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Physiological Systems > FINAL > Flashcards

FINAL Flashcards

1
Q

What is the purpose of the eye?

A

collect light + focus light onto the retina
- visible spectrum = 400-750 nm (purple to red)

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2
Q

What are the main functional components of the eye and what is their purpose?

A
  1. cornea: does most of the focusing
  2. pupil: controls how much light goes in
  3. lens: shape modified by ciliary fiber contraction: changing shape = “accommodation” –> allows fine focus
    - rounding increase focal power + enables viewing of near objects
  4. fovea: pit/focus point in the center of the macula of the retina where light is focused; high cone density –> high spatial contrast detection at the center of gaze
  5. retina: part of the CNS; composed of light detecting cells (photoreceptors) and other neurons
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3
Q

What are the common vision abnormalities?

A
  1. myopia (nearsightedness): light focuses in front of the retina
  2. hyperopia (farsightedness): light focuses behind the retina
  3. astigmatism: light does not focus and causes distorted vision
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4
Q

Explain the pupillary response.

A

Dilation: sympathetic
- relaxes ciliary muscles
Constriction: parasympathetic
- contracts ciliary muscles

Control of the pupils in the two eyes is “yoked” = work together, only one needs to be stimulated

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5
Q

What are the structures and functions of the main cells in the retina?

A
  1. Photoreceptors: rods (low light), cones (brighter light, color)
    - send signals to ganglion cells which carry light responses deeper into the brain
  2. Interneurons: horizontal, bipolar, and amacrine cells modify retinal response
  3. Pigment epithelium prevents light from bouncing around inside the eye
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6
Q

What are receptive fields?

A

portion of the retina innervated by a single ganglion cell

receptive fields are much larger for individual ganglion cells in the retina periphery than at the fovea (more rods/cones innervated by 1 ganglion)

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7
Q

What happens to photoreceptors in response to dark?

A

rods: depolarized, high transmitter release (glutamate)
- high cGMP concentration keeps nonselective cation channel open

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8
Q

What happens to photoreceptors in response to light?

A

rods: hyperpolarized, low transmitter release (glutamate)
- low cGMP concentration closes cation channel

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9
Q

Explain the visual transduction pathway.

A
  1. Rhodopsin = GPCR with retinal embedded in the membrane of PRs; cis-trans isomerization when it absorbs a photon
  2. Activates the G-protein called transducin (GαT); changes GDP to GTP; separates from βγ subunits
  3. Transducin activates phosphodiesterase (PDE) enzymes which converts cGMP to GMP
  4. cGMP levels drop, CNG channels close, reducing Ca2+/Na+ influx; hyperpolarizing membrane
    - guanylyl cyclase generates cGMP from GTP opening channels in the dark; inhibited by Ca2+; controls adaptation
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10
Q

What is the basis of color vision?

A

differences in the primary structure of opsins
- Short cones: violet
- Medium cones: yellow-green
- Long cones: yellow-red

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11
Q

How are images formed from retinal signals?

A
  • visual field is split left-right in nerves from each eye
  • contralateral visual fields are sent to each half of the cortex (nasal); cross at optic chiasm
  • temporal halves are ipsilateral
  • relay signals to LGN of the thalamus
  • V1 combines signals from both eyes
  • Visutopic maps in the brain correspond to a specific spot in the retina to maintain spatial organization of the visual field
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12
Q

Olfaction facts

A

uses 350 olfactory receptors to detect various odors located on olfactory receptor cells (specialized neurons in the nasal cavity)
- each detects specific group of odor molecules

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13
Q

Different cells in the nasal cavity?

A
  1. olfactory-binding proteins: facilitate diffusion
  2. olfactory receptor cells: transducers; only expresses single type of receptor
  3. support cells: produce mucus
  4. basal cells: stem-cells that differentiate into new receptor cells
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14
Q

What is the cellular mechanism of odor sensation?

A
  1. odorant molecules bind to olfactory receptors (GPCR) in the nasal cavity
  2. produces cAMP which opens nonselective cation channels (Na+/Ca2+), Cl- channels open, depolarizes
  3. all receptors of the same type project to the same glomerulus in the olfactory bulb
  4. mitral cells receive input from glomerulus and relay signals through the olfactory tract

each odorant activates different subset of glomeruli

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15
Q

What are the features of hair cells? What is the mechanism of transduction?

