Lab 6 (Exam 2)

What are the specific receptor types, transduction mechanisms, and cranial nerves responsible for taste (gustation)?

• Receptor Type: Chemoreceptors housed in taste buds on the lingual papillae.

• Transduction Mechanisms:

  • Sweet, bitter, and umami: Act via G-protein coupled receptors (GPCRs).

  • Salty: Acts via direct ion channels where Na+ enters through epithelial sodium channels (ENaC).

  • Sour: Acts via direct ion channels where H+ acts on sour-sensing channels

• Afferent Cranial Nerves:

  • CN VII (Facial nerve): Anterior two-thirds of the tongue.

  • CN IX (Glossopharyngeal nerve): Posterior one-third of the tongue.

  • CN X (Vagus nerve): Epiglottis and pharynx.

What is the anatomical and physiological basis of the fovea centralis providing the highest visual acuity?

• Location & Receptor Composition: Located at the center of the macula lutea and contains cones only at the highest density in the retina

• Neural Convergence: Each cone has nearly a 1:1 connection with its own bipolar and ganglion cell —> minimal convergence —> tiny receptive fields

• Optical Clarity: Overlying retinal layers and blood vessels are displaced to the side to form the foveal pit —> light hits photoreceptors directly without scattering

What is the role of the middle ear in normal hearing, and why does air conduction (AC) normally exceed bone conduction (BC)?

Role: Acts as an impedance-matching amplifier that boosts sound intensity by 20–30 dB.

Mechanism: The tympanic membrane has roughly 17 times the surface area of the stapes footplate, and the malleus and incus function as a mechanical lever —> concentrates force onto the oval window —> makes AC > BC in normal ears.

What is the optical defect behind astigmatism, and how is it corrected clinically?

Optical Defect: Unequal curvature of a refracting surface (usually cornea, sometimes lens) across perpendicular meridians (shaped like the back of a spoon rather than a sphere).
Clinical Correction:

• Regular astigmatism: Corrected with an axis-specific cylindrical (toric) lens (spectacles, toric soft contacts, or toric intraocular lenses)

• Irregular astigmatism: Corrected with rigid gas-permeable (RGP) or scleral lenses, where the tear film beneath the rigid lens creates a new smooth refracting surface.

What are the eight neural and receptor-level mechanisms sensory systems use to prevent information overload?

• Receptor adaptation: Phasic receptors decrease firing during constant stimulation (largest filter).

• Thresholds: Discard subthreshold background noise.

• Convergence: Compresses neural information in low-acuity regions.

• Lateral inhibition: Removes redundancy and sharpens spatial edges.

• Relative coding: Reports deviation from an adapted baseline rather than absolute stimulus magnitude.

• Thalamic gating: Filters all sensory modalities except olfaction before they reach the cortex

• Selective attention: Suppresses unattended sensory channels.

• Central habituation: Dampens repeated, non-threatening stimuli in the CNS.

6. How does olfactory adaptation occur at the cellular level, and how does the receptor reset upon odor removal?

• Adaptation Mechanism: Odorant binds to Ca2+ enters through the cyclic nucleotide-gated (CNG) channel—> binds calmodulin —> desensitizes the CNG channel. Simultaneously, phosphodiesterase (PDE) breaks down cAMP → receptor potential falls below threshold → action potentials cease even though the odorant remains bound (supplemented by slower central habituation in the olfactory bulb and piriform cortex).

• Recovery (Reset) Mechanism: Stimulus removed → odorant dissociates and clears from mucus →Na+ / Ca2+ exchangers extrude Ca2+ calmodulin releases the channel and cAMP resets → restores channel sensitivity and resting membrane potential.

7. Why does the central olfactory pathway trigger vivid emotional memories faster than other senses?

• Thalamic Bypass: Olfaction is the only sensory system that does not relay through the thalamus before reaching the cortex.

• Direct Limbic Pathway: Olfactory epithelium (CN I) → crosses cribriform plate → olfactory bulb → olfactory tract →projects directly within 1–2 synapses to the piriform cortex, amygdala (emotion), and hippocampus (memory).

• Result: Unfiltered odor signals activate emotional and memory centers before conscious odor naming occurs.

How does tactile adaptation occur with a single coin on the forearm, and why does stacking two additional coins immediately restore perception?

• Tonic Merkel discs and Ruffini endings maintain low firing that is suppressed by central habituation.

