what is the most common cause of hyperthryoidism?
what is important to knwo about this?
who is it common in?
what causes this?
3 things it leads to?
MOST COMMON CAUSE OF HYPERTHYROIDISM
women more common 20-40 years old!!
autoimmune TSH-R AB-IgG antibodies aka TSI directed to TSH receptor over-activate gland leading to hypersecretion
leads to: hypertrophy, hyperplasia, commonly goiter!!
2 3 key ones you need to remember
1. hyperactivity, irritability, restlessness
2. heat intolerance, sweating
4. increased appetite, weight loss
7. fine tremor
9. warm, oily hair
10. proximal muscle weakness
3 things causes?
unique to graves disease
1. proptosis/exopthalmos "lid lag"
2. conjunctival inflammation/edema
3. corneal drying
******occurs because the lympocytes infiltrate the orbit, muscles, eyelids and may cause diplopria and compression of optic nerve*****
what is the name for this?
what does this cause?
*******noninflammatory induration and plaque formation of the pre-tibial area leading to thickened skin, and orange skin appereance*****
2 tests to check
what don't you need to check?
1. very low TSH
since the T3 and T4 high, negative causes this to be low
2. total and T4 elevated
**don't need to check TSH-R AB for dx**
9 tx options?
what is the toc?
who do you use each in?
1. endocrinology consult essential
2. propanolol for sxs
3. methimazole (thiourea) -MILD TO MOD 12-18 months!
-inhibits thyroid peroxidases and block organification of iodine to decrease hormone production
-monitor WHB, pruirits, and FT4
4. propylithiouricil (PTU) (thiourea) if pregnant
5. saturated iodine solution- severe
6. iodinated contrast agens- severe or thyroid storm
-prevents conversion of T4 to T3
8. radioative iodine-DEFINITIVE TX and TREATMENT OF CHOICE IN THE US!!
-destroys the overactive gland because concentrates here
no longer TOC but used in children or pregnancy or those that can' be controlled with medication
what do you need to keep in mind about the toc for this? what is it? what might worsen?
used to destroy the gland because it concentrates here
permanent hypothyroidism often develops within 1 year and may need replacement tx FOR LIFE!!!!
***opthalmopathy may worsen esp in smokers with this tx***
what is important to remember about this?
what type of disease?
how does it show up?
2 things ath cause this
what to keep in mind?
MOST COMMON CAUSE OF HYPOTHYROIDISM
AUTOIMMUNE, with insidious onset
thyroperoxidase and thyroglobulin antibodies present in high titers
*****keep in mind, this can itially cause a hyperthyroidism from release of stored hormone, but the end result is hypothyroisim*****
5 early sxs
8 late sxs
1. cold intolerance
2. dry hair, hair loss
5. thin, brittle nails
1. slow speech
2. hoarse voice
3. weight gain
4. facial and eyelip puffiness
6. edema non pitting
8. pleural/pericardial effusion
in txing it with thiourea drugs what percent will have reccurance?
(propylithiouricil or methimazole)
reccurence are common if tx is only with thiourea, propylthiouracil or methimazole
what are 4 complications that can come from graves disease?
3. psychological complications
4. post tx hypothyroidism common, but easily txed
what is this?
3 tx options?
rare, but life-threatening of extreme hyperthyroidism, can be fatal and need to be admitted and txed STAT
elevated T3 and T4
1. satruated iodine solution
2. iodinated contrast agents
what are the 5 causes of hypothyroidism?
1. hasimotos thyroiditis
2. congenital hypothyroidism
5. drug induced- amiodarone
why is it key to identify?
screening of TSH in newborns should elimate disease
early detection is key to prevent cretinism and hypodevelopment
what can this lead to?
abnormal interstitial fluid acculuation in skin giveing it a waxy/coarsened (non-pitting) appearence
can lead to mydxedema crisis EMERGENCY:
severe form of hypothyroidism
-CNS depression (coma)
- respiratory depression
1. High TSH
2. low T3/T4
3. increased triglycerides
4. decreased HDL
5. anti-thyroid antibodies
what is the tx?
how is it dosed?
goal? time frame?
levothyroxine (synthetic T4)
a. start 50-100 ug/day and titrate to full dose over time, following TSH levels
b. recheck TSH levels every 2-3 months until normal
GOAL: clinically euthyroid state (normal)
**sxs improve slowly over months**
iatrogenic (we caused it)
radioative iodine for initial hyperthyroidism that leads to gland destruction
what is this caused by?
caused by gram positive bacteria
1. tender thyroid
fine needle aspiration
De quervains aka granulomatous
what is this?
when is it most common?
when does it occur?
explain the progression?