A
  • located in the inner ear and exposed to endolymph and perilymph
  • cilia oriented in specific directions to detect mechanical stimuli
  • transduction mechanism: cilia motion (caused by sound vibrations or fluid movement)

positive mechanical deformation: to the right (kinocilium) opens K+ channels, depolarization, opens V-gated Ca2+ channels, vesicle fusion and NT release

negative mechanical deformation: to the left closes K+ channels, hyperpolarization

mechanosensitive channels exhibit K+ leak into the cell to allow for electrical response to movement

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16
Q

What is the anatomy of the ear?

A

outer ear: pinna and ear canal collect sound

middle ear: malleus, incus, and stapes convert transmission medium from air to fluid

inner ear: cochlea converts sound pressure into electrical (neural) signals; vestibular system for balance

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17
Q

How does the middle ear transform air into fluid?

A
  1. tympanic membrane moves inward pushed by compression of a sound wave
  2. pushes malleus (longer) into incus
  3. pushes fluid inward
  4. tympanic membrane pulled by the rarefaction phase of a sound wave
  5. pulls malleus + incus back
  6. pulls fluid out
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18
Q

How are inner hair cells stimulated by a drop of pressure in the outer ear?

A
  1. Air pressure wave travels down ear canal; rarefaction portion of pressure wave strikes
    tympanic membrane causes movement of malleus, incus and stapes to pull oval window
    outward
  2. Pressure drops in scala vestibuli (below scala tympani) round window moves inward
  3. Basilar membrane bows upward
  4. Outer hair cells deflect toward longer stereocilia
  5. Transduction channels open in outer hair cells (Organ of Corti) and depolarize cells
  6. Outer hair cells contract (shorten), amplifying movement
    of basilar membrane
  7. Endolymph flows out of the inner sulcus
  8. Inner hair cells move toward longer stereocilia and open transduction channels, depolarizes inner hair cells
  9. Depolarization opens calcium channels and causes glutamate release from inner hair cells
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19
Q

What is the anatomy of the vestibular system and its functions?

A

maintains balance; part of the inner ear

saccule and utricle detect linear acceleration, gravity, and head position based on the movements of stereocilia stuck in otolithic membrane
- saccule = vertical movement
- utricle = horizontal movement
hair cells oriented oppositely = push-pull (active/inhibit)
- positioned to cover all angles

3 semi-circular canals detect head rotation (angular acc) through fluid movement that bends hair cells
- ampulla at base of each canal have hair cells that are oriented in the same direction

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20
Q

What are the general features of sensory systems?

A
  1. sensory cells detect a stimulus and convert it into a receptor potential (voltage change)
  2. amplification
  3. NT release to convey signal to neurons
  4. adaptation to adjust sensitivity based on stimulus intensity/duration
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21
Q

Describe sensory field and its importance in touch sensation.

A

the “region” of stimulus space that can stimulate a sensory neuron
- smaller allow for greater spatial resolution (fingers)
- larger allow for general detection (back)
- overlapping fields enhance touch sensitivity

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22
Q

Describe the design of sensory neurons.

A

unipolar neurons with cell bodies in a peripheral ganglion (i.e. dorsal root ganglion)
- have rapidly adapting, intermediate adapting, and slow adapting responses to mechanical stimuli

2 projections: one to sensory receptors in tissues; other connect to spinal cord
- nerve endings contain ion channels that respond to mechanical stimuli by opening cation channels

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23
Q

What is the difference between rapidly adapting and slowly adapting receptors?

A

RA: detect transient stimuli (higher frequency vibrations)
SA: detect sustained stimuli (constant pressure); prolonged firing for duration of stimulus

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24
Q

What is the role of Piezo2 and TRP channels in mechanoreception?

A

Piezo2: channels detect mechanical force, triggering receptor potentials in touch-sensitive cells

TRP channels: nonselective cation channels that respond to specific stimuli like pressure, temperature, or chemicals

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25
Q

What are the different mechanoreceptors in the skin?

A

depth, size, and branching affect function
- hair follicle nerve endings: slowly or rapidly adapting; deformation of hair
- Merkel cells: fine touch and texture; slow adapting
- Meissner’s corpuscles: light touch; rapidly adapting, small receptive fields
- Free nerve endings: intermediate adapting, temperature and pain
- Ruffini endings (deep): skin stretch; slow adapting
- Pacini’s corpuscles (deepest) : 20-80 layers of lamelli; deep pressure and vibrations; rapidly adapting; big receptive fields

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26
Q

How is temperature sensed in the body?

A

single sensory neurons respond to cold or heat, but not both; not uniformly distributed

thermoreceptors (TRP) on the bare nerve endings of temperature-sensitive neurons found in hypothalamus and skin
- TRPV1-4 sense heat (#1 is capsaicin receptor spicy)
- fires within certain T range

  • TRPM8 senses cold (menthol receptor)

firing rate based on temperature and duration of exposure

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27
Q

What is proprioception?

A

information about where parts of the body are located and effort being employed by muscles via mechanoreceptors

2 sensors = Golgi tendon organs (GTOs) in the tendon for force (series) and muscle spindle inside muscle for length and rate of stretch (parallel) – adjust sensitivity

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28
Q

What is the spinal reflex circuit and the relay pathway to the cortex?

A

knee-jerk response (simple motor reflex)

tapping patellar tendon–> stretch quad muscle –> muscle spindle detects –> sensory neuron–> spinal cord–> motor neuron to contract quad to counter initial stretch, inhibits MN in flexor muscle

sensory neuron–> spinal cord–> brainstem–> thalamus–> sensory cortex

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29
Q

How do different fiber types carry sensory information?

A

Aalpha: largest diameter, myelinated, fastest conduction velocity
- proprioception; motor neurons to skeletal muscle
Abeta: second largest diameter, myelinated, fast conduction velocity, touch and pressure
- sensory afferents from mechnoreceptors
Adelta: small diameter, thin myelin, slow conduction velocity
- sensory afferents from sharp pain and temperature
C: smallest diameter, no myelin, slowest conduction velocity
- sensory afferent from dull pain, temperature, and itch

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30
Q

How is sensory information organized in the cortex?

A

pathway: arm–> spinal cord–> medulla–> pons–> midbrain–> thalamus–> postcentral gyrus

body areas map to specific cortical regions; primary somatosensory cortex (S1) processes touch, pressure, and proprioception
- larger cortical areas are devoted to regions requiring fine discrimination (hands/lips)

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31
Q

What are the 5 main types of taste sensation and how are taste buds organized?

A

sweet (sugar), sour (H+), salty (Na+), bitter, umami (MSG, protein)

taste buds are clusters of receptor cells (50-150) on the tongue’s papillae

signals from taste cells are sent to the brain via cranial nerves

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32
Q

What is the mechanism by which salt stimulates NT release? Sour? Sweet/umami/bitter?

A
  1. Na+ enter taste cells via ENaC
  2. Depolarizes cell
  3. AP opens ATP channel
  4. ATP release signal to gustatory nerve to brain
  5. H+ enters the cell
  6. blocks K+ channel
  7. depolarization
  8. Na+ channels open, Ca2+ channels open
  9. tastant binds to GPCR
  10. internal Ca2+ release from ER
  11. opens TRPM5 channel (K out, Na in)
  12. depolarization (Na+ channels open, Ca2+ channels open)
  13. release of ATP
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33
Q

Use partial pressure and Henry’s Law to describe O2 and CO2 concentrations in body fluids.

A

Px = Fx * Ptot
-Px: partial pressure of gas
- Fx: fraction in air
- Ptot: total pressure of has mixture (atmospheric, 760 mmHg)

Henry’s Law: concentration of O2 dissolved = s * PO2

O2 diffuses from high partial pressure (alveoli) to low (blood; CO2 diffuses in the opposite direction

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34
Q

Describe the branching anatomy of the lungs and the functional differences of airways by generation.

A

lungs branch in generations (levels of branching)

conducting zone: generations 0-16; trachea, bronchi, bronchioles, no gas exchange

Respiratory zone: generations 17+; alveolar ducts/sacs; gas exchange

branching increases surface area

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35
Q

What does a spirometer measure?

A

Measures lung volumes
- Tidal volume: air moved in/out during normal breathing
- Residual volume: air remaining after maximum exhalation
- Inspiratory reserve volume: air forcefully inhaled after normal tidal inhale
- Expiratory reserve volume: air forcefully exhaled after normal tidal exhale

  • IC: max amount of air inhale = TV + IRV
  • FRC: volume of air remaining in lungs after normal expiration
  • Vital capacity: max exhale after max inhale = TV+IRV+ERV
  • TLC: max amount of air in the lungs after max inspiration = TV + IRV + ERV + RV
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36
Q

What is the role of intrapleural pressure, elastic recoil of the lung, and elastic recoil of the chest wall?

A

intrapleural pressure: negative pressure between the lung and chest wall keeps the lungs inflated

lungs want to collapse, chest wall want to expand; opposing elastic recoils balance each other

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37
Q

Describe the static mechanics of the lung in terms of a pressure-volume diagram.

