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First AId 2CK > Endocrinology - MTB > Flashcards

Endocrinology - MTB Flashcards

0
Q

Panhypotpituitarism: presentation

A

symptoms dependent of deficiency of a specific hormone

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1
Q

Panhypopituitarism

A
  • caused by any condition that compression or damage to pituitary gland
  • look for tumors (e.g. metastatic cancer, adenomas, Ranthke cleft cysts)
  • look for conditions (e.g. hemachromatosis, sarcoidois)
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2
Q

Prolactin deficiency

A
  • in women, prolactin deficiency inhibits lactation after childbirth
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3
Q

Deficiency of LH and FSH

A
  • women are unable to menstruate (become anovulatory)
  • men unable to produce sperm and have erectile dysfunction
  • both men and women have decreased libido and decreased axillary, pubic, and body hair
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4
Q

Kellman syndrome

A
  • decreased FSH and LH from decreased GnRH
  • anosmia
  • renal agenesis
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5
Q

Growth hormone deficiency

A
  • children present with short stature and dwarfism

- adults have few symptoms b/c catecholamines, glucagon, and corticol act as stress hormones

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6
Q

Adult presentation of GH deficiency

A
  • Central obesiry
  • increased LDL and cholesterol levels
  • reduced lean muscle mass
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7
Q

Growth hormone diagnostic tests

A
  • Hyponatremia (2/2 hypothyroidism and isolated glucocorticoid underpoduction)
  • potassium remains levels b/c aldosterone is not affected
  • MRI detects compressing mass lesions
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8
Q

Low TSH and low thyroxine

A

confirm w/ decreased TSH response to TRH

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9
Q

decreased ACTH and decreased cortisol level

A

normal response to cosyntropin stimulation of adrenal, cortisol will rise in recent disease and cortisol is abnormal b/c of adrenal atrophy

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10
Q

Metyrapone

A

inhibits 11- B hydroxlase

  • decreases output of adrenal gland
  • should cause ACTH to rise b/c cortisol goes down
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11
Q

Insulin stimulation

A
  • insulin decreases glucose levels so GH should rise

- failure to rise in response to insulin indicates pituitary insufficiency

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12
Q

Posterior pituitary

A
  • produces ADH and oxytocin

- no deficiency disease for oxytocin

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13
Q

Oxytocin deficeiency

A
  • aids with uterine contraction

- delivery still occurs even if active

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14
Q

Diabetes Inspidus

A
  • decrease in amt of ADH from pituitary (central DI) or decease in response to ADH on collecting tubules (nephrogenic DI)
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15
Q

Central DI

A

any destruction of brain from stroke, tumor, trauma, hypoxia, or infiltration of gland from sarcoidosis or infection

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16
Q

Nephrogenic DI

A

Kidney diseases (e.g chronic pyelonephritis, amyloidosis, myeloma, and sickle cell disease) damaged kidney enough to inhibit effect of ADH

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17
Q

Electrolyte abnormalities that can cause nephrogenic DI

A
  • Hypercalcemia

- Hypokalemia

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18
Q

DI: presentation

A
  • presents with high volume urine and excessive thirst resulting in volume depletion and hypernatremia
  • hypernatremia sx (condusion, disorientation, lethargy then later seizures, coma)
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19
Q

classic cause of nephrogenic DI

A

Lithium

- look for bipolar patients

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20
Q

Diabetes inspidus

A
  • serum sodium is elevated

- decreased urine osmolality and urine sodium is decreased

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21
Q

Difference btwn central DI and nephrogenic DI

A

Response to vasopressin (desmopression(

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22
Q

Central DI: Treatment

A
  • treated with long term vasopression
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23
Q

Nephrogenic DI: treatment

A
  • correct underlying cuase (e.g. hypokalemia or hypercalcemia)
  • treat with thiazides, amiloride, or prostiglandin inhibitors (NSAIDS)
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24
Q

Acromegaly

A

overproduction of growth hormone leading to soft tissue overgrowth

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25
Q

Acromegaly: Etiology

A
  • often cuased by pituitary adenoma
  • can be associated with MEN (e.g. parathyroid or pancreatic disorders)
  • rarely caused by ectopic GH or GHrH production from lymphoma or bronchial carcinoid
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26
Q

Acromegaly: presentation

A
  • increased hat, ring, and shoe size
  • carpal tunnel syndrome and sleep apnea from enlarged soft tissues
  • body odor from sweat gland hypertrophy
  • coarsening facial features
  • colonic polyps and skin tags
  • arthralgias
  • hypertension
  • cardiomegaly and CHF
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27
Q

Best initial test for suspected acromegaly?

