Homeostasis Flashcards
endocrine, excretory, nervous
What is the purpose of homeostasis
to keep enzymes in their optimal conditions (keep them happy)
- high priority is invested into maintaining favorable internal conditions
Negative FBL
- what are they
- provide an example
- works against change
- maintains dynamic eq
- wave function when graphed
ex: insulin and glucagon, reaction to cold, response to dehydration, respiration
Positive FBL
- what are they
- provide an example
- reinforces change by AMPLIFYING affect
- exponential, linear, geometric
ex: child birth, blood clotting,
explain the positive feedback loop in child birth
baby head pushed on cervix (stimulus) –> cervix tissue tension –> stretch receptors stimulated –> hypo stimulates ant. pit –> ant. pit releases oxytocin –> smooth muscle tissue contracts –> baby is pushed MORE = cervix is stressed –> cervix tissue tension
what are the components of a FBL
stimulus, sensor, control centre, effector
hypothalamus
- main control centre
- receives information from PNS (sensory) and sends appropriate instructions often through the pituitary gland
pituitary gland
- posterior and interior portions
- sits underneath hypothalamus
- receives signals from hypothalamus and sends signals to wherever they need to go through HORMONES
- controls growth, H2O levels (ADH)
what are hormones
- chemical signals that influence cell activities
what are target cells
cells with matching receptors to hormones
- similar to substrate-enzyme concept
endocrine glands
- secreted INTO body
- travel throughout body via circulatory system to its target cells
- EMPTIES its contents into blood stream
exocrine glands
secreted OUT of body through ducts
TRH
- name
- released by ___
- stimulates ____
- purpose
thyrotropin-releasing hormone
- released by hypothalamus
- stimulates pituitary gland
- allows glands to communicate with each other
TSH
thyrotropin stimulating hormone
- released by pit. gland
what connects the hypothalamus to the pituitary gland
infundibulum
thyroid gland purpose
regulate metabolism
parathyroid gland purpose
control Ca levels in blood
what causes abnormal growth
pituitary tube
Steroid Hormone
- characteristics
- how does it work
- non polar = diffuses right into cell membrane
- diffuses into cell
- binds with receptor in CYTOPLASM
- HORMONE-RECEPTOR COMPLEX enters nucleus and goes thru protein synthesis
Peptide Hormones
- characteristics
- how do they work?
- polar –> cannot diffuse thru cell membrane easily
- binds to receptor ON cell membrane
- produces G-PROTEIN
- interacts with ADENYLATE CYCLASE
- activates cAMP
- activates protein kinase
- reduced ATP (2 PO4)- metabolic changes in cell
Transduction/Phosphorylation Cascade
each protein activates the next like a domino effect thru phosphorylation and the last step is when the very last protein causes an effect on the cell
Explain Cell Signaling with Insulin & GLUT4
when blood sugar is high, insulin is released from liver which binds to receptor on GLUT4 membrane allowing the gates to open and glucose to rush into cell
Local signalling
- nearby cells effected
- uses NRTMS
- immune cells use DIRECT CONTACT
Long distance signalling
- distance cells effected
- release hormones into blood and carry it thru out body (endocrine signaling)
BMR
- basal metabolic rate
- baseline/reference point of a persons rate of metabolism
what are the conditions that must be met when finding a persons BMR
awake, fasted for 12 hours, rested
what does BMR affect
insulin, sex hormones, etc but doesnt regulate them
what regulates BMR
thyroid glands
what do thyroid glands control?
prolonged stress and cold exposure, BMR
thyroid hormones
iodine + tyrosine = thryoid hormone
use FBL to explain how thyroid hormones work
cold (stimulus) –> hyp stimulated –> releases TRH –> pit. gland stimulated –> releases TSH –> thyroid stimulated –> releases T3/T4 –>inc BMR, glucose levs = H+ leak in mitochondria = thermal energy produced
goiter
occurs when theres low iodine
- low I = low T4 = inc TSH to stimulate hormones to make more T4 = builds up in thyroid
cretinism
no t3/t3 in babies = developmental delays
primary hypothyroidism
thyroid cant produce the hormone orders from pit gland
secondary hypothyroidism
thyroid isnt stimulated by pit gland to make hormones
hyperthyroidism
overactive thryoid = inc bmr = weight loss
graves disease
autoimmue bodies mimic TSH and overstimulate thyroid
relation b/w insulin and glucagon
- antagonistic
- both peptide based hormones
- respond to [blood sugar] directly –> dont need hypo. or pit. gland
- neg FBL
- their effects trigger e/o
what happens if ur blood sugar is too high?