A

Ptp = Pa - Pip
transplural pressure (inflation/deflation of lung) = alveolar pressure (amount of flow) - intrapleural pressure

inspiration: Pip becomes more negative, transiently making Pa negative, drawing air into lungs

expiration: Pip becomes less negative, transiently making Pa more positive, pushing air out of lungs

hysteresis: difference between inspiration and expiration due to surface tension
- very small in tidal breathing

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38
Q

How does surface tension affect lung mechanics? What is the role of surfactant?

A

surface tension collapses alveoli, increasing the effort needed to inflate the lungs

surfactant has hydrophobic tails that pull it upward and decrease the density of H2O molecules–> reduces surface tension, prevents alveolar collapse, and lowers the work of breathing
deficiency in pre-term babies

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39
Q

How does lung compliance change in lung fibrosis or emphysema and why?

A

compliance is slope of volume pressure graph

fibrosis: decreased compliance, stiffer lungs; scar tissue reduces elasticity

emphysema: increased compliance, floppy lungs; alveolar wall destruction, airways collapse
smoking

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40
Q

What is pH and what is the range in the human body?

A

pH = -log[H+]
normal body: 7.4
strong acid: completely dissociates
weak acid~buffer keeps pH stable

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41
Q

What is the Henderson-Hasselbach equation?

A

pH = pKa + log([HCO₃⁻]/[CO₂])
pH = 6.1 + log ([HCO₃⁻]/0.03 X PCO2)
- increase PCO2, lowers pH
- increase HCO3- (buffer), increases pH

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42
Q

What is buffering power and how do closed buffer (non-CO2) systems resist pH changes?

A

ability to resist pH changes by absorbing or releasing H+
B = change (strong base)/change in pH
B = -change (strong acid)/change in pH

fixed amount of buffer, limited capacity
multiple systems work together to stabilize pH over a range

43
Q

Explain the buffering power of an open system (CO2 buffer).

A

open-system buffering power increases exponentially with pH because there is more bicarbonate in the system
Bopen = 2.3 [HCO3-]

if you double PCO2, drops by 0.3 = respiratory acidosis
- increase [bicarb]
if you double HCO3-, increase by 0.3 = respiratory alkalosis

44
Q

Explain the Davenport Diagram.

A
  • Higher CO2 = left-shifted curve towards lower pH; need more [HCO3-] to maintain normal pH
  • Lower CO2 = right-shifted curve towards higher pH; need less [HCO3-] to maintain normal pH
  • If no non-CO2 buffers, black point shifts horizontally
  • If buffering capacity is infinite, point shifts up (i.e. pH
    does not change, even if CO2 increases)
  • Combined CO2 and non-CO2 buffers are the combination of these cases
  • Shifts in the curve regulated by ventilation
  • Movement along curve regulated by [HCO3-] balance
    (e.g. kidney reabsorption/excretion)
45
Q

What is the composition of blood?

A
  1. plasma = 55%
    - water, ions, proteins, nutrients, hormones
  2. Red blood cells = 45%
    - contain hemoglobin for O2 transport
  3. White blood cells and platelets = <1%
    - immunity and clotting
46
Q

What is the role of hemoglobin in O2 transport and what does its saturation curve look like?

A

Hb = tetrameric Fe-containing protein with 4 binding sites

hematocrit (HCT) = height of RBC / Total height
- following centrifuge
- volume fraction in blood

sigmoidal shape from cooperative binding; plateau from saturation

47
Q

How does hemoglobin respond to physiological variables?

A

shift in saturation curve:
1. right shift (lower O2 affinity, higher O2 delivery to tissues): increased, T, pCO2, [H+], 2,3-DPG (drives O2 into placenta)
exercise: CADET
2. left shift (higher O2 affinity, less O2 delivery to tissues): decreased T, pCO2, [H+]

“smart” because O2 is delivered in metabolically active tissue and retained in the lungs

48
Q

In what forms is CO2 carried in the blood and which is most important?

A
  1. Dissolved CO2 (10%)
  2. Carbonic acid
  3. **Bicarbonate (69%)
    - carbonic anhydrase converts CO2 into bicarb in RBCs
  4. Carbonate
  5. Carboamino compounds (21%) (CO2 with protein complex)
49
Q

What is the diffusing capacity (DL) of the lung and what influences it?

A

How effectively gases diffuse across the alveolar-capillary membrane

influenced by:
1. surface area and thickness of the membrane
2. solubility and molecular weight of gases
3. partial pressure gradient

Vnet (net airflow) = -AD (delta s * P/a)
A: area of barrier
D: diffusion constant
s: Henry’s Law constant
P: pressure
a: thickness of barrier

at the end of inspiration, stretch maximizes area and minimizes thickness

50
Q

What are perfusion and diffusion limitation and how are they represented along the alveolar capillary?

