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BMS200 > week 3, lecture 3 > Flashcards

week 3, lecture 3 Flashcards

1
Q

when thinking of HPA axis and endocrine pathologies how can the dysfunctions be divided into 3 categories

A

primary, secondary and tertiary

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2
Q

primary dyfunction

A

in the “final” endocrine organ i.e. adrenal glands

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3
Q

secondary dysfunction

A

in the pituitary gland

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4
Q

tertiary dysfunction

A

in the hypothalamus

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5
Q

what is hyper function in the adrenal glands?

A

▪ secondary causes are quite common
▪ Can involve increased levels of cortisol or aldosterone

  • Disorders that are associated with elevated levels of androgens usually also involve decreased levels of glucocorticoids and/or mineralocorticoids
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6
Q

diseases of hyper function in the adrenal glands

A

▪ Cushing’s syndrome (Hypercortisolism)
▪ Hyperaldosteronism
▪ Pheochromocytoma

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7
Q

diseases of hypofunction in the adrenal glands

A

▪ Adrenocortical
insufficiency
▪Congenital adrenal hyperplasia

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8
Q

what is Cushing syndrome an excess of?

A
  • Disorder caused by any condition that produces an elevation in glucocorticoid levels (cortisol)
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9
Q

4 common sources of excess cortisol in Cushing syndrome

A

▪ Iatrogenic (i.ed drugs/meds/ exogenous)

▪ hypothalamic-pituitary diseases associated with hypersecretion of ACTH

▪ Hypersecretion of cortisol by an adrenal adenoma, carcinoma or nodular hyperplasia

▪ Secretion of ectopic ACTH by a nonendocrine neoplasm – aka paraneoplastic syndrome

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10
Q

is hyper secretion of ACTH mostly endogenous or exogenous? men or women effected more?

A

mostly women

exogenous from drugs

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11
Q

what is the main cause of hyper secretion of ACTH in Cushing disease

A

pituitary gland contains an ACTH- producing microadenoma

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12
Q

ectopic ACTH production - paraneoplastic syndrome (could be a cause of Cushings)

A
  • Paraneoplastic syndrome

▪Main tumours are small cell lung cancer and a
renal adenocarcinoma
▪Represent about 10% of cases of endogenous Cushing syndromes
▪Usually involve rapid increases in the levels of ACTH and evolution of symptoms/signs

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13
Q

primary Cushing syndrome (ACTH independent cushings)

A

▪10 to 20 % of cases of endogenous hypercorticolism are due to an adenoma in the adrenal glands themselves

  • Adenomas are usually well-differentiated, more common in women, and functional (i.e. secrete cortisol)
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14
Q

adrenocortical carcinom

A

-uncommon cause
-rare and aggressive tumor
* Typically large mass with excess production glucocorticoids & androgens

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15
Q

Iatrogenic Cushing Syndrome

A

Exogenous administration of glucocorticoids (such as hydrocortisone, prednisone, methyl-prednisolone or dexamethasone) prescribed by a health care practitioner to treat other diseases

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16
Q

what is the most common cause of Cushing syndrome

A

Iatrogenic Cushing Syndrome (exogenous drugs)

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17
Q

what form of exogenous glucocorticoids must be given To develop Iatrogenic Cushing Syndrome

A

Needs to be systemically administered to cause Cushing syndrome – topical or inhaled will not cause significant increases in serum glucocorticoids

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18
Q

Cushing ACTH dependent vs independent diagram

A

slide 12

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19
Q

CUSHING mnemonic

A

– C - Central obesity, Cervical fat pads,
Collagen fibre weakness, Comedones (acne)
– U - Urinary free cortisol and glucose increase
– S - Striae, Suppressed immunity
– H - Hypercortisolism, Hypertension,
Hyperglycemia, Hirsutism
– I - Iatrogenic (Increased administration of corticosteroids)
– N - Noniatrogenic (Neoplasms)
– G - Glucose intolerance, impaired Growth

