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EMED Unit II > 4 Endocrine Emergencies > Flashcards

4 Endocrine Emergencies Flashcards

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1
Q

How would a T1DM in hypoglycemia present?

A 
Irritable
Diaphoretic
Tachycardic
Blurred vision
Weakness
\+/- AMS/confusion
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2
Q

What diagnostic studies should you order if a patient presents with symptoms of suggestive of T1DM hypoglycemia?

A

Finger stick glucose (looking for low blood sugar)

U/A and Microscopy

+/- urine pregnancy if female

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3
Q

What is the laboratory alert definition of hypoglycemia?

A

<70 mg/dL

Some favor a cut-off of <54 mg/dL

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4
Q

Why do some providers prefer to use a lower threshold for hypoglycemia?

A

To avoid over diagnosis in asymptomatic patients (some are used to living at a lower blood glucose)

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5
Q

Patients with Type 1 DM average _____ episodes of severe hypoglycemia per year and less severe episodes (54-70 mg/dL) once every ______.

A

3x

Several days

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6
Q

Potential causes of hypoglycemia?

A

Delay in eating (esp after administering insulin)

Poor caloric intake (dieting/vomiting)

Increased or unusual physical exertion or physiologic stress (ie infection, trauma)

Impaired counter-regulatory hormone axis

Alterations in therapeutic regimen

If using insulin, variable absorption at injection site

Excessive insulin release caused by sulfonylurea

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7
Q

In general, hypoglycemia is much more common in ______ diabetics

A

Type I

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8
Q

How do you manage asymptomatic hypoglycemia?

A

“Defensive actions”

Repeat measurement in near future
Avoid critical tasks (ie driving)
Ingest carbs
Adjust treatment regimen

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9
Q

Managing hypoglycemia in awake but symptomatic patients

A

15-20g oral carbs
• 3-5 glucose tablets/hard candies
• 1/2 c. juice/non-diet soda
• This is usually enough to raise blood sugar to a safe level without inducing hyperglycemia

Can be followed by a long-acting carb to prevent recurrence of symptoms

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10
Q

Managing severe hypoglycemia/AMS

A

Typically unable to safely swallow oral glucose

SQ or IM 0.5-1.0mg of glucagon

Consciousness usually recovered in less than 15 min but may have marked N/V

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11
Q

Alternative to SQ/IM glucagon for treatment of hypoglycemia

A

“1 amp of D50”

25 grams of 50% glucose (dextrose) IV

Follow w subsequent glucose infusion or if mental status allows, give them food

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12
Q

What happens once a hypoglycemia patient’s blood glucose increases to a normal range?

A

Usually the patient’s mental status normalizes, diaphoresis and tachycardia typically resolve

Some patients exhibit stroke-like symptoms with focal neuro exam - these findings also resolve

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13
Q

What warning should you give your hypoglycemic patient once they recover?

A

The condition may reoccur - it’s best to observe patient for some time, checking serial blood sugaring and doing patient ed to “fix the problem”

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14
Q

What must you do differently to manage your hypoglycemic patient if their condition was caused by a sulfonylurea?

A

MUST admit them - b/c the half-life of the drug is so long that the condition will most certainly reoccur in a short time

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15
Q

How might diabetic ketoacidosis present?

A

Like metabolic acidosis

Severe abdominal pain
Vomiting
Confusion
Frequent urination
Tachycardia
Tachypnea
Hypotension
Dehydration
Urinary ketones, protein
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16
Q

You see a super low bicarb on a CMP. What do you immediately think?

A

Metabolic acidosis

May also have electrolyte imbalance, elevated BUN/Cr, elevated glucose

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17
Q

If you get a super low bicarb on CMP, what is the first thing you do next?

A

ABG - will probably show metabolic acidosis

Calculate anion gap too

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18
Q

Causes of elevated anion gap metabolic acidosis

A 
MUDPILES
Methanol
Uremia
Diabetic, alcoholic, or starvation ketoacidosis
Paracetamol, propylene glycol, paregoric
Iron, Ibuprofen, Isoniazid
Lactic Acid
Ethylene glycol
Salicylates (aspirin)
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19
Q

What are the two hyperglycemia crises of DM?