A

Insulin growth factor (IGF -1) levels

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28
Q

Acromegaly: lab testing

A
  • Glucose interolerance and hyperlipidemia, which contribute to cardiac dysfunction
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29
Q

Most accurate test for acromegaly

A

Glucose suppression test

- normally glucose suppreses GH levels

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30
Q

When is the MRI done in diagnosis of acromegaly?

A

Only after lab identification of acromegaly

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31
Q

Acromegaly: Treatment

A
  1. Surgery: transphenoidal resection of pituitary
  2. Medications
    - cabergoline
    - octreotide or lanreotide
    - pegvisomant
  3. Radiotherapy
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32
Q

Cabergoline

A

dopamine will inhibit GH release

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33
Q

Octreotide or lanreotide

A

somatostatin inhibits GH release

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34
Q

Pegvisomant

A

Gh receptor antagonist, inhibits IGF release from the liver

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35
Q

Hyperprolactinoma

A
  • prolactin can be cosecreted with GH and increase simply b/c of acromegaly
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36
Q

Physiologic cause of hyperprolactinoma

A
  • Pregnancy
  • Intense exercise
  • Renal insufficiency
  • Increased chest wall stimulation
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37
Q

Drug induced hyperprolactinoma

A
  • Antipsychotic meds
  • Methyldopa
  • Metoclopromide
  • Opioids
  • TCAs
  • Verapramil
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38
Q

Which the only CCB that raises prolactin levels?

A

Verapramil

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39
Q

Hyperprolactinoma: presentation

A
  • women present with galactorrhea, amenorrhea, and infertility
  • men experience erectile dysfunction and decreased libido
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40
Q

Hyperprolactinoma: Diagnostic tests

A
  1. Thyroid fxn tests
  2. Pregnancy tests
  3. BUN/Cr (kidney disease elevates prolactin)
  4. Liver fxn test (cirrhosis elevates prolactin)
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41
Q

When is the MRI done in diagnosis of hyperprolactinemia

A
  1. High prolactin level is confirmed
  2. Secondary causes such as meds are exclused
  3. Patient is not pregnant
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42
Q

Hyperprolactinemia: Treatment

A
  1. Dopamine agonitsts: cabergoline
  2. Transphenoidal surgery: when refractory to meds
  3. Radiation is rarely indicated
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43
Q

Hypothyroidism

A
  • often of failure of thyroid gland from burn out (e.g Hashimoto thyroiditis)
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44
Q

Less common causes of hypothyroidism

A
  • Dietary deficiency of iodine

- Amiodarone

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45
Q

Hypothyroidism: common sifns

A
  • all bodily processes being slowed

- high TSH (2x upper limit) with T4

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46
Q

If patient has hypothyroidism and TSH is less than double normal, what’s next step?

A
  • Get antithyroid peroxidase/antithyroidglobulin antibodies

- if antibodies are positive, replace thyroid hormone

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47
Q

Hypothyroid: presentaiton

A
  • Bradycardia
  • Constipation
  • Weight gain
  • Fatigue, lethargy, coma
  • Cold intolerance’
  • Hypothermia (hair loss, edema)
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48
Q

Hyperthyroidism

A
  • Tachycardia, palpitations, arrhythmia
  • Diarrhea
  • Weight loss
  • Anxiety, nervousness, restlessness
  • Hyperreflexia
  • Heat intolerance
  • Fever
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49
Q

Best diagnostic test for suspected thyroid disorders

A

TSH levels

  • if TSH is suppressed then meausre T4 levels
  • if TSH is markedly elevated then gland has likely failed
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50
Q

Hypothyroidism: treatment

A

Thyroid hormone replacement

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51
Q

Pt has hyperthyroidism and presents with proptosis (eye drooping) and skin findings. Likely diagnosis?

A

Graves disease

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52
Q

Pt has hyperthyroidism and presents with a tender thyroid. What’s the most likely diagnosis?

A

Subacute thyroiditis

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53
Q

Patient has low TSH and high T4 but presents with nontender thyroid and normal exam results. Likely diagnosis?

A

Painless “silent” thyroiditis

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54
Q

Pt has high T4 levels and low TSH with an involuted gland that is not palpable. Likely diagnosis?

