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Phar300 > lect 12 corticosteroids > Flashcards

lect 12 corticosteroids Flashcards

1
Q

what is inflammation

A

body’s immune response to an irritant or foreign object

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2
Q

changes leading to inflammation at site of injury

A

blood flow, increase in blood flow permeability, recruitment of proteins, white blood cells, microphages, neutrophils from circulation to site of injury

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3
Q

what diseases involve unwanted inflammation and why

A

almost all because diseases change your inflammatory response to grow and thrive

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4
Q

class of drugs that lower inflammation in body and reduce immune system

A

corticosteroids

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5
Q

doctors often prescribe corticosteroids for which two disease

A

asthma and arthritis

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6
Q

Biologically active compound with four rings arranged in a specific molecular configuration

A

steroids

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7
Q

2 principal functions of steroids

A
  1. are signalling molecules

2. important component in cell membrane that can alter membrane fluidity

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8
Q

corticosteroids = ? + ?

A

glucocorticoids + mineralocorticoids

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9
Q

class of corticosteroids produced in adrenal cortex that influence salt water balance

A

mineralocorticoids

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10
Q

primary mineralocorticoid

A

aldosterone

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11
Q

immune response of cortico.

A

pain induces hypothalamus to release hormones that stimulate adrenal gland to release cortico to reduce pain and inflammation

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12
Q

system that is the circuit board of the body through which cell communicate. Complex network of glands and organs

A

endocrine system

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13
Q

how does endocrine system use hormones (7)

A

to control and coordinate body metabolism, energy level, reproduction, growth, response to injury, stress, resolution of inflammation

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14
Q

cell produces ligand which interacts with receptor on same cell

A

autocrine

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15
Q

cell’s ligand interacts with receptor in nearby cell

A

paracrine

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16
Q

cell’s chemical messenger circulates in body and affects speecific receptors on distant cells

A

endocrine

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17
Q

Major components of endocrine system

A

brain
hypothalamus
target organs: thyroid, pancreas, adrenal glands, ovaries, testes

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18
Q

forward path in response to stress, illness ect

A

Hypothalamus –> CRH release –> Pituitary –> ACTH release–> adrenals –> Cortisol

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19
Q

how does cortisol work

A

comes back and interacts with glucorticoid receptors in pituitary and hypothalamus and dowregulate the drive to increase itself (negative feedback)

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20
Q

41 aa peptide prohormone produced in hypothalamus. amino acids are cleaved for activation

A

Corticotrophin-releasing hormone (CRH)

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21
Q

how does CRH act in the pituitary

A

acts on g-protein coupled receptors in the anterior pituitary to stimulate POMC synthesis which is processed to release ACTH and beta LPH

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22
Q

roles of ACTH

A
  1. increases delivery of cholesterol to inner mitochondrial membrane
  2. increase transcription of steroidogenic enzymes
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23
Q

what happens to adrenal glands in forward pathway

A

ACTH regulates glucocorticoid synthesis in adrenal cortex

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24
Q

places in adrenal cortex that make corticosteroids and which type

A

both zona fasciculata/reticularis make glucocorticoids but only zona glomerusola makes mineralocorticoids

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25
Q

process where cholesterol becomes steroids

A

steroidogenesis

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26
Q

first critical step of steroidogenesis

A

CYP11A that cleaves side chain then make different steroids

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27
Q

enzyme involved in aldosterone formation

which regulates salt secretion

A

CYP11beta2

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28
Q

enzyme involved in cortisol formation

which affect metabolism and regulates glucose levels

A

CYP11beta1

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29
Q

turning cholesterol to glucocorticoids needs what to make cortisol from prior metabolites

A

CYP17 and CYP11beta1

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30
Q

issues with feedback mechanism of cortisol can cause what

A

diseases

31
Q

true or false? external corticosteroids can affect loop mechanism of cortisol

A

true

32
Q

explain mechanism of action of glucocorticoids to receptor

A

they bind to ligand-binding domain of steroid hormone receptors. the ligand-bound receptor moves from cytoplasm to nucleus and initiate signal transduction for steroid hormones which lead to changes in gene expression for hours to days

33
Q

dna-binding domain of steroid hormone receptors binds to what

A

specific areas of the genome like glucocorticoid response element

34
Q

transcription-activating domain of steroid hormone receptor does what

A

turns on transcription of very specific genes that are related to the effects of the hormone

35
Q

up to 20% of immune cell genes are regluated by what

A

glucocorticoids

36
Q

Glucocorticoids can transactivate or transrepress genes by binding to what receptor

A

GRalpha

37
Q

what can block the action of GRalpha by blocking transactivation and transrepression

A

GRbeta

38
Q

mechanism of tolerance with glucocorticoid relating to GRalpha

A

when one becomes tolerant to glucocorticoids, more GRbeta is produced and inhibits more GRalpha which causes decrease effect of glucocorticoid

39
Q

summary of glucocorticoid mechanism and gene

A

glucocorticoid bind steroid hormone receptor like GRalpha or GRbeta. This interacts then areas of genome like GRE (gluco. resp. element) to transactivate or transrepress