A 
Diabetic Ketoacidosis (DKA)
Hyperosmolar Hyperglycemic State (HHS)
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20
Q

Both DKA and HHS can be precipitated by…

A 
Infection (ie UTI, PNA)
Trauma or surgery
MI, stroke
Insulin omission
Undiagnosed DM
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21
Q

DKA almost always occurs in ______ DM as a result of _________

A

Type 1

Insulin insufficiency in the setting of a precipitation

Often the PRESENTING symptom of DM

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22
Q

SSx of DKA

A

Tend to develop over hours/days

Abdominal pain/N/V
Hyperventilation (Kussmaul respiration’s)
Hypotension/shock/dehydration
Metabolic acidosis with increased anion gap
Elevated glucose
Elevated serum ketones
Polyuria, polydipsia, weight loss

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23
Q

DKA is the presenting sign of DM in ______ of Type 1 diabetics

A

~25%

The lack of DM Hx does NOT exclude DKA from your DDx

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24
Q

Glucose in DKA is typically…

A

Between 350-500 mg/dL

Diagnosis NOT based on elevation of glucose - need other lab abnormalities

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25
What other lab abnormalities must be present to diagnose DKA in the face of elevated glucose?
KETONES - urine and serum positive Potassium may be high, low, or normal but MONITOR CLOSELY - May be elevated at presentation but tends to fall precipitously with treatment so WATCH IT and supplement as needed Sodium FALSELY LOWERED Extremely low BICARB Elevated BUN/Cr (2˚ to dehydration) Elevated ANION GAP Elevated serum OSMOLARITY (not as high as HHS though) Overall ACIDOSIS
26
Therapeutic goals for DKA patients
``` Make Dx and address ABCs Restore circulatory volume Correct serum osmolarity CLEAR SERUM KETONES*********** Correct electrolytes and anion gap Treat underlying causes REDUCE BLOOD GLUCOSE (But slowly and not first) ```
27
Initial management of DKA
ABCs ISOTONIC SALINE IV Correct electrolyte disorders • Replete potassium (monitor closely) • Follow sodium • Replete phosphate if severe deficit Control blood glucose Reverse acidosis and ketogenesis • Insulin bolus IV —> continuous IV insulin infusion
28
Fluid management for DKA
15-20 mL/kg lean body weight per hour (~1L/hr for the first couple hours) Max of ~50mL/kg in the first 4 hours Beyond 2-3 hours - replacement depends on hydration state (monitor I&Os) Add dextrose to saline when blood glucose reaches 200-250 mg/dL
29
When do you add dextrose to DKA patients and why?
When glucose reaches 200-250mg/dL B/c the goal is to reverse ketogenesis, not attain normoglycemia
30
Should you give bicarb to a DKA patient to increase pH?
Nope It can cause hypernatremia, hypokalemia, paradoxical CSF acidosis**** and a residual serum alkalosis RISK OF INTRACELLULAR CEREBRAL ACIDOSIS —> CEREBRAL EDEMA —> BRAIN DAMAGE Also, it might slow recovery of kenos is
31
What is one setting when it would be appropriate to give bicarb to a DKA patient?
When significant hyperkalemia is evident The bicarb will quickly lower serum K+
32
What are the mainstays of reversing ketoacidosis in DKA patients?
Fluid administration and insulin With insulin present, glucose will enter cells and body will discontinue lipolysis —> lower blood glucose —> clearance of ketones
33
What if the DKA patient’s glucose normalizes but an elevated anion gap is still evident?
Continue the insulin administration B/c it’s the presence of insulin that stops lipolysis
34
HHS occurs mainly in Type _____ DM and in the presence of ______
Type 2 Precipitation - Infection, MI, other stressors Think older nursing home patients or homeless dudes
35
SSx of HHS
Insidious onset (days to weeks) Altered state of consciousness (more likely than in DKA) Weakness - both generalized and focal Polydipsia and polyuria Dehydration
36
What is the pathophysiology of HHS?
Hyperglycemia —> glycosuria —> dehydration —> Hemoconcentration —> worsening hyperglycemia Glucose will usually be 500+ Dehydration - plasma osmolality >320 (5-10 L deficient!) Relative insulin deficiency but NO KETONES and NO ACIDOSIS