A

Exogenous thyroid hormone use

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55
Q

Patient has has T4 and high TSH. Likely diagnosis?

A

Pituitary adenoma

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56
Q

Graves disease: lab findings

A
  • low TSH
  • high RAIU
  • positive antibody testing
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57
Q

Subacute thyroiditis: lab findings

A
  • low TSH
  • low RA iodine uptake
  • confirm with tender thyroid
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58
Q

Painless “silent” thyroiditis: lab findings

A
  • low TSH
  • low radioactive iodine uptake
  • no confirmatory testing
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59
Q

Exogenous thyroid hormone: lab findings

A
  • low TSH
  • low radioiodine uptake
  • confirm with hx and involuted thyroid nonpalpable gland
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60
Q

Pituitary adenoma

A
  • high TSh
  • radioactive iodine uptake not dones
  • confirm with MRI of head
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61
Q

Graves disease: treatment

A

Radioactive iodine

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62
Q

Subacute thyroiditis: treatment

A

Aspirin

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63
Q

Painless “silent” thyroiditis: treatment

A

None

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64
Q

Exogenous thyroid hormone: tx

A

Stop use

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65
Q

Pituitary adenoma: tx

A

Surgery

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66
Q

Thyroid Storm / Acute hyperthyroidism: Treatment

A
  1. Propranolol
  2. Thiourea drugs (methimazole and PTU)
  3. Iodinated contract material
  4. Steroids
  5. Radioactive iodine
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67
Q

Propranolol in thyroid storm

A
  • blocks target organ effect, inhibits peripheral conversion of T4 to T3
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68
Q

Thiourea drugs: Methimazole and Propylthiouracil) in management of thyroid storm

A
  • Blocks hormone production
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69
Q

Use of iodinated contrast material (iopanoic acid and ipodate) in thyroid storm mgmt

A

Blocks peripheral conversion of T4 to T3 (more active)

- blocks release of existing hormone

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70
Q

Graves Ophthalmopathy: Treatment

A

Steroids are best initial therapy

- radiation used when pt is unresponsive to steroids

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71
Q

Which is preferred in management of thyroid storm? Methimazole or PTU

A

Methimazole

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72
Q

Thyroid nodules

A
  • extremely common
  • 95 % benign (adenoma, colloid nodule, cyst)
  • rarely associated with hyperfunctioning and hypofunction
73
Q

46 y.o woman comes to the office b/c of small mass she found on palpation of her own thyroid. A small nodule is found in thyroid. No tenderness. Otherwise symptomatic and uses medications. Next step for management of this patient?

A

Check T4 and TSH levels

74
Q

If patient has thyroid nodule > 1 cm and has normal thyroid fxn (T4/TSH). What’s the next step?

A

FNA

- no need for U/S or radionucleotide because they cannot exclude cancer

75
Q

When patient has a nodule… next steps?

A
  1. Perform thyroid function tests (TSH and T4)

2. If tests are normal, biopsy the gland

76
Q

46 y.o woman with thyroid nodule is found to have normal thyroid function testing. The FNA comes back as “indeterminant for follicular adenoma. What is the most appropriate next step?

A

Surgical removal (excisional biopsy)

77
Q

Hypercalcemia

A
  • most common cause in hyperparathyroidism
  • most patients are asymptomatic
  • symptomatic patients have high prevalence of cancer and hypermalignancy of malignancy
78
Q

Other causes of hypercalcemia

A
  • Vitamin D intoxication
  • Sarcoidosis and other granulomatous disease
  • Thiazide diuretics
  • Hyperthyroidism
  • Metastases to bone and multiple myeloma
79
Q

Hypercalcemia: Presentation

A
  • acute, symptomatic hypercalcemia presents with confusion, stupor, lethargy, and constipation
80
Q

CV presentation: hypercalcemia

A
  • short QT syndrome and hypertension
81
Q

Hypercalcemia: Treatment

A
  1. Saline hydration at high volume

2. Bisphosphonate: pamidronate, zoledronic acid

82
Q

75 y/o man with a hx of malignancy is admitted with lethargy, confusion, and abdominal pain. He is found to have a a markedly elevated calcium level. After 3 liters of normal saline and pamidronate, his calcium level is still markedly elevated the following day. What is the most appropriate next step in management?

