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Emergency Med Exam 3 > Endocrine Emergencies > Flashcards

Endocrine Emergencies Flashcards

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1
Q

Hypoglycemia defined

A

Glucose < 70 mg/dL
Symptomatic hypoglycemia with levels <50

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2
Q

Risk factors for hypoglycemia in type II diabetes

A

Age
PMHx of vascular disease
Renal failure
Decreased food intake
Alcohol use
Drug interactions
Non compliance

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3
Q

Hypoglycemia sympathomimetic symptoms

A

Sweating, tremor, pallor, nausea,
anxiety, palpitations

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4
Q

Hypoglycemia Neuroglycopenia symptoms

A

Dizziness, psychosis, confusion, coma,
agitation, seizures

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5
Q

Hypoglycemia additional causes

A

● Insulinoma- Pancreatic islet cell tumor (90% benign)
● Medications/Drugs/Alcohol
● Extrapancreatic neoplasm
● Hepatic disease(depletion of glycogen stores)
● Deficiency of counterregulatory hormones
● Critically ill, stressed infants, hypothermia
● Dumping syndrome
● Artifactual

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6
Q

Hypoglycemia treatment

A

Standard treatment options
- Oral Glucose
Sugar Water
- D50 (50% dextrose in water) - 50 mL bolus provides 25gm of glucose (500mg/mL)
- D25 (peds)
- D10 (neonates)
- Maintain glucose at > 100 mg/dL
Recheck blood sugar q30 mins
- IV infusion of D10 (10% dextrose in water) or oral to maintain blood sugar
Glucagon 1mg IM/IV
- Stimulates glycogenolysis
- Can raise BS by ↑ 100mg/dL
- Works slower (10-15 minutes)

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7
Q

secondary causes of hypoglycemia if failure to respond to initial therapy

A

Sepsis, toxin, insulinoma, hepatic failure, adrenal insufficiency

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8
Q

Octreotide (Sandostatin)

A
  • Inhibits insulin secretion
  • Helps prevent rebound hypoglycemia in setting of glucose Infusion treatment and persistent symptoms refractory to
    sulfonylurea-induced hypoglycemia (As an antidote)
  • 50-100 mcg SC or IV
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9
Q

Give _____ with glucose in malnourished hypoglycemic patients

A

thiamine

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10
Q

Diagnosis of DM

A
  • Fasting glucose (100-125 mg/dL)
  • Random glucose (>200 mg/dL)
  • 2 hour oral glucose tolerance (>200 mg/dL)
  • HbA1c of >6.5%
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11
Q

Severe Hyperglycemia (>300 mg/dL) treatment

A
  • Fluids IV
  • Insulin -Regular insulin at 0.1- 0.15 units/kg IV or SC (IV better absorption)
    Appropriate to initiate Metformin 500 mg qDay
  • Make sure creatinine is normal
  • If modest elevation, inform patient of concern, F/U PCP
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12
Q

Hypoglycemic medications

A
  • Sulfonylurea agents:
  • (2nd gen) Glipizide, glimepiride, glyburide
  • Stimulate pancreatic insulin secretion
  • Cause profound hypoglycemia in OD
  • Long duration of action
  • Repaglinide (Prandin)
  • Stimulates insulin secretion
  • Can also cause hypoglycemia
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13
Q

Antihyperglycemic Agents (less likely to cause hypoglycemia in overdose)

A

Metformin
- Rarely causes lactic acidosis
Less risk of hypoglycemia
GLP-1 agonist
SGLT2 inhibitors
DPP-4 inhibitors
Thiazolidinediones

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14
Q

Diabetic Ketoacidosis Pathophysiology

A

Defined as cellular starvation due to relative or a
complete lack of insulin:
- Hyperglycemia
- Osmotic diuresis
- Prerenal Azotemia
- Ketone formation
- Wide anion gap metabolic acidosis

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15
Q

Free Fatty acids are converted to Ketones
in the liver → ______

A

Metabolic Acidosis

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16
Q

Hyperglycemia effects on the body

A

Glycosuria
Osmotic diuresis
Decreased GFR
Intracellular dehydration
Impaired consciousness
Shock
(Table on slide 20)

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17
Q

Loss of islet cell function in DKA causes what effects on the body?

