Endocrine Flashcards
down regulation
medication may act as hormones
body recognizes excess and cells will down regulate the number of receptors
causes desensitization
cells less responsive to the hormone
endocrine negative feedback mechanism
endocrine system works by negative feedback
endocrine tissue will stop secreting hormone when homeostasis is restored
Diabetes
syndrome characterized by hyperglycemia resulting from an absolute or relative impairment in insulin secretion/ action
disorder of carbohydrate metabolism: deficiency of insulin, resistance to action of insulin
body system of diabetes
liver, pancreas, skeletal muscles
role of liver in diabetes/ sugar
turns stored glycogen into glucose
Glucose
most important energy source
brian is highly dependent on it for energy, other tissues as well
comes from food and from production by liver( glycogenesis)
2 hormones exert most influence: glucagon and insulin
glucagon
hormone produced by alpha cells of pancreas
released when glucose levels in blood are too low
cause liver to convert stored glycogen into glucose and release into blood stream
raises blood sugar levels
how does the body respond to high blood glucose
pancreas releases insulin
liver produces glycogen, cells take up glucose from blood
blood glucose falls
how does the body respond to low blood glucose
pancreas releases glucagon
liver breaks down glycogen
blood glucose rises
glycogen
storage form of glucose
function as a shrt term energy storage
can be quickly mobilized to meet sudden need of of glucose
made primarily in liver
Insulin
hormone that regulates carbohydrate metabolism
lower blood glucose
released rapidly in response to high glucose levels
stimulates uptake of glucose into cells, especially in muscle and fat
insulin in the liver
stores glucose in form of glycogen
converts excess glucose into fat
suppresses hepatic glucogenesis and glycogenolysis
insulin release
plasma- glucose in most important factor in controlling release
quick so carbs are absorebed/ used/stroed in liver to prevent serum glucose levels from rising to high
postprandial
after eating, typically refers to the increase in glucose that causes insulin to be released by beta cells
what happens without insulin
blood glucose levels elevate, causing increased urination, hunger, thirst
muscle used for energy: weight loss
fat is used for energy: ketones, which can cause diabetic ketoacidosis
3 Ps of insulin shortage/ resistance
polyuria (increased urination)
polyphagia (increased hunger)
polydipsia (increased thirst)
Indications for insulin
type 1/2 diabetes
DKA
hyperosmolar hyperglycemic state
surgery
use of glucocorticoids/ corticosteroids and vasopressors
illness/ infection
stress
parental/enteral nutrition
pancreatitis and diseases that decrease beta cell function
hyperkalemic pt
gestational diabetes
DM type 1
absolute deficiency of Insulin
autoimmune destruction of pancreatic beta cells
increased glucose cant get into cells, body mistake that there isnt enough glucose
body break down lipid and proteins to gain energy
insulin is indicated in all cases of Type 1
occurs mainly in childhood or puberty, but can happen anytime
rapid onset
underweight
DM type 2
insulin resistance
plasma insulin normal or increased
tissues resistant to insulin
adult onset, linked to obesity, sedentary lifestyle, lack of exercise, race
initially controlled with lifestyle changes, may need oral drug therapy, than insulin
gradual onset
overweight
T1 symptoms
polydipsia, polyuria, polyphagia, weight loss
T2 symptoms
3 Ps, blurred visions, fatigue recurrent infections
pregnancy effecting diabetes
placenta produces hormone that antagonize the action of insulin
production of cortisol increases threefold
glucose can pass freely from the maternal to the fetal circulation (fetak hyperinsuliinemia)
Gestational diabetes
diabetes that devlops during pregnancy
2-10% of pregnancies in US
subsides rapidly after delivery