MOST COMMON CAUSE OF PAINFUL THYROID GLAND
***peaks in the summer....weird****
MC POST VRAL INFECTION
thyrotoxicosis initially presents followed by hypothyroidism and euthyroid within 12 months
1. markedly increase ESR
2. very low anti-thyroid bodies
ionated constrast agent
drug induced amiodarone
what does the medication contain?
what percent get this?
3 progression steps?
contains 37% iodine by weight or 75 mg per tablet
causes thyroid dysregulation in 20% of patients
1. can cause rise in T4 during first month of tx
2. causes cellular resitsance to T4
3. hypothyroid picture ensues with elevated TSH
fibrous thryoiditis (riedel)
who is this in?
what hapens to the thyroid?
what happens to RAI?
1 dx method
1 tx method?
rarest form of thyroiditis, 80% are in females
formation of dense fibous tissue in the thyroid
hard "woody" asymmetric thyroid feeling
the fibrosis can spread outside of the thyroid
radioactive iodine is decreased in involved areas of the thyroid
antibodies may be present in 45%
what are 2 most common causes?
what is hypersecreted?
2 hallmark lab findings?
what are 5 things this can lead to?
1. MC cause parathyroid adenoma
2. parathyroid hyperplasia/enlargement
hypersecretion of PTH
1. elevated PTH
2. elevated serum total and ionized Ca
1. increased excretion of Ca and PO4 by the kidney overwhlems the tubular Ca absorptive capacity leading to hypercalciURIA
2. chronic bone reabsorption
3. sever leads to
how is this normally found?
pneumonic for sxs?
leads to what what 6 presentations?
often discovered as incidental lab finding
"moans, groans, stones, bones"
1.skeletal: loss of cortical bone with bone pain and arthalgias
2. nephrologic disorders:
-decreased sensitivity to ADH with polyuria and poly dipsea
-increased calcium stones from saturation
5 lab findings
what is important to do?
1. serum Ca over 10.5
2. increased ionized calcium over 5.4
3. PO4 low
4. alk phos increase if presence of bone disease
5. PTH assay via radioimmunoassay
**important to do a 24 hour urine to quantify***
4 tx options
what are the indications for the last?
1. normal saline to increase intravascular space
2. furosemide facilitates Ca excretion
3 biphosphonate stop osteoclast bone resorption
presence of bone or kidney disease
1. hypercalcemia with significant hypercalcuria
2. BD ovr 2 SD below normal
3. age less than 50
what is a complication from thyroidectomy used to tx hyperparathyroidism?
rapid drop of PTH levels and can lead to acute hypocalcemia post-op
RX: calcium supplements
until parathyroid resumes function
what are five complications of hyperparathyroidism?
1. pathologic fractures, esp in women
2. urinary stones, obstruction, UTIs
3. if Ca rises rapidly-CNS changes, renal failure
4. PUD and pancreatitis form high CA levels
what are the 3 causes?
1. MC-post-thyroidectomy or removal of parathyroid adenoma
2. rarely polyglandular autoimmune
3. chronic magnesium deficiency which impairs PTH release
low ionized Ca
6 acute sxs
5 chronic sxs
paresthesias of hands and feet
1. personaity changes
2. decrease cognitive function
4. dry brittle nails
4. chevosteks sign-twitching of facial nerve with tapping
5. trousseaus sign-blow up BP cuff around arm and hand will twitch
IV CALCIUM GLUCONATE
do until tetant and other sxs resolve
1. oral calcium
2. active metabolite of vitamin D 1,25-dihyrdroxycholecalciferole AKA CALCITROL
3. magnesium supplement
**goal: maintain serum Ca in low normal range**
4 lab findings
1. low serum total and ionized Ca
2. elevated PO4
3. decreased PTH
4. prolonged QT and arrythmias
what is the overall effect?