HYPERtonic solution –> RBC water LEAVES = BV inc = BP inc = inc dehydration
why do we feel dehydrated when our [blood sugar] is high
- in order to secrete the excess glucose, we pee alot of it out along with the h2o that left our cells to enter out hypertonic blood
what happens if ur blood sugar is too low?
- lose consciousness bc vital processes/organs prioritized
- lose body mass thru protein/lipid catabolism to get more glucose
insulin
- secreted by?
- what does it do?
- how does it work?
- secreted by beta cells, triggered by high blood sugar conc
- stops sending glucose to gluconeogenesis and lipolysis. stores glucose as glycogen in liver
- binds to cell receptor on membrane -> transduction–> inc GLUT4 production –> inc glucose intake in cells
Gluconeogenesis
making new glucose molecules by taking the glycogen stored in the liver (glycogen –> glucose)
lipolysis
breaking white fat down thru beta-oxidation for more glucose
Glucagon
- secreted by?
- what does it do?
- how does it work?
- secreted by alpha cells when low [blood sugar]
- a-cells activated = released glucagon in blood stream –> go to liver to do gluconeogenesis and lipolysis
- inc blood sugar
Type 1 Diabetes (Juvenile)
pancreas doesnt produce enough insulin = too much gluc in blood stream = hypertonic solution = dehydration, fatigue, weight loss (cells go to lipolysis for glucose)
Type 2 Diabetes (Adult Onset)
- desensitized insulin receptors
- GLU4 doesnt open
- high blood sugar
what is the pancreas’ role?
- endocrine and exocrine function
- acts as both sensor and control centre
- endocrine fn: release insulin/glucagon to control blood sugar levels
- exocrine: digestive enzymes
3 key characteristics of stress are….
- stress calls for action
- our body responds to physical/mental stress the same way
- can cause structural/physiological changes to our body temporarily or long term
what do our adrenal glands to when activated by stress? (3 marks)
- move blood away from extremities and to core organs
- vasoconstrict = inc BP = inc HR
- open up lungs = inc o2
what is our adrenal medulla responsible for?
fight or flight response
- releases epinephrine/norepinephrine
what does epinephrine/norepinephrine release cause/do
- inc HR, BP
- lipolysis (more gluc = more energy)
- narrow veins
- open lungs (adrenaline)
- muscle glycogen –> muscle glucose (adrenaline)
what part of the NS is the adrenal medulla in? what is this part responsible for?
sympathetic
- alarm stage
- fight or flight
- short term
how does our ant pit contribute to our stress response?
secrete ACTH and beta- endorphins (pain)
- resistance stage
- sustained response
what is our adrenal cortex responsible for?
- long term stress
- creates/synthesizes CORTICOSTEROIDS
what effect do glucocorticoids (cortisol) have?
- MAINTAINS high blood gluc levels to help brain fn and have enough energy to SUSTAIN FOF response
- breaks down fats EVEN MORE
- suppresses immune fn and inhibit inflammatory response
- released during intense physical exercise
what effect does mineralocorticoids (aldosterone) have?
- maintain electrolyte balance
- reabsorb na/h2o in kidneys
- inc BV/BP
- release stimulated by dehydration, low na, blood loss
using a flow chart, explain how our body reacts to LONG TERM stress
stress/rhythm –> hyp –> CRH –> ant pit -> ACTH –> adrenal cortex –> cortisol –> inc blood gluc, a.a, f.a
what occurs in exhaustion stage?
- no more F.O.F
- long term effects of glucocorticoids
- prediabetic (long term blood gluc levs)
- lose muscle mass/strength
- impaired congnitive fn (memory, emotion, decision making)
cortical sex hormones
- creates sex hormones before gonads develop
- determines how gonads will develop through its levels in developing embryo
where does intercellular waste come from
cellular rxns
- cell resp/metabolism
- CO2, H2O, NH4+, PO4+
- breakdown of a.a,f.a,n.a
- drug/toxin metabolism
what is oxidative deamination?
removing an NH2 group from proteins turning it into NH4
- the remaining C molecule goes to krebs
what is the diff between single cells and clusters when it comes to excreting intercellular waste?
