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Emergency Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Intentional tremor- postural, bilateral ACTION tremor of the hands, forearms, head, neck, or voice is known as ______.

A

Essential familial tremor

  • Benign
  • *Worsened with emotional stress (finger to nose testing the tremor intensifies as finger reaches target)
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2
Q

Essential tremors are shortly relieved with ____ ingestion.

A

ETOH

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3
Q

Treatment for essential tremor is usually not needed. However, ______ may help if severe or situational.

A

Propranolol

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4
Q

_____ presents with hair loss, fatigue, cold intolerance, muscle cramps, weight gain, constipation, pallor, nonpitting edema, delayed DTRs, etc.

A

HYPOthryroidism

  • Pts with myxedema coma have hypothyroidism and present with hypothermia, bradycardia, hypotension, and AMS–> MC seen in elderly women with long standing hypothyroidism in winter
  • *Lab abnormalities may include hypoglycemia and hyponatremia
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5
Q

Key characteristics of HYPOthyroidism include:

A
  1. Cold intolerance
  2. Loss of outer 1/3 of eyebrow
  3. Hypoactivity
  4. Bradycardia and decreased CO
  5. Menorrhagia
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6
Q

Key characteristics of HYPERthyroidism include:

A
  1. Heat intolerance
  2. Hyperactivity
  3. Tachycardia, palpitations
  4. High-output HF
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7
Q

______ is a potentially fatal complication of hyperthyroidism. Leads to a hypermetabolic state causing palpitations, tachycardia, A fib., high fever, N/V, tremors, and psychosis.

A

Thyroid storm

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8
Q

Management of thyroid storm involves:

A
  1. PTU IV or Methimazole and Beta Blockers

* AVOID ASA!

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9
Q

______ is the MC cause of Hyperthyroidism that is MC in women 20-40.

A

Graves Disease

*Worse with stress, pregnancy

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10
Q

Clinical manifestation so Graves are:

A
  1. Ophthalmopathy- lid lag, EXOPHTHALMOS/PROPTOSIS
  2. Thyroid bruits
  3. Pretibial myxedema- nonpitting, edematous, pink to brown plaques/nodules on shin
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11
Q

_____ is the MC therapy used for Graves.

A
  1. Radioactive Iodine
    * Will need hormone replacement
  2. PTU and Methimazole
  3. Beta blockers
  4. Thyroidectomy
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12
Q

See p.311 for more HYPERthyroidism

A

FYI

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13
Q

_____ is the MC cause of HYPOthyroidism in the US. 6x MC in women.

A

Hashimoto’s thyroiditis

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14
Q

Clinical manifestations of Hashimoto’s are:

A
  1. Painless, enlarged thyroid

2. May present in euthyroid state

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15
Q

How is Hashimoto’s diagnosed?

A

+ Thyroid Ab present: thyroglobulin Ab, antimicrosomial and Thyroid Peroxidase Ab

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16
Q

How is Hashimoto’s treated?

A

Levothyroxine therapy!

*Synthetic T4. Monitor TSH levels @ 6 week intervals when initiating/changing dose. Slow, small increases in >50y and patients with CVD. Monitor elderly, patients with angina, MI, or CHF for ADRs.

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17
Q

The MC cause of HYPOthyroidism worldwide is _____.

A

Iodine deficiency

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18
Q

See p. 312 for more cases of HYPOthyroidism and Thyroiditis

A

FYI

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19
Q

_____ is defined as the excess release of PTH.

A

Primary Hyperparathyroidism

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20
Q

_____ is the MC cause of primary hyperparathyroidism (80%).

A

Parathyroid adenoma

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21
Q

Increased production of PTH due to hypocalcemia or vitamin D deficiency is known as ______.

A

Secondary hyperparathyroidism

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22
Q

______ is the MC cause of secondary hyperparathyroidism.

A

CKD

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23
Q

What are the clinical manifestations of primary hyperthyroidism?

*Hint- think signs of hypercalcemia

A

Hypercalcemia- “stones, bones, abdominal groans, psychic moans,” decreased DTRs

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24
Q

How is primary hyperparathyroidism diagnosed (triad)?

