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BIOM 3200 > The endocrine system > Flashcards

The endocrine system Flashcards

1
Q

what is homeostasis

A

a state of balance among all body systems needed for the body to survive and function correctly

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2
Q

what 4 factors does homeostatic control rely on

A
  1. sensor: constant monitoring
  2. integration center: to coordinate
  3. response system: to change
  4. Negative feedback
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3
Q

homeostasis furnace analogy

A

house temp falls - thermostat detects it (sensory system) - furnace turns on (response system) - heat is produced - house temp rises - thermostat detects - furnace turned off

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4
Q

homeostasis and blood pressure: lying down to standing up

A

stimulus: blood pressure falls
sensor: blood pressure receptors respond
effector: heart rate increases
Negative feedback response: rise in blood pressure

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5
Q

basic endocrine dysfunctions

A

hyper-function: too much hormone
hypo-function: too little hormone
resistance: too little effect of hormone

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6
Q

connections between the endocrine system and disease statistics

A
  • diabetes Mellitus is the 6th leading cause of death in Canada
  • thyroid disorders affect around 5% of the population, increasing with age
  • endocrine ovarian disorders affect around 6% of the female population and are the e#1 cause of infertility
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7
Q

what is a hormone

A

a regulatory molecule secreted into the blood by endocrine glands

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8
Q

what is an endocrine gland

A

a tissue that releases a substance into the bloodstream
- the substance then travels via the blood stream to influence target cell

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9
Q

what did banting and best identify

A
  • contributed to insulin
  • an antidiabetic substance in pancreatic extracts, injecting this extract prevents symptoms of diabetes
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10
Q

what is insulin

A

a peptide hormone produced by beta cells in the pancreas
- promotes the absorption of glucose from blood to skeletal muscle and fat tissue

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11
Q

active vs inactive form of insulin

A

active: a monomer
inactive: a heximer - made of zinc held together by histidine residues

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12
Q

what are the 4 types of hormones

A
  1. polypeptides and proteins (most common)
  2. steroids (cholesterol derivatives)
  3. amines (catecholamines)
  4. amines (thyroid)
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13
Q

3 levels of effect of hormones

A
  1. autocrine: secretory cell is also the target cell
  2. paracrine: secretory cell is adjacent to its target cells
  3. endocrine: secretory cell send the molecule through the bloodstream to reach the target cell
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14
Q

characteristics of peptide hormones

A

synthesis: in advance
storage: in secretory vesicles
release from cell: exocytosis
transport in blood: dissolved in blood plasma
half life: short
example: insulin

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15
Q

characteristics of steroid hormones

A

synthesis: on demand
release from cell: diffusion
transport in blood: bound to carrier proteins
half life: long
example: estrogen/androgen

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16
Q

characteristics of amine hormones (Cat)

A

synthesis: in advance
storage: secretory vesicles
release from cell: exocytosis
transport in blood: dissolved in plasma
half life: short
example: epinephrine/norepinephrine

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17
Q

characteristics of amine hormones (thyroid)

A

synthesis: in advance
storage: secretory vesicles
release from cell: diffusion
transport in blood: bound to carrier proteins
half life: long
example: T4

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18
Q

where are the receptors of hormones located

A

most hormones: transmembrane
thyroid hormones: nucleus
steroid hormones: the cytoplasm

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19
Q

specific binding of hormones to receptors

A
  • hormones have specific receptors they bind to at their target cells (don’t actually enter the cell)
  • non-specific binding is known as hormone “overspill”
  • there is a continuous turnover of the receptor-hormone complex
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20
Q

transmembrane receptor binding

A
  • hormone binds the extracellular domain of the receptor and activates one or more cytoplasmic signalling pathways
  • many pathways involve phosphorylation and enzyme activation
  • some pathways lead to the DNA/mRNA/protein pathway response and others just have a local effect in the target
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21
Q

