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Emergency Medicine > Endocrine Emergencies > Flashcards

Endocrine Emergencies Flashcards

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1
Q

Pathophysiology of DKA

A 
Body's response to cellular starvation
Relative insulin deficiency
Counterregulatory excess (glucagon)
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2
Q

Why does one become acidotic in DKA?

A

Relative insulin deficiency
Cellular starvation
Lipolysis with subsequent fatty acid transport to hepatocytes
Formation of ketoacids
Ketonuria
Anion gap metabolic acidosis with capensatory tachypnea
Vomiting

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3
Q

Why does one become dehydrated in DKA?

A

Relative insulin deficiency
Hyperglycemia increases osmotic load and leads to glycosuria
Water drawn out of cells via oncotic pressure
Impaired consciousness
Shock

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4
Q

Presentation of DKA

A

Hyperglycemia
Acidosis from ketoacids
Volume loss

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5
Q

Presentation of Hyperglycemia

A

Polydipsia

Polyuria

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6
Q

Presentation of Acidosis from Ketoacids

A

Tachypnea

Fruity odor of breath

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7
Q

Signs of Dehydration

A

Dry membranes
Poor skin turgor
Delayed capillary refill
Mental confusion

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8
Q

Management of DKA

A 
Aggressive fluid therapy (NS)
Place monitor
2 large bore IVs
Bedside glucose, urine dipstick, EKG
CBC, CMP, phosphate, and magnesium
ABGs
Blood cultures/other labs as indicated
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9
Q

Fundamentals of Treatment of DKA

A

Volume repletion
Reversal of metabolic consequences of insulin insufficiency
Correction of electrolyte and acid-base imbalances
Treatment of precipitating cause
Avoid complications

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10
Q

Why does fluid administration help with a decrease in blood glucose and ketone concentration?

A

Increases GFR

Allows for glucose and ketones to be excreted

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11
Q

Insulin Therapy in DKA

A

0.1 units/kg/hr after fluid bolus
Use infusion pump for less complications, flexibility in adjusting dose
AVOID IM and subQ doses

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12
Q

What is the most life-threatening electrolyte derangement during treatment of DKA?

A

Hypokalemia

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13
Q

Goals of Potassium Therapy in DKA

A

Maintain normal extracellular K during acute phase

Replace intracellular K over several days

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14
Q

Hypokalemia in DKA due to Therapy

A

Cardiac arrhythmias
Respiratory paralysis
Paralytic ileus
Rhabdomyolysis

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15
Q

Complications of DKA

A 
Hypoglycemia
Cerebral edema
Hypokalemia
Hypophosphatemia
Adult respiratory distress syndrome
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16
Q

Reasons for DKA in NOT a New Onset Diabetic

A

Compliance issues
Discontinuation of insulin
Insults to the body such as infection, MI, PE

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17
Q

What condition occurs in patients with poorly controlled or undiagnosed type II DM?

A

Hyperosmolar hyperglycemic state

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18
Q

Define Hyperosmolar Hyperglycemic State

A 
Serum glucose: 600+ mg/dL
Plasma osmolality: 315+ mOsm/kg
Bicarbonate: 15+
Arterial pH: 7.3+
Serum ketones negative
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19
Q

Shared Symptoms of DKA and Hyperosmolar Hyperglycemic State

A 
Hyperglycemia
Hyperosmolality
Severe volume depletion
Electrolyte imbalances
Acidosis??
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20
Q

Mortality Rates in DKA and Hyperosmolar Hyperglycemic State

A

DKA: 5%
HHS: 15-30%

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21
Q

Risk Factors of Hyperosmolar Hyperglycemic State

A

Inability to access water

Non-ambulatory patients

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22
Q

Presentation of Hyperosmolar Hyperglycemic State

A 
Elderly
Abnormalities in vitals or mental status
Precipitated by acute illness
\+/- baseline cognitive impairment
Weakness
Anorexia
Fatigue
Cough
Dyspnea
Abdominal pain
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23
Q

Treatment of Hyperosmolar Hyperglycemic State

A 
Volume repletion
Correction of electrolyte abnormalities
Treat precipitating cause
Correction of hyperglycemia
Judicious management of concurrent illness
24
Q

Neurogenic (Increased ANS Activity) Hypoglycemia Signs and Symptoms

A 
Sweating
Pallor
Tachycardia
Palpitations
Tremor/shaking
Nervousness/anxiety
Tingling, paresthesias
25
Q

Neuroglycopenic (Lack of Sugar to Brain) Hypoglycemia Signs and Symptoms

A 
Headache
Drowsiness
Lightheadedness or syncope
Mental dullness or confusion
Amnesia
Seizure
Coma
26
Q

At what glucose level do neurogenic symptoms appear?

A

Approximately less than 54 mg/dL

27
Q

At what glucose level do neuroglycopenic symptoms appear?

