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Endocrine > Adrenal Gland Disorders > Flashcards

Adrenal Gland Disorders Flashcards

1
Q

What makes up the adrenal glands?

A

They are composed of two regions: Adrenal Cortex & Adrenal Medulla

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2
Q

What cells make up the cortex?

A

3 Zones:

  1. Zona glomerulosa
  2. Zona fasiculata
  3. Zona reticularis
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3
Q

What cells make mineralocorticoids (aldosterone)?

A

Zona glomerulosa

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4
Q

What cells make glucocorticoids (cortisol)?

A

Zona fasiculata

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5
Q

What cells make androgens: androstenedione, DHEA and DHEA-S?

A

Zona reticularis

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6
Q

What cells make catecholamines (epi and norepi)?

A

Medulla (10-20%)

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7
Q

What is the site of action for aldosterone?

A

Distal nephrons of the kidneys

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8
Q

What is the function of aldosterone?

A
  • reabsorb Na+ and Cl-
  • secrete K+ & H+
  • water homeostasis
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9
Q

Where is renin stored?

A

Renin is produced and stored in the juxtaglomerular cells surrounging the afferent arterioles of glomeruli in the kidneys.

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10
Q

What does aldosterone help retain?

A

Aldosterone enhances renal sodium retention and thus results in expansion of the extracelular fluid volume thus dampening the stimulation for renin release.

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11
Q

Describe the renin angiotensin pathway.

A

Renin acts on angiotensinogen (Alpha 2 globulin produced in the liver) in the kidney and peripherally to form angiotensin 1.

Angiotensin 1 is transformed by ACE (angiotensin converting enzyme-particularly present in the pulmonary vascular endothelium) to angiotensin 2. Angiotensin 2 is a potent pressor agent and exerts it’s action by direct effect on arteriolar smooth muscle.

Angiotensin 2 also stimulated production of aldosterone by the zona glomerulosa (adrenal cortex).

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12
Q

What stimulates renin synthesis?

A

Renin synthesis occurs in the juxtaglomerular cells of the kidney and is released in response to:

  • low sodium
  • low renal blood flow
  • high K
  • increased sympathetic nerve stimulation
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13
Q

What stimulates the release of cortisol and androgens?

A

Release stimulated by ACTH.

The release of ACTH, and thus of cortisol and androgens, occurs episodically throughout the 24 hour cycle in a circadian pattern.

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14
Q

What stimulates the secretion of ACTH?

A
  • stress (trauma, surgery, anxiety, emotional disturbance)

- low circulating levels of cortisol

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15
Q

What inhibits the secretion of ACTH?

A
  • high circulating levels of cortisol

- presence of synthetic glucocorticoids

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16
Q

What are the physiological effects of gluccocorticoids?

A
  • Stimulate gluconeogenesis
  • Induce insulin resistance
  • Increase release of amino acids and fatty acids
  • Elevate RBC and platelet levels
  • Maintain normal vascular response to vasoconstrictors
  • Stimulation of PMN leukocytosis
  • Depletion of circulating eosinophils and lymphocytes.
  • Decrease macrophage adherence to endothelium
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17
Q

What is Hyperaldosteronism (Conn’s Syndrome)?

A

Elevated levels of aldosterone causing HTN and hypokalemia

18
Q

What is the most common etiology of Hyperaldosteronism (Conn’s Syndrome)?

A

Aldosterone producing adenomas (60-70%)

19
Q

How is hyperaldosteronism diagnosed?

A

Screening: Measure 8 AM plasma aldosterone (PA) & plasma renin activity (PRA) levels. Obtain PA/PRA ratio.
Ratio 4-10 = normal
Ratio > 20 = primary aldosteronism

Confirmatory testing: Saline or salt loading test fails to suppress aldosterone. Aldosterone >10 ng/dL leads to a positive diagnosis.

20
Q

What are the types of adrenal insufficiency?

A

Primary (Addison’s disease): originates at the adrenal gland

Secondary: Pituitary problem (ACTH)

21
Q

What is the etiology of Primary Adrenal insufficiency (Addison’s disease)?

A

Autoimmune (most common cause), TB is another cause

Caused by the dysfunction or absence of the adrenal cortices. Characterized by a chronic deficiency of cortisol. ACTH levels are elevated.

22
Q

What are the clinical features of chronic adrenal insufficiency?

A 
Weakness, Weight loss, small heart
Anorexia, nausea 
Abdominal pain, Diarrhea or constipation
Postural hypotension – dizziness, syncope
Salt craving
Skin hyperpigmentation
23
Q

What causes hyperpigmentation?

A

Increase of ACTH

24
Q

Where do we see hyperpigmentation in Primary AI?

A

dorsal surface and palmar creases, elbows and knees

25
Q

What causes Iatrogenic Adrenal Insufficiency?

A

Caused by: chronic exogenous steroid use

Degree of suppression depends on
dosage, schedule, and duration of administration

suppression rarely occurs with dosages of HC (or its equivalent) of <21 days usually do not result in adrenal insufficiency

26
Q

What is adrenal crisis?

A

Acute adrenal insufficiency is an emergency caused by insufficient cortisol. Crisis may occur in the course of treatment of chronic insufficiency, or it may be the presenting manifestation of adrenal insufficiency.

Can occur during stress or in withdrawal of adrenocortical hormone.

27
Q

What are the clinical features of adrenal crisis?

A

Headache, N/V, abdominal pain, and often diarrhea. BP is low. May see sparse axillary hair (if hypogonadism is also present). Hyponatremia, hyperkalemia

No hyper-pigmentation in acute failure

28
Q

How is adrenal crisis treated?

A

Treat with hydrocortisone, glucose and IV saline immediatley, with out waiting for results.

29
Q

How is adrenal insufficiency diagnosed?

A

Cosyntropin stimulation test, Anti adrenal antibodies are present in 50% of patients.

30
Q

How is primary adrenal insufficiency treated?

A

Combination of corticosteroid and mineralcorticoid. Hydrocortisone is the drug of choice with fludrocortisone acetate.

Alert bracelet

31
Q

What is cushings syndrome?

A

The term Cushings refers to the manifestations of excessive corticosteroids commonly dure to supraphysiologic doses of corticosteroid drugs and rarely due to spontaneous production of excessive corticosteroids by the adrenal cortex.

40% due to ACTH hypersecretion by pituitary

32
Q

How is cushings syndrome different from cushings disease?

A

Cushing’s disease: Pituitary source of high ACTH

Cushing’s syndrome: Adrenal source of high cortisol levels

33
Q

What causes cushings syndrome?

A

Ectopic source: ACTH or CRH production by tumors

Exogenous steroids: Most common

34
Q

What are the clinical findings for cushings syndrome?

A 
Central obesity
Muscular weakness,proximal
Moon facies and facial plethora
Buffalo hump, Purple straie
Hirsutism, Acne
Polyuria, nocturia
Hypertension 
DM or Impaired glucose tolerance (IGT)
Osteoporosis
Avascular bone necrosis
35
Q

What is Ectopic ACTH syndrome?

A

Marked wasting and skin pigmentation are present

36
Q

How is cushings diagnosed?

A

Dexamethasone Suppression Test

37
Q

Determining ACTH-dependent vs. ACTH-independent.

A

Check plasma ACTH level. Suppressed (200) then suggests an ectopic source.

38
Q

What is Pheochromocytoma?

A

Chromaffin tumors that usually arise in the adrenal medulla, can be extra-adrenal, along the sympathetic chain in the abdomen, thorax, or neck, and rarely in sympathetic tissue in the walls of the urinary bladder.

39
Q

What are the clinical features of Pheochromocytoma?

A

Headaches occur in 80% of cases

Other common symptoms:
excessive perspiration (70%)
palpitations (64%)
tremors (30%)

Catecholamine excess often causes pallor (due to vasoconstriction) and not flushing (due to vasodilation)

40
Q

How is Pheochromocytoma diagnosed?

A

Urinary measurements of:
free catecholamines
urinary metabolites– metanephrines, and VMA.

Diagnostic yield increased significantly if obtained after or during paroxysm

41
Q

How is Pheochromocytoma treated?

A

Surgical excision of the tumor is curative

Medical treatment:
preoperatively (to decrease perioperative morbidity and mortality) and on a chronic basis in surgical failures
α – adrenergic blockade-cornerstone of medical therapy

Should be instituted as soon as the diagnosis is made

Phenoxybenzamine is the drug of choice

ß-blockade to control tachyarrhythmias
use only after adequate α –blockade

42
Q

How is Cushings treated?

A

Best treated with transsphenoidal selective resection of the pituitary adenoma. Give hydrocortisone/ prednisone until return to normal functioning.

Endocrine (8 decks)

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