Adenylate cyclase (AC) pathway

A
  1. hormone attaches to the receptor and G-proteins dissociate
  2. alpha subunit activates AC
  3. AC turns ATP in the cytosol to cAMP
  4. cAMP binds to inhibitor protein on protein kinase and releases them
  5. protein kinase activates many other molecules (hormonal response)
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22
Q

phospholipase C-Ca2+ (PIPLC) pathway

A
  1. hormones attach to receptor
  2. G-proteins dissociate and activates phospholipase C (PLC)
  3. the phosphate bearing head-group is cleaved from the membrane to get IP3
  4. IP3 binds endoplasmic reticulum and releases stored Ca2+ into the cytoplasm
  5. Ca2+ activates other molecules (hormonal response)
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23
Q

beta-adrenergic vs alpha-adrenergic receptors

A

activate AC (via Gq) , mediate vasodialation and smooth muscle relaxation = beta-adrenergic
activate PIPLC (via Gs), mediate smooth muscle contraction and vasoconstriction= alpha-adrenergic
- G-alpha subunits fall into several subtypes (Gq-alpha and Gs-alpha)

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24
Q

Cytoplasmic receptor binding: steroid hormones

A
  1. steroid hormone is transported bound to plasma carrier protein
  2. steroid hormone binds to receptor in the cells cytoplasm
  3. hormone translocates to the nucleus and binds to DNA
  4. transcription happens then protein synthesis
  5. steroid hormone releases response
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25
Q

nucleus receptor binding: thyroid hormone

A
  1. T4 (thyroxine) binds to a carrier protein in the blood plasma
  2. T4 enters the target cell and becomes T3 (triiodothyronine)
  3. T3 uses binding proteins to enter the nucleus and get to the receptor
  4. hormone bind to the receptor which binds to DNA
  5. transcription makes a new mRNA then a protein
  6. thyroid hormone response
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26
Q

how does the hypothalamus control hormones

A
  • hormones that start in the hypothalamus must travel through blood vessels to the anterior pituitary then go through the circulation to reach the target tissue
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27
Q

6 major hormones from the anterior pituitary and their target tissues

A
  1. prolactin - mammary gland (breasts)
  2. thyroid stimulating hormone (TSH) - acts on the adrenal cortex
  3. Adendocorticotropic hormone (ACTH) - acts on the adrenal cortex
  4. growth hormone (GH) - acts on bone, muscle and adipose tissue
  5. folicle-stimulating hormone (FSH) - acts on the ovaries and testes
  6. luteinizing hormone (LH) - acts on the ovaries and testes
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28
Q

what do inhibitory hormones do

A

provide an alternate pathway - signals are prevented instead of produced

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29
Q

what are the 3 parts of the anterior pituitary

A
  • pars tuberalis
  • pars intermedia (skin colouring, other things)
  • pars distalis
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30
Q

7 major hormones from the hypothalamus and what they regulate

A
  1. Dopamine (PIH) - inhibits secretion of prolactin
  2. Prolactin-releasing hormone (PRH) - stimulates the release of
  3. thyrotropin-releasing hormone (TRH) - regulates the secretion of TSH
  4. Corticotropin-releasing hormone (CRH) - regulates the secretion of ACTH
  5. Growth hormone inhibiting hormone (GHIH) - inhibits secretion of GH
  6. Growth hormone releasing hormone (GHRH) - stimulates secretion of GH
  7. Gonadotropin-releasing hormone (GnRH) - regulates secretion of LH and FSH
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31
Q

adrenal cortex axis

A

hypothalamus - releases CRH - acts on anterior pituitary - releases ACTH - acts on adrenal cortex - secretes cortisol - acts on many tissues