A
  • Autoimmune destruction → Type I
  • Leads to inability of cells to use glucose for fuel, despite
    increased levels of intravascular glucose
  • Breaks down protein and adipose stores
  • Increased counterregulatory hormones further leads to
    ketonemia and increased hyperglycemia (Osmotic Diuresis)
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18
Q

Precipitants of DKA

A

Noncompliance with Insulin
Infection
Myocardial Infarction
Pregnancy (IUP)
CVA
Trauma
Hyperthyroidism
Pancreatitis
Any acute stressor

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19
Q

Metabolic acidosis causes compensatory ____

A

hyperventilation
- Kussmaul breathing
- Acetone leads to fruity breath smell

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20
Q

Avenues of volume loss in DKA

A
  • Osmotic Diuresis
  • Vomiting (Acidosis)
  • Loss of potassium
  • Leads to further hyperglycemia
  • Poor absorption of SC Insulin
  • Leads to poor Hemodynamics
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21
Q

Diabetic Ketoacidosis diagnosis

A
  • Glucose >250 mg/dL
  • Anion gap > 10 mEq/L
  • Bicarbonate < 15 mEq/L
  • pH < 7.3
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22
Q

Initial Goals and goal labs in treating DKA

A
  • 1st - Volume replacement
  • 2nd- Potassium Correction
  • 3rd- Insulin Therapy

Goal labs:
- Glucose <200
- Lower Glucose 75 mg/dL/ hr
- >18 mEq/L
- pH >7.3

23
Q

Fluids / Bicarbonate in DKA - treatment

A
  • Initial fluid resuscitation for hypovolemia
  • Replace electrolytes
  • Insulin drip
  • Sodium bicarbonate is rarely indicated
  • As glucose normalizes, start Dextrose
24
Q

What is Pseudohyponatremia

A

Sodium is artifactually decreased 1.6 mEq/L for every
100 mg/dL increase in glucose over 100
- After initial bolus, if eunatremic, then switch to 0.45% saline

25
Q

Complications of DKA Treatment

A

Hypoglycemia- due to excess insulin
Begin giving glucose when glucose = 200-250
Hypokalemia- from insulin, bicarbonate, hydration
CSF acidosis- bicarbonate
Cerebral edema- Neurologic change

26
Q

How to treat neurologic changes in DKA

A

50% of fatalities in DKA
Possibly over-hydration, hypoxemia,
Bicarbonate, rapid osmotic changes
Tx- Mannitol, restrict fluid, intubation

27
Q

Alcoholic Ketoacidosis

A
  • Binge drinking with heavy
    alcohol,
  • decreased food intake
  • starvation ketosis
  • EtOH metabolism inhibits
    gluconeogenesis
  • Depletes Glycogen stores
  • Abdominal pain, nausea,
    vomiting, dehydration,
    disorientation
28
Q

Treatment for alcoholic ketoacidosis

A
  • D5 Normal Saline
  • Thiamine
  • Electrolyte correction
29
Q

Anion Gap Metabolic Acidosis causes (MUDPILES)

A

Methanol/ Metformin
Uremia
Diabetic Ketoacidosis, Alcoholic Ketoacidosis
Paraldehyde
Iron, Isoniazid, Inhalants
Lactic Acidosis
Ethylene Glycol (AntiFreeze)
Salicylates

30
Q

Hyperosmolar Hyperglycemic Syndrome is similar to DKA except:

A
  • Triggered with concurrent
    inflammatory condition
  • Hyperosmolar, No ketoacidosis
  • Glucose usually higher(>1000)
31
Q

Precipitating factors for HHS

A

Infection, especially pneumonia
Myocardial infarction
CVA
GI bleed
Pyelonephritis
Pancreatitis
Uremia
Subdural hematoma
Peripheral vascular occlusion
Any stressor

32
Q

Common comorbid conditions with HHS

A

Renal insufficiency, vascular disease, poor access to water

33
Q

Common associated medications with HHS

A

Diuretics, B-Blockers, Corticosteroids, Ca++ channel blockers
Phenytoin, Cimetidine

34
Q

Physical findings for HHS

A
  • Dehydration, Altered, coma rare
    Focal neurologic findings
35
Q

Treatment of HHS

A

Similar balancing act to DKA
Normal saline(average fluid deficit 8-12 liters)
½ deficit over first 12 hours, the rest over next 24 hours
1-2 liter bolus clinically indicated
Insulin infusion (lower doses than DKA)

36
Q

Hyperthyroidism causes

A

-Graves’ disease (most common)-an autoimmune disorder
thyroid-stimulating immunoglobulins mimic TSH action
-Toxic thyroid adenoma, toxic multi-nodular goiter
-Thyroiditis
-Pituitary adenoma
-Drug Induced
-Excess iodine in diet