40
Q

anti-inflammatory effects of glucocorticoids in body

A
  1. change in cell proliferation, migration, survival
  2. decreases proinflammatory cytokines, interleukins, prostaglandins
  3. Block things at transcriptional level of proinflammatory molecules
41
Q

metabolic effects of glucocorticoids in body

A
  1. increase glucose to protect brain, heart by transcriptional activation.
  2. Increase blood glucose by increasing glycogen breakdown (glycogenolysis), increasing glucose synthesis (gluconeogenesis), decrease fat deposit (increase lipolysis), increase protein catabolism
42
Q

pharmacokinetics of glucocorticoids

A

administered to most routes because small and lipid soluble but local administration preferred to minimize adverse effects

43
Q

glucocorticoids bind to what for circulation

A

steroid hormone binding globulins

44
Q

Cortisol is 80-90% bound by what and why

what about the 5-10%

A

bound to corticosteroid-binding globulin (CBG, transcortin) for better circulation.

5-10% loosely bound to albumin

45
Q

problem with bioavailabilty of CBG bound glucocorticoids

A

hormone is transported but CBG modulates availability of hormone so another reaction is needed to make it available

46
Q

which synthetic glucocorticoids can CBG bind or not bind

A
  1. Can bind to prednisone and prednisolone

2. cant bind to dexamethasone so 100% plasma dexamethasone bioactive

47
Q

absorption of glucocorticoids

A

absorbed rapidly from GI tract, synovial (joints) and conjunctival (eyes) due to lipophilic but slowlly absorbed from skin

48
Q

what hormone increases CBG biosynthesis in liver and requires increased plasma cortisol to maintain correct bioavailability

A

elevate estrogen concentrations

49
Q

can circadian rythm affect endogenous corticosteroids levels

A

yes

50
Q

glucocorticoids as grugs structure

A

backbone: 4 rings

structurally modified side chain to increase bioavailabilty, half life

51
Q

what changes were made to synthetic glucocorticoids betamethasone and dexamethasone and why

A

adding methyl group at C16 to increase activation of glucocorticoid receptor and virtually eliminate mineralocorticoid receptor activity. Increases duration of action of these compounds

52
Q

introduction of other side chain than methyl c16 and on who enhances gluco and mineralo activities

A

Fluorine at C9
prednisone, prednisolone, methylprednisolone,
dexamethasone,
betamethasone

53
Q

which gluco. has longer-acting and higher half-life over which gluco.

A

beta/dexamethasone over pednisone, prednisolone

54
Q

asthma treatment

A

inhalers targeting the inflammation in lungs

55
Q

eczema treatment

A

cream form to prevent inflammation on skin or pill to be systemic

56
Q

EVALI (vaping) treatment

A

vitamin E acetate is not the cause of high inflammation. glucocor. can help breath and better prognosis on ventilator

57
Q

immunosupressive action use of glucocor. example

A

for organ transplants

58
Q

Rare adrenal insufficiency disease where glands do not make enough aldosterone and cortisol

A

Addison’s Disease

59
Q

treatment of addisons disease

A

systemic glucocorticoid therapy over period of time. Replacement drugs (gluco. and mineralo.) given on schedule time to mimic 24hr fluctuation of cortisol

60
Q

types of blood cancer that cant be cured that begin with abnormal mutation in stem cell and causes overproduction of white b cells and reduction of RBC’s

A

myeloproliferative diseases

61
Q

treatment of myeloproliferative diseases

A

glucocorticoids to keep RBC count up and increase lifespan

62
Q

low treatment of cortisol effects (7)

A

hariness, acne, greasy skin, irregular periods, fatigue, tiredness reduced fertility

63
Q

high treatment of cortisol effects (8)

A

increased appetite, weight gain, muscle weakness, thin skin, easy bruising high BP, diabetes, osteoperosis

64
Q

Adverse effects of prolonged gluco. therapy (7)

A

osteoporosis decreased bone density, glucose intolerance diabetes, central obesity, muscle weakening, increase risk of infections, depression, cataracts

65
Q

oral candidiatis is what and how can it be avoided

A

adverse effect when using inhaler. avoided by rinsing mouth after using inhaler

66
Q

what is HPA axis supression and how avoided

A

long term steroid use shutting down hypothalamus, pituitary, adrenal axis and adrenal atrophy. no more ACTH to keep adrenal functioning. avoid by slowly decreasing amount taken

67
Q

growth inhibition of steroid use how to avoid

A

important in having right dose in inhaler for prepubertal patients to keep glucocort. in lungs and prevent systemic effects

68
Q

oral corticosteroid used for extreme cases and short duration

A

prednisone

69
Q

genetic disease caused by excess cortisol

A

cushing’s syndrome

70
Q

causes of cushing syndrom (2)

A
  1. overuse of steroids
  2. cancer, ectopic production of ACTH
  3. inhibition of HPA axis, exogenous cortisol act like endogenous overproduction so excess intake of cortisol that cannot be controlled
71
Q

people using corticosteroids are more susceptible to develop what famous disease and why

A

COVID 19 and dut to imunnosupressant nature of glucortocoids

72
Q

people with obesity need more or less glucocorticoid?

A

more to have right blood concentration as the fat absorbs

73
Q

common features in cushing syndrome (6)

A

obesity, hump shoulder blades, mood face, muscle wasting, weakness, psychiatric issues

Phar300 (18 decks)

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