Endocrine Flashcards

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1
Q

What is the cut off value to define hypoglycemia

A

< 70 mg/dl

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2
Q

in general, is hypoglycemia more common in type I or type 2 diabetics

A

type 1 diabetics

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3
Q

management of asymptomatic hypoglycemia

A
  • defensive actions
    • repeating measurement in near future
    • avoid critical tasks (driving)
    • ingest carbs
    • adjusting tx regimen
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4
Q

management of symptomatic hypoglycemia (able to swallow)

A
  • 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
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5
Q

management of symptomatic severe hypoglycemia (unable to swallow)

A
  • 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
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6
Q

25 g of 50% glucose (dextrose) IV should be followed with

A
  • subsequent glucose infusion or if mental status allows, food should be given
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7
Q

tx of hypoglycemia caused by a sulfonylurea

A

patient must be admitted because half-life of drug is so long that condition will certainly reoccur

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8
Q

what is equation for anion gap? what is the normal range?

A
  • Na - Cl + HCO3
  • normal < 10
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9
Q

List causes of elevated anion gap metabolic acidosis (mneumonic)

A

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
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10
Q

clinical presentation

  • hyperglycemia
  • hypotension
  • hyponatremia
  • hypokalemia
  • hyperventilation
  • elevated serum keytones
  • dehydration
  • AMS
  • diffuse abd pain
  • acidosis
  • elevated anion gap
A

diabetic ketoacidosis

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11
Q

hyperglycemic crisis in DM (diabetic ketoacidosis and hyperosmolar hyperglycemic state) are both precipitated by what conditions

A
  • infection (think UTI or pna)
  • trauma, surgery
  • MI
  • Insulin omission
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12
Q

DKA signs/symptoms tend to develop over what time period

A

hours/days

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13
Q

What is commonly the presenting sign of diabetes in type I diabetics

A

DKA

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14
Q

describe the physics behind why DKA occurs

A
  • insulin deficiency -> relative glucagon excess
    • increase in lipolysis -> glycerol + FFA
      • glycerol -> inc gluconeogenesis -> hyperglycemia
      • FFA -> ketogenesis
        • hypergycemia -> osmotic diuresis
          • dehydration
          • Metabolic acidosis
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15
Q

what diagnostics must be present to diagnose someone with DKA

A
  • hyperglycemia: generally > 250 mg/dl
  • Keytones: urine and serum positive
  • Bicarbonate: Low
  • Anion gap: elevated
  • ABG: acidosis
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16
Q

What electrolyte must you watch for when you give insulin in a patient with DKA

A
  • Potassium
    • insulin causes potassium to enter cells -> significant K+ deficit
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17
Q

List therapeutic goals of DKA

A
  • restore circulatory volume
  • correct serum osmolarity
  • clear serum keytones
  • reducing blood glucose is last
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18
Q

Treatment of DKA

A
  1. isotonic saline IV: give fluids aggressively
  2. correct electrolyte disorders
    • follow K+ closely
  3. reverse acidosis and ketogenesis
  4. control blood glucose
    • continuous IV insulin infusion
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19
Q

would you use bicarbonate to treat patients in DKA

A
  • 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
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20
Q

what are adverse effects of administering bicarbonate

A
  • paradoxical CSF acidosis
    • -> severe cerebral edema and brain damage
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21
Q

When should the insulin infusion be stopped when treating patients in DKA

A
  • If there is still an elevated anion gap, insulin administration must continue
    • presence of insulin will stop lipolysis
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22
Q

Hyperosmolar Hyperglycemic State is mainly seen in type I or type 2 diabetics

A

type 2

23
Q

signs/symptoms of Hyperosmolar Hyperglycemic State present in what time period

A
  • days to weeks
24
Q

clinical presentation

  • altered state of consciousness
  • weakness: both generalized and focal
  • polydipsia and polyruia
  • dehydration
A

