Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endo Repro Midterm > The Adrenal Gland _PV > Flashcards

The Adrenal Gland _PV Flashcards

1
Q

Describe the organization of the adrenal gland in terms of its functional layers and the principal hormones secreted from them.

LO1

A

Adrenal Cortex

1) Zona Glomerulosa
- mineralcorticoids (aldosterone)
2) Zona fasciculata
- glucocorticoids (cortisol)
- androgens (DHEA)
3) Zona reticularis
- glucorticoids (cortisol)
- androgens (DHEA)

Adrenal Medulla
- Catecholamines ( Epi and NE)

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

What does steroidogenesis start with?

A

cholesterol

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

Describe the pathways that control steroid hormone production?

LO2

A

Cholesterol-> Prenganglone via desmolase-> progesterone -> 11b deoxycorticosterone via 21 hydroxylase and 17a hydroxyprogesterone via 17 hydroxylase -> androgens via 17,20 lyase

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

HPA axis is under what type of control?

  • stimulated by
  • target organs and effects (4)
A

negative feedback

stimulatory factors: stress and circadian rhythm

Target Organs

1) immune system- immune suppression
2) liver- gluconeogenesis
3) muscle- protein catabolism
4) adipose tissue- lipolysis

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

Circadian rhythm of cortisol

A

high in morning

low in late evening

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

Glucocorticoids

  • what type of control?
  • examples
A

negative feedback

  • cortisone
  • prednisone
  • methylprednisone
  • dexamethasone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

21 hydroxylase deficiency

  • describe
  • symptoms

LO2a

A

CYP21A2

  • most common
  • decrease cortisol
  • decrease mineralcorticoid
  • increase sex hormones

Symptoms

  • hypotension
  • decrease aldosterone
  • sodium and volume loss (salt wasting)
  • hyperkalemia
  • elevated renin
  • Female: virilization and sexual ambiguity
  • Male: phenotypically normal, precocious psuedo-puberty, premature epiphyseal plate closure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

11B hydroxylase deficiency

  • describe
  • symptoms

LO2a

A

CYP11B1

  • increased androgens
  • virilization of female fetuses
  • increase 11 deoxycorticosterone

Symptoms

  • HTN
  • hypokalemia
  • suppressed renin secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

17a hydroxylase deficiency

  • describe
  • symptoms

LO2a

A

CYP17A1

  • extremely rare
  • decreased androgens and cortisol
  • excess mineralocorticoids
  • diagnosed at puberty

Symptoms

  • HTN
  • hypokalemia
  • hypogonadism
  • male: undescended testes
  • female: lack of secondary sexual development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Actions of mineralcorticoids

LO3

A

influence sodium and potassium levels

aldosterone

  • kidney fxn
  • secreted in response to low BP or blood volume
  • controlled by RAAS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Actions of Corticosteroids

LO3

A

influence glucose metabolism and immune system

ACTH
- stimulated by stress and mediates glucose metabolism

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

Actions of Androgens

LO3

A
  • influence secondary sex characteristics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cortisol

  • describe
  • target organ
  • action
  • diseases
A

target tissue: body wide

Actions: numerous

  • glucocorticoid response elements (GRE)
  • non-genomic actions( endocannabinoids)

Glucocorticoid excess= Cushing syndrome or disease

Glucocorticoid defiency= Addison disease

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

Effects of cortisol on:

Liver

A

increases gluconeogenesis

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

Effects of cortisol on:

muscle

A

breakdown of muscle protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Effects of cortisol on:

fat

A

promotes lipolysis in extremities

promotes central fat deposition

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

Effects of cortisol on:

cutaneous

A

skin thins

fragile blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Effects of cortisol on:

immune system

A

increase infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Effects of cortisol on:

endocrine

A

insulin resistant

glucose intolerant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Effects of cortisol on:

GI

A

interferes with calcium absorption

- risk of osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the regulation of cortisol secretion
-steps

LO5

A

1) CRF (CRH)
2) release from PVN
3) brinds CRF1 receptor (GPCR)
4) stimulates release of ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the pattern of ACTH and cortisol release.

