Nephron Map Assignment

Nephron Map Checklist | Human Anatomy

📚Abbreviations Key

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Structural + Anatomic

L/R = Left / Right

PCT = Proximal Convoluted Tubule

DCT = Distal Convoluted Tubule

CD = Collecting Duct

LoH = Loop of Henle

TAL = Thick Ascending Limb

tDL = Thin Descending Limb

JGA = Juxtaglomerular Apparatus

JG cells = Juxtaglomerular (granular) cells

UPJ = Ureteropelvic Junction

UVJ = Ureterovesical Junction

IVC = Inferior Vena Cava

Physiology + Pressures

GFR = Glomerular Filtration Rate

NFP = Net Filtration Pressure

HP = Hydrostatic Pressure

OP / π = Oncotic (colloid osmotic) Pressure

BP = Blood Pressure

MAP = Mean Arterial Pressure

TGF = Tubuloglomerular Feedback

RBF = Renal Blood Flow

Hormones + Regulators

RAAS = Renin-Angiotensin-Aldosterone System

Ang I / Ang II = Angiotensin I / II

ACE = Angiotensin Converting Enzyme

ADH = Antidiuretic Hormone (Vasopressin)

ANP = Atrial Natriuretic Peptide

BNP = Brain Natriuretic Peptide

PTH = Parathyroid Hormone

EPO = Erythropoietin

Transporters + Channels

AQP2 = Aquaporin 2 (water channel)

ENaC = Epithelial Na+ Channel

ROMK = Renal Outer Medullary K+ Channel

NKCC2 = Na/K/2Cl Cotransporter (TAL)

NCC = Na/Cl Cotransporter (DCT)

NHE3 = Na/H Exchanger (PCT)

SGLT = Sodium-Glucose Cotransporter

GLUT = Glucose Transporter

TRPV5 = Transient Receptor Potential Vanilloid 5 (Ca2+ channel, DCT)

V2 receptor = Vasopressin type 2 receptor (principal cells)

Clinical

DI = Diabetes Insipidus

SIADH = Syndrome of Inappropriate ADH

UTI = Urinary Tract Infection

AKI = Acute Kidney Injury

CKD = Chronic Kidney Disease

Lab Structures Progress

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Rubric

Anatomy 10 pts

Histology + Micro 10 pts

Flow Pathways 5 pts

Function 5 pts

Visual + Effort 10 pts

Accuracy 10 pts

📄 How to Build Your Nephron Map -- Read This First

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🎨 This is a Visual, Not a List

Your Nephron Map is a single-page illustrated diagram, not an outline, not a study guide written in bullet points, and not a paragraph essay. If your final product looks like a table or a numbered list, start over. The goal is a hand-drawn or digitally designed map that traces a single nephron from renal corpuscle to collecting duct, with annotated structures, zoom-in boxes, and brief labels. Think of it as a page out of a medical atlas that you made yourself.

You are not being graded on artistic ability. Rough sketches, imperfect circles, and uneven lines are completely fine. What matters is that you drew something, a real visual representation, not that it looks beautiful.

📷 What "Visual" Actually Means

Every region of the nephron should be drawn as a shape on the page, even a simple tube or oval. From that shape, you pull out and annotate. Here are the three visual tools you should be using:

🔍 Zoom-In Boxes

Draw a small box or circle that zooms in on a specific region. For example, draw the renal corpuscle as an oval, then draw a magnified box off to the side showing the three-layer filtration membrane with labeled fenestrated endothelium, basement membrane, and podocyte slit diaphragms. Connect it to the main diagram with a line. This is how you show histology without cluttering your main diagram.

▣ Cross-Sectional Boxes

At least one segment should include a small cross-section showing the epithelial cell type and key transporters. The PCT is a great choice, draw the lumen, brush border, basal striations, and label the transporters (SGLT2, NHE3, Na-K ATPase on basolateral side). This is also where you can show the principal cell vs intercalated cell difference in the collecting duct.

→ Arrows and Brief Captions

Every label on your map should be a short phrase of 1 to 5 words, connected by an arrow to the structure it describes. Captions can be slightly longer (one sentence max) but should be written as annotations, not prose. Example: "Podocyte -- filtration slit" is a good caption. A paragraph explaining podocyte function is not.

