Endocrinology Flashcards
1
Q
principles of endocrinology
A
- hormones are secreted by ductless glands, and allow distant cells to communicate
2
Q
hormone function
A
- chemical messengers
- by transmitting information via blood borne chemicals, that will regulate and coordinate distant organs
3
Q
endocrine vs nervous
A
nervous system: fast, precise, short, constant and works within an external environement
endocrine system: slow generalized, long, amplified and workins within an internal enviornment
- both pathways working together are called neuroendocrine interactions
4
Q
hormones are in 3 distinct classes of chemicals
A
- peptides and proteins
- amines
- steriods
5
Q
peptides and proteins
A
- chains of amino acids (can be short or long)
- contains the majority of animal hormones (insulin)
6
Q
amines
A
- derived from tyrosine (the amino acid), secreted by thyroid and adrenal medulla
7
Q
steriods
A
- neutral lipids derived from cholesterol
- secreted bt adrenal cortex and gonads
8
Q
cholesterole
A
- different hormones mat be derived from a common precursor
- they will share chemical similarities
- however small changes in chemical composition can have huge changes in biological responses
9
Q
why is structure important
A
- knowing the structure will tell you about the solubility, synthesis, storage, secretion, transport, effect type, duration of response and half-life
- structure
- if struture is know, we can synthesize them exogenously and fix deficiencies (growth and insulin hormones) and trick the body to perform functions
10
Q
peptide and catecholamines
A
- hydrophilic ( they like water)
- highly soluble in water, do not like lipids
11
Q
steroids and thyroid hormones
A
- lipophilic ( they like lipids)
- poor water solubility and high lipid solubility
- dont want to be in the plasma, cant store it in the cell
12
Q
hormone synthesis
A
- peptides: produced just like any other proteins (ribosomes on rough endoplasmic reticulum)
- but because they need to be released on demand, they need to be kept separated from other proteins
1. preprohormone is synthesized
2. pruned to a pro hormone and then an active hormone in the golgi complex
3. final hormone gets concentrated in golgi complex, packaged into vesicles
4. released via exocytosis upon stimulation. allows the release of large quantities of hormones in short notice
(fuse with cell membrane and get released through excocytosis
13
Q
peptide synthesis
A
- the bits from the pruning are often secreted with the hormones for functions
- cleave and stay together for either:
- hormone controlling melanin production (affects appetite and sexual arousal)
- hormone stimulating secretion of gluccocorticoid hormones
14
Q
steroid synthesis
A
- all start with cholesterol as precursor. either from diet or synthesis it from LDL
- enzymes are required to modify the cholesterol framework (to make it function) enzymes are found in mitochondria or endoplasmic reticulum, but cells/organs can only produce the hormone for which it has the completeed enzymes
- once produced steroid hormones cannot be stored, the are lipholic so they diffuse through the plasma membrane. rate of production is limited by synthsis
- some get further modified (different hormones or more modified hormones) in the blood or other organs
15
Q
amine hormone synthesis
A
- unique pathway
- they are derived from tyrosine
- both thyroid and catecholamines are stored until they are secreted
- thyroid hormones also undergos further processing after being released
ex. bodt cannot produce t3 so we produce t4 and cleave it to t3 for body to use
16
Q
hormone transport peptides
A
- travel most often freely in the plasma or sometimes bound to a specific carrier protein
17
Q
hormone transport steroids and amines
A
- lipophilic cant dissolve in large enough quantities, they are dragged around by plasma proteins
18
Q
protein carriers
A
- some can only carry specific hormones
- others like albumin only take hitchhikers
- only free lipophilic hormones are active. bound hormones cant diffuse and bind to a receptor with no effect
19
Q
hormone transport inactivation
A
- once a free H has interacted with its target cell it gets inactivated
- hormones that are bound to a carrier protein act as a reserve pool in the bloodstream
- the goal is to maintain hormonal equilibrium through feedback loops - need to focus on the free active portion of H, not the bound protion
20
Q
tropic hormones
A
- the sole function of a H is to regulate the production and secretion of another hormone
- target: endocrine tissue
21
Q
non tropic hormone
A
- primarily act as a non-endocrine target tissue
target: non endocrine tissue
