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Emergency Medicine > Endocrine and Metabolic Emergencies > Flashcards

Endocrine and Metabolic Emergencies Flashcards

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1
Q

Fundamentals of tx of DKA?

A
  • volume repletion
  • insulin
  • correction of lytes and acid-base imbalance
  • tx precipitating cause
  • avoid complications
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2
Q

Most impt initial step in tx of DKA?

A
  • Rapid fluid admin
  • NS recommended initially
  • then alt w/ 0.45% NS
  • BG and ketone conc will fall after fluid admin andb/f implementation of any other therapeutic modality (rise in GFR allows for glucose and ketone body clearance)
  • increased insulin perfusion facilitates action of insulin
  • *insulin and fluid key to tx
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3
Q

Insulin therapy in DKA?

A

***- admin at 0.1 units/kg/hr after fluid bolus
- continus IV infusion of small doses through pump:
less complications
- loading dose not necessary
- monitor freq.
- DONT do IM or SubQ (erratic absorption)

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4
Q

What causes K+ def in DKA?

A
  • combo of acidosis, osmotic diuresis, and vomiting
  • initial serum conc usually normal or high due to:
    intracellular exchange of K+ for H+
    total body fluid deficit
    diminished renal fxn
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5
Q

K+ therapy in DKA?

A
  • necessary for replacement in 1st 24-36 hrs - don’t have to replace as much as previously thought
  • will normalize w/ fluid tx
  • if tx rapidly - K+ conc will fall rapidly -
    can lead to cardiac arrhythmias, resp paralysis, parlytic ileus and rhabdo
  • development of severe hypokalemia is potentially most life threatening lyte derangement during tx of DKA
  • want to maintain extracellular K conc during acute phase and replace intracellular deficit over days
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6
Q

Complications of DKA?

A
  • hypoglycemia
  • cerebral edema
  • hypokalemia
  • hypophosphatemia
  • adult resp distress syndrome
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7
Q

Causes of DKA?

A
  • new onset diabetic
  • compliance issues
  • d/c of insulin
  • insults to body: infection (Pneumonia, UTI) or MI, PE
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8
Q

What is hyperosmolar hyperglycemic state? Who does it occur in?

A
  • AKA nonketotic hyperosmolar state
  • occurs in pts w/ poorly controlled or undx type II DM
    syndromes:
    -severe hyperglycemia
    -hyperosmolality
    -relative lack of ketonemia
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9
Q

How is hyperosmolar hyperglycemic state defined?

A
  • serum glucose usually over 600 mg/dL
  • elevated plasma osmolality of over 315 mOsm/kg
  • bicarb over 15
  • arterial pH over 7.3
  • serum ketones that are negative to mildly positive
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10
Q

Shared sxs b/t DKA and hyperosmolar hyperglycemic state?

A
  • hyperglycemia, hyperosmolality, severe vol depletion, lyte disturbances, and sometimes acidosis (usually due to hypoperfusion - lactic acidosis)
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11
Q

Diff b/t DKA and hyperosmolar hyperglycemic state?

A
  • DKA:
    glucose: over 250
    pH: lower than 7.3
    bicarb: less than 15
    urine ketone: +
    serum osmolarity: variable
    anion gap: greater 10
    AMS: alert/drowsy to stupor/coma

-HHNS:
glucose: over 600
pH: greater than 7.3
bicarb: greater than 15
urine ketone: small
serum osmolarity: over 320
anion gap: less than 12
AMS: stupor/coma

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12
Q

Epidemiology of HHNS?

A
  • poorly controlled or undx DM II
  • less freq than DKA
  • mortality rates higher than DKA:
    15-30% compared to 5% in DKA
    Increases w/ advanced age
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13
Q

Who is at greatest risk for HHNS?

A
  • iability to access water

- nonambulatory nursing home pt

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14
Q

Presentation of HHNS?

A
  • elderly, often brought in by caretaker due to abnorm VS and AMS
  • often precip by acute illness: pneumonia, UTI (50% cases)
  • most have some levels of baseline cog impairment
  • sxs: weakness, anorexia, fatigue, cough, SOB, abd pain
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15
Q

Tx of HHNS?

A
  • volume repletion
  • correct lytes
  • ID and tx precip cause
  • gradual correction of hyperglycemia
  • manage concurrent illnesses
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16
Q

S/S of hypoglycemia?

A

Neurogenic (increased ANS activity):

  • sweating
  • pallor
  • tachy
  • palpitations
  • tremor/shaking
  • nervousness/anxiety
  • tingling, paresthesias (mouth and fingers)

Neuroglycopenic (not enough sugar to feed brain):

  • HA
  • drowsiness
  • lightheadedness/syncope
  • mental dullness/confusion
  • amnesia
  • seizures
  • coma
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17
Q

Hypoglycemia thresholds - assoc manifestations?

A

Vary depending on individual

  • drop 65-68 mg/dl: secretion of insulin counter-reg hormones glucagon and epi
  • 54 mg/dL: neurogenic sxs
  • 47 mg/dL: sxs of cog dysfxn (neuroglycopenic)
  • Danger zone: under 50 mg/dL
  • poorly controlled diabetes w/ persistent hyperglycemia results in higher glucose thresholds
  • lower thresholds w/ repeated hypoglycemia episodes
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18
Q

What is hypoglycemia unawareness? Pts at greatest risk?

A
  • development of low serum sugar values w/o physiologic ability to react:
    places pts at greater risk for coma and other neuro sequelae
  • pts at greatest risk:
    extremes of age
    comorbidities
    meds
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19
Q

Hypoglycemia tx for outpt?

A
  • 15-20 g of glucose (effects should be noticeable in 15 min)
  • may only be transient so retest plasma glucose in 15 min w/ add txs as necessary
  • glucagon should be Rx for all pts at sig risk
  • alt of insulin regimen or dosage adjustment of ral med may help
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20
Q

Hypoglycemia tx in ED?

A
  • take blood sugar on anyone who comes in w/ AMS!
  • initial: admin 1g/kg dextrose, D50W in adults and infusion of D10W to follow for maintenance of glucose above 100 mg/dL
  • repeat glucose q 30 min for 2 hrs
  • oral replacement (300 g carb given PO)
  • glucagon 1 mg IM or IV, (slower response than dextrose)
  • octreotide can be given after glucose therapy has been initiated in pt w/ sulfonylurea ingestion
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21
Q

Other etiologies of hypoglycemia if pt not a diabetic?

A
  • ETOH

- sepsis

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22
Q

Fxn of adrenal medulla?

A
  • controlled by nervous system

- when stim secretes epi and NE into adrenal veins

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23
Q

adrenal cortex - components and hormones secreted?

A
  • glomerulosa: mineralocorticoids: aldosterone
  • fasciculata: glucocorticoids- cortisol
  • reticularis: sex hormones
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24
Q

Fxn of ACTH?

A
  • stim synthesis and secretion of adrenocortical hormones (cortisol, androgens, aldosterone)
  • primarily stim cortisol
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25
Q

What is adrenal insufficiency?

A
  • failure of adrenal glands to produce essential basal secretion of steroids - not enough cortisol
  • insidious wasting disease
  • addison’s disease:
    wt loss
    skin tanning
    amenorrhea and early menopause, craving salty food
26
Q

What is adrenal crisis?

A
  • failure to respond to increased demands caused by stress or sudden inability to secrete essential steroids
  • life threatening
27
Q

2 forms of adrenal insufficiency?

A
  • primary (Addison’s): results from destruction or dysfxn of adrenal cortex
  • secondary: results from inadeqaute stim of adrenal cortex by ACTH (MC cause is chronic admin of exogenous steroids!!!)
28
Q

Lab work of Addisons?

A
  • Na: low - 126
  • K: high - 5.7
  • glucose: low - 50
  • cortisol: decreased
  • ACTH: increased
  • low BP, inreased HR
29
Q

Etiology behind decreased cortisol in Addisons?

A
  • cortisol up-regulates alpha1-adrenergic receptors on vascular smooth muscle so decreased amt leads to lack of vasoconstriction
30
Q

Etiology behind decreased aldosterone in Addisons?

A
  • aldosterone increases Na reabsorption by renal cells, leading to increases in extracellular fluid vol and blood vol, venous return, CO, and arterial pressure so decrease in aldosterone would do just the opposite
31
Q

Etiology behind increased HR in Addisons?

A

compensatory mechanism as a result of:
- decreased vol
we have decreased arteria pressure - baroreceptor refles - leads to increased sympathetic outflow and therefore an increase in HR

32
Q

Etiology behind decreased blood glucose in Addisons?