A

**perfusion-limited (Q = CO): gas exchange depends on blood flow
- O2 equilibrates quickly

diffusion-limited (Dl): gas exchange depends on diffusion rate
- slow rise in partial pressure along capillary

gradient for CO2 is much smaller because its DL is 3-5x greater than O2

51
Q

What is minute ventilation and alveolar ventilation?

A

minute ventilation: total volume of air entering or leaving the lungs per minute
V = tidal volume * respiratory rate (f)

alveolar ventilation: volume of air reaching alveoli per minute, which participates in gas exchange
V = (tidal volume - dead space volume) * respiratory rate

52
Q

What is dead space? How is it measured? What is the difference between Bohr’s and Fowler’s method?

A

volume of air that does not participate in gas exchange
- anatomic: air in conducting airways (trachea, bronchi)
- physiologic: anatomic + alveoli not perfused

physiologic (Bohr) = anatomic (Fowler) + alveolar

Bohr’s: physiologic dead space using CO2 concentrations in exhaled air

Fowler’s: anatomic dead space by using nitrogen washout after single breath of 100% O2

53
Q

What is the relationship between alveolar CO2 and alveolar ventilation?

A

inverse relationship: increased V decreases alveolar CO2

PAco2 = 0.863(Vco2/VA)
Vco2: volume of CO2 leaving alveoli
VA: volume of air leaving alveoli

54
Q

Describe how alveolar O2 is related to alveolar CO2.

A

inverse relationship: as alveolar CO2 increases, the alveolar decreases

PAO2 = PIO2 - PACO2

55
Q

Describe the basis of non-uniformity of ventilation and perfusion in the lung.

A

Apex
- PaO2 higher: better ventilation relative to blood flow
- PaCO2 lower: lower alveolar CO2 because less CO2 is delivered by the blood
- ventilation and perfusion reduced at apex, but Q is reduced more than V, but Q more than V –> HIGH V/Q ratio

Base
- PaO2 lower: poor ventilation compared to blood flow
- PaCO2 higher: more CO2 delivered by blood
- ventilation and perfusion higher at the base, but Q increased more than V –> LOW V/Q ratio

56
Q

Describe the lung mechanisms for compensation of ventilation-perfusion mismatch in the lung.

A

Bronchoconstriction: happens in response to poor perfusion (blockage), reducing ventilation to match

Vasocontriction: happens in response to poor ventilation (hypoxia), redirection blood flow to well-ventilated alveoli

57
Q

Important terms for different types of breathing.

A

Eupnea: pattern of alternating inspiratory and expiratory activity that occurs under normal conditions at rest

Dyspnea: short of breath

Apnea: absence of breath

58
Q

Describe how inspiration and expiration depend on signals sent to the muscles of respiration through cranial and spinal nerves.

A

inspiration:
- diaphragm contraction via phrenic nerve
- external intercostal muscles activated via intercostal nerves

expiration:
- rest: passive due to elastic recoil
- active expiration (exercise): signal to abdominal muscles and internal intercostals via spinal nerves

59
Q

Describe the flow chart for control of ventilation.

A
  1. control centers in the CNS: medulla = central pattern generator (pre-Botzinger complex) has specialized neurons that fire to control RR
    pons = breathing rhythm
  2. efferent signals send through motor neurons to the muscles of respiration (diaphragm, intercostals)
  3. chemical and mechanical sensors that send afferent signals to the CNS control centers
    peripheral: detect PCO2, PO2, and pH in blood
    central: changes in brain interstitial fluid pH
  4. sensory integration centers that collect and process information
60
Q

Describe the groups of neurons in the medulla that fire in phase with activities of the respiratory muscles.

A
  1. Dorsal respiratory group (DRG): fires during inspiration to signal diaphragm and intercostals
  2. Ventral respiratory group (VRG): fires during active expiration and inspiration; signals accessory muscles of breathing
    - three regions with specialized function including pre-Botzinger complex
61
Q

Describe how ventilation is regulated by PCO2, PO2, and pH through the action of peripheral and central chemoreceptors.

A

arterial PCO2 is most important

peripheral chemoreceptors: located in cartoid and aortic bodies and respond to decreased PO2, increased PCO2, and decrease in pH
- Glomus cells generate APs

central chemoreceptors: located in the medulla and respond to increased PCO2 that crosses the BBB and lowers pH
- adjusts RR

62
Q

What are the differences between nervous system and endocrine system?