• Phasic receptors act as differentiators (encoding relative change per Weber's law),

10. Why does room-temperature water feel warm to a cold-adapted hand and cool to a warm-adapted hand simultaneously?

• Mechanism: Thermoreceptors are phasic receptors that encode the direction of temperature change relative to their own adapted baseline rather than absolute temperature.

11. Why does a vibrating tuning fork placed on the midline of the skull (Weber test) lateralize in opposite directions for conductive versus sensorineural hearing loss?

• Midline Delivery: Bone conduction delivers equal vibrational energy to both cochleae simultaneously.

• Conductive Loss → Lateralizes to Affected (Bad) Ear: A block in the outer/middle ear traps bone-conducted low-frequency sound energy inside the canal (occlusion effect) and shields the healthy cochlea from ambient airborne masking noise → sounds louder in the bad ear.

• Sensorineural Loss → Lateralizes to Normal (Better) Ear: The damaged cochlea or CN VIII on the affected side cannot transduce the skull vibration → only the healthy ear registers the full signal.

13. How is visual field information routed from the retina to the primary visual cortex?

• Pathway Sequence: Retina →

  • Optic nerve (CN II) →

  • Optic chiasm (where nasal retinal fibers cross to the opposite side and temporal retinal fibers stay ipsilateral)→

  • Optic tract (now carrying the complete contralateral visual hemifield from both eyes) →

  • Lateral geniculate nucleus (LGN) of the thalamus →

  • Optic radiations →

  • Primary visual cortex (V1) around the calcarine sulcus in the occipital lobe.

• Optic Radiation Split:

  • Meyer's loop: Sweeps through the temporal lobe carrying the contralateral superior visual field.

  • Parietal fibers: Travel through the parietal lobe carrying the contralateral inferior visual field.

15. Why must a subject avoid squinting during the Snellen visual acuity test, and why must the untested ear be covered during the distance hearing test?

• No Squinting (Vision): Squinting acts as an artificial pinhole, reducing the aperture and increasing depth of field → falsely improves measured visual acuity on the Snellen chart.

• Covering Untested Ear (Hearing): Because hearing is binaural and airborne sound waves can travel across the skull to the opposite ear, an uncovered normal ear will mask a unilateral hearing loss in the tested ear.

16. What happens to flavor perception if a patient has severe sinus inflammation, and why do they describe food as "bland" rather than completely "tasteless"?

• Pathway Disrupted: Sinus inflammation swells the olfactory cleft and thickens mucus→ physically blocks airborne odorants from reaching CN I (olfactory nerve) receptors at the roof of the nasal cavity (similar to pinching the nose to block retronasal airflow in Lab Exercise 1).

• Classification: Conductive olfactory loss (the CN I axons crossing the cribriform plate to the olfactory bulb remain intact).

• Bland" vs. "Tasteless": Because 80% of flavor is olfactory, losing retronasal smell strips away complex flavor notes (causing confusion between Coca-Cola, Pepsi, and Mtn Dew in the lab). However, the gustatory nerves (CN VII, IX, and X) are unaffected, so the five basic tastes (sweet, salty, sour, bitter, umami) remain intact → food tastes bland, not tasteless.

17. What happens to the Rinne and Weber tests if a patient has otosclerosis (stapes fixation) or middle ear effusion in the LEFT ear?

• Diagnosis: Left conductive hearing loss.

• Left Rinne Test Result: Negative Rinne (BC > AC). Once the tuning fork stem goes silent on the left mastoid process, moving the tines 2 cm in front of the left ear canal produces no audible sound because middle ear amplification is lost while bone conduction bypasses the blockage.

• Weber Test Result: Lateralizes to the LEFT (affected) ear because the conductive block traps bone-conducted sound via the occlusion effect and blocks ambient room noise.

18. What happens to a patient's Rinne test if they suffer cochlear hair cell damage (from ototoxic drugs or noise) in the right ear, and why can't the Rinne test alone diagnose it?

• Right Rinne Test Result: Positive Rinne (AC>BC)

• Why: In sensorineural hearing loss, the outer and middle ear amplifying apparatus is completely intact, and both AC and BC share the same damaged final common pathway (cochlea / CN VIII) → both AC and BC are reduced equally, preserving the normal AC > BC ratio.

• Why Weber is Required: A positive Rinne only proves the middle ear works. Adding the Weber test separates normal hearing (equal bilaterally) from right sensorineural loss (lateralizes to the left/better ear).

Why are some body regions more sensitive?

Receptor density + receptive field size.

