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Endocrinology Flashcards

1
Q

What are hormone plasma carriers?

A

A reservoir of inactive hormone, providing hormone reserve. Don’t degrade or get uptaken and thus allow smooth fluctuations in hormones over time. Only the free hormone contributes to feedback and is biologically active

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2
Q

Which type of hormones are transported freely in plasma?

A

Catecholamines
Steroid hormones are hydrophobic-bound to steroid binding protein. Only small amounts of free hormone dissolved in plasma

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3
Q

Which receptors do hydrophilic or hydrophobic hormones bind to?

A

Hydrophilic-cell surface receptors

Hydrophobic-nuclear receptors

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4
Q

What are the main functions of the hypothalamus?

A

Temperature regulation (anterior hot, posterior, cold)

Neuroendocrine function: Catecholamines, ADH, oxyocin, TSH, ACTH, FSH, LH, prolactin, growth hormone

Appetite behaviours Thirst, hunger and sex

Defensive reactions: fear and rage

Control of body rhythms

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5
Q

How does the hypothalamus sense the thirst response?

A

Hypertonicity via osmoreceptors. Hypovolemia sensed by baroreceptors releases angiotension II.
Both of which act on hypothalamus to produce thirst.
Thirst may occur without decreased osmolality due to haemorrhage

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6
Q

What is released in the posterior pituitary?

A

Oxytocin
ADH (vasopressin)
Both PRODUCED in posterior pituitary but also exist in neurones
Both not bound in plasma

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7
Q

What are the key actions of oxytocin?

A

Contraction of myoepithelial cells allowing milk expression
Smooth muscle contraction of uterus
Inhibited by progesterone
Increased number of oxytocin receptors in uterus rather than increased oxytocin levels in labour

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8
Q

Which hormones are secreted by the anterior pituitary?

A

ACTH: aldosterone +sex hormones
GH: somatomedins. Produces a fall in blood urea nitrogen
TSH: thyroxine
FSH: growth of ovarian follicle/maintenance of corpus luteam/ testes
LH: growth of ovarian follicle/maintenance of corpus luteam/ testes. Acts on theca internal cells.
Prolactin: breast milk

No nerves involved in anterior pituitary

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9
Q

Why do dopaminergic drugs cause breast development?

A

Prolactin is under constant inhibition by hypothalamus via dopamine, reducing inhibition causes secretion

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10
Q

Why do patients with Addison’s disease/primary adrenal insufficiency get tanned?

A

ACTH binds to melanotropin, acts as MSH (melanocyte stimulating hormone). With adrenal insufficiency there increased release of ACTH

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11
Q

What are the actions of growth hormone?

A

A proportion of GH is protein bound in plasma

Decreased insulin sensitivity

Na+ retention

Lipolysis

Erythropoesis

Protein synthesis

Epiphysial growth (mitosis)

Does not affect carbohydrate utilization. Does not stimulate pancreatic B cells to release insulin, just increases ability of pancreas to respond to insulinogenic stimuli. Can produce ketosis in excessive amounts

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12
Q

Which stimuli increase/decrease GH release

A

Hypgylcemia, exercise, fasting, going to sleep, protein meal, stressful stimuli, L-dopa, estrogens and androgens, glucagon all increase GH release

REM sleep, glucose, cortisol, GH and IGF-1 all decrease GH release

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13
Q

What are the effects of hypopituitarism?

A

Decreases activity of other endocrine glands
Increased insulin sensitivity
Diabetes insipidus: increased osmotic load due to ACTH deficiency, TSH deficiency causes low metabolic rate and GH deficiency causes depression of glomerular filtration rate
Glucocorticoid deficiency

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14
Q

How does the histology of the thyroid change when it is active vs inactive?

A

Inactive: colloid( glycoprotein and thyroglobulin) abundant, follicles are very small cubiod cells
Active: Follicles columnar and larger with much smaller areas of colloid with reabsorption lacunae

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15
Q

What is the difference between T4 and T3?

A

T4: primary hormone secreted
T3: greater activity, generated at sites of action by peripheral tissues by deiodination
Iodine required to make thyroid hormones. Taken up by the thyroid across basement membrane by Na/I symporter and across apical membrane by Cl/I exchanger

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16
Q

How does colloid serve as a reservoir for thyroid hormone?

A

Thryocytes make thryoglobulin. Thryoid hormones produced are bound to thyroglobulin until required to be released as T3 and T4

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17
Q

What are the functions of thyrocytes?

A
  1. Collect and transport iodine
  2. Synthesis thryoglobulin and endocytosis into colloid
  3. Fix iodine to thyroglobulin and generate thyroid hormones
  4. Remove thyroid hormones from thyroglobulin and secrete them into the circulation
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18
Q

How do thyroid hormones travel in plasma?

A

Protein bound as lipophilic

Free forms in plasma are in equilibrium with protein bound hormones

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19
Q

Which proteins bind to thyroid hormones?

A

TBG: highest affinity but smallest capacity. Raised in pregnancy
Transthyretin
Albumin: greatest binding capacity

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20
Q

How do hyperthyroidism, hypothyroidism, estrogens and glucocorticoids/androgens affect thyroid levels?

A

Hyperthyroid: binding N total plasma H free plasma H

Hypothyroid: binding N total plasma L free plama L

Estrogens/heroin: binding H total plasma H free plasma L

Glucocorticoids/androgens: binding L total plasma L free plasma N

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21
Q

Which tissues do thyroid hormones NOT increase O2 consumption in?

A 
Brain
Testes
Uterus
Spleen
Lymph nodes
Anterior pituitary
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22
Q

Why does hyperthyroidism lead to increased urine K+ and uric acid secretion?

A

Catabolism of endogenous protein and fat stores without increased food intake. Also causes low circulating cholesterol

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23
Q

How does hyperthyroidism affect the kidneys?

A

Raised body temperature-> cutaneous dilation-> decreased peripheral resistance-> increased reabsorption of Na and H20
Affect erythropotein

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24
Q

How do increased thyroid hormones affect the heart?

A

Increased cardiac output
Increased heart rate
Increased contractility and pulse pressure

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25
Q

How does hyperthyroidism affect the CNS?

A

Rapid mentation
Irritability
Restlessness
Shortens stretch reflexes

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26
Q

How does hyperthyroidism affect the GI tract?

A

Increased absorption of carbohydrates

Plasma glucose increases rapidly after a meal then decreases rapidly again

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27
Q

Why do beta blockers work in thyrotoxicosis?

A

Thyroid hormones have a similar action to catecholamines

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28
Q

What are the 3 layers of the adrenal cortex and what do they excrete?

A

From outside to inside, salt, sugar sex

zona glomerulosa: Aldosterone

Zona fasciulata: Glucocorticoids/ cortisol

Zona reticularis: Androgens

All made from cholesterol

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29
Q

What does the adrenal medulla excrete?

A

Adrenaline, noradrendaline and dopamine
Both made from tyrosine
Secretion initiated by ACh

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30
Q

What are the affects of catecholamines?

A

Glycogenolysis in liver and skeletal muscle
Mobilisation of free fatty acids
Increased plasma lactate
Stimulation of metabolic rate
Increased cardiac contractility and heart rate, increased excitability

NA: vasoconstriction (a1), HTN, stimulating baroreceptors producing rflex bradycardia, decreasing CO and increasing TPR=normal pulse pressure

A: Vasodilation in skeletal muscle and liver (b1). Usually overbalances constriction affect of NA and decreases TPR

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31
Q

What causes adrenal hyperplasia?

A

Any enzyme deficiency in adrenal system

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32
Q

What happens in cholesterol desmolase deficiency?

A

Adrenal hyperplasia

Female genitalia regardless of sex

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33
Q

What happens in 3bhydoxysteroid dehydrogenase deficiency?

A

Increased DHEA

Not sufficient to cause masculisation in females but hypospadias in males

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34
Q

What happens in 17a-hydoxylase deficiency?

A

No sex hormones
Female external genitalia
elevated corticosterone and aldosterone thus HTN & hypokalaemia

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35
Q

What happens in 21b-hydoxylase deficiency?

A

Decreased cortisol and aldosterone

Virilisation due to androgens

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36
Q

What happens in 11b-hydoxylase deficiency?

