1/44
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
adaptation
changing genotype, changing phenotype
genetic variation
role for the environment
long term (between generations, affects species/population)
evolution
population genotypes and phenotypes change over time
variation
genotypic differences result in phenotypic differences
selection
environmental pressures affect reproduction
acclimation
short term (within generation, affects individual)
phenotypic plasticity
regulated gene epxresion
role for environment
endocrine system
homeostatic regulation of other physiological systems
autocrine signals
act on same cell and secretes them
not very efficient
paracrine signals
diffuse locally and act on neighboring cells
endocrine signals
hormones carried between cells by blood or other body fluids
neural signals
diffuse a short distance between neurons
neuroendocrine signals
released from neurons but are carried by blood or other body fluids and act on distant cells
pheromones
released into the environment and act on a different individual
hypothalamus
antidiuretic hrmone (ADH)
promotes reabsorption of H2O by kidneys
ACTH (adrenocortiotropic hormone)
stimulates adrenal glands to secrete glucocorticoids such as cortisol
epinephrine
produces effects related to short term response
HPA axis
hypothalamic pituitary adrenal axis
regulates stress response
cortisol
ACTH, adrenal cortex —> produces glucocorticoids
amplification of hormonal signal
signaling cascade
not in one cell, in many!
negative feedback loop
homeostasis
stop signal by stopping the production of the signal
more cortisol —> negatively affects HPA axis to stop releasing hormones
regulation of blood sugar
hormones: insulin and glucagon
type 1 diabetes
juvinile, insulin dependent
insufficient insulin - deficiency of siignal
autoimmune destruction of endocrine cells in pancreas (beta cells in islets of langerhans)
type 2 diabetes
decreased responsiveness to insulin signaling → deficiency of receptor
lipid-mediated/increase in protein kinase C activity reduces efficiency of signaling from insulin receptor
pancrease
insulin and glucagon expression limited to this
glucagon receptors
binds to gpcr receptor (g protein coupled)
signal cascade
amplification done by secondary messenger AND kinases
insulin receptor
tyrosine receptor kinase (dimer)
regulation by alternative splicing
glucagon signaling
low glucose level seen by pancreas
glucagon stimulates to increase blood glucose
negative feedback to pancreas to no longer release glucagon
hyperthyroidism
hormone: thyroxine
effects: increased basal metabolic rate, increased heat production, increased sensitivity to adrenaline
symptoms: weight gain, increased heart rate, hair loss, sweating, nervousness
treatment: dietary (eat iodine), radioactive iodine, beta blockers, surgery
thyroxine synthesis
tyrosine: chemical basis of thyroxines
iodine: unique use of this element in physiology
selenium: cofactor in enzymes used to convert T4 into active hormone
increases HR, increases
sensory neuron
dendrites (top)
cell body (middle)
axon (bottom)
interneuron
more dendrites
connected to thousands of neurons
motor neuron
astrocytes
care and protection of neurons
oligodendrocytes and schwann cells
forms myelin sheaths
ependymal cells
produces cerebrospinal fluid
microglial cells
acts as immune cells
Na+/K+ pump
direction of ion flow
energy used
regulated by
K+ channel
direction of ion flow
energy used
regulated by
voltage gated Na+ channel
direction of ion flow
energy used
regulated by
Voltage gated K+ channel
direction of ion flow
energy used
regulated by
voltage gated Ca2+ channel
direction of ion flow
energy used
regulated by
voltage gated (forgot)
direction of ion flow
energy used
regulated by
action potential
resting potential (-70) → voltage gated Na+ channels open and Na+ enters cell causing positive spike in membrane potential (positive inside relative to outside) → (electrical gradient brings to 0 but chemical brings it to +40) → at +40mV, Na+ channels close and voltage gated K+ channels open which allows K+ ions to leave cell and causes membrane potential to become more negative → overshoot in amount of K+ ions that leave the cell causes cell membrane to be hyperpolarized (leading to refractory period where nerve can’t fire another action potential) → membrane gradually returns to resting (Na+/K+ pump) as excess K+ ions are returned to cell AND potassium channel changes direction it moves potassium
axon helic