• High density → small, non-overlapping fields → the two tips excite two different afferents → felt as TWO. Low density → large overlapping fields → one afferent → felt as ONE.

• Add cortical magnification — fingertips and face occupy a huge share of S1 (the sensory homunculus) — and lateral inhibition, which sharpens the contrast between the points.

• Our data: fingertip 0.3 cm vs below elbow 3.0 cm — a 10× difference, exactly the expected gradient.

Which receptor types detect fine touch?

• Merkel discs (SA I) — fine form, edges, texture; best spatial resolution, so they drive two-point discrimination. Meissner corpuscles (RA I) — light touch and flutter.

• Both use large myelinated Aβ fibers → dorsal column–medial lemniscal pathway → VPL → postcentral gyrus.

• EXAM TRAP: free nerve endings = pain and temperature (spinothalamic tract), not fine touch.

Endocrine

Q. Which hormones are lipophilic, where are their receptors, and what is the thyroid-hormone exception?

• Lipophilic hormones are steroids made from cholesterol : cortisol, aldosterone, estrogen, progesterone, testosterone .

• They cross the cell membrane and bind receptors inside the cell (cytoplasm or nucleus) , which changes gene transcription.

• Thyroid hormone is an amine, but it is nonpolar , so it also uses an inside receptor (so do vitamin D and retinoic acid)

• Nonpolar molecules slip through the lipid membrane.

• Polar molecules can't, so they need a receptor on the membrane.

• Thyroid hormone sits in the amine (hydrophilic) family, yet it acts like a lipophilic hormone

• Estrogen is a steroid (lipophilic).

• FSH and calcitonin are peptides (hydrophilic)

Name the 3 classes of hydrophilic hormones with examples. How do they signal?

• Amines from tyrosine (epinephrine, norepinephrine, dopamine, thyroid hormone) or tryptophan (serotonin,melatonin)

• Polypeptides/proteins (ADH, insulin, GH)

• Glycoproteins (FSH, LH). They are polar, so they bind receptors on the cell membrane and act through second messengers .

They are polar, so they bind receptors on the cell membrane and act through second messengers.

Why: There are three membrane systems:

• G-protein-coupled receptors

• Guanylate cyclase receptors

• Tyrosine kinase receptors.

Lab Note:

• Insulin, FSH, ACTH are hydrophilic

• Cortisol and estrogen are lipophilic

Q. How does a G-protein-coupled receptor turn on, and how does it turn itself off?

• The hormone binds, the α subunit releases GDP and binds GTP (GRFs help), splits off and activates an enzyme.

• The α subunit has GTPase activity (GAPs help), so it turns GTP back into GDP and the signal shuts itself off .

• The αs activates adenylyl cyclase (↑ cAMP),

• The αi inhibits it, and αq activates phospholipase C (IP₃/Ca²⁺).

Why: GRFs and GAPs are the two “assistants” that keep the switch from staying on forever.

• ADH: V2 uses cAMP and V1 uses IP₃/Ca²⁺

• PTH on bone uses cAMP

Q. What do cAMP and cGMP activate, and which enzyme breaks down both?

• cAMP activates protein kinase A (PKA)

• cGMP activates protein kinase G (PKG)

• The enzyme that breaks down BOTH is phosphodiesterase (PDE) .

Q. How is a guanylate-cyclase receptor different from a tyrosine-kinase receptor? Give an example of each.

• Guanylate cyclase: the receptor itself is the enzyme (no G protein)

  • It turns GTP into cGMP which activates PKG

  • Nitric oxide (NO) enters cell, activates soluble guanylate cyclase, so PKG activates myosin phosphatase and causes vasodilation 

• Tyrosine kinase: When insulin binds, the two receptor halves merges and phosphorylate their own tyrosines. Then phosphorylate other proteins. Prolactin, GH and growth factors (EGF, PDGF, IGF) use this type too.

 Lab Note: Insulin works through a tyrosine-kinase receptor

Q. Which 6 hormones does the anterior pituitary make? Which 2 does the posterior pituitary release, and where are they made?

• Anterior pituitary (6):

  • Prolactin (Target/Effect = Breast (held down by dopamine)

  • GH (Target/Effect = Liver → IGF-1; all cells)

  • ACTH (Target/Effect = Adrenal cortex → cortisol)

  • TSH (Target/Effect = Thyroid →(T3/T4)

  • LH and FSH (Target/Effect = Gonads → (Testosterone, Estrogen)

• Posterior pituitary (2): (Made in hypothalamus)

  • ADH  = Supraoptic nucleus → V2 kidney

  • Oxytocin (vasopressin) = Paraventricular nucleus

    • Oxytocin cause milk ejection and uterine contractions

Which pituitary hormones share a subunit, and what precursor does ACTH come from?

