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