37
Q

Hyperthyroidism S/S

A

Nervousness, tremor, insomnia
Heat intolerance, sweating
Weakness, weight loss, hair loss
Tachycardia, palpitations
Diarrhea
Irregular menses
Goiter / thyroid bruit
Exophthalmos (Graves’ only)
Lid lag (lids move slower than eyes)
Pretibial Myxedema

38
Q

Thyroid Storm

A

A life-threatening complication of hyperthyroidism
Essentially a severe form of Thyrotoxicosis
- Most common cause is Graves Disease

39
Q

Precipitating events for Thyroid storm

A

Withdrawal of antithyroid meds
Administration of IV contrast
Thyroid hormone overdose
Pneumonia
CVA
Pulmonary embolism
Toxemia of pregnancy
Diabetes

40
Q

clinical diagnosis of thyroid storm

A

Hallmark is CNS dysfunction
- Temperature > 38 C
- Tachycardia out of proportion to fever
- Exaggerated peripheral manifestations of thyrotoxicosis
- Including tremor and weakness
- GI-Hepatic Dysfunction
- Atrial Fibrillation
- Congestive Heart Failure

41
Q

T/F No lab tests distinguish thyroid storm from simple hyperthyroidism

A

T

42
Q

5 step treatment approach to Thyroid storm

A

1)General supportive care-
IV fluids
Correct electrolyte imbalance
No ASA(displaces thyroid hormone from thyroglobulin)
2) Blockade of thyroid hormone synthesis-
- PTU 1000 mg PO (also inhibits peripheral conversion of T4 to T3
3) Blockade of thyroid hormone release
Iodine given 1 hour after PTU
4) 𝛃- adrenergic receptor blockade of peripheral thyroid hormone effects-
- Propranolol
5) Prevent peripheral conversion of thyroxine to triiodothyronine
- Corticosteroids(decrease peripheral conversion T4 to T3)

43
Q

Hypothyroidism causes

A
  • Treatment of Graves’ disease
  • After ablation
  • Iodine deficiency in diet
  • Autoimmune destruction of thyroid gland
    (e.g. Hashimoto’s)
  • Lithium therapy for bipolar disorder
  • Amiodarone
  • Pituitary and hypothalamic disorders (rare)
  • External Radiation
44
Q

Hypothyroidism S/S

A

● Weakness, lethargy
● Cold intolerance
● Hypothermia
● Weight gain
● Constipation
● Dry, thick skin
● Prolonged, heavy periods
● Generalized nonpitting edema
● (myxedema)

45
Q

Myxedema Crisis (severe hypothyroidism) signs

A

Dermatologic: Coarse, waxy skin, scant pubic hair,
Loss of lateral third of eyebrows, puffy face and extremities
CNS: Slowed mentation, altered mental status, coma,
psychosis(myxedema madness)
Cardiac: CHF, bradycardia, hypotension, cardiomegaly,
Pericardial effusion, low voltage(ECG)

46
Q

Hypothyroidism - myxedema coma signs

A

Non-pitting generalized and periorbital edema
Altered mental status
Hypoxemia
Hypothermia
Bradycardia
Hypotension

47
Q

Myxedema Coma precipitating factors:

A

Stressors- MI, infections, trauma, cold exposure
Drugs metabolized slower, increased effects
Non-compliance with thyroid replacement

48
Q

Myxedema Coma treatment

A

Supportive care: rewarming, fluid support, underlying cause

Specific treatment
IV thyroxine(T4)- may require large doses
IV T3 is not recommended(causes V- tach)

Corticosteroids- possible unrecognized adrenal/pituitary
Insufficiency
Search for underlying cause

49
Q

Adrenal Crisis clinical findings

A
  • Acute stressors with underlying insufficiency
  • Destruction of hypothalamic-pituitary or adrenal gland
  • Hypotension refractory to vasopressors
  • Abdominal pain, nausea, vomiting
  • Confusion, lethargy
  • Look for sepsis
50
Q

Adrenal Insufficiency treatment

A
  • D5NS IV
  • Hydrocortisone
  • Pressors
  • Future maintenance for anticipated stressors
  • Surgery, etc
51
Q

Adrenal insufficiency labs

A

Chest X-ray
Abdominal CT to look at Adrenal glands
Brain CT or MRI
HIV Screen

52
Q

Acute presentation of adrenal insufficiency

A

Fever and refractory hypotension

53
Q

Clinical manifestations of adrenal insufficiency

A
  • Cortisol- metabolism of most tissues, glucose regulation
  • Aldosterone(renal Na+ reabsorption, K+ excretion)

Emergency Med Exam 3 (7 decks)

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