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NPB 130 M2 > ACTH in the adrenal gland and Effects of Glucocorticoids > Flashcards

ACTH in the adrenal gland and Effects of Glucocorticoids Flashcards

1
Q

ACTH originates from…?

A

Larger precursor molecule
- make large proteins and are cut at different spots to make different active proteins

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2
Q

What does POMC stand for?

A

Proopiomelanocortin

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3
Q

POMC is produced in …?

A

Corticotropes
Intermediary lobe
Arc
Keratinocytes

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4
Q

What are the three (tissue-specific) molecules that are the result of the cleavage during the post translational processing

A

ACTH
alpha MSH
BMSH
B-Endorphin

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5
Q

Cleaving both alpha MSH and CLIP give you ??

A

ACTH

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6
Q

when are precursor molecule cleaved??

A

post-translational processing

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7
Q

activated PKA is start 4 short term effects …

A
  1. LDLR
  2. CHO Esterase
  3. StAR
  4. P450scc
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8
Q

post translation processing is tissue-specific and result in …??

A

molecules with different biological activity
(ACTH, MSH, and B-endorphin

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9
Q

Increase of LDLR , result of activated PKA

A

helps LDLR go to the membrane to being LDL into the cell (bad cholesterol)

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10
Q

CHO Esterase

A

Breaks Cholesterol (LDL)

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11
Q

StAR

A

picks up free Cholesterol and takes it into the mitochondria (but must be phosphorated before doing so)

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12
Q

P450scc

A

breaks side chain of Cholesterol to make pregnenolone
occurs in the mitochondria
start of steroidogenesis

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13
Q

What is a long term effect of activated PKA in the nucleus

A

increase gene expression
+ making the proteins in the short term effects

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14
Q

Congenital Adrenal Hyperplasia (CAH)

A
  • effect in cortisol synthesis
  • lack of negative feedback
  • 90-95% caused by mutation of P450c21
  • Results: adrenal hyperplasia & excess production of adrenal androgen
  • Problem&raquo_space; female fetuses = masculinization (androgenization)
  • Mild to sever&raquo_space; complete absence of cortisol and aldosterone
  • deficiency of mineralocorticoid
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15
Q

Corticosteroids

A

Steroid hormones (Glucocorticoids, mineralocorticoid, adrenal androgens)

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16
Q

Corticosterone

A

intermediary molecule in aldosterone synthesis pathway
- main glucocorticoid in birds, reptiles, amphibians

17
Q

Cortisone

A

Cortisol synthetic

18
Q

Dexamethasone

A

Potent synthetic corticosteroid

19
Q

Name 4 Effects of Cortisol to increase blood glucose

A
  1. inhibits glucose uptake by peripheral tissues
  2. Myostatin&raquo_space; break down proteins from the muscle to obtain Amino Acids
  3. Adipose tissues stimulates Hormone Sensitive Lipase (HSL)&raquo_space; breaks down triglycerides to FA and glycerol
  4. Liver stimulates PEPCK and Glucose 6-Phosphatase (to do into gluconeogenesis)
20
Q

Name two enzymes used in gluconeogenesis

A

PEPCK
Glucose 6- Phosphatase
(G-6-P)

21
Q

In order for the Liver to reach glucose homeostasis it need to (3 specific things)

A
  1. Stimulate gluconeogenesis (PEPCK & G-6-P)
  2. increase glycogen deposit (make an easier way to get glucose)
  3. Decrease glycogen mobilization (not breaking down glycogen)
22
Q

In order for the adipose tissue to reach glucose homeostasis it need to (2 things)

A
  1. Activate HSL
  2. inhibition of glucose uptake
23
Q

In order for the Muscle to reach glucose homeostasis it need to (3 things)

A
  1. decrease synthesis of muscle fibers
  2. simulate myostatin
  3. inhibition of glucose uptake
24
Q

Cortisol affects

A

every body system
has a widespread negative consequence

25
Q

Negative affects from cortisol

A
  • Endocrine system&raquo_space; decrease (LH, FSH, TSH, GH)
  • Immune system (anti-inflammatory action, immunosuppression)
  • Brain/CNS (depression, psychosis, negative cognition, less activity at CNS)
26
Q

Why would it be better to use a nonsteroidal anti inflammatory drug instead of a steroidal one?

A

Steroidal dug (cortisol) will block the entire inflammatory pathway

27
Q

If you take a steroidal anti inflammatory drug what effects will it have??

A

You won’t have any signs of inflammation
NO….
- redness
- warmth
- Swelling
- pain
- loss of function

28
Q

Regulation of immune system by glucocorticoids (cortisol) in INNATE IMMUNITY

A

Decreases …
(cell- mediate innate immune response)
- vascular permeability
- mast cell numbers
- APC numbers
(pro-inflammatory molecules)
- PG (prostaglandins) synthesis
- Cytokine Production

29
Q

Regulation of immune system by glucocorticoids (cortisol) in ACQUIRED IMMUNITY

A

Decreases&raquo_space;
- T and B lymphocytes in circulation
- Synthesis of immunoglobulins

Increases
- Lymphocyte apoptosis

30
Q

An excessive amount of cortisol (effects on acquired immunity)

A

results to autoimmune diseases
- antibodies against own B cells
- Diabetes Mellitus Type 1

31
Q

Cortisol Consequences of dysregulation of immune response

A

Exaggerated allergies
Autoimmune disease
- rheumatoid arthritis
- Type 1 Diabetes

32
Q

Clinical use of Glucocorticoids
- dexamethasone
- triamcinolone
-prednisolone

A

Tropical, anti-itch medication
Autoimmune disease
chronic inflammatory diseases
Inhibition of the immune system after tissue transplant
Anaphylactic shock

33
Q

Primary

A

when the original problem is at the endocrine gland (producing the hormone

34
Q

Central or secondary

A

when the original problem is at higher centers (Brain or pituitary)

35
Q

Hyperadrenocortism
AKA Cushing Disease

A

Increase cortisol or glucocorticoids

  • ACTH- independent (most commonly iatrogenic)
  • ACTH- dependent ( pituitaryprimary & non pituitary tumors secreting CRH/ACTH&raquo_space; Cushing disease
36
Q

Excess circulating Cortisol
(hyperadrenocortism) signs

A
  • skin thinning and alopecia (inhibition of collogen & hair growth)
  • centripetal obesity (effects regulation of triglyceride synthesis and adipose tissue in abdomen)
  • Dehydration (inhibition of H2O absorption)
  • Osteoporosis (effects CA 2+ deposition in bone)
  • Muscle weakness ( proteolytic effect to release AA)
37
Q

Cushing’s Disease

A

Pituitary Tumors increasing ACTH-dependent
Ectopic ACTH expression by nonpituitary tumor cells
Bilateral hyperplasia of Zona Fasciculata and Zona Reticularis
ACTH-independent causes include adrenal tumors

38
Q

Addison’s disease
( Hypoadrenocorticism)

A
  • cortisol deficiency
  • expect high levels of ACTH
  • primary hypoadrenocorticism&raquo_space; low levels of adrenal cortex hormone
  • associated with mineralocorticoid deficiency
  • Causes&raquo_space; autoimmune, infectious, congenital, iatrogenic & hyperpigmentation

NPB 130 M2 (4 decks)

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