37
Treatment of HHS
Fluid and electrolyte replacement (same guidelines as DKA) Insulin IV if fluids alone doesn’t decrease glucose Transition to home insulin regime or optimize outpatient therapy TREAT UNDERLYING PROBLEM
38
What is the difference between hyperthyroidism and thyrotoxicosis?
Hyperthyroidism refers to inappropriately elevated thyroid function Thyrotoxicosis is excessive amount of circulating thyroid hormone - NOT synonymous with hyperthyroidism (can be from exogenous source)
39
What is thyroid storm?
Rare and potentially fatal complication of hyperthyroidism that typically occurs in patients with untreated or partially treated thyrotoxicosis
40
Diagnostic criteria for thyroid storm
Presence of severe and life-threatening Sx (hyperpyrexia, CV dysfunction, AMS) in a patient with biochemical evidence of hyperthyroidism Elevation of free T4 and/or T3 Suppression of TSH There are no universally accepted criteria or validated clinical tools for diagnosing it
41
Who gets thyroid storm?
Patients with long-standing untreated/undertreated hyperthyroidism (Graves’ disease, TMG, solitary toxic adenoma) Often precipitated by an acute event such as thyroid or non-thyroidal surgery, trauma, infection, acute iodine load, or post-parting state
42
Presentation of thyroid storm
All the normal hyperthyroid symptoms plus: Hypermetabolism - weight loss/diarrhea Excessive adrenergic response ``` May have: Hyperpyrexia Atrial fib w/ possible HF Goiter, exophthalmos, tremor, moist skin Shock Confusion —> agitation —> coma Death ```
43
Supportive care for thyroid storm
ICU admission and ABCs Cooling measures - antipyretic and cooling blankets Appropriate IV fluid resuscitation Electrolyte replacement Nutritional support
44
Thyroid specific meds therapy for thyroid storm
Prevent thyroid hormone release Decrease peripheral action of circulating thyroid hormone (reduce HR and support circulation) Treat the precipitating condition
45
Therapeutic options for thyroid storm are the same as those for uncomplicated thyrotoxicosis except...
The drugs are given in higher doses and more frequently
46
Drugs for thyroid storm
1st give a Beta blocker - PROPRANOLOL (not atenolol) Then a Thionamides - PTU and/or Methimazole 1 hour after thionamide, give Iodine solution - Lugol’s solution or SSKI (super saturated potassium iodide) Glucocorticoids Bile acid sequestrants
47
Why propranolol instead of atenolol for thyroid storm?
Atenolol is great for treating non-emergent hyperthyroidism but propranolol also inhibits the type 1 deiodinase, which may help reduce serum T3 levels
48
Why must iodine solution be given 1 hour AFTER thionamides?
To prevent the iodine from being used as a substrate for new hormone synthesis
49
Why might you prefer to use PTU over Methimazole in Thyroid storm?
PTU works by decreasing thyroid hormone synthesis AND blocks the conversion of T4 to T3 Methimazole only decreases synthesis Because of it’s converting action, PTU results in lower serum T3 levels for the first few days of treatment
50
Why might Methimazole be preferred over PTU in severe but not life-threatening hyperthyroidism (not thyroid storm)?
Longer half-life Lower risk of hepatic toxicity Ultimately restore euthyroidism more quickly than PTU Patients initially treated with PTU should be transitioned to Methimazole before discharge from the hospital
51
Why are glucocorticoids used in adjunct therapy for thyroid storm?
To reduce T4 to T3 conversion, promote vasomotor stability, and possible treat an associated relative adrenal insufficiency
52
Why are bile acid sequestrants used as an adjunct therapy in thyroid storm?
To decrease enterohepatic recycling of thyroid hormones
53
What are the five Bs for our approach to treating thyroid storm?
``` Block synthesis (antithyroid drugs) Block release (iodine) Block T4 to T3 conversion (PTU, propranolol, corticosteroid) Beta-blocker Block enterohepatic circulation ```
54