  • produced where
  • derived from
  • component
  • type of control

LO4

A

produced in anterior pituitary (PEPTIDE HORMONE)

principle hormone that stimulates adrenal glucocorticoids

derived from POMC

contains MSH activity (excess ACTH= hyperpigmentation)

negative feedback

  • glucocorticoid exert negative feedback onto CTH adn ACTH secretion
  • GC inhibit POMC
  • GC inhbit mRNA synthesis of CRH and ACTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Dexamethasone suppression test

-types and describe

A

1) Low dose
- determines whether a problem is present
- overnight
- differentiates pts with Cushing of any cause from patients who do not have Cushing
- no ACTH suppression= Cushing
- normal response= suppression of ACTH and cortisol secretion

2) High Dose
- distinguishes patients with Cushing
- help determine source of the problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cosyntropin (synthetic ACTH) stimulation tests

  • test for what
  • steps
A

for adrenal gland insufficiency

1) adminster ACTH
2) results
- healthy= cortisol should increase from baseline
- adrenal unresponsive and cortisol remains the same= adrenal insuffiency
- adrenal responds dramatically and cortisol increases too= secondary adrenal insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Etiologies of Cushing’s syndrome

A

1) exogenous glucocorticoid excess
- latrogenic
- decrease cortisol but symptoms of excess
2) psuedo cushing syndrome
- major depression
- anxiety
- acute/chronic illness
- alcoholism
3) ACTH dependent
- cushing disease
- ectopic acth- secreting tumors
- CRH secreting tumors
4) ACTH- independent
- adrenal adenoma/carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Primary action of aldosterone

- steps

A

Renal sodium absorption

  1. Aldosterone combines with cytoplasmic receptor
  2. hormone-receptor complex initiates transcription in nucleus
  3. translation and protein synthesis makes new protein channels and pumps
  4. aldosterone-induced proteins modulate existing channels and pump
  5. increase Na reabsorption and K secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Symptoms and signs of Cushing’s syndrome

LO7

A
  • truncal obestity
  • moon face
  • buffalo hump
  • easy bruising
  • HTN
  • edema
  • osteoporosis
  • hirsutism
  • acne
  • virilization
  • diabetes
28
Q

Cushing Syndrome

  • describe
  • clinical lab results

LO7

A

hypercortisolism

hypersecretion of CORTISOL
- adrenal neoplasm

elevated cortisol but LOW ACTH

  • Adrenal problem

Test
- if inject exogenous glucocorticoid (dexamethasome)-> ACTH undetectable and dexamathasone FAILS to suppress cortisol secretion (negative feedback works but hypercortisolism still persist)

29
Q

Cushing Disease

  • descrive
  • clinical lab results

LO7

A

Hypercortisolism

*pituitary problem

hypersecretion of ACTH

  • pituitary gland tumor
  • can be non-pituitary neoplasm (cell carcinoma)

overstimulates adrenal cortex and excess cortisol is secreted

HIGH ACTH HIGH CORTISOL

Test
- if inject exogenous glucocorticoid (dexamethasome)-> ACTH normal or slightly elevated and SUCCESSFULLY suppresses cortisol secretion (abnormal negative feedback)

30
Q

Addison Disease

  • describe
  • clinical lab results

LO7

A

primary adrenal insufficiency
* adrenal problem

chronic, progressive destruction of adrenal gland

HIGH ACTH LOW CORTISOL
- adrenal response is blocked from signal

Test
- if inject synthetic ACTH (cosyntropin)-> no change in plasma cortisol level (bc adrenals can’t respond to ACTH)

31
Q

Secondary Adrenal Insufficiency

  • describe
  • clinical lab results

LO7

A
  • pituitary problem
  • caused by exogenous glucocorticoid administration

ACTH deficiency

LOW ACTH LOW CORTISOL

Test
- if inject synthetic ACTH (cosyntropin)-> increase in plasma cortisol level (bc adrenals are functional)

