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Emergency EOR > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

DDX for palpitations

A 
Hyperthyroidism
Thyroid storm
Hypoglycemia
Anemia
Electrolyte disorders
Cardiac disease
Alcohol withdrawal
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2
Q

DDX for tremors

A

Hypoglycemia
Hyperthyroidism
Thyroid storm

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3
Q

Primary hyperparathyroidism

A

Excess (inappropriate) PTH production

Most common type

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4
Q

Most common cause of primary hyperparathyroidism

A

Parathyroid adenoma

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5
Q

Primary hyperparathyroidism occurs in 20% of pts taking _______

A

Lithium

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6
Q

Secondary hyperparathyroidism

A

Increased PTH due to hypocalcemia or vitamin D deficiency

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7
Q

Most common cause of secondary hyperparathyroidism

A

Chronic kidney failure - kidneys convert vitamin D to its usable form

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8
Q

Tertiary hyperparathyroidism

A

Prolonged PTH stimulation after secondary hypothyroidism, leading to autonomous PTH production

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9
Q

Signs/Symptoms of hypercalcemia

A 
Stones
Bones
Abdominal groans
Psychic moans
Decreased DTRs
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10
Q

Diagnosis of hyperparathyroidism

A 
Hypercalcemia
Elevated PTH
Decreased phosphate
Increased 24 hour calcium excretion, increased vitamin D
Imaging studies for parathyroid adenoma
Osteopenia on DEXA
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11
Q

Management of hyperparathyroidism

A

Acute - saline, calcitonin, bisphosphonates

Definitive - Parathyroidectomy - remove overactive (if all 4, remove 3.5 glands)

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12
Q

Most common cause of hyperthyroidism

A

Grave’s disease - autoimmune disease that leads to TSH receptor antibodies

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13
Q

Signs/Symptoms of hyperthyroidism

A 
Anxiety
Heat intolerance
Menstrual irregularities
Weight loss
Palpitations
Tachycardia
Hyperdefecation
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14
Q

Specific signs/symptoms for grave’s disease

A 
Eye (proptosis, chemosis, lid retraction)
Skin abnormalities (pretibial myxedema)
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15
Q

Diagnosis of hyperthyroidism

A
  1. R/o pregnancy if menstrual irregularities
  2. Low TSH, high T4
  3. Radioactive iodine uptake (will show decreased uptake in all forms except graves - elevated)
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16
Q

Treatment of thyroid storm

A

PTU or methimazole
Beta blockers
High dose corticosteroids

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17
Q

Treatment of grave’s disease

A

Beta blockers
PTU or methimazole
Definitive tx: radioactive iodine
Steroids for ophthalmopathy

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18
Q

Treatment for grave’s in pregnant pts

A

PTU first trimester

Switch to methimazole after

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19
Q

S/E of methimazole

A

Leukopenia/agranulocytosis

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20
Q

S/E of PTU

A

hepatotoxicity

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21
Q

Most common cause of acute thyroiditis

A

Staph aureus

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22
Q

Signs/symptoms of acute thyroiditis

A

Painful, fluctuant thyroid.

Usually very ill, febrile

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23
Q

Diagnosis of acute thyroiditis

A

Increased WBC w/ left shift

Usually euthyroid

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24
Q

Tx of acute thyroiditis

A

Abx, drainage if abscess present

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25
Q

Adrenal insufficiency secondary to autoimmune destruction (most common cause)

A

Addison’s Disease

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26
Q

Signs/Symptoms of Addison’s disease

A

Fatigue, weakness, anorexia, nausea, weight loss
Hyperpigmentation
Hypotension, hyponatremia, hypoglycemia, hyperkalemia, metabolic acidosis

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27
Q

Cause of hyperpigmentation in adrenal insufficiency

A

Long-standing elevated ACTH levels

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28
Q

Diagnosis of adrenal insufficiency/Addison’s

A
  1. Low cortisol levels (<3)(measure early morning)
  2. ACTH stimulation test
  3. ACTH level - increased levels = primary, decreased levels = secondary
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29
Q