A

nervous: wired, NT, very short distance, dependent on anatomy, rapid, brief duration of action, coordinate rapid, precise responses

endocrine: wireless, hormones, very long distance, dependent on chemistry of binding, slow response, long duration of action, coordinates activities of long duration

63
Q

Structure/function relationship of hypothalamus and pituitary and difference between anterior and posterior.

A

hypothalamus receives inputs from stress, daylight, season, hormones, glucose and connects CNS to the pituitary directly via the stalk
- close to optic chiasm
- anterior: hypothalamic neurons release releasing hormones and inhibiting hormones into portal vessels, then the AP secretes ACTH, GH, MSH, TSH, gonadotropins (FSH, LH), prolactin
- posterior: does not synthesize its own hormones; receives oxytocin and ADH directly

64
Q

What are the hypothalamic nuclei and how do they relate to the posterior pituitary?

A

collection of neurons releasing certain hormone

paraventricular nucleus (PVN): secretes oxytocin
- uterine contraction, milk ejection
supraoptic nucleus (SON): secretes vasopressin (ADH)
- water reabsorption in kidneys (AQP2 insertion), raise blood pressure

nuclei–> axons of hypothalamic neurons –> capillaries

65
Q

How does the hypothalamus-anterior pituitary axes work?

A
  1. hypothalamus releases releasing hormones and secretes them into capillaries
  2. anterior pituitary releases hormones into general circulation
  3. negative feedback from the final hormones on the upstream
66
Q

Which hypothalamic-anterior pituitary hormone axes do you have to know?

A
  1. TRH-TSH–thyroid (T3/T4)
  2. CRH-ACTH–adrenal (cortisol)
    - high in morning, declines throughout the day
  3. GnRH-FSH and LH-ovary/testis
  4. GHRH-growth hormone –multiple target tissues
    (somatostatin inhibits)
  5. dopamine-prolactin-breast
    (suckling inhibits dopamine–> prolactin release –> milk production)
    anti-psychotic drugs inhibit dopamine
67
Q

Differences between GH and TH.

A

both regulate growth and metabolism

GH: bone growth and glucose metabolism
- controls linear growth in youth and maintains muscle/bone mass and glucose metabolism in adults

TH: basal metabolic rate, GI tract activity, HR
- abnormalities early in life = growth of developing fetus, normal brain development and later in life = metabolism

68
Q

What is the chemical structure of the thyroid hormones?

A

T3: more biologically active (converted in peripheral tissue)
T4: converted to T3 by deiodinase (95%)

69
Q

What are the steps of thyroid hormone synthesis?

A
  1. active transport of I- through the thyroid epithelial cell into colloid via Na+ cotransport and I- channels
  2. synthesis of thyroglobulin
  3. iodination and coupling of tyrosyl residues in thyroglobulin (TG) via thyroid peroxidase to yield T3 and T4
  4. endocytosis and proteolysis of TG in lysosomes, releasing T3 and T4
70
Q

What happens when you have an iodine deficiency?

A

decreased T3/T4–> increased TRH and TSH –> thyroid gland enlargement = goiter

71
Q

How does the thyroid hormone act in the cell?

A
  1. enter the cell via diffusion or via carrier-mediated transport
  2. once inside, T4–>T3
  3. T3 binds to intracellular thyroid hormone receptors in the cell nucleus to activate gene expression
72
Q

What are the tissue effects of thyroid hormone?

A
  1. fetal development: development of fetal brain and growth of skeleton
  2. regulates basal metabolic rate: increases Na-K ATPase in muscles and brown adipose tissues
  3. increases beta-adrenergic receptors in the heart, adipose, and skeletal muscle –> increases contraction strength and HR
  4. increases catecholamine production in adrenals
  5. generates more energy by increasing hepatic gluconeogenesis and glycogenolysis, increase absorption of glucose from intestine, increase cholesterol degradation, increase lipolysis
73
Q

Growth hormone regulation and feedback?

A

stimulated by GHRH and inhibited by somatostatin
- GH release is pulsatile and stimulated by sleep
- IGF-I inhibits GH release

74
Q

What are the direct actions of GH?

A
  1. acts on long bones in children to cause growth
  2. makes energy available in tissues by mobilizing TG from fat cells, blocks insulin’s ability to lower blood sugar, increases gluconeogenesis by liver
  3. increases protein synthesis in tissues
75
Q

What are the indirect actions of GH?

A

stimulates release of IGF-I from the liver which binds to many cells throughout the body and increases glucose transport into cells, protein synthesis, cell proliferation, and improves cell survival

76
Q

How do you treat GH hypersecretion?