32
Q

Primary vs Secondary/ Tertiary adrenal insuffiency

A

Primary

  • both cortisol and aldosterone DECREASES
  • RAAS damafed

Secondary/Tertiary

  • cortisol decreases
  • but RAAS STILL exists
33
Q

Causes of Primary adrenal insufficiency

- Symptoms

A

Addison’s disease
- autoimmune disease

Adrenal hemmorhage
- can be caused by anticoagulant

infection

  • tuberculosis
  • meningitidis

Tumor metastases to adrenal gland

Symptoms:

  • hyperpigmentation
  • hypoglycemia
  • weight loss
  • muscle weakness
  • hypotension
  • hyponatremia
  • hyperkalemia
34
Q

Treatment for Adrenal insufficiency

A

cortisol is replaced with corticosteroid

aldosterone in replaced with mineralcorticoid hormone (fludrocortisone)

  • people with secondary adrenal insufficiency normally maintain aldosterone production-> do NOT require mineralcorticoid replacement therapy
35
Q

Primary excess (adrenal)

  • cortisol
  • CRF
  • ACTH
  • hyperpigmentation?
A
  • cortisol: increase
  • CRF: decrease
  • ACTH: decrease
  • hyperpigmentation: No
36
Q

Secondary excess (pituitary )

  • cortisol
  • CRF
  • ACTH
  • hyperpigmentation?
A
  • cortisol: increase
  • CRF: decrease
  • ACTH: increase
  • hyperpigmentation: Yes
37
Q

Primary excess (adrenal)

  • cortisol
  • CRF
  • ACTH
  • hyperpigmentation?
A
  • cortisol: decrease
  • CRF: increase
  • ACTH: increase
  • hyperpigmentation: yes
38
Q

Secondary deficiency (pituitary)

  • cortisol
  • CRF
  • ACTH
  • hyperpigmentation?
A
  • cortisol: decrease
  • CRF: increase
  • ACTH: derease
  • hyperpigmentation: no
39
Q

Exogenous glucocorticoid treatment

  • cortisol
  • CRF
  • ACTH
  • hyperpigmentation?
A
  • cortisol: decrease
  • CRF: derease
  • ACTH: decrease
  • hyperpigmentation: no
40
Q

Aldosterone

  • describe
  • regulator
  • overall results

LO9

A

principal mineralcorticoid controlling Na/K exchange in distal nephrin

Major regulator of K body storage

increases synthesis and activity of :

  • Na channels in APICAL membrane
  • Na/K ATPAse in basolateral membrane in distal tubule

Overall result: increase in Na reabsorption and increase in K excretion

41
Q

Actions of aldosterone in kidney (3)

A
  1. increases Na reabsorption
  2. Increases K+ secretion
  3. Increases H+ secretion
42
Q

Aldosterone pathologies

  • Hyperaldosteronism
  • Hypoaldosteronism

LO10

A

Hyperaldosteronism

  1. Primary
    - excessive release of aldosterone from adrenal cortex
    - exm. Conn’s syndrome: adenoma in adrenal cortex
  2. Secondary
    - excessive renin secretion by juxtaglomerular cells in kidney

Hypoaldosteronism

  • destruction of adrenal cortex
  • defects in aldosterone synthesis
  • inadequate stimulation of aldosterone secretion
43
Q

High-dose dexamethaosone

- two paths

A

1) decrease ACTH-> pituitary tumor
- effect mediated by negative feedback on pituitary
2) no change in ACTH-> ectopic tumor
- no negative feedback effect on ectopic source of ACTH

44
Q

All congenital adrenal enzyme deficiencies are characterized by what?