small cells: diffusion
large cells: transport system
what is a waste transport system made up of
circulatory system: prevents hypertonic solution of waste and how things actually leave
excretory system
what type of animal excretes ammonia? what are characteristics of ammonia that can explain this
aquatic animals
ammonia is: highly soluble (can diffuse in h2o quickly) & high toxic (its alright bc its flushed out by currents in sea)
highly toxic: due to it being highly toxic, animal wants to excrete it quickly, often losing water. this is fine bc it lives IN water so can easily be replenished
what type of animal excretes urea? what are characteristics of urea that can explain this
terrestrial animals
urea = processed nh4 (in liver)
- mid-soluble: larger molecule
- less toxic: less urgent to get rid of = can hold in more water
WATER SHOULD BE PRESERVED BC ITS NOT EASILY ACCESSIBLE
what type of animal excretes uric acid? what are characteristics of uric acid that can explain this
egg laying animals
- low solubility: excreted as solid, once it leaves embryo in egg, wont come back in, protects embryo
-lox toxicity: doesnt damage embryo
- even larger molecule
- flying animals want to minimize weight, solid waste means less water loss/less need to drink more water = LIGHT!
what are the 3 main job of the kidney?
- filtering out waste from blood
- maintain key conditions
- excrete hormones
ADH (Anti-Diuretic Hormone)
purpose: reabsorb H2O, decrease urine output
- secreted by post. pit
stimulus: low bp, high osmorality
controls: collecting ducts, bp, osmorality
effect: makes collecting ducts more permeable to h2o by pushing aquaporins to membrane and allow more h2o to be absorbed = inc bv = inv bp = dc osmorality
RAAS (Renin - Angiotensin - Aldosterone System)
renin: kindeys
angiotensin 1: liver
renin + angiotensin 1 = angiotensin 2
aldosterone: adrenal cortex (mineralocorticoids)
- Na/H2O reabsorption
stimulus: dehydration (low bv = low bp)
controls: juxtaglomerular cells, bp, bv
effect: angio2 inc bp aldosterone = inc h2o = inc v= inc bp
EPO (erthyropoetin)
- comes from BONE MARROW
- secreted in KINDNEYS
- promotes RBC production
stimulus: low o2 (hypoxia)
controls: RBC production
effect: inc RBC = inc O2 brought everywhere = dec hypoxia-inducible factor = stop hypoxia
Bright’s Disease
cause: autoimmune disorders\diseases
response: inc bp, inflammation of tissues, protien in urine
treatment: low protein diet, ACE inhibitors, diuretics
Nephritis
cause: autoimmune diseases/UTIs
response: inflamed nephron = inc pressure = nephron damaged = RBC in urine = improper waste secretion (escaping from the glomerulus)
activates RAAS = inc bp
Treatment: antibiotics, steroids, antiinflammatory
hypertension
cause: high bp
response: high bp = damage blood vessel = damage nephron
- vasoconstriction inc = flexibility dec
adh/raas: more salt = more h2o = more v = more bp
Treatment: ACE, diuretics
Diabetes Insipidus
cause: improper secretion/response to ADH
response: improper response = not enough water being reabosrbed = water treated as waste = peeing a lot
treatment: synthetic adh drugs
kidney stones
cause: crystallization of salts in urine (uric acid, ca, oxalate)
response: stones in collecting ducts
treatment: diuretic, pain medicine, break them apart
purpose of nervous system
gathers, interprets and transmits info between cells
central nervous system
- what does it do
- what body parts are included
receives input from PNS (sensory), processes info and coordinates a response (sometimes sent to PNS (motor))
- brain and spinal cord
what parts of the brain are apart of the CNS
cerebrum, cerebellum, brain stem
white matter
bundles of myelinated axons
- continuous
grey matter
unmyelinated axons, nuclei and dendrites
- where synapses occur
- what surface of brain is mostly made of
what would happen if the brains grey matter was somehow damaged
synapses wouldnt occur properly, nerves wouldnt be able to communicate to each other, vital signals wouldnt be sent out, we die
cerebrospinal fluid
shock absorber
- blood brain barrier: blood doesnt actually come in contact with the brain
- allows nutrients to circulate in the CNS
Peripheral nervous system
- what does it do
- what parts are involved
connects CNS to muscles/other organs
- sensory receptor: responds to internal/external stimulus
- motor output: receives response from cns and uses effector cells to act on them
autonomic nervous system
automatic response we do without thinking
parasympathetic nervous system
rest and digest
sympathetic nervous system
fight or flight
somatic nervous system
voluntary movement
neruons
bundles of cells that make up nerves, carrying impulses in ONE direction through synapses and action potential