2 ways it accomplishes this
INCREASES BLOOD CA LEVELS
1. STIMULATES RELEASE OF CA FROM BONE (RESORPTION)
2. STIMULATES VITAMIN D ACTIVATION BY KIDNEY TO INCREASE INTESTINAL CA ABSORPTION
what secretes this?
3 ways it accomplishes this?
secreted by the thyroid c-cells
**decreases blood Ca levels**
1. inhibits intestinal Ca absorption
2. inhibits osteoclast and stimulates osteoblast activity
3. inhibits renal tubular reabsorption of Ca
what is this?
what type of bone is lost more commonly?
MOST COMMON METABOLIC BONE DISEASE
comprimised bone strength leading to an increased risk for fracture
bone resorption occurs most commonly in the trabecular bone "spongy bone" than the corical bone
Net bone loss over 10 years:
trabecular 25-30% and MC!!
describe the progression throughout life? 5
what do people suggest about the tx based on this progression?
1. increases dramatically in puberty due to gonadal steroids
2. peaks in early 20s
3. bone loss beings before menses creases
4. accelerated bone loss in the 1st 5-10 years post menopause
5. slows after age 60
***this is why people think that you could theoretically prevent with estrogen, and might be helpful in subsets like hypogonadism or premature menopause but NOT as long term option due to adverse outcome risks****
what are 7 conditions that increase the risk someone will develop osteoporosis?
1. sex hormone deficiency, esp post menopause
2. excess glucocorticoids (cushings)
3. hyperparathyroidism-increased PTH stimulates bone breakdown
4.thyrotoxicosis-increased bone metbolism
7. vit d deficency
BMD 1-2.5 SD below peak bone density
BMD over 2.5 SD from normal
when classifying between osteopenia, osteoporosis, or just normal person, what do you NEED to keep in mind?
presence of fracture without S&S or trauma indicates severe osteoporosis regardless of what the SD is!!
do men get osteoporosis?
1 out of 5 dxed people are men
hip fracture is a significant predictor for mortality!!
what are 7 RF that increase your risk for osteoporosis?
1. prior fractures
2. FH of osteoporosis related fractures
3. low body weight
4. cigarette consumption
5. excessive ETOH use
6. chronic inflammation: RA
7. patients at high risk for falls or frailty
what are 4 sxs you may see with this?
what is usually the inital presentation?
1. many asymptomatic till fracture (often spontaneous)
2. ******may see back pain, decrease in height, or kyphosis***
3. dietary calcium, vit D deficiency
4 texts for dx
1 TOC? interpretation
1. DEXA is TOC!!!
includes spine, femur
T-score: SD away from young healthy adults
over 2: osteopenia
2. check calcium levers
3. check vitamin D levels (25-hydroxy vit D)
4. consider checking putuiary hormones when indicated
who do you screen for osteoporosis in?
1. early menopause
can you reverse established osteoporosis?
can increase BD, decrease fractures, and hald or slow progression
what are the 5 drug classes used to tx this? First DOC? how is it taken? key things to know?
ALENDRONATE: take 30 mins before AM meal with 8ox water and remain upright 30 minutes after
-increased risk of unusual fracture so not longer than 5 years
dental care important-jaw issues
very long half-life, in bone 10 years
serum estrogen receptor agonist/antagonist
alternative to estrogen in postmenopausal woman with decreased risk of adverse effects since no BC risk
4. Vitamin D; calcium
always supp vit D, Ca only if it is low!
5. PTH synthetic analog
***normally PTH stimulates osteoclasts BUT when given in synthetic form it increases osteoblast activity and new bone formation=paradox**
INCREASES BONE DENSITY MORE THAN ANY OTHER DRUG BUT IS NEW AND CAN LEAD TO BONE CANCERS SO NOT USED AS MUCH NOW
only used in patients with premature menopause or hypogonadism...dose related issues and increased risk for BC, DVT, endometrial cancer etc and short term use only
what are the percent prevalence of T1DM and T2DM?
what are 5 brief features you find in Type 1 diabetes?
what are 4 brief features of T2DM?
what is the clinical importance of the insulin structure?
contrains C peptide
this is present only on endogenous insulin so measuring this will tell you how much insulin the Beta cells are actually producing and how much of their function is lef
WE MEASURE THIS TO TELL US HOW WELL THE BETA CELLS ARE WORKING
what are 5 overall broad functions of insulin secretion?
