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Emergency Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

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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
Q

How is primary hyperparathyroidism treated?

A

Parathyroidectomy

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26
Q

______ is due to adrenal gland failure, resulting in cortisol and aldosterone deficiency.

A

Adrenal Insufficiency/Addison’s Disease

*MC cause is autoimmune destruction of the adrenal cortex

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27
Q

ACTH stimulates the adrenal cortex to secrete cortisol, cortisol has a negative feedback on the pituitary to inhibit secretion of ACTH

A

some axis info…

28
Q

Manifestations of Adrenal Insufficiency are…

A

Weakness, dehydration, HYPOtension, anorexia, nausea, vomiting, weight loss, abdominal pain

-Hyperpigmentation of the skin is seen

29
Q

______ is the acute, life-threatening form of adrenal insufficiency.

A

Adrenal crisis

30
Q

Addison’s is defined by an aldosterone and cortisol problem. Similar clinical manifestations as those with Adrenal Insufficiency with myalgias and arthralgias as well.

A

Also orthostatic hypotension, Delayed DTRs, Salt craving

31
Q

Addison’s is associated with ____(hypo/hyper)natremia and ______(hypo/hyper)kalemia.

A

HYPOnatremia and HYPERkalemia

*Also hypoglycemia

32
Q

How is Addison’s diagnosed?

A
  1. AM cortisol
  2. Cosyntropin Stimulation Test (ACTH)
    * Low levels of ACTH at AM cortisol suggest secondary disease
33
Q

Secondary adrenal insufficiency will not have findings of hyperkalemia as there is not a deficiency of ______.

A

Aldosterone

34
Q

The MC cause of acute adrenal insufficiency is:

A
  • Adrenal suppression from prolonged steroid use with either abrupt steroid withdrawal or
  • Exposure to increased physiologic stress such as injury, illness, or surgery.
35
Q

Causes of primary adrenal insufficiency:

A

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
Q

Causes of secondary adrenal insufficiency:

A

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
Q

How do you treat an adrenal crisis?

A
  • 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
Q

_____ is caused by the absence of ADH (vasopressin). Lease to polyuria, polydipsia (esp at night).

A

Diabetes Insipidus

  • Can lead to HYPERnatremia :(
  • *Glucose is normal!
39
Q

Causes of Central DI:

A

Idiopathic, familial, infiltrative disease, tumor, trauma, surgery

*Image the pituitary!!!

40
Q

How is central DI treated?

A

Vasopressin, DDAVP

41
Q

DKA defined…

A
  • Diabetic- blood sugar over 250
  • Keto- ketones in the urine or blood
  • Acidosis- pH of 7.3 or lower
42
Q

The lack of insulin in DKA leads the body to burn ___ for fuel. Which leads to ketone production and acidosis.

A

Fat

43
Q

DKA v. HHS

A
  • DKA: 4-6 L volume down

- HHS: 9-10 L volume down, often with AMS

44
Q

Some PE findings with DKA include:

A
  1. Kussmaul respirations

2. Fruity odor to breath

45
Q

The 7 I’s to DKA

A

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
Q

Many patients w/ DKA have N/V/abdominal pain

A

fyi

47
Q

Initial management of DKA…

A
  • 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
Q

_____ is initially much more important than insulin.

A

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
Q

DKA can lead to ____ (hypo/hyper)kalemia.

A

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
Q

Once serum glucose is < _____ you want to reduce insulin drip by 1/2 and switch to D5 1/2 NS to prevent HYPOglycemia.

A

200

*But DON’T stop insulin until anion gap is normal

51
Q

For peds you want to limit fluid boluses to one ___ cc/kg bolus

A

20

52
Q

Non-Ketotic Hyperglycemia is the same as Hyperosmolar Hyperglycemic State (HHS). It is characterized by:

A

Profound dehydration, hyperglycemia, hyperosmolarity, and decreased mental status that can progress to coma

*Ketosis is absent!!

53
Q

HHS is a common presentation in _____ (what population).

A

New-onset type-2 diabetics

54
Q

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 _____.

A

HHS

55
Q

Defining labs for HHS are:

A
  1. Serum glucose > 600
  2. Serum osmolarity > 320
  3. pH > 7.3
  4. Negative or mildly elevated ketones
56
Q

Patients with DM, sepsis, adrenal insufficiency, hypothyroidism, or malnutrition are at risk for severe ______.

A

Hypoglycemia

57
Q

Symptoms of hypoglycemia are:

A

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
Q

Management of hypoglycemia entails…

A
  • 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
Q

______ is caused specifically by pituitary increasing ACTH secretion.

A

Cushing’s Disease

*Syndrome- S&S related to cortisol excess

60
Q

Clinical manifestations of Cushing’s are:

A
  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
Q

MC exogenous cause of Cushings is ______.

A

Long-term high-dose corticosteroid therapy

62
Q

MC endogenous cause of Cushings is ______.

A

Benign pituitary adenoma or hyperplasia

63
Q

______ test is used for diagnosing Cushings.

A

Low-dose dexamethasone suppression test

*Dexamethasone is 4x more potent than cortisol. Normal response is cortical suppression. No suppression= Cushing’s syndrome

64
Q

Other tests of diagnosing Cushings are:

A
  • 24 hour urinary free cortisol levels

- Salivary cortisol levels

65
Q

Understanding ACTH levels…

A
  1. Decreased ACTH–> adrenal tumors

2. Normal/Increased ACTH–> Cushing’s disease or ectopic ACTH-producing tumor

66
Q

How is Cushing’s managed?

A
  1. Transsphenoidal surgery
  2. Ectopic ACTH-secreting or adrenal tumors- tumor removal
  3. Iatrogenic steroid therapy

Emergency Medicine (11 decks)

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