A

decreased cortisol- one action of cortisol is to increase blood glucose conc by promoting gluconeogenesis and decreasing glucose uptake by the tissues and therefore a decrease in cortisol would lead to decreased glucose and - possible hypoglycemia

33
Q

Etiology behind hyperkalemia in Addisons?

A
  • decreased aldosterone -
    in add. to stim Na reabsorption, aldosterone stim K secretion by renal principal cells and therefore a decrease in aldosterone would lead to decreased K secretion and hyperkalemia
34
Q

Etiology behind hyponatremia in Addisons?

A
  • decreased aldosterone:
    aldosterone increases Na reabsorption by renal principal cells. So if there is decreased aldosterone: there is decreased Na reabsorption - leads to hyponatremia
35
Q

Primary manifestation of adrenal crisis?

A
  • hypotension

- replace cortisol

36
Q

What pts usually present w/ adrenal crisis?

A
  • previously undx pts w/ primary adrenal insufficiency who has been subjected to serious infection or other acute, major stress
  • in pt w/ known primary adrenal insufficiency who doesn’t take more glucocorticoid during an acute infection like the flu
  • after bilateral adrenal infarction or bilateral adrenal hemorrhage
  • rarely in pts w/ secondary adrenal insufficiency, can be seen in pts withdrawn abruptly from suppressive doses of corticosteroids
37
Q

Presentation, dx, tx of adrenal crisis?

A
  • presentation:
    marked hypotension
    abd and flank pain
  • dx:
    clinically oriented for abrupt withdrawal from exogenous steroids.
    For primary adrenal insufficiency, a short cosyntropin test (measure in 60 min, primary adrenal insufficiency excluded if poststim level over 550 nmol/L)
  • tx:
    if adrenal crisis suspected or dx, IV glucocorticoids
    D5NS may be reqd to correct hypovolemia and hypoglycemia
38
Q

51 yo female comes in complaining of severe menopausal symptoms. She has been having attacks where her heart races and pounds along with a throbbing HA. She feels hot during these episodes even though her hands and feet are cold. She was rx hormone replacement and now she is having attacks daily . Her vital signs in office are 200/110 and 110bpm. Yesterday at walmart her BP was 140/90 .
What does she most likely have?

A
  • pheochromocytoma
39
Q

What is a pheochromocytoma?

A
  • tumor derived from neural crest cells of SNS that is responsible for about .1-2% of cases of HTN. Tumor releases catecholamines, which cause episodic or sustained s/s such as palpitations, sweating, HA, fainting spells, HTN emergencies
  • it is a surgically correctable form of HTN
  • majority of time: located in adrenal medulla
40
Q

Effects of catecholamines?

A
  • Heart: 2 major effects, each mediated by B1 receptor
  • increased HR
  • increased contractility
  • blood vessels:
  • vasoconstrictionof cutaneous blood vessels via alpha1 receptor
  • vasodilation of skeletal muscle blood vessels via Beta2 receptor
41
Q

90% tumor - pheochromocytoma?

A
  • 90% of the time they arise from the adrenal medulla (other 10% from mediastinumor abdomen)
  • 90% of time adrenal pheo will be unilateral
  • 90% of time it isn’t malignant
  • 90% of time it occurs in adults
42
Q

Dx of pheochromocytoma?

A
  • hx is impt: pt usually has episodes of HTN, HA, palpitation sweating
  • dx made by demonstrating elevated urinary excretion of catecholamines or their metabolites (metanephrines and vanillylmandelic acid) during period of HTN
  • once dx is made hunt for source: CT w/ focus on adrenal glands
  • BP has to be controlled prior to surgery
43
Q

Onset of hypothyroidism? Lab findings?

A
  • primary hypothyroidism has insidious onset:

lab findings include low T4 and high TSH, usually no urgency when suspecting primary

44
Q

Feedback of hypothyroidism?

A
  • low circ levels of Thyroid hormone stim hypothalamus and ant pituitary to stim TSH to produce T3, T4 from thyroid (where disease process is: this step isn’t occuring)
45
Q

When does Myxedema coma occur?

A
  • in individuals w/ long-standing preexisting hypothyroidism presents w/ life-threatening decompensation
  • rare, potentially life threatening
  • correct dx rqrs high degree of suspicion
  • affected pts commonly in geri pop
46
Q

Presentation of myxedema coma?