A

Calcitonin

  • inhibits osteoclasts
  • onset of action of calcitonin is very rapidly
83
Q

Hyperparathyroidism

A
  • Solitary adenoma (** most common cause**)
  • Hyperplasia of all 4 glands
  • Parathyroid malignancy
84
Q

Hyperparathyroid: presentation

A
  • Asymptomatic elevation in calcium levels found on routine testing
    Slower manifestations
  • osteoporosis
  • nephrolithiasis and renal insufficiency
  • muscle weakness, anoreia, nausea
  • peptic ulcer disease
85
Q

Hyperparathyroidism: diagnostic tests

A
  • high calcium and high PTH
  • low phosphate levels
  • EKG shows short QT
  • alkaline phosphotase may be elevated due to PTH effect on bone
86
Q

Best test to determine PTH effect on bone

A

DEXA scan

87
Q

Hyperparathyroidism: Treatment

A

Surgical removal of gland

- if surgeon is poor surgical candidate

88
Q

Primary hypoparathyroidism

A
  • often a complication of prior neck surgery (e.g. thyroidectomy)
89
Q

Common causes of hypoparathyroidism

A
  • prior neck surgery (most common)
  • hypomagnesemia
  • renal failure
90
Q

Hypocalcemia 2/2 hypomagnesemia

A

Mg is necesssary for PTH to be released from gland

- low Mg levels also leads to increased urinary loss of calcium

91
Q

Hypoparathyroidism 2/2 renal failure

A

Leads to hypocalcemia

- kidney converts 25 hydroxy vitamin D to 1,25 dihydroxy Vitamin D

92
Q

Calcium correct with albumin levels

A

For every 1 point decrease in albumin, decrease calcium by 0.8

93
Q

Discuss low albumin and low total calcium

A

Lab testing measures calcium bound to albumin thus less albumin means less calcium

94
Q

Hypocalcemia: presentation

A

Signs of neural hyperexcitability in hypocalcemia:

  • Chvostek sign (facial nerve hyprexcitability)
  • Carpopedal spasm
  • perioral numbess
  • mental instability
  • seizures
  • tetany (Trousseau)
95
Q

Hypocalcemia: treatment

A

Replace with vitamin D and calcium

- only done orally if symptoms are severe

96
Q

Hypocalcemia: diagnostic testing

A
  • Low Ca levels
  • EKG shows prolonged QT that can cause arrhythmia
  • slit lamp may show early cataracts
97
Q

Low calcium: presentation

A

Twitchy and hyperexcitable

98
Q

High calcium: presentation

A

Lethargic and slow

99
Q

Diabetes Mellitus

A
  • persistently high fasting glucose levels greater than 125 on at least 2 separate occasions
100
Q

Type 1 DM

A
  • onset in childhood
  • insulin dependent from early age
  • not related to obesity
  • defined as insulin deficiency
101
Q

Type 2 DM

A
  • onset in adulthood
  • directly related to obesity
  • defined as insulin resistance
102
Q

Diabetes Mellitus: presentation

A
  • polyuria, polyphagia, and polydipsia
  • type 1 diabetics usually thinner than type 2
  • type 2 diabetics less likely to present with polyphagia
103
Q

Diabetes Mellitus: Diagnostic Tests

A
  • Two fasting blood glucose measurements > 125 mg/dL
  • Single glucose level > 200 mg/dL with above symptoms
  • Increased glcose level on oral glucose tolerance test
  • Hemoglobin A1c > 6.5% is a diagnostic criterion and best to follow response to therapy for the past few months
104
Q

Diabetes Mellitus: Treatment

A
  • weight loss since less adipose tissue decreases insulin resistance
105
Q

Best initial medical treatment for diabetes mellitus

A

Oral metformin

- blocks glucogenesis

106
Q

Contraindications of metformin

A

In DM pts with renal dysfunction because it can accumulate and cause metabolic acidosis

107
Q

Why aren’t sulfonyureas first line drugs for DM?