A
  1. Hypercalcemia
  2. Increased intact PTH
  3. Decreased phosphate
  • Increased 24h urine calcium excretion
  • *Osteopenia on bone scan
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25
How is primary hyperparathyroidism treated?
Parathyroidectomy
26
______ is due to adrenal gland failure, resulting in cortisol and aldosterone deficiency.
Adrenal Insufficiency/Addison's Disease *MC cause is autoimmune destruction of the adrenal cortex
27
ACTH stimulates the adrenal cortex to secrete cortisol, cortisol has a negative feedback on the pituitary to inhibit secretion of ACTH
some axis info...
28
Manifestations of Adrenal Insufficiency are...
Weakness, dehydration, HYPOtension, anorexia, nausea, vomiting, weight loss, abdominal pain -Hyperpigmentation of the skin is seen
29
______ is the acute, life-threatening form of adrenal insufficiency.
Adrenal crisis
30
Addison's is defined by an aldosterone and cortisol problem. Similar clinical manifestations as those with Adrenal Insufficiency with myalgias and arthralgias as well.
Also orthostatic hypotension, Delayed DTRs, Salt craving
31
Addison's is associated with ____(hypo/hyper)natremia and ______(hypo/hyper)kalemia.
HYPOnatremia and HYPERkalemia *Also hypoglycemia
32
How is Addison's diagnosed?
1. AM cortisol 2. Cosyntropin Stimulation Test (ACTH) * Low levels of ACTH at AM cortisol suggest secondary disease
33
Secondary adrenal insufficiency will not have findings of hyperkalemia as there is not a deficiency of ______.
Aldosterone
34
The MC cause of acute adrenal insufficiency is:
- Adrenal suppression from prolonged steroid use with either abrupt steroid withdrawal or - Exposure to increased physiologic stress such as injury, illness, or surgery.
35
Causes of primary adrenal insufficiency:
Primary --> autoimmune, adrenal hemorrhage or thrombosis, drugs, infections involving adrenal glands, infiltrative disorders involving adrenal glands (sarcoidosis, lymphoma, amyloidosis, etc.), surgery (bilateral adrenalectomy), hereditary, idiopathic
36
Causes of secondary adrenal insufficiency:
Secondary --> sudden cessation or prolonged glucocorticoid therapy, pituitary necrosis or bleeding, exogenous glucocorticoid administration, brain tumors, pituitary surgery/irradiation, infiltrative disorders of the pituitary or hypothalamus, infectious diseases involving organs away from adrenal
37
How do you treat an adrenal crisis?
* DO NOT WAIT FOR PENDING LAB RESULTS BEFORE BEGINNING EMPIRIC TX * Treat HYPOTENSION with volume → 2 to 3 L of NS or D5NS- if hypoglycemic * Give IV DEXAMETHASONE 4mg or IV HYDROCORTISONE 100mg -Vasopressors if unresponsive to fluid therapy (norepinephrine, dopamine, etc) •If less ill, can give oral hydrocortisone (20mg/kg) -Patients may require lifelong glucocorticoids and/or mineralcorticoids
38
_____ is caused by the absence of ADH (vasopressin). Lease to polyuria, polydipsia (esp at night).
Diabetes Insipidus * Can lead to HYPERnatremia :( * *Glucose is normal!
39
Causes of Central DI:
Idiopathic, familial, infiltrative disease, tumor, trauma, surgery *Image the pituitary!!!
40
How is central DI treated?
Vasopressin, DDAVP
41
DKA defined...
- Diabetic- blood sugar over 250 - Keto- ketones in the urine or blood - Acidosis- pH of 7.3 or lower
42
The lack of insulin in DKA leads the body to burn ___ for fuel. Which leads to ketone production and acidosis.
Fat
43
DKA v. HHS
- DKA: 4-6 L volume down | - HHS: 9-10 L volume down, often with AMS
44
Some PE findings with DKA include:
1. Kussmaul respirations | 2. Fruity odor to breath
45
The 7 I's to DKA
o Infection- signs/symptoms of pneumonia, UTI, appendicitis/cholecystitis? o Infarction- CVA or MI o Iatrogenic- change in insulin dose by provider o Incision- surgery can be a precipitating cause o Intoxication- ETOH or illegal drugs o Initial- initial diagnosis of Type 1 DM o Insulin- too little or no insulin being taken by the patient
46
