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Physiology > Theme C > Flashcards

Theme C Flashcards

1
Q

Describe the metabolic adaptations during pregnancy.

A

Pregnant women have increased insulin synthesis & secretion due to increased beta-cell proliferation & hypertrophy.

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2
Q

What happens to blood volume during pregnancy?

A

It increases, beginning at 6 weeks and peaking at 32 weeks.

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3
Q

What happens to plasma volume during pregnancy?

A

It increases.

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4
Q

What happens to red cell mass during pregnancy?

A

It increases.

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5
Q

What happens to white blood cell concentration during pregnancy?

A

It increases in the first trimester, plateauing in the second and third.

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6
Q

What happens to cardiac output during pregnancy?

A

It increases.

Heart rate increases from 5 weeks and stroke volume increases from 8 weeks.

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7
Q

What happens to blood pressure during pregnancy?

A

It decreases.

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8
Q

What are some of the renal adaptations that take place during pregnancy?

A
  • renal blood flow increases
  • GFR increases
  • kidney size increases by 1 cm
  • water & salt retention increase
  • plasma volume increases
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9
Q

Why don’t the vessels in the blood lakes of the placenta respond to the same stressors that the mother’s vessels will respond to?

A

Blood needs to flow to the foetus unimpeded, but the mother still needs to respond to normal stressors. If the mother is exposed to vasoconstrictors, we don’t want this vasculature to constrict as well.

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10
Q

Describe some of the fetal cardiovascular adaptations.

A
  • lower oxygen saturation
  • higher haemoglobin concentration
  • higher affinity for oxygen
  • umbilical circulation
  • ductus venosus
  • foramen ovale
  • ductus arteriosus
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11
Q

What are the the immediate cardiovascular changes that occur upon birth which form the intact adult cardiovascular system?

A
  • umbilical cord is clamped
  • ductus venosus closes (trigger unknown)
  • foramen ovale closes
  • ductus arteriosus closes
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12
Q

Babies weighing less than ___ are considered low term birth weight.

A

2500 g

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13
Q

When is a baby considered SGA?

A

They are below the 10th percentile for the gestational age.

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14
Q

What is the common feature of babies that are born small?

A

Decreased nutrient delivery across the placenta.

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15
Q

What is fetal programming?

A

Exposure of the fetus to a suboptimal environment causes adaptations that may help it survive in the short term but leads to increased susceptibility of developing some diseases in adulthood.

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16
Q

How can IUGR affect the kidneys?

A

Nephron number is decreased.

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17
Q

How can IUGR affect the heart?

A

Cardiomyocyte number is decreased.

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18
Q

How can IUGR affect vasculature?

A
  • endothelial function decreased
  • increased vessel stiffness
  • predisposition to atherosclerosis
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19
Q

How can IUGR affect the pancreas?

A

Insulin secretion is decreased.

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20
Q

Why is the postnatal growth trajectory important when it comes to cardiovascular disease?

A

Babies that are born small but have accelerated growth & get fatter are at higher risk of developing cardiovascular disease.

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21
Q

How can IUGR affect the HPA axis?

A
  • higher plasma cortisol levels
  • altered mineralocorticoid and glucocorticoid receptors
  • greater HPA axis response to stress
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22
Q

___nucleated cardiomyocytes transition to the mature ___nucleate phenotype in late fetal development and around birth.

A

Mono; bi.

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23
Q

How does the critical period for cardiomyocyte development differ from humans in rats?

A

It continues postnatally.

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24
Q

What happened to the heart in hypoxic chicks?

A
  • larger left ventricular lumen
  • thinner left ventricular wall
  • dilated cardiomyopathy
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25
Q

What happened to the cardiomyocytes in IUGR sheep?

A
  • decreased relative heart weight

- less binucleate cardiomyocytes (suggesting retarded maturation)

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26
Q

What are the results of uteroplacental inefficiency and how do they affect the fetus in later life?

A
  • small offspring
  • altered maternal endocrine environment (decreased progesterone)
  • impaired mammary development
  • triggers early lactogenesis
  • decreased milk quality & quantity during lactation

Impaired lactational nutrition compromises post-natal growth and has consequences for adult disease development.

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27
Q

Early accelerated growth is ___.

Late accelerated growth is ___.

A

Protective against disease; detrimental.

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28
Q

What happens if you cross-foster restricted males onto control mothers?

A

Post-natal body weight is improved due to early accelerated growth.

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29
Q

What happens to restricted pups suckled by restricted mothers? How can this be reversed?

A
  • cardiomyocyte number decreased
  • hypertension

These are restored when the pups are suckled by control mothers.

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30
Q

Name the three pairs of excretory organs that form during development and when they develop.

A
  • pronephroi (21-22 days then regresses)
  • mesonephroi (begins at 25 days then regresses)
  • metanephroi (permanent kidney)
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31
Q

From which structures does the metanephros form?

A

The ureteric buds.

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32
Q

From which portion of the nephric duct does the metanephros form?

A

The distal portion.

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33
Q

Is the kidney essential for fetal survival?

A

No.

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34
Q

Describe the process of branching morphogenesis.

A
  • outgrowth of ureteric bud at caudal end of Wolffian duct at day 30
  • ureteric bud invades metanephric mesenchyme
  • reciprocal induction occurs between ureteric bud & metanephric mesenchyme
  • ureteric tree forms collecting duct, calyces & renal pelvis
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35
Q

Describe the process of nephrogenesis.

A
  1. The ureteric bud induces metanephric mesenchyme to condense & form a cap, which turns into the pretubular aggregate.
  2. The pretubular aggregate undergoes metanephros, forming the renal vesicle.
  3. The vesicle undergoes morphological changes and becomes comma shaped, then S-shaped.
  4. The upper portion of the S becomes the distal convoluted tubule.
  5. The central portion becomes the proximal tubule, the loop of Henle & the distal straight tubule.
  6. The lower portion becomes the renal corpuscle.
36
Q

Which structure arises from the upper portion of the S-shaped renal vesicle?

A

The distal convoluted tubule.

37
Q

Which structures arise from the central portion of the S-shaped renal vesicle?

A

The proximal tubule, the loop of Henle & the distal straight tubule.

38
Q

Which structure arises from the lower portion of the S-shaped renal vesicle?

A

The renal corpuscle.

39
Q

What are the consequences of bilateral renal agenesis?

A

An absence of kidneys leads to low amniotic fluid and gross abnormalities. You won’t die from a lack of kidneys as they are not vital in the fetus, but you will die from lung issues.

40
Q

What happens when Wnt4/Wnt9b are “knocked out” and what do the results imply?

A

When these genes are knocked out, there is a significant reduction in branching, so they must be important for this process.

41
Q

Where is GDNF expressed?

A

The intermediate mesoderm.

42
Q

What are the consequences of a double knockout of GDNF?

A

Bilateral renal agenesis or small, disorganised rudimentary kidneys.

43
Q

What are the consequences of GDNF +/-?

A

30% reduction in nephrons.

44
Q

What is the function of bone morphogenetic proteins (BMPs)?

A

They are important for the growth of the ureteric bud and branching morphogenesis.

45
Q

Can any new nephrons be formed after nephrogenesis?

A

No.

46
Q

What are some of the renal consequences for adults who are born small?

A
  • decreased perinatal nephron endowment
  • increased glomerular volume (hyperfiltration)
  • increased concentrations in RAS system
  • increased risk of kidney disease
47
Q

Describe what happens during albuminiria.

A

Structural changes to the glomerulus allow larger proteins to enter. The proximal tubule is unable to cope with the increased load and becomes dysfunctional.

48
Q

Describe some of the renal consequences in rats who were born small.

A
  • immature glomeruli
  • decreased nephron number
  • increased glomerular volume (males at 6M, females at 18M)

MALE ONLY:

  • dysregulated RAS
  • kidney disease
  • hypertension
49
Q

What is the primary role of leptin?

A

Appetite suppression & increased energy expenditure.

50
Q

What happens to leptin in growth restricted babies?

A
  • leptin transporter expression is dysregulated
  • reduced leptin concentration
  • reduced post-natal leptin surge
51
Q

What happened to IUGR piglets who were administered leptin from birth to Day 5?

A
  • accelerated growth
  • increased organ weight
  • improved immune function
  • NO CHANGE in glomerular number
52
Q

What happens to the leptin of mothers who suckled restricted pups?

A

They have more leptin but no change in milk leptin concentration.

53
Q

What are the consequences of cross-fostering a restricted pup onto a control mother in terms of leptin?

A

Plasma leptin concentration is restored.

54
Q

Is leptin likely to control nephrogenesis?

A

No.

55
Q

Describe the pathway of the Brenner Hypothesis.

A

Prematurity & low birth weight > reduced nephron number > hyperfiltration & glomerular hypertension > systemic hypertension & proteinuria > nephron loss & glomerulosclerosis > chronic kidney disease.

56
Q

Describe the pathway from diabetes to cardiovascular disease.

A

Diabetes > elevated blood glucose > endothelial damage > weakened blood vessels > cardiovascular disease.

57
Q

Describe the normal glucose homeostasis process.

A

Increased blood glucose > increased insulin secretion > glucose utilisation > decreased blood glucose.