• TSH, FSH and LH (and placental hCG) have a similar α subunit and a unique β subunit.

• ACTH is cut from POMC (pro-opiomelanocortin) , which also yields MSH and β-endorphin.

  • This explains Addison's skin darkening later: more POMC → more ACTH → more MSH. 

• GH and prolactin form a third family (that is why GH has some milk-making activity).

Q. Trace each hypothalamus → pituitary → target axis, and say where negative feedback acts.

Releasing hormones reach the anterior pituitary through the portal capillaries:

• TRH → TSH → T3/T4 

• CRH (+AVP) → ACTH → cortisol

• GnRH → LH/FSH → sex hormones 

• GHRH → GH → IGF-1 from the liver

  • Somatostatin inhibits GH (and TSH),

  • Dopamine inhibits prolactin

The final hormone gives negative feedback to BOTH the pituitary and the hypothalamus

The pituitary is called the “master gland,” but the hypothalamus is the real boss: it tells the pituitary what to do.

What is a tropic hormone? Give the lab examples?

• A tropic hormone stimulates another endocrine gland to secrete its hormone. for example:

  • TRH and TSH (thyroid axis),

  • CRH (acts on the anterior pituitary)

  • ACTH (acts on the adrenal cortex)

  • FSH (acts on ovarian follicles)

• Negative feedback: the final hormone shuts off the hormones above it.

• T4 inhibits TRH and TSH;

• Cortisol inhibits CRH and ACTH;

• Estrogen holds FSH down.

TRAP:

• CRH has a tropic effect on the adrenal gland” is wrong.

• CRH acts on the anterior pituitary; ACTH acts on the adrenal.

What does “Hypox” mean, what is the rat missing, and how is it different from a Tx rat?

• Hypophysectomized = pituitary removed

  • No TSH , and no ACTH, GH, FSH, LH, prolactin, ADH or oxytocin either.

  • Its thyroid is intact but not stimulated , so T4 is low and BMR is low.

• Tx = thyroidectomized = thyroid removed , so there is no T4, T3 or calcitonin .

• Hypox = the gland is there but nobody tells it to work. Tx = no gland at all.

• Expected symptom in a Hypox rat = decreased BMR . Weight loss, hyperactivity and high body temperature are HYPERthyroid signs

How does growth hormone do its job, and when is it released most?

• GH (somatotropin) works like a contractor

  • It makes the liver produce “subcontractors” called somatomedins mainly IGF-1 (insulin-like growth factor 1)

  • GH is released in a pulsatile way (about every 2 hours); the biggest burst is within 1 hour of falling asleep (stage III) . High IGF-1 gives negative feedback to stop more GH.

• The professor's tip:

  • insulin and IGF-1 are both “builders.”

  • Babies sleep 16–17 hours a day partly to make growth hormone.

What raises GH secretion and what lowers it?

• GH goes UP with low glucose, low fatty acids, arginine, fasting, exercise, stress, stage III–IV sleep, puberty hormones, ghrelin and α-adrenergic agonists .

• GH goes DOWN with high glucose, high fatty acids, obesity, aging, somatostatin, somatomedins, GH itself, β-adrenergic agonists and pregnancy .

Common sense:

• GH rises when the raw materials for growth are LOW, so it can raise them.

• Ghrelin (the hunger hormone from an empty stomach) boosts GH.

• α-agonists RAISE GH;

• β-agonists LOWER GH.

Why is GH called diabetogenic, and why does GH need thyroid hormone?

• GH causes insulin resistance : cells take up less glucose, so blood glucose rises .

• GH mobilizes fatty acids from fat and increases protein synthesis, organ growth and linear growth.

• GH and thyroid hormone need each other:

  • hypothyroid patients have low GH and low IGF-1 (restored by T3/T4), and T3/T4 have little growth effect without GH .

• This is one reason every newborn's thyroid hormone is tested: without it, GH can't do its job

• GH is one more hormone that RAISES blood glucose, along with glucagon and cortisol 

Q. What controls prolactin, and how does prolactin block ovulation?

• Prolactin is held down all the time by hypothalamic dopamine.

• It is the ONLY pituitary hormone that is released without restraint when dopamine is absent.

