Diabetes Mellitus Flashcards
glycogen
stored glucose
glycogenesis
formation of glycogen
glycolysis
breakdown of glucose by enzymes
gluconeogenesis
reverse of glycolysis (formation of glucose)
glucose metabolism
glycogen, glycogenolysis, gluconeogenesis
fat metabolism
lipolysis, metabolic acidosis, ketoacidosis
lipolysis
breaking down of triglycerides to fat
glycogenolysis
breaking down stored glucose from glycogen
protein metabolism
proteins broken down to amino acids
insulin
lowers blood glucose levels
-causes glucose uptake by target cells
-stores glucose as glycogen or fat
glucose-regulating hormones
insulin, somatostatin, amylin, gut-derived hormones
-glucagon, epinephrine, GH, glucocorticoid
alpha cells in pancreatic langerhans
secrete glucagon
beta cells in pancreatic langerhans
create insulin
delta cells in pancreatic langerhans
secrete statin
glucagon with glucose, fat, protein metabolism
glucose:
-glycogen breakdown
-increase gluconeogenesis
fat:
-adipose lipase makes fatty acids usable for energy
proteins:
-increased amino acid uptake by the liver
-amino acids>gluconeogenesis>glucose
insulin with glucose, fat, protein metabolism
glucose:
-increase transport to muscle, fat tissue
-glycogen synthesis
-decreases gluconeogenesis
fat:
-triglyceride synthesis by the liver
-increased fatty acids into adipose cells
-converts fatty acids to triglycerides
-stores fat by stopping triglyceride breakdown
proteins:
-amino acids go into cells (AT)
-increase protein synthesis
-decreases protein breakdown
insulin-dependent glucose transporter (GLUT-4)
insulin binds to insulin receptors>intracellular signal>GLUT-4 receptor comes to cell membrane>glucose is transported
classifications of diabetes mellitus
prediabetes
type 1
type 1
gestational
DM from other causes
prediabetes (type 2)
blood glucose is elevated but not enough for a diagnosis
-IFG 100-125 mg/dL
-IGT 140-199 mg/dL (2 hour test)
treated with lifestyle modifications
diabetes mellitus type 1
total lack of insulin-beta cells destroyed
-glucose won’t enter muscle or fat tissue
-autoimmune
-decreased glucose uptake
-hyperglycemia
treated with insulin injections, diagnosed usually in childhood
diabetes mellitus type 2
dysfunctional beta cells-impaired insulin
-defective insulin receptors
-insulin destruction before effective
-beta cell exhaustion/dysfunction from hypertrophy (become atrophic)
-genetic component and obesity/inactivity
-hyperglycemia
-increased glucose output by liver
treated with diet/exercise, medication
type 1 and 2 manifestations
3 Ps:
-polyuria from osmotic diuresis (excessive H20 loss)
-polydipsia from dehydration
-polyphagia from hunger (fat, protein broken down for energy)
fatigue, paresthesia (tingling), infections
type 1 manifestations
nausea, severe vomiting, abdominal pains and cramping
type 2 manifestations
muscle wasting, blurred vision, hand and foot numbness/tingling, dry skin, slow healing of skin damage
diagnostic testing
HbA1c >/= 6.5%
FPG >/= 126 mg/dL
2 hour PG >/= 200 mg/dL
random glucose >/= 200 mg/dL (hyperglycemia)
type 1 vs type 2 onset
type 1:
-childhood, younger age
-abrupt symptoms
-recent weight loss
-uncommon family history
-autoimmune
-early or late islet problems
-almost no beta cells
-almost no insulin
-insulin required
type 2:
-usually adulthood
-gradual symptoms/asymptomatic
-obesity
-common family history
-late islet problems
-slightly reduced beta cells
-elevated/normal insulin
-insulin not needed AT FIRST
-can be improved
metabolic syndrome
preventable X factors: abdominal obesity, hyperglycemia, hypertension, lipid intake
-hypertrophy+hyperpigmentation in skin
-muscle dysfunction
-atherosclerosis
gestational DM
abnormal glucose regulation during 2nd-3rd trimester of pregnancy
-mom at risk for diabetes postpartum
causes fetal abnormalities:
-macrosomia (large bodies)
-hypoglycemia (<45 mg/dL)
-hypocalcemia
-polycythemia
-hyperbilirubinemia
acute complications of DM
ketoacidosis, hyperosmolar hyperglycemic state, hypoglycemia
-life threatening
diabetic ketoacidosis
primarily type 1:
-increased lipolysis, ketones
-from an absence of insulin
-hyperglycemia (>250 mg/dL)
-low bicarbonate
-low arterial pH
-+urine, serum ketones
in type 2:
-from severe stress: stroke, sepsis, myocardial infarction
low arterial pCO2
-acidosis-induced hyperkalemia
-hyperventilation
diabetic ketoacidosis process
low insulin, high glucagon
-glucagon causes gluconeogenesis, ketogenesis by the liver
-high blood glucose levels from excess
-free fatty acids in adipose tissue produces ketones
fruity breath-big sign
hyperosmolar hyperglycemic state (HHS)
insulin deficiencies reduce glucose use but cause hyperglucagonemia and glycogenolysis
-glycosuira causes dehydration
-blood glucose>600 mg/dL
-hyperosmolarity>310
-no ketoacidosis
mostly in type 2
hypoglycemia manifestations
altered CNS function
-headaches, lethargy, altered behavior, coma, seizures
ANS activation
-hunger, anxiety, tachycardia, sweating, constricted skin vessels (clammy skin)
hypoglycemia treatment
15-15 rule
-repeat if blood glucose<70 mg/dL
glucagon IM, 50% dextrose IV, oxygen
