Endocrine Flashcards
DDx for unexplained weight loss
Malignancy - especially in the elderly
Uncontrolled type 1 DM - more so in younger patients
Adrenal insufficiency - pituitary adenoma or Addison’s Disease
Pheochromocytoma - inappropriate catecholamine release
Hyperthyroidism
DDx for bone pain and pathologic fractures
Disorders of the parathyroid gland can cause alterations in bony reabsorption, leading to excessive bony demineralization
—-hyperparathyroidism is considered in cases of bone pain and hypercalcemia
Osteopenia - especially when encountered before age 60
–hyperthyroidism
–Cushing’s Syndrome - disorder of cortisol
Difference between type 1 and type 2 diabetes
DM I - presents in childhood
-Caused by pancreatic islet Beta cell destruction predominantly by an autoimmune process
–Islet autoantibodies are often present
-polyuria, polydipsia and weight loss associate with a random serum glucose >200
DM II - presents in adulthood
-Caused by insulin resistance with a defect in compensatory insulin secretion
—So much sugar/carbs in the diet that the body just begins to ignore the amount of insulin that is being made
What does insulin do?
Transport glucose to the cells for use
In DM I, there is not enough insulin to move the glucose, due to islet cell destruction
In DM II, the body is making a lot of insulin because there is so much glucose, therefore the cells are insensitive to the insulin so the glucose builds up
Diagnosis of DKA
Diagnosis:
-Hyperglycemia >250
-Acidosis pH <7.3
-Serum bicarb <15
-Serum positive for ketones: beta hydroxybutyrate >1.5
-Anion gap >15
-Elevated serum osm >330
-Kussmaul’s breathing - faster, deeper breathing
-Hypotension and tachycardia
-Parched mucous membranes
-Abd pain, n/v
Treatment of DKA
Intubate if pt is too altered to maintain airway
Give insulin: ALWAYS regular human insulin
—0.15 units/kg IV bolus
—0.1 units/kg/hr IV as gtt
—–Insulin gtt gets calculated hourly according to the change in glucose
Restore fluid deficit: usually 4-5L in an adult - NS preferred
—Once glucose is <250, change fluid to D5%W to maintain serum glucose 250-300
No need to treat hyperK. As you give insulin the K will come down because it will be pushed into the cell
Treat severe acidosis with bicarb until pH is >7.1
What electrolytes should you monitor in DKA
Watch for K
–Could present initially hyperK or normal K but the K will always drop during treatment so you might need to supplement
—check BMP every 4 hours
Also keep eye on bicarb - likely will be low initially but if you replete fluids, the bicarb will normal out
Treatment of hypoglycemia
If awake and alert, give sugary foods/drinks
If the pt has AMS: Given D50% 50cc IV, recheck glucose shortly after
—Feed as soon as possible, well balanced
If patient took overdose of metformin:
–Give Octreotide 75mcg SC/IM
–Feed the patient
–Observe for 12-24 hours given long half life
Lab findings in hyper- and hypothyroidism
Hyperthyroidism:
TSH will be low
T3 will be elevated
123I uptake and scan will be elevated
Antithyroglobulin will be elevated
Hypothyroidism:
TSH will be high
Free T4 will be elevated
If antithyroglobulin is high and TSH is high - Hashimoto’s
Thyroid nodules: High risk and low risk
Less worrisome:
-High TSH, low FT4
-Older women
-Cystic appearance on US
-Family hx of goiter
More worrisome:
-vocal changes
-Young men
-Hx of radiation exposure
-Any solitary, firm nodule
Causes of goiter
Iodine deficiency
Congenital hypothyroidism
Clinical features of hypothyroidism
fatigue
cold intolerance
constipation
depression
weight gain
puffy appearance to the face
Myxedema: Causes, clinical presentation, treatment
Usually occurs when a hypothyroid patient is placed under physiological stress (infection)
Clinical presentation:
-decreased LOC
-hypothermia
-hypoNa
-hypoglycemia
-hypotension
-hypoxia/hypercapnia
-Often coexists with acute adrenal insufficiency
Treatment:
Levothyroxine 400mcg IV once and then 100mcg IV daily
If adrenal insufficiency is present then hydrocortisone 100mg IV then 25-50mg IV every 8 hours
Fluid replacement
Slowly rewarm with blankets
Treatment of hyperthyroidism
Methimazole 30-60mg Daily until FT 4 levels return to normal
Propranolol as symptomatic relief
131I to destroy the thyroid and then thyroid hormone replacement for life
Clinical presentation and labs of hypoparathyroidism
Paraesthesias start first followed by abd cramping and tetany
Labs will show low serum and ionized calcium, high phosphate
Clinical features of diabetes insipidus
Intense thirst with a specific craving for cold drinks
Correspondingly large urine output
Weight loss
Fatigue
tachycardia
Hypotension
SIADH: What is it? Causes?