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32
Q

CRH synthesis and release from the hypothalamus

A
  • produced by paraventricular cells in the nucleus
  • central stimulatory control of the hypothalamus is noradrenergic which stimulates pre-pro CRH gene protein expression
  • pre-pro CRH is processed from 196 AA to 41 AA which is released in a pulsatile manor
  • released at the median eminence from their neurosecretory nerve terminals into the blood vessels
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33
Q

inhibitory influences of CRH release

A
  • ## physiological levels of cortisol inhibit the release of CRH (possibly inhibit pre-pre CRH gene expressions)
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34
Q

ACTH synthesis and release from the anterior pituitary

A
  • ACTH comes from the POMC family and regulates adrenal cortex function
  • convertases cleave POMC to give rise to ACTH
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35
Q

hormones from the adrenal cortex

A

synthesizes 3 main types of steroid hormones
1. glucocorticoids (cortisol) - controlled by ACTH
2. mineralocorticoids (aldosterone) - not controlled by ACTH
3. sex steroids (testosterone) - controlled by ACTH

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36
Q

3 regions of the adrenal cortex

A
  • Z glomerulosa
  • Z fasciculata (secretes cortisol)
  • Z reticularis
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37
Q
A
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38
Q

how does cholestrol get converted to cortisol in humans vs rodants

A

humans: cholesterol - 17 hydroxypregnenolone - 17 hydroxyprogesterone - deoxycortisol - cortisol
rodants: cholesterol - pregnenolone - prohesterone - deoxycorticosterone - corticosterone

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39
Q

why is cortisol essential

A
  • protects against hypoglycemia (low blood sugar)
  • protects gluconeogenesis ( increased blood sugar)
  • plays a role in the immune system, bone, muscle, etc.
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40
Q

why can having too much cortisol be bad?

A
  • breaks down skeletal muscle (for gluconeogenesis)
  • suppresses the immune system
  • catabolic on bone
  • affects brain function (mood memory, learning)
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41
Q

Cushings syndrome: primary

A
  • high levels of corticosteroids in the blood
  • prolonged exposure to high levels of cortisol
  • caused by taking glucocorticoid drugs, or diseases that result in excess cortisol, ACTH or CRH levels
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42
Q

Cushing’s disease: secondary

A
  • the cause is pituitary-dependent, a tumour in the pituitary gland produces large amounts of ACTH, causing adrenals to make excess cortisol
  • ACTH levels are higher in the secondary form
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43
Q

What are the effects of Cushing’s syndrome

A
  • changes carbohydrate and protein metabolism, hyperglycemia, hypertension, muscular weakness
  • metabolic problems give rise to puffy appearance and CNS disorders (depression, decreased learning, memory etc.)
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44
Q

treatments for Cushing’s syndrome

A
  • surgery to remove pituitary or adrenal gland
  • medical management of signs and symptoms
  • if not treated, disease worsens and any other health problems will also get worse
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45
Q

Why might cortisol be too low?

A

Addison’s disease is the primary cause of hypocortisolism
- adrenal insufficiency: many causes including genetic, autoimmune destruction of adrenal cortex
- high-dose steroids > 1 week begins to suppress adrenal glands by suppressing CRH and ACTH (and feedback pathways)

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46
Q

how does adrenal cortex secretion work?

A
  • continuous: in the blood 24v hours a day
  • pulsatile: released in little spurts
  • circadian rhythm: highest when you wake, lowest in deep sleep
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47
Q

the adrenal cortex: Insomnia and the HPA axis

A

people with insomnia secrete more cortisol around sleep time, elevated levels make it harder to sleep

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48
Q

PPID - pituitary pars intermedia dysfunction

A
  • Cushing’s disease in horses
  • mostly affects older
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49
Q

signs and causes of PPID in hoses

A

Signs: hypertrichosis, abnormal hair coat, muscle atrophy, excessive sweating, fat pads on top of neck tail head and eyes, pot-bellied appearance
causes: impaired pituitary gland - hyperlasia and hypertrophy in the pars intermedia, results in high blood glucose and suppression of the immune system