A

severe decline in metabolic fxn:

  • AMS
  • hypothermia
  • bradycardia
  • hypotension
  • hypoventilation
  • cardiovasc collapse
  • decreased drug clearance
  • usually pt has hx of primary hypothyroidism of previous thyroid surgery
 - often a precip factor:
med noncompliance
cold exposure
severe infection
add of new meds
47
Q

lab findings in myxedema coma?

A
  • anemia, hyponatremia, hypoglycemia, elevated transaminases, elevated CPK, elevated lactate dehyddrogenase, hypercholesterolemia, decreased PO2, increased PCO2
  • EKG: may demonstrate sinus bradycardia, prolong of QT interval, and low voltage w/ flattening or inversion of T waves
48
Q

Tx of myxedema coma?

A
  • stabilization: may rqr intubation, mechanical ventilation
  • correction of hypothermia w/ cautious use of gentle passive external rewarming
  • IV levo initial bolus followed by reduced daily dose until orals tolerated
  • routine admin of glucocorticoid
  • gentle fluid restriction to correct dilutional hyponatremia
49
Q

Sxs in hyperthyroidism?

A
  • heat intolerance, palpitations, sweating, tremor, nervousness, weakness, and fatigue
  • if sxs are mild: can do outpt eval, high clinical suspicion may warrant empiric sx therapy (BBs)
50
Q

Diff b/t thyroid storm and hyperthyroidism?

A
  • usually precip in previously unrecognized or poorly tx hyperthyroidism pt by:
    infection, trauma, DKA, MI, CVA, thromboembolic disease, surgery, withdrawal of thyroid meds, iodine admin
  • rare but medical emergency
  • tx initiated empirically
  • sxs that may be seen in thyroid storm and not necessarily in hyperthyroidism:
    fever
    arrhythmia
    CNS dysfxn: agitation, confusion, delirium, stupor, coma, seizure
51
Q

Tx of thyroid storm?

A
  • stabilization, airway protection, O2, IV fluids, monitoring
  • BBs for severe adrenergic sxs
  • antithyroid agents such as PTU or methimazole
  • admin of iodine to decrease performed thyroid hormone
52
Q

What is thyrotoxicosis?

A
  • referring to any accelerated thyroid state
53
Q

MC cause of acute adrenal insufficiency?

A
  • sudden withdrawal of exogenous steroids
54
Q

Why do you have hyperpig in addisons?

A
  • increased ACTH
55
Q

hypotension in adrenal crisis is typically resistant to? What needs to be replaced?

A
  • resistant to catecholamines and IV fluid admin

- if missing cortisol isn’t replaced - death will ensue!

56
Q

What does unexplained hyponatremia, hyperkalemia and hypotension unresponsive to catecholamine and IV fluids suggest?

A
  • adrenal crisis
57
Q

Sxs of thyroid storm?

A
  • hyperthyroid sxs
    +
  • fever
  • CNS disturbances
58
Q

PP of DKA?

A 
- body's response to cellular starvation (not organism starvation):
relative insulin deficiency
counterregulatory excess (think glucagon)
59
Q

Why do you become acidotic in DKA?

A
  • cellular starvation results since insulin deficiency (cant drive glucose into cells) - then lipolysis occurs - formation of ketoacids - and then ketonuria, anion gap metabolic acidosis w/ compensatory tachypnea, and vomiting
60
Q

Why do you become dehydrated w/ DKA?

A
  • insulin deficiency leads to increased serum levels of glucose (hyperglycemia) this increases osmotic load and spills into urine (glycouria) water is then drawn out of cells via oncotic pressure (occurs at BG of 200) - this leads to impaired consciousness, shock
61
Q

Why is there hypotension in DKA?

A
  • initially increase in vol of vascular compartment b/c pulling fluid into vascular compartment w/ osmotic load but as glucose starts to spill into urine there is massive osmotic diuresis
62
Q

What is the presentation of DKA?

A
  • hyperglycemia: polydipsia, polyuria
  • acidosis from ketoacids:
    tachypnea (to diminish CO2 and resture pH), fruity odor of breath
  • vol loss: dehydration signs - dry membranes, poor skin turgor, delayed cap refill, mental confusion

Emergency Medicine (22 decks)

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