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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
Aldosterone is what type of adrenal hormone?
Mineralocorticoid
26
What is function of aldosterone
Conservation of Na, Cl and water Blood volume and pressure
27
Aldosterone's structure is similar to...
that of cortisol
28
Aldosterone Mechanism of action
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
29
What happens when too much aldosterone stimulation in renal cell?
Inflammation Extracellular matrix accumulation Increased blood pressure Overall: renal damage
30
Effect of aldosterone
retain Na and water Excrete K in urine
31
Results of aldosterone
Increased BP
32
Pathologies in aldosterone, too much too little
Deficiency: loss of sodium, water, hyperkalemia Excess: elevated Na, retention of water, hypokalemia
33
Selectivity of aldosterone and cortisol if both are so similar?
GCR selective for cortisol, MCR not selective
34
Which compound converts from cortisol to cortisone
Cortisol bio active --> 11beta-HSD2 NAD+ --> Cortisone: bio inactive
35
which compound converts cortisone --> cortisol
Cortisone --> Cortisol 11 beta HSD1 NADPH
36
which compound does aldosterone-sensitive tissues have?
11-beta HSD2 NAD+
37
Active compound in black licorice?
Glycyrrhetinic acid
38
Action of black licorice compound?
Inhibits 11-beta-HSD2 result: too much bioactive cortisol, MCR overstimulated, increase blood pressure and volume overstimulated
39
Primary and secondary adrenal pathology
Primary - Addison's autoimmune disease Secondary adrenal insufficiency
40
Third adrenal pathology mentioned?
Congenital adrenal hyperplasia
41
what is the reason for cong. adrenal hyperplasia?
21 hydroxylase insufficiency 11 hydroxylase insufficiency
42
Two people with Addison's
Jane Austen JFK
43
Addison's autoimmune symptoms + reasons
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
Why there is hyperkalemia when addison's?
Lack of Na+ due to no aldosterone Na+ out, K+ in Higher K+
45
Commonly used corticosteroids
Hydrocortisone/cortisol Dexamethasone Fludrocortisone
46
Hydrocortisone - type, administration
short to med acting glucocorticoids Oral, injectable, topical
47
Dexamethasone - type + administration
Long-acting glucocorticoids Oral, injectable, topical
48
Fludrocortisone - type+ administration
Mineralocorticoid Oral
49
Most common use for corticosteroids
Anti-allergic, anti-inflamm, rheumatic, respiratory, dermatological conditions
50
Mechanism of c-steroid effects?
inhibition of proteolytic enzymes inhibition of leukocyte response inhibition of FGF (fibroblast growth factor)
51
Corticosteroids and cancer treatment
Lymphoma/leukemia - with antineoplastics Anti-lymphocytic actions Androgen dependent tumours - impression of ACTH Hypercalcemia of malignancy - Anti vitamin D receptor and PTH receptor
52
Disorder resulting from glucocorticoid excess/etymology
Cushing's disease: from glucocorticoid therapy or ACTH secreting pituitary adenoma
53
Symptoms of Cushing's
Moon face Acne Weight gain Slow would healing thin skin
54
Therapeutics against Cushing's
Inhibitors of ACTH secretion Adrenal related inhibitors
55
ACTH inhibitors list
Pasireotide somatostatin rec 5 agonist, inhibits corticotropin
56
List of adrenal related inhibitors
Ketoconazole - inhibits CYP17 and CYP11A Mitotane - targets adrenal proteins Mifeprisone - RU 486 Spironolactone - MR antagonist
57
Which drug is used for inoperable adrenocarcinoma
Mitotane
58
Which drug is more glucocorticoid receptor antagonism
Mifepristone
59
drug against hyperaldosteronism
Sprionolactone
60
Steps of thyroid hormone secretion 7
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
Thyroid hormone wrt HPA axis
Thyrotropin-releasing hormone TRH (hypothalamus) TRH-R pituitary release TSH alpha-beta
62
Actions of TSH
binds receptor Gs AC and Gq PLC Stimulates all steps in synthesis of thyroid hormones?
