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PHASE 1 OWN STUFF > SUGER > Flashcards

SUGER Flashcards

1
Q

what is the renal corpuscle made of?

A

the glomerular tuft and Bowman’s capsule

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2
Q

what are some of the functions of the renal corpuscle?

A
  • structural support for capillary
  • production of extracellular matrix protein
  • contraction; regulates flow and filtration, Tubuloglomerular feedback
  • phagocytosis of breakdown products
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3
Q

what is the total glomerular surface area?

A

1m^2

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4
Q

what is the charge of the membrane of the kidney?

A

it is negatively charged

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5
Q

what are some of the features of the glomerulus?

A

formed of 3 layers:

  • has endothelial cells - these are fenestrated
  • has a basement membrane - it is the fusion of two basement membranes (that of capillary and podocyte) and is negatively charged
  • podocytes are present
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6
Q

what are the two mechanisms of autoregulation of glomerular perfusion?

A

myogenic

tubuloglomerular constriction

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7
Q

what happens during myogenic auto regulation of glomerular perfusion?

A

smooth muscle contracts in response to an external stretching force
this occurs in capillary walls and is a passive mechanism

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8
Q

what happens during tubuloglomerular feedback in terms of auto-regulation?

A

afferent arterioles constrict in order to increase sodium chloride concentration.
they dilate in response to decreased concentration
this response is fast via GFR but slow via RAAS

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9
Q

what happens during tubuloglomerular feedback?

A
  1. blood regulates itself through the detection of Na+
  2. macula dense cells detect Na+ concentration levels through the NKCC2 transporter
  3. signals go through adenosine and nitric oxide to the walls of the arterioles
  4. the afferent arterioles are effected greater than the efferent
  5. if flow rate is high then constriction of the afferent arteriole causes GFR to fall
  6. if flow rate is low then the dilation of the afferent arteriole causes GFR to rise
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10
Q

how is blood flow rate controlled in the glomerulus?

A
  • there is neural and hormonal input to afferent and efferent arterioles which cause changes in net glomerular filtration pressure
  • glomerular capillaries are unique and they sit between two sets of arterioles
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11
Q

how do you increase GFR?

A
  • constrict efferent arteriole (build up pressure before)

- dilate the afferent arteriole (build up pressure after)

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12
Q

how do you decrease GFR?

A
  • constrict the afferent arteriole (reduce blood flow)

- dilate the efferent arteriole (allows blood to escape easier)

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13
Q

what is GFR?

A

the glomerular filtration rate

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14
Q

what is glomerular filtration?

A

the passage of fluid from the blood into the Bowman’s space

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15
Q

what determines GFR?

A
  • pressure gradients
  • size of the molecule
  • charge of the molecule
  • rate of blood flow
  • surface area; directly proportional to membrane permeability and surface area
  • binding to plasma proteins
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16
Q

what does the normal GFR equal?

A

125ml/min

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17
Q

what substance is used to measure GFR?

A

marker substance, M which is creatinine

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18
Q

why is creatinine used as the marker substance for GFR?

A

it is used as it is freely filtered by the glomerulus, is not secreted or absorbed in tubules and is not metabolised
it is also constantly produced as a muscle metabolite which means amount depends on muscle mass

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19
Q

what is constant across the length of the glomerular capillary?

A

hydrostatic pressure

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20
Q

what are some of the functions of the kidney?

A
  1. regulation of water, ions and acid-base balance
  2. removal of metabolic waste products and foreign chemicals from blood and excretion in urine
  3. gluconeogenesis
  4. production of enzymes/hormones:
    - EPO
    - renin
    - active vitamin D
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21
Q

what is oogenesis?

A

the growth + differentiation process in which an oogonia becomes a mature ovum

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22
Q

what are oogonia homologous with?

A

spermatogonia

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23
Q

at what point in fetal development do fetal oogonia stop dividing?

A

at around the 7th month of gestation

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24
Q

in fetal life, what do all oogonia differentiate into?