✅ Use This Checklist the Right Way

The checklist in this tool is organized by region and category, anatomy, histology, cells, transport, neural/hormonal, and function. Work through each region on your actual map first, then come back and check off what you included. Do not write out every checklist item as text on your map, that defeats the purpose. Each item on this list should correspond to a label, a zoom-in box, a symbol, or an arrow on your drawing.

A good gut check: if you can fold your map and all the information is still readable as prose without the drawing, you have not made a map. You have made a document. Go back and draw.

💡 Practical Layout Tips

●Start by sketching the full nephron as a winding tube on your page, renal corpuscle at the top, collecting duct at the bottom draining toward the papilla. Show a clear border between cortex (top) and medulla (bottom) so segments can be located regionally.

●Draw the blood supply alongside the tubule, afferent arteriole into glomerulus, efferent arteriole out, peritubular capillaries hugging the PCT and DCT, vasa recta running parallel to the loop of Henle. Use a different color for blood.

●The juxtaglomerular apparatus deserves its own zoom-in, draw the triangular contact zone where the DCT touches the afferent arteriole, and label all three cell types (macula densa, JG cells, extraglomerular mesangial cells).

●Use color to differentiate categories, one color for histology labels, another for transporters/secretions, another for hormones. A simple legend in the corner is enough.

●Reserve at least one corner or side margin for your cross-section or zoom-in boxes. These do not need to be large, a 2 inch box is sufficient if it is clearly labeled.

●For the physiology panel (A&P course): feedback loops should be drawn as small circles or loops with arrows marked "+" (stimulates) and "-" (inhibits). A RAAS loop that is one inch in diameter and clearly labeled beats a paragraph of text every time.

●Scan or photograph your finished map at high resolution before submitting. Make sure all labels are legible in the digital version.

Bottom line: The rubric rewards completeness and accuracy, not beauty. A clean, clearly labeled sketch that includes the renal corpuscle, all tubular segments, cell types, transporters, and the JGA will score well. A gorgeous digital illustration that is missing the macula densa or forgets to label the loop of Henle limbs will not. Draw first. Label accurately. Keep text short.

🔍 Urinary System Lab Identification List

This is the full structural checklist from your lab handout. Use this panel when you are working with cadaveric specimens, models, or imaging to identify the gross and microscopic structures of the urinary system. Check off each structure as you locate and correctly identify it in the lab. This is a separate task from your Nephron Map, which is graded on the 50 pt rubric and covered in the next two tabs.

Note for BIO 004 students: This panel is your priority. The Nephron Map Anatomy tab is the drawing assignment. The Physiology tab is optional reference.

Note for BIO 431 students: Work through all three panels. Lab identification first, then build your Nephron Map across the anatomy and physiology tabs.

Identify

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Left kidney + Right kidney (retroperitoneal, right sits lower due to liver)
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Suprarenal (adrenal) gland -- sits on superior pole of each kidney
Not functionally part of the urinary system but anatomically paired
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Renal capsule -- thin fibrous layer directly on kidney surface
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Perirenal fat (adipose capsule) + renal fascia (Gerota's) + pararenal fat
Three support layers surrounding the kidney
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Renal cortex -- outer region, contains renal corpuscles + convoluted tubules
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Renal medulla -- inner region, contains loops + collecting ducts
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Renal column -- cortical tissue extending between pyramids (contains interlobar vessels)
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Renal pyramid -- triangular medullary masses; 8 to 18 per kidney; apex = papilla
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Renal sinus -- the hollow fat-filled cavity housing calyces, pelvis, vessels, nerves
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Minor calyx -- cup-shaped, collects urine from one papilla
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Major calyx -- formed by 2 to 3 minor calyces merging
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Renal pelvis -- funnel formed by merged major calyces; continuous with ureter
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Hilum -- indentation where renal artery, renal vein, ureter, nerves, lymphatics enter/exit
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Ureter -- ~25 to 30 cm muscular tube from renal pelvis to bladder (retroperitoneal)
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Urinary bladder -- identify trigone, detrusor muscle, rugae
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Urethra -- female ~4 cm; male ~20 cm (prostatic, membranous, spongy regions)

