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(C) CM 1A: Heme/Onc/Endo > Lecture 14: Adrenal Disorders Part 1 > Flashcards

Lecture 14: Adrenal Disorders Part 1 Flashcards

1
Q

Where are adrenal glands located?

A

Atop the kidneys

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2
Q

What makes up the adrenal cortex layers?

A

Zona Glomerulosa
Zona Fasciculata
Zona Reticulairs

Superficial to deep: GFR

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3
Q

What are the 3 layers of the adrenal gland?

A

Capsule
Cortex
Medulla

Superficial to deep

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4
Q

What is made in the Zona Glomerulosa?

A

Mineralcorticoids (Aldosterone)

Go Find Rex, Make Good Sex

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5
Q

What are the 4 functions of aldosterone?

A
  • Sodium Retention
  • Water Retention
  • Potassium Excretion
  • Increases BP and blood volume
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6
Q

What happens to renin in aldosterone deficiency and excess?

A

Aldosterone def: Increased renin
Aldosterone excess: Decreased renin

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7
Q

What is secreted in the Zona Fasciculata?

A

Glucocorticoids (Cortisol)

Go Find Rex, Make Good Sex

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8
Q

What are the 3 functions of cortisol?

A
  • Gluconeogenesis in the liver
  • Immune system suppression
  • Inflammation suppression
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9
Q

When is our serum cortisol highest and lowest?

A

Highest in the morning.
Lowest at night.

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10
Q

What overall mechanism controls cortisol release?

A

HPA Axis

Hypothalamus-Pituitary-Adrenal

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11
Q

What kind of feedback is cortisol controlled by?

A

Negative feedback

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12
Q

What does the Zona Reticularis secrete?

A

Gonadocorticoids (DHEA)

RGD

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13
Q

What does DHEA do?

A

Controls/stimulates the development of sexual characteristics.

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14
Q

What does the adrenal medulla secrete?

A

EPI
NE

MEN

Chromaffin cells make up the adrenal medulla

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15
Q

What would cause a chronic increase in ACTH and CRH levels?

A

Adrenal gland destruction.

Lack of cortisol = lack of negative feedback to the hypothalamus

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16
Q

What does ACTH stimulate adrenals to do? What does it need?

A

Stimulates steroid synthesis.

It requires cholesterol to synthesize steroid hormones.

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17
Q

What is the precursor to all steroid hormones besides cholesterol?

A

Pregnenolone.

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18
Q

What does a 21A-2 deficiency result in?

A

Cortisol deficiency
Aldosterone deficiency
Androgen excess

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19
Q

What is unique about primary adrenal insufficiency vs the other 2 types?

A

It includes aldosterone insufficiency as well.

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20
Q

What is the MCC of addison’s disease and what specific CYP deficiency is it?

A

Autoimmune (80%)

CYP21A2 (21-hydroxylase) MC autoantigen

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21
Q

What does a CYP11A1 deficiency result in? CYP17A1?

A

11A1: Excess Cholesterol, deficient in everything else.
17A1: Excess Aldosterone, deficient in everything else.

11A1 is #1, because cholesterol is the precusor steroid.

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22
Q

When does addison’s typically present? Why?

A

10-40 y/o, because adrenal function decreases over time into insufficiency.

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23
Q

What is adrenoleukodystrophy?

A

Genetic disorder, resulting in accumulation of very long FA chains in adrenal cortex, inhibiting ACTH effects.

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24
Q

What is congenital adrenal insufficiency/hyperplasia?

A

Genetic mutation or absence of adrenal cortex.

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25
Q

Although rare to cause addison’s, what is the MC infection that can cause it?

A

TB

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26
Q

What are the 4 etiologies that result in chronic addison’s?

A
  • Autoimmune (80%)
  • Adrenoleukodystrophy
  • Congenital adrenal insufficiency/hyperplasia
  • Infection
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27
Q

In what 4 ways can drugs induce chronic addison’s?

A
  • Inhibiting cortisol synthesis
  • Accelerate metabolism of cortisol
  • Adrenocorticolytic drug that inhibit cortisol synthesis
  • Suppressing CRH or ACTH release
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28
Q

What drug is used to treat adrenocortical carcinoma and can result in addison’s?

A

Mitotane

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29
Q

Why does using glucocorticoids suppress CRH and ACTH?

