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PCL469 > Steriods/Adrenal/Thyroid > Flashcards

Steriods/Adrenal/Thyroid Flashcards

1
Q

What triggers the stress response HPA

A

Circadian rhythm
Stress
Trauma
Infection
Hypoglycemia

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2
Q

Cortisol release pathway

A

Stress-> Hypothalamus: CRH, corticotropin-releasing hormone –> pituitary gland: ACTH, adrenocorticotropic hormone –> Adrenal gland: Cortisol

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3
Q

Mediators of HPA axis, 2 glands

A

Hypothalamus, anterior pituitary

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4
Q

Amino acids, activation of hypothalamic hormone in HPA

A

CRH- 41 aa polypeptide
GPCR CRHR activates Gs (corticotropin-releasing hormone receptor, involved in cAMP)

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5
Q

amino acid, activation of a. pituitary hormone in HPA axis

A

POMC - ACTH 39 aa polypeptide
GPCR ACTHR activate Gs

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6
Q

What does POMC stand for?

A

Pro-opiodmelanocortin

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7
Q

step 1 of all three pathways activated by POMC

A

gamma-MSH
ACTH (glucocorticoids)
beta-lipotropin

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8
Q

What does ACTH branch out to from POMC?

A

alpha-MSH (melanin)
CLIP

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9
Q

what does beta-lipotropin produce from POMC?

A

gamma-lipotropin –> beta-MSH
beta-endorphin

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10
Q

Adrenal hormones and from which portion

A

Aldosterone - zona glomerulosa
Cortisol - zona fasciculata

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11
Q

layers of adrenal gland

A

Capsule
Zona glomerulosa
Zona fasciculata
Zona reticularis
Adrenal medulla

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12
Q

Cortisol vs aldosterone concentrations compare

A

cortisol&raquo_space; aldosterone

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13
Q

Adrenal steroid synthesis in zona fasciculata, humans vs rodents

A

Cholesterol –> Pregnenolone –> 17Oh-Pregnenolone –> 17OH progesterone –> 11-deoxycortisol –> Cortisol measured in humans
or
Progesterone –> 11-deoxycorticosterone –> corticosterone

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14
Q

Zona glomerulosa adrenal steroid synthesis

A

Cholesterol –> z.g –> Pregnenolone –> Progestrone –> 11-deoxycorticosterone –> Corticosterone–> aldosterone

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15
Q

Zona reticularis adrenal synthesis

A

Cholesterol –> zr –> Pregnenolone –> 17OH pregnenolone –> DHEA –> Andtrostenedione or DHEA-s

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16
Q

Cortisol regulation/effect in zona fasciculata

A

ACTH binds to adrenal GPCR –> alpha g protein binds to GTP + AC –> cAMP –> activates PKA –> PKA phosphorylates CREB –> enters nucleus –> Steroidogensesis

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17
Q

Cortisol activation pathway, now with the enzymes

A

Cholesterol: CYP11a1 –> Pregnenolone: Cyp17 –> 17OH pregnenolone: 3betaHSD2 + Cyp21 –> 11-deoxycortisol: Cyp 11 beta–> Cortisol CBG

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18
Q

Where is cortisol bound afterwards?

A

90% bounds to CBG
5 to albumin
5 free, active in cells

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19
Q

Glucocorticoid functions

A

Intermediary metabolism - increase glucose and free fatty acids
Cardiovascular - increase HR
Immune system - decrease inflammation
Growth - is inhibited

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20
Q

Cortisol mechanism of action

A

Cortisol bounds to protein –> enters cell –> binds to glucocorticoid receptor –> with chaperone complex dimerizes + enters nucleus –> glucocorticoid receptor * cortisol *2 binds to GRE (g-c response element) –> Transcription –> altered cellular protein function

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21
Q

Cortisol effects

A

Catabolic effect on muscle protein - muscle wasting
Increased glycogen and blood glucose - anti insulin
Lymphocytes and eosinophils decreased in blood
Anti-inflammation
Increased cardiac contraction and vascular tone

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22
Q

Where is aldosterone produced?

A

Zona glomerulosa of adrenal gland

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23
Q

Regulation of aldosterone 2 organs

A

Liver –> Angiotensinogen –> converted to Angiotensin I (via renin prod. by kindey) –> Angiotensin 2 via ACE
Angiotensin 2 stims adrenal gland via K+ –> aldosterone released from zona glomerulosa

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24
Q

Angiotensin Regulation of Aldosterone

A

see slide 12 lecture 3

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25
Q

Aldosterone is what type of adrenal hormone?