What is the treatment of choice for thyroid storm if a patient has a contraindication or is allergic to thionamides or if treatment is refractory to meds?
Thyroidectomy
55
Rare complication of severe hypothyroidism due to severe deficiency in thyroid hormone —> encephalopathy
Myxedema coma Can occur as the culmination of severe, long-standing hypothyroidism (either under-treated or undiagnosed)
56
Myxedema coma may be precipitated by...
An acute event Infection, MI, COLD exposure, admin of sedative drugs (ie - opioids)
57
Hallmark features of myxedema coma
``` Hypothermia CNS depression/coma Hypotension Bradycardia Hyponatremia Hypoglycemia Hypoventilation ``` Onset may be rapid or insidious
58
Who is at greatest risk for myxedema coma?
Elderly, esp women
59
What is myxedema anyway?
Puffiness of the hands and face, a thickened nose, swollen lips and an enlarged tongue secondary to nonpitting edema with abnormal deposits of mucin in the skin and other tissues
60
When should you think of myxedema coma?
Clinical manifestations or Hx of Hypothyroidism are accompanied by disturbances of consciousness, hypothermia, hypoventilation, and hypotension
61
What are the diagnostic studies for myxedema coma?
TSH: Usually high (primary hypothyroidism) - it’s possible to be low too if the hypothyroidism is secondary to hypothalamic or pituitary dysfunction FT4: Low or undetectable FT3: Low or undetectable
62
How do you manage myxedema coma?
MAKE THE FUCKING DIAGNOSIS FIRST ABCs Thyroid hormones Glucocorticoids given until adrenal insufficiency ruled out IVF, correct electrolyte imbalances, rewarm Find the precipitating cause and treat
63
How may thyroid hormone should you give someone with myxedema coma?
T4 - initial dose of 200-400 mcg IV, followed by daily IV doses of 50-100 mcg until the patient can take T4 orally T3 - controversial - can reverse the condition more rapidly but can also precipitate MI or arrhythmias (start with lower doses) - but still give it
64
Potentially life-threatening condition that occurs when there is a lack of cortisol, produced by the adrenal glands
Adrenal insufficiency
65
How does primary adrenocortical insufficiency occur?
The adrenal gland is damaged/not functioning and it cannot produce glucocorticoids or mineralocorticoids This is Addison’s disease btw
66
How does secondary adrenocortical insufficiency occur?
Involves a defect of the pituitary gland inhibiting proper release of ACTH May be isolated or occur in conjunction with other pituitary hormone deficiencies (ie panhypopituitarism)
67
How does tertiary adrenal insufficiency occur?
Caused by suppression of HPA axis Most common cause by far is from abrupt withdrawal of chronically administered high dose glucocorticoids (think COPD and chronic prednisone use)
68
In tertiary adrenal insufficiency, ________ secretion is nearly normal
Mineralocorticoid B/c this function depends mostly on the renin-angiotensin system rather than on ACTH
69
Acute adrenal crisis in a patient with primary adrenal insufficiency) is usually....
An acute exacerbation of chronic insufficiency caused by sepsis or surgical stress Can be caused by adrenal hemorrhage, adrenal infarction, anticoagulation complications or congenital abnormalities
70
Presentation of acute adrenal crisis
``` N/V/D/Abd pain Confusion/coma Fever Hyponatremia Hypoglycemia Weight loss PROFOUND HYPOTENSION***** ``` Must be distinguished from other forms of shock
71
What is Waterhouse-Friderichsen syndrome?
Adrenal infarction due to meningococcemia Think of this with FEVER, MENTAL STATUS CHANGES, PURPURA
72
Management of acute adrenal crisis
ABCs and IVF Correct electrolytes and monitor closely Administer 100mg IV Hydrocortisone q6h Administer Mineralocorticoid (Florinef) - usually 0.1mg PO qd ID/Tx underlying cause
73
If there is reason to suspect adrenal crisis in any patient, you should...
Treat immediately with hydrocortisone and considered mineralocorticoids
74
Think of adrenal crisis when...
Shock is otherwise unexplained and inadequately responsive to vasopressors and volume replacement

EMED Unit II (5 decks)

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