A

hypersecretion: acromegaly (GH-secreting tumor of pituitary) treated with somatostatin-like drugs

77
Q

Anatomy of the adrenal gland?

A

sits on top of the kidneys
cortex = outer layer, produces steroid hormones
medulla = inner layer, produces catecholamines (epinephrine, norepinephrine)

78
Q

How does the adrenal medulla produce catecholamines? When are they released?

A
  • synthesized from tyrosine and stored in granules within chromaffin cells
  • release stimulated by stress
  • innervation from the sympathetic nervous system
    1.) neurons release norepi directly at target tissue
    2. adrenal medulla releases epi into bloodstream for widespread effects
79
Q

What are adrenergic receptors?

A

GPCRs of catecholamines
alpha 1: increases intracellular Ca2+ and PKC
alpha 2: inhibits cAMP and PKC
- vasoconstriction
beta: activates cAMP and PKC
- vasodilation

80
Q

What steroids does the adrenal cortex produce?

A

derived from cholesterol

1.) glucocorticoids: gene regulation following the binding of intracellular receptors that regulates metabolism, fight inflammation
- cortisol
2.) mineralocorticoids: regulates fluid volume, BP, Na+/K+ balance
- aldosterone (Na+ reabsorption, K+ excretion)
- synthesis triggered by the renin-angiotensin-aldosterone system (low BP) and high K+ levels
3.) androgens: puberty
- testosterone

81
Q

What is the difference between the exocrine and endocrine pancreas?

A

exocrine = directly aids digestion via enzymes

endocrine = help body decide how to use stuff that has been digested and absorbed via hormones
- glucose increases, pancreas releases insulin, liver = glucose into glycogen, cells absorb glucose
- glucose decreases, pancreas releases glucagon, liver = glycogenolysis, gluconeogenesis, ketogenesis

82
Q

How is the pancreas organized?

A

islets: secrete hormones
- beta cells in the center secrete insulin
- alpha cells produce glucagon in the periphery = make energy available between meals
- delta cells produce somatostatin (interspaced) = inhibit glucagon release when senses glucose, delay of nutrients into the circulation by slowing gastric emptying

83
Q

What is the mechanism of insulin secretion in beta cells?

A
  1. glucose enters the cell via GLUT transporter (facilitated transport, does not require ATP)
  2. glucokinase detects intracellular glucose levels and phosphorylates it
  3. G6P enters glycolysis and the Krebs cycle, producing more ATP
  4. ATP closes K+ channel, depolarizes cell
  5. Ca2+ enters from V-gated channels, granules with insulin are exocytosed

First: stored insulin released (big spike), then newly-synthesized insulin causes steady rise

84
Q

What are other regulators of insulin release ?

A

parasympathetic stimuli, gut hormones/amino acids/lipids amplify

inhibitors = sympathetic + somatostatin

85
Q

What are the actions of insulin?

A

STORAGE OF ENERGY
- liver: promotes glycogen synthesis, inhibits gluconeogenesis
- muscle: increases glucose uptake and protein synthesis
- adipose tissue: stimulates fat storage by enhancing TG synthesis

86
Q

Mechanisms of diabetes? Long term consequences?

A

Type 1: autoimmune destruction of beta cells treated with insulin injections
Type 2: insulin resistance, islet cells fail later

long-term high blood sugars causes failure of the vasculature = blindness, kidney failure, CVD

87
Q

What is the role of incretins in insulin secretion?

A

gut glucose effect: oral glucose stimulates insulin more than IV glucose

incretins produced by cells in the gut:
- GIP + GLP-1 (suppresses glucagon, slows gastric emptying, suppresses appetite): bind to GPCRs on beta cells that amplify insulin release

88
Q

What are the key hormones in mineral homeostasis?

A

parathyroid hormone (PTH): increases blood calcium by stimulating bone resorption, increasing renal calcium reabsorption, and activating vitamin D
- very short half life

Vitamin D: increases intestinal calcium and phosphate reabsorption

FGF-23: reduces blood phosphate by inhibiting renal reabsorption and decreasing vitamin D activation

89
Q

Calcium and its flux?

A

99% bones, 1% in blood + EC fluid

forms: ionized, protein bound, complexed (other ions)

diet, absorption (small intestine), excretion and reabsorption by kidneys

90
Q

Phosphorous and flux?

A

85% bone, 14% soft tissue, 1% in blood

hydroxyapatite = Ca5(PO4)3(OH)

diet, absorption (small intestine), excretion and reabsorption by kidneys
- PTH: increases excretion
- FGF-23: lowers phosphate by reducing reabsorption and Vitamin D activation

91
Q

How does the parathyroid cell know what the EC calcium concentration is?

