Endocrine Flashcards
What is the cut off value to define hypoglycemia
< 70 mg/dl
in general, is hypoglycemia more common in type I or type 2 diabetics
type 1 diabetics
management of asymptomatic hypoglycemia
- defensive actions
- repeating measurement in near future
- avoid critical tasks (driving)
- ingest carbs
- adjusting tx regimen
management of symptomatic hypoglycemia (able to swallow)
-
15-20 g oral carbohydrate
- 3-5 glucose tablets/hard candies
- 1/2 c juice
- sufficient to raise blood sugar to a safe level without inducing hyperglycemia
management of symptomatic severe hypoglycemia (unable to swallow)
-
subcutaneous or intramusclar injection of 0.5 to 1.0 mg of glucagon
- recovery in 15 min
- may be followed by N/V
- 25 g of 50% glucose (dextrose) IV
25 g of 50% glucose (dextrose) IV should be followed with
- subsequent glucose infusion or if mental status allows, food should be given
tx of hypoglycemia caused by a sulfonylurea
patient must be admitted because half-life of drug is so long that condition will certainly reoccur
what is equation for anion gap? what is the normal range?
- Na - Cl + HCO3
- normal < 10
List causes of elevated anion gap metabolic acidosis (mneumonic)
MUDPILES
- Methanol
- Uremia (renal failure)
- Diabetic, alcoholic, or starvation ketoacidosis
- Paracetamol, propylene glycol, paregoric
- Inborn errors of metabolism: iron, ibuprofen, isoniazid
- Lactid acid
- Ethylene glycol
- Salicylates
clinical presentation
- hyperglycemia
- hypotension
- hyponatremia
- hypokalemia
- hyperventilation
- elevated serum keytones
- dehydration
- AMS
- diffuse abd pain
- acidosis
- elevated anion gap
diabetic ketoacidosis
hyperglycemic crisis in DM (diabetic ketoacidosis and hyperosmolar hyperglycemic state) are both precipitated by what conditions
- infection (think UTI or pna)
- trauma, surgery
- MI
- Insulin omission
DKA signs/symptoms tend to develop over what time period
hours/days
What is commonly the presenting sign of diabetes in type I diabetics
DKA
describe the physics behind why DKA occurs
-
insulin deficiency -> relative glucagon excess
- increase in lipolysis -> glycerol + FFA
- glycerol -> inc gluconeogenesis -> hyperglycemia
- FFA -> ketogenesis
- hypergycemia -> osmotic diuresis
- dehydration
- Metabolic acidosis
- hypergycemia -> osmotic diuresis
- increase in lipolysis -> glycerol + FFA
what diagnostics must be present to diagnose someone with DKA
- hyperglycemia: generally > 250 mg/dl
- Keytones: urine and serum positive
- Bicarbonate: Low
- Anion gap: elevated
- ABG: acidosis
What electrolyte must you watch for when you give insulin in a patient with DKA
- Potassium
- insulin causes potassium to enter cells -> significant K+ deficit
List therapeutic goals of DKA
- restore circulatory volume
- correct serum osmolarity
- clear serum keytones
- reducing blood glucose is last
Treatment of DKA
- isotonic saline IV: give fluids aggressively
- correct electrolyte disorders
- follow K+ closely
- reverse acidosis and ketogenesis
- control blood glucose
- continuous IV insulin infusion
would you use bicarbonate to treat patients in DKA
- general rule: bicarbonate should NOT be used to tx patients in DKA even when there is a severe acidosis present
- however, approprate to administer bicarb when significant hyperkalemia is present
- bicarb will push potassium into cells
what are adverse effects of administering bicarbonate
-
paradoxical CSF acidosis
- -> severe cerebral edema and brain damage
When should the insulin infusion be stopped when treating patients in DKA
- If there is still an elevated anion gap, insulin administration must continue
- presence of insulin will stop lipolysis
Hyperosmolar Hyperglycemic State is mainly seen in type I or type 2 diabetics
type 2
signs/symptoms of Hyperosmolar Hyperglycemic State present in what time period
- days to weeks
clinical presentation
- altered state of consciousness