There is a negative feedback loop which decreased insulin secretion as blood glucose levels decrease.

58
Q

Describe the impaired glucose homeostasis process.

A

Increased blood glucose > impaired insulin secretion > impaired glucose utilisation (body not responding to insulin) > glucose levels remain elevated > no negative feedback loop.

59
Q

What is the difference between insulin resistance and insulin sensitivity?

A

Insulin resistance: body does not respond to insulin signals.

Insulin sensitivity: to what degree does the body respond to insulin signals?

60
Q

How is IUGR associated with insulin?

A

It is associated with increased insulin resistance.

61
Q

Why does diabetes emerge with advanced age in IUGR individuals?

A

The pancreas compensates during childhood by secreting more insulin to maintain blood glucose.

62
Q

Describe the insulin resistant concept.

A

Pancreatic beta-cells increase insulin secretion in response to a decline in insulin sensitivity until a point of beta-cell exhaustion, leading to increased apoptosis & decreased insulin secretion.

63
Q

Describe the beta-cell apoptosis concept.

A

Pancreatic beta-cell mass is decreased from increased apoptosis due to exhaustion.

64
Q

Describe the islet malformation concept.

A

Beta-cells are found in the pancreatic islet. With islet malformation, there is an intrinsic beta-cell deficit. The impaired development limits insulin secretion upon age-related increases in insulin resistance.

65
Q

What does the second hit of pregnancy unmask in growth restricted female rats?

A

A susceptibility to impaired glucose tolerance.

66
Q

What happened to IUGR rats after 4 weeks of exercise in terms of beta cell mass?

A

It was restored.

67
Q

What kind of placenta do horses and pigs have?

A
  • diffuse
  • epitheliochorial
  • no pooling of maternal blood
68
Q

What kind of placenta do ruminants have?

A
  • cotyledonary
  • epitheliochorial
  • individual placentomes
69
Q

What kind of placenta do carnivores have?

A
  • zonary

- endotheliochorial

70
Q

What kind of placenta do humans, apes, monkeys & rodents have?

A
  • discoid

- hemochorial

71
Q

What kind of placenta do marsupials have?

A
  • choriovitelline

- blastocyst lies in endometrium depression but does not embed

72
Q

Describe what is meant by optimal placental weight.

A

For every fetal weight, there is an optimal placenta weight.

Large placenta + a small baby = inefficient.
Small placenta + a big baby = poorly developed.

73
Q

What is the placenta’s function?

A
  • nutrient transport
  • endocrine function
  • immune function
  • barrier
74
Q

What kind of hormones does the placenta secrete?

A
  • growth hormones (regulation of insulin levels)
  • progesterone
  • leptin
75
Q

How does the placenta aid immune function?

A

The placenta must modulate the maternal immune system to prevent rejection. It secretes Neurokinin B, which parasites use to evade the immune system.

76
Q

How does the placenta act as a glucocorticoid barrier?

A

There is a gradient of glucocorticoids from the mother to the fetus, with higher levels in the mother. 11HSD beta-2 converts glucocorticoids from their active form into their inactive form, protecting the fetus from excess maternal glucocorticoids.

77
Q

Define placenta accreta, increta & percreta.

A

Placenta accreta: partial invasion of the myometrium
Placenta increta: penetrates myometrium but not uterine serosa
Placenta percreta: penetrates myometrium AND uterine serosa

78
Q

What is placental abruption?

A

Detachment of the placenta from the uterine wall.

79
Q

What is placenta praevia? How would it affect the birth?

A

The placenta blocks the cervix. The mother would have to get a C-section.

80
Q

Explain the concept of placental efficiency. How is it calculated?

A

Placental efficiency is calculated by fetal weight/placental weight x 100.

Small baby + big placenta = inefficient, as it has to grow in size to meet fetal demands = low ratio.

Big baby + small placenta = very efficient, however may be poorly developed = high ratio.

81
Q

How is placental ratio related to risk of health conditions in the future?

A

Both low & high placental ratios are associated with cardiovascular disease IN MEN.

A high placental ratio is associated with increased blood pressure, increased cardiovascular disease and increased glucose intolerance in BOTH GENDERS.

82
Q

Are sex-specific differences confounded by obesity?

A

No.

83
Q

What does soluble FLT-1 do?

A

It mops up any VEGF (which promotes healthy vessels) in the maternal circulation.

84
Q

What is the difference between multigenerational and transgenerational programming?

A

Multigenerational programming is when the offspring are directly impacted by the initial insult.

Transgenerational programming is the study of the first generation that is NOT exposed to the initial insult.

85
Q

What effect does F1 maternal & paternal growth restriction have on their F2 children?

A

Increased risk of low birth weight.

Physiology (1 decks)

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