2- Endocrine Emergencies Flashcards
Pt with a hx of T1DM presents with diaphoresis, blurry vision, weakness, irritability, and confusion. PE shows tachycardia. What are you concerned for?
Hypoglycemia
What value is defined as hypoglycemia?
< 70 mg/ dL
Delay in eating, poor caloric intake, increased or unusual physical exertion, increased physiologic stress, impaired counter-regulatory hormone axis, alterations in therapeutic regimen, accidental excessive dose of exogenous insulin, variable insulin absorption at injection site, and excessive insulin release caused by sulfonylurea are possible causes of what?
Hypoglycemia
Is hypoglycemia more common in T1 or T2DM?
T1
What is the tx for asx hypoglycemia (drug-treated DM and glucose < 70)?
Defensive actions
(repeat measurements, avoid critical tasks, ingest carbs, adjust tx regimen)
What is the tx for a pt who is hypoglycemia but awake?
15-20g oral carbohydrate followed by long acting carb
(raises blood sugar to a safe level w/o inducing hyperglycemia)
What is the pt who is severely hypoglycemia and has AMS who is unable to safely swallow oral glucose?
Subcutaneous or IM injection of 0.5- 1.0mg of glucagon
What is a SE of subcutaneous of IM injection of glucagon in the tx of hypoglycemia?
N/V
Aside from tx with subcutaneous/ IM glucagon, how can severe hypoglycemia be treated more quickly?
25g of 50% glucose (dextrose) intravenously, followed by subsequent glucose infusion or food (if possible)
Stroke-like sxs evident on a focal neuro exam of a pt with hypoglycemia will likely resolve with what?
Resolution of hypoglycemia
Under what circumstances would a pt with hypoglycemia need to be admitted?
If due to sulfonylurea
(half life of drug makes reoccurence very likely)
Pt presents with severe abd pain, vomiting, confusion, and frequent urination. On PE you note an unusual, “fruity” odor to breath. What might you be concerned for?
Hyperglycemia/ DKA
What diagnostics/ labs should be ordered for a pt if there is suspicion for hyperglycemia/ DKA?
CBC, CMP, EKG, urine
What will CMP and UA show for a pt in hyperglycemia/ DKA?
Bicarb decreased = metabolic acidosis
UA (+) for ketones
How will anion gap appear for a pt with hyperglycemia/ DKA?
Elevated anion gap
What are the 2 types of hyperglycemic crises seen in pts with DM?
DKA and hyperosmolar hyperglycemic state (HHS)
What are the 2 most common precipitating causes of DKA and HHS? (hyperglycemic crises in DM)
Infection and insulin omission
Pt presents with abd pain/ N/V, Kussmal respirations (hyperventilation), hypotension, metabolic acidosis, elevated glucose, hypotension/ shock/ dehydration, and elevated serum ketones. What are you concerned for?
DKA
Pt presents with falsely lowered sodium, low chloride and bicarb, elevated BUN/Cr, anion gap, WBC, acidosis on ABG, evidence of MI on EKG, electrolyte abns, arrhythmias, and evidence of stroke on head CT. What are you concerned for and what additional, more specific, lab values would support this dx?
DKA
- Glucose: 350-500 mg/dL
- Ketones: urine and serum (+)
- K+ levels changing
(glucose cannot be only finding to dx)
How will K+ levels change from presentation and w/ treatment for DKA?
- @ presentation- elevated (insulin def and hyperosmolality = K+ movement out of cells into EC fluid)
- w/ treatment- K+ falls (must monitor and prepare for supplementation)
What are the therapeutic goals for tx of DKA aside from dx, ABCs, restore circulatory volume, correct serum osmolarity, correct electrolytes and anion gap, and tx underlying condition?
Reverse ketogenesis, not attain normoglycemia (although you still want to reduce blood glucose)
What is included in the management of DKA aside from ABCs and correct electrolyte disorders? (4)
- Isotonic saline (0.9 NS) IV
- Control blood glucose
- Reverse acidosis and ketogenesis
- Aggressive IV fluids
How do you reverse acidosis/ ketogenesis in DKA?