• TRH, VIP and estrogen (pregnancy) increase it.

• Prolactin blocks ovulation by inhibiting GnRH , so LH and FSH fall.

Q. What is the most SENSITIVE stimulus for ADH, and what is the most POWERFUL one?

• Most sensitive: plasma osmolarity. A rise of only 1% (normal ≈ 300 mOsm) is sensed by osmoreceptors in the hypothalamus , and ADH rises.

• Most powerful (overriding): loss of blood volume/pressure (about 10%), sensed by baroreceptors (left atrium, carotid artery, aortic arch).

The professor's ER case: a bleeding patient given lots of water has LOW osmolarity, yet ADH stays high. Survival (volume) beats osmolarity.

Sensitive ≠ powerful. Osmolarity is the most sensitive; volume loss is the most powerful.

Where and how does ADH save water? What does it do at high doses?

• ADH binds V2 receptors on principal cells of the late distal tubule and collecting duct.

• cAMP rises, PKA inserts aquaporin-2 water channels, and water moves back into the blood.

• In large amounts ADH also causes vasoconstriction through V1 receptors (IP₃/Ca²⁺) , which is why it's called vasopressin

No ADH → no aquaporins → water goes down the drain as lots of dilute urine.

The only question here in this slide is what is the receptor? And the receptor is V2.”

What is BMR, how was it measured in the lab, and which hormone is its main regulator?

• BMR = (ml O₂/min × 60) ÷ weight in kg

• BMR (basal metabolic rate) is the energy the body uses at rest , measured as oxygen consumed per kg per hour (ml O₂/kg/hr) 

• The main regulator is thyroxine (T4) from the thyroid

• Axis:

  • TRH → TSH → T4 → ↑ BMR 

  • High T4 inhibits TRH and TSH

  • Low T4 removes the brake, so TSH rises

• Lab:More thyroid hormone → cells burn more fuel → they use more O₂. So O₂ use is a direct readout of thyroid function.

• Lecture: thyroid hormone raises BMR by making more Na⁺/K⁺-ATPase pumps

Q. Walk through how the follicle cell makes and releases T3/T4. Name each transporter and enzyme.

• I⁻ enters with 2 Na⁺ through the Na⁺/I⁻ symporter (NIS) , then crosses into the colloid through pendrin

• Thyroid peroxidase (TPO) , using H₂O₂ made by thyroid oxidase (TO) , turns I⁻ into iodine and attaches it to tyrosines on thyroglobulin 

• 1 iodine = MIT , 2 = DIT , MIT + DIT = T3 , DIT + DIT = T4 

• TSH makes the cell take colloid back in by endocytosis

• Lysosomes free T4/T3 into the blood.About 85% is T4 , 15% is T3.

• Lec

• Leftover MIT and DIT are recycled for their iodine (iodotyrosine deiodinase). Every step needs TPO, which is why drugs target it.

• TPO… the most important enzyme that you have to know.

• Lab:

  • PTU blocks T4 synthesis

How does T4 travel, what is the active form, and what do Graves' disease and excess iodide do?

Most T4 rides on thyroxine-binding globulin (TBG) ; only the free (unbound) hormone is active. In target cells T4 becomes active T3 (45%, by 5'-deiodinase) or inactive reverse T3 (55%). Graves' disease: IgG antibodies i ic TSH → the gland enlarges and overproduces. Large excess iodide shuts the gland down

(used to treat

hyperthyroidism). Somatostatin also blocks TSH.

Q. What does thyroid hormone do in the body? Predict the signs of hypo- vs hyperthyroidism.

 It raises BMR, O₂ use and heat (more Na⁺/K⁺-ATPase) increases glucose absorption, glycogenolysis,gluconeogenesis, lipolysis and protein synthesis; raises heart rate (acts on β-adrenergic receptors in the heart) needed for brain

maturation 

• Hypothyroid → listless, slow, sleepy, poor memory 

• Hyperthyroid → hyperexcitable, hyperreflexia, irritable, weight loss 

  • the hyperthyroid rats are the ones with BMR above 1800.

What is a Tx rat missing, and how would you make it function normally?

• Its thyroid was removed, so it has no T4, T3 and calcitonin , To fix it, give T4 (thyroxine) supplements , TRH,TSH, iodine and tyrosine all need a thyroid to work , so they do nothing.

The C cells that make calcitonin are in the thyroid too

A normal rat weighs 249 g and uses 7.0 ml O₂ in 1 m. Find its BMR and category.