ACTH stimulation test

A

Addison’s disease
Give pt ACTH (cosyntropin) if cortisol levels do not rise, adrenal insufficiency is confirmed

Once low cortisol has been confirmed, draw ACTH level

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30
Q

Increased levels of ACTH with adrenal insufficiency

A 
Primary insufficiency (adrenal problem)
CT of adrenal gland. Will also see elevated renin and decreased aldosterone
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31
Q

Decreased levels of ACTH with adrenal insufficiency

A

Secondary (pituitary problem) or tertiary insufficiency (hypothalamus).
MRI of the brain.
Renin and aldosterone levels will be unaffected

32
Q

Treatment of primary adrenal insufficiency

A

Hydrocortisone and fludrocortisone

33
Q

Treatment of secondary adrenal insufficiency

A

Hydrocortisone

34
Q

Adrenal Crisis: presentation and tx

A
  1. Present with shock, n/v, abd pain, ams

2. Volume repletion and high dose IV glucocorticoid administration

35
Q

Diabetes insipidus is caused by:

A
  1. ADH (vasopressin) deficiency (central) - MC

2. Insensitivity to ADH (neprhogenic) - inability of kidneys to concentrate urine

36
Q

Signs/symptoms of diabetes insipidus

A
  1. Polyuria (up to 20 L/day)
  2. Polydipsia
  3. Nocturia
  4. Hypernatremia (if severe)
37
Q

Diagnosis of diabetes insipidus

A
  1. Fluid deprivation test

2. Desmopressin (ADH) stimulation test

38
Q

Fluid deprivation test for diabetes insipidus

A

Establishes diagnosis
Normal response - progressive urine concentration
DI: continued production of dilute urine (low s.g. < 1.005)

39
Q

Desmopressin (ADH) stimulation test

A

Differentiates nephrogenic from central DI
Administer ADH
1. Central: reduction in urine output indicating a response to ADH
2. Nephrogenic: continued production of dilute urine (no response to ADH)

40
Q

Management of central DI

A

Desmopressin/DDAVP

Intranasal, injection or oral form

41
Q

Management of nephrogenic DI

A

Na+/protein restriction

Hydrochlorothiazide, indomethacin

42
Q

Results of insulin deficiency and counterregulatory hormonal excess in diabetes as a direct response to stressful triggers

A

DKA

Hyperosmolar hyperglycemic syndrome (HHS)

43
Q

Stressful triggers that can cause DKA/HHS

A

Infection (MC)
Infarction
Noncompliance with insulin/dosage change
Undiagnosed diabetes

44
Q

DKA and HHS differ in:

A

DKA has presence of ketoacidosis

Severity of hyperglycemia (higher in HHS)

45
Q

Signs/Symptoms of DKA

A

Hyperglycemia, abdominal pain, hypotension

Thirst, polyuria, polydipsia, nocturia, weakness, fatigue

46
Q

Signs/Symptoms of HHS:

A

Hyperglycemia, mental status changes, hypotension

Thirst, polyuria, polydipsia, nocturia, weakness, fatigue

47
Q

DKA specific physical exam

A

Ketotic breath

Kussmaul’s respirations

48
Q

Kussmaul’s respirations

A

Deep continuous respirations as lung attempts to blow off excess CO2 to reduce acidemia

49
Q

Diagnosis of DKA

A
  1. Plasma glucose > 250
  2. pH < 7.30
  3. Bicarb < 18
  4. Ketones (urine/serum)
50
Q

Diagnosis of HHS

A
  1. Plasma glucose > 600
  2. > 7.30
  3. Bicarb > 15
  4. Small ketones
51
Q

Management of DKA/HHS

A
  1. IV Fluids
  2. Insulin
  3. Potassium (verify renal output) if potassium low/normal
  4. Bicarb if severe
52
Q