Insulin bolus IV vs continuous IV insulin infusion
What is included in fluid management for DKA?
- 15-20 mL/ kg lean body weight per hour (monitor urine output)
- Add dextrose to saline when blood glucose reaches 200-250 mg/dL
What should you NOT use to tx patients in DKA because K+ will go into cell?
Bicarb (also may slow the rate of ketosis/ accelerate ketogenesis)
What are the complications of bicarb used to raise pH levels in DKA? (4)
Hypernatremia, hypokalemia, paradoxical CSF acidosis, residual serum alkalosis
The following is the pathophysiology for what complication with the use bicarb to tx patients in DKA:
Increased uptake of CO2 by cells = IC cerebral acidosis = neuro deterioration = edema/ brain damage
Paradoxical CSF acidosis
What is the one setting where bicarb is an appropriate tx for DKA?
Significant hyperkalemia (lowers K+ quickly)
What is the mainstay of reversing ketoacidosis?
Fluid admin + insulin
In treating a pt with ketoacidosis with insulin infusion… do you stop insulin infusion when glucose normalizes?
NOT if there is still elevated anion gap
Is serum osmolarity elevated more in HHS or DKA?
HHS
Is HHS seen more with T1 or T2DM?
T2DM (in presence of precipitant)
Pt presents with insidious onset (days to weeks) of AMS, weakness (generalized and focal), polydipsia and polyuria, and dehydration. What are you concerned for?
HHS
What is the pathophysiology for HHS?
Hyperglycemia > glycosuria > dehydration > worsens hyperglycemia
Pt presents with plasma osmolality > 320 and 5-10 fluid deficiency. What are you concerned for?
HHS
Does a pt with HHS have ketones?
NO because only relative insulin deficiency (sufficient to prevent significant lipolysis/ ketogenesis)
What does the absence of ketones indicate?
NO ACIDOSIS
What is tx for HHS?
Fluid + electrolyte replacement, insulin IV, tx underlying
Pt presents with fever, palpitations, diarrhea, hypervigilant, agitated, high HR/ RR/ BP/ temp, prominent eyes, tremor, hyperreflexia in LE’s, confusion. What are you concerned for?
Hyperthyroidism
In addition to hyperthyroidism sxs on PE, what specific finding might contribute to your suspicion for dx?
Prominent, tender, thyroid
What will labs show for hyperthyroidism?
TSH low, FT3/4 high
(should also order EKG)
What is defined as a rare and potentially fatal complication of hyperthyroidism?
Thyroid storm
How is a thyroid storm diagnosed?
Severe and life threatening sxs, biochemical evidence of hyperthyroidism
(hyperpyrexia, CV dysfunction, AMS)
Pt with long-standing untreated/ undertreated hyperthyroidism (Grave’s, TMG, solitary toxic adenoma) + precipitation (surgery, trauma, infection, acute iodine load, post-partum) is at risk for what?
Thyroid storm
Pt presents with the following:
Hyperthyroid sxs + hypermetabolism, excessive adrenergic response
(+/- hyperpyrexia, a-fib/ HF, goiter/ exophthalmos/ tremor/ moist skin, shock, confusion/ agitation/ coma, death)
What are you concerned for?
Thyroid storm
What is included in supportive care of thyroid storm tx? (5)
ICU, cooling measures, IV fluids, electrolyte replacement, nutrition support
Aside from supportive care, what are the specific tx goals for thyroid storm?
Prevent thyroid hormone release, decrease peripheral action of circulating thyroid hormone, tx precipitating conditions
What meds are used in the tx of thyroid storm? (3)
- BBs (propranolol)
- Thionamides (PTRU/ methimazole)
- Iodine solution (Lugol’s solution, SSKI)
(adjunct: glucocorticoids, bile acid sequestrants (cholestyramine))
What pharm tx for thyroid storm has the following MOA?
Decreases TH synthesis and blocks conversion of T4 to T3
PTU
What pharm tx for thyroid storm has the following MOA?
