Home
Browse
Create
Search
Log in
Sign up
Upgrade to remove ads
Only $2.99/month
241 exam 2 Diabetes
STUDY
Flashcards
Learn
Write
Spell
Test
PLAY
Match
Gravity
Terms in this set (41)
Blood glucose
-glucose via circulation required for brain and nervous system function
-blood glucose levels vary throughout the day
Glycogenolysis
breakdown of glycogen to release glucose
Gluconeogenesis
synthesis of glucose from amino acids, glycerol, and lactic acid
Glycogen
major stored carbohydrate
Glycerol
an alcohol that is a component of fats
Glucagon
hormone produced by the alpha cells in the pancreas
- stimulates conversion of glycogen to glucose by the liver
Blood Glucose
2/3 of glucose ingested is stored as glycogen in liver
*glycogenolysis and release of glucose occurs between meals
Liver can synthesize glucose
-gluconeogenesis
-from amino acids, glycerol, and lactic acid
Actions of insulin
glucose from blood moves inside cells for energy needs
-certain tissues require insulin for glucose transport into cells
-promotes glucose uptake by target cells; glucose storage; protein synthesis
-prevents or inhibits fat and glycogen breakdown; gluconeogenesis
Counter regulatory mechanisms
Hormones secreted to counteract hypoglycemia
-Glucagon
*secreted by alpha cells in pancreas as blood glucose falls
*increases glycogenolysis, gluconeogenesis, lipolysis
Epinephrine
-secreted from adrenal medulla in stress, hypoglycemia
-inhibits release of insulin
-mobilizes stored glycogen and fatty acids to conserve glucose
Growth hormone
-secreted from anterior pituitary in exercise, fasting, stress, trauma, and low blood glucose
-opposes use of glucose for energy
Glucocorticoid hormones
Cortisol
-secreted from adrenal cortex in hypoglycemia due to fasting, starvation, stress due to infection, pain, surgery, anxiety, prolonged exercise
-gluconeogenesis by liver
-reduced tissue use of glucose
Measures of blood glucose
Fasting blood glucose
- 80-100 mg/dl- normal
100-125- impaired
Over 125- diabetes
-random (casual) blood glucose
>/= 200 mg/dl diabetes
Diabetes Mellitus
"the running through of sugar"
-disorder of carbohydrate, protein, and fat metabolism
-imbalance in insulin availability and insulin need
-when uncontrolled- glucose can not enter fat and muscle cells causes hyperglycemia and cellular "starvation"
Type 1
absolute insulin deficiency
-autoimmune (type 1a) or idiopathic (tybe 1b)
-catabolic disorder- breakdown of body and protein...weight loss
-ketosis- ffa from fat cells release and convertes to ketones by liver
-required exogenous insulin replacement
Type 2
-Fasting hyperglycemia despite availability of insulin
-more common in older persons who have upper body obesity--increases ff.
-impaired insulin secretion, increased glucose production by liver and resistance to insulin (burnout of beta cells)
Epidemiology of diabetes
-sixth leading cause of death
-39% increase in adult diabetes between 1990 and 2000
-18 mil affected in 2003- 22 million in 2025
-70% rise in 30-39 yr olds
-costs > $132billion/ year
Metabolic syndrome
-syndrome caused by obesity and lack of physical exercise
-insulin resistance
-increased triglycerides
-decreased HDL's
-central obesity
-hypertension
-increased c-reactive protein
Secondary diabetes mellitus
-Endocrine disease: Acromegaly (GH), Cushing's (cortisol), pheochromocytoma (epinephrine)
-drug associated
-pancreatitis, cystic fibrosis
Gestational diabetes
-diabetes during pregnancy
-glucose intolerance in 1-14% of pregnancies
-Risk factors of GDM:
*family history of diabetes
*glycosuria
*large or heavy-for date infant
*obesity
*advanced maternal age
*Hx of miscarriage or fetal anomalies
Consequences of uncontrolled GDM
-complications in pregnancy
-increased mortality
-fetal abnormalities- marcrosomia, hypoglycemia, hypocalcemia, hyperbilirubinemia, etc
-increased maternal risk for developing diabetes
Manifestations of diabetes mellitus
-Rapid (type 1) or insidious (type 2) onset
-Three Polys-
*polyuria- glycosuria and water loss
*polydipsia-intracellular dehydration
*polyphagia-cellular starvation
Type 1 manifestations
weight loss, vomiting, lethargy (DKA)
Type 2 manifestations
obesity, blurred vision, fatigue, parathesias, skin and vaginal infections
Diagnosing and monitoring of diabetes
-Fasting blood glucose >125 mg/dl
-Random blood glucose >200 mg/dl
-Glucose tolerance test 2hr postload glucose >/= 200mg/dl
-glycosylated hemoglobin test
*A1C
*normal 4-6%
*<7% recommended in diabetes
Acute complications of diabetes
-diabetic ketoacidosis
-hyperglycemic hyperosmolar state
-hypoglycemia (insulin shock)
Diabetic ketoacidosis
-ketone (energy) production by liver exceeds cellular use and renal excretion
-more common in type 1
-common at onset of disease
-precipitated by infection, emotional/physical stress
-increased ffa causes increased ketone production by liver
-ketoacids cause metabolic acidosis
-characterized by hyperglycemia, ketosis, and metabolic acidosis
Manifestations of DKA
-hyperglycemia (over 250mg/dl)
-onset: SLOW- 1-2 days of polyuria, polydipsia
-nausea and vomiting
-fatigue, lethargy, stupor
-abdominal pain and tenderness
-may progress to coma
-breath has fruity smell
-skin warm and dry
-hyperventilation (Kussmaul's respirations)
-tachycardia
total potassium depletion may occur due to polyuria and vomiting
-serum potassium may be normal or high. Why?