Arterial (in order)

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Renal artery -- enters kidney at hilum; branches from abdominal aorta
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Segmental arteries -- first branches inside renal sinus
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Interlobar arteries -- travel through renal columns between pyramids
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Arcuate arteries -- arch along the base of each pyramid (cortex/medulla junction)
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Cortical radiate (interlobular) arteries -- ascend radially into the cortex
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Afferent arteriole -- delivers blood to glomerulus
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Efferent arteriole -- carries blood AWAY from glomerulus (unique portal system feature)

Capillary beds

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Glomerular capillaries -- tuft between afferent + efferent arterioles; high pressure, filtration
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Peritubular capillaries -- wrap PCT + DCT of cortical nephrons; low pressure, reabsorption
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Vasa recta -- long straight vessels parallel to loop of Henle (juxtamedullary nephrons); preserve medullary gradient

Venous (reverse order)

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Cortical radiate (interlobular) veins
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Arcuate veins
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Interlobar veins
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Renal vein -- exits at hilum; drains into IVC
No segmental vein; venous return mirrors arterial tree minus segmental level

Identify

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Glomerulus -- tuft of fenestrated capillaries
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Glomerular (Bowman's) capsule -- double-walled epithelial sac surrounding the glomerulus
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Parietal layer of glomerular capsule -- simple squamous epithelium (outer wall)
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Visceral layer of glomerular capsule -- podocytes (inner wall, directly on capillaries)
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Bowman's (capsular) space -- between parietal + visceral layers; filtrate collects here
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Vascular pole (afferent/efferent arterioles enter) vs tubular pole (PCT begins)

Identify

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Proximal convoluted tubule (PCT) -- coiled tubule in cortex, immediately exits glomerular capsule
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Loop of Henle -- U-shaped, dips into medulla; descending limb + ascending limb
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Distal convoluted tubule (DCT) -- coiled tubule in cortex, returns near its own corpuscle
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Collecting duct -- receives filtrate from multiple DCTs; descends through medulla
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Papillary duct -- distal-most portion of collecting duct; opens at renal papilla into minor calyx

JGA Cells

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Juxtaglomerular apparatus (JGA) -- found where the DCT contacts the afferent arteriole of its own corpuscle
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Macula densa cells -- modified DCT epithelial cells; sense NaCl delivery in filtrate
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Granular (juxtaglomerular) cells -- modified smooth muscle cells in afferent arteriole wall; secrete renin

Trace the flow

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Step 1: PCT (proximal convoluted tubule)
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Step 2: Loop of Henle (descending then ascending limb)
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Step 3: DCT (distal convoluted tubule)
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Step 4: Collecting duct
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Step 5: Papillary duct
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Step 6: Minor calyx → Major calyx → Renal pelvis
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Step 7: Ureter (~25 to 30 cm, peristaltic contractions push urine)
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Step 8: Urinary bladder (storage)
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Step 9: Urethra (through internal then external urethral sphincter) to outside

Memorize this one-liner

PCT → Loop of Henle → DCT → CD → papillary duct → minor calyx → major calyx → renal pelvis → ureter → bladder → urethra → outside

Trace the flow

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Abdominal aorta → renal artery (enters at hilum)
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Segmental artery → interlobar artery (in renal column)
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Arcuate artery (base of pyramid) → cortical radiate artery
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Afferent arteriole → glomerular capillaries → efferent arteriole
This is the portal-like system -- capillaries between two arterioles
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Peritubular capillaries (cortical) OR vasa recta (juxtamedullary)
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Cortical radiate vein → arcuate vein → interlobar vein → renal vein → IVC

Memorize this one-liner

Aorta → renal a. → segmental → interlobar → arcuate a. → cortical radiate → afferent arteriole → glomerulus → efferent arteriole → peritubular / vasa recta → cortical radiate v. → arcuate v. → interlobar → renal v. → IVC

Category: Anatomy Histology Cells Transport Neural/Hormonal Function

Draw on your map

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Afferent arteriole entering glomerulus at the vascular pole
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Glomerular capillary tuft (fenestrated); label as the high-pressure filtration bed
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Efferent arteriole leaving glomerulus at the vascular pole
This is the hallmark portal-like arrangement -- capillaries between two arterioles
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Peritubular capillaries wrapping the PCT and DCT (cortical nephrons)
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Vasa recta running parallel to the Loop of Henle (juxtamedullary nephrons)