treated with Insulin, diet, exercise
fasting blood glucose levels
70-110
normal non fasting blood glucose
less than 140
pre diabetes blood glucose fasting
110-125
diabetes blood glucose fasting
greater than 126
diabetes non fasting blood glucose levels
more than 200
diabetes complications
renal failure
cardiovascular complication
blindness
nerve damage
amputation
non-pharm diabetes treatment
lifestyle modification
diet
exercise
weight loss
Drugs used in conjunction for DM
ace inhibitors or ARB for hypertension
statins for lipida
insulin sources
From pork: differs from human by 1 amino acid
Human: made from recombinant tech, human like
should be non-allergenic
synthetic insulin analogs
basal insulin
continuous secretion that maintains glucose
bodys baseline of level of insulin
prandial insulin
insulin secretion in response to meals
correctional supplemental insulin
correct any elevation in blood glucose usually due to illness or stress
rapid/short acting insulin
covers meal intake
used for elevated BG
intermediate/ long acting insulin
used for basal insulin needs
not intended to cover meals
rapid acting insulin kinetics
Onset: 10-30 min
peak: 1hr
duration: 3-5 hr
clear
before eating or with meals
types of rapid acting insulin
Humalog: lispro
NovoLog: aspart
Apidra: glulisine
short acting insulin kinetics
onset: 30-60 min
peak: 1-5 hrs
Duration: 6-10hr
IM
IV: half life of 4-5 min`
short acting insulin types
regular: humulin, novalin
intermediate acting inulin kinetics
onset: 1-2 hrs
peak: 6-14hrs
duration: 16-24hrs
cloudy appearance
BID
TID
only given SubQ
cannot be mixed with short acting insulins
intermediate acting insulin
type: NPH insulin
N, Humulin N, Novolin N
long acting insulin kinetics
onset 1-2 hrs
peak: flat
duration: 12-24hrs
clear
not given IV
used with other Insulins
why are long acting insulins not mixed
they do not mix because of low pH
long acting insulin types
Lantus (glargine)- qd U-1100
Levemir (detemir) qd, Bid dosing
lantus duration
18-24 hrs
levemir
12-24 hrs
concentrated insulin
for large amounts of insulin
500 U/ml
can cause severe hypoglycemia
what insulin is cloudy
NPH
sliding scale
for correctional insulin treatment
rapid or short acting insulin to correct BG
before meals
not effective as sole source of insulin
treat BG post hyperglycemia
insulin general kinetics
destroyed by gastric acid, not given orally
subq- abdomen fastest rate of absorption, then arm,tthigh, buttocks
in IV- up to 80% absorbed by IV tubing
Insulin storage
refrigerate, kept up to 1 month without significant loss of activity
out of direct sunlight and extreme heat
S/S of hypoglycemia
tachycardia
tremulousness, confusion, agitation, seizures, muscle weakness, blurred vision, diaphoresis, seizures, LOC, Death
treatment of hypoglycemia
if swallow: sugar (OJ, candy, glucose)
no swallow: IV glucose or D5W, glucagon IM
Lipohypertrophy
increased fat mass at injection site causing spongey area
insulin absorption delayed from this site
lipoatrophy
antibody formation causes destruction of fat at injection site
can cause depression in skin and dleayed absorption
insulin on potassium
helps move potassium inside the cells
Insulin used for treatment of hyperkalemia, can also couse hypokalemia
Insulin drug-drug interaction
any hypoglycemic agent, diuretics, glucocorticoids, phenytoin, beta blockers
barriers to insulin
fear of needles/unknown, cost, inconvenience, weight gain
agb A1C to blood glucose
goal of under 7
insulin monitoring
by self, or HgbA1C over span of time
Insulin Pens
hold 150-300 units
reusable or disposable
dial dosage and inject
insulin pen pros
portable, discreet, convenient, saves time, accurate dosing
insulin pen cons
expensive, waste, cant mix insulins, size of numbers on dial, strength/ dexterity to use
insulin pump
usually rapid/short acting insulin
basal insulin over 25 hrs
mimics physiological secretion of insulin
insertion site q3 days, same as injection
insulin pump candidates
