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Endocrine > Disorders Of Adrenal Glands 1/2 > Flashcards

Disorders Of Adrenal Glands 1/2 Flashcards

1
Q

What are the secretory products from the adrenal medulla?

A

Peptides:
- Somatostatin and substance P

Catecholamines:
- epinephrine and norepinephrine

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2
Q

What are all the functions that adrenal gland hormones play a part in?

A

BP regulation

Salt and water balance

Control blood sugar levels

Energy production

Sex organ development

Stress response

Heart rate

Attention

Inflammation

Fetal development

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3
Q

How do catecholamines axis and CRH-ACTH axis differ?

A

Catecholamines
1) nerve impulses from hypothalamus -> middle horn of the spinal cord and synapse

2) middle horn of the spinal cord -> directly on adrenal medulla and synapse on the ganglion.
- this is the preganglionic sympathetic nerves.

3) postganglionic sympathetic goes directly to adrenal medulla cells and releases catecholamines into blood stream

CRH-ACTH
1) hypothalamus releases CRH in response to circadian rhythms and stressors which moves down the infundibulum the corticotroph cells in the anterior pituitary/ adenohypophysis.

2) cells release ACTH into blood and go to adrenal cortex to bind to cells in the Zona fasiculata. These cells release glucocorticoids (primarily cortisol/sortisone) into blood

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4
Q

Cushing syndrome/adrenal excess/hyperadrenalism/hypercortisolism

A

Excessive levels of adrenocortical hormones (specifically cortisol)

Effects 13 in 1 million
- more common in women and occurs primarily between ages 25-40 (endogenous)

  • more common in males who use high levels of exogenous steroids and then cease (exogenous)
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5
Q

Common symptoms from excess Mineralcorticoids

A

Hypertension

Hypernatremia

Hypokalemia

Expanded blood volume

Edema

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6
Q

Common symptoms from excess cortisol

A

Symptoms:

  • weight gain
  • deposition of adipose tissue in abnormal areas
  • proximal muscle weakness
  • osteoporosis
  • mental disturbances
  • thin skin and bruises with “striae”
  • “moon-facies”
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7
Q

Common symptoms from excess androgens

A

Hirsutism

Atrophy of breasts

Amenorrhea

Masculinization of voice and virilization of body

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8
Q

Why does hyperpigmentation appear in both excess cortisol and deficiency of cortisol

A

Hyperpigmentation is caused by excess ACTH
- this is more common in Addison disease but is possible in cushings since it could be a secondary issue releasing too much ACTH and leads to excess cortisol

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9
Q

When is work up for cushings needed?

A

Specific features to cushings gets worse

Adrenal masses are noted on imaging or physical exam

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10
Q

Diagnosis of cushings

A

Low dose dexamethasone suppression

  • inject dexamethasone 1mg at evening and wait until morning, then pull levels of cortisol
  • if cortisol is low = normal (the dexamethasone will suppress the ACTH)
  • if cortisol is high = cushing syndrome)

Can also use imaging studies (CT or MRI (MRI is better)

Can also measure a 24hr urine free cortisol count
- a level >140 mmol/d it’s suggestive of cushing syndrome

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11
Q

Difference between Cushing syndrome and disease

A

Syndrome = primary (adrenal cortex is the issue)

Disease = secondary (pituitary gland is the issue)

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12
Q

How to tell difference between ACTH secreting pituitary tumor (adenoma) and ectopic ACTH secretion with only labs?

A

1 = dexamethasone suppression high dose

  • if cortisol stays high = ectopic ACTH secretion
  • if cortisol stays low = ACTH pituitary tumor

Can check Serum hypokalemia
- if serum potassium is low it is more likely ectopic (75%) chance vis pituitary

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13
Q

Surgical management for cushing disease and syndrome

A

Cushing disease = transsphenoidal hypophysectomy

Cushing syndrome = adrenalectomy via adrenal adenoma

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14
Q

Prognosis of Cushing

A

Without treatment = 50% mortality at 5 years

- usually CV risks and HTN

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15
Q

Addison disease

A

Deficiencies of cortisol/ glucocorticoids

Most common affects people between ages 30-50
- more common in women than men

Primary = inability of the adrenal cortex to secrete sufficient cortisol
- will show hyperkalemia, high ACTH and eosinophila