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50
Q

diagnosis, treatment and management of PPID in horses

A

Diagnosis: measuring resting (basal) ACTH and fasting insulin
Treatment: Drug (pergolide) that acts on the pituitary gland to decrease circulating ACTH
Management: exercise, weight loss (if obese), limit starch/sugar in diet

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51
Q

thyroid axis

A

hypothalamus - releases TRH - acts on the anterior pituitary - releases TSH - acts on the thyroid
- releases thyroid hormones - act on many tissues

52
Q

what is the thyroid

A
  • located just below the larynx (voice box)
  • 2 lobes on either side of the trachea
  • connected by the isthmus (bridge)
  • largest purely endocrine gland
53
Q

what is thyroglobulin

A

long peptide chain with lots of tyrosine side chains found in the colloid, responsible for iodide storage and thyroid homeogenesis

54
Q

why is iodine important to the thyroid

A

It helps make thyroxine
- follicles take up iodine from the blood into the follicular cells by a sodium-iodide transporter, then into the colloid by a pendrin transporter
- in the colloid TPO converts iodide to iodine and helps attach it to a tyrosine residue in thyroglobulin

55
Q

how are different forms of iodotyrosine formed?

A
  • attaching one iodine = MIT
  • attaching 2 iodines = DIT
    when tyrosine molecules are joined together by enzymes in the colloid their structures modify
  • MIT + DIT = T3
  • DIT + DIT = T4
56
Q

thyroid hormone mode of secretion

A
  • thyroid receptors are in the nucleus, hormones are made in advance and stored until needed
  • T3 and T4 receptors are still attached to thyroglobulin, so it must be cut up so that T3 and T4 hormones are separated
  • endocytosis is stimulated by TSH and T3 and T4 are secreted out of the thyroid where they find a carrier protein
57
Q

how are thyroid hormones produced?

A
  1. the enzyme TPO removes an electron from iodide to produce iodine
  2. iodine binds tyrosine residues in thyroglobulin to form MIT and DIT
  3. condensation of MIT and DIT residues form T3 and T4
58
Q

how does a thyroid hormone become active

A
  • it has to lose its carrier protein to produce an effect on the target cell
  • > 99% of THs in the blood circulation are bound to carrier proteins - inactive
59
Q

how is secretion of thyroid hormones regulated?

A
  • pulsed secretion of TRH (only releases hormone when it reaches thyroid)
  • more is secreted in young animals than in older animals
  • increased secretion when stresses or cold
  • highest between 10am and 2pm
60
Q

hyper and hypothyroidism

A

hypothyroidism: abnormally low BMR (weight gain), lethargy, intolerance to cold
- common in dogs
hyperthyroidism: increased BMR (weight loss), muscular weakness, nervousness, protruding eyes (exophthalmos)
- common in cats

61
Q

what is cretinism

A

congenital deficiency of thyroid hormone during maternal hypothyroidism
- individuals born suffer from reduced physical growth and sever mental deficiency
- treatment with T4 soon after birth can almost completely restore development of intelligence as measured by IQ by age 5
- can also arise from a diet deficient in iodide

62
Q

terminal brain differentiation due to thyroid hormone

A
  • thyroid-dependent development of the brain begins in utero but is completed after birth
  • dendritic and axonal growth, myelin formation and synapsis formation
  • neuronal migration
  • maternal thyroid hormones first supply the needs of the fetus
63
Q

what can cause hyper/hypothyroidism

A
  • insufficient dietary iodide
  • thyroid gland defect
  • impaired thyroid hormone pathway
  • insufficient AP TSH or hypothalamus TRH
  • mutant TSH or TRH receptors (genetic)
  • mutant TH proteins
    -autoimmunity
64
Q

Hypothyroidism: Goiters

A
  • abnormal growth of the thyroid
  • low iodide intake = thyroid can’t produce enough hormones
  • lead to low plasma T3 and T4, high TRH, high TSH, stimulates excess growth of thyroid
65
Q

