human phys exam 4

what are the functions of the kidney?

functions of the kidney: 

• regulation of water, inorganic ion balance, acid-base balance

• removal of metabolic waste products & foreign chemicals from blood + excretion in urine

• gluconeogenesis

• production of hormones/enzymes (erythropoietin, renin, vitamin D)

what is the renal cortex vs. renal medulla?

renal cortex: outer region

renal medulla: inner region pyramids

distinguish between the two types of nephrons

cortical nephron: located mostly in cortex; performs filtration & bulk reabsorption

juxtamedullary nephron: located deep into medulla; responsible for urine concentration & creating osmotic gradient

what is the difference between filtration, secretion, and reabsorption?

• filtration: blood → glomerulus → Bowman’s capsule

• reabsorption: kidney (tubule) → blood (peritubular capillaries)

• secretion: blood (peritubular capillaries) → tubule (kidney); will be excreted via. urine

what is the organization of the nephron?

glomerulus → Bowman’s capsule → proximal convoluted tubule (PCT) → Loop of Henle → distal convoluted tubule (DCT) → cortical collecting duct

 why are some molecules actively secreted vs. reabsorbed?

homeostatic control

secreted - eliminate molecules that the body doesn’t need (e.g., waste products, toxins, in excess)

reabsorbed - conserve molecules that are valuable to the body (e.g., glucose, amino acids)

secreted & reabsorbed - regulation of pH, K⁺

what is the sequence of blood flow in the glomerulus?

afferent arteriole → glomerular capillaries → efferent arteriole

**highest blood pressure/hydrostatic pressure in the glomerulus

what are podocytes?

• foot processes that create filtration slits

• provide selective barrier for size & charge

what is Bowman’s capsule?

• surrounds glomerulus to collect filtrate and send to PCT

what is juxtaglomerular apparatus (JGA)?

• controls filtration & blood pressure

• composed of…

  • macula densa: senses NaCl concentration to regulate renin & GFR

  • juxtaglomerular cells: modified smooth muscle cells that secrete renin to regulate blood pressure

what are mesangial cells?

• modified smooth muscle

• can contract → ↓ surface area → ↓ GFR

what molecules can and can not be filtered through podocytes?

filtered: H₂O, electrolytes, glucose, amino acids, vitamins, urea, uric acid, creatinine

NOT filtered (large molecules): blood cells, plasma proteins, large anions, minerals (e.g., Ca²⁺), hormones

what factors are involved in glomerular filtrate rate.

• podocyte pores - filtration barrier affecting what can and can’t be filtered

• hydrostatic (blood) pressure - pressure of blood in glomerular capillaries that pushes filtrate OUT to Bowman’s capsule; driving factor of filtration

• forces opposing filtration (↓ GFR)

  • bowman’s capsular hydrostatic pressure: pressure in Bowman’s capsule pushing fluid back into glomerular capillaries

  •  glomerular oncotic pressure: caused by plasma proteins pulling water back into glomerular capillaries

• arterial diameter

  • ideally wide afferent arteriole & narrow efferent arteriole

*net glomerular filtration rate (GFR) = glomerular hydrostatic pressure - bowman’s hydrostatic pressure - glomerular oncotic pressure

what factor regulates the glomerulus filtration rate?

arteriole diameter

• afferent arteriole

  • ↓ diameter (constriction) → ↓ GFR (less blood/filtration)

  • ↑ diameter (dilation) → ↑ GFR (more blood/ filtration)

• efferent arteriole

  • ↓ diameter (constriction) → ↑ glomerular pressure → ↑ GFR

  • ↑ diameter (dilation) → ↓ glomerular pressure → ↓ GFR

what is the PCT?

Proximate Convoluted Tubule (PCT): major site of water and solute reabsorption in blood

How is water and sodium reabsorbed in the PCT?

sodium

1. Na⁺ moves down concentration gradient from lumen → PCT/tubule cell

2. Na⁺ is actively transported/pumped into interstitial fluid

water

• water follows sodium via. osmosis

how are molecules reabsorbed and secreted in the PCT?

• *driven by Na⁺ gradient (created by Na⁺/K⁺ ATPase

• Cotransport (symport) → reabsorption of glucose & amino cells from lumen → cell

• Countertransport (antiport) → secretion of H⁺ from cell → lumen

how does PCT regulate pH?