-What will happen when acidosis is reversed?
Hypoglycemia
-blood glucose less than 45-60 mg/dl
-most common in type 1
-caused by any situation with too much insulin and not enough food
-rapid onset of manifestations reflect glucose needs of the nervous system
-give concentrated sugar, glucagon
manifestations of hypoglycemia
-headache
-confusion
-coma
-tremors, shakiness
-seizures
-anxiety
-tachycardia
-cool, moist skin
dizziness
-hunger
Hyperosmolar hyperglycemic state
-high plasma osmolarity (electrolyte-water balance)
-high blood glucose (>600 mg/dl)
-dehydration
-no ketoacidosis
-depressed sensorium, coma
-seen in type II diabetes only
-caused by increased resistance to insulin effects and excessive carbohydrate intake
-dehydration of brain cells causes neurological S&S's
-may be mistaken for stroke or intoxication
Somogyi effect
-counterregulatory hormones secreted after insulin-induced hypoglycemia
- "hypoglycemia brings rise to hyperglycemia"
- in addition- insulin resistance develops
Dawn phenomenon
increased levels of fasting blood glucose between 5am and 9am
-caused by increase in growth hormone in early AM
-may combine with Somogyi effect to produce profound hyperglycemia
Chronic complications
-microvascular disorders
*neuropathies
*nephropathies
*retinopathies
-macrovascular disorders
*coronary artery disease
*cerebrovascular disease
*PVD
-foot ulcers
-incidence can be greatly reduced by intensive diabetic treatment
Microvascular complications
-occur in insulin-dependent tissues that do not require insulin for glucose to enter cells
*lens, kidneys, nerves, blood vessels
Pathogenesis:
-glucose--sorbitol--osmotically active--swelling, opacity in lens
-abnormal glycoproteins cause structural defects in basement membrane of small vessels
-decrease in oxygen delivery
Neuropathies
mechanism
*ischemia of vessels supplying oxygen to nerves
*impairment of nerve conduction due to demyelinization
-Peripheral
*loss of feeling, touch, position sense (falls, burns, injury)
-impaired GI function
-postural hypotension
-bladder disorders
-30-60% male diabetics have impotence
Diabetic nephropathies
-leading cause of end-stage renal failure
-causes- thickening of capillary basement membrane in glomerulus
*diffuse sclerosis
*nodular glomerulosclerosis
RF for nephropathies
genetic predisposition, HTN, poor glycemic control, and smoking
-proteinuria causes loss of plasma proteins, edema
-can result in complete renal failure
Retinopathies
-diabetes is the leading cause of acquired blindness in the US
-causes vascular permeability in retina, microaneurysms, hemorrhage, neovascularization, scarring, retinal detachment
-without good blood glucose control
*after 20 years with type 1- 100% have some degree of retinopathy- 50% with some loss of sight
-*after 20 years 60% of those with type 2 have retinopathy
Macrovascular complications
CAD, cardiovascular disease, cerebrovascular disease, PVD
-risk is two to four times higher in diabetics
-50 to 75% of type 2 diabetics will die from a microvascular complication
Diabetic foot ulcers
-due to effects of neuropathies (decreased pain sensation) and vascular insufficiency
-reason for over one half of all non traumatic amputations of lower extremities
YOU MIGHT ALSO LIKE...
Nursing 121 Diabetes Nursing Management in Alterat…
44 terms
patho CH41
70 terms
Pathophys, Exam 2: Diabetes Mellitus (9.15)
82 terms
Integrated Pathophysiological Concepts
78 terms
OTHER SETS BY THIS CREATOR
Thea241 exam 2
78 terms
241 exam 2 AIDS
26 terms
NURS241 exam 2 acid/base balance
35 terms
241 Exam 2 neoplasia
58 terms