22
Q
hormones effect
A
- only specific target cells can respond to each H because only they have the receptors for binding with a particular H
- cell receptors on outside can accept or deny
- receptor in cell lipophatic
23
Q
membrane receptors
A
- hydrophilic peptides and catecholamines cant pass through lipid membranes of their target cells
- they bind to the receptor outside the plasma membrane
- open an ion channel (Na or Ca)
- activate secondary messanger systems
- messangers change protein activity in the cell (enzymes) to get the effect
24
Q
internal receptors
A
- lipophilic steroids and thyroid H (when free ) pass through plasma membrane, and binds to specific receptors inside the cell
- typically those receptors are transcription factors that regulate gene expression and protein production (rate and type) in that cell
these H usually increase the rate of transcription
BUT: some reactions are too quick to require gene transcription. steroid H have receptors in the plasma membrane, which change ionic fluxes or enzymes activity
25
Q
receptors
A
- receptor needs the H to bind to the DNA: No H, no NDA access
- binding occurs at a very specific site on the DNA: the HRE, which is specific to each H
- when its memebrane binding = quick
- when its steroids = slow
26
Q
hormone regulation
A
- H effects are proportional to their concentration in the blood - [H] should be under control responding to homeostatic needs
1. rate of secretion into the blood
2. rate of metabolic activation
3. extent of protein binding
4. rate of removal for circulation
5. number of receptors on target cell
27
Q
negative feedback loops
A
- most common type of control in biological systems
- negative feedback exists when the output of a system counteracts a change in input
- stops over production
- final product is inhibiting the product that follows it
28
Q
control rate of secretion
A
- neuroendocrine reflexes:
- many endocrine systems involve neuroendocrine reflexes
- neural and hormonal components
- typically used to produce a sudden increase in hormone secretion in response to an external stimulus
29
Q
circadian and other biological rhythms
A
– haing negative feedback loops does not necessarily mena that the [H] concentration is constant - secretions will fluctuate with time
- circadian control: anticipatory regulation allows your body to adjust to these cyclical changes
30
Q
what problems can arise with with controlled rate of secretion
A
- hypersecretion: too much hormones
- hyposecretion: not enough hormones
31
Q
control of H transport, metabolism and excretion
A
- not physiologically regulated or controlled (triggers are different)
- but changes in transport, metabolism or excretion can affect the size of the effectiveness pool
- metabolism: peptides and catecholamines (hydrophilic) quickly inactivate in blood enzymes - stay active mins to hours
- lipophilic thyroid H and steroids are bound and protected - stay in blood for hours (steroids) up to a week (thyroid)
- hormones are eliminated primarily through urinary excretion. urine sample : non invasive way to assess endocrine function
32
Q
control of hormone receptors
A
- the response of a cell to a H is correlated with the number of receptors filled with H molecules on that cell
- down-regulation: process where the presence of H reduces the number of H receptors on teh cells (endocytosis and destruction )
33
Q
pineal gland
A
- control circadian rythm (day/night)
- secretes melatonin 10x higher during periods of darkness
- takes three days for brain to adjust to an 8 hour shift
- seasonal melatonin release influenced by the cyclic changes in a day length as seasons change
for reproduction - long day breeds: horses, breed with low melatonin
- short day breeds: sheep breed with high melatonin
34
Q
central endocrine glands
A
posterior pit has direct neural connection to the hypothalamus
two hormones are produced by the hypothalamus and are stored and released (upon neuron excitement) by post pit
- vasopressin and oxytocin
35
Q
Vasopressin (ADH)
A
- two roles:
- enhances retention of water by kidneys
- contraction of arteriolar smooth muscles (vasopressin effect)
- input: hypothalamis osmoreceptors (increased plasma osmolarity = increase of vassopressin secretion)
- angiotensin II also causes the release of ADH which increases water uptake and increases blood pressure
- ADH deficiency : diabetes insipidus (DI) making you always thirsty and dilutes urine)
- central DI: no secretion of ADH
- nephrogenic DI: kidneys dont respond to ADH
36
Q
oxytocin
A
- stimulates contraction of uterine smooth muscle during birth
