Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

REVISION EXTRAS > BLOCK 11 > Flashcards

BLOCK 11 Flashcards

1
Q

What inhibits oxytocin release?

A

catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what inhibits prolactin release

A

dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

where is oxytocin secreted from? what else is secreted from here?

A

supraoptic and paraventricular nuclei in the hypothalamus

vasopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what stores oxytocin?

A

herring bodies which are dilatations in the length in the axons from hypothalamus to posterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what synthesises prolactin?

A

lactotrophs in the anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how does the hypothalamus keep prolactin ;levels controlled?

A

releases dopamine which binds to specific receptors on lactotrophs, inhibiting prolactin release
also secretes thyrotropin releasing hormone which stimulates prolactin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

outline the physiology of why women tend to not ovulate or have menstrual periods whilst breastfeeding?

A

as prolactin inhibits the release of GnRH which decreases FSH and LH levels which are needed for the development of follicles and ovulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are risk factors of mastitis?

A 
breast feeding difficulty
mastitis with a previous Childs
severe, prolonged, unilateral engorgement 
poor milk drainage
nipple excoriation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how does mastitis present?

A

unilateral
redness, swelling, tenderness
fever, myalgia, chills, flu-like symptoms
may be axillary pain and swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

why is colostrum so important?

A

rich in IgA so helps fight infections
a laxative so can rid of meconium, preventing physiological jaundice
full of vits and minerals e.g. vit A and carotenoids
helps baby transition to outside world as its similar to amniotic fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is mammogeneiss? when doe sit start and when is it complete?

A

the process of growth and development of the mammary gland in preparation for milk production. This process begins when the mammary gland is exposed to estrogen at puberty and is completed during the third trimester of pregnancy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is lactogenesis

A

the process of developing the ability to secrete milk and involves the maturation of alveolar cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is galactokinesis?

A

milk let down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is galactopoeisis?

A

the maintenance of lactation once lactation has been established.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is involution?

A

removes the milk-producing epithelial cells when they become redundant at weaning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

outline the 2 stages of involution?

A

During the first phase, remodelling is inhibited and apoptotic cells can be seen in the lumen of the alveoli. In the second phase, apoptosis is accompanied by remodelling of the surrounding stroma and re-differentiation of the adipocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

whats the period of maximal susceptibility to teratogenic effects?

A

first 10 weeks after conception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

whats the critical period for CNS development?

A

up to 16 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

whats the critical period for heart development?

A

up to 5.5 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

whats the critical period for upper limb development?

A

weeks 4 to 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

whats the critical period for eye development?

A

weeks 4 to 8.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

whats the critical period for lower limb development?

A

weeks 4 to 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the fetotoxic effects of the mother taking androgens during the first trimester?

A

virilisation of female foetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the fetotoxic effects of the mother taking oestrogen during the first trimester?

A

feminisation of male foetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the fetotoxic effects of the mother taking warfarin during the first trimester?

A

craniofacial abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the fetotoxic effects of the mother taking retinoids during the first trimester?

A

craniofacial defects, CV defects, CNS defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the fetotoxic effects of the mother taking diethylstilboestrol during the first trimester?

A

uterine lesions/ vaginal clear cell adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the fetotoxic effects of the mother taking antiepileptics during the first trimester?

A

facial defects, mental retardation and neural tube defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the fetotoxic effects of the mother taking antiepileptics after the first trimester?

A

mental retardation

autism or aspergers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the fetotoxic effects of the mother taking ACEi?

A

renal dysgenesis

craniofacial abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are the fetotoxic effects of the mother taking alcohol?

A

craniofacial abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are the fetotoxic effects of the mother taking ahminoglycosides?

A

ototoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are the fetotoxic effects of the mother taking carbamazepine?

A

neural tube defects

craniofacial abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are the fetotoxic effects of the mother taking cocaine?

A

preterm labour and IUGR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

whats the best choice of pharmacological management of nausea and vomiting in pregnancy?

