Endo step Up Flashcards
when is insuline released
response to glucose intake
secreted by pancreatic beta islet cell
effects of insulin
induce glucose and aa uptake by muscle, adipose and liver
glucose to glycogen fatty acids and pyruvate
inhibits lipolysis
where and when is glucagon released
by alpha islet cells in response to decreased glucose and protein intake
promotes breakdown of glycogen and fatty acids
What HLA is assoc with DM I
HLA DR3 DR4 and DQ
signs of DM I
polyuria polydipsia, polyphagia, weight loss
rapid onset
labs of DMI I
hyperglycemia, glycosuria, serum and urine ketones, increase HbA1c
what happens if DM I patient gives too much insulin
hypoglycemia
what illnesses are associated with onset beta cell destruction
rubella
coxsackie virus and mumps
risk factors DM II
FMH obesity metabolic syndrome, lack of exercise, gestational DM
Dx criteria DM
random plasma glucose >200 with Sx
fasting glucose >126 on 2 separate occasions
plasma glucose >200 2 hrs after 75 g oral glucose load
HbA1c>6.5%
what are the rapid acting insulin
lispro, asoart and glulisine
what are the long acting insulins
NPH, glargine and detemir
diabetic ketoacidosis is complication of what
DM I only
complication dM II
hyperosmolar hyperglycemic nonketotic syndrome retinopathy nephropathy neuropathy atherosclerosis
what leads to DKA
low insulin
glucagon excess leading to dehydration of TG that eventually turn to ketoacids
so not taking insuline or have infection,stress, MI or high alcohol use
signs DKA
weakness, polyuria, polydipsia, abdominal pain, vomiting, dry mucous membranes, decreased skin turgor, fruity odor on breath, hyperventilation, kussmaul breathing, mental status changes from dehydration
how does metformin work
decrease hepatic gluconeogenesis
increase insulin sensitivity
side effects metformin
GI
dec B12 absorption
CI in those with hepatic or renal insufficiency
what are the sulfonylurea drug names
glyburide glimepriride, glipizide
how do sulfonlyureas work
stimulate insulin release from beta cells, reduce serum glucagon, increase binding insulin to tissue R
adverse effects of sulfonylureas
hypoglycemia. CI in those with hepatic or renal insufficiency
Mechanism of thiazolidinediones
decrease gluconeogenesis
increase insulin sensitivity
thiazolidinediones are CI in what patients
CHF
what are the gliptins
DDP-IV inhibitors that inhibit degradation of incretin. cause decreased glucagon and increased insulin
delay gastric emptying so can cause diarrhea or constipation
what are the gliflozins
SGLT-2 inhibitors that inhibit renal reabsorption of glucose, lowering BP
can cause fungal infections or recurrent UTI
how does acarbose work
alpha glucosidase inhibitor that decrease GI absorption of starch
cause flatulance
what drugs stimulate insulin release
meglitinides
can cause hypoglycemia
and sulfonylureas
what drug promotes satiety in DM
pramlintide, delays gastric emptying
labs in DKA
high glucose like 300-800, decreased Na normal or inc K (total body K decreased) so pseudohyperkalemia dec phosphate high anion gap acidosis serum and urine ketones
Tx DKA
IV saline, insulin, KCl
labs in hyperosmolar hyperglycemic state
glucose >800 and commonly above 1000
what are signs of DM retinopathy
AV nicking, hemorrhages, edema and infarcts
type of nephropathy in DM
glomerulosclerosis, mesangial expansion and BM degeneration
signs of DM nephropathy
proteinuria, renal insufficiency later turns into nephrotic
labs in DM nephropathy
hypoalbuminemia, increased Cr, increased BUN, UA showing proteinuria and microalbuminuria, EM show thickening and kimmelstiel wilson nodules
Autonomic neuropathy in DM
postural hypotension, impotence and incontenence and gastroparesis
why are DM at highger risk silent MI
altered pain sensation from neuropathy
greatest cause of death in DM patients
cardiac
macrovascular disease
signs of hypoglycemia
fainting, weakness, diaphoresis, palpitations (from epinephrine release)
headache, confusion, mental changes, decreased consciousness
causes of hypoglycemia
reactive- post eating iatrogenic (too much insulin) insulinoma (beta islet cell tumor) fasting (under production glucose) alcohol induced pituitary/adrenal insufficiency- decreased cortisol leads to insuffiecient hepatic gluconeogenesis
what stiulates and inhibits TRH
cold stimulates
stress inhibits
TSH comes from where
ant pituitary
which thyroid hormone is more potent
T3
what increase TBG levels
pregnancy and OCP
free T4 stays same
what decrease TBG levels
nephrotic syndrome and androgen use
normal free T4
signs of thyroid storm
severe diaphoresis, vomiting, diarrhea, tachy, fever and mental changes
what happens in graves
autoimmune TSI Ab bind to TSH R and stimulate hormone production
what is toxic multinodular goiter or toxic adenoma
single or multiple
produce excess thyroid hormones
increased uptake at nodules on scan
What is subacute thyroiditis
de quervain enlarged thyroid maybe from virus painful goiter neck pain, fever, increased ESR decreased uptake!!!!
Tx subacute thyroiditis
NSAIDs, beta blockers
silent thyroiditis
temporary may follow pregnancy low uptake on scan Bx will show inflammation beta blockers for sx. self limited
factitious hyperthyroid
taking hormones for thyroid
how does IV sodium iodine help hyperthyroid
block thyroid hormone release
how does hydrocortisone help hyperthyroid
inhibits conversion T4 to T3
Hashimoto
Autoimmune antithyroid peroxidase anti-TPO and antithyroglobulin Ab
also have lymphocytic infiltrates
thyroid scan of hashimoto
decreased uptake “cold”
chronic use of what can cause hypothyroidism
chronic lithium and chronic iodide
which type thyroid nodules have higher risk malignancy
cold nodule and solid on US
signs of thyroid carcinoma
nontender mass in neck. dysphagia hoarseness and maybe lymphadenopathy
Tx thyroid carcinoma
surgery, radioablation and postop replacement of hormones
malignant need resection and radioiodine ablation
chemo for mets
decreased TSH and hypothyroid
pituitary or hypothalamic
complications thyroid surgery
hypoCa from loss PTH
hoarseness from recurrent laryngeal nerve
most common thyroid carcinoma
papillary
has follicular variant
follicular has worse prognosis
which thyroid CA produces calcitonin
medullary in parafollicular cells
!! MEN 2A and 2B
most aggressive thyroid CA
anaplastic
PTH is screted in response to what and what does it do
low Ca reabsorb bone and increase Ca induce kidneys to conver Vit D decrease phosphate reabsorption (lose phosphate) increase Ca reabsorption
active Vit D does what
increase intestinal reabsorption Ca
calcitonin does what
inhibits bone reabsorption
hypercalcemia
bones stones abdominal groans and psychiatric overtones
labs in primary hyper PTH
increase Ca, decreased phosphate, increased urine Ca, increased PTH
decreased Ca. but high PTH
hyperparathyroidism secondary to malnutrition, malabsorption, renal disease or Ca wasting drugs
Tx hypercalcemia
IV fluids and bisphosphonates
most common cause hypoPTH
surgery
signs hypoPTH
hypo Ca
tingling in lips and fingers, dry skin, weakness, abdominal pain, tetany, dyspnea, tachycardia, seizures, movement disorders, cataracts, dental hypoplasia, Trousseau sign, Chvostek sign
increased phosphate, decreased PTH
Tx hypoPTH
Ca and Vit D
pseudohypo PTH
tissue does not respond to elevated PTH
Albright hereditary osteodystrophy
Sx of pseudohypo PTH
hypoCa symptoms, short stature, seizure, poor mental development
labs in pseudohypo PTH
decreased Ca, increased phosphate and increased PTH!!
Tx pseudohypo PTH
Ca and Vit D
ant pituitary secretes
ACTH, TSH, GH, FSH and LH
post pituitary secretes
ADH and oxytocin
what drugs can cause hyperprolactinemia
phenthizines, risperidone, haloperidol, methyldopa, verapamil
Tx prolactinoma
dopamine agonists like cabergoline and bromocriptine and pergolide
most common pituitary tumor
prolactinoma
acromegaly
excess secretion GH from anterior pituitary
effect of glucose on GH
should decrease it
Tx for acromegaly
surgical resection adenoma, dopamine agonists or octreotide to lessen effects
complications acromegaly
cardiac failure, DM, spinal cord compression, vision loss
child with advanced growth
check GH for gigantism
why do those with acromegaly have higher risk DM
also have increased insulin R
decreased LH FSH causes what
no estrogen
no testosterone in men impotence and testicular atrophy
decreased libido, infertility, decreased pubic hair, amenorrhea and genital atrophy in women
how to check for hypopituitary
no menstruation after medroxyprogesterone
no GH after give insulin
dec TSH
dec prolactin
cortisol does not increase after insulin from no ACTH
Sx low ACTH MSH
adrenal insufficiency causing fatigue, weight loss, dec appetite, poor response to stress, decreased skin pigment!!!!
how to determine cause of cortisol excess
low DXM test
low cortisol is usually found
if there is no decrease in cortisol then cushings
high dose DXM test– determine cause of cortisol excess
what causes cushings
excess corticosteroid- most common
pituitary adenoma
paraneoplastic from ACTH production
adrenal tumor
signs cushing
weakness, depression, menstural irregularities, polydipsia, polyuria, increased libido, impotence, HTN, acne, increased hair growth, central obesity - buffalo hump and moon facies
purple striae on abdomen and cataracts
labs in cushings
hyperglycemia, glycosuria and decreased K
complications cushings
increased risk CV or DVTs
increased infection
increased avascular necrosis of hip
hypopituitarism or adrenal insufficiency post surgery
conn syndrome
primary hyperaldosteronism from adenoma
secondary hyperaldosteronism
activation RAAS from perceived LBP from kidneys (renal a stenosis, heart failure cirrhosis, nephrotic syndrome)
signs of hyperaldosteronism
HA, weakness, paresthesias, recalcitrant HTN, tetany
labs hyperaldosteronism
DECREASED K metabolic alkalosis increased Na decreased renin in conns increased 24 urine aldosterone high ratio plasma aldosterone to plasma renin
Addison
primary adrenal insufficiency
autoimmune destruction adrenal cortices
secondary corticoadrenal insufficiency
insufficient ACTH production by pituitary
tertiary corticoadrenal insufficiency
deficient CRH release from hypothalamus
usually from chronic corticosteroid
signs of adrenal insufficiency
weakness, fatigue, anorexia, weight loss, nausea and vomiting
myalgia arthralgias
decreased libido, memory impairment and depression
hypotension
increased skin pigmentation!!!(only addison)
labs adrenal insufficiency
decreased Na
increased K from low aldosterone
decreased cortisol
increased ACTH if addisons
ACTH in secondary and tertiary adrenal insufficiency
decreased
give ACTH and if cortisol increases
secondary or tertiary insufficiency
what is addisonian crisis
severe weakness, fever, mental status changes, vascular collapse
what is congenital adrenal hyperplasia
defect in synthesis cortisol causing low cortisol
increased ACTH, adrenal hyperplasia and androgen excess from shunting
17 a hydroxylase deficiency
get cortisol androgen and estrogen deficiency so see amenorrhea, ambiguous genitalia in men
HTN
decreased K, increased Na
21 alpha hydroxylase deficiency
insufficient cortisol and aldosterone,
most common form!!!!
shifts to androgen
ambiguous genitalia in female, virilization
mactogenitosomiand precocious puberty in men
dehydration and hypotension in more severe cases
labs in 21 alpha hydroxylase def
decreased Na and increase K
what causes ambiguous genitialia in women, precocious puberty in men and HTN
11 beta hydroxylase deficieny from excess deoxycorticosterone
Tx 17 a hydroxylase def
cortisol replacement to suppress ACTH
Tx 21 a hydroxylase def
cortisol for ACTH suppresion.
fludorcortisone for mineralocorticoids
Tx 11 b hydroxylase def
cortisol replacement and anti-HTN
mutation in RET
most MEN 2A 2B
Tx pheo
alpha and beta blockers before and durign surgical resection
give alpha before beta!!!!!!!!!!!! to avoid HTN crisis
MEN1
Parathyroid hyperplasia
Pituitary
Pancreas
possible zollinger ellison
Men2A
Medullary thyroid hyperplasia
Parathyroid hyperplasia
Pheo
MEN2B
Medullary thyroid
Mucosal neuroma
Pheo
can have marfinoid body habitus
Cretinism
congenital hypothyroid froms evere iodide deficiency or hereditary
signs cretinism
poor feeding, lethargy, large fontanelles, thick tongue, constipation, umbilical hernia, poor growth, hypotonicity, dry skin, hypothermia and jaundice
labs in cretinism
decreased T4 increased TSH
Tx cretinism
levothyroxine shortly after birth
prolonged jaundice
first sign cretinism