- inpit : cervix afferent nerves detecting stretching
- promotes release of milk by mammary glands (but arent repsonsible for milk secretion)
- input = suckling
- has a behavioural effect
37
Q
prolactin
A
milk production
- increases during pregnancy to cause mammary gland enlargement in preparation of milk production
- hihg progesterone levels during pregnancy blocks milk production. progesterone drop post patum - milk secretion activation
- increases post coitus: sexual gratification - sexual refractory period
- too much = loss of libido and impotence
- tole in immunity, myelin production, regulates cell cycles
38
Q
anterior pituitary
A
- produces 6 H
- hypothalamus produces tropic H that control the release of H from the ant pit
- hormones travelling though a portal system
39
Q
what is a portal system
A
- two capillaries back to back that skip over the heart and leave it to the end
- will pick up hormones - release to the ant pit - drop hormones into veins and at last take them to the heart = hypothalamus-hypophyseal portal system
40
Q
hypothalamus
A
- secretes its own tropic H
-direct neural connection within the brain - sensing the blood chemistry, not part of the blood brain barrier - negative feedback loops to maintian homeostasis
41
Q
HGH development
A
- growth depends on HGH and other factors
- diet - need the nutrients to sustain growth
- no stress - corticosteroids have antigrowth effect (protein breakdown, inhibition of bone growth, decrease GH)
- normal levels of growth influencing hormones, such as thyroid H, insulin, sex hormones
42
Q
GH and metabolism
A
- GH has metabolic effects by binding directly with receptors on its target organs: adipose tissues, skeletal muscle and liver
- increased breakdown of fat, increased fatty acids in the blood
- increased blood glucose level: reducing the intake of glucose by the muscles (by using fatty acids rather than glucose) increasing output by the liver
- overall effect: mobilize fat storage as major energy source, keeps glucose from the brain
- during period of fasting, GH increases to ensure fat, rather than glucose, gets metabolized so that glucose is saved for the brain
43
Q
GH and growth
A
- GH has indirect growth promoting actions
- indirect because effects are mediated via (insulin-like growth factors)
there are 2 IGFs
44
Q
IGF-2
A
- independent of GH
- important during fetal development
- does not increase during puberty
- produced continuously throughout life, involved in muscle growth
- mutation that increases IGF-2 gene activity in pig muscles:
- pigs will have 3-4% more growth in muscel mass
- super muscular pigs are a result of a IGF-2 mutation
45
Q
IGF-1
A
- the more important IGF for growth
- stimulated by GH - to be released
- produced everywhere (mostly for local - paracrine effects), the main source of circulating IGF-1 is the liver (acting as a peripheral endocrine gland)
- production of IGF-1 a peripheral endocrine gland)
- production of IGF-1 affected by: nutrition, age, factors specific to tissues
- eg. sex H - IGF-1 increases reproductive organs (testes for males, ovaries and uterus for females)
- the peak of IGF-1 is puberty, causing growth sperts
46
Q
effects of GH/IGF-1 on soft tissues
A
- hyperplasia: increase number of cells, increases cell division ( mitosis), decrease programmed cell death (apoptosis )
- hypertrophy increase size of cells
- increase synthesis of proteins (main structural component of cells), decreased protein degration, increased uptake of AA by the cell to make proteins, increased everything needed to make proteins
47
Q
double muscle cows
A
- economic return = more meat
- increased feed expense
- longer to slaughter
- increase work, expense
- is it ethical?
48
Q
growth of bones
A
- bones is a living tissue: cells + extracellular matrix
- like cartilage, but calcified ( calcium phosphate) to make it stronger
- structural strength of bones - that of reinforced concrete
49
Q
a long bone is made up of
A
- a cylindrical shaft - the diaphysis
- a flared articulating knob at eitherend - the epiphysis
- a layer of cartilage separating the two: the epiphyseal plate
- bones grow thicker by adding new bone on top of the old bone
- bones grow longer by proliferation of cartilage cells in the epiphyseal plates
50
Q
GH regulation
A
- complex dual hypothalamic control loops
- GHRH - stimulatory
- GHIH (somatostatin) - inhibitory
- negative feedback loops participate in the regulating GH secretion
the finale product (IGF-1) inhibits the production of the primary and secondary products (GHRH and GH) - BUT:
- the secondary and opposing loop gets activated
- the final prodcut IGF-1 also stimulate the production of GHIH