Hyperthyroidism: Graves disease

A
  • auto Abs activate the thyroid gland
  • high plasma thyroid hormones T3 and T4, low TRH, low plasma TSH
66
Q

Hypothyroidism in dogs (primary and secondary)

A

Primary: lymphocytic thyroiditis - 50% of affected dogs are doberman’s, idiopathic atrophy of the thyroid (thyroid tissue lost and replaced by adipose cells)
Secondary: thyroid destruction secondary to neoplasia (40% of dogs with cancer), congenital hypothyroidism/cretinism/pituitary dwarft
- > 75% of both lobes are non-functional by the time clinical signs show

67
Q

treatment of thyroid disorders in pets

A
  • surgery (hemithyroidectomy)
  • hormone supplimentation
  • radiation
  • blockers ( thiouracil derivatives: decrease iodination and T4 -> T3)
  • stimulants (furosemide, increase T4 -> T3)
  • diet, exercise, infusions etc.
68
Q

somatotropic axis

A

hypothalamus - releases GHRH - acts on the anterior pituitary - releases GH: 2 PATHS FROM HERE
1. GH acts on liver - releases IGF-1 - acts on cartilage, bone, muscles and other organs (growth)
2. GH acts on adipose tissue (lipolysis and release of fatty acids) and other tissues (decreased glucose utilization)

69
Q

what does IGF-1 do?

A
  • hormones that promotes growth along with GH
  • IGF-1 is almost entirely bound to transport proteins (IFG-1 BPs)
  • some IFG-1 transport proteins have an endocrine function
  • transported through the blood
70
Q

What are insulin-like growth factors?

A
  • hormones produced by the liver
  • IFG-1 and IFG-2 are somatomedins
  • have 40% homology to insulin
71
Q

how do GH and IGF-1 work together

A
  • GH stimulates the synthesis and release of IGF-1 in many tissues (not just the liver)
  • they exert opposite actions in some tissues which shows they have independent roles
72
Q

body function and result of GH and IGF-1

A

liver glucose release: GH = incr, IGF = decr
plasma glucose concentration: GH = incr, IGF = decr
sensitivity of tissue to insulin: GH = decr, IGF = incr
lipolysis in adipocytes: GH = incr, IGF = decr
muscle amino acid uptake: both incr

73
Q

how do children grow?

A
  • they have 2 periods of growth: postnatal and puberty
  • they both grow in height and change in body proportion
74
Q

Why wouldn’t children grow without GH

A
  • GH is needed to stimulate growth of bbone and cartilage as well assoft tissue growth
75
Q

types of soft tissue growth

A

hypertrophy: increased cell size
hyperlaysia: increased cell number

76
Q

how is bone formed?

A
  • calcified ECM is formed when calcium phosphate crystals precipitate and attach to lattice support
  • most common form of calcium in bone is hydroxyapatite
77
Q

2 ways that bone is built up

A
  1. diameter increases: growth occurs around the bone, matrix deposits on the outer surface
  2. length increase: growth occurs at the epithyseal plates
78
Q

Bone growth from the epiphyseal plates

A
  • located near the end of the bone and contains chondrocytes: columns of collagen-producing cells
  • as collagen thickens old cartilage calcifies and chondrocytes degenerate
  • osteoblasts invade and lay bone matrix on top of cartilage bone
79
Q

how does growth hormone stimulate bone growth

A
  • GH directly stimulates chondrocytes as well as the production of IGF-1 in the liver
  • IGF-1 helps stimu,late the chondrocyte and osteoblast activity to promote bone
80
Q

GH related disorders in growing mammals

A

dwarfism: underproduction of GH of GHR
- small size and proportions
pygmies: laron-type dwarfism, GH receptor deficiency
pituitary gigantism: over production of GH