Hyperosmolar Hyperglycemic State

25
Q

what plasma osmolarity is seen in Hyperosmolar Hyperglycemic State

A

plasma osmolarity > 320

26
Q

is there acidosis in Hyperosmolar Hyperglycemic State

A
  • No acidosis due to relative insulin deficiency
    • amount of insulin present is insufficient to prevent hyperglycemia but sufficient to prevent lipolysis and ketogenesis
27
Q

treatment of Hyperosmolar Hyperglycemic State

A
  • fluid and electrolyte replacement
  • insulin IV if fluid replacement alone is inadequate
  • treat underlying problem
28
Q

who gets thyroid storm

A
  • 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
29
Q

Diagnostic criteria for thyroid storm includes what categories

A
  • thermoregulatory dysfunction
  • CNS effects
  • GI-hepatic dysfunction
  • cardiovascular dysfunction
  • heart failure
  • precipitant history
30
Q

PTU and methimazole are examples of

A

Thionamides

31
Q

In thyroid storm treatment, what is given first to control tachycarida

A

beta blocker

32
Q

List treatment steps of thyroid storm

A
  1. beta blocker
  2. PTU or methimazole
  3. 1 hr after thionamide is given, administer iodide solution
  4. give glucocorticoids and bile acid sequestrants simultaneously
33
Q

function of PTU

A
  • decreases thyroid hormone synthesis AND blocks the conversion of T4 to T3
    • results in lower serum T3 levels and thus may be preferred
34
Q

function of Methimazole

A

decreased thyroid hormone synthesis

35
Q

function of glucocorticoids in tx of thyroid storm

A
  • reduce T4 to T3 conversion
  • promote vasomotor stability
  • possibly treat an associated relative adrenal insufficiency
36
Q

function of bile acid sequestrants in tx of thyroid storm

A

decrease enterohepatic recycling of thyroid hormones

37
Q

if patient is allergic to or has a contraindication to the use of thioamides, what is the treatment of choice

A

thyroidectomy

38
Q

What is Myedema coma

A
  • severe deficiency in thyroid hormones leads to encephalopathy
39
Q

causes of Myedema coma

A
  1. culmination of severe, long-standing hypothyroidism
  2. precipitated by an acute event
40
Q

what are the cardinal features of Myedema coma

A
  • Hypothermia
  • CNS depression/coma
41
Q

who is at the highest risk for Myedema coma

A
  • elderly
  • women
42
Q

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
A

Myedema coma

43
Q

Pretibial myxedema is commonly seen in what condition

A

hyperthyroid state: graves disease

44
Q

mortality associated with Myedema coma

A

30-40%

45
Q

Treatment of Myedema coma

A
  1. administer thyroid hormone: T4
  2. glucocorticoids-hydrocortisone- given until adrenal insufficiency is ruled out
  3. recovery is slow
46
Q

primary adrenocortical insufficiency

A
  • adrenal gland is damaged/not functioning and cannot produce glucocorticoids or mineralocorticoids
  • addisons disease
47
Q

secondary adrenocortical insufficiency

A
  • defect of the pituitary gland inhibiting proper release of ACTH
48
Q

tertiary adrenocortical insufficiency

A
  • suppression of hypothalamic-pituitary-adrenal function
49
Q

most common cause of tertiary adrenocortical insufficiency

A

abrupt withdrawal of chronic administration of high doses of glucocorticoids

50
Q

what are mineralocorticoid levels affected in tertiary adrenocortical insufficiency

A
  • mineralcorticoid secretion is nearly normal because this function depends mostly on renin-angiotensin system rather than on ACTH
51
Q

common symptom associated with acute adrenal crisis

A

profound hypotension

  • think of adrenal criss when shock is othewise unexplained and inadequatly responsive to vasopressors and volume replacement
52
Q

what is Waterhouse-Friderichsen syndrome

A
  • adrenal infarction due to meningococcemia
  • think of this with
    • fever
    • mental status changes
    • purpura
53
Q

managment of adrenal crisis

A
  • administer hydrocortisone and mineralocorticoid