1. decrease blood glucose
2. decrease blood fatty acid
3. decrease blood amino acid
4. increase protein syntheisi
5. increase fuel storage
Stimulation of glycogen synthesis
breakdown of glycogen to glucose
(occurs at liver, and less commonly muscles)
**WHAT TO KEEP IN MIND...WHAT DOES THIS OCCUR WITH?***
generation of glucose from glycogen (most commonly from the liver)
****KEEP IN MIND THAT GLYCOGENOLYSIS AND GLUCONEOGENESIS BOTH OCCUR AT THE SAME TIME BECAUSE THE FIRST MUST OCCUR TO ALLOW THE SECOND!!!***
1 anit- catabolic
increase glucose uptake
increase triglyceride synthesis
increase fatty acid uptake and synthesis
inhibition of lipolysis
1. increase glucose uptake
2. increase glycogen storage
3. increase protein synthesis
4. increase amino acid uptake
1. inhibition of proteolysis
2. decrease amino acid output (wants to build)
what cells secrete glucagon?
alpha cells of the pancreas when blood glucose was low
if there is a decrease in blood sugar...what is released and ffrom where? what does it cause
glucagon is released from the alpha cells of the pancrease which causes liver glycolysis and gluconeogenisis
**negative feedback once BS increase**
causes relase of stored glycogen (glucose stored) into the blood
who do you typically find diabetic ketoacidosis in?
(can be in late stage 2)
who do you typically find acute hypoglycemia in?
type 1 post insulin without eating
if you find a diabetic in a stoke like coma or passed out...what can you almost always believe it is?
5 risk factors
1. abdominal obesity
4. fasting glucose
***must have 3 of the five qualifications***
what is this called?
what does it indicated for the patient?
what type of diabetes?
aka insulin resistance; syndrome X
classified as a constellation of sxs findings that significantly increase risk of athlerosclerosis
associated with T2DM
waist circumference RF
men over 102
women over 88
men less than 40
women less than 50
over 130 SBP
over 85 DBP
fasting glucose RF
what does it do? (hence why bad)
4 steps that make this bad!
bad because it secretes adipokines/cytokines
theses increase insulin resistance
insulin resistance can also increase DYSLIPDEMIAS
dyslipidemias lead to
MI, STROKE, HYPERTENSION
what are they ment to work like?
what do they do?
what are 3 things they cause as SE?
minic the function of insulin by closing the K channels so that insulin is secreted
since made to act like insulin can cause:
increased body weight
what is the goal preprandial glucose?
post: less than 180
what part do they work on?
what type of diabetic do you use this in
what are the two drugs name
what are the 3 side effects that you might see with this!
THIS IS THE SECOND DRUG OF CHOISE AFTER METFORMIN
work on the K pump as well but are less likely to cause hypoglycemia but are very expensive
T2DM, in adjunct to metformin
****caution can cause hypoglycemia, hyperinsulinemia, and weight gain***
what to keep in mind?
4 things that it does in the body?
who do ou not use this in? 3 senarios? why?
what is a senariou you don't want to give this medication?
first drug you give for T2DM
1. decreases hepatic glucose production
2. increases insulin sensitivity and promotes uptake by skeletal muscle (what is left will work better)
3. improves lipid profile
4. decrease carbohydrate absorption in the gut
MC common SE is GI distrubances so start low go slow to get to max dose of 2000-2500
*****contraindicated for patients with renal insufficiency, liver failure, and major surgery because of increased risk of lactic acidosis***
(so hold on same day as contrast and 48 hours after so if kidneys shut down don't get poisioned)
GLP-1 receptor agonist
what is this?
how is it given?
what is unique that this is thought to do?
4 things it stimualtes
3 things it decreases
since thought that GLP-1 can cause Beta cell proliferation it is though that this medication could help to regain beta cell function when the beta cells start to burn out
**alternative to insulin w/o weight gain** SC admin
1. insulin secretion
3. insulin production
4. increase beta cell production
5. muscle uptake and and storage
6. decreased gastric empyting
7. decrease appetite
8. decrease glucagon release
what do they do?