• normal conditions:

  • H⁺ recycled back into lumen

  • HCO_3^- reabsorbed into blood

• alkalosis: more HCO₃^- > H⁺ in lumen

  • ↓ H⁺ secretion, ↑ HCO₃⁻ excretion

  • some reform H₂CO₃ → CO₂ + H₂O, rest of HCO₃^- stays in lumen and excreted out via. urine

• acidosis: more H⁺ > HCO₃^-

  • ↑ H⁺ secretion via. urine, ↑ buffers (phosphate, ammonia), ↑ new HCO₃⁻ reabsorbed

  • HPO₄^2- (buffer) + H⁺ → H₂PO₄^- → urinated out

  • NH₃ (buffer) +H⁺ → NH₄⁺ → urinated out

what is the Loop of Henle? what are the two parts of it?

• creates gradient (countercurrent multiplier) via. active transport (pump)

• descending limb: goes into renal medulla

  • permeable to water → water leaves descending limb to interstitial fluid

  • filtrate/urine becomes more concentrated (hyperosmotic)

• ascending limb: goes back to renal cortex

  • impermeable to water

  • actively pumps ions (Na⁺, K⁺, Cl^-) out to interstitial fluid via. NKCC

  • filtrate becomes dilute (hypoosmotic), interstitial fluid becomes hyperosmotic

• medulla gradient: further down medulla = saltier

how to loop diuretics work?

• targets NKCC in Loop Henle to treat hypertension

• blocking NKCC → less salty medulla → less water reabsorbed into interstitial fluid, more water retained in kidney → more water urinated, lower blood volume, lower blood pressure

what is the vasa recta?

vasa recta: capillary network that runs parallel to loop of Henle

• maintains osmotic gradient in medulla (countercurrent exchange) via. passive transport

• collects water from interstitial tissue

• both limbs permeable to water but not permeable to colloid proteins

what are the two portions of the vasa recta?

• descending portion (going into medulla): NaCl diffuses INTO blood, water diffuses OUT of blood → blood becomes more concentrated (hyperosmotic)

• ascending portion: NaCl diffuses OUT of blood, water diffuses INTO blood → blood becomes diluted

which nephron structures are regulated via. osmosis vs. hormones?

osmosis: PCT, Loop of Henle, vasa recta

hormones: DCT, collecting duct

what effects do vasopressin have on collecting duct?

• vasopressin = anti-diuretic hormone (ADH)

• controls water permeability by inserting aquaporins (water channels) into membrane to allow movement of water from lumen → interstitium

• dehydration → sensed by osmoreceptors in hypothalamus → hypothalamus signals to posterior pituitary gland to release vasopressin/ADH → add aquaporins → urine becomes concentrated/less urination, blood volume increases

when is ADH inhibited? what effect does that have on the body?

• inhibited when…

  • blood is too dilute → ↓ signaling of osmoreceptors in hypothalamus → ↓ ADH release from posterior pituitary

  • blood volume/pressure is too high → ↑ baroreceptor firing → siginal ↓ ADH release

  • alcohol

• effects:

  • fewer/no aquaoprins → ↓ water reabsorption → ↓ blood volume, ↑ urine volume → frequent urination & dehydration

what effect does aldosterone have on collecting duct?

• aldosterone: increases Na⁺ reabsorption and K⁺ secretion → retains water & increases blood volume/pressure

what controls aldosterone release?

• low Na⁺ → activates RAAS (indirect) → ↑ aldosterone release

• high Na⁺ → inactivates RAAS (indirect) → ↓ aldosterone release

• high K⁺ → ↑ aldosterone release (direct control) → ↑ K⁺ excretion, ↓ plasma K⁺

• low K⁺ → ↓ aldosterone release (direct control) → ↓ K⁺ excretion, ↑ plasma K⁺

How is aldosterone regulated by renin system?

1. macula densa senses low Na⁺ 

2. triggers JG (juxtaglomerular) cells to release renin

3. triggers RAAS pathway (renin-angiotensin-aldosterone system)

   1. ACE converts angiotensin I → angiotensin II → vasoconstriction → ↑ blood pressure

   2. aldosterone → Na/K⁺ ATPase pumps Na⁺ out (lumen → blood) and K⁺ in (blood → lumen) → ↑ Na⁺ reabsorption + ↑ K⁺ secretion → more water reabsorption in blood → ↑ blood volume → ↑ blood pressure

what influences JGA renin secretion?