- weakness: both generalized and focal
- polydipsia and polyruia
- dehydration
Hyperosmolar Hyperglycemic State
what plasma osmolarity is seen in Hyperosmolar Hyperglycemic State
plasma osmolarity > 320
is there acidosis in Hyperosmolar Hyperglycemic State
-
No acidosis due to relative insulin deficiency
- amount of insulin present is insufficient to prevent hyperglycemia but sufficient to prevent lipolysis and ketogenesis
treatment of Hyperosmolar Hyperglycemic State
- fluid and electrolyte replacement
- insulin IV if fluid replacement alone is inadequate
- treat underlying problem
who gets thyroid storm
- can develop in patients with long standing untreated hyperthyroidism
- BUT often is precipitated by an acute event
- surgery, trauma, infection, acute iodine load, post-partum
Diagnostic criteria for thyroid storm includes what categories
- thermoregulatory dysfunction
- CNS effects
- GI-hepatic dysfunction
- cardiovascular dysfunction
- heart failure
- precipitant history
PTU and methimazole are examples of
Thionamides
In thyroid storm treatment, what is given first to control tachycarida
beta blocker
List treatment steps of thyroid storm
- beta blocker
- PTU or methimazole
- 1 hr after thionamide is given, administer iodide solution
- give glucocorticoids and bile acid sequestrants simultaneously
function of PTU
- decreases thyroid hormone synthesis AND blocks the conversion of T4 to T3
- results in lower serum T3 levels and thus may be preferred
function of Methimazole
decreased thyroid hormone synthesis
function of glucocorticoids in tx of thyroid storm
- reduce T4 to T3 conversion
- promote vasomotor stability
- possibly treat an associated relative adrenal insufficiency
function of bile acid sequestrants in tx of thyroid storm
decrease enterohepatic recycling of thyroid hormones
if patient is allergic to or has a contraindication to the use of thioamides, what is the treatment of choice
thyroidectomy
What is Myedema coma
- severe deficiency in thyroid hormones leads to encephalopathy
causes of Myedema coma
- culmination of severe, long-standing hypothyroidism
- precipitated by an acute event
what are the cardinal features of Myedema coma
- Hypothermia
- CNS depression/coma
who is at the highest risk for Myedema coma
- elderly
- women
clinical presentation
- nonpitting edema with abnormal deposits of mucin in the skin and other tissues
- puffiness of hands and face
- thickened nose
- swollen lipds
- enlarged tongue
Myedema coma
Pretibial myxedema is commonly seen in what condition
hyperthyroid state: graves disease
mortality associated with Myedema coma
30-40%
Treatment of Myedema coma
- administer thyroid hormone: T4
- glucocorticoids-hydrocortisone- given until adrenal insufficiency is ruled out
- recovery is slow
primary adrenocortical insufficiency
- adrenal gland is damaged/not functioning and cannot produce glucocorticoids or mineralocorticoids
- addisons disease
secondary adrenocortical insufficiency
- defect of the pituitary gland inhibiting proper release of ACTH
tertiary adrenocortical insufficiency
- suppression of hypothalamic-pituitary-adrenal function
most common cause of tertiary adrenocortical insufficiency
abrupt withdrawal of chronic administration of high doses of glucocorticoids
what are mineralocorticoid levels affected in tertiary adrenocortical insufficiency
- mineralcorticoid secretion is nearly normal because this function depends mostly on renin-angiotensin system rather than on ACTH
common symptom associated with acute adrenal crisis
profound hypotension
- think of adrenal criss when shock is othewise unexplained and inadequatly responsive to vasopressors and volume replacement
what is Waterhouse-Friderichsen syndrome
- adrenal infarction due to meningococcemia
- think of this with
- fever
- mental status changes
- purpura
managment of adrenal crisis
- administer hydrocortisone and mineralocorticoid