A

Our body thinks we are making cortisol, so it sends negative feedback to the hypothalamus and pituitary.

This is why we should taper steroid use down if > 10d.

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30
Q

What are the two etiologies of acute addison’s?

A
  • Adrenal hemorrhage
  • Adrenal addisonian crisis
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31
Q

What causes adrenal hemorrhage?

A
  • Sepsis
  • HIT
  • Anticoag
  • APS
  • Trauma
  • Surgery
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32
Q

What is the pathophysiology behind an addisonian crisis?

A

Insufficient cortisol.

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33
Q

How would an addisonian crisis present?

A
  • Profound fatigue
  • Dehydration
  • Vascular collapse (decreased BP)
  • Renal shut down
  • Hyponatremia
  • Hyperkalemia

Results of aldosterone and cortisol deficiency.

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34
Q

How does someone with addison’s generally present?

A
  • Bronze pigmentation of skin
  • Hypogylcemia
  • Postural hypotension
  • Weight loss
  • Weakness
  • GI disturbances
  • Changes in distribution of body hair
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35
Q

Why is hyperpigmentation common in addison’s?

A

ACTH has affinity for melanin. If the adrenal gland is not functioning, the ACTH binds to melaninotic receptors instead.

It is often the first and only symptom!

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36
Q

Why does vitiligo/hypopigmentation occur in addison’s?

A

Autoimmune destruction of dermal melanocytes

Not related to ACTH affinity for melaninotic receptors.

10% of pts

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37
Q

What are the the typical first symptoms of chronic addison’s?

A
  • Anorexia
  • Weight loss
  • Fatigue
  • Decreased stamina
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38
Q

Why do people with addison’s present with lymph tissue hyperplasia?

A

Increased immune system responses since lack of modulation.

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39
Q

Deficiency in which CYP would cause excess pubic/axillary hair growth in women?

A

21A2, excess testosterone

40
Q

Why do people in addison’s commonly complain of generalized pain?

A

Inflammation everywhere, since cortisol normally modulates it.

41
Q

How would someone with addison’s present in terms of psychiatric symptoms?

A
  • Anxious
  • Irritable
  • Depressed
42
Q

Which CYP deficiency results in amenorrhea in addison’s?

A

21A2 (excess androgens)

43
Q

What generally differentiates adrenal crisis from adrenal hemorrhage?

A

Crisis involves a severe febrile state of > 105F.

44
Q

What is a common DDx for adrenal crisis?

A

Abdominal complaints like appendicitis.

Adrenal crisis presents with acute abdominal symptoms, like pain, N/V.

45
Q

What are the two reasons people with adrenal crisis get hypotensive?

A
  • Lack of aldosterone
  • Vomiting
46
Q

What would I expect in a CBC and CMP for addison’s?

A

CBC: eosinophilia, lymphocytosis

CMP: hypoN, hyperK, elevated BUN/Cr, low BG.

HyperK can be masked by vomiting.

47
Q

What is the overall concern with treating an addisonian crisis?

A

Finding the underlying cause. Order cultures.

48
Q

What lab values of plasma cortisol and ACTH would suggest addison’s?

A

Low cortisol + high ACTH.

8am Cortisol < 3mcg + elevated ACTH is usually diagnostic.

49
Q

When does a random cortisol rule out addison’s?

A

> 25 mcg/dL

50
Q

How do I perform a rapid ACTH stimulation test? What finding confirms addison’s?

A

Step 1: Measure serum cortisol

Step 2: Administer synthetic ACTH 0.25mg IM

Step 3: Measure serum cortisol 45 mins post IM.

Positive Finding: Rise in serum cortisol < 20 mcg.

Only used when serum cortisol and ACTH are non-diagnostic.

51
Q

Use of what drug would give false readings on a rapid ACTH stimulation test?

A

Any exogenous steroid use.

If on dexamethsasone, must be switched to hydrocortisone prior to test.

52
Q

When do we order a plasma renin test? What kind of findings do I expect in addison’s?

A

Monitor treatment.

Plasma renin is typically increased in addison’s, which indicates the need for mineralcorticoid replacement.

Non-diagnostic test.

53
Q

What kind of CT abdomen finding suggests autoimmune addison’s?