81
Q

GH related disorders in adults

A

alopecia: in dogs - thin skin, hair loss
cushing’s syndrome: in humans - increased cortisol inhibits GH synthesis
acromegaly: over secretion of GH
- thickening of bones/joints and skin, enlargement of internal organs (tounge, liver, spleen)

82
Q

Treatment for children with low GH

A
  • rHGH is given to the bottom 1% of children
  • daily injections ~ 2 years gives 1.3 ft increase in height
  • side effects: glucose intolerance, pancreatitis, physiological height problems
83
Q

types of specialty cats

A

miniture: selective breeding, runts
dwarf: genetic mutation munchkin (chondrodysplastic, short legged)
tea cup: dwarf breed but normal proportions, have bone muscle and endocrine problems

84
Q

types of specialty dogs

A

dwarf: GH deficiency, small all over
brachycephalic: shortened skill bones, short muzzle
micromelic: short legged

85
Q

why is GH controversial for athletic enhancement?

A

it is good at maintaining muscle mass due to AIDS

86
Q

GH application in agriculture

A
  • feeding GH to cows increases milk yield by 30%, faster growth, leaner meat
  • adverse effects on reproduction
  • concern for humans who consume their products
87
Q

what are intra and extra cellular Ca2+ essential for?

A
  • neuromuscular excitation
  • blood coagulation
  • hormone secretion
  • enzyme activity
  • fertilization
88
Q

how is Ca2+ tightly regulated in the body?

A

intracellular: largely associated with membranes in mitochondria, ER and plasma membrane
extracellular: 50% ionized calcium, 40% protein-bound and 10% calcium complexed with phosphate and citrate

89
Q

how is total body calcium maintained?

A
  • intake calcium through diet; about 1/3 is absorbed in the small intestine
  • body can’t make calcium and must replace it
  • output through kidneys
90
Q

how can you calculate total body calcium?

A

intake - output OR intracellular + extracellular (ECF/plasma and bone)

91
Q

how does the endocrine system control calcium concentration?

A

3 hormones regulate movement of calcium between bone, kidney and intestine
1. Parathyroid
2. calcitriol
3. calcitonin

92
Q

parathyroid hormone (PTH)

A
  • made in the parathyroid gland and helps regulate calcium
  • parathyroid cannot be removed (essential for life)
  • 2 cell types found: chief cells (produce PTH) and oxyphils (unknown)
  • when plasma Ca2+ decreases PTH raises blood Ca2+ back to normal
93
Q

3 mechanisms of PTH that raise blood calcium when it is low

A
  1. stimulates osteoclasts to reabsorb bone
  2. PTH stimulates kidneys to reabsorb Ca2+
  3. PTH stimulates kidneys to produce enzyme needed to activate vitamin D
94
Q

secretion of PTH

A
  • secreted continuously (not stored)
    hypocalcemia (too low): PTH secretion up
    hypercalcemia (too high): PTH secretion down
95
Q

how does PTH stimulate bone to reabsorb calcium?

A

bone resorption: osteoclasts dissolve the hydroxyapatite and returns the bone calcium to the blood
bone deposition: osteoblasts secrete matrix or collagen protein which hardens and builds up bone

96
Q

how does PTH stimulate the Kidneys to reabsorb calcium?

A
  • reabsorption by kidneys increases clood Ca2+ and decreases urinary excretion of calcium
97
Q

how does PTH help our body activate vitamin D3

A
  1. vitD is produced from 7-dehydrocholestrol under the influence of sunlight
  2. vitD is secreted into the blood and is a PREhormone, goes to the liver and is chemically changed
  3. hydroxyl group is added to carbon 1 to activate it
98
Q

phosphate homeostasis

A
  • phosphate metabolism is controlled by the same mechanisms that regulate calcium, but not as tightly
99
Q

how does vitamin D3 regulate movement of calcium

A
  • humans: synthesize vitD from 7-dehydrocholestrol with UV light in the skin and obtain it by dietary sources
  • dogs and cats: only obtain it from diet
  • vitD stimulates intestinal absorption of Ca2+
  • directly stimulates bone reabsorption by promoting formation of osteoclasts
100
Q

how does calcitonin regulate movement of calcium

A
  • made in the C cells of the thyroid in response to high calcium
  • minor in adults because patients can have thyroid gland removed and still be ok
101
Q

what are the possible effects of hyperparathyroidism?