Function + Annotation

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Two-capillary-bed design: glomerular (high pressure, filtration) + peritubular/vasa recta (low pressure, reabsorption)
Key annotation to include on your map near each bed
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Arteriole diameter changes modulate GFR: constrict afferent → GFR drops; constrict efferent → GFR rises
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Vasa recta form countercurrent exchange loops that preserve the medullary osmotic gradient

Histology Note

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Glomerular capillaries: fenestrated endothelium with ~70 to 100 nm pores
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Peritubular capillaries: continuous capillaries with low hydrostatic pressure + high oncotic pressure (favors reabsorption)

Not on the map: the larger arterial tree (renal → segmental → interlobar → arcuate → cortical radiate) lives on the Lab Structures tab. Your Nephron Map only needs the microvasculature around the nephron itself.

Anatomy

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Glomerulus: tuft of fenestrated capillaries
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Bowman's capsule: double-walled epithelial sac surrounding glomerulus
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Parietal layer (simple squamous) + visceral layer (podocytes) + Bowman's space between
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Vascular pole (afferent + efferent arterioles enter/exit) + urinary pole (PCT begins here)

Histology

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3-layer filtration membrane: fenestrated capillary endothelium + glomerular basement membrane (GBM) + podocyte slit diaphragms
Key zoom-in box on your map
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GBM is negatively charged (heparan sulfate) -- repels anions; this is why albumin (negative) is excluded despite being near the size cutoff
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Size cutoff: freely filtered < ~5 kDa; restricted 5-70 kDa; excluded > 70 kDa (albumin is ~69 kDa)

Cells

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Podocytes: visceral layer cells with primary processes extending pedicels (foot processes); slit diaphragms bridge between adjacent pedicels (nephrin/podocin proteins)
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Intraglomerular mesangial cells: structural support, phagocytose debris, contract to regulate Kf (filtration coefficient)
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Fenestrated endothelial cells: ~70-100 nm pores (block RBCs, platelets, large proteins)

Function

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Ultrafiltration of blood: filters by size + charge; produces ~125 mL filtrate/min (GFR)

Anatomy

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Most convoluted segment of the nephron; located entirely in the cortex
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Receives filtrate from Bowman's space at urinary pole; drains into descending limb of loop of Henle

Histology

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Simple cuboidal epithelium with prominent apical brush border (dense microvilli) -- tallest brush border in the nephron
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Basal striations from densely packed mitochondria (high ATP demand for active transport)
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"Leaky" tight junctions: permits paracellular movement of water and small ions

Cells Transport

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PCT epithelial cells: Na/K ATPase (basolateral) drives secondary active transport of glucose (SGLT2, SGLT1), amino acids, phosphate
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Reabsorbs: ~65% Na+, 65% water, 65% Cl-, 100% glucose, 100% amino acids, 85% HCO3-, 65% K+, phosphate
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Secretes: H+ (via NHE3), organic acids (PAH, urate, penicillin), organic bases, creatinine, drugs

Function

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Bulk isosmotic reabsorption: filtrate leaves PCT at the same osmolarity it entered (~300 mOsm), but volume is reduced ~65%
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Major site of drug excretion (secretion) and reclaiming of valuable solutes

Anatomy

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U-shaped hairpin loop descending into medulla then ascending back to cortex; three segments: descending limb > thin ascending limb > thick ascending limb (TAL)
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Cortical nephrons (~85%) have short loops; juxtamedullary nephrons (~15%) have long loops reaching deep medulla
Juxtamedullary = deep concentrating power

Histology

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Thin descending + thin ascending = simple squamous epithelium
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Thick ascending limb (TAL) = simple cuboidal; abundant mitochondria (active transport)