A
  • Sulfonyureas increase insulin release from pancreas, thereby driving glucose intracellularly and increasing obesity
  • goal of therapy < 7%
108
Q

Thiazoledinediones (glitazones)

A
  • provide no clear benefit over the other hypoglycemic conditions
  • contraindicated in CHF because they increase fluid overload
109
Q

Nateglinide and repaglinide

A
  • stimulators of insulin release from pancrease

- don’t contain sufa

110
Q

Alpha glucosidase inhibitors (e.g. acarbose, miglitol)

A
  • block glucose absorption in the bowel
  • add about 1/2 point decrease in HgA1c
  • can cause flatus, diarrhea, and abdominal pain
  • can be used with renal insuffiency
111
Q

Incretins (exenatide, sitagliptin, saxagliptin, linagliptin)

A
  • part of mechanism by which oral glucose normally produces rise in insulin and decreases glucagnon levels
  • decreases gastrin motlity and help in weight loss, decreasing Type 2 diabetes
112
Q

Exenatide: side effects

A

Pancreatitis

113
Q

Pramlinitide

A
  • analog of protein called amylin that is secreted normally with insulin
  • amylin decrease gastric emptying
  • decreases glucagon levels and decreases appetitie
114
Q

Insulin use in Type 2 DM

A

used when oral hypoglycemics cannot control

115
Q

Short acting insulin

  • lispro
  • aspart
  • glulisine
A
  • onset in 5 - 15 minutes
  • peak action in 1 hr
  • lasts for 3-4 hrsw
116
Q

Regular insulin

A
  • onset in 30 to 60 minutes
  • peak action in 2 hrs
  • duration of 6 - 8 hrs
117
Q

NPH

A
  • onset in 2 to 4 hrs
  • peak action in 6 to 7 hrs
  • lasts for 10 - 20 hrs
118
Q

Glargine

A
  • onset in 1 to 2 hrs
  • peak action in 1 to 2 hrs
  • lasts for 24 hrs
119
Q

Diabetic ketoacidosis

A
  • more common in type 1 diabetics
  • Patients present w/
    • hyperventilation
    • possibly AMS
    • metabolic acidosis w/ increased anion gap
    • acetone odor on breath
    • polydipsia and polyuria
    • hyperkalemia in blood but decreased total body K
    • increased anion gap on blood testing
    • serum positive for ketones
    • nonspecific abdominal pain
120
Q

DKA: Treatment

A

Large volume saline and insulin replacement

  • replace K when potassium level comes down to a level approaching normal
  • correct underlying cause: meds, infection, pregnancy
121
Q

57 y.o man is admitted to ICU with AMS, hyperventilation and markedly elevated glucose level. Which is the following is the most accurate measure of the severity of the condition?

A

Serum bicarbonate

  • measure of anion gap acidosis
  • the lower the bicarb, the more severe the acidosis
122
Q

DM patients should receive the following for health maintenance:

A
  • Pneumococcal vaccine
  • Yearly eye exam for proliferative neuropathy
  • statin meds if LDL > 100
  • ACEis or ARBS if BP is > 130/80 mm Hg
  • ACEis or ARBS if microalbuminuria is present
  • Aspirin if diabetic patients > 50
  • foot exam for neuropathy
123
Q

Complications of DM

A
  • CV risk
  • Diabetic nephropathy
  • Gastroparesis
  • Retinopathy
  • Neuropathy
124
Q

CV complications of DM

A
  • DM patients are at increased risk of MI
  • CHF from premature atherosclerotic disease
  • why BP goal is < 130/80
  • target LDL goal < 100 mg/DL when initiating stain treatments
125
Q

Diabetic Nephropathy

A
  • DM can lead to microalbuminuria (30 - 300 mg per 24 hrs)
  • should be screened annually for microalbuminuria
  • if detected, DM pt should be started on ACEis and ARBs by decreasing intraglomerylar HRn and decreasing kidney damage
126
Q

Gastroparesis

A
  • immobility of bowels that leads to bloating, constupation and early satiety
  • DM decreases ability of gut to sense the stretch of walls of bowel, important as stretch stimulates gastric motility
127
Q

Gastroparesis: Treatment

A

Metoclopromide
Erythromycin
– increases gastric motility

128
Q

Diabetic nonproliferative retinopathy

A
  • DM affects nonproliferative retinopathy for tighter control of glucose
129
Q

Diabetic proliferative retinopathy

A
  • neovascularization and vitreous hemorrhages are present

- treat with laser photocoagulation, which markedly retards progression to blindness

130
Q

Diabetic neuropathy

A
  • damage to microvasculature damages vasonervorum that surrounds large peripheral nerves
  • decreased sensation in the feet - main cause of skin ulcers
131
Q

