Endocrine Lecture 3: Adrenal Gland Flashcards

1
Q

Adrenal Anatomy:

The Cortex of the adrenal gland refers to the ____, the Medulla refers to the ____.

A

Outer “bark” = Cortex

inner region = Medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The Adrenal Medulla is directly connected to the _____ branch of the nervous system via nerves.

A

Sympathetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The Adrenal Medulla releases ______, which are responsible for activation of our fight or flight responses.

A

Catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What cells in the adrenal medulla are responsible for creating catecholamines?

A

Chromaffin cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Catecholamines are derived from what substance?

A

Tyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 4 catecholamines that are produced in the Adrenal Medulla?

A

DOPA [Aromatic L-amino acid decarboxylase (AADC or AAAD), also known as DOPA decarboxylase]

Dopamine
Epinephrine
Norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

_____ is the principal product of the Adrenal Medulla and is ONLY made in the Adrenal Medulla.

A

Epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Of the catecholamines made in the Arenal Medulla, 80% is ______ and 20% is ______ . Only a scant amount of ____ is made in the Adrenal Medulla as well.

A

80%= Epinephrine
20%= Norepinephrine
scant amount = Dopamine

Norepinephrine and Dopamine are primarily made elsewhere in the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Epinephrine and Norepinephrine have strong alpha-1 effects which results in ______?

A

Arterial vasoconstriction most importantly

  • Bronchoconstriction
  • Inhibits insulin secretion
  • Stimulates glycogenolysis (↑blood sugar) and gluconeogenesis
  • Mydriasis-eyes open wide
  • GI relaxation
  • Activation increases intracellular Ca (neurotransmitter release)
  • Smooth muscle contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Epinephrine has stronger beta-1 effects which results in ____ and _____.

A

Increased HR
and
Contractility

Beta-1 (Target for Beta blockers)
-↑HR, ↑Conduction velocity, ↑myocardial contractility (inotropy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Norepinephrine is converted to Epinephrine by what enzyme?

A

Phenylethanolamine N-Methyltransferase (PNMT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PNMT expression is regulated by ________, which accounts for ______’s role in affecting BP.

A

Glucocorticoids (cortisone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

_________ is a tumor either caused by adrenal medullary hyperplasia or extra-adrenal chromatin tissue

A

Pheochromocytoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pheochromocytoma tumors make and release _______ in an unregulated fashion.

A

Catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Symptoms of pheochromocytoma include:

A
paroxysmal HTN
tachycardia
HA
sweating
anxiety
tremor
glucose intolerance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T/F: Most pheochromocytoma (85-90%) are solitary tumors localized to a single adrenal gland (usually the R side)

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

10-15% of Pheochromocytomas are extra-medullary, of these most are found in the _______.

A

Abdomen

18
Q

Diagnosis of Pheochromocytoma is made by testing _____ for the presence of _______.

A

Urinary Vanillymandelic acid (VMA) through a 24 hour urine collection.

Both Epi and Norepi are degraded into VMA

19
Q

The introduction of alpha adrenergic antagonist preoperatively reduces the incidence of _______

A
preoperative blood pressure fluctuations
MI
CHF
Dysrhythmias
CVA
20
Q

Alpha blockers phenoxybenzamine or parson should be started _____ days prior to surgery to normalize BP.

A

10-14 days before surgery

21
Q

Once alpha blockage is established, beta blockage can begin. Why is this?

A

Beta blockage is delayed B/C of the risk of unopposed alpha mediated vasoconstriction.

When arteries do relax, volume expansion is necessary.

22
Q

What medications should be avoided intraoperatively to prevent provocation of pheochromocytomas?

A

Histamine releasing agents
metoclopramide
glucagon

23
Q

When a Pheochromocytoma tumor is removed, ______ can happen.

A

abrupt hypotension
(as catecholamine levels drop and alpha and beta blockade are unopposed), blood resuscitation may be required sometimes pressers are needed.

24
Q

Following removal of pheochromocytoma tumor removal, catecholamine levels return to normal after a few days and about ____% of patients become normotensive within _____ days.

A

75%

10 days

25
Q

T/F: Medullary Hyposecretion= not a serious physiologic problem.

A

TRUE

The SNS compensates for cardiovascular regulation.
Other regulatory hormones compensate for metabolic effects.

26
Q

What are the 3 zones/layers of the adrenal cortex? (from outer to inner)

A

Zona glomerulosa (outer)

Zona Fasciculata (middle)

Zona reticularis (inner)

27
Q

What is produced in each of the zones/layers of the adrenal cortex?

A

Zona glomerulosa (outer)= mineralocorticoid (Aldosterone)

Zona Fasciculata (middle)= glucocorticoid (Cortisol)

Zona reticularis (inner)= Androgens (Androstenedione)

28
Q

The primary mineralocorticoid produced in the zona glomerulosa is ______. What are it’s primary functions?

A

Aldosterone

Aldosterone effects salt and water balance and therefore BP. Aldosterone effects the distal convoluted tubule and collecting ducts of the nephrons. It causes water and sodium retention and excretion of potassium and hydrogen.

If unopposed = HTN, extracellular fluid expansion, hypokalemia, and alkalosis.

Aldosterone is primarily regulated by the renin-angiotensin system and by potassium levels.

29
Q

The primary glucocorticoid produced in the zona fasciculata is _______.

A

Cortisol

  • named glucocorticoid b/c it has effects of glucose metabolism
  • essential for life and regulates a variety of CV, metabolic, immunologic, and homeostatic functions.
  • regulates gluconeogenesis (formation of glucose in the liver as proteins are converted into carbohydrates.)
  • High cortisol levels have anti-inflammatory effects. (useful in autoimmune diseases or allergic reactions)
30
Q

The primary Androgen produced in the zona reticular is _____.

A

Androstenedione

31
Q

All of the steroid hormones produced in the Adrenal Cortex are synthesized from ______.

A

Cholesterol

32
Q

Conn’s syndrome is ______.

A

Hyperaldosteronism- Primary
Caused by aldosterone secreting tumors or hyperplasias.
Dx: low renin from negative feedback. Tx: surgical
s/s: HTN, extracellular fluid expansion, hypokalemia, and alkalosis.

Secondary Hyperaldosteronism

  • Caused by CHF, cirrhosis w/ ascites & nephrosis
  • ECF list to extravascular space
  • total body volume overload and intravascular volume depletion, triggers release of renin by kidneys. exacerbates fluid retention and Na retention.
33
Q

Hypoaldosteronism/Adrenal insufficiency:

A
  • Na lost in urine, K retained

- plasma volume decreases, hypotension & hyperkalemia may lead to circulatory collapse

34
Q

Almost any stress (physical or neurogenic) can use an immediate release of ______ from the anterior pituitary gland followed by greatly increased secretion of cortisol (glucocorticoids)

A

ACTH
Adrenalcorticotropic Hormone

ACTH stimulates cortisol secretion almost entirely.
ACTH release is controlled by corticotropin-releasing hormone (CRH) from the hypothalamus.

High cortisol levels causes negative feedback loop and inhibits ACTH and CRH release

CRH, ACTH, and cortisol are released in relation to circadian rhythms with higher levels in the AM.

35
Q

Cushing Disease:

Cushings syndrome:

A

Cushing disease= ACTH secreting tumor of the pituitary causing high cortisol levels

Cushings syndrome= sequela of symptoms caused by excessive cortisol secretion.

36
Q

Cushing syndrome symtoms:

A

Integument: thin skin, stria, poor healing, bruising, acne

Bone: inhibition of GI Ca absorption, decreased serum Ca, increased PTH, decreased bone formation, osteoporosis

muscle: wasting, weakness, fatiguability

Endocrine: impaired glucose tolerance, amenorrhea, turncal obesity, moon mace, buffalo hump

Renal: salt/water retention, hypokalemia from mineralocorticoid activity and excessive glucocorticoids

CV: HTN

CNS: moody

37
Q

Addison’s Disease/Adrenal insufficiency:

A

Results from failure to produce adrenocortical hormones (mineralocorticoids and glucocorticoids)

  • Primary: adrenal nonfunction= autoimmune
  • Secondary: hypothalamic or pituitary nonfunction (shock/sepsis)
38
Q

Symptoms of Addison’s disease:

A

Lack of glucocorticoids: Hypoglycemia, fatigue, weakness, WT loss, anorexia
hyper pigmentation of skin d/t increased ACTH
severe deterioration to stress

lack of mineralocorticoids: dehydration, polyuria, hypotension, low sodium, hyperkalemia, metabolic acidosis

Risk of cardiovascular collapse (Addisonian Crisis)

39
Q

What is an Addisonian Crisis and how is it treated?

A

Risk of cardiovascular collapse from lack of adrenocorticol hormones (mineralocorticoids and glucocorticoids-cortisol)

Tx: give cortisol

Death in 4 days - 2 weeks if untreated.

40
Q

Etomidate is a induction drug used often times for hemodynamically unstable patients, why is Etomidate contraindicated for patients with adrenal insufficiency/ addison’s disease?

A

Etomidate causes profound suppression of cortisol for at least 24 hours and contribute to deterioration of patient. Can cause profound hypotension.