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20
Q

other clinical features of cushings

A

-psychiatric (anxiety, depression, paranoia, depressive psychosis)
-infection
-irregular menses
-long term hypercortisolism can cause osteoporosis and subsequent fractures

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21
Q

endogenous vs exogenous (iatrogenic) Cushing time course

A

endogenous- slow –> start with hypertension and weight gain
(exception: paraneoplastric can be rapid)

iatrogenic is rapid

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22
Q

labs for cushing

A

24 hour free urine cortisol and low dexamethasone suppression test

▪ Often cortisol is measured as 24-hour free urine cortisol and/or serum cortisol within a low dexamethasome suppression test
* Since cortisol secretion varies so much over the course of a day, doing a 24-hour urine collection gives you a rough idea of the “average” secretion
▪ Salivary cortisol is also used sometimes as well * But there is wide diurnal variation

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23
Q

dexamethasone suppression test - low dose

A
  • A small dose of dexamethasone is given the night before & endogenous glucocorticoid levels are assessed the next morning
    ▪ In a healthy patient we would expect dexamethasome to inhibit the anterior pituitary gland and supress endogenous glucocorticoids.
    ▪ No suppression is indicative of Cushing syndrome
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24
Q

if healthy, what are the results of dexamethasone test

A

inhibit the anterior pituitary gland and supress endogenous glucocorticoids.

no suppression=cushing

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25
Q

high dose dexamethasone suppression test is used for what

A
  • Used to differentiate Cushing’s disease from other causes of Cushing’s syndrome
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26
Q

high dose dexamethasone suppression test

suppression means what disease and no suppression means what disease

A

▪ Suppression of endogenous glucocorticoids => Cushing’s disease
▪ No suppression => ectopic ACTH-dependent

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27
Q

CHART ON SLIDE 18

A

differente for Cushing labs

28
Q

can adrenocortical insufficiency be primary, secondary or tertiary

and what does that mean

A

primary (adrenals) or secondary (pituitary-ACTH)

  • Caused by primary adrenal disease or decreased stimulation of the adrenals due to a deficiency of ACTH
29
Q

acute or chronic adrenocortical insufficiency

A

▪Those with chronic adrenal insufficiency may show signs similar to acute insufficiency if their need for steroids (stress, infection) suddenly increases
▪Acute can be iatrogenic – people being weaned off of high doses of glucocorticoids too quickly

30
Q

what are the 3 patterns of primary and secondary adrenal insuffieicieny

A

–Primary acute adrenocortical insufficiency (Adrenal crisis)
–Primary chronic adrenal insufficiency (Addison Disease)
–Secondary adrenocortical insufficiency

31
Q

what is Addison disease AKA

A

primary chronic adrenal insufficiency

32
Q

etiologies (causes) of primary acute adrenocortical insufficiency

A

-stress that precipitates chronic adrenocortical insufficiency
-exogenous corticosteroids
- adrenal hemorrhage

▪ In patients with chronic adrenocortical insufficiency precipitated by any form of stress that requires an increased in steroid output from glands incapable of responding

▪ In patients on exogenous corticosteroids
* Rapid withdrawal of steroids or failure to increase steroid doses in response to acute stress may precipitate an adrenal crisis
* = inability of atrophic adrenals to produce glucocorticoid hormones

▪Adrenal hemorrhage
▪ Newborns after a prolonged & difficult delivery
▪ Anticoagulant therapy
▪ Post-surgical disseminated intravascular coagulation (aka DIC)
▪ Waterhouse-Friderichsen syndrome (rare)

33
Q

clinical features of acute adrenal insufficiency

A

▪ Hemodynamic instability (inability to maintain bloodpressure, shock, severe postural
hypotension)
▪ Abdominal pain, nausea, vomiting, fever ▪ Hypoglycemia and hyponatremia
▪ Decreased level of consciousness, stupor