• macula densa senses NaCl concentration in tubular fluid

  • low NaCl → ↓ GFR, ↓ flow → stimulates JG cells to ↑ renin release

  • high NaCl → afferent arteriole constriction + ↓ renin release

• afferent arteriole pressure (baroreceptor mechanism)

  • low pressure → ↓ stretch → ↑ renin release

  • high pressure → ↑ stretch → ↓ renin release

• sympathetic nervous system (β₁)

  • ↑ sympathetic (β₁) → ↑ renin

what is the difference between endocrine vs. exocrine glands?

• endocrine: secrete hormones directly into bloodstream; does not have ducts; acts on distant targets

• exocrine: secrete via. duct to lumen/surface; local effects (e.g., sweat, digestive enzymes)

what are the three major classes of hormone molecules?

• amines - derived from amino acids (e.g.,  tyrosine)

• peptides - protein-based hormones

  • water-soluble → travels freely without needing a carrier

  • acts on cell surface receptor (bc can’t to through plasma membrane)

• steroids - cholesterol-based

  • lipid soluble → travels bound to hormone binding protein to form hormone-protein complex

  • acts on intracellular receptors

what are examples of amino hormones?

• e.g., dopamine, epinephrine, norepinephrine

what are examples of peptide hormones?

• e.g., vasopressin, oxytocin, insulin

what are examples of steroid hormones?

e.g., cortisol, aldosterone, testosterone, estradiol

what is congenital adrenal hyperplasia?

congenital adrenal hyperplasia: inherited genetic disorder that impairs the adrenal glands’ ability to produce essential hormones (cortisol and aldosterone) and overproduce androgens

how are levels of testosterone vs. estradiol regulated?

• **ratio of testosterone to estradiol is dependent on amount of aromatase (enzyme that converts testosterone to estradiol)

what is the significance of cholesterol being the base molecule for steroid

• interconnected pathways

• lipid-soluble → cross cell membrane and bind to intracellular receptors

• slower onset but long-lasting effects

• bound to carrier proteins to be transported in blood

what is the difference between total vs. free hormone levels?

total hormone = free hormone + protein-bound hormone

free hormone = unbound hormone

what are the types of hormone interactions?

• Synergistic: effect of each hormone is independent, but combined effect is greater/additive

• Antagonistic: one hormone opposes/inhibits another

• Permissive: one hormone enhances/affects another hormone’s effect/physiology

what is an example of synergistic interaction?

• ex: combo of epinephrine + norepinephrine have a greater increase on heart rate together than independently

what is an example of antagonistic interaction?

• ex: insulin + glucagon → maintains blood sugar levels

what is an example of permissive interaction?

• ex: epinephrine + thyroid hormone

• ex: peak in estrogen/estradiol in uterus causes increase in progesterone receptors

what is the difference between physiologically relevant and pharmacological level?

physiologically relevant levels: normal concentration of hormone in the blood that naturally occurs in the body

• controlled by feedback mechanisms to maintain homeostasis

• reflects balance of secretion, circulation, uptake and removal

• pulsatile secretion release hormones in bursts rather than constantly to prevent excess hormone buildup

pharmacological levels: higher than natural/physiological levels

what is the initial vs. long-term effect of pharmacological levels of hormones?

• initial effect: higher binding → ↑ activity

• long term effect: 

  • stress → ↓ sensitivity (downregulation)

  • binding to unintended low-affinity receptors → change other hormone levels → downstream effects

what inputs regulate endocrine cell secretions?

• ions/nutrients, neurotransmitters, hormones

• **key idea: each input can act independently or dependently (permissive effects, influence/interact with each other)

• ex: high blood sugar → insulin release → lowers blood sugar → releases glucagon

what mechanisms limit hormone concentrations in blood?

• negative feedback

• uptake by target tissues

• hormone half-life (time it takes hormone levels to drop by 50%)

• liver metabolism/degradation into inactive forms

• receptor regulation (up/downregulation)

• naturally avoid downregulation through pulsatile secretions

what are tropic vs. trophic hormones?

• tropic: any hormone that acts on other endocrine glands as their target

• trophic: any hormone that causes tissue growth

what are the two parts of the pituitary gland?