A

Virilisation and salt retention

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37
Q

How are glucocorticoids bound in plasma and when to the inhibit the pituitary?

A

Bound to CBG in plasma

Only free cortisol inhibits anterior pituitary

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38
Q

Who is adrenal estrogen most important for?

A

Men and postmenopausal women

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39
Q

What are the affects of gluccocorticoids (cortisol)?

A

Increased protein catabolism, hepatic glycogenesis and gluconeogenesis
Raises plasma glucose
Allows for vascular smooth activity
Decreases lymphocyte, eosinophil and basophil count, increases neutrophils, platelets and RBC
Low GCs causes irritability, apprehension, defective water excretion

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40
Q

What are the signs of cushing syndrome?

A 
Protein catabolism
Thick skin and hair
Poor muscle
Poor wound healing
Acne
Hirsituism
Fat redistribution 
Striae
HTN
DM
Osteoporosis
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41
Q

What do mineralocorticoids/aldosterone do?

A

Increases reabsorption of sodium from urine, sweat, saliva and colon thus retention of Na in ECF

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42
Q

What are some conditions that increase aldosterone secretion?

A 
Surgery
Anxiety
Trauma
Haemorrhage
(All have increased glucocorticoid secretion as well)
High K+ intake
Low Na+ intake
Constrictin of inferior vena cava in thorax
Standing
Secondary hyperaldosetonism (HF, CKD)
(Glucocorticoid secretion unaffected)
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43
Q

What are the key elements involved in changing dehydrocholesterol into calcium?

A

Sunlight
Liver
Kidney
Cholesterol is converted into Vitamin D by sunlight. Vitamin D increases calcium and phosphate uptake from the GIT. High calcium inhibits renaal 1a-hydroxylase so less 1,25-DHC is produced

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44
Q

Describe the parathyroid hormone and calcium feedback loop?

A

Plasma calcium drops
Increased PTH secretion
Acts to increase Ca reabsorption in kidney and bone plus increase 1.25-DHC formation in kidney
Decreases urinary excretion of Ca (increased phosphate excretion)
Increased release of calcium into plasma
High circulating Ca and 1,25-DHC decrease PTH

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45
Q

Where is PTH produced?

A

Chief cells of parathyroid gland

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46
Q

What is renal hyperparathyroidism?

A

Hypocalcemia due to inability of kidneys to produce 1,25-DHC

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47
Q

Where is calcitonin produced and what are its actions?

A

Produced by parafollicular (c-cells) of thyroid
Lowers circulating Ca and Po4 levels
Lowers Ca by inhibiting bone resorption

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48
Q

What affect does cortisol have on the stomach?

A

Increases HCL secretion and pepsin

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49
Q

Why is the adrenal medulla considered a modified sympathetic ganglion?

A

Receives preganglionic input

Embryologically arises from same origin as sympathetic nerve

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50
Q

What are the key effects of adrenaline?

A 
Increased glyconeogenesis from liver and muscle
Mobilise FFA from adipocytes
Increase BMR
Increase pulse pressure
No effect on protein synthesis
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51
Q

What is the physiological response to activation of adrenergic nervous system?

A
  1. Increase circulating renin levels
  2. arteriolar coronary dilation
  3. hepatic glycogenolysis
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52
Q

Where are alpha adrenergic receptors found?

A

Intestinal smooth muscle
Cutaneous vascular smooth muscle
Pupils
Sweat glands

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53
Q

What are the effects of a B2 antagonist?

A

Bronchoconstriction
Coronary constriction
Peripheral vasoconstriction
Bradycardia

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54
Q

Why are alpha adrenergic blockers used in refractory shock?

A

Increase renal blood flow

Prevent imbalance between pre capillary and venular tone

55
Q

What is the effect of injected dopamine?

A

Renal vasodilation
Inotropic affect on heart via B1 receptors
General vasoconstriction, hence net increase in total peripheral resistance
Decrease appetite via dopaminergic receptors
NO effect on prolactin

56
Q

Why does the thyroid enlarge in pregnancy?

A

HCG looks similar to TSH in structure

57
Q

How is iodine utilised by the thyroid?

A

Essential for making thyroid hormone
About 80 micrograms enters thyroid per day by active transport via NIS symporter and pendrin
Most of the iodine ingested is just excreted by the kidneys

58
Q

How does thyroid affect growth?

A

Essential for bone growth and epiphyseal closure

59
Q

Where is most calcium in the body?

A

99% in the bone
Some readily exchangeable
Most is slowly exchanged by bone resorption and absorption

60
Q

What facilitates absorption of calcium?

A

1,25 dihydroxycholecalciferol

61
Q

How is calcium filtered by the kidney?

A

99% reabsorbed
60% in proximal tubule
PTH acts at distal tubules to reabsorb calcium

62
Q

Which hormones affect calcium levels in the blood?

A

1, 25 dihydoxycholecalciferol: increases calcium absorption from intestine
PTH: from parathyroid gland, releases Calcium from bones and increases phosphate excretion in urine
Calcitonin: decreases osteoclasts and decreases calcium levels

63
Q

How does pH affect calcium?

A

High pH-> plasma proteins more ionised->easier for Ca+ to bind-> worse hypocalcemia
ie. patient with tetany hyperventilates, becomes more alkalotic, worsens tetany

64
Q

What are the key actions of phosphorus?

A

Used in ATP cAMP
Absorbed in the duodenum and small intestine by active transport and passive diffusion
85-90% reabsorbed in the kidney

65
Q

What are the 2 types of bone?

A

Cortical bone: 80% of all bone, outer layer, haversian canals
Spongey bone: 20%, nutrition via diffusion

66
Q

What are the 2 ways bones form?

A

Chondral ossification; cartilage first, then bone

Membranous ossification; tissue first, then bone

67
Q

Which hormones affect the width of the epiphyseal plate between epiphysis and diaphysis?

A

GH
IGF-1
Bone continues to grow as long as the plate does not fuse with the shaft (cartilage cells proliferate, release VEG-F-> causes ossification)

68
Q

What are the haematological origins of osteoclasts and osteoblasts?

A

Osteoblast: from fibroblasts, lays down bone
Osteoclast: from monocytes, eats away bone

69
Q

How much of the adult skeleton is remodelled?

A

18% per year

70
Q

Why does menopause cause osteoporosis?

A

Estrogen increases production of TGF-B-> apoptosis of osteoclast
Estrogen decreases production of TNF-A->osteoclasts break down bone

Low estrogen->hormones act unopposed-> osteoclasts get out of control->osteoporosis

71
Q

What are the key actions of calcitriol/vit D?

A

Increase Ca-H ATPase -> Increase calcium and phosphate reabsorption
Via intestinal cells and kidney
Decreases pTH secretion

72
Q

Factors that increase 1,25 dihydoxycholecalciferol

A 
PTH
Low calcium
prolactin
growth hormone
calcitonin
73
Q

What increases release of PTH?

A 
Low levels of calcium
Low Mg
cAMP
High phosphate
Chronic renal disease
74
Q

What are the actions of PTH?

A

Mobilise calcium
Increase calcium absorption from intestine
Increase distal reabsorption of kidney
Increases proximal reabsorption of phosphate, in excess can cause hypophosphatemia

75
Q

How does chronic kidney disease cause secondary hyperparathyroidism?

A 
Vit D can't be activated
Reduced calcium absorbed from intestine
Plasma Ca chronically low
PTH chronically high
Causes hypertrophy and hyperparathyroidism
76
Q

What causes hypercalcemia of malignancy?

A

20% due to bone lesions

80% due to elevated PTHrP (common in cancer of breast, ovary, kidney, skin)

77
Q

What causes calcitonin secretion?

A

High calcium
Gastrin
CCK
Secretin

Calcitonin lowers calcium

78
Q

What are the 4 types of cells in the pancreas? What do they secrete?

A

A: Glucagons (catabolic, moves glucose and FFA into blood stream)
B: Insulin (moves glucose into cells)
D: Somatostatins (turn everything off)
F: Pancreatic polypeptides

79
Q

Where is insulin made?

A

Rough endoplasmic reticulum
Transported to golgi apparatus
Packed as proinsulin
Once activated, split by C-protein into insulin

80
Q

What stimulates insulin release?

A

Glucose >5mmol/L
Anything that increases cAMP (glucagon + theophylline+B-agonists)
Vagal stimulation (via Ach)
GIT hormones (GIP, enteroglucagon, secretin, CCK)
Oral hypoglycemic drugs

81
Q

What decreases insulin release?

A 
Somatostatin
Beta blockers
Sympathetics
K+ depletion
Galanin
Insulin (via negative feedback)
82
Q

What are the actions of insulin on lipids?

A

Brings glucose and K+ into cell
Increase lipoprotein lipase so increases FFA storage
Decreases enzyme lipase which normally breaks down fat

83
Q

What is the action of insulin on muscles?

A

Brings glucose, K+ and ketones into the cell
Makes glycogen for storage
Makes more proteins and decreases protein catabolism
Decreases release of glucogenic amino acids

84
Q

What action does insulin have on the liver?

A

Increased protein synthesis and fat deposit
Decreased ketogenesis
Decreased glucose output due to increased glycogen synthesis
Increased cell growth

85
Q

How does insulin differ from growth hormone?

A

decreases hormone sensitive lipase in fat cells

increases lipoprotein lipase in the vicinity of fat cells

86
Q

What are the key effects of insulin deficiency?

A

Diminished growth
Reduced lipogenesis
Diabetes mellitus

87
Q

What are the 4 places where glucose uptake is not affected by diabetes mellitus?

A

Intestinal absorption ->via SGLT1 and 2
Reabsorption of glucose in proximal tubule ->via SGLT 1 and 2
Brain
RBC

88
Q

What is the fate of most ingested glucose?

A

50% of ingested glucose is burned to CO2 and H2O
5% converted to glycogen
30-40% converted to fat to be deposited
Therefore with increased glucose in diet, most will be stored as fat
In diabetes glucose just stays in the blood, hardly any converted to fat

89
Q

Why do diabetics drink a lot?

A

Blood full of glucose so hyperosmolar
Glycosuria and polyuria due to osmotic diuresis. Increased Na and K+ lost in urine with glucose
Causes dehydration and polydipsia

90
Q

Why do diabetics get muscle wasting?

A

Cells have no glucose
Body thinks it’s starving
Liver releases glucose and so does skeletal muscle
Diminished protein synthesis and wasting

91
Q

Why do diabetics have increased ketones?

A 
Fat catabolism is increased
Increased FFA
Excess acetyl CoA is fomred
Acetyl CoA is converted into ketones 
Ketones cause acidosis
92
Q

What increases glucagon release from the gut?

A

Hypoglycemia (exercise, stress, infection)
Amino acids (alaine, serine, glycine)
CCK and gastrin
Cortisol
Vagus nerve activity
Alpha receptors (-) and beta receptors (+) ->balance is stimulation

93
Q

What decreases glucagon release?

A 
Glucose and insulin
GABA (released along with insulin)
Somatostatin
Secretin
FFA and ketones
Alpha adrenergic agents
94
Q

What are the key actions of glucagon?

A 
Main site of action liver
Glycogen breakdown
Gluconeogenesis
Ketogenesis in liver
Increased lipolysos in adipose
In large dose it is a +ve inotrope
Increased secretion of insulin and GH
Calorigenic via increased hepatic clearance of amino acids
NO EFFECT ON MUSCLE
95
Q

what controls GH release?

A

GHrH (+)

Somatostatin (-)

96
Q

Which receptors does GH act on?

A

Tyrosine kinase activities
Type 1->binds IGF-1 > IGF-II> insulin

Type 2 -> binds IGF-II > IGF-1

Insulin receptors -> binds insulin > IGF 1

IGF-II more important in fetus

97
Q

What does the prolactin?

A

Promotes milk secretion (not ejection)
Decreases actions of LH and FSH. Can cause infertility in males and females
Role in males unknown

98
Q

What increases prolactin release?

A 
Nipple stimulate in non-lactating women (via T5)
Stress
Pregnancy
TRH
Vasopression
Estrogen
99
Q

What decreases prolactin release?

A

L-dopa
Bromocriptine
Apomorphine

100
Q

What are the key actions of ADH/vasopression?

A

Inserts aquaporin into collecting duct of kidney
No affect on distal tubules
Water reabsorption is passive
Increases permeability of inner medulla of kidney to urea
Vasoconstriction in vasa recta of renal medulla causing decreased blood flow
Increases ACTH release by anterior pituitary

101
Q

What increases ADH/vasopressin release?

A

Mild hyperosmolality of ECF
Severe hypovolemia
Mild hypovolemia and mild hyperosmolality of the ECF
Severe hypovolemia + severe hypoosmolality of ECF
Drugs (morphine, nicotine, chlorpropamide)
Stress, pain, exercise, sleep
Standing, N+v
Post op (pain, morphine and loss of ECF)

102
Q

What decreases ADH/vasopressin release?

A

Alcohol (water + alcohol in beer inhibit ADH release). Has no effect on tubular Na reabsorption
Increased plasma volume
Decreased plasma osmotic pressure
Controlled by osmoreceptor in hypothalamus and low pressure receptor in veins and atria

103
Q

Why in SIADH may urine volume/day be normal?

A

With SIADH secretion the GFR may be increased

104
Q

What are the two types of diabetes insipidus and how are they different?

A

Central : not enough ADH released

Nephrogenic: Kidney doesn’t respond to ADH

105
Q

What causes thirst?

A 
Controlled by hypothalmic mechanism
Caused by intracellular dehydration
Caused by extracellular dehydration
Increased with haemorrhage/low CO
Increased by High ANGII levels
Increased by increased osmolarity due to high sodium
106
Q

Why can thirst occur without a change in plasma osmolarity?

A

Haemorrhage increases thirst via angiotensin via osmoreceptors

107
Q

What happens if you drink 10L of water in 5 minutes?

A

Immediate expansion of ECF
Increase in interstitial fluid volume
Altered consciousness as cerebral neurons swell
Spontaneous haemolysis will occur when osmolarity <20mOsm/kg
Urea is freely diffusible and obtains equilibrium with ECF without any significant changes in its concentration in plasma

108
Q

What increases secretion of oxytocin?

A

Mechanical distension of vagina

Stimulation of nipples

109
Q

What does the pineal gland do?

A

Outside blood brain barrier
Secretes melatonin (made from tryptophan via serotonin)
Has no influence over K+ metabolism

110
Q

How does GnRH affect LH?

A

In general increased GnRH will increase LH +FSH secretion from anterior pituitary
Constant GnRH high is ineffective due to receptor downregulation
An hourly pulse will increase LH secretion

111
Q

What does FSH do in the male?

A

Stimulates seminiferous tubules to make sperm
Stimulates sertoli cells to control maturation of spermatids to spermatozoa
Increases production of inhibin which acts as negative feedback on pituitary

112
Q

What does LH do in the male?

A

Trophic on interstitial leydig cells-> stimulates androgen production

113
Q

What does FSH do in the female?

A

Accelerates growth of 6-12 primary follicles with proliferation of granulosa cells +theca interna and externa (follicle maturation)
In the hours before ovulation there is a rapid spike in LH +FSH

114
Q

What does LH do in the female?

A

Acts via receptors on theca interna cells_> stimulate ovulation and luteinisation of ovarian follicle
For final development of the follicle and ovulation
LH converts the granulosa and theca interna cells into a progesterone secreting type of cell

115
Q

What are the effects of testerone?

A

Increases growth, protein synthesis
Retention of Na, K, phosphate, Calcium and water
Increase libido
Maturation of wolffian ducts and male internal genitalia

116
Q

Where is testerone excreted?

A

Metabolised in liver and excreted in urine

Can also be converted into DHT from 5a-reductase

117
Q

How is testerone related to development?

A

Elaborated in male embryo from 7th to 12th weeks
Almost absent in the male up to 10 years
Excreted in the female in small amounts
Necessary for normal spermatogensis
Produced from cholesterol in leydig cells

118
Q

What are the key affects of estrogen?

A
  1. Increases uterine muscle and amount of contractile proteins
  2. Changes vaginal epithelium from cuboidal to squamous
  3. Makes cervical mucus thinner and alkaline
  4. Makes boobs grow in puberty
  5. Increases osteoblastic activity
  6. Increased secretion of thyroid binding globulin ->euthyroid
  7. Slight increase in total body protein
  8. Increased secretion of angiotensinogen
  9. Sensitises myometrium to oxytocin
  10. Increases deposition of subcutaneous fat
  11. Causes skin to be softer, smoother and more vascular
  12. Decreases FSH and may increase/decrease LH
119
Q

Where is progesterone secreted?

A

Placenta and corpus luteum
In last half of pregnancy the placenta secretes enough progesterone to keep pregnancy going so corpus luteum secretion not necessary

120
Q

What are the key effects of progesterone?

A

Decreased excitability of myometrial cells
Thickens mucus and makes cervix firmer
Stimulates breast lobules and alveoli
Causes vaginal epithelial proliferation and thick viscous mucus production
Raises temperature and probably responsible for temp rise at ovulation

121
Q

Why does oophorectomy before the 6th week of pregnancy lead to abortion?

A

The placenta is not able to produce enough estrogen and progesterone to maintain pregnancy

122
Q

What occurs during the follicular phase of the menstrual cycle?

A

Progesterone levels are depressed
Oestradiol secretion is steady NOT inhibited
Vaginal mucus is thin and alkaline
Basal body temperature is not elevated

123
Q

How do LH and FSH develop the ovarian follicle?

A

Both essential for ovulation
Granulosa cells initially have FSH receptors, but later develop LH receptors
Both rise in hours before ovulation
LH converts granulosa cells and theca interna cells into progesterone secreting type of cell

124
Q

When are plasma oestrogen levels the highest?

A

24-48 hours pre ovulation

125
Q

How does the ovary self regulate?

A

Theca interna provides androgens to granulosa cells and estrogens which inhibit GnRH, LH and FSH
Granulosa cells secrete inhibin which inhibits FSH release
LH regulates thecal cells, granulosa cells regulated by both LH and FSH

126
Q

When is the number of oxytocin receptors the highest?

A

The amount of oxytocin receptors in the myometrium abd decidua increase 100 fold during pregnancy and reaches a peak during early labour

127
Q

What is relaxin and what does it do?

A

Relaxin is produced by corpus luteum, uterus, placenta and mammary glands in women and prostate glands in men. During pregnancy it relaxes the pubic symphysis and dilates uterine cervix.
In men it is found in semen

128
Q

How do endocrine glands change in pregnancy?

A

Anterior pituitary: 50% increase in size with increased secretion of corticotrophin, thyrotropin and prolactin
Adrenal: increased glucocorticoid secretion,2x increased aldosterone secretion
Thyroid:50% increase in size and production of thyroxine (from increased human chorionic gondotropin and placental human chorionic thyrotropin)-but euthyroid
Parathyroid: increased size and secretion of PTH (especially in lactation)

129
Q

What are the key physiological changes noted in pregnency?

A

Uterus increases 22x

15% increase in basal metabolic rate in second half of pregnancy

Increased absorption and storage of protein

Minute ventilation increases 50% with a fall in arterial pCO2

RR increases as diaphragm squished by baby

Increased urine production, increased fluid, Na and Cl reabsorption

CO increased by 30-40% by 27th week, but then normalises

Blood volume increases in 2nd half of pregnancy

Decreased maternal antibody production

130
Q

What are the actions of human horionic somatomammotropin?

A

Similar to that of GH

131
Q

Where is oestiol synthesized during pregnancy?

A

Combined effect of fetal and placental tissue

Level is higher at 36th week than 20th week

132
Q

What is the theory behind why the maternal body does not reject the fetus?

A

Placental trophoblast lies between fetal and maternal tissue and does not express MHC genes so antibodies to fetal proteins do not develop

133
Q

What are the key placental hormones?

A

Placenta secretes, hCG, progesterone, estrogen, corticotropin releasing hormone, melanocyte stimulating hormone, leptin, human chorionic somatomammotropin
hCG vital to prevent expulsion of implanted ovum

134
Q

Why does lactation only start after birth?

A

Breast duct growth is stimulated by estrogens, but this estrogen antagonises the milk producing affect prolactin
After expulsion of placenta, levels of estrogen and progesterone abruptly decline which initiates lactation

Physiology (7 decks)

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