Lecture 8 - Endocrine Flashcards
DKA
hyperglycemia –> ketosis –> metabolic acidosis
most common acute life threatening complication of diabetes
MC in type 1 than type 2
What is the pathophysiology behind DKA?
decreased insulin –> decreased glucose utilization –> body in starvation mode
starvation –> promote gluconeogensis and glycogenolysis –> increase glucose leves
(convert adipose to free fatty acids)
fatty acids make blood highly osmotic
fatty acids oxidized to ketones –> metabolic acidosis
What causes DKA?
precipitating event, commonly: infection (MC) injury/trauma MI, CVA, TIA pancreatitis ethanol, drug use gastroenteritis noncompliance with meds
What are the signs and sxs of DKA?
general fatigue/weakness abdominal pain, can include N/V Kussmaul's respiration (deep and fast, trying to compensate for acidosis) fruity breath polyuria, polydipsia, polyphagia AMS
What lab findings do you see in a pt with DKA?
serum glucose >250 serum ketones serum bicarb <15 arterial pH <7.3 anion gap BUN elevated
always be sure to check serum potassium (this needs to be corrected before you give insulin)
Why do you need to correct potassium before giving insulin in a pt with DKA?
acidosis drive K out of the cell, raising serum K+
when insulin is given, it drives K into the cells, causing HYPOkalemia –can lead to lethal arrhythmia
What is the treatment for DKA?
1) Fluids
2) Potassium
3) Insulin
ABCs
monitor glucose hourly
monitor VBG every 2 hours
determine underlying cause of DKA
Fluids - expand extracellular volume and stabilize cardiovascular status
If shock: give isotonic saline bolus
if NO shock: give IV isotonic saline 15-20ml/kg/hour
If a pt is not in shock but is in DKA< what is the rate of NS we give?
15-20ml/kg/hour
after volume restored:
five 1/2NS at 4-14ml/kg/h
when serum glucose reaches approx 200, add dextrose
potassium replacement:
<3.3: HOLD insulin, KCL 20-40 mEq/h
>3.4 - <5.3: start IV and PO KCL at 20-30 mEq/L
>5.3: no K, monitor K every 2 hours
insulin:
Bolus 0.1 units/kg IV then start continuous IV infusion fo 0.1units/kg/hr
HHS
hyperglycemic hyperosmolar non-ketone syndrome
dehydration! you have enough glucose
unlike DKA, HHS have sufficient insulin to prevent lipolysis and ketogenesis
HHS results from gradual diuresis causing significant dehydration, leading to electrolyte deficiencies and ultimately mental status changes
HHS caused by physiological stressors like DKA (infections, MIs, CVA, trauma, decreased PO intake or medications)
Who gets HHS?
> 65, chronic care facility, dementia
change in DM medications, new medications (especially steroids)
infection hx
What are the signs and sxs of HHS?
polydipsia, polyphagia, polyuria
generalized weakness
AMS
dry mucus membrane
What labs do you expect see for someone in HHS?
fluid deficit (9L vs 3–5L in DKA)
serum glucose >600 mg/dl
glycosuria is prominent
serum osmolality is 320-380 mOsm/kg
serum bicarb usually >15mEg/L, pH is usually >7.3, usually no anion gap
What is the treatment for HHS?
1) Fluids
2) Potassium
3) Insulin
FLUIDS
usually 1-1.5 L of NS over the first hour, then
correct 1/2 fluid deficit in first 8 hours and then the other 1/2 over the next 24 hours
if sodium is high: use 1/2NS at rate of 250mml/h after initial bolus
if sodium is normal or low: continue NS
once serum glucose reaches 250mg/dl 5% dextrose in 1/2NS at rate 250ml/h if sodium is high, if normal sodium or low sodium 5% NS
potassium (same as DKA, basically correct potassium before insulin)
insulin IV only
goal: decrease glucose by 50-70mg/dl/hr
Hypoglycemia
serum glucose less than 50mg/dL
severe hypoglycemia is <30mg/dl
What are the most common causes of hypoglycemia?
exogenous insulin
others:
pancreatic B cell tumor
EtOH
What are the signs and symptoms of hypoglycemia?
initially: increased catecholamine release: tachycardia, irritable, diaphoresis, paresthesia's, hunger, and decreased concentration AMS visual disturbances hallucinations seizures
What is the treatment for hypoglycemia?
give 50cc of 50% dextrose (amp of D50)
remember to give thiamine 100mg IV /IM in alcoholics to prevent Wernicke’s encephalopathy
What is the most common cause of hyperthyroidism?
grave’s disease
autoimmune disorder resulting from thyroid stimulating hormone receptor antibodies that stimulate thyroid gland growth and thyroid hormone synthesis and release
What are the signs and sxs of hyperthyroidism?
“high/fast”
changes in vision, dry eyes, increased neck size, palpitations, heat intolerance, tremor, moist skin, weight loss, diarrhea, fatigue, anxiety
tachycardia HTN anxious/agitated tremor ophthalmopathy pretibial myxedema lid lag diffuse goiter thyroid nodule brisk reflexes
How do you dx hyperthryoidism?
suppressed serum TSH
elevated T3/T4
What is the treatment for hyperthyroidism?
supportive
beta blockers (atenolol 25-50mg) for symptom control
long term treatment: antithyroid drugs (thionamides), radioiodine, or surgery
MC thionamides: MMI or PTU
Thyroid storm
hx of hyperthyroidism often thyrotoxic sxs over many months prior AMS recent thyroid surgery/treatment D/c MMI or PTU
precipitating factors:
infection, trauma, MI, radioiodine, pregnancy
What are the signs and sxs of thyroid storms?
tachycardia (SVT) tachypnea systolic HTN hypotension from cardiac collapse FEVER (can be greater than 104, don't let this throw you off your track of endocrine etiology) hyperthermia AMS N?V?D dehydration
How do you dx thyroid storm?
TSH low T4 elevated hyperglycemia leukocytosis abnormal LFTs