A

Mineralocorticoid

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26
Q

What is function of aldosterone

A

Conservation of Na, Cl and water
Blood volume and pressure

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27
Q

Aldosterone’s structure is similar to…

A

that of cortisol

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28
Q

Aldosterone Mechanism of action

A

Aldosterone binds to mineralocorticoid receptor + chaperone –> enter nucleus –> alter transcription –> affect Na-K ATPase, SGK1, increased collagen, TGF beta
affect NADPH oxidase and increase ROS
Without nucleus:
mineral.cort receptor on membrane –> non-genomic transactivation –> ERK1/2 phosphorylation

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29
Q

What happens when too much aldosterone stimulation in renal cell?

A

Inflammation
Extracellular matrix accumulation
Increased blood pressure
Overall: renal damage

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30
Q

Effect of aldosterone

A

retain Na and water
Excrete K in urine

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31
Q

Results of aldosterone

A

Increased BP

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32
Q

Pathologies in aldosterone, too much too little

A

Deficiency: loss of sodium, water, hyperkalemia
Excess: elevated Na, retention of water, hypokalemia

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33
Q

Selectivity of aldosterone and cortisol if both are so similar?

A

GCR selective for cortisol, MCR not selective

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34
Q

Which compound converts from cortisol to cortisone

A

Cortisol bio active –> 11beta-HSD2 NAD+ –> Cortisone: bio inactive

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35
Q

which compound converts cortisone –> cortisol

A

Cortisone –> Cortisol
11 beta HSD1 NADPH

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36
Q

which compound does aldosterone-sensitive tissues have?

A

11-beta HSD2 NAD+

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37
Q

Active compound in black licorice?

A

Glycyrrhetinic acid

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38
Q

Action of black licorice compound?

A

Inhibits 11-beta-HSD2
result: too much bioactive cortisol, MCR overstimulated, increase blood pressure and volume overstimulated

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39
Q

Primary and secondary adrenal pathology

A

Primary - Addison’s autoimmune disease
Secondary adrenal insufficiency

40
Q

Third adrenal pathology mentioned?

A

Congenital adrenal hyperplasia

41
Q

what is the reason for cong. adrenal hyperplasia?

A

21 hydroxylase insufficiency
11 hydroxylase insufficiency

42
Q

Two people with Addison’s

A

Jane Austen
JFK

43
Q

Addison’s autoimmune symptoms + reasons

A

Hyperpigmentation - decreased cortisol, inhibition of ACTH, more aMSH/melanin
Salt craving - loss of aldosterone, Na
Fatigue - decreased blood pressure
Dizziness when standing - orthostatic hypotension - BP unregulated
Nausea and vomiting - hyperkalemia
Weight loss - nausea, vomiting, loss appetite

44
Q

Why there is hyperkalemia when addison’s?

A

Lack of Na+ due to no aldosterone
Na+ out, K+ in
Higher K+

45
Q

Commonly used corticosteroids

A

Hydrocortisone/cortisol
Dexamethasone
Fludrocortisone

46
Q

Hydrocortisone - type, administration

A

short to med acting glucocorticoids
Oral, injectable, topical

47
Q

Dexamethasone - type + administration

A

Long-acting glucocorticoids
Oral, injectable, topical

48
Q

Fludrocortisone - type+ administration

A

Mineralocorticoid
Oral

49
Q

Most common use for corticosteroids

A

Anti-allergic, anti-inflamm, rheumatic, respiratory, dermatological conditions

50
Q

Mechanism of c-steroid effects?

A

inhibition of proteolytic enzymes
inhibition of leukocyte response
inhibition of FGF (fibroblast growth factor)

51
Q

Corticosteroids and cancer treatment

A

Lymphoma/leukemia - with antineoplastics
Anti-lymphocytic actions

Androgen dependent tumours - impression of ACTH

Hypercalcemia of malignancy - Anti vitamin D receptor and PTH receptor

52
Q

Disorder resulting from glucocorticoid excess/etymology

A

Cushing’s disease:
from glucocorticoid therapy or
ACTH secreting pituitary adenoma

53
Q

Symptoms of Cushing’s

A

Moon face
Acne
Weight gain
Slow would healing
thin skin

54
Q

Therapeutics against Cushing’s

A

Inhibitors of ACTH secretion
Adrenal related inhibitors

55
Q

ACTH inhibitors list

A

Pasireotide
somatostatin rec 5 agonist, inhibits corticotropin

56
Q

List of adrenal related inhibitors

A

Ketoconazole - inhibits CYP17 and CYP11A
Mitotane - targets adrenal proteins Mifeprisone - RU 486
Spironolactone - MR antagonist

57
Q

Which drug is used for inoperable adrenocarcinoma

A

Mitotane

58
Q

Which drug is more glucocorticoid receptor antagonism

A

Mifepristone

59
Q

drug against hyperaldosteronism

A

Sprionolactone

60
Q

Steps of thyroid hormone secretion
7

A

1 Iodine trapping
2 synthesis of thyroglobulin
3 Oxidation of iodide into iodine
4 Iodination (of thyroglobulin) and coupling of tyrosine
5 endocytosis of colloid into thy. cell from lumen
Proteolysis of coupled T3 T4
7 secretion of thyroid hormone into blood stream

61
Q

Thyroid hormone wrt HPA axis

A

Thyrotropin-releasing hormone TRH (hypothalamus)
TRH-R pituitary
release TSH alpha-beta

62
Q

Actions of TSH

A

binds receptor Gs AC and Gq PLC
Stimulates all steps in synthesis of thyroid hormones?