51
Q
what affect the secretion of GHRH and GHIH
A
- circadian rythm ( peaks 1h after deep sleep)
- exercise, stress, hypoglycemia descreases blood sugar
- when energy demands > glucose reserves:
- conserve glucose for the brain
- get fatty acids as alternate energy source for muscles
Minor inputs: - high amino acids in the blood after a high protine meal increase GH
- low fatty acids in the blood increase GH
- ghrelin ( hunger hormone released by the stomach
52
Q
growth hormone deficiency
A
- main causes: pituitary issues (tumours, damage, inflammation) or congenital
53
Q
GH deficiency effect on newborns
A
- no issues before birth (micropenis in males) hypoglycemia. if untreated it could result in dwarfism
54
Q
GH deficiency effect on Adults
A
- reduced muscle mass and bone mass (osteoporosis), reduced energy, baldness, increased body fat, high cholesterol, cardiac dysfunction
treatment: injection of GH
55
Q
growth hormone hyperproduction
A
- main causes: pituitary issues tumours or congenital
56
Q
GH hyperporduction in children
A
- causes gigantism
- easily detected with glucose ( low blood glucose - GH is released, so to test increase blood glucose measure would be 0)
- but with hyperporduction - high blood sugar can still measure GH but it would always have a value greater than 0 because its always on
57
Q
GH hyperprodution in adults
A
- causes acromegaly
- wont be taller - plates are closeed but parts of the body will be continuing to grow
- wide nose, cheek bones and brow bones noticible
- treatment : injection of synthetic GHIH
58
Q
not all growth defects are due to growth hormones
A
- short proportional limbs = hormonal
- short unproportional limbs = genetics
59
Q
thyroid gland
A
- thyroid H produced by endocrine cells arranged in thyroid follicles
mammals: 2 lobes joined by narrow portion (looks like a bowtie)
non-mammalian: clusters of thyroid follicles, central or paired, around the ventral region of the head
structure highly conserved
60
Q
follicular cells
A
- secretory cells = follicular cells
- arranged in spheres, full of fluid = colloid (storage of TH)
- collide made of large glycoprotein thyroglobulin (Tg)
- Tg serve as building platform for TH
- unique mode of storage (extracellular ) - reflects the evolutonary origin of the thyroid (endostyle: exocrine secreting digestive organ)
- stores iodine (I) (80% thyroid, 20% eyes, ovaries and mammary glands)
61
Q
synthesis of thyroid horome
A
- follicular cells produce 2 iodine -containing hormones:
- tetra-iodothyronine aka thyroxine T4
- tri iodothyronine T3
- T3+T4 = thyroid hormone
- to make thyroid hormone you need tyrosine and iodine
62
Q
step 1 in synthesizing thyroid hormones
A
- Tg(containing tyrosine) are produced in the thyroid follicular cell by the ER and Golgi complex
- it is then expoted by exocytosis
63
Q
step 2 in synthesizing thyroid hormone
A
- iodine is carreid by active transport from the blood into the follicular cell
- use atp to gte salt and keep iodine
64
Q
step 3 in synthezing thyroid hormone
A
- in the cell, iodide is oxidized into an active form by TPO
65
Q
step 4 in synthezing thyroid hormone
A
- active iodine goes into the colloid through a luminal channel
66
Q
step 5
A
- TPO attaches to iodide to tyrosine within the Tg molecule
Tg+I MIT = (mono-iodo tyrosine)
MIT+I DIT = ( di-iodo-tyrosine)
67
Q
step 6
A
- coupling of molecules to form hormones
- MIT + DIT = T3 (3 iodides attached)
- DIT + DIT = T4 (4 iodides attached)
68
Q
step 7,8,9
A
- on stimulation, follicular cells engulf colloid with Tg in it by phagocytosis
- lysosomes (contained degradative enzymes) attack the vesicles and split the Tg from the other iodinated products)
- T3 and T4 diffuse into the blood MIT and DIT are deionated and the free I is recycled
69
Q
transport
A
- more that 99% of TH is bound to plasma proteins (ineffective)
- thyroxine binding globulin (TGB - T3 and T4), albumin and others
- varies by species: fish and amphibians: transthyretin (TTR for T4)
- <1% T3 and less than 0.1% T4 remains unbound (free)
- most often thyroid produces more t4 than the T3
- regardless more T4 is converted to T3 in the kidneys and liver
T3 is the major biologically active form of TH - deactivation: type 1 deiodinase (T4-rT3 )
- control of biological effect
70
Q
effects
A
- Th are lipophilic hormones: cross the plasma membrane without transporter
- binds to intracellular nuclear receptors, that sits on the thyroid repsonse elemnent(TRE) of DNA) affect the transcripton of MRNA and alter protein production
- slow reaction - TH is often refered to as sluggish
- hours or days later