A

cyclising or promethazine

36
Q

whats the best choice of pharmacological management of constipation in pregnancy?

A

bulk forming laxatives e.g. isphagula husk

37
Q

whats the best choice of antibiotics to use in pregnancy?

A

penicillins and cephalosporin

38
Q

what are the main medications you should avoid in pregnancy?

A 
ACEi after first trimester
anti epileptic drugs
alcohol
antibiotics - particularly streptomycin, tetracyclines in 3rd trimester and trimethoprim
vitamin A e.g. retinoid acid
warfarin
lithium
39
Q

whats the fetotoxic effect of the mother smoking?

A

preterm labour

IUGR

40
Q

whats the fetotoxic effect of the mother taking sodium valproate?

A

neural tube defects and craniofacual abnormalities

41
Q

when do GHRH levels peak?

A

1 hour after sleep

42
Q

what are some stimuli that increase GHRH release?

A

exercise
hypoglycaema
rising oestrogen and testosterone in puberty

43
Q

what inhibits growth hormone release? I,e. what are the negative feedback loops?

A

increased GH inhibits GHRH release from hypothaamys

when growth hormones reaches tissues, they make somatomedin which signal anterior pituitary to stop making GH

somatomedin and increased GH signal to hypothalamus to produce somatostatin

44
Q

what is the growth hormone inhibiting hormone called?

A

somatostatin

45
Q

where is somatostatin release?

A

hypothalamus and delta cells o the pancreas

46
Q

what are the effects of somatostatin?

A

it blocks GHRH from acting on somatotropin cells on the pituitaru
inhibits insulin, glucagon, vasoactive intestinal peptide and gastrin

47
Q

how does growth hormone directly stimulate growth?

A

promotes lipolysis
promotes gluconeogenes and glycogenolysis
increases insulin resistance n tissues

48
Q

how does GH indirectly stimulate growth?

A

liver/muscles/bones/kidneys release somatomedin C which binds to IGF-1 and insulin receptors to promote cellular metabolism, prevent cell death and increase rate of cell division and differentiation

49
Q

after GnRH is released from the hypothalamus, what does it cause?

A

stimulates gonadotrophic cells in anterior pituitary to release gonadotrophic hormones

50
Q

in intrauterine life, when does GnRH secretion begin?

A

week 4

51
Q

in intrauterine life, when does Lh and FSH secretion begin?

A

weeks 10-12

52
Q

whats higher in childhood… FSH or LH levels?

A

FSH

53
Q

when do pulsatile secretions of GnRH begin?

A

in puberty
10-14 girls
12-16 boys

54
Q

how does GnRH levels change during puberty?

A

released in pulses at night

as puberty develops pulsatile release happens in day too and becomes more frequent

55
Q

how do FSh and LH levels compare in puberty?

A

LH levels higher than FSH

56
Q

which male cells do LH and FSH act on? whats the response?

A

LH acts on leydig cells to cause testosterone release

FSH acts on Sertoli cells to kickstart sperm production

57
Q

which female cells do LH and FSH act on? whats the response?

A

LH acts on theca cells to cause androstenedione production

FSH acts on granulosa cells to convert androstenedione to oestrogen and progesterone

58
Q

why do females get variations in Lh and FSH levels over the menstrual cycles but males dont?

A

males dont have the cyclic centre in the hypothalamus that females do

59
Q
  • Whats the difference between primary/secondary sex characteristics?
A

Primary are those directly involved in reproduction e.g. genitals - penis and vagina. Secondary is pubic hair, breast development, deeping of voice etc

60
Q
  • How do we evaluate sex characteristics?
A

with Tanner stages

61
Q

what are the 2 independent criteria of Tanner stages?

A

Pubic hair

Testis/penis development and Breast development

62
Q

outline the Tanner stages

A

1 - No pubic hair, small testes and flat chest

2- Soft pubic hair, testes growing, breast buds

3 - Pubic hair coarser, penis begins to enlarge, breasts mounds form

4 - Pubic hair covers region, penis widens, breast mounds continue

5 - Pubic hair reaches inner thigh, breast take on adult contour, penis and testes and fully enlarged

63
Q

what is constitutional growth delay?

