Endocrine Pt 1 Flashcards
where is the primary source of endogenous glucose production via glycogenolysis and gluconeogenesis
liver
a normal glucose level requires
a balance between glucose usage and endogenous production or dietary carb intake
what percent of glucose released by the liver is metabolized by insulin-insenstive tissues such as the brain, GI tract, and RBCs
70-80%
how long after meals is there a transition from exogenous glucose usage to endogenous production
2-4 hours - this is necessary to maintain a normal plasma glucose
which hormones can cause hyperglycemia (4)
glucagon, epinephrine, growth hormone, and cortisol
glucagon ______ glycogenolysis and gluconeogenesis; while _____ glycolysis
glucagon stimulates glycogenolysis and gluconeogenesis; while inhibiting glycolysis
Diabetes mellitus results from
an inadequate supply of insulin and or an inadeqaute tissue response to insulin
increased circulating glucose levels leads to eventual
microvascular and macrovascular complications
Type IA Diabetes is caused by
T-cell mediated autoimmune destruction of beta cells within pancreatic islets, resulting in minimal or absent circulating insulin levels
1a - autoimmune
Type 1B diabetes is a rare disease of
absolute insulin deficiency not immune mediated
Type 2 diabetes results from
defects in insulin receptors and post-receptor intracellular signaling pathways
also not immune-mediated
with type I diabetes, how long is the pre-clinical period of B-cell antigen production before onset of symptoms
9-13 years
what percent of Beta cell function is lost before hyperglycemia ensues in Type I diabetes
at least 80-90%
hyperglycemia over several days/weeks associated symptoms (7)
fatigue, weight loss, polyuria, polydipsia, blurry vision, hypvolemia, ketoacidosis
since type II diabetes is very underrecognized, how long do patients go before being diagnosed
4-7 years
in the inital stages of type II diabetes, insensitivity to insulin in peripheral tissues leads to
increased pancreatic insulin secretion
as DM progresses, pancreatic function decreases and insulin levels become
inadequate
what are the 3 abnormalities seen in DM2
increased hepatic glucose release (caused by reduction in insulin’s inhibitory effect on the liver)
impaired insulin secretion
insufficent glucose uptake in peripheral tissues
in DM2, where is insulin resistance characterized to
skeletal muscle, adipose, and liver
causes of insulin resistance (3)
abnormal insulin molecules
circulating insulin antagonists
insulin receptor defects
what are 2 contributing factors to DM2
obesity and sedentary lifestyle
diagnosis of DM
fasting blood glucose
HbA1C
diabetes diagnostic HbA1C criteria
normal?
Prediabetes?
Diabetes?
normal < 5.7%
prediabetes 5.7-6.4%
diabetes >6.5%
other criteria for diagnosis of diabetes
fasting blood glucose > 126 mg/dL
2-hour plasma glucose > 200 mg/dL during an oral glucose tolerance test (OB)
symptoms of hyperglycemia with a random plasma glucose > 200 mg/dL
DM2 treatment
diet
exercise/weight loss
PO antidiabetic drugs
metformin - biguanide
enhances glucose transport into tissues
decreases triglycerides and LDL levels
sulfonylureas
stimulate insulin secretion
enhances glucose transport into tissues
not effective long term due to progressive loss of B cell function
:( hypoglycemia, weight gain and cardiac effects
hypoglycemia with insulin can be exacerbated by what substances (6)
ETOH
metformin
sulfonyureas
ACE-Is
MAOIs
non-selective BB
repetitive hypoglycemic episodes can lead to what?
hypoglycemia unawareness - patient becomes desensitized to hypoglycemia and doesn’t show autonomic symptoms
what are signs of neuroglycopenia and treatment
fatigue, confusion, headache, seziures, coma
PO/IV/IM glucose
Kahoot Q
DKA is more common in which type of diabetes, what is its trigger
DM1, triggered by infection/illness
Kahoot Q
high glucose exceeding the threshold for renal reabsorption creates a
osmotic diuresis and hypovolemia
why does the liver start producing ketoacids in DKA
tight metabolic coupling of gluconeogenesis and ketogenesis
in DKA, excessive glucose - counterregulatory hormones with glucagon activate what?
lipolysis and free fatty acids which are substrates for ketogenesis
diagnostic features of DKA
serum glucose ?
pH ?
HCO3?
serum osmol ?
serum and urine ketones?
serum glucose > 300 mg/dL
pH < 7.3
HCO3 < 18 mEq/L
serum osmol < 320 mOsm/L
serum and urine ketones mod to high
DKA treatment
IV volume replacement
insulin
correct acidosis - NaHCO3
lyte replacement (K+, Phos, Mg++, Na+)
kahoot Q
insulin dose for treating DKA
loading dose 0.1 units/kg Regular Insulin
infusion @ 0.1 unit/kg/hr
T/F correction of glucose without correcting Na+ may result in cerebral edema
True
characteristics of hyperglycemic hyperosmolar syndrome
severe hyperglycemia, hyperosmolarity, and dehdyration
who is most likely to experience hyperglycemic hyperosmolar syndrome
DM2 > 60 years old
hyperglycemic hyperosmolar syndrome evolves over days to weeks with persistent glucosuric diuresis… why
when glucose loads exceeds max renal glucose absorption, mass solute diuresis occurs
symptoms of HHS
hyperglycemic hyperosmolar syndrome
polyuria, hypovolemia, HypoTN, tachycardia, organ hypoperfusion
pts have some degree of acidosis but not DKA
treatment of HHS
fluid resuscitation, insulin bolus and infusion, electrolyte replacement
mortality 10-20%
DM complications
nephropathy occurs because the kidneys develop what 3 things
glomerulosclerosis, arteriosclerosis, and tubulointerstitial disease
symptoms of nephropathy
HTN, proteinuria, peripheral edema, decreased GFR
GFR < 15-20; no longer clearing K+ patient becomes hyperK and acidotic
what drug can slow the progression of proteinuria and the rate of GFR slowing
ACE inhibitors
transplantaion of what organ with the kidney can help prevent recurrent nephropathy
pancreas
peripheral neuropathy is distal symmetric diffuse sensory motor polyneuropathy.. where does it start and progress
starts in toes/feet and progresses proximally
loss of large sensory and motor fibers produces
decreased light touch and proprioception
loss of small nerve fibers leads to
decreased pain/temp perception leading to neuropathic pain
treatment for peripheral neuropathy
optimal glucose control, NSAIDs, antidepressants, anticonvulsants
retinopathy with DM is caused by (4)
microvascular changes including vessel occlusion, dilation, increased permeability and microaneursysms
what are the visual changes with retinopathy
color loss to blindness
glycemic control and BP management reduces the progression
autonomic neuropathy is caused by
damaged vasoconstrictor fibers, impaired baroreceptors, ineffective cardiovascular activity
CV symptoms of autonomic neuropathy
abnormal HR control and vascular dynamics, resting tachycardia, loss of HR variability, orthostatic hypotension and dysryhtmias
autonomic neuropathy in the GI tract cause decreased gastric secretion, and motility leading to what
what are symptoms and treatment
gastroparesis
symptoms: N/V, early satiety, bloating, epigastric pain
treatment: glucose control, small meals, prokinetics