- effects broken into (metabolic effects, cardiovascular effects, growth and nervous system)
71
Q
metabolic rate and heat production
A
- evolution of endothermy = need a way to control temperature
- TH does that by modulating basal metabolic rate (BMR)
- effects mediated by regulation of mitochondrial function and protein that generate heat
72
Q
metabolic rate and heat production
A
- endotherms have high levels of TH
- ectotherms have selectively high level of TH, during time of high metabolic demands (mating and migration)
- when endotherm body temp drops - theres a drop in TH
73
Q
metabolic rate and nutrients
A
- concentration-dependent effects:
- low [TH] anabolic effects buildup
- glucose - glycogen (for storage)
- protein synthesis
- store fat
High [TH] catabolic effects (breakdown) - glycogen - glucose (released into blood)
- protein breakdown/wasting - AA in blood
-breakdown of fat - fatty acids in blood
74
Q
cardiovascular effects
A
- TH increases heart responsiveness to catecholamines
- increase of HR
- force heart contraction and increased cardia output
- increased heat production and increase of vasodilation to get rid of the heat
75
Q
growth and nervous system
A
Th essential for normal growth:
- indirect effect:
- need TH for GH secretion
- promotes GH and IGF effects on synthesis of new proteins and skeletal growth
- note: low [TH]- stunted growth high [TH] excess growth
- Th required for normal nervous system:
- allows for normal development
- needed for normal transmission of AP through nerves
76
Q
dermatological effects
A
- Th increase associated with molt process in mammals and birds
growth of new feather, horns and hair - TH required for normal skin and hair cell turnover
hair: - low Th: more telogen (inactive) hair follicles
- dry coat, excess shedding, spot baldness
skin: - low Th thikened skin (myxedema
77
Q
sympathomimetic effects
A
TH increase target cell responsiveness to catecholamines (epinephrine and norepinephrine)
fight or flight response
78
Q
more (but poorly understood effects)
A
- immune system
- hematology
- reproduction
79
Q
regulation of TSH
A
- from the ant pit is the most important regulator of TH secretion
- TSh also maintain the integrity of the gland itself
- no TSh - atrophy of the thyroid gland. low TH secretion
- too much TSh - hypertrophy (increased size of follicles) and hyperplasia (increased number of follicles) = goiter
- TH inhibits the release of TSh ( negative feedback)
- TSh is stimulated by TRH (thyrotropin-releasing H) from the hypothalamus
80
Q
hyperthyroidism
A
- not enough thyroid hormone produced
- hypothalamus issue, ant pit issue
thyroid not responding to TSH, poor amount of iodine, autoimmune attacks thyroid - increased TSh and Th, resulting in goiters
81
Q
hypothyroidism
A
- decreased BMR (cold intolerant)
- weight gain
- lack of energy
- poor pulse, slow heart rate
- decreased CNS alertness and memory
- poor skin, hair loss and puffiness
- from birth = cretinis, (impaired physical and mental growth)
- from adulthood = myxedema - puffy face and extremitites (treated by iodine and H defficienct - T4
82
Q
hyperthyroidim in cats
A
- increased BMR ( heat intolerant)
- weight loss
-irritability - heart failure due to increased cardiac output
- bilateral hair loss
83
Q
treatment of hyperthyroidism in cats
A
radioactive iodine (I131) selectively kills the thyroid, but safe for other tissues
- surgical removal of thyroid
- anti-thyroid drugs (lower T4 levels)
- very low iodine diets
84
Q
adrenal glands
A
- mammals have 2 adrenal glands (next to the kidney) on top of each kidney
- for most species:
- outer layer: adrenal cortex - secretes steroids (cells: steroidogenic cells)
- inner layer: adrenal medulla (secretes catecholamines)(cells: chromaffin cells)
85
Q
adrenal cortex
A
- 80% of the adrenal gland of most mammals is made of cortex, that has 3 layers
1. zona glomerulosa (outermost layer)
2. zona fasciculata (middle and largest)
3. zona reticular (innermost) - the adrenal cortex produces different adrenal-corticoids, all of which are steroids derived from the common precursor cholesterole
- all steroidogenic cells are filled with droplets of cholesterole
- cholesterol - pregnolone (in all cells)
- each tissue has a set of enzymes to produce one or several, but not all steroids
86
Q
mineralocorticoids
A
- mostly aldosterone: influence electrolyte balance (na and K mainly)
- produced only in the zona glomerulosa
- part of the RAAS: aldosterone release stimulated by angiotensin II
87
Q
glucocorticoids
A
- mostly and corticosterone: major role in glucose metabolism, and lipid and protein metabolism
- produced mostly by zona fasciculata and a bit by zona reticularis
