Diabetes Flashcards
(26 cards)
type 2 diabetes in children
there is an increased amount, especially in america, related to food choices and environmental factors
Diabtes risk factors
age, ethnicity and family histroy, body weights, hypertension, dyslipidemia, metabolic syncdrom, gestational diabetes, PCOS, pre diabetic
Metabolic syndrom
increased risk fo diabetes and surrounding risks
central, visceral fat obesity, high BP, high triglycerides, low HDL cholesterol, insulin resistance
Testing criteria
have any risk factors, overweight w/ BMI over 25, 45 or older
Normal insulin physiology
meal ingested- increasing plasma glucose and amino acids- insulin is secreted, causing glucose uptake into muscle cells and adipocytes, glycogen synthesis, amino acid uptake and protein synthesis, triglyceride synthesis
peaks with meal times, hase constant basal, non 0 rate
Diabetes pathophysiology
Decreased insulin supply/use- decreased transport of glucose in cells causing cellular starvation causing
- fight or flight increase of cortisol, epinephrin, and growth hormone, leading to glycogen catabolis in liver and muscle leading to hyperglycemia
- protein catabolism and gluconeogenesis which leads to hyperglycemia
- Fat catabolism FFA and glycerol produces then causing ketones to be produced as a product of fat metabolism
impaired glucose tolerance
glucose peaks to high with eating, a sign of prediabetes
impaired fasting glucose
glucose is too high while fasting, sign of prediabetes
Type 1 diabetes pathopysiology
dysfunction of beta cells leading to alsolute deficiency of insulin
Type 2 diabetes
insulin resistance
Decreased insulin receptors or inability to bind to muscle and adipose cells leading to inability to transport glucose into cells
defect in pancreatic beta cell secretion
live pushes out too much glucose
Factos that contibute to hyperglycmeia
decreased insulin secretion i nthe pancreas
increased glucose reabsorption in the kidneys
neurotranmistter dysfunction in the brain
increased lipolysis of adipose tissue
decreased incretin effect in the digestive system
increased hepatic glucose production and decreased hepatic glucose uptake in the liver
decreased glucose uptake in muscle
Type 1 clinical manifestations
polyuria- excessive urination
polydipsia
plyphagia
hyperglycemia
ketonuria
weight loss, weakness, fatigue, dizziness
Type 2 clinical manifestation
3ps
blurry vision, skin infections, vaginitis
hyperglycemia
target organ damage
What are a1c level best for
seeing average blood sugars rather than immediate
fasting plasma glucose
prefferd diagnostic test
greater/equal than 126- diabetic
100-125 prediabetic
less than 100 normal
oral glucose tolerance test
only really used in pregnancy
a1C test
more than 6.5% diabetic
5.7-6.4 pre diabetic
less than 5.7 non diabetic
monitors amount of glucose stuck to red blood cells- increased makes blood sticky
test for assessing and managing diabetes
blood glucose
glucose tolerance test
A1C
ketonuria- ketones from metabolizing protein
proteinuria- increased from breaking down fat
BUN, creatinine, GFR
Diabetes complications
Erectile dysfunction
renal disease
peripheral neuropathy
retinopathy/ macular edema
autonimc neuropathy
hypertension
CV disease
dyslipidemia
gastropathy
PVD
diabetes treatment
glucose control
diet- lower lipids, lower cardiovascular risk
exercise- help lower BP, decrease strok risk
weight loss
diabetes medication
blood pressure control (ACE, ARBs, can also help kidneys)
blood lipidc ontrol
eye, kidney, feet, teeth, gums preventative care factors
aspirin
Glucose monitoring
plasma glucose in venous (most accurate)
capillary- typically lower, not as accurate
dexcom continuous monitoring
Glycemic control goals
a1c less than 7
pre-prandial glucose 90-130
postprandial less than 180
glycemic control in older adults
higher potential for hypoglycemia from over aggressive treatment can create more adverse effects than positive ones
impatient glycemic targets
critically ill: 140-180, tigheter in CABG or certain other populations
non-critically ill: glucose less than 180