Syndrome of inappropriate antidiuretic hormone secretion
Excessive unsurpressible release of antidiuretic hormone either from the posterior pituitary gland or an abnormal non-pituitary source
Result is low serum osm, profound hyponatremia and very concentrated urine
Causes:
CNS diseases that stimulate hypothalamus
Various cancers
Various lung disease
Numerous drugs that chemically stimulate the hypothalamus
Inherited mutations
Treatment of SIADH
Mild and asymptomatic hypoNa:
Treat with adequate solute intake and fluid restriction to 1000mL/day
Moderate and symptomatic hypoNa:
Raising serum sodium level by 0.5 to 1/hr for a total of 8 during the first day with the use of lasix and replacing Na and K losses with NS
Severe symptoms (confusion, convulsions, coma):
Hypertonic saline and lasix - slow. Monitor Na and K losses
Clinical features of Addison’s Disease
Disease caused by destruction or dysfunction of the adrenal glands resulting in deficiency in cortisol, aldosterone and adrenal androgens
Low ACTH
Symptoms include:
Weakness
Easy fatiguability
Anorexia
Weight loss
N/v/d
amenorrhea
Hyperpigmented skin
sparse axillary hair
Labs show hypoNa, hyperK and neuropenia
Presentation of acute Addisonian Crisis
Hypotension
Hypothermia
Hypoglycemia
HyperK
Treated with hydrocortisone 50-100mg IV every 6-8hrs depending on response
Causes and Clinical features of Cushing’s Disease
Excessive circulating cortisol which can be caused by chronic glucocorticoid use, pituitary adenoma
Clinical features:
Moon face
buffalo hump
central obesity
muscle waisting
Hirsutism
Purple striae
Amenorrhea
Polyuria and polydipsia
Labs show hyperglycemia, hypernatremia, hypoK, elevated serum cortisol in the AM
How to work someone up for pheochromocytoma - Clinical presentation and labs
Rare condition wherein a tumor forms in the adrenal glands and secretes catecholamines inappropriately
Pt will have attacks of headache, perspiration, palpitations, nausea, chest pain, tremors
Acutely hypertensive, tachycardic
TSH and FT4 would be normal
Should collect a 24 hour urine metanephrine (metabolite of norepinephrine and epinephrine)
CT is the confirmatory test to localize the tumor
What is the diagnostic criteria for diagnosis of DMI
Serum fasting (at least 8 hours) blood glucose >126 on more than one occasion
or
Random plasma glucose >200 with signs of hyperglycemia (polyuria, polydipsia and weight loss)
or
A1c >6.5
Standard initiation of treatment for newly diagnosed DMI
Basal insulin + mealtime boluses of a rapid-acting or short-acting insulin
Basal could be intermediate acting (NPH) or long-acting (Lantus) or could be a short acting continuous monitoring insulin pump
What are the risk factors for metabolic syndrome - related to DMII
Waist circumference >40in for men and >35 for women
BP>130/85
Triglycerides >150
FBG >100
HDL<40 in men and <50 in women
If you have two of these you are at significant increased risk for cardio-embolic stroke
If you draw a glucose that is over 1,000, is it HHS or DKA?
Often HHS
DKA does not go that high usually
What are the lab results typical in Hyperosmolar hyperglycemic state (HHS)
Greatly elevated serum glucose
Hyperosm
Elevated BUN and Cr
Elevated A1c
Relatively normal pH (could be ever so slightly acidotic but normal for the most part)
Normal Anion Gap
Treatment of HHS
Almost identical to treatment of DKA
Protect the airway
Administer O2 as needed
Isotonic fluids (NS) at least 1L in the first hour, then 500mL/hr
Then switch to 1/2NS after the first hour and watch glucose levels
Once glucose is <250, switch to D5 1/2 NS to prevent hypoglycemia
0.1 unit/kg regular insulin IV bolus
Then give 0.1 units/kg/hr drip
In hyperthyroidism, what do the labs look like?
Low TSH
Elevated T3, sometimes elevated T4
High iodine uptake is consistent with Grave’s Disease
Low iodine uptake is consistent with subacute thyroiditis
Labs results in hypothyroidism
TSH is elevated
T4 is low or low normal
Often also see hypoNa and hypoglycemia
Treatment of thyroid crisis
Complication of hyperthyroidism
Propylthiouracil 150-250mg every 6 hours
or
Methimazole 15-25mg every 6 hours with the following in 1 hour:
-Lugol’s solution 10gtts three times daily
or
-sodium iodine 1g slow IV with
-Propranolol 0.5-2g IV every 4 hours or 20-120mg PO every 6 hours with
-Hydrocortison 50mg every 6 hours with rapid reduction as situation improves
Avoid ASA
How do you work someone up for Cushing’s Syndrome
Dexamethasone suppression test and check plasma cortisol in the AM
Serum ACTH
Treatment of Cushing’s Syndrome
Determine the cause
-Discontinue medications (steroids) that may be causing sxs
-Transsphenoidal resection of a pituitary tumor
-Surgical removal of adrenal tumors
-Resection of ACTH secreting tumors
Manage electrolyte imbalances
What is a test to rule out Addison’s Disease?
Cosyntropin stimulation test
Outpatient treatment of Addison’s Disease
Glucocorticoid (hydrocortisone)
Mineralocorticoid (Fludrocortisone acetate (Florinef)
Labs and diagnostics for SIADH
Euvolemic hypoNa
Decreased serum osm
Increased urine osm
Urine sodium >20
Renal, cardiac, thyroid function is normal
Causes of Diabetes Insipidus
Central:
Related to pituitary or hypothalamus damage resulting in ADH deficiency
-Idiopathic causes
-Damage to hypothalamus or pituitary
-Surgical damage
-Accidental trauma
-Infections
-Metastatic carcinoma
Nephrogenic:
Defect in the renal tubules resulting in renal insensitivity to ADH
Psychogenic
Laboratory findings and diagnostics in Diabetes insipidus
HyperNa
Elevated BUN and Cr
Serum osm >290
Urine osm <100
Urine spec grav low
Should conduct Vasopressin challenge to determine if central DI or nephrogenic - positive in central DI
If no cause can be found, then should order Brain MRI to look for mass/lesion
Management of Diabetes Insipidus
If serum Na >150, given D5W IV to replace 1/2 volume deficit in 12-24 hours
When Na <150, switch to 1/2NS or NS
DDAVP 1-4mcg IV or SW every 12-24 hours for acute situations and then switch to IN