IV fluids for management of DKA/HHS

A
  1. Give 0.9% NS until hypotension resolves, then 0.45% NS

2. When glucose reaches 250, switch to D5 0.45% NS to prevent hypoglycemia from insulin

53
Q

Treatment goals of DKA

A

Close anion gap

54
Q

Treatment goals of HHS

A

Normal mental status

55
Q

Autoimmune destruction of the pancreatic beta cells, which will result in insulin dependence

56
Q

Characterized by insulin resistance related to obesity

57
Q

Main distinction b/w type 1 and type 2 diabetes

A

Presence of antibodies

58
Q

Risk factors for DM type II

A 
> 45 y/o
BMI > 25
DM in 1st degree relative
Sedentary lifestyle
Gestational DM
Hx of child delivery > 9 lb
Dyslipidemia
HTN
PCOS
59
Q

Signs/Symptoms of DM

A
  1. Polyuria
  2. Polydipsia
  3. Fatigue
60
Q

Screening options for DM

A
  1. Two fasting glucose levels > 126
  2. One glucose level > 200 with symptoms
  3. HgA1c > 6.5%
  4. Positive 2 hour oral glucose tolerance test
61
Q

Diabetic follow up care

A
  1. Yearly eye exam to screen for retinopathy
  2. Yearly urine microalbumin screening
  3. LDL > 100 (statin first line)
  4. BP > 140/90 (ACE/ARB first line)
  5. Yearly comprehensive foot exam
  6. ASA for prevention if 10 year risk . 10% and > 30 y/o
62
Q

Increased pituitary ACTH secretion leading to cortisol excess

A

Cushing’s Disease

63
Q

Signs/Symptoms of Cushing’s Disease

A
  1. Redistribution of fat - moon face, buffalo hump, supraclavicular fat pads
  2. Catabolism (breakdown of protein) - thin extremities, skin atrophy
  3. Hypertension
  4. Mental - depression, mania, psychosis
  5. Androgen excess - hirsutism, oily skin, acne, amenorrhea
64
Q

Most common cause of cushing syndrome

A

Exogenous - long-term high dose corticosteroid therapy

65
Q

Endogenous causes of cushing’s disease

A
  1. Benign pituitary adenoma or hyperplasia (secretes ACTH)

2. Adrenal tumor - cortisol-secreting adrenal adenoma (or rarely carcinoma)

66
Q

Diagnosis of cushing’s disease

A
  1. Low-dose dexamethasone suppression test
  2. 24 hour urinary free cortisol levels
  3. salivary cortisol levels
67
Q

Low-dose dexamethasone suppression test

A

Cushing’s disease

Normal response is cortical suppression. No suppression = cushing’s disease

68
Q

24 hour urinary free cortisol levels

A

Cushing’s disease

Increased urinary cortisol = cushing’s syndrome

69
Q

Salivary cortisol levels

A

Cushing’s disease
Increased cortisol in cushing’s syndrome
usually performed at night

70
Q

Decreased ACTH with cushing’s syndrome

A

Adrenal tumor

71
Q

Management of cushing’s disease

A

Pituitary - transsphenoidal surgery
Adrenal - tumor removal
Iatrogenic steroid therapy - gradual steroid taper

72
Q

Most common etiology of hypothyroidism

A

Hashimoto’s thyroiditis

73
Q

Signs/Symptoms of hypothyroidism

A
  1. Constipation
  2. Weight gain
  3. Fatigue
  4. Decreased reflexes (on relaxation phase)
  5. Cold intolerance
  6. Menstrual irregularities
  7. Hair loss
74
Q

Diagnosis of hypothyroidism

A

Elevated TSH, decreased T4

Hashimotos: thyroid peroxidase antibodies

75
Q

Treatment for hypothyroidism

A

Levothyroxine - take fasting and wait 4 hours before taking iron or calcium supplements

Emergency EOR (12 decks)

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