Transport

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Descending limb: permeable to water (AQP1), impermeable to NaCl -- filtrate concentrates as it descends
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Thin ascending: impermeable to water, permeable to NaCl (passive) -- filtrate dilutes
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TAL: impermeable to water; NKCC2 (Na+/K+/2Cl- cotransporter) actively pumps out NaCl; ROMK recycles K+ to lumen (creates + lumen voltage)
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TAL paracellular reabsorption of Ca2+, Mg2+ (driven by + luminal charge)
Loop diuretics block NKCC2 here

Function

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Countercurrent multiplication: establishes medullary osmotic gradient (300 mOsm at corticomedullary junction > 1200 mOsm at papilla)
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Reabsorbs ~25% of filtered NaCl; TAL is the "diluting segment" -- filtrate leaves hypoosmotic (~100 mOsm)

Anatomy

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Located entirely in the cortex; begins at the macula densa; less convoluted than PCT
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Early DCT (NCC-expressing) transitions to late DCT (principal + intercalated cells begin here)

Histology

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Simple cuboidal; few or no microvilli (no brush border -- key distinction from PCT)
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Abundant mitochondria; smaller lumen than PCT in cross-section

Cells Transport

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DCT cells: NCC (Na+/Cl- cotransporter, thiazide-sensitive) on apical side; reabsorbs ~5-7% of filtered Na+
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Ca2+ reabsorption: TRPV5 apical, calbindin cytoplasm, NCX/PMCA basolateral; PTH-stimulated
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Impermeable to water (like TAL) -- continues diluting the filtrate

Function

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Fine tuning of Na+ and Ca2+ reabsorption; major site of hormone-regulated Ca2+ handling (PTH, vitamin D)

Anatomy

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Cortical collecting duct > outer medullary > inner medullary > papillary duct (ducts of Bellini) > minor calyx
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Multiple nephrons drain into a single collecting duct (convergence point)

Histology

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Simple cuboidal in cortex, transitioning to simple columnar in inner medulla (cells get taller as duct descends)
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Cells have distinct, well-defined cell borders on histology slides (easy to identify)

Cells Transport

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Principal cells (~70%): ENaC (aldosterone-sensitive, apical Na+), ROMK (K+ secretion apical), AQP2 (ADH-sensitive water channels)
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Alpha (Type A) intercalated cells: H+-ATPase + H+/K+-ATPase apical (secrete H+); AE1 (Cl-/HCO3- exchanger) basolateral (reabsorb new HCO3-)
Active in acidosis
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Beta (Type B) intercalated cells: pendrin (apical HCO3- secretion); H+-ATPase on basolateral side (reabsorb H+)
Active in alkalosis

Hormonal

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ADH (vasopressin): binds V2 receptor on principal cells > cAMP > AQP2 inserted into apical membrane > water reabsorbed
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Aldosterone: upregulates ENaC, ROMK, and Na/K ATPase in principal cells > Na+ retention, K+ secretion

Function

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Final regulation of water balance (ADH), Na+/K+ balance (aldosterone), and acid-base status (intercalated cells)

Anatomy

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Triangular zone at vascular pole where DCT of a nephron contacts the afferent arteriole of its OWN glomerulus
This is a dedicated zoom-in box on your map

Cells

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Macula densa: specialized tall, narrow DCT epithelial cells that sense luminal NaCl via NKCC2
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JG cells (granular/juxtaglomerular cells): modified smooth muscle cells in the afferent arteriole wall containing renin granules
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Extraglomerular mesangial cells (Lacis cells): sit in the triangle between macula densa + afferent + efferent arterioles; relay signals between them

Hormonal

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Renin release triggers: low perfusion pressure (afferent baroreceptor), low NaCl at macula densa, sympathetic stimulation (β1 on JG cells)

Function

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Tubuloglomerular feedback (TGF): local GFR regulation via macula densa > adenosine > afferent constriction
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RAAS initiation: systemic BP regulation via renin release > angiotensin II > aldosterone

Neural

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Sympathetic innervation (T10-L1): renal plexus around renal artery; innervates afferent + efferent arterioles, JG cells (β1 -- renin), PCT/TAL (Na+ reabsorption)
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Parasympathetic (S2-S4, pelvic splanchnic): primarily innervates bladder (detrusor contraction); minimal role in nephron function
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Somatic motor (pudendal nerve): external urethral sphincter voluntary control