Secondary = inability of pituitary to secrete adequate ACTH
- will show normal potassium, low ACTH, and no eosinophila

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16
Q

Etiology of Addison disease

A

Most common overall = autoimmune adrenalitis

  • can also be idiopathic
  • genes associated are HLA-DR3 and CTLA-4

Other casues

  • TB , Funchal, viral infections with AIDS patinets
  • metastatic cancers
  • CAH’s
  • surgical/iatrogenic
  • drug induced
  • Waterhouse-friedrichson syndrome or anti phospholipid syndrome
  • Sheehan syndrome (traumatic blood loss casues infarctions most common = pregnancy)
17
Q

Symptoms of Addison disease

A

Fatigue

Weight loss/anorexia**

Fever

Myalgia

Hyperpigmentation of skin and mucous membranes**

Normochromic anemia/lymphocytosis and eosinophils

Orthostatic hypotension**

Hyponatremia And hypoglycemia**

Hyperkalemia**

Osteoporosis**

Abdominal pain and nausea/vomiting**

18
Q

Adrenal crisis

A

Acute Addison disease

Most commonly caused by steroid withdrawal or intense stress with underlying Addison disease present

Symptoms:

  • profound fatigue
  • dehydration
  • super low hypotension
  • hyperkalemia
  • severe hyponatremia
  • sudden extreme back/leg cramps
  • cyanosis
  • refractory fluid treatment without hydrocortisone therapy ;

looks a lot like sepsis

19
Q

How to diagnosis Addison disease

A

Serum levels of glucose, electrolytes

  • hypoglycemia
  • hyponatremia
  • hyperkalemia

Blood levels of hormones

  • primary = high ACTH and renin. Low aldosterone
  • secondary = low ACTH/renin and normal aldosterone

CBC
- shows eosinophil and Normocytic anemia

Presence of adrenal autoantibodies = autoimmune adrenalitis
- if these aren’t there get a chest xray and CT to look for masses of TB infection

20
Q

Management for adrenal crisis

A

Give IVs and glucose as needed to replace

Also needs to replace steroids with hydrocortisone in order tor place

After stablizing = corticosteroids and Mineralcorticoid replacement therapy for life

21
Q

Congenital adrenal hyperplasia (CAH)

A

A group of 5 different enzyme disorders that result in varying effects

ALWAYS shows cortisol Deficiency

VARIES with Mineralcorticoids and androgen excess of Deficiencies

21a-deficiency is the most common (90%)

Treatments = glucocorticoid replacement
- if salt wasting is present = Mineralcorticoid as well

22
Q

21-hydroxylase deficiency

A

Gene mutation in CYP21A2

Causes glucocorticoids and Mineralcorticoid deficiency. Androgen excess

Diagnostic markers: all in blood and are high

  • 17-hydroxyprogesterone ***
  • 21-deoxtcortisol
  • 17-hydroxyurea a loose

Should suspect in both true/pseudo hermaphroditism

Simple virilizing form = 25%

  • shows ambiguous genitalia and virilization of females and males
  • linear growth is accelerated by plates fuse shut eagerly = short stature

Salt wasting form = 75%

  • presents with adrenal crisis at 1-4 wks old
  • may present with some charactistics of virilization but is less pronounce compared to the simple virilization form
23
Q

11B-hydroxylase deficiency

A

Gene mutation in CYP11B1

Causes glucocorticoid deficiency
Mineralcorticoid and androgen excess

Diagnostic markers: all high in blood

  • 11-deoxycortisol
  • 11-deoxycorticosterone
24
Q

17a-hydroxylase deficiency

A

Gene mutation in CYP17A1

Glucorticoid and androgen deficiency
Mineralcorticoid excess

Diagnostic markers: all high in blood

  • 11-deoxycorticosterone
  • pregnenolone
  • progesterone
25
Q

Hyperaldosteronism

A

Most common cause is bilateral adrenal hyperplasia
- most common = adrenal adenoma (conn-syndrome)

Other causes of primary (shows elevation of aldosterone)

  • over use of glucocorticoid and then acute withdrawal
  • carcinomas
  • CAH (17a and 11b only)
  • cushing syndrome
  • Liddell syndrome (mutant ENaC channels which increases ENaC function)