A

Approximately less than 47 mg/dL

28
Q

Define Hypoglycemia Unawareness

A

Development of low serum sugar values without physiologic ability to react

29
Q

Patients at Greatest Risk for Hypoglycemia Unawareness

A

Extremes of age
Co-morbidities
Medications

30
Q

Outpatient Recommendations for Treatment of Hypoglycemia

A

15-20 g of glucose
Retest glucose in 15 minutes
Prescribed glucagon
Alter insulin or dosage adjustment of oral medication

31
Q

ED Management of Hypoglycemia

A 
1 g/kg body weight dextrose
Retest glucose q30 for 2 hours
Oral replacement (300g)
Glucagon 1 mg IM/IV
Octreotide
32
Q

Other Considerations for Hypoglycemia in Non-Diabetic Patients

A

ETOH

SEpsis

33
Q

What does the adrenal medulla secrete?

A

Epinephrine

Norepinephrine

34
Q

What does the adrenal cortex secrete?

A

Mineralocorticoids (aldosterone)
Glucocorticoids (cortisol)
Sex hormones

35
Q

Function of Adrenocorticotropic Hormone (ACTH)

A

Stimulate synthesis and secretion of adrenocortical hormones

36
Q

Define Adrenal Insufficiency

A

Failure of adrenal glands to produce essential BASAL secretion of steroids

37
Q

Symptoms of Insidious Wasting Disease in Adrenal Insufficiency

A 
Weight loss
Fatigue
Lack of ambition
Hypotension
Hyper-melanoma
38
Q

Define Adrenal Crisis

A

Failure to RESPOND to the increased demands caused by stress or SUDDEN INABILITY to secrete essential steroids

39
Q

Define Primary Adrenal Insufficiency

A

Results from destruction or dysfunction of the adrenal cortex

40
Q

Define Secondary Adrenal Insufficiency

A

Results from inadequate stimulation of adrenal cortex by ACTH

41
Q

Where is adrenal crisis seen?

A

Undiagnosed primary adrenal insufficiency subjected to major stress
Known adrenal insufficiency who doesn’t take extra steroids during major stress
After bilateral adrenal infarction or hemorrhage

42
Q

Presentation of Adrenal Crisis

A

Marked hypotension

Abdominal and flank pain

43
Q

Treatment of Adrenal Crisis

A

IV glucocorticoids

D5NS: correct hypovolemia and hypoglycemia

44
Q

Signs and Symptoms of a Pheochromocytoma

A 
Episodic or sustained
Palpitations
Sweating
Headaches
Fainting spells
HTN emergencies
45
Q

Key History of Pheochromocytoma

A

Episodes of HTN, headache, palpitation, and sweating

46
Q

Diagnosing a Pheochromocytoma

A

Demonstrating elevated urinary excretion of catecholamines or metabolites DURING a hypertension period

47
Q

Lab Levels in Hypothyroidism

A

TSH: high

T4, T3: low

48
Q

When does myxedema occur?

A

In individuals with long-standing preexisting hypothyroidism presents with life-threatening decompensation

49
Q

Most Common Patient Population

A

Geriatric patients

50
Q

Presentation of Myxedema

A 
Alteration in mental status
Hypothermia
Bradycardia
Hypotension
Hypoventilation
Cardiovascular collapse
Decreased drug clearance
History of primary hypothyroidism, previous thyroid surgery, or hypercholesterolemia
51
Q

What is myxedema coma generally preceded by?

A

Medication non-compliance
Cold exposure
Severe infection
Addition of new medications

52
Q

Laboratory Findings in Myxedema Coma

A 
Anemia
Hyponatremia
Hypoglycemia
Elevated transaminases
Elevated CPK
Elevated lactate dehydrogenase
Hypercholesterolemia
Decreased PO2
Increased PCO2
53
Q

Treatment of Myxedema Coma

A 
Stabilization
Correction of hypothermia (passive external rewarming)
IV levothyroxine
Routine administration of glucocorticoid
Gentle fluid restriction
54
Q

Hyperthyroidism Symptoms

A 
Heat intolerance
Palpitations
Weight loss
Sweating
Tremor
Nervousness
Weakness
Fatigue
55
Q

What is a thyroid storm potentially preceded by?

A 
Infection
Trauma
DKA
MI
CVA
Thromboembolic disease
Surgery
Withdrawal of thyroid medications
Iodine administration
56
Q

Symptoms Seen in Thyroid Storm but not Hyperthyroidism

A

Fever
Arrhythmias
CHF
CNS dysfunction: agitation, confusion, delirium, stupor, coma, seizure

57
Q

Treatment of Thyroid Storm

A

Stabilization
Beta-blockers: severe adrenergic symptoms
Antithyroid agents
Iodine: decrease preformed thyroid hormone

Emergency Medicine (17 decks)

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