Hormonal

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Renin (JG cells) > Angiotensin I > ACE > Angiotensin II > Aldosterone + ADH + thirst + vasoconstriction
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ADH (posterior pituitary): V2 receptor on principal cells > AQP2 insertion > water reabsorption
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ANP/BNP (atrial/ventricular stretch): dilates afferent, constricts efferent; inhibits renin/aldosterone/ADH; opposite of RAAS
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PTH (parathyroid): stimulates Ca2+ reabsorption in DCT; activates 1-alpha-hydroxylase in PCT (calcitriol synthesis); inhibits phosphate reabsorption in PCT
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Erythropoietin (peritubular fibroblasts): released in response to hypoxia; stimulates RBC production in bone marrow

Drawing Reminders: Single page, front side only. Use arrows and brief captions, avoid paragraphs. Color-code your nephron segments, blood vessels, and hormones separately. Include at least one zoom-in box of the filtration membrane and one zoom-in of the JGA. Label the cortex/medulla boundary clearly so segment locations make sense. Optional: add mnemonics or brief clinical correlations (kidney stones, diabetes insipidus, SIADH).

Rubric | 50 pts Total

Anatomical Accuracy

10 pts

Histology + Cell Types

10 pts

Vascular + Tubular Flow

5 pts

Functional Annotations

5 pts

Visual Organization

10 pts

Accuracy + Effort

10 pts

How to use this panel: Each card is a pressure, transporter, or regulatory loop. Check it off as you add it to your map. For each one, your map should show the ON stimulus, the EFFECT, and the OFF signal. A tiny labeled loop is enough, no paragraphs needed.

Chips: ON triggers response EFFECT what it does OFF what stops it LINK draw this

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Net Filtration Pressure (NFP)

ONBlood flow into glomerular capillaries under pressure; afferent arteriole delivers blood at ~55 mmHg (P_GC)

EFFECTNFP = P_GC (55) minus P_BS (15) minus osmotic pull of plasma proteins pi_GC (30) = ~10 mmHg favoring filtration into Bowman's space

OFFLow BP drops P_GC; ureteral obstruction raises P_BS; dehydration raises pi_GC; all three decrease filtration

LINKDraw all three pressure arrows at the glomerulus: P_GC pushing out, P_BS pushing in, pi_GC pulling back. NFP is the net vector.
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Glomerular Filtration Rate (GFR)

ONGFR = Kf (filtration coefficient) times NFP; Kf depends on filtration membrane permeability and surface area

EFFECTNormal GFR ~125 mL/min = ~180 L/day; entire plasma volume filtered ~60 times per day

OFFMesangial cell contraction reduces Kf; glomerular damage reduces surface area; low NFP reduces GFR

LINKClinical: GFR is the best measure of kidney function. Creatinine clearance approximates GFR because creatinine is freely filtered but minimally secreted.

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Myogenic Mechanism

ONIncreased arterial pressure stretches afferent arteriole smooth muscle cells

EFFECTStretch activates Ca2+ channels > smooth muscle contracts > afferent arteriole constricts > resistance rises > GFR held stable

OFFPressure normalizes > stretch decreases > smooth muscle relaxes > afferent dilates back

LINKIntrinsic to the vessel (no nerves or hormones). Works over BP range ~80 to 180 mmHg. Why you can change posture without fainting or shutting down GFR.
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Tubuloglomerular Feedback (TGF)

ONIncreased GFR > increased flow past macula densa > increased NaCl delivery detected by NKCC2

EFFECTMacula densa releases adenosine (and ATP) > afferent arteriole constricts > GFR decreases back to set point

OFFGFR normalizes > NaCl delivery normalizes > adenosine release stops; macula densa can also signal JG cells to release renin when NaCl is LOW

LINKDraw the closed loop: sensor (macula densa) > signal (adenosine) > effector (afferent arteriole). Classic negative feedback.