• Step 1: 7.0 × 60 = 420 ml O₂/hr

• Step 2: 249 g ÷ 1000 = 0.249 kg

• Step 3: 420 ÷ 0.249  = 1686.75 ml O₂Kg/hr

• Which is euthyroid (1650–1750).

bmr= (ml O2/min × 60) ÷ body weight in kg

Q.Give the BMR cut-offs. A 250 g rat uses 6.0 ml O₂ per minute. What is its BMR and category?

6.0 × 60 = 360 ml/hr

250 / 1000 = 0.25kg

360 / 0.25 kg = 1440 , which is hypothyroid .

Hypothyroid: below 1600

Euthyroid: 1650–1750

Hyperthyroid: above 1800 .

What is a goiter, and what 2 things does it need?

• A goiter is an enlarged thyroid (palpation result: “Mass”)caused by too much TSH stimulation .

• it needs a thyroid gland AND high TSH 

  • Tx rat: no gland, so never

  • Hypox rat: no TSH, so only if TSH is injected

  • Thyroxine injection: TSH falls, so never

Q.After injections, Tx + T4 = 1885.71, Hypox + T4 = 1942.62 and Hypox + TSH = 1893.44. Was the dose too small, just right or too large?

• Too large . All are above 1800, which means hyperthyroid , past normal. A just-right dose would land at 1650–1750 .

• Review answers: the fastest baseline BMR was the normal rat (1686.75), the only one with normal thyroxine. Both surgical rats were lower because both lack thyroxine.

Q. Compare insulin and glucagon: source, effect on blood glucose, effect on glycogen.

• insulin: beta cells of the pancreatic islets; lowers blood glucose by moving glucose into cells; builds glycogen .

• Glucagon: alpha cells ; raises blood glucose; breaks glycogen down

• Both are released into the blood. Insulin-mediated glucose uptake acts as negative feedback when glucose rises.

  • glucose is stored as glycogen in liver and muscle;

  • glucose is the main fuel for nerve cells.

Q. What is the difference between type 1 and type 2 diabetes? Can a glucose reading tell them apart?

• Type1:pancreas don’t make enough insulin(beta cells destroyed),insulin is low. 

• Type 2: cells are unresponsive to insulin (insulin resistance), so insulin is normal or high .

 A glucose reading cannot tell the type : it shows that glucose is high, not why.

Diabetics have EXCESS glucose in the urine, not too little.

Lecture: GH causes insulin resistance

Q.Give the fasting plasma glucose cut-offs. Diagnose a man with 115, 110, 122 mg/dl and a woman with 130, 140,128 mg/dl

• Below 100 = normal

• 100–125 = impaired / borderline (prediabetes)

• 126 or higher = diabetes

• 134, gestational diabete

• 146, diabetic 

Q.Give the source, chemical type and action of FSH, estrogen and calcitonin.

FSH: anterior pituitary , peptide , stimulates ovarian follicle development .

Estrogen: developing ovarian follicles , steroid , stimulates bone growth and protects against osteoporosis .

Calcitonin: thyroid C cells , peptide , inhibits osteoclasts and stimulates Ca²⁺ uptake and deposition in long bones .

Q.Give the T-score categories. As bone density increases, what happens to the T score? Classify −2.31 and −2.61.

• +1 to −0.99 = normal

• −1.0 to −2.49 = osteopenia (bone thinning)

• −2.5 and below = osteoporosis 

• As density increases, the T score becomes less negative .

  • −2.31 = osteopenia ; 

  • −2.61 = osteoporosis 

Why were ovariwctomized rats used? Predict their estrogen, FSH and bone density before treatment.

• Removing the ovaries stops estrogen , which mimics menopause.

• Estrogen is low . FSH is high , because there is no estrogen negative feedback. Bone is lost, so all three rats started with osteoporosis (T score −2.61) .

• TRUE statement: the ovaries stop secreting estrogen after menopause

Q. Where are PTH receptors in bone, and how can PTH both build and break bone?

• PTH receptors are on osteoblasts , not osteoclasts (PTH uses cAMP).

• Brief, intermittent PTH causes bone formation , which is why it is used to treat osteoporosis.

• Chronically high PTH makes osteoblasts release cytokines ( RANKL ) that activate osteoclasts → bone resorption → Ca²⁺ released into the blood. OPG is a decoy that grabs RANKL to keep osteoclasts in check.

The phosphate released from bone would bind Ca²⁺ and limit the rise, which is why PTH also makes the kidney dump phosphate