  • Often exacerbated by concomitant illness and physiologic stress (shock, infection, surgery, trauma)
    ▪ Can occur on a background of slowly progressive chronic insufficiency
34
Q

Addison disease: Chronic primary Adrenal Insufficiency

A

▪ Uncommon disorder resulting from progressive destruction of
adrenal cortex
▪ Clinical manifestations do not appear until 90% of adrenal cortex compromised

35
Q

what are the 4 main disorders that cause Addison disease/ Chronic primary Adrenal Insufficiency

A

▪ Autoimmune destruction of the adrenal cortex (60-70% in
developed countries)
▪ TB (less common now, but most common cause worldwide)
▪ AIDS
▪ Sarcoidosis or malignancy
(usually lung or breast metastases)

36
Q

autoimmune causes of Addison disease

A

-autoimune polyendocrine syndrome (APS) type 1
-APS type 2
-idiopathic

37
Q

APS 1 vs APS 2 (Addisons autoimmune)

A

APS1- autosomal recessive

APS2- more common, no skin or dental findings

38
Q

clinical features of Addisons disease

A
  • Begins insidiously- at least 90% of cortex of both glands destroyed
  • Initial manifestations: progressive weakness and easy fatigability
  • GI disturbances: anorexia, nausea, vomiting, weight loss, diarrhea
  • Hyperpigmentation
  • Loss of sodium: Hypotension, hyperkalemia, hyponatremia, volume depletion
  • Stress (infection, trauma, or surgery) can cause an acute adrenal crisis
  • Death can occur rapidly unless corticosteroid therapy begins immediately
39
Q

what is a secondary adrenocortical insuffcieicny? possible causes?

A
  • Any disorder of hypothalamus and pituitary that reduces the output of ACTH → syndrome of hypoadrenalism

▪ Possible etiologies include: metastatic cancer, infection, infarction, irradiation

40
Q

how does secondary adrenocortical insuffieicny differ from primary Addisons? what steroid hormones are deficient and what is normal?

A
  • With secondary disease, hyperpigmentation of primary Addison is absent
  • Deficient cortisol and androgen output but normal aldosterone levels (therefore no hyperkalemia, hyponatremia)
41
Q

what labs if suspect ACTH deficiency?

A

▪ Insulin tolerance test: after insulin administration cortisol &
ACTH secretion should increase
▪ CRH administration should also show increased cortisol and ACTH plasma levels

42
Q

labs for adrenal insufficiency

A

▪ Often ACTH & cortisol is measured (as 24-hour free urine
cortisol and/or serum morning cortisol)

43
Q

how to distinguish between primary and secondary adrenal insufficiency in labs?

A

ACTH stimulation test can be done
▪ Exogenous ACTH (cosyntropin) is given

44
Q

CHART ON SLIDE 28

A
45
Q

primary hyperaldosteronism –> what does chronic excess secretion of aldosterone cause (hint: Na+ and K+)

A
  • Causes sodium retention and potassium excretion
  • Resulting in hypertension and hypokalemia
46
Q

how does hyperaldosteronism after the renin-angiotensin system?

A

autonomous overproduction of aldosterone, with resultant suppression of the renin-angiotensin system and decreased plasma renin activity

47
Q

causes of primary hyperaldosteronism

A

▪Adrenocortical neoplasm: usually a solitary aldosterone secreting adenoma
*–> Conn Syndrome

▪Bilateral hyperplasia of adrenals

48
Q

secondary hyperaldosteronism- why is the excess aldosterone released?

A
  • Aldosterone release in response to activation of the renin-angiotensin system
  • Characterized by increased levels of plasma renin
49
Q

what conditions can cause secondary hyperaldosteronism?