63
Which steps does TSH stimulate?
Iodine trapping synthesis of thyroglobulin oxidation of iodide-iodine Binding and iodination of tyrosine Endocytosis into cell proteolysis release of T3 and T4
64
Which of thyroid hormones most prevalent?
In circulation 90% T4 - bound to thyroxine binding globulin T4 more tightly bound
65
Conc of free T4 free T3 TSH
free T4: 11-24 pmol/: free T3 3.3-6.5 pmol/L TSH 0.5-5 mU/mL
66
T4 vs T3 activity
T3 is active form T3 is mostly from deiodinated T4
67
Action of thyroid hormone
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
Infantile hypothyroidism, prevalence, how dealt with
Infantile cretinism 1:4000 incidence Screened and treated
69
Symptoms of infantile cretinism
Mental retardation deaf mute dwarfism poor thermogenesis accumulation of mucopolysaccharides in lungs CV disturbances
70
Adult hypothyroidism etymology
Iodine deficiency Hashimoto's disease (autoimm)
71
Adult hypothyroidism symptoms
dry skin cold intolerance constipation fatigue weight gain hair loss daytime somnolence
72
Thyroid hormone drugs list
Synthroid Eltroxin Levo-thyroxine
73
Which is preferred drug for Thyr. analogue, what is monitored, dose
Levathyroxine preferred monitored for TSH, T3 and T4 Average dose 110-125 micrograms
74
Quickness of levothyroxine effect
takes several weeks for full effect patients started on low dose and monitored for TSH T3 and T4 Dose adjusted until TSH normal
75
In which cases is Levo-T ineffective
due to ineffective conversion to T3
76
Difference in Liothyronine/cytomel vs levothyroxine
T3 vs T4 analogue T3 more readily available and potent than L-thyroxine
77
Half-life, free [], and relative activity of L-thyroxine
7 days 0.05% 1
78
Half-life, % free and relative activity of Liothyronine
1.5 days 0.5% 10
79
Why is liothyronine preferred during hypothyroidism in pregnancy?
Threat to fetus during hypothyroidism requires increased T4 doses during pregnancy low T3, need more T3
80
Why can L-thyroxine be ineffecitve alternative
problem with conversion to T3 possible increased conversion to reverse T3 (inactive form) Thyrolar, Liotric 4:1 T4:T3
81
Potential toxicities of thyroid drugs
Hyperthyroidism
82
Cause of hyperthyroidism
Mostly caused by Graves disease
83
What is Graves disease?
autoimmune stimulation of TSH receptor
84
Symptoms of Graves disease
Bulging eyes Heat intolerance HR increased, Increase BP weight loss sleep problems anxiety goiter 3x higher in women
85
Treatment of graves' disease
Thiourea Propylthiouracil Methimazole
86
Propylthiouracil half life and potency
2H 1
87
Methimazole half life and potency
6hours 10
88
Thionamides action
Inhibit thyroid peroxidase, block iodination of tyrosine groups, block thyroid hormone
89
Pharmacokinetics of thionamides
peak plasma concentration 1 h maximal effect - several weeks
90
Thionamides and pregnancy
Crosses placenta use in pregnancy low
91
Thionamides and toxicities
Agranulocytosis 0.5 drug rash arthralgia edema 2% Rarely hepatitis Swollen lymph nodes loss of taste
92
Alternative therapy of hyperthyroidism
Thyroid ablation
93
Principle of thyroid ablation side effect?
radioactive sodium iodide solution/capsules concentrates in thyroid follices kills cells by local radiation treatment may cause hypothyroidism
94
Other alternatives for hyperthyroidism
surgery or radiofrequency ablation/endoscopy
95
Fludrocortisone type and admin
mineralocorticoid Oral

PCL469 (6 decks)

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