• Anterior pituitary (adenohypophysis) → makes hormones

• Posterior pituitary (neurohypophysis) → stores & releases hormones made in hypothalamus

what hormones are secreted from the anterior pituitary gland?

tropic hormones:

• TSH (thyroid stimulating hormone) - targets thyroid gland for T3/T4 production

• ACTH (adrenocorticotropic hormone) - targets adrenal cortex for cortisol section (+ androgens)

• LH (luteinizing hormone) - targets gonads for ovulation & testosterone production

• FSH (follicle-stimulating hormone) - targets gonads for follicle development + sperm production

direct/non-tropic hormones:

• growth hormone

• prolactin - targets mammary glands to produce milk

what hormones are secreted from the posterior pituitary gland?

• ADH (Antidiuretic hormone/vasopressin) - targets kidney for water reabsorption

• oxytocin - uterine contractions + milk ejection

what are the hormones produced and secreted by the thyroid gland?

T4 (thyroxine) hormone (80%): longer half-life → travels longer distances than T3

T3 (triiodothyronine) hormone (20%): 4x as potent as T4; strong effect but degrades faster (short half-life)

what is the pathway to make thyroid hormone?

1. follicular cells secrete thyroglobulin into colloid/lumen

2. thyroglobulin + iodine → MIT (1 iodine) or DIT (2 iodine)

3. DIT + DIT → T4

4. MIT + DIT → T3

what are the structures of the thyroid?

thyroid follicles: main unit made of follicular cells (outer layer) and central lumen filled with colloid

• follicular cells: produce thyroglobulin, takes up iodine, process/release T3/T4

• colloid: gel-like material inside follicles; site of hormone synthesis + storage

• parafollicular cells: located between cells; secrete calcitonin

what is TSH?

TSH (thyroid stimulating hormone): tropic hormone that stimulates iodine uptake +  TG synthesis → leads to synthesis + release of T3/T4

What are the functions of thyroid hormone?

• binds to intracellular receptors → induce gene transcription

• ↑ metabolism - stimulates carb absorption in small intestine, fat breakdown, protein turnover

• ↑ heat production - stimulates Na⁺/K⁺ pump activity → heat byproduct to maintain body temp

• improves muscle performance via. myosin ATPase

• Permissive effects

  • T3 + epinephrine → fatty acid + glycerol release

  • b-adrenergic receptors respond to thyroid hormone → ↑ heart rate

what is hypothyroidism?

hypothyroidism: underactive thyroid; low T3/T4

what is hyperthyroidism?

hyperthyroidism: overactive thyroid; high T3/T4

what is goiter? how can it present as both hyper and hypothyroidism?

goiter: thyroid enlargement

• if caused by hyperthyroidism: overactive thyroid → excess trophic hormones (T3 + T4) → cell enlargement

• if caused by hypothyroidism: underactive thyroid → stimulates TSH release (trophic effect) → tumor growth

what are parafollicular cells?

• secrete calcitonin (hormone)

• inhibits osteoclast activity (breakdown bone)

• opposite effect of PTH (parathyroid hormone)

• ↓ blood Ca²⁺ → ↓intestine Ca²⁺ absorption, ↓ bone resorption (osteoclast activity), ↓ renal Ca²⁺ reabsorption, ↑ Ca²⁺ secretion, ↓ vitamin D synthesis

what are parathyroid glands?

• release PTH (parathyroid hormone)

• opposite effect of calcitonin

• ↑ blood Ca²⁺ → ↑intestine Ca2+ absorption, ↑ bone resorption (osteoclast activity), ↑ renal Ca²⁺ reabsorption, ↓ Ca²⁺ secretion, ↑ vitamin D synthesis

what are all the hormones related to the thyroid?

what is the pathway of Vitamin D?

1. Skin: UV light converts 7-dehydrocholesterol → Vitamin D₃ (cholecalciferol)

2. Liver: converts Vitamin D₃ → 25-hydroxyvitamin D (25(OH)D) (circulating inactive form)

3. Kidney: 1α-hydroxylase (enzyme) converts 25(OH)D → 1,25-dihydroxyvitamin D (calcitriol) (active form)

how does PTH and kidney play a role in Vitamin D synthesis?

kidney - activation site

PTH - regulator of activation’

• Low Ca²⁺ → ↑ PTH

• PTH → ↑ 1α-hydroxylase activity → ↑ active Vitamin D (calcitriol) → ↑ Ca²⁺ absorption

what is the function of Vitamin D?