Decreases TH synthesis (does not inhibit T4 to T3 so = lower T3 levels)
Methimazole
What pharm tx for thyroid storm has the following MOA?
Reduce T4 to T3 conversion, promote vasomotor stability, tx associated relative adrenal insufficiency
Glucocorticoids
What pharm tx for thyroid storm has the following MOA?
Decrease enterohepatic recycling of thyroid hormones
Bile acid sequestrants
What is the sequence of tx for thyroid storm?
- BB
- Thionamide
- Iodine solution (1 hour after thionamide to prevent for use as substrate)
When is methimazole vs PTU preferred for tx of thyroid storm due to longer half life, lower risk of hepatic toxicity and restores euthyroidism more quickly?
Severe but not life-threatening hyperthyroidism
What should be done for pts initially treated with PTU prior to d/c from hospital?
Transitioned to methimazole
What is the tx of choice for thyroid storm IF allergic or c/i to thionamides or refractory to meds?
Thyroidectomy
What is the mortality for thyroid storm?
10-30%
Pt presents with lethargy, weakness, hx of sleeping more than normal, cool to touch, slowed speech with delayed response, hyporeflexia, hx of thyroidectomy. What are you concerned for?
Myxedema coma
What will labs show for pt with myxedema coma?
Markedly elevated TSH, markedly depressed T4/ T3
What is defined as a rare complication of hypothyroidism/ occurs as culmination of severe, long-standing hypothyroidism + precipitation by acute event that has the potential to lead to encephalopathy?
(acute event = infection, MI, cold exposure, opioids)
Myxedema coma
What are the hallmark features of myxedema coma?
Hypothermia, CNS depression/ coma
(others: hypotension, bradycardia, hyponatremia, hypoglycemia, hypoventilation)
What is considered the highest risk population for myxedema coma?
Elderly women
What is defined as puffiness of hands/ face, thickened nose, swollen lips, enlarged tongue, secondary to nonpitting edema, abn deposits of mucin?
Myxedema
What is the mortality for myxedema coma?
30-40% (not always easy to dx)
What is included in the management for myxedema coma (aside from dx, ABCs, IV fluids, correct electrolyte abns, rewarming blankets, tx underlying)?
- Thyroid hormones (IV T4, T3 controversial)
- Glucocorticoids (hydrocortisone) until adrenal insufficiency r/o
Is the recovery from myxedema coma fast or slow?
SLOW
Pt presents with profound hypotension, fever, vague abd pain, N/V, intermittent confusion, hx weight loss, recent hx of surgical procedure. What are you concerned for?
Adrenal insufficiency
What is defined as a potentially life-threatening condition that occurs when there is a lack of cortisol produced by adrenal glands?
Adrenal insufficiency
What is the result of adrenal gland damaged/ not functioning and it cannot produce glucocorticoids or mineralocorticoids (possible acute exacerbation of chronic insufficiency)?
(possible exacerbation = adrenal hemorrhage, adrenal infarction, anticoag complications, congenital abns)
Primary AI (Addison’s)
What is defined as a defect of pituitary gland inhibiting proper release of ACTH?
Secondary AI
What is defined as suppression of HPA function and caused by abrupt withdrawal of chronic admin of glucocorticoids, mineralocorticoid secretion ~ N?
Tertiary AI
What is adrenal infarction due to meningococcemia and p/w fever, AMS, and purpura?
Waterhouse= Friderichsen syndrome
What is the management for adrenal insufficiency (aside from ABCs, IV fluids, correct electrolyte abns, tx underlying)?
- Hydrocortisone (100 mg IV q 6 hrs) (MOST IMPORTANT in acute stages of disease)
- Mineralocorticoid- Florinef (0.1 mg po qd)
What additional management should be done for AI if bacterial etiology of acute adrenal crisis is suspected (sepsis)?
Blood cultures and empiric abx
If there is reason to suspect adrenal crisis in ANY pt then what should you do?
Tx immediately w/ hydrocortisone
What should you be concerned for if shock is otherwise unexplained and inadequate response to vasopressors and volume replacement?
Adrenal crisis