A

primary oocytes

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25
Q

describe (in brief) the stages of differentiation from an oocyte to an ovum

A
  1. primary oocytes undergo meiosis 1 in utero
  2. meiosis 1 is arrested at metaphase 1 until puberty
  3. resumption occurs after puberty and meiosis 1 is complete just before ovulation
  4. in this division, one of the two daughter cells (the secondary oocyte) retains nearly all of the cytoplasm, and the other daughter cell is the first polar body and is very small + non-functional
  5. meiosis 2 then occurs by which the secondary oocyte develops into the ovum
  6. meiosis 2 is arrested at metaphase 2 until fertilisation
  7. it is only completed in the Fallopian tube after fertilisation
  8. one daughter cell, called the ovum retains all the cytoplasm - the other becomes the second polar body
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26
Q

what is the net result of oogenesis?

A

the production of one ovum from one primary oocyte

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27
Q

where are spermatozoa produced?

A

in the testis

28
Q

what are male undifferentiated germ cells called?

A

spermatogonia

29
Q

when do spermatogonia begin to mitotically divide?

A

at puberty

30
Q

what types of daughter cells do spermatogonia produce when they divide?

A

two types - type A and type B

31
Q

what are type A spermatogonia daughter cells?

A

cells that remain outside of the blood-testis barrier and produce more daughter cells until death

32
Q

what are type B spermatogonia daughter cells?

A

cells that differentiate into primary spermatocytes (this occurs entirely in the basal compartment)

33
Q

how do primary spermatocytes pass through the blood testis barrier?

A

they pass through the tight junctions of Sertoli cells

34
Q

what happens during meiosis 1 of type B spermatogonia cells?

A

they undergo meiosis 1 to produce 2 secondary spermatocytes

35
Q

what happens to the secondary spermatocytes?

A

they undergo meiosis 2 and differentiate into 4 spermatids

36
Q

what happens to spermatids?

A

they differentiate into spermatozoa
(grow a tail + discard cytoplasm to become lighter). this occurs while they are contained in recesses formed by the invaginations of the Sertoli cell plasma membranes

37
Q

define spermiogenesis

A

the transformation of spermatids into spermatazoa

38
Q

what happens when sperm formation is complete?

A

the cytoplasm of the Sertoli cells around the sperm retracts and the sperm are released in the lumen to be bathed in luminal fluid

39
Q

what are the three main differences between spermatogenesis and oogenesis?

A
  • 1 spermatocyte becomes 4 spermatozoa whereas 1 oocyte becomes 1 ovum
  • both maturations occur in testsis for spermatogenesis, whereas one occurs in the ovaries and one occurs in the Fallopian tube after fertilisation
  • spermatogenesis is a continuous process whereas oogenesis is a disjointed process
40
Q

what is the difference between spermiogenesis and spermatogenesis?

A 
spermiogenesis = the transformation of spermatids to spermatozoa 
spermatogenesis = the transformation of spermatogonia to spermatids
41
Q

what is included in the HPG axis?

A

the hypothalamus, pituitary gland and gonads

42
Q

what are Gonadotrophins?

A

the hormones produced to control the reproductive system

LH + FSH are gonadotrophins

43
Q

what hormones are involved in the HPG axis?

A
  • gonadotrophin-releasing hormone (GnRH) - secreted from the hypothalamus
  • LH
  • FSH
  • oestrogen
  • testosterone
44
Q

what are the stages of the male HPG axis?

A
  1. GnRH is released by the hypothalamus
  2. GnRH travels to the anterior pituitary gland where it binds to receptors
  3. LH and FSH are released by the anterior pituitary and travel to the testes
  4. FSH acts primarily on Sertoli cells to stimulate the secretion of paracrine agents required to initiate spermatogenesis
  5. LH acts primarily on Leydig cells to stimulate testosterone secretion
  6. testosterone acts to reduce amount of GnRH released from the hypothalamus and also reduces the amount of LH released from the anterior pituitary gland
  7. Sertoli cells release inhibin which acts on the anterior pituitary to inhibit the release of FSH
45
Q

what are the stages of the female HPG axis?

A
  1. hypothalamus secretes GnRH
  2. GnRH travels down to the anterior pituitary gland where it binds to receptors
  3. this promotes the release of LH and FSH
  4. LH and FSH travel in the bloodstream to the ovaries
  5. when LH and FSH bind to the ovaries, they stimulate the production of oestrogen and inhibin
  6. increasing levels of oestrogen and inhibin have a negative feedback effect on the anterior pituitary and hypothalamus
  7. this leads to decreased production of GnRH, LH and FSH
  8. this in turn results in decreased production of oestrogen and inhibin
46
Q

what is the menopause?