1 drug we use?
2 problems with them?
avoid in? 1
improves insulin sensitivity and signaling
weight gain (don't wanna give to type 2 patients)
heart failure from edema around the the hear***favoritism going out because of this!!!
AVOID: liver dysfunction, so need to get a LFT before intitiating
***try staying away from these drugs because of the side effects but if you have to go with one of them go with pioglitazone***
what do they do?
what is the drug name?
because of this what are you at increased risk for?
why is one benefit to this drug and who can this help?
WHAT IS THERE A WARNING ABOUT?
blocks reabsorption of glucose in the proximal tubule and causes it to be excreted in the urine
BENEFIT: can cause weightloss of 5-10 pounds since diuresis, lowers bp (good for T2DM!)
UTIS since increasing sugar excretion
*****FDA WARNING ABOUT KETOACIDOSIS since more sugar secreted in the urine****
what is this?
when is it normally secreted?
what does it improve?
which diabetes do you use it in?
synthetic analogue of amylin
amylin is normally co-secrete with insulin and
-suppresses glucagon secretion
-slows gastric emptying
-improves glycemic control
**modulates post prandial glucose**
type 1 and type 2
stages of resistance for Type 2 diabetes
1. obesity leads to insulin resistance
body pumps out a lot of insulin to overcome the resistance and initially it is able to keep the BS within normal range
2. impaired glucose tolerance
eventually resistance increase to a point where B cells work overtime to pump out more insulin through Beta cell hyperplasia to try to get sugar down but the resitance grows so despite elevated insulin, the surgar stays high
3. early diabetes-B cell burn out
B cells start to burn out so the insulin production decreases but the sugar is still high EARLY DIABETES CAN'T MEET DEMANDS
4. late diabetes
BETA CELLS BURN OUT!!
name of the drug?
what does ths drug do?
why is complance better?
how is this drug used?
breaks down the DDP-4 enzyme that breaks down GLP-1 increasing increatin hormones
(stimulates insulin, inhibits glucagon)
overall, this drug decreases blood sugar
**oral so better compliance...but used as an adjunt
what is more efffective than any oral antidiabetic drug?
what are the ABCDEs of diabetes?
A=aspirin reduce platelets
B=bloood pressure ACE
D=diet, diabetes control
E=exercise, improves glucose and lipids
what is insulin resistance?
feuled by proinflammatory respons from cytokines and adipokines
what are 3 microvascular long term complications of diabetes?
1 macrovacular long term complication of diabetes?
(CHD, CVD/stroke, PAD)
what are the 2 types?
what is each characterized by?
what is key to prevent this?
microaneurysms, hemorrhases, exudates, retinal edema
formation of new blood vessels leading to BLINDNESS
*********TIGHT GLYCEMIC CONTROL ESSENTIAL TO PREVENTION OF RETINOPATHY*****
worse with HTN and smoking
how often do diabetics need eye exams?
what are 2 things that cause this?
who is this worse in?
what is important to know as a fact abou prevalance in the US?
3 tx options?
developes from chronic hyperglycemia and uncontrolled HTN
***to prevent...control both of these***
worse in smokers!!
leading cause of ESRD in the US!!!!! diabetic nephropathy
1. tight glycemic control
2. tight BP controll less than 140/90
3. early institution of ACEI
how do you check for nephropathy in diabetic?
want to check MICROALBUMINURIA 30-300
BUT A DIPSTICK ISN'T SENSITIVE ENOUGH SO NEED TO ORDER A RADIOIMMUNOASSAY SPOT AM URINE
normal less than 30
albumenmia: over 300
what are two ways to tx diabetic nephropathy once they have reached ESRD?
2. transplantation from living related donor is preferable to dialysis
ACE initiation in diabetics
who do you start in and when?
what are 4 things it prevents the progression of?
start in Type 1 and Type 2 with the presence of microalbuminuria
EVEN IF THE BP IS NORMAL!!!!!
decreases risk for
GOAL: less than 140/90, often requires multipe agents
diabetic complications: athlerosclerosis
what are 5 things this can lead to?
what is diabetes a equivalent to?
what should you consider putting them on?
diabetes is a coronary risk equivalent
***put patient on ASA if they these RF***
diabetes is a...
CVD risk factor equvalent!!
Periphreal vascular disease in diabetics
what vessels effected?
lleads to 4 things?
4 tx options?
Large and small vessel disease
regular foot exams
tight glycemic contro.
3 tx options for medication?
1. distal symmetric polyneuropathy-decrease sensation in "stocking glove" distribution
2. motor involvement late
3. PAIN COMMON
1. gabapentin (neurontin)
2. duloxetine (cymbalta)
3. pregabalin (lyrica)
slow gastric emptying incuding early saiety, nausea, and vomitying 1-3 hours after meal
3. orthostatic hypotension
fludrocortisone and elastic stockings
4. impotence, sexual dysfunction
5. decreased bladded sensation
5 general sxs?
once havd it for a while....6 sxs? 1 buxx word!!
1. decrease mentation
5. RAPID BREATH WITH FRUITY BREAHT (accumulation of ketones)
6. kussmauls respiration
form of hyperventilation to blow off the CO2
what is this?
who does it occur in?
4 potenital causes?
2 critical things it can lead to?
TYPICALLY TYPE 1 DM
need for insulin increases from trigger
can progress to coma and death
diabetic ketoacidosis pathophysiology
1. inadequate insulin resulting in increased BS that promps increase in abnormal fat breakdown
2. increase in BS also increases catechols, cortisol, glucagon, and GH resulting in gluconeogenisis and glycogenolysis
3. fat breakdown or lipolysis produces free fatty acids and conversion of acetoacetic (ketoacid) and B=hydroxybutyric acid leading to ACIDOSIS
4. increases ketogenesis in the liver also contributes to ketoacidosis
results in metabolic acidosis with increase anion gap
what 2 products does the fat breakdown or lipolysis create for products?
production of FFA and conversion to
1. acetoacetic (ketoacid)
2. B-hydroxybutyric acid
2 things it leads to because of glycosuria from glucse wasting from hyperglycemia?
1. osmotic diuresis
2. volume and electrolyte loss/imbalance
7 lab findings
1. pH less that 7.3
2. low HCO3 with increased anion gap
3. increased urine osmolarity
4. BS usually over 300
5. elevated amylase
6. elevated WBC over 10,000 without infxns
7. initial serum K often high but total body ky low from fluid and electrolyte losses
diabetic ketoacidosis tx:
4 tx options
1. estalish flowsheet ot measure all levels
2. insulin regular
3. replace lost fluids with 0.9% NaCL***give 3-4 L over 8 hours***
4. replace K by KCL IB
hyperglycemic nonketotic hyperosmolar state
which diabetics is this in?
what is the patho of this?
what is the sugars like? what isn't present?
type 2 DM
adequate circulate insulin to breakdown fat but not enough to control hyperglycemia **aka there is some insulin so the body doesn't think it is starving itself**
progressive development of very high BS 600-2400 in absence of ketoacidosis
hyperglycemic hyperosmolar nonketoic acidosis:
what happens here that complicates thsi?
2 tx options?
the profound ostmotic diuresis causes severe dehydration (10-11L) is complicated by the ensuring pre-renal azotemia
1. 0.9% normal saline
what is the mortality seen with hyperglycemic hyperosmolar nonketotic acidosis?
explain why diabetic ketoacidosis is INCREASED ANION GAP ACIDOSIS?
the anion gap equation is
in diabetic ketoacidosis, the HCO3 decreases to buffer the acid produced by the muscle breakdown to make the intermediate, since this is decreases according toe the equation the total amount is increase
Henced increases metabolic acidosis
what is the differences between DKA and HHNK?
DKA=TYPE 1, presensce of ketones
HHNK= TYPE 2, way higher BS
type 1 DM
what promps this start of this?
infectious or toxic insult
in genetically predisposed people causing autoimmune response against altered pancreatic B cell antigens
Type 1 DM
what is your typical patient? 2
what is the primary cause of this? (what happens)
what type of disorder is this? lead s to 2 things?
non-obese and insulin dependent
mediated with presence of islet cell antibodies that lead to destruction of the B cells in pancrease
catabolic disorder where absence of insulin leads to:
2. fat and protein breakdown lead to
type 1 DM treatment
what is the medication you tx with?
combination and percent of diffreent insulins? 2
tx: INSULIN only!!
SMBG 4-6x daily
basal insulin= 40-50% intermediate/long acting
(NpH, glargine, detemir)
short term or rapid (regular or INSULIN LISPRO)
**alernative is insulin pump**
what do you use as insulin to tx Type 1 DM?
combination of basal (Long acting) and prandial (shorter acting) insulin
covers them throughout the day and also when they have their specific meals
what is the total insulin need for someone with T1DM?
what is the most common seen complication with insulin or sulfonylurea use?
what are two drugs that are known for doing this?
what sugar correlates with this?
most common complication seen with insulin or sulfonylurea
less than 50 BS
what drug can mask hypoglycemia because it produces similar sxs
non selective beta blockers
Type 2 DM
characteristics of patient? 4
what is the goal? how to accomplish? 2
2 first line tx options?
MOST IMPORTANT TO REGAIN INSULIN SENSITIVITY
1. WEIGHT REDUCTION
2. DIET AND EXERCISE
1. LIFESTYLE THEN
explain the role of central/visceral obesity in T2DM?
increased central visceral fat causes increased waist/hip fat of the omentum and this contributes to insulin resitsance which snowballs and makes the central obesity worse
what does this come from?
what mechanism does it cause to be faulty? what does this lead to?
comes from chronic hyperglycemia that inhibits the increase in insulin secretion normally seen in response to hyperglycemia
worsens insulin resistance and destroys the B cell function
**THE MECHANISM GETS RUINED WITH CHRONIC INCREASED GLYCEMIA**
how does diet and exercise improve insulin resistance?
exercise increases blood flow to the muscles
increases muscle mass and decreases muscle fat storage
***this improves glucose resistance because of the decreased fats that release the cytokines and adipokines***
Type 2 DM
7 sxs associated with this?
1. often no sxs early
4. skin infections
6. abnormal fat distribution
glycated HB (A1c)
what does this show you?
how often should you check in diabetic?
what are the values for normal, prediabetic, and diabetes?
what is the goal for diabetic?
describes the state of glycemia over prior 8-12 weeks, recheck every 3-4 months
****goal in diabetic for A1c is less than 7%*****
what are the values for A1c?
what are the four qualifications/options for diabetes dx?
1. FBS over 126 (normal under 100)
2. A1C over 6.5%
3. 2 hr GTT over 200
4. Random BS over 200 (need fasting to confirm but highly likely)
what are the 3 qualifications/options for imparied glucose tolerance aka pre diabetes?
1. FBS 100-125
2. 2 hr GTT BS of 140-199
3. A1c 5.7-6.4%
what is the 3 tx algorithm used fot T2DM?
Step 1 treat at dx: lifestyle and metformin
metformin + basal insulin (long)******(this is the better option according to handler lecture)
metformin + sulfonylure
step 3: metformin + intensive insulin (basal + prandial)
what are the goal levels for:
postprandial=less than 180
a1c=less than 7
rapid acting insulin
what is the name?
what is it ideal for?
how can it be used?
onset: 5-15 mins, peak 1-2 hours
ideal for pre-meal and rapidly deals with glucose load
**can be used with insulin pump**
how long does it take?
how is it delivered? unique fact?
onset: 30-60 mins
only IV so used to tx diabetic ketoacidosis
how long does this last?
onset: 1-3 hours
duration: 14-18 hours
how long does this last?
how long is the coverage?
when is it dosed?
why is this good?
what can' you do?
long acting insulin
24 hour coverage with steady state insulin levels
dosed at bedtime
**causes less hypo/hyperglycemia**
**can't mix with other insulins**
what insulin can you use it with?
how does it work?
can be used with lispro or regular
continuous SQ insulin infusion, maintains basal insulin infusion and times bolus delivery before meals
Benefits: tight glycemia control
drawbacks: cost, skin infections, and DKA
things you should be checking every 3-6 months and annuually for diabetics?