A
  • hypercalcaemia
  • increased bone reabsorption of calcium (fractures)
  • mineralization of soft tissues
  • increased thirst and urination (calcium blocks ADH effects)
102
Q

what are the possible effects of hypoparathyroidism?

A
  • hypocalcaemia
  • muscle weakness, ataxia
  • cardiac arrythmias
103
Q

osteoporosis - the most common bone disorder

A
  • reduction of bone quality due to excess absorption (increased risk of fractures)
  • known risk factors: female, lack of exercise, calcium deficient diet, age
  • prevalence: 1 in 3 women and 1 in 5 men
  • treatments: calcium and vitamin D intake, hormone therapy (may cause other diseases)
  • best treatment: PREVENTION with exercise, vitamin D etc
104
Q

vit D deficiency disorders

A
  • rickets in children: bone pain, stunted growth, disformaties
  • osteomalacia in adults: bone pain, fractures
105
Q

what types of cells do the testes

A

sperm (sertoli cells)
testosterone (leydig cells)

106
Q

MALE reproduction axis

A

hypothalamus - releases GnRH - acts on the anterior pituitary - produces FSH and LH - @ different paths from here…
1. FSH acts on sertoli cells - produce inhibin - negative feedback to anterior pituitary
2. LH acts on leydig cells - produce testosterone - negative feedback to the hypothalamus and anterior pituitary

107
Q

Where does testosterone act in different stages of life?

A

fetal: masculinizes tract and external genitalia
puberty and adulthood: growth and maturation of reproductive system, sex drive, secondary sex characteristics, bone, muscle and brain

108
Q

why is there an increased risk of infertility in males taking steroids

A
  • AAS mimics the effects of testosterone
  • excess testosterone shuts down the pathway
  • testes stop producing sperm and testosterone which decreases libido and fertility
109
Q

Male contraceptives

A
  • vasectomies may be irreversible
  • condoms can be ineffective
  • new tests have been done where men are given excess testosterone, effective for 4 months but not for 6
110
Q

FEMALE reproduction axis

A

hypothalamus - secretes GnRH - acts on the anterior pituitary - releases FSH and LH - act on the ovaries - produce estrogen and progesterone - act on the uterus

111
Q

what do the ovaries produce

A
  • eggs - go to the falopian tube
  • hormones - act on the uterus which gets ready for pregnancy, then is stripped of lining if implantation doesn’t occur
112
Q

mestural discharge

A

~ 80mL of blood, fluid, cell debris from the outer layer of the uterine endometrium
- endometrial arteries are responsible for mentural bleeding
- animals that lack these arteries do not bleed when they shed ednometrium

113
Q

which 2 female reproductive cycles occur at the same time?

A

ovarian cycle: regulated by FSH and LH
uterine (menstrual) cycle: regulated by estrogen and progesterone
- occur simultaneously since they are coupled by GnRH from the hypothalamus and FSH/LH from the anterior pituitary

114
Q

in the female reproductive cyles, what 3 phases occur over 28 days

A

Ovarian cycle: follicular phase (day 7), ovulation (day 14), luteal (day 21)
menstrual cycle: mestruation (day 1-5), proliferative (day 5-14), secretory (day 14-28)