63
Q

Which steps does TSH stimulate?

A

Iodine trapping
synthesis of thyroglobulin
oxidation of iodide-iodine
Binding and iodination of tyrosine
Endocytosis into cell
proteolysis
release of T3 and T4

64
Q

Which of thyroid hormones most prevalent?

A

In circulation 90% T4 - bound to thyroxine binding globulin
T4 more tightly bound

65
Q

Conc of free T4
free T3
TSH

A

free T4: 11-24 pmol/:
free T3 3.3-6.5 pmol/L
TSH 0.5-5 mU/mL

66
Q

T4 vs T3 activity

A

T3 is active form
T3 is mostly from deiodinated T4

67
Q

Action of thyroid hormone

A

Growth skeleton
Growth and development and function of CNS
Protein synthesis
Carb absorption
Adrenal and gonadal function
Cardiac and renal functions

Regulation of basal metabolic rate

68
Q

Infantile hypothyroidism, prevalence, how dealt with

A

Infantile cretinism
1:4000 incidence
Screened and treated

69
Q

Symptoms of infantile cretinism

A

Mental retardation
deaf mute
dwarfism
poor thermogenesis
accumulation of mucopolysaccharides in lungs
CV disturbances

70
Q

Adult hypothyroidism etymology

A

Iodine deficiency
Hashimoto’s disease (autoimm)

71
Q

Adult hypothyroidism symptoms

A

dry skin
cold intolerance
constipation
fatigue
weight gain
hair loss
daytime somnolence

72
Q

Thyroid hormone drugs list

A

Synthroid
Eltroxin
Levo-thyroxine

73
Q

Which is preferred drug for Thyr. analogue, what is monitored, dose

A

Levathyroxine preferred
monitored for TSH, T3 and T4
Average dose 110-125 micrograms

74
Q

Quickness of levothyroxine effect

A

takes several weeks for full effect
patients started on low dose and monitored for TSH T3 and T4
Dose adjusted until TSH normal

75
Q

In which cases is Levo-T ineffective

A

due to ineffective conversion to T3

76
Q

Difference in Liothyronine/cytomel vs levothyroxine

A

T3 vs T4 analogue
T3 more readily available and potent than L-thyroxine

77
Q

Half-life, free [], and relative activity of L-thyroxine

A

7 days
0.05%
1

78
Q

Half-life, % free and relative activity of Liothyronine

A

1.5 days
0.5%
10

79
Q

Why is liothyronine preferred during hypothyroidism in pregnancy?

A

Threat to fetus during hypothyroidism
requires increased T4 doses during pregnancy
low T3, need more T3

80
Q

Why can L-thyroxine be ineffecitve
alternative

A

problem with conversion to T3
possible increased conversion to reverse T3 (inactive form)
Thyrolar, Liotric 4:1 T4:T3

81
Q

Potential toxicities of thyroid drugs

A

Hyperthyroidism

82
Q

Cause of hyperthyroidism

A

Mostly caused by Graves disease

83
Q

What is Graves disease?

A

autoimmune stimulation of TSH receptor

84
Q

Symptoms of Graves disease

A

Bulging eyes
Heat intolerance
HR increased, Increase BP
weight loss
sleep problems
anxiety
goiter
3x higher in women

85
Q

Treatment of graves’ disease

A

Thiourea
Propylthiouracil
Methimazole

86
Q

Propylthiouracil half life and potency

A

2H
1

87
Q

Methimazole half life and potency

A

6hours
10

88
Q

Thionamides action

A

Inhibit thyroid peroxidase, block iodination of tyrosine groups, block thyroid hormone

89
Q

Pharmacokinetics of thionamides

A

peak plasma concentration 1 h
maximal effect - several weeks

90
Q

Thionamides and pregnancy

A

Crosses placenta
use in pregnancy low

91
Q

Thionamides and toxicities

A

Agranulocytosis 0.5
drug rash
arthralgia
edema 2%
Rarely hepatitis
Swollen lymph nodes
loss of taste

92
Q

Alternative therapy of hyperthyroidism

A

Thyroid ablation

93
Q

Principle of thyroid ablation
side effect?

A

radioactive sodium iodide solution/capsules
concentrates in thyroid follices
kills cells by local radiation
treatment may cause hypothyroidism

94
Q

Other alternatives for hyperthyroidism

A

surgery or radiofrequency ablation/endoscopy

95
Q

Fludrocortisone type and admin

A

mineralocorticoid
Oral

PCL469 (6 decks)

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