diabetes mellitus Flashcards
what is diabetes mellitus
systemic metabolic disorder in which there is chronic hyperglycemia
what are the two reasons for diabetes mellitus
- decrease in production/secretion of insulin (t1)
2. a decrease in the cells ability to utilize the insulin-receptor problem (t2)
insulin deficiency results in
impaired use of CHO, fats and proteins
chronic hyperglycemia causes
structural abnormalities in the vasculature of many organs
in the lock and key concept, insulin is which
key
where does insulin come from
pancreas (beta cells)
what is glute 4
glucose transporter protein
where does insulin and glucose bind on a cell?
to the tyrosine kinase receptors
glute 4 allows glucose and insulin to ender cells by what
facilitated diffusion
type one is also called what
juvenile onset
type two is also called what
adult onset
which type of DM is most common
type 2 (85-90%)
what is the age of onset for type one
usually before 30 (abrupt)
why does type one happen?
theory is that beta cells are destroyed by an inappropriate autoimmune response supported by the presence of islet cell antibities
what is the cause of type two
resistance to insulin in the cell membrane receptors or a decrease in the number of receptors
what are the risk factors for type two
age
obesity
heredity
what are the manifestations of type one
polyuria polydyspia (thirst) polyphagia (hunger) weight loss (gluconeogenisis) weakness/fatigue
what are the clinical manifestations of type two
same as type one or may be asymptomatic
what is the management of type one
insulin
diet/exercise
what is the management of type two
diet/exercise
oral hypoglycemic meds
insulin possibly
which DM type is easy to control
type two if adhere to diet
how do they diagnose DM
FBS > 126
presence of islet cell antibodies
glycosylated hemoglobin >5.5%
glucose tolerance test
What is the criteria for good DM control
- maintain optimal weight
- glycosylated hgb <7%
- FBS under 140
4, Postprandial bs no higher than 180
What is diabetic ketoacidosis (diabetic coma)
hyperglycemia of 300-800 with ketonuria
what is the patho of diabetic ketoacidosis
marked decrease in insulin
not enough insulin
illness
psychologic stress
what is the patho chain for diabetic ketoacidosis
body senses lack of cellular fuel-> glycogenolysis and gluconeogenisis-> makes things worse because we don’t need more glucose
what happens due to the high blood sugar in DK
osmotic diruesis
what does osmotic diuresis in DK
fluid moves toward glucose causing increase in BV
leads to dehydration as kidneys pee out extra BS
what is increased lipolysis (breakdown of lipids) in DK
ketone production and accumulation of acids leads to ketonuria and acidosis when then leads to hyperkalemia via ion switch
what is the breakdown product of lipolysis
ketones
how does the body in DK get rid of ketones
excretion of ketone acids by lungs (hard, deep, fast)
what kind of breathing is seen with those in DK
kussmaul’s
hard, deep, fast
gets rid of excess ketone acids
what is increased proteolysis in DK
increase in gluconeogenisis
what are the clinical manifestations of DK
hyperglycemia ketonurea polyuria, polydipsia, polyphagia N/V, abdominal pain, kussmauls respirations osmotic diuresis (tachy, hypot, shock, cardiac arrhythmias)
what is the management of someone in DK
- shift from fat catabolism to CHO catabolism
- Correct fluid and electrolyte imbalances
- correct the cause
what is hypoglycemia
BS level less than 60
how does hypoglycemia happen
OD of insulin
inadequate food intake
increased amts of exercise
what are the 2 clinical manifestations of hypoglycemia
- neurogenic reaction when the hypothalamus senses decreased glucose levels
- cellular malnutrition
what is the neurogenic reaction when the hypothalamus sensies decreased glucose levels in hypoglycemia
increaded HR and RR diaphoresis palor tremors cool skin
what happens due to cellular malnutrition in hypoglycemia
(mostly brain things)
HA, dizziness, irritability, confusion, fatigue, vision changes, hunger, seizures, coma
what is the management with a hypoglycemic person
give glucose
correct fluid and electrolyte imbalance
correct cause
What are the 4 chronic complications of DM
- microvascular degenerative changes
- microvascular disease (degenerative change)
- neuropathy
- Infection
What is macrovascular degenerative change
In the major vessels
Lipolysis-> hyperlipidmia->atherosclerosis-> CAD/DVD/CVA
what is microvascular disease
Affects the Capillary
thickening of the basement membrane leading to vascular cell proliferation of cap wall
what two things cause microvascular disease
- glycoslation of protein/collagen (glucose binds with no enzyme) forms/deposits advanced glycosylation end product in vessel walls
- Protein kinase c (enzyme) is inappropriately activated by high BS
what is the patho chain of microvascular disease
vascular cell prolif-> thickens basement membrane of caps-> decreased perfusion-> hypoxia/ischemia
what does microvascular disease mainly affect
retina (diabetic retinopathy)
kidney (nephropathy, renal failure)
also affects extremities
what is neuropathy related to
microvascular disease
what causes neuropathy in DM
vascular ischemia-> nerve endings are destroyed in the ischemic areas
what is peripheral neuropathy mani in DM
pain and tingling in extremities
decreased sensation
what is autonomic nervous system mani of nuropathy in DM
gastropanesis (delayed emptying of GI) neurogenic bladder (decreased bladder emptying) sexual dysfunction CV- no HR variability
why does infection occur with DM
glucose is a good media for growth
decreased sensation/decreased possible prevention
hypoxia/ischemia causes poor wound healing