88
Q
sex steroids
A
- identical or similar to the ones produced in the gonads. most abundant and important one is DHEA
- produced by zona fasciculata and zona reticulous
89
Q
transport of steroids
A
- they are lipophilic - all of them are carried in the blood bound to plasma proteins but wide variations
- 60% aldosterone is bound to proteins, most non-specific albumin
- 90% glucocorticoids are bound, mostly to corticosteroid binding globulin
- 98% DHEA is bound, just to albumin
90
Q
mode of action for steroids
A
- all steroids bind to a receptor specific for it within the cytoplasm of the target cells:
- MR (mineralocorticoidoid), GR (glucocorticoid), AR (androgen)
- carried in the blood, as soon as carrier let it go, floats through blood stream
- the receptor needs the H to bind to the DNA: no H DNA access
- binding occurs at a very specific site on the DNA: the HRE which is specific to each H
91
Q
glucocorticoids metabolic effects
A
- overall effects: increase the concentration of blood glucose at the expense of protein and fat storage
- stimulates gluconeeogenesis: conversion of non-carb in to carb) during fasting glycogen in liver becomes depleted (broken down to maintain blood glucose level)
- gluconeogenesis - to replenish those hepatic glycogen reserves
- inhibits glucose uptake: in all tissue but in brain, help to keep the reserves of glycogen for the brain only
- stimulates proteins degration, especially in muscles (breaks down muscle - increases AA in the blood)
- allows repair of damage tissue. helps build new cellular structures
- facilitates lipolysis (break down fat)
- release fatty acids in blood, used for fuel
92
Q
permissiveness glucocorticoids
A
- one H must be present in adequate amount for full exertion of another H effects
- glucocorticoids are extremely important for their permissive actions
93
Q
brain effects glucocorticoids
A
- affect neural function
- cortisol exposure during a learning even may help or impede the consolidation of these events
- cortisol also interferes with information recall
- too much cortisol (stress) is linked to memory loss in humans
94
Q
what is stress
A
- generalized non specific response to any factor that overwhelms, or threatens to overwhelms the bodys ability to maintain homeostasis
- stressors can be physical, chemical physiological and social
- measure of cortisol in the blood is a good indicator of stress: the greater the increase the greater the stress
95
Q
anti-inflammatory and immunosuppressive effects
A
- stress and issue injury:
- if stress + injury happens: increased inflammation and increased immune response
- cortisol: anti-inflammatory + immunosuppressive effect - keeps bodys response in check (too much inflammation is bad)
- partially blocks production of inflammatory chemicals such as prostaglandins
- stops migration of neutrophils to injured site
- interferes with phagocyte activities
- stop production of fibroblasts
- interferes with antibody production
cortisol and immunity interact - helps to keep homeostasis
96
Q
dose-dependent effects
A
- normal dose (low ) = no anti-inflammatory effects
- normal dose (high) = anti-inflammatory effects (immunosuppression)
- stressed animals are more susceptible to infections
97
Q
how do we stress animals
A
- handling techniques, manipulations in domesticated and wild animals can increase cortisol release
98
Q
medical applications of glucocorticoids
A
- low dose for anti-inflammatory effects
- decreased swelling after calving, sprains and strains
- decreased respiratory inflammation: necrotic laryngitis (caves) asthma (fluticasone)
- allergic reactions
- high doses : immunosuppressive effects,
99
Q
negative effects of glucocorticoids
A
- anti-inflammatory effects + metabolic effects
- increased chance of infection
- increased fat and protein breakdown in the long term
- hypothalamus pituitary adrenal axis suppression
- inhibits CRH and ACTH release
- abortion in pregnant animals
100
Q
regulating pathway glucocorticoids
A
- HPA
- hypothalamus release CRH
- stimulates anterior pituitary to release ACTH
- ACTH stimulates adrenal cortex to release cortisol
- ACTH stimulates both the growth nd secretory output of the 2 inner layers of the cortex
101
Q
sex hormones
A
- adrenal cortex in both sexes produce both androgens (male sex hormones) and estrogens (female sex hormones)
- under normal conditions, those secretions are not enough to induce masculinizing or feminizing effects
- the only adrenal sex hormone that has significant biological effects is the androgen DHEA
- overpowered by testicular testosterone in males
- important for females who otherwise lack androgens