Diabetic neuropathy: treatment

A
  • Preglabin
  • Gabapentin
  • Tricyclic antidepressants
132
Q

Cushing syndrome

A
  • aka hypercortisolism

- can be cased by prednisone or other glucocorticoid

133
Q

Cushing disease

A
  • pituitary overproduction of ACTH from carcinoid or cancer or from overproduction autonomously in the the adrenal gland
  • can be caused by prednisone or other glucorticoids
134
Q

Most common cause of hypercorticolism

A

Pituitary ACTH (Cushing disease)

135
Q

Cushing syndrome: presentation

A
  • Fat redistribution: “moon facies” , truncal obesity
  • Skin: striae
  • Osteoporosis
  • Hypertension
  • Menstrual disorders in women
  • Erectile dysfunction in men
  • Cognitive disturbance
  • Polyuria
136
Q

Best initial test for presence of hypercorticolism

A

24 hr urine cortisol

137
Q

Test for hypercorticolism other than 24 hr urine cortisol

A
  • 1mg overnight dexamethasone suppression test

** if suppression doesn’t occur, hypercorticolism can be excluded

138
Q

More specific test of hypercorticolism

A

24 hr urine cortisol

139
Q

Causes of false positive 1 mg dexamethasone suppression testing

A
  • Depression
  • Alcoholism
  • Obesity
140
Q

Best initial test to determine the cause (source) or location of hypercortisolism

A

ACTH testing

141
Q

If ACTH level is high in someone with suspected hypercortisolism, the source could be from:

A
  • Pituitary (suppresses w/ high dose dexamethsone)

- Ectopic production: lung cancer, carcinoid (dexamethasone doesn’t suppress)

142
Q

If the ACTH level is elevated and doesn’t suppress with high dose dexamethasone

A
  • Scan the brain MRI
143
Q

If patient has suspected hypercortisolism and the MRI does not show pituitary lesion. What’s the next step?

A

Sample the inferior pretrosal sinus for ACTH, possible after the stimulating the patient with CRH

144
Q

Why should the petrosal venous sinus must be sampled in cases of suspected hypercortisolism when head MRI is negative?

A

Some pituitary lesions are too small detected on RI

145
Q

If patient has suspected hypercortisolism and the ACTH is levated and cannot find defect in pituitary either by MRI or petrosal sinus sampling, what’s the next step?

A

Scan chest for ectopic source of ACTH production

146
Q

Patient has suspected hypercortisolism but low ACTH. Source of cortisol?

A

Adrenal srouce

147
Q

Patient has suspected hypercortisolism but has high ACTH and has been given high dose dexamethasone. Source?

A

If dexamethasone test suppresses: pituitary source

If dexamethasone test does not suppress: ectopic + cancer

148
Q

Effects of hypercortisolism

A
  • Hyperglycemia
  • Hyperlipidemia
  • Hypokalemia
  • Metabolic alkalosis
  • Leukocytosis (from demargination of WBC cells)
149
Q

Why does hypercortisolism cause hypokalemia and metabolic alkalosis?

A

Cortisol has an aldosterone-like effect on distal tubules in which potassium and hydrogen ions are excreted

150
Q

Hypercortisolism: Treatment

A

Surgically remove the source of hypercortisolism

  • transsphenoidal surgery is done for pituitary sources
  • laparoscopic removal is adrenal sources
151
Q

Evaluation of adrenal incidentaloma (unexpected, asymptomatic adrenal lesion found on CT)

A
  • metanephrines of blood or urine to exclude pheochromocytoma
  • renin and aldosterone levels to exclude hyperaldosternism
  • 1 mg overnight dexamethasone suppression test
152
Q

Adrenal source hypercortisolism: findings

A
  • low ACTH
  • petrosal sinus not does
  • no suppression of high dose dexamethasone
153
Q

Pituitary source hypercortisolism: findings

A
  • high ACTH
  • high ACTH found on petrosal sinus
  • high dose dexamethasone suppresses ACTH
154
Q

Ectopic source hypercortisolism findings

A
  • high ACTH level
  • low ACTH in petrosal sinus
  • no suppression on high dose dexamethasone
155
Q

Addison disease

A
  • chronic hypoadrenalism

- caused by autoimmune destruction of the gland in more than 80% of causes

156
Q

Most common cause of hypoadrenalism

A

Addison disease

157
Q

Less common causes of hypoaldrenalism

A
  • Infection (tuberculosis)
  • Adrenoleukodystrophy
  • Metastatic cancer to the adrenal gland
158
Q