dendrites
receives info from other neurons, carries impulse towards axon
axon terminals
connect neuron to many other neurons, glands or muscles
- brings impulse AWAY from axon
reflex arc
stimulus –> sensory neuron (PNS) –> interneuron (spinal cord - CNS) –> motor neuron (PNS) –> response
gyri
bumps/ridges
SULCI
crevices/valleys
purpose of gyri/sulci
folding increases SA and represents the synapses
corpus callosum
- where left and right brain hemisphere connect
- thick bundle of axons (white matter)
parts of forebrain
– diencephalon
- cerebrum
diencephalon
- major relay centre
- monitors homeostasis
cerebrum
largest part of the brain
- split into 4 main sections: temporal, parietal, occipital, frontal
frontal lobe
responsible for speech, emotions, motor controls and DECISION MAKING
parietal lobe
responsible for speech, taste, reading, sensory
temporal lobe
balance and hearing
occipital lobe
- vision
thalamus responsibility
- switching centre for nerve messages
- sensory info (except smell) goes here first
what does pons and medulla oblongta do
control our HR, vasoconstriction, digestion, swallowing, vomitting and respiration
what is in the hindbrain
- brain stem
- medulla oblongta
- pons
- cerebellum
brain stem
- connects brain to spinal cord
- smallest, oldest, most primitive part of body
- autonomic nervous system
- responsible for essential body functions
cerebellum
fine motor control and balance
cerebral cortex
thin layer of gray matter covering the cerebrum
what parts of the brain are in the limbic system
- hippocampus
- amygdala
- thalamus
- hypothalamus
what does limbic system do
stores emotions and emotional memories
hippocampus
short term —> long term memory
amygdala
survival type of emotions
- fight or flight
- hippocampus turned off when amygdala is active
what is the purpose of the diencephalon in the limbic system
provides pathway for info going to limbic system
the reticular system, arousal and sleep
- regulates sleep and arousal
- acts as sensory filter
- the reticular activating system of reticular formation
what is reticular formation
major switching centre and filter for sleep cycles
sleep paralysis
mismatch between sleeping and awake areas of brain
rem antonia
NRTMS paralyze all muscles during sleep, preventing o2 intake trigged by FOF during sleep paralysis
what do these sleep waves mean?
- alpha
- beta
- delta
alpha: awake but quiet
beta: awake during intense mental activity
delta: deep sleep
dopamine
pleasure
- becomes addictive
- main NRTM in reward pathway
serotonin
happy
GABA
inhibitory NRTM
- calms firing nerves in CNa
- contributes to motor control/vision
- increases focus
glutamate
excitatory
- cognitive functions, synapses
epinephrine
- inhibits memory
- dilates airways, inc HR, Blood flow, o2
norepinephrine
attention and response
- fight or flight
- contracts vessels = inc blood flow
acetylcholine (Ach)
- learning, thought, memory
- enhancement of sensory perception when walking
heroin
- before drug: dopamine NRTM inhibited
- heroin mimics natural opiates and binds to opiate receptor allowing dopamine to flood into synapse
marijuana
- before: dopamine released inhibited by inhibitory NRTM in synapse
- THC mimics anandamide and binds to cannabinoid receptors allowing dopamine to flood into synapse
- anadamide removes unnecessary short term memory and relaxation of muscles —> forgetfulness and sluggishness
LSD
LSD builds to serotonin receptors instead of actual serotonin resulting in an inhibitory or excitatory response depending on the receptor it binds with
- results in hallucinations and distress
alcohol
- interacts with GABA receptors making the even more inhibitory
- binds to glutamate receptors = preventing glutamate from exciting the cell —> cannot rmr or make good decisions
ecstasy
ecstasy mimi’s serotonin and is taken up by serotonin receptors instead —> confuses transporters —> actual serotonin is transported out of cell and trapped in cleft —> continuously binds to it’s receptors —> overstimulation
cocaine
coke blocks dopamine transporters —> dopamine trapped in cleft —> keeps binding with receptors —> overstimulation
methamphetamine
meth mimics dopamine —> transporters take meth instead —> meth kicks dopamine out after entering vesicles —> dopamine stuck in cleft, keeps on binding to its receptors —> overstimulation
what determines the effect a NRTM will have
- its time spent in cleft
- concentration
- IPSP vs EPSP
what is the order of a synapse
- Ca++ enters axon terminal (presynaptic cell)
- entry causes vesicles carrying NRTMs to move towards membrane, leaving thru excocytosis
- gates open on post synaptic cell
- graded potential created