A

the cessation of menstruation, usually occurring between 48-52 years, when the ovaries stop releasing eggs

47
Q

what is the mechanism by which the menopause occurs?

A
  1. there is depletion of primordial follicles at roughly 40 years old
  2. there isa decrease in follicular oestrogen production
  3. there is a gradual increase in FSH and LH (due to lack of negative feedback provided by oestrogen)
  4. the decline in inhibin results in a further increase in FSH
  5. increase in FSH results in the rapid increase in oestrogen secretion from existing follicles
  6. this leads to shorter menstrual cycles
  7. as fewer follicles remain, the increase in FSH no longer stimulates the increase in oestrogen
    8, the decrease in oestrogen and lack of ova results in the menopause
48
Q

what are some of the short term signs of the menopause?

A
  • hot flushes, sweats, palpitations, headaches
  • irritability, lethargy, panic attacks + depression
  • shorter menstrual cycle
  • altered blood loss
  • skin dryness
49
Q

what are some of the long term signs of the menopause?

A
  • vaginal dryness
  • decreased libido
  • hair loss/thinning
  • diminished urethral seal + loss in compliance
  • general aches and pains
  • increased risk of osteoporosis
50
Q

what are the two phases of the menstrual cycle?

A

follicular phase
luteal phase
these are separated by ovulation

51
Q

when during the menstrual cycle are FSH levels high?

A

at the start of the follicular phase

52
Q

when are levels of oestrogen high in the menstrual cycle

A

during the follicular phase - specifically when the first follicle has fully matured

53
Q

what is the impact of high levels of oestrogen on the follicular phase of menstruation

A
  • initially it inhibits the growth of other competing follicles
  • increasing amounts of circulating oestrogen then cause:
  • -> endometrial thickening
  • -> thinning of the cervical mucus (to allow easier passage of sperm)
  • -> inhibition of LH production by the pituitary gland
54
Q

when is LH produced?

A

when oestrogen levels in the follicular phase surpass the threshold levels

55
Q

when is the secondary oocyte released?

A

when the Graafian follicle ruptures, following high levels of LH

56
Q

what takes the ovum into the Fallopian tube?

A

the fimbriae

57
Q

what is the first stage of the luteal phase?

A

the development of the corpus luteum from the Graafian follicle due to LH + FSH

58
Q

what does the corpus luteum produce?

A

progesterone

59
Q

what do increased levels of progesterone result in?

A
  • the endometrium becoming receptive to implantation of the blastocyst
  • negative feedback causing decreased FSH and LH
  • increase in woman’s body temperature
60
Q

when does the corpus luteum degenerate?

A

when levels of LH + FSH in the luteal phase fall

61
Q

what stimulates stretch receptors in the bladder wall?

A

increasing pressure in the bladder due to filling with urine

62
Q

what are the stages of micturition?

A
  1. stretch receptors are stimulated in bladder wall
  2. afferent neurones of these receptors enter spinal cord + stimulate parasympathetic neurones (pelvic splanchnic nerve S2-S4)
  3. these cause the detrusor muscles to contract
  4. when the detrusor muscle contracts, the change in bladder shape pulls the internal urethral sphincter open
  5. the afferent input from the stretch receptors reflexively inhibits the sympathetic neurones (hypogastric nerve T12-L2) to the internal urethral sphincter which further contributes to the opening
  6. the afferent input also inhibits the somatic motor neurones (pudendal nerve S2-S4) to the external urethral sphincter, causing it to relax
  7. this activity results in the opening of both of the sphincters, and the contraction of the detrusor muscles is then able to produce urination
63
Q

what is the sympathetic supply to the bladder?

A 
hypogastric nerve (T12-L2)
causes relaxation of the detrusor muscle, promoting urine retention
64
Q

what is the parasympathetic supply to the bladder?

A

pelvic splanchnic nerve (S2-S4)

increased signals from this nerve causes contraction of the detrusor muscles - therefore stimulating micturition

65
Q

what is the somatic supply to the bladder?

A

via pudendal nerve (S2-S4)

gives voluntary control over micturition - can cause external urethral sphincter to contract or relax

66
Q

what is the sensory (afferent) supply to the bladder?

A

nerves that are located in the bladder wall and signal (to the brain) the need to urinate when the bladder becomes full

PHASE 1 OWN STUFF (7 decks)

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