A
  1. Calcium sensing receptor (CaSR): GPCRs located on the surface of parathyroid cells
    - increases intracellular Ca2+ concentration, reducing PTH release
  2. PTH receptor: GPCR located on cells in the kidney and bone; triggered by low Ca2+
  3. Vitamin D: steroid-like hormone stimulated by PTH
92
Q

How is Vitamin D formed?

A
  1. skin: UV light converts to vitamin D3 (or from diet)
  2. liver: converts vitamin D3 to 25-OH-D3
  3. kidney: converts 25-OH-D3 to calcitriol (active form)
    - main site of regulation via PTH and low Ca2+/PO43- levels
    - 98% of filtered calcium reabsorbed into blood (30% in distal convoluted tubule, PTH HERE)
    - 80-99% of phosphate is reabsorbed (high PTH/FGF-23 increase excretion)
93
Q

How does Vitamin D act?

A

targets intestinal epithelial cells, increases synthesis of calcium-binding proteins (calbindin) for enhanced calcium absorption via Ca-ATPase

promotes bone resorption to release calcium and phosphate

94
Q

FGF-23 and phosphate regulation

A

produced by osteocytes in bone in response to high phosphate
- inhibits phosphate resorption in kidneys, absorption in bowels, 1,25-D synthesis in the kidney

95
Q

Co-regulation of Ca2+ and phosphate?

A

critical for bone mineralization and preventing soft tissue calcification

PTH: increases calcium while lowering phosphate via renal excretion

Vitamin D: enhances absorption of both in the intestines

FGF-23: reduces phosphate

96
Q

Osteoclasts vs. osteoblasts.

A

Osteoclasts: break down bone, releasing Ca/P
- RANKL promotes
- PKA inhibits

Osteoblasts: build bone

97
Q

Mitosis vs. meiosis

A

mitosis: somatic cells, produces two genetically identical, diploid daughter cells

meiosis: germ cells, produces gametes, 4 genetically unique haploid cells in men and 1 in women (recombination)

98
Q

Hypothalamic-pituitary-gonadal (HPG) axis MEN

A
  1. hypothalamus secretes GnRH
  2. anterior pituitary secretes LH and FSH
  3. LH stimulates Leydig cells to produce testosterone
  4. FSH stimulates Sertoli cells to produce growth factors
  5. Regulation of anterior pituitary via testosterone, inhibin
  6. Regulation of hypothalamus via testosterone
99
Q

Spermatogenesis and oogenesis.

A

Continuous from puberty throughout life; driven by testosterone; Sertoli cells envelope spermatocytes

  1. primordial germ cell
  2. spermatogonium undergoes mitotic divisions until asymmetric division
  3. undergoes meiosis: primary spermatocytes, secondary spermatocytes, spermatids
  4. spermatids mature into spermatozoa

proliferation of germ cells occurs before birth; meiotic divisions produce 1 ovum

100
Q

Hypothalamic-pituitary-gonadal (HPG) axis FEMALE

A
  1. hypothalamus secretes GnRH
  2. anterior pituitary, stimulated by GnRH, secretes LH and FSH
  3. LH stimulates theca cells to produce progestins
  4. FSH stimulates granulosa cells to produce sex steroids, inhibins, activins
  5. Regulation of anterior pituitary via inhibins, activins, sex steroids
  6. regulation of hypothalamus via sex steroids
101
Q

Gonadotropin levels in females

A
  1. surges during fetus and infancy
  2. low during childhood
  3. nighttime pulsatile GnRH secretion marks onset of puberty
  4. increase in pulsatile leads to LH surge, first menstrual cycle
102
Q

Hormonal changes during the menstrual cycle. Ovarian and uterine cycles.

A

Ovary
1. Follicular phase: FSH stimulates follicle growth; estradiol rises
2. Ovulation: positive feedback by high estradiol triggers LH surge
3. Luteal phase: progesterone secretion from empty follicle

Uterus
1. menses: shedding occurs if no fertilization
2. proliferative phase: estradiol promotes thickening
3. secretory phase: progesterone stabilizes and prepares for implantation

103
Q

Fertilization of an Oocyte

A
  1. sperm binds to zona pellucida
  2. sperm releases enzymes from acrosome to penetrate
  3. membranes fuse
  4. cortical reaction hardens the zona pellucida to prevent polyspermy
  5. oocyte completes meiosis 2
  6. fusion of pronuclei, producing a zygote

Physiological Systems (3 decks)

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