• increase blood Ca²⁺

• intestine - ↑ Ca²⁺ absorption from diet

• bone - works with PTH to ↑ Ca²⁺ release

• kidney - supports Ca²⁺ reabsorption

what is the morphology/structure of the adrenal gland? what hormones are released?

adrenal cortex (outer): made of epithelial cells; produces steroid hormones

• zona glomerulosa: salt → aldosterone

• zona fasciculata: sugar → glucocorticoids (cortisol)

• zona reticularis: sex steroids (androgens)

adrenal medulla (inner): functions like modified sympathetic ganglion; produces amine hormones

• epinephrine

• norepinephrine

what is the relationship between glucocorticoids with innate and humoral/adaptive immune function?

innate → reduced inflammation & decrease activity of macrophages & neutrophils

adaptive → lymphocyte suppression and ↓ cytokine signaling → reduced antibody response and immune coordination

How is glucocorticoid stress response adaptive and maladaptive?

adaptive (short-term): prevents excess inflammation, protects tissues during stress/injury, conserves energy for survival

maladaptive (chronic): long-term cortisol elevation leads to immunosuppression, increased infection risk, and poor wound healing

what is the function of cortisol in daily physiological maintenance?

**maintains homeostasis (baseline regulator) by…

• maintains blood glucose

• supports normal metabolism (protein, fat)

• maintains vascular tone + blood pressure

• regulates immune activity

what is Addison’s Disease?

• Addison’s Disease: hyposecretion of adrenal cortex

• low cortisol → leads to fatigue, weight loss, low blood pressure

  • feedback response: ↑ ACTH

• ↓ aldosterone → Low blood pressure + Electrolyte imbalance

what is Cushing’s Syndrome/Disease?

• Cushing’s Syndrome: hypersecretion of ACTH in pituitary gland

• ↑ ACTH → excess cortisol → leads to muscle/bone breakdown, high blood glucose, immunosuppression, hypertension, androgens

• leads to adrenal hyperplasia

how is cortisol related to diabetes?

• cortisol causes ↑ gluconeogenesis (makes new glucose), ↓ insulin sensitivity, ↑ fat & protein breakdown

• elevated cortisol causes ↑ blood glucose level + ↑ insulin requirements (especially during stress/infection)

how is cortisol related to respiratory distress syndrome (RDS)?

• cortisol stimulates surfactant production in lungs → reduces surface tension + prevents lung collapse

• low cortisol → ↓ surfactant → RDS

how does cortisol relate to congenital adrenal hyperplasia?

adrenal hyperplasia = enlargement of adrenal gland

↓ cortisol production → signals ↑ ACTH → ↑ androgens

what are the gonadotropic hormones?

follicle stimulating hormone (FSH): stimulates gamete production (eggs, estrogen, sperm)

luteinizing hormone (LH): triggers ovulation (production of progesterone) + production of testosterone

what enzyme is responsible for oxidizing iodides and attaching them to tyrosines on thyroglobulin?

thyroid peroxidase

what are the two target organs of parathyroid hormone?

• kidney

• bone

what is Graves’ disease?

• autoimmune disease that activates TSH receptors

• results in hyperthyroidism + goiter

what is the difference between primary and secondary adrenal conditions?

primary - affects adrenal glands (e.g., Addison’s)

secondary - affects pituitary gland (ACTH) (e.g., Cushing’s)

what is the difference between primary and secondary hyposecretion?

primary (Addison’s disease) - ↓ cortisol, ↓ aldosterone, ↑ ACTH (due to loss of feedback)\

• Hyperpigmentation (↑ ACTH → melanocyte stimulation)

• Low blood pressure (↓ aldosterone)

• Electrolyte imbalance

secondary - ↓ cortisol, normal aldosterone (mostly), ↓ ACTH

• No hyperpigmentation

• Less severe electrolyte issues

what is the difference between primary and secondary hypersecretion?

primary (e.g., adrenal tumor/overactivity): ↑ cortisol, ↓ ACTH (negative feedback)

secondary (Cushing’s disease): ↑ ACTH, ↑ cortisol, Adrenal hyperplasia