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Flashcards in Diabetes Deck (21):

Diffference between type 1 and type 2 diabetes

insulin dependent diabetes mellitus- type I; insulin therapy is required to prevent ketoacidosis

non-insulin dependent diabetes mellitus- type II; insulin therapy is not required


type I insulin insufficient

occurs at any age, characterized by the progressive inability of the pancreas to secrete insulin
-autoimmune destruction of beta cells(type 1A)
-LADA is slow adult type I diabetes
-if insulin is withdrawn, then ketosis and ketoacidosis will develop
-entirely dependent on exogenous insulin


Type 1A diabetes: immune-mediated

-cellular mediated autoimmune disease characterized by production of auto-antibodies causing B-cells destruction and insulin deficiency
-measuring of islet auto-antibodies can assist in diagnosis
- cause is unknown, perhaps genetics


Type 1B diabetes: idiopathic- diabetes of unknown origin

tests for islet cell antibodies will come up negative
-insulin deficiency and experience ketoacidosis, but injection of insulin comes and goes
-Asians, hispanics, african more likely to develop it
- cause is unknown


Type 2 diabetes mellitus

insulin is produced by body resist the effects
-develops slowly and progressively
-treated with lifestyle changes in diet, weight
-doesn't develop ketoacidosis or ketosis, but can happen under great stress



when blood glucose levels are higher than normal, but not high enough to be diagnosed as type 2 diabetes


IGT (impaired glucose tolerance) and IFG (impaired fasting plasma glucose)

When a disease process may be present, but not severe enough to cause hyperglycemia aka pre-diabetes


provisional diabetes

based on fasting plasma glucose: less than 5.6 is normal, greater than 7 is diagnosis


secondary diabetes mellitus

pancreatic disease such as pancreatitis CF and neoplasms
-endocrine disorders such as Cushing, hyperthyroidism (grave), acromegaly


MODY ( mature-onset diabetes of the young)

hereditary form of diabetes caused by mutation in a sex-dependent autosome dominant gene disrupting insulin production
-referred as monogenic diabetes since it involved other factors like genes and environment
- usually acts as Type I

Clinical presentation:
- significant hyperglycemia: increase thirst and urination
-usually have no symptom or sign, are diagnosed by accident


Gestational Diabetes Mellitus

-during pregnancy, like type II
-placental hormone and weight gain
- screened at 24-28 weeks
- infant can have metabolic abnormalities, stillbirth
- mother can develop type II in life


signs and symptoms of diabetes

1. polyuria- excessive urination; high glucose level, amount of glucose filtered by glomeruli exceed amount that can be reabsorbed by renal tubules- causes glycosuria ( glucose in urine) and dehydration
2. polydipsia- excessive thirst; dehydration as blood glucose level goes up
3. polyphagia- excessive hunger; type I common; low cellular stores of carbs, fat, protein



caused by damage to blood vessels of the retina, most common complication of diabetes
1. non-proliferative: blood vessels in eyes become larger and becomes blocked. Small amount of bleeding and fluid may leak into retina, cause eyesight problem
2. proliferative: more severe, new blood vessels start to grow in the eye, can fatigue and bleed the hemorrhage, vision loss



Diabetic nephropathy

persistent albuminuria, decline in glomerular filtration rate and increase blood pressure, cause of chronic renal failure
-mostly in type 2 diabetes
-hyperlipidemia:high lipid levels
-microalbuminuria: when kidney exhibits an abnormally high permeability for albumin
-cause is unknown


earliest cell abnormality of diabetic nephropathy

thickening of glomerular basement membrane and expansion of mesangial matrix. Change in basement membrane allows plasma protein to escape the urine, causing protenuria and development of hypotenomia.


Coronary artery disease

plaque and clot formation, stroke, high bp, leg and foot infection
-growth of yeast organism
-breakdown of fat, increase acid and chemical substances


hyperosmolar hyperglycemic state (HHS)

coma occurs because endogenous insulin suppresses ketone formation and prevents ketoacidosis
- results in persistent glycosuria with osmotic diuresis
-dehydration develops with high osmolarity and hemoconcentration of erythrocytes, proteins, and creatinine


oral glucose tolerance test

measures body's ability to store glucose by removing it from the blood


capillary blood glucose monitoring (glucometer)

fasting blood glucose test, random blood glucose test


glycated hemoglobin testing (glycohemoglobin)

hemoglobin A1C ( 120 days of RBC, hemoglobin becomes glycated)


Urine tests

assess kidney function, estimate glucose levels, detect complications such as kidney disease, infection, ketoacidosis, and cardiovascular condition. It can include visual, microscopic, test strip exams, culture.
Testing urine for sugar might be too late as patient already needs high blood glucose levels. Ketone is more effective