Other causes of secondary (shows elevation of aldosterone and renin)

  • Bilateral renal stenosis
  • cirrhosis of liver
  • CHF
  • nephrotic syndrome
26
Q

What the easiest way to differentiate primary hyperaldosteronism from secondary hyperaldosteronism

A

Check renin levels

Secondary = high 
Primary = low
27
Q

Symptoms of hyperaldosteronism

A

Often asymptomatic but is most commonly suspected with unexplained HTN/edema, hyperkalemia and hypokalemia***

Labs

  • hypokalemia
  • hypernatremia
  • metabolic alkalosis
28
Q

Treatment of hyperaldosteronism

A

If surgery = laparoscopic adrenalectomy

If medical drug therapy = spironolactone/amiloride or eplernone
- spironolactone is #1

29
Q

Definition of orthostatic hypotension

A

Decrease of 20 systolic and/or 10 diastolic BP after laying/sitting down to standing up quickly

30
Q

What is primary, secondary and tertiary adrenal insufficiency etiology

A

Primary = adrenal gland hypoproduction of cortisol
- injection of ACTH = NO CHANGE cortisol

Secondary = pituitary gland hypoproduction of ACTH
- injection of ACTH = INCREASED cortisol

Tertiary = hypothalamus hypoproduction of CRH
- injection of ACTH = INCREASED cortisol

31
Q

How to differentiate 21b/17a/11b CAH from each other based on symptoms

A

21b-hydroxylase (most common)

  • HYPOTENSION*
  • HYPERKALEMIA*
  • HYPONATREMIA*
  • INCREASED PLASMA RENIN*
  • virilization and hermaphroditism
  • precocious puberty

17a-hydroxylase

  • HYPERTENSION*
  • HYPOKALMEIA*
  • NORMAL OR HYPERNATREMIA*
  • NO VIRULIZATION*
  • NORMAL PLASMA RENIN*
  • NO PRECOCIOUS PUBERTY*

11b-hydroxylase

  • HYPERTENSION*
  • HYPONATREMIA*
  • HYPERKALEMIA*
  • VIRULIZATION*
  • NORMAL PLASMA RENIN*
  • precocious puberty
32
Q

How does 11B cause hypertension

A

11-deoxycortisol even though it is not cortisol it does have weak Mineralcorticoid actions
- therefore excess 11-deoxycortisol acts like excess aldosteronism and leads to HTN, Hypernatremia and hypokalmeia

33
Q

Medications used to treat cushings (excess cortisol levels)

A

Ketoconazole = inhibits glucocorticoid production via 17-20 desmolase inhibition.

Metyrapone = reversibly inhibits 11B-hydroxylase in steroid synthesis pathway

Aminoglutethimide = inhibits p450scc which prevents cholesterol eating -> pregnenolone

34
Q

Review how aldosterone is regulated

A

Via the RAAS axis and ACTH levels

- angiotensin 2 is a potent stimulator of aldosterone synthase enzymes

35
Q

Causes of secondary HTN

A

Renal artery stenosis

  • more commonly seen between 25-50yrs
  • causes are usually atherosclerosis or fibromuscular dysplasia

Pheochromocytoma

  • adrenal medulla tumor that secretes excess catecholamines
  • will present with episodic intensive headaches/sweating and tachycardia

Conn syndrome

  • unilateral adrenal cortex tumor that secretes aldosterone excess
  • will present with HTN, hypokalemia and metabolic alkalosis

Cushing syndrome: excess ACTH that causes excess cortisol

Primary renal disease:
- typically unilateral renal parenchyma disease

36
Q

What is the most common ECG finding in hyperaldosteronism

A

Prominent flattening of U waves
Flattened T waves
ST-segment depression

**this is because of the hypokalmeia

37
Q

Sheehan syndrome

A

Caused by some sort of massive blood loss which leads to ischemia and necrosis of the pituitary gland

this is most common in pregnancy because during pregnancy, other factors promote hyperplasia of both the anterior and posterior pituitary. However during pregnancy, extreme blood loss occurs which causes ischemia due to focal volume loss

Symptoms:

  • inability to breast feed after pregnancy**
  • intense fatigue
  • mental sluggishness
  • tachycardia and orthostatic HTN
  • symptoms related to loss of pituitary hormones

Endocrine (46 decks)

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