motivated for better control, can be type 1/2
test BG QID
high A1c
blood glucose swings
those with frequent hypoglycemia
Pros of insulin pumps
less needle pricks
dose calculations
convenience and spontaneity
imporoves A1C and glucose control
bettery quality
Cons of insulin pumps
cost
steep learning curve
complication
worn all the time
skin infections/rash
biguanides
drug of choice for most type 2
P-metformin
metformin MOa
decreases hepatic glucose production
sensitizes insulin receptors
decreases intestinal glucose absorption
does dot increase insulin secretion
insulin must be present already for drugs to work
metformin kinetics
absorption: orally, absorbed slowly but incompletely results in bioavailability of 50-60%
food delays absorption
Onset: peak in 2-3 hrs
metabolism: does not undergo hepatic metabolism
elimination: excreted unchanged by kidneys, bad for renal
metformin adverse effects
GI distress most common
decreased appetitie, nausea, diarrhea
metallic taste
not associated with hypoglycemia in therapeutic doses
Metformin BBW
can cause lactic acidosis- can keep lactic acid from being destroyed
LA risk increased with renal insufficiany patients
S/S hyperventilation, myalgia, malaise, GI distress
hold before/ after studies using iodine IV contrast
avoid alcohol
metformin drug interactions
cimetidine, digoxin, procainamide, vancomycin
increased metformin concentration due to competition for renal tubular secretion
W/ iodine, increased incidence of lactic acidosis
W/ herbals increased incidenc of hypoglycemia
pearls of metformin contraindications
with liver disease, alcoholics, acute or chronic metabolic acidosis, chronic heart failure, renal impairment
with meals
drug of choice with new diagnosis
first generation sulfonylureas
chlorpropamide
tolbutamide
second generation sulfonyleureas
P- glyburide (diabeta, micronase)
glipizide
glymepiride
sulfonylureas MOA
stimulate pancreatic beta cells to secrete insulin, aka secretagogue
reduces glucose output from liver by decreasing glycogenolysis and gluconeogenesis
increases insulin sensitivity at cellular sites
only used in Type 2
sulfonyereus kinetics
half life- 10 hrs
onset 2 hrs
peaks 2-4 hrs
duration 24 hrs
sulfonylereus adverse effects
hypoglycemia
weight gain
hyponatremia
skin rash
GI upset
cholestasis
hemolytic anemia
pearls of sulfaneyrleurus
warning with sulfa allergiea, thiazide diuretic
caution with renal/hepatic disease
30-60 min before meals, in morning
avoid alcohol, supplements, alternative therapies because increased risk of hypoglycemia
meglitinides
P- repaglinide (prandin)
nateglinide (starlix)
meglitinides MOA
stimulate secretion of insulin
provide quick insulin burst with onset of action in 20 minutes
minimal renal exretion, good for renal pts
for lowering post prandial glucose levels
thiazolidinediones
p- piogllitazone ( actos)
rosiglitazone ( avandia)
thiazolidinediones MOA
reduces insulin resistance (insulin sensitizer)
insulin must be present for it to work
inhibit hepatic cluconeogenesis
adverse effects: edema, weight gain, HF, decreased liver function, anemia
may increase ovulation in women
Alpha- glucosidase inhibitors
P- acarbose (precose)
miglitol (glyset)
alpha- glucosidase inhibitors MOA
do not secrete nor sensitize to insulin
inhibits glucosidase in small intestine
leads to delayed absorption of carbs
decreased post-prandial blood glucose rise
takes 2-3 months
w/ first bite of meal
cannot use candy if become hypoglycemis b/c will not be absorbed
alpha- glucosidase inhibitors adverse effects
flatuence, cramps, diarrhea, abdominal pain, iron deficiency anemia, increased hepatic enzymes
Incretin hormone (GLP-1)
released by small intestine
increases amount of insulin secreted
decrease amount og glucagon secreted
delay gastric emptying
decrease food intake
GLP-1 agonists
p- exenatide (byetta)
exenalide (bydureon)
lireglutide (victoza)
dulaglutide (trulicity)
albigluitide (tanzeum)
samaglutide (ozempic)
