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Physio Exam 2 > Jackson Lectures 6 > Flashcards

Jackson Lectures 6 Flashcards

1
Q

Congenital adrenal hyperplasia is an

A

adrenal enzyme deficiency results in excess production of adrenal androgens

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2
Q

Congenital adrenal hyperplasia is caused by more than

A

one mutation and severity varies depending on mutation

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3
Q

Congenital adrenal hyperplasia: example:

A

21α hydroxylase mutation impairs synthesis of cortisol → decreased negative feedback of cortisol on ACTH secretion → increased stimulation of adrenal cortex → increased production of adrenal androgens

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4
Q

Congenital adrenal hyperplasia: genotype is

A

XX; phenotype is virilized or more male than female depending on severity

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5
Q

5α-reductase deficiency (guevodoces): development of the

A

penis, scrotum and prostate gland is DHT-dependent

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6
Q

5α-reductase deficiency (guevodoces): enzyme deficiecy results I failure of differentiation of the

A

external genitalia early in life, but increased T secretion with the onset of pubery completes differentiation.

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7
Q

5α-reductase deficiency (guevodoces): phenotype is female at birth until

A

early puberty

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8
Q

Testicular feminization or androgen insensitivity: lack

A

functional androgen receptor (used by both T and DHT)

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9
Q

Testicular feminization or androgen insensitivity: no differentiation of

A

genitalia

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10
Q

Testicular feminization or androgen insensitivity: genotype is

A

XY

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11
Q

Testicular feminization or androgen insensitivity: phenotype is

A

female; condition often diagnosed at puberty

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12
Q

There is a dramatic increase in circulating concentrations of steroid hormones during pregnancy due to

A

placental production

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13
Q

CL regresses after

A

~ 3 months and hCG supports luteal steroidogenesis

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14
Q

placental E2 stimulates

A

growth of myometrium

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15
Q

placental P reduces

A

uterine contractility and stimulates vasodilation

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16
Q

Endocrine regulation of growth

First, there are

A

non-endocrine factors that regulate growth

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17
Q

Genetics is the principle factor controlling the potential for

A

growth.

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18
Q

Disease damages tissue and activates the

A

HPA axis. Stress axis.
• This takes energy from growth processes
• Activates stress axis; cortisol inhibits growth

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19
Q

cortisol inhibits

A

growth

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20
Q

The hormones of the growth axis (GHRH → GH → IGF-1) control growth by their actions in

A

somatic tissue and the liver. (has direct actions in muscle, fat, and bone to stimulate growth)

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21
Q

• The relative importance of

A

IGF-1 and GH varies during development.

22
Q

IGF-1 is necessary for

A

fetal growth; GH becomes important later in development.

23
Q

• IGF-1 is like insulin in terms of

A

structure, not action

24
Q

• Growth axis:

A

Hypothalamus, pituitary and muscle/fat/bone

25
Q

• Growth axis:

A

Hypothalamus, pituitary and muscle/fat/bone

26
Q

Thyroid hormone is required for synthesis of

A

GH and manifestation of GH effects. (permissive effect on GH)

27
Q

Growth is also controlled by

A

glucose-regulating hormones.

28
Q

Glucocorticoids inhibit

A

GHRH secretion.

29
Q

Insulin has actions that oppose

A

GH and IGF-1

30
Q

Gonadal steroids (T and E2) also have a role in growth. (conversion of testosterone to estradiol that causes

A

stoppage of growth)

31
Q

At puberty, the epiphyseal plates ossify due to the actions of

A

E2

32
Q

Lacks estradiol receptors (alpha receptor), kept on

A

growing

33
Q

GHRH – from hypothalamus, stimulate

A

GH secretion; comes from arcuate nucleus, stimulated with exercise, stress, fasting, sleep

34
Q

Somatostatin (SS) – inhibits

A

GH secretion, comes from paraventricular nucleus, but is secreted in pulsile manner of these hormones due to feedback mechanisms

35
Q

Need thyroxine to stimulate

A

growth

36
Q

GH also acts in somatic tissue (muscle and bone) to stimulate

A

protein synthesis. (Anabolic, does this through stimulation of AA uptake and ribosome stimulation)

37
Q

GH acts in opposition to

A

insulin (on muscle and fat); makes glucose available for growth

38
Q

The principle indirect effect of GH on growth is to stimulate the secretion of

A

insulin-like growth factor 1 (IGF-1, powerful mitogen) from the liver and other tissues (bone and cartilage). (stimulates gluconeogenesis)

39
Q

GH • LL feedback from

A

IGF-1

40
Q

• IGF-1 and GH inhibit

A

GH and GHRH secretion, but stimulate SS secretion (this will further decrease GH secretion)

41
Q

o GHRH elevated during

A

sleep, relative to day time levels

42
Q

o SS elevated during the

A

day

43
Q

Somatic growth is the result of interactions between

A

GH and IGF-1

44
Q

GH stimulates maturation of

A

chondroblasts into chondrocytes and upregulates IGF-1 receptor expression

45
Q

IGF-1 stimulates cell division (secreted by

A

chondrocytes)

46
Q

There are no known defects in

A

IGF-1 synthesis or for the IGF-1 receptor (insufficient IGF-1 is a lethal mutation)

47
Q

Malnutrition impairs IGF-1 synthesis independent of

A

GH

48
Q

Sex steroid stimulate

A

GH and IGF-1 synthesis, but have contrasting effects on skeletal growth.

49
Q

Steroids stimulate the

A

prepubertal spurt in bone growth, but ultimately causes fusion of the epiphyseal plates by inhibiting bone growth.

50
Q

Thyroid hormone regulates

A

GH synthesis, and is required for GH effects.

51
Q

Cortisol/glucocorticoids have

A

anti-growth effects. (inhibition of DNA synthesis; breakdown of bone, high levels of cortisol can inhibit growth axis)

52
Q

Glucocorticoid therapy- for things like asthma, you are impairing/inhibiting

A

growth due to effects of cortisol on growth axis

Physio Exam 2 (11 decks)

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