Acute adrenal crisis

A
  • caused by hemorrhage, surgery, hypotension, or trauma that rapidly destroys the gland
  • sudden remove of high dose prednisone (steroid) can precipitate episode
159
Q

Hypoadrenalism: presentation

A
  • weakness, fatigue, AMS
  • hypotension
  • hyponatremia
  • hyperkalemia
  • hyperpigmentation from chronic adrenal insufficiency
160
Q

Acute adrenal crisis

A
  • presents with profound hypotension, fever, confusion, and coma
161
Q

Hypoadrenalism: diagnostic test

A
  • Hypoglycemia
  • Hyperkalemia
  • Metabolic acidosis
  • Hyponatremia
  • High BUN
  • Eosinophilia
162
Q

Most specific test of adrenal function

A

Cosyntropin test

  • cosyntropin is synthetic ACTCH
  • measure the cortisol level before and after the administration of cosyn
163
Q

Hypoadrenalism (acute adrenal crisis): treatment

A
  1. Replace steroids with hydrocortisone
  2. Fludrocortisone is steorid hormone that is particularly high in mineralicorticoid or aldosteroine-like effect
    • fludrocortisone most useful in cases of postural instability
    • mineralocorticoid supplements shoud be used in primary adrenal insufficiency
164
Q

Patient is brought to the ED after a MVA in which he sustains severe abdominal trauma. On the 2nd hospital day, the patient necomes markedly hypotensive w/o evidence of bleeding. There is a fever, high eosinophil count, hyperkalemia, hyponatremia, and hypoglycemia. What is the most appropriate next step in management?

A

Draw cortisol level and administer hydrocortisone

- in suspected acute adrenal insufficiency, treatment is more important than diagnosis

165
Q

Primary hyperaldosteronism

A
  • autonomous overproduction of aldosterone despite high pressure with low renin activity
  • 80% are from solitary adenoma
  • other causes are from bilateral hyperplasia
166
Q

Most common cause of primary hyperaldosteronism

A

Solitary adenoma

167
Q

Risk factors for secondary hypertension

A
  • under age 30 or after age 60
  • not controlled by 2 anti-BP meds
  • has characteristic finding on hx, physical, or labs
168
Q

Primary hyperaldosteronism findings

A
  • high blood pressure in association with low potassium level
  • low K found on routine lab testing or b/c of symptoms of muscular weakness or diabetes insipidus from hypokalemia
169
Q

Best test to measure primary hyperaldosteronism

A

Ratio of plasma aldosterone to plasma renin

- elevated plasma renin excludes primary aldosteronism

170
Q

Most accurate test to confirm unilateral adenoma in primary hyperaldosteronism

A
  • Sample of venous blood draining the adnreal

- it will show high aldosterone levels

171
Q

Diagnostic order in suspected hyperaldosteronism

A
  1. ratio of plasma aldosterone to plasma renin

2. CT scan of adrenals (only AFTER biochemical confirmation of low K, high aldosteronism, low plasma renin)

172
Q

High BP + hypokalemia =

A

Primary hyperaldosteronism

173
Q

Hyperaldosteronism: Treatment

A
  • Unilateral adenoma is resected by laparascopy

- Bilateral hyperpaslia is treated with eplerenone or spironolactone

174
Q

Phemochromocytoma

A
  • nonmalignant lesion of adrenal medulla autonomously overproducing catecholamines despite high BP
175
Q

Pheochromocytoma: presentation

A
  • Hypertension that is episodic in nature
  • Headache
  • Sweating
  • Palpitations and tremor
176
Q

Best initial test for pheochromocytoma

A

Plasma level of free metanephernes

177
Q

Pheochromocytoma: diagnostic testing

A
  1. plasma level of free metanepherines
    • confirmed with 24 hr urine collection for metanepherines
  2. imaging of adrenal glands w/ CT or MRI done after bio chemical testing
178
Q

MIBG scanning

A

nuclear isotope scan that detects location of pheochromocytoma that originates outside of gland

179
Q

Pheochromocytoma: treatment

A
  1. Phenoxybenzamine (alpha blocker) is best initial therapy
  2. CCBs and B-blockers are used afterwards
  3. Pheochromocytoma is removed surgically or by laparscopy
180
Q

Spironolactone: side effects

A
  • causes gynecomastia and decreased libido b/c it is antiadrenogenic

First AId 2CK (22 decks)

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