A

–Decreased renal perfusion
–Arterial hypovolemia and edema: CHF, cirrhosis, nephrotic syndrome
–Pregnancy: due to estrogen induced increases in plasma renin substrate

50
Q

2 main symptoms of hyperaldosteronism

A

hypertension and hypokalemia

  • Hypertension:
    ▪ sodium retention increases total body sodium and expands
    the extracellular fluid * Hypokalemia:
    ▪ due to renal potassium wasting and can cause variety of neuromuscular manifestations
51
Q

what labs to do for hyperaldosteronism?

A

▪ Serum aldosterone & renin can be measured for an
aldosterone: renin ratio (ARR)

52
Q

congenital adrenal hyperplasia

A
  • Autosomal recessive defect in enzyme in cortisol synthesis pathways (to make cortisol and aldosterone)
53
Q

what is the most common deficiency enzyme in congenital adrenal hyperplasia ? what step cannot be done?

A

21-Hydroxylase

progesterone cannot be converted into cortisol (or way less)

54
Q

what are the types of congenital adrenal hyperplasia

A

classic (affects newborns)
non-classic (later onset)

▪Classic: affects newborns
* Salt-wasting:
▪complete inactivation of 21-hydroxylase
* Simple virilizing:
▪significantly reduced
function of 21-hydroxylase

▪ Non-classic
* Milder & later onset (late childhood/early adulthood)
* Partial deficiency in 21- hydroxylase

55
Q

classic forms of congenital adrenal hyperplasia: salt wasting vs simple virilizing

A

salt wasting= complete inactivation of 21-hydrolase enzyme
simple virilizing= reduced enzyme activity

  • Salt-wasting
    ▪ No synthesis of aldosterone causes hyponatremia, hyperkalemia, dehydration, hypotension, & increased renin secretion
  • Can be fatal if not treated
    ▪ Virilization of female infants
  • Simple virilizing
    ▪ Female infants often have ambiguous genitalia at birth
    ▪ Male infants show no abnormalities of sexual organs at birth
    ▪ Adult women typically experience infertility
  • Adult men can be fertile or experience azoospermia
56
Q

what happens to female babies with congenital adrenal hyperplasia?

A

females show male characteristics (virilization or ambiguous genitalia)

because too much aldosterone, but how because progesterone is not being converted into aldosterone or cortisol??e???

57
Q

non classic/late onset congenital adrenal hyperplasia

A

▪ No abnormalities at birth, symptoms typically present at puberty
▪ In women, late-onset CAH can often mimics poly cystic ovary syndrome (PCOS)
* Hirsutism, acne, menstrual irregularities, infertility ▪ Men are often asymptomatic

58
Q

what is the most common form of congenital adrenal hyperplasia?

A

late onset/non- classic

59
Q

what labs to run for congenital adrenal hyperplasia

A

17 hydroxyprogesterone (17-OHP) levels

60
Q

what cells do pheochromocytoma effect?

A

Rare tumour of chromaffin cells
▪ Most of the time secretes elevated quantities of catecholamines (NE and E)

61
Q

where are the tumors in pheochromocytoma?

A

▪ Most of the time tumours arises in the adrenal medulla (which is where chromaffin cells are)
▪ In about 10% of cases they can be malignant and will invade

62
Q

what is the main feature of pheochromocytoma?

A

hypertension

-paroxysmal hypertension
* enormous acute increases in blood pressure, often precipitated
by stress or even posture changes
* Large changes in blood pressure can result in cerebrovascular accidents, heart failure, and eventual hypertrophy of the heart

-surgical excision to treat

63
Q

which conditions have increased levels of cortisol

A

▪ Cushing disease, Cushing syndrome
▪ Stress (physiologic or psychologic)
▪ Hyperthyroidism (increased cortisol to meet needs of metabolism)

64
Q

which conditions have decreased levels of cortisol

A

▪ Congenital adrenal hyperplasia
▪ Addison disease
▪ Hypopituitarism, hypothyroidism

65
Q

what does dexamethasone work on

A

inhibits ACTH at anterior pituitary

66
Q
A

BMS200 (19 decks)

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