A

enlargement of both adrenal gland

bc increase ACTH stimulation due to low cortisol

45
Q

Cortisol-cortisone shunt

A

11B HSD2 metabolizes cortisol to cortisone in kidney

protects the MR from cortisol binding

keeps MR available for aldosterone

11B HSD2 is inhibited by glcyrrhizic acid (licorice)

  • cortisol has free access to MR
  • MR is overwhelemed by cortisol, especially in hypercortisomelic conditions (Cushing)
46
Q

Primary Hyperaldosteronism

- describe

A

aka Conn Syndrome

  • hypersecretion of aldosterone
  • adrenal neoplasm
  • adrenal problem
47
Q

Secondary Hyperaldosteronism
- describe

LO10

A

hypersecretion of rennin

excess renin from juxtaglomerular cells of the kidney

KIDNEY problem

48
Q

Primary hypoaldosteronism
- describe

LO10

A

hyposecretion of aldosterone

destruction of adrenal cortex

defects in aldosterone synthesis

ADRENAL problem

49
Q

Secondary hypoaldosteronism
- describe

LO10

A

hyposecretion of renin

deficient renin from juxtaglomerular cells of kidney

inadequate stimulation of aldosterone

KIDNEY problem

50
Q

Primary adrenal failure

-general characteristics

A

deficient cortisol AND aldosteron

51
Q

ACTH deficiency

- general characterisitc

A

cortisol deficiency but NOT change in Aldosterone

52
Q

Adrenal androgen

  • hormone
  • precursor
A

DHEA
precursor to human sex steroids

relies on 3B hsd superfamily to exert androgenic and estrogenic activities

adrenal carcinomas that secrete androgens
- females may feature virilization, hirsutism, clitoromegaly, acne

53
Q

Cathecholamines

  • produced where
  • breakdown
A

produced in adrenal medulla

80% epinephrine
- responder to stress (hypoglycemia/exercise)
-influence energy metabolism and cardiac output
20% noepinephrine

54
Q

Epi and NE pathway

A
  1. SNS release Ach
  2. Ach binds nicotinic receptor
  3. ACH increases synthesis of tyrosine hydroxylase and activity of dopamine
  4. VMAT moves EPi into specialized storage vesicles in chromaffin cells
55
Q

Synthesis of catecholamines

-controlled by

A

under the control of CRH-ACTH-cortisol axis

  1. ACTH stimulate synthesis of DOPA
  2. Cortisol increase PNMT enzyme
  3. release is triggered by CNS control
56
Q

Rate limiting step of NE/E synthesis

A

tyrosine hydroxylase

57
Q

degradation of catecholamines

- describe enzymes

A

1) monoamine oxidase
-oxidizes stuff
- used to treat neuropsychiatric disorders
NE or E=> dihydroxymandelic acid

2) COMT
- methylates
- primary enzymes that inactivates catecholamines released from the adrenal gland

both enzymes located in CNS and peripheral tissue

58
Q

Pheochromocytoma

  • describe
  • symptoms
  • receptors
A

benign, unilateral tumor on chromaffin tissue
-produces excess catecholamines

Symptoms

  • HTN
  • orthostatic hypotension
  • headaches, sweat, palpitation, chest pain
  • anxiety

Catecholamines secreted by pheochromocytoma stimulate both a & B adrenergic receptors

59
Q

Adrenergic receptors

- which one responds better to NE than E? vice versa? same?

A

a receptors and B3 respond better to NE than E

B1 receptors respond equally to NE and E

E is more potent than EN for B2 receptors

60
Q

a1 receptor

  • primary mechanism
  • action
A

ip3/ca/dag

increase vascular SM contraction

61
Q

a2 receptor

  • primary mechanism
  • action
A

decrease camp

inhibit NE and insulin

62
Q

b1 receptor

  • primary mechanism
  • action
A

increase camp

increase CO

63
Q

b2 receptor

  • primary mechanism
  • action
A

increase camp

increase hepatic glucose output

dilation for bronchioles,, uterus, vessels

64
Q

b3 receptor

  • primary mechanism
  • action
A

increase camp

increase hepatic glucose output

increase lipolysis

65
Q

Stress Response and HPA axis

  • short term
  • long term
A 
1) short term
nerve impulse
catecholamines (Epi/NE)
- increase HR, BP
- dilate bronchioles
- BMR increase
- glycogen to glucose
2) long term 
mineralocorticoid and glucocorticoid
- sodium and h2o retentin 
- increase BP, BV
- immune system suppressed
- blood glucose increase

Endo Repro Midterm (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions