotic damage areas of affect |
|
Definition
| retinopathy, cataracts ,and nueorpathy |
|
|
Term
| most common complciation of TYE I DM |
|
Definition
| insulin idnucedh ypoglycemia |
|
|
Term
| goljan:mostimportant mechanis of hyperglycmeia in DKA- |
|
Definition
| increased gluconegoenesis due to decresed insulin and inresaed glucagon and epineprhine |
|
|
Term
|
Definition
| Acetyl CoA derived from b-ox of fatty acids |
|
|
Term
| mechanism of hypertrichlyeridemia in DKA |
|
Definition
| decrased insulin decrases capillary LP lipase, decrasing lipolysis of chylomicrons and vldl - (different from adipose tissue lipolysis, which is stimualted by lack f insulin) |
|
|
Term
|
Definition
leads to hyeprkalemia- due to protons going into itnracelluar space in exchagne for potassium going out, and lack of insulin effect shutnign potassium into cells
however Total body poatasisum is actually reduced, due to urinary excretion. |
|
|
Term
| Goljan:GEstational diabetes |
|
Definition
| anti insulin effect of human placental lactogen (HPL0, cortisol and progesterone) |
|
|
Term
| newborn risks of diabetic mother:hyperglycemis |
|
Definition
macrosomia- hyperglycemia in newborn causes icnresaed insulin releas, and fat store accumulation as aresult, and msucle stoers.
Respiratory distress sydnrome- insulin inhbiits surfactant produciton.
neonatal hypoglycemia- due to increased insulin driving glucose down |
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|