- females: repsonsible for androgen-dependent processes:
- growth of pubic hair
- growth of armpit hair
- increased growth spurt at puberty
- development and maintenance of female sex drive
102
Q
to much cortisol
A
- cushings (common in older dogs, horses)
- cause by too much CRH and ACTH - pituitary tumours are most common, rarely : adenal tumour
symptoms: too much gluconeogenesis (high blood glucose, protien shortage )- muscle loss - glucose end up in urine and thirst (mimic diebetes mellitus)
- increased appetite, weight gain
- poor skin, loss of hair
- increased chances of infection
- high blood pressure
103
Q
treatment of cushings
A
- treatment:
- destroy the adrenal cortex
- inhibits cortisol (steroid) synthesis
- reduce steroid use
104
Q
addisons disease
A
- not enough corticol
- common in certian dog breeds, body destroys cortex - results in low cortisol and low aldosterone
- aldosterone deficiency is most risky (low bp hypovolemia) could be fatal
- animals often weak and lethargic weight loss low BP low blood sugar
- treatment: exogenous glucocorticoids and mineralocorticoids (aldosterone)
105
Q
adrenal medulla is a modified sympathetic ganglion
A
- preganglionic neuron: originating in teh CNS whose axon ends up in the postganglionic neuron which terminates in the effector organ
- the post ganglionic neurotransmitter released is norepinephrine which binds to target receptors called adrergic receptors
- the adrenal medulla has a modified postganglionic called chromatin cells
- they dont have axons, they dump chemical transmitters directly in the blood neurohormones
- some NE but mostly epihephrine is released in mammals
- belong to catecholamines derived from tyrosine
106
Q
storage
A
- synthesis of catecholamines in the cytosol of medullary cells
- epiphrine and NE produced are stored in chromatin granules
- released by exocytosis of chromaffin granules
- once released, degration in fast (minutes)
107
Q
control
A
- catecholamines secretion: control by sympathetic input into the gland
- short term fear/stress - catecholamines released
- increase preganglionic sympathetic impulses to adrenal medulla
- physical/environmental distrubances hemorrhage illness exercise hypoxia cold exposure hypoglucemis
108
Q
epinephrine
A
- repsonsible for the fight or flight response and metabolic effects: imminent danger (short term stress): need to mobolize resources to sustain peak physical exertion
- caridac effects: increase rate and strenth of cardian contraction - increase cardian output activates B 1 receptors using both epi and norepinephrine
109
Q
vascular effects for epinephrine
A
- a-1 receptor: causes vasoconstriction increases systemic blood pressure - both epi and norepi
- skin abdominal organs - redirect blood critical organs
- B-2 receptors: causes selective vasodilation, muscle brian and heart vessels - epinephrine only
- divert blood flow to vital fight or flight organs
110
Q
respiratory effects
A
- b-2 receptor activation (epinephrine only) causes bronchodilation allowing for increased ventilation
111
Q
metabolic effects
A
- working at low concentration (lower than that ti change HR)
- mobalization of stored carbs and fat to provide energy to muscles
- increase blood glucose via gluconeogenesis and glycogenolysis (break down of glycogen into glucose ) in the liver
- stimulates glycogenolysis in the skeletal muscles: BUT glycogen is not broken down into glucose for the blood. rather glycogen is broken down into lactate burst of ATP for muscles ( anaerobic)
- increased blood fatty acid levels by promoting lipolysis
- pancreas: decreased insulin and increase glucagon release
- increase overall metabolic rate (tissue metabolize faster) similar effects that TH
112
Q
other effects
A
affects CNS: promote state of arousal and increased alertness (adrenal rush)
- causes sweating to eliminate heat
- decreased salivation
- dilates pupil flatten the lends increases panoramic vision
- decreased digestive activity and inhibits bladder
113
Q
catecholamine function
A
- requires other hormones for maximum effect
- thyroid hormone will increase adrenergic recptors
- cortisol increase catecholamine induced vasoconstriction
- other hormones in involved in stress response
114
Q
what is the prolonged stress response
A
- decreased long term energy stores
- proteolysis (cortisol)
- lipolysis (cortiosole epinephrine)
- immunosuppression (cortisol)
- decreased parasympathetic function (GI tract)
- psychological effects - maladptive stress response
- epigenetic effects: infant rearing modifies activation of HPA axis
- affect resilience to and control of stress reponse
115
Q
A