A

Small without calcifications on adrenal gland.

54
Q

When is a CXR ordered to evaluate addison’s?

A

Suspected TB etiology or pneumonia

55
Q

What is the overall goal in treating addison’s?

A

Baseline therapy using oral glucocorticoids to replace the lack of endogenous cortisol production.

Lifelong treatment

56
Q

How do we dose hydrocortisone for addison’s?

A

15-30mg daily.
2/3 morning, 1/3 night (mimicking natural cortisol levels)

Alternatives: prednisone or methylprednisolone

57
Q

What is glucocorticoid stress therapy? Why do we do it?

A

Increasing steroid dose in anticipation of incoming stress.

Designed to prevent adrenal crisis.

58
Q

When we give glucocorticoid stress therapy, what is the main secondary concern?

A

Infection. Increasing steroid intake means a weakened immune system.

59
Q

In what situations do we add mineralcorticoid therapy to an addison’s patient? What is the DOC?

A

If they are on LOW doses of hydrocortisone, they probably need supplementation.

Fludrocortisone 0.05-0.3mg.

Monitor with PRA. High PRA = need more fludrocortisone.

60
Q

If a patient presents with suspected adrenal crisis with no prior Hx of addison’s, what are the first steps for treating them?

A

Order Serum cortisol + ACTH.
Initiate treatment, do not wait for results.

61
Q

What is the treatment protocol for adrenal crisis?

A

1: Loading dose of IV hydrocortisone
2: Continuousn IV hydrocortisone
3: Switch to oral hydrocortisone (if PO tolerable)
4: Broad spectrum ABX
5: Treat any electrolyte/glucose/volume abnormalities.

62
Q

What electrolyte abnormalities are common in Addison’s?

A

HyperK is likely
HypoN is likely

63
Q

What are we monitoring for in addison’s besides cortisol levels?

A
  • No development of Cushing’s
  • WBC diff and electrolytes returning to normal
  • DEXA scan for osteoporosis
64
Q

What are some patient education/recommendations for addison’s?

A
  • Medical alert bracelet
  • All infections must be treated immediately.
  • Injectable hydrocortisone
65
Q

What is the MCC of Cushing’s Syndrome?

A

Iatrogenic (99%)
Excessive corticosteroids.

66
Q

What is the MCC of Cushing’s Disease?

A

Benign anterior pituitary adenoma

More common in females

67
Q

What is Cushing syndrome also known as etiology-wise?

A

ACTH independent hypercortisolism

68
Q

What is Cushing Disease also known as etiology-wise?

A

ACTH dependent hypercortisolism

Disease for dependent

69
Q

What are the 4 etiologies of ACTH dependent hypercortisolism?

A
  • Pituitary hypersecretion of ACTH
  • Ectopic secretion of ACTH
  • Ectopic secretion of CRH
  • Iatrogenic/factitious Cushing’s syndrome
70
Q

What is often the first & long lasting symptom of Cushing’s?

A
  • Fatigue
  • Reduced physical endurance
71
Q

What are the 4 main locations for fat deposition in Cushing’s?

A
  • Central obesity
  • Moon face
  • Supraclavicular fat pads
  • Buffalo hump (back of the neck)
72
Q

What is a key difference between an obese person and an obese person with Cushing’s?

A

Cushing’s typically have thin extremities.

73
Q

What is the typical clinical presentation symptoms of someone with Cushing’s besides the weight gain?

A
  • Skin atrophy with large, purple striae
  • Easy bruisability
  • Proximal muscle weakness
  • Immune system suppression (frequent infections)
  • Females only: menstrual irregularities

Proximal muscle weakness often presents as difficulty carrying things overhead.
Difficulty sitting up from seated position

74
Q

What are some of the common symptoms associated with increased ACTH?

A
  • Hyperpigmentation
  • Elevated BP
  • Hirsutism, male pattern hair loss
75
Q

What would I expect to see on a CBC and CMP of a Cushing’s pt?

A

CBC: leukocytosis with neutrophilia but lymphocytopenia and decreased eosinophils

CMP: elevated BG, possible hyperN, hypoK

76
Q

What are the 3 diagnostic goals for Cushing’s?

A

Determine if its exogenous/endogenous.
Establishing the presence of hypercortisolism.
Determine the underlying cause.

77
Q

Which Cushing’s type requires a work-up?

A

Endogenous/disease only.

78
Q

How do we establish the presence of hypercortisolism?

A

2 out 3 first line tests must be positive.
* Dexamethasone suppression test
* 24 Urine Free cortisol (2 separate measurements)
* Late night salivary cortisol (2 separate measurements)

79
Q

How do I perform a dexamethasone suppression test? What is a positive finding?

A
  1. Take dexamethasone 1mg PO at 11pm.
  2. Serum cortisol at 8AM.
  3. <5mcg likely rules OUT Cushing’s syndrome
80
Q

What can cause a false-negative or false-positive in a dexamethasone suppression test?

A

False-Neg: 8% of cushing’s disease have normal cortisol suppression, antiseizure drugs, rifampin, and estrogens.

False-Pos: 20-30%, psychiatric disorders, stress

81
Q

How do I perform a 24 Urine Free Cortisol? What is a positive finding?

A
  1. After first morning void, begin collection.
  2. Document time of first morning void.
  3. Collect all urine, including next morning void.

Positive = 3x UNL on BOTH occasions.

82
Q

How do I perform a late night salivary cortisol? What is considered positive?

A
  1. Saturate a swab in your mouth for 90 secs between 11pm and midnight.
  2. Both readings must be > 100ng to be positive.
83
Q

What can interfere with a late night salivary cortisol test?

A
  • Steroid use
  • Brushing teeth
  • Oral intake of anything
  • Inadequate collection
  • Night shift people
  • Pregnancy
  • anticonvulsants
  • stress
84
Q

What do I do if both of my Cushing’s tests are negative? What if only 1 is positive? What if both are positive?

A

2 Negatives = no further workup, but if you are very suspicious still, send to endo.
1 Negative (24UFC or saliva), 1 positive = repeat test at random intervals and consider a cyclic cushing disease. Refer to endo.

2 positive = refer to endo

Always refer to endo :)

85
Q

How do we determine the cause of hypercortisolism?

A

Serum ACTH.

86
Q

How do we order a serum ACTH and interpret it?

A

6-9AM collection in an EDTA tube stored at -20C until assay.

<20 pg = adrenal CT

> 20 pg = Pituitary MRI

Low ACTH + high cortisol suggests adrenal tumor
High ACTH + high cortisol suggests a source making ACTH.

87
Q

What are the red flags for a malignant carcinoma of the adrenal gland?

A
  1. > 4cm
  2. Growth of nodule (if previous CT)
  3. Density > 10 Hounsfield Units
88
Q

What MRI results indicate treatment for a pituitary adenoma? What indicates more testing?

A

Lesion > 5mm = treatment.

Lesion < 5mm = Inferior petrosal sinus sampling. (elevated ACTH = pituitary)

If sampling is negative, CT chest/abd.
If CT neg, order whole body PET.

89
Q

How do we manage Exogenous Cushing’s syndrome?

A

Slowly titrate down exogenous glucocorticoid/ACTH therapy.

Rapid withdrawal can cause adrenal insufficiency

90
Q

What are the two treatment options for adrenal or pituitary adenomas?

A

Surgical removal (requires lifelong glucocorticoid replacement therapy)

Pituitary radiation

91
Q

If my patient is waiting for surgery/has a CI for an adrenal adenoma, what can we do for them?

A

11-beta-hydroxylase inhibitor: blocking cortisol steroidogenesis (metyrapone and osilodrostat)

Ketoconazole: inhibits early steps of steroidogenesis

92
Q

If my patient is waiting for surgery for their pituitary tumor, what drug can they take?

A

Pasireotide: somatostatin analog that inhibits ACTH secretion.

PasieroTide = Pituitary Tumor

93
Q

What are the DOCs for mineralcorticoid hypertension?

A

Spironolactone or eplerenone.

Second: ACEI

94
Q

What is the DOC for hyperandrogenism in women?

A

Flutamide, which inhibits androgen uptake.

Female

95
Q

What are some common cortisol-related complications to monitor?

A
  • Osteoporosis
  • CVD
  • Psychiatric disorders
  • DM
  • HypoK
  • Muscle weakness
  • infections
  • Sleep apnea

(C) CM 1A: Heme/Onc/Endo (28 decks)

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