115
Q

stages of the HPG-axis in the ovarian and menstration cycle

A
  1. gonadotropin secretion from the anterior pituitary increases
  2. Folicular phase: estrogen inhibits GnRH, FSH, LH (prevents more follicles from the same cycle)
  3. Ovulation: LH surge is stimulated by estrogen
  4. Early/Mid luteal phase: corpus luteum produces progesterone and estrogen, negative feedback supresses gonadotropins
  5. Late luteal-menstruation: estrogen and progesterone secretion decreases which removes negative feedback on HPG, FSH and LH increase
116
Q

Stages of the ovarian cycle

A
  1. just before day 1: FSH influences several ovarian follicles to begin maturation
  2. follicular phase: FSH declines and LH increases
  3. ovulation: egg is released, whats left behind forms the corpus luteum
  4. early/mid luteal phase: corpus luteum develops and then regresses of no pregnancy
    4: late luteal (menstruation): corpus luteum likes 12 days then apoptosis happens
117
Q

stages of the uterine cycle

A
  1. just before day 1: day 1 of menstrual bleeding begins
  2. follicular phase: estrogen stimulates endometrial growth
  3. ovulation: egg is released, whats left behind forms the corpus luteum
  4. early/mid luteal phase: endometrium anticipating pregnancy, progesterone causes a cervical mucosal barrier which thickens to block pregnancy
    4: late luteal (menstruation): endometrium requires progesterone or else vasculature contracts and dies, sloughs off and menstration starts (14 days post ovulation)
118
Q

why do women who want to know when they ovulate check their temperature?

A
  • starting at day 1 after the LH prak, basal body temperature sharply rises
  • progesterone goes up and is responsible for the BT change
119
Q

why do women get PMS

A
  • decreased mood, anxiety, bloating, breast tenderness, weight gain, difficulty concentrating
  • temporal correlation with luteal phase
  • requires ovulation and formation of corpus luteum (disappears at menopause)
  • link with neurotransmitter actions with hormones
120
Q

What are contraceptive pills

A
  • synthetic estrogen and progesterone (peak them so ovulation doesn’t occur because your body thinks it already happened)
  • elevation of these howmones causes negative feedback inhibition of gonadotropin section
  • stimulates false luteal phase
121
Q

what happens during menopause?

A
  • ovaries depleted of follicles, stop secreting estrogen (change is at ovarian, not pituitary level)
  • weak form of estrogen is made in adipose tissue (women with more have higher levels and less propensity to osteoperosis)
122
Q

hormone replacement therapy

A
  • menopause is associated with an increased risk of osteoporosis, hot flashes and aging
  • estrogen-progesterone study increased breast cancer risk and cardiovascular complication
  • estrogen only study increased stroke risk
123
Q

13 components in the melanocortinin system

A

4 posttranslational products of proopiomelanocortin (POMC): ACTH, a-MSH, b-MSH, g-MSH
5 melanocortin receptors: MC1R, MC2R, MC3R, MC4R, MC5R
2 antagonists: Agouti, AGRP
2 modulators of melanocortinin activity: mahogany and syndecan 3

124
Q

tissue specifity of POMC

A
  • different POMC peptidesare produced by different cell types which provides control of physiological fynctions by the same pro-hormone
125
Q

mutations in different peptides of POMC

A

a-MSH produced in the brain inhibits food intake: mutation causes early onset obesity
a-MSH in skin acts on melanocytes: mutation causes altered pigmentation
MCR acts on adrenal, skin, brain, penis, etc: mutation causes sexual function/dysfunction

126
Q

how does a-MSH increase brown/black pigment in skin?

A
  • binds to receptors MCR
  • activate signal pathways (G protein coupled reactions, cAMP, PKA, CREB)
  • synthesis of MITF
  • transcription tyr, DCT, influence pigmentation
127
Q

how can mutation in a-MSH result in yellow and obese mice

A
  • these mice have a mutated gene and overproduce agouti protein
  • agouti is an antagonist to MCR1 which means it interferes with and block it
  • overeat because agouti protein blocks MC4R in the brain

BIOM 3200 (7 decks)

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