Many patients w/ DKA have N/V/abdominal pain
fyi
47
Initial management of DKA...
- Finger stick glucose, 2 large bore IVs, blood draw for labs and STAT VBG - Labs: CBC, Chem 10, VBG, UA, Serum Ketones, Serum or urine HCG
48
_____ is initially much more important than insulin.
IV fluids!! 1. Signs of shock --> 2-3 L of NS as fast as possible! 2. W/O signs of shock --> 1L NS over 1 hr
49
DKA can lead to ____ (hypo/hyper)kalemia.
HYPOkalemia * Total body stores of potassium are depleted in DKA- insulin is needed to drive potassium into cells, without insulin lots of K is lost in the urine * If K is < 3.3 you want to add 20-30 meq of K+ per L of IV fluids **DON'T START INSULIN UNTIL K IS > 3.3 (otherwise too much K in cells and fatal arrhythmia is possible) ***If K> 5 no extra is needed
50
Once serum glucose is < _____ you want to reduce insulin drip by 1/2 and switch to D5 1/2 NS to prevent HYPOglycemia.
200 *But DON'T stop insulin until anion gap is normal
51
For peds you want to limit fluid boluses to one ___ cc/kg bolus
20
52
Non-Ketotic Hyperglycemia is the same as Hyperosmolar Hyperglycemic State (HHS). It is characterized by:
Profound dehydration, hyperglycemia, hyperosmolarity, and decreased mental status that can progress to coma *Ketosis is absent!!
53
HHS is a common presentation in _____ (what population).
New-onset type-2 diabetics
54
An elderly patient with DM2 who presents with complains of weakness or mental status changes, and has preexisting renal or heart disease is a common presentation of someone with _____.
HHS
55
Defining labs for HHS are:
1. Serum glucose > 600 2. Serum osmolarity > 320 3. pH > 7.3 4. Negative or mildly elevated ketones
56
Patients with DM, sepsis, adrenal insufficiency, hypothyroidism, or malnutrition are at risk for severe ______.
Hypoglycemia
57
Symptoms of hypoglycemia are:
Sweating, shakiness, anxiety, nausea, dizziness, confusion, slurred speech, blurred vision, headache, lethargy, coma *Dx not based on blood glucose alone. The diagnosis is based on the glucose level in conjunction with typical symptoms that resolve with treatment
58
Management of hypoglycemia entails...
- If patients have hypoglycemia with an altered mental status, treat with 50% dextrose 50 mL IV. A continuous infusion of 10% dextrose solution may be required to maintain the blood glucose above 100 mg/dL. Provide a carbohydrate meal if the patient can tolerate PO - If there is no IV access, administer glucagon 1mg IM or SC - Refractory hypoglycemia secondary to the sulfonylureas may respond to octreotide 50-100 µg SC. A continuous infusion of 125µ/hr may be required
59
______ is caused specifically by pituitary increasing ACTH secretion.
Cushing's Disease *Syndrome- S&S related to cortisol excess
60
Clinical manifestations of Cushing's are:
1. Redistribution of fat- central obesity, "moon faces," buffalo hump, supraclavicular fat pads 2. Catabolism- breakdown of proteins. Wasting of extremities, skin atrophy, increased infections 3. HTN- weight gain, HYPOkalemia, acanthosis nigricans 4. Androgen excess
61
MC exogenous cause of Cushings is ______.
Long-term high-dose corticosteroid therapy
62
MC endogenous cause of Cushings is ______.
Benign pituitary adenoma or hyperplasia
63
______ test is used for diagnosing Cushings.
Low-dose dexamethasone suppression test *Dexamethasone is 4x more potent than cortisol. Normal response is cortical suppression. No suppression= Cushing's syndrome
64
Other tests of diagnosing Cushings are:
- 24 hour urinary free cortisol levels | - Salivary cortisol levels
65
Understanding ACTH levels...
1. Decreased ACTH--> adrenal tumors | 2. Normal/Increased ACTH--> Cushing's disease or ectopic ACTH-producing tumor
66
How is Cushing's managed?
1. Transsphenoidal surgery 2. Ectopic ACTH-secreting or adrenal tumors- tumor removal 3. Iatrogenic steroid therapy

Emergency Medicine (11 decks)

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