A

A normal variation of development where there is a temporary delay in growth. Eventually the person will end up their normal adult height

64
Q

what is achondroplasia?

A

An autosomal dominant genetic condition where the primary feature is dwarfism

65
Q

whats the pathophysiology of achondroplasia?

A

heterozygous mutation in FGFR gene on chromosome 4 (codes for FGFR protein) which makes the FGFR gene constituently actve = strong signal to inhibit bone growth

66
Q

what does the FGFR protein do?

A

FGF binds to it and it causes slowed growth of certain bones

67
Q

which bones are typically affected in achondroplasia? what does this mean?

A

endochondrial bone formation is affected the most e.g. humerus - i.e. bones that form from cartilage
this means head and trunk size are largely preserved

68
Q

whats the main risk factor for sporadic achondroplasia and why?

A

increasing paternal age

increased chance for sperm progenitor cells to undergo mutations

69
Q
  • What if a child gets homozygous achondroplasia?
A

They will get an extremely severe form and will not survive the birth or will die very soon after

70
Q

what is acromegaly?

A

A hormonal disorder in adults where there is excess growth hormone which leads to continued growth of extremities = large face, hands and feet

71
Q

what is acromegaly called in children?

A

gigantism

72
Q

whats the main cause of acromegaly?

A

Pituitary adenoma - somatotroph cells produce too much GH

73
Q

what syndrome can acromegaly be associated with?

A

MEN-1 syndrome

74
Q

what health problems can acromegaly cause?

A

Carpal tunnel syndrome, diabetes mellitus, gastrointestinal cancer and congestive heart failure

75
Q

how can acromegaly be treated?

A

Surgical resection of a tumour (or radiotherapy.) Sometimes somatostatin analogues or GH receptor antagonists can be given

76
Q

when is puberty considered delayed?

A

13 in females and 14 in males (when you have not begun development through the tanner scale by the time 95% of your peers have)

77
Q

what is hypogonadism?

A

When you have low levels of sex hormones from low gonad activity which leads to undeveloped sex characteristics

78
Q

what is primary hypogonadism?

A

When the cause is in the gonads themselves and they do not respond to LH and FSH. Or they may not have healthy cells capable of producing hormones
e.g. trauma to gonads or turners syndrome

79
Q

why is primary hypogonadism known as hypergonadotropic hypogonadism?

A

oestrogen and progesterone and testosterone levels are low because of low release from gonads so there is no negative feedback on GnRH release and we get overprudtcion levels of LH and FSH

80
Q

why is primary hypogonadism known as hypogonadotropic hypogonadism?

A

low levels of LH, FSH or GnRH leads to low levels of oestrogen and progesterone

81
Q

what are some causes of secondary hypogonadism?

A

Causes are stress, radiotherapy exposure, trauma, kallmann syndrome, panhypopituitarism, chronic illness, excessive exercise, malnutrition, obesity

82
Q

what is precocious puberty?

A

Puberty which begins before 95% of your peers do. i.e. you begin moving through the tanner stages
In females, this is before 8 and males before 9

83
Q

what is central precocious puberty?

A

Gonadotropin dependant - when hypothalamic-pituitary-gonadal axis is prematurely activated so there is an early rise in LH and FSH which causes an increase in sex hormones e.g GnRH releasing tumour, infection, radiation which imapirs negative feedback. Mostly idiopathic and considered a normal variation

84
Q

what is peripheral precocious puberty?

A

Gonadotropin independent when the issue is with the gonads themselves overproducing sex hormones e.g tumour, cysts, mccune alright syndrome, exogenous sex steroids

85
Q

whats the treatment for precocious puberty?

A

GnRH analogues to suppress LH and FSH please with reduces level of sex hormones and slows puberty
Or surgery to remove tumors

REVISION EXTRAS (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions