endocrine Flashcards
Type one
ketone development occurs
weight loss
believed to be the result of an ifectious or toxic envrionment insult to pancreatic B cells
type two
random over 200
fasting x 2 > 126
bun
10-20 fluctuates indipendant of kidney function
creat
.5-1.5
metabolic syndrome
waist circumferance >40 in men and 35 in women BP >130/85 Triglycerides >150 FBG >100 HDL <40 in men and <50 in women
any 3 equals + diagnosis
super high rish of sudden cardiac death
AIC
5.5-7 6 is goal
normal fasting glucose
60-99
dm diet
total carbs 55-60%
fats 20-30
fiber 25g or 1000ca
protein 10-20%
if pt presents with ketons then
insulin is most likely warented
insulin admin split dose
05u kg/da 2/3 am (2/3 nph and 1/3 R)pm (1/2 nph 1/2 regular)
type two therapy for obese
start with weight loss
consider early oral antidiabetics
oral antadiabetics sulfonyureas
most widley prescribed stimulate pancreasee to produce insulin (glipizide, glyburide lglimiperide)
biguanides
good adjunc but can be used alone for obese pts
standard of care oral on type two diagnosis
etformin (biguininide-glucaphage) Lactic acidosis is a potential side effect.
symogi effect
nocturnal hypoglycemia leads to surge of counter regulatory hormones which increase the blood sugar, low at 0300 but high at 0700 - dc or reduce bedtime dose
dawn phenomenon
tissue becomes desentized to insulin nocturnally progressive increase through the day and elevated glucose at 0700 the dawn is rising - add or increase pm insulin dose.
syndrome x
HTN obesity and abnormal liid profile Hig trig and low HDL’s
DM 2 beyond the polys
recurrant vaginitis
blurred vision
neruopathy
chronic skin infections including prutius
sulfonyureas
stim pancreas to release insulin
alpha glucosidase inhibitors -
less sugar absorption in the gut
thiazolidediones
decrease glycogeniss - less production of glucose
avandia - increase in heart failure
actos same
non sulfonurea insulin reales stims –
mimics the effect of insulin - prandid and starliz
Major complication of Type 1
DKA
Type one DKA what is it
intracellular dehydration as a result of elevated blood glucose levels
type one DKA S&S
poly and nocturia weak N&V Kussmals altered LOC orthostatic hypo poor turgur
Type one DKA labs and diagnosits
Hyperglycemia- serum glu >250-300 Ketones acidosis ph <7.30 low bicarb low pco2 elevated hct elevated BUN Hyperkalemia leukocytosis Hyperosmololity 2(nameq/L +Kmeq/L+Glucose/18)
type one DKA managemnt
protect airway
admin 02
isotonic flu (NS) at least 1 L in he frist hr and then 500ml per hr
is glu is less that 500 use 1/2 after first hour
when glu is below 250 change to d51/2 to preent hypoglycemia
0.1u/kg rugular insulin bolus followed by 0.1u/kg/hr if glucose dose not fall bu at least 10% after the first hours, repeat the bolus
correct acidosis- if PH <7.1 with bicarb gtt 44-48meqin 900ml 1/2nss untill ph goes >7.1
do not treat hyperkalemia
monitor hourly uop
normal serum osmo
thumbnail is like 2 times the NA 140x2 is 280
HHNK
no ketones greatley elevated glu like >1000
HHNK (2) signs
normal anion gap,crazy high glucose
HHNK treatment
NS IV for massive fluid recussitation
ns then 1/2 then D51/2
may give insulin but this is contraversial
HHNK II
HYPER thyroid
most common in women 8:1
young onset 20-40
GRAVES DISEASE IS MOST COMMON PRESENTATION
other causes of hyper- toxic adenoma, subacute thyroiditis, TSH secreting tumor of pituitary, high dose amiodarone
HYPER thyroid S and S
UP - nervous sweaty (tired) emotion temor hyper reflexes increased appetite weight loss SMOOTH WARM MOIST VELVETY SKIN FINE/THIN HAIR lid lag tacchy heat intolerance increased a-fib
Labs, diagnostics for HYPER thryroid
TSH assay is the most sensitive test and is LOW in most cases
sometimes T4 is normal but T3 is elevated 80-230ng/dl)
sereum ANA usually up (no lupus or collagen disease)
HYPER thyroid and iodine
high iodine uptake is graves
low iodine uptkae is subacute thyroiditis
prefered exam to visualize the eyes in graves
MRI of the orbitz
HYPO thyroid
primary disease of the tyroid gland pituitary defficiency of tsh hypothalmic defficiency of TRH iodine deficiency hashimotos thryroiditis damage to gland
HYPOTHYROID
down extreme weakness muscle fatigue arthalgias COLD INTOLERANCE briiittle nails edema in hads and face slowed DTRs
HYPO thryoid LABS
TSH is elevated in HYPO
T4 is low or normal
hyponatremia and hypoglycemia
most common presentation of hyper thryorid
graves
most common presentation of HYPO thyroid
hashimotos thyroids
HYPERthyroid labs
TSH down T3 is up
Hyperthyroid meds-
propanolol - 10-80mg four times daily treats the shakes
thiourea drugs for small goiters and fear of isotopes
Hyper thyroid meds methimazole
tapazole - 30-60 daily in 3 divided doses
HYPERTHYROID meds radioactive iodine
131 used to destroy goiters
HYPERTHYROID meds lugols solution
2-3 drops por every day x10 days to reduce vascularity of the gland
patients with subacute thyroiditis are treated with
propanolol
treatment of thyroid crisis
propylthiouracil 150-250- q6 or
methimazole or tapazole 15-25mg q6 with the followign in one hour
lugols solution 10gtt
sodium iodine 1g slow iv
propanolol 05-2gm iv q4 or 20-120 po q6
hydrocortizone 50 q6 with reduction on improvment.
HYPER THYROID cRISIS Avoid
ASA
HYPO thyroid meds
SYNthroid, 50-100 mcg Qday, increasing dose by 25mcg, every 1-2 weeks untill symptoms stabelize, >60 years of age decrease dose
HYPO thyroid in patient manageet of myxedema coma
protect airway fluid replacement synthroid 400mcgIVx1 then 100mcg qday support hypotension slow rewrm
cushings
ATCH is hyperselected by the pituitary
adrenal tumors
chronic admin of glucocorticoids
Cushings s and s
central obesity MOON FACE AND BUFFALO HUMP acne poor wound healing purple straie hirstuism hypertension weakess amenorrhea impotence headache polyuria and thirst labile mood frequent infections
lab and diagnostics cushings
hyperglycemia hypernatremia hyperkalemia glycosuria leukocytosis ELEVATED PLASMA CORTISOL IN AM serum ACTH Dexamethasone supression test to differentiate cause
cushings treatment
depends on the cause discontinue meds inducing the symptoms transphenoidal resection of a pituitary adenoma surgical removal of adrenal tumor resection of ACTH secreting umor treat E imbalance
myxedema is functionally
a varried breathing state
Adreno cortico trophic hormone
ACTH
cushings pressure
high
cushings lab triad
HIgh sodium K and sugar
addisons cause
low cortisone (rare)
destriction of adrenal glan
defficiencey of cortisol , aldosterone and androgen
anticoag adrenal hemmorage
Addisons s and s
hyperpigmentation in the buccal mucosa and skin creases: knuckels nipples skin creases palms
diffuse tanning anf freckles,
orthostasis and hypotension
scant axillary and pubic hari
addisons acute
fever, change in LOC, rapid change in chronic symptoms
addisons lab
Low sugar, NA and K
elevated ESR
PLASMA CORTICOL <5mcg/dl at 8a
cosyntropin
addisons management
secilist referral
GLUCOCORTICOID AND MINERALOCORTICOID REPLACEMENT
hyrodcortisone
flroinef
addisons inpatient management
HYDROCORTISONE (SOLUCORTEF 100-300MCG iv WITH NSS
REPLACE VOLUME WITH d5nss at 500cchr/4hrs and then taper
addisons and vasopressors
usually dont work
assisons common underlying cause
infections
SIADH
release of ADH occurs independent of osmolaity or volume dependent stim INNAPRORIATE WATER RETENTION tumors producing ADH skull frx or head trauma CNS disorder chronic lung disease
Siadh
low NA and temp
COLD INTOLERENCE
decreased DTR
SIADH volume and sodium
euvolemic by low sodium
SIADS serum osmo vs urine osmo
<280mOsm/kg (Low)
urine osmo >100mOsm/kg (high)
normal renal cardiac and thyroid function
DI Central
related to pituitary or hypothalmus damage resulting in ADH defficiency
damage to above
infection
surgical damage
metastatic tumor
Di Nephrogenic
due to a defect in the real tubules where renal tubules are insensitive to ADH antidiuretic hormone
x-link trait
aquired due to pylenephrotis, sickle cell anemia, chronic hyper K
SIADH treatmet >120
If serum NA is Less than 120 1000ml fluid restrictions for24hrs
SIADH NA 110-120
without symptoms 500 fluid restriction q24
SIADH NA <110
or neuro symptoms present
replace with hypertonic na and lasix
at 1-2meq/hr
monitor NA and k
DI s and S
Thirst 5-10 L per day 2-20L per day peeing weigh loss fatigue changes in LOC dizzy HIGH TEMP tacchy hypotension poor turgor and dry
THIRST
PEEING
DRY
Nephrogenic DI caused by meds
lithium and methicillin
DI labs
DRY
HIgh NA
elevated BUN and creat
DI LABS
serum osmo high >290
urine osmo is low <100
urine specific gravity <1.005 peeing water
DI determination if central is suspected
DDAVP vasopressen test- 0.05-0.1ml nasally or 1 uq sq or iv with measurement of urine volume. if urine osmo goes up its central if it does not then its nephro
urine normal specific gravity
1.10-1.03
if no clear cause for DI then
MRI
DI tx NA over 150
if serum na is over 150 then D5w to replace 1/2 volume deficit in 24 hours, dont lower na quickly can cause neuro damage
DI tx NA less than 150 substitute 1/2 or .9nss
substitute 1/2 or .9nss
DI maintence dose of DDAVP
10ug every 12-24hrs intranasal
DI acute DDAVP dose
1-4ug IV or sq Q24
pheocromocytoma
rare but serious disease from excess catecholamine release causing parox or sustained HTN almost always from ADRENAL MEDULLA TUMOR
pheocromocytoma S and S
labile HTN sweating high sugar SEVERE HA palpitations tremor tacchy postural hypotension
pheocromocytoma LAB AND DIAG
TSH NORMAL
NORMATENEPHRINE AND METANEPHERINELEVATED
pheocromocytoma DIAG
CT OF ADRENALS USED TO CONFIRM AND LOCALIZE TUMOR
Pheocromocytom vs hyperthyroid differentiation
check TSH
pheocromocytoma lab test
plasma free metanephrine
pheocromocytoma non emergent
test urine 24hrs chatacholimine creat VMA and metaniphrine
pheocromocytoma TX
surgical removal of tumor is treatment of choice
Pheocromocytoma
alpha adrenergic meds can be used pre op
Pheocromocytoma post op
HYPOtension
adrenal insufficiency (HYpotension)
hemmorhage