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Na/K ATPase -- The Primary Pump

ONBasolateral Na/K ATPase on every PCT cell constantly pumps 3 Na+ out, 2 K+ in (uses ATP)

EFFECTCreates a low intracellular Na+ environment, which drives secondary active transport of glucose, amino acids, phosphate, and H+ from the lumen via various cotransporters/antiporters

LINKNearly every reabsorption event in the kidney depends on this one pump. It is why the kidney has such high O2/ATP demand. Draw it on the basolateral side with a star.
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Glucose Reabsorption (SGLT + GLUT)

ONFiltered glucose in PCT lumen; Na+ gradient maintained by Na/K ATPase

EFFECTSGLT2 (early PCT, ~90%) and SGLT1 (late PCT, ~10%) cotransport Na+ and glucose into cell; GLUT2 basolateral releases glucose to blood. Normally 100% reabsorbed.

OFFPlasma glucose greater than 180 to 200 mg/dL exceeds Tm (~375 mg/min) > transporters saturate > glucosuria

LINKDiabetes: glucosuria is diagnostic because transport is saturated. SGLT2 inhibitors (empagliflozin, dapagliflozin) therapeutically block reabsorption to lower blood glucose.
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HCO3- Reabsorption (PCT)

ONFiltered HCO3- arrives in PCT lumen; ~85% of filtered HCO3- reclaimed here

EFFECTPCT secretes H+ (NHE3) > H+ + HCO3- forms H2CO3 > carbonic anhydrase IV splits to CO2 + H2O > CO2 enters cell > reverse reaction > HCO3- exits basolateral via Na-HCO3 cotransporter

OFFAcetazolamide (carbonic anhydrase inhibitor) blocks this > HCO3- lost in urine > metabolic acidosis

LINKImportant: PCT RECOVERS existing HCO3- (no net new bicarb made). Draw H+ cycling in and out while HCO3- moves from lumen to blood.
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Obligatory Water Reabsorption

ONSolute reabsorption creates osmotic gradient across PCT cells

EFFECTWater follows solutes passively via AQP1 and paracellular route; ~65% of filtered water reabsorbed isosmotically (not hormone-regulated)

LINK"Obligatory" = happens regardless of body's water status. "Facultative" = water reabsorption in collecting duct, regulated by ADH. Map both separately.

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Countercurrent Multiplication (Loop of Henle)

ONActive NaCl transport out of TAL (NKCC2) into medullary interstitium, creating a steep osmotic gradient

EFFECTDescending limb is water-permeable (AQP1): water exits > filtrate concentrates. Ascending limb is water-impermeable but NaCl-permeable: NaCl exits > filtrate dilutes. Net result: medullary gradient 300 mOsm (cortex) to 1200 mOsm (papilla).

OFFLoop diuretics (furosemide, bumetanide) block NKCC2 > no gradient > impaired urine concentrating ability

LINKDraw the loop with opposing arrows: water out of descending, NaCl out of ascending. This gradient is what ADH later uses to pull water out of the collecting duct.
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Countercurrent Exchange (Vasa Recta)

ONVasa recta capillaries run parallel to loop of Henle in hairpin loops through the medulla

EFFECTDescending vasa recta: gains solute, loses water. Ascending vasa recta: loses solute, gains water. Net: solutes are recycled in the medulla, gradient is preserved, but O2/nutrients still reach medullary cells.

OFFHigh medullary blood flow (vasodilation) can wash out the gradient, reducing concentrating ability

LINKCritical distinction: loop of Henle CREATES the gradient; vasa recta PRESERVES it. Both are needed. Map them as parallel hairpins with different colors.
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Urea Recycling Amplification

ONInner medullary collecting duct urea transporters (UT-A1/A3) activated by ADH

EFFECTUrea concentrated in inner medullary interstitium; urea then diffuses into thin descending loop and cycles back; contributes ~50% of deep medullary osmolarity at max concentrating state

LINKThis is why low protein diet can reduce urine concentrating ability: less urea available for recycling.

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Renin Release -- JG Cells

ONThree triggers: (1) decreased renal perfusion pressure (afferent arteriole baroreceptor); (2) decreased NaCl at macula densa; (3) sympathetic β1 stimulation of JG cells

EFFECTJG cells release renin into blood; renin cleaves angiotensinogen (liver) to Angiotensin I

OFFRestored BP, restored NaCl at macula densa, decreased sympathetic tone, high Ang II (negative feedback)

LINKRenin is the RATE-LIMITING step of the entire cascade. Three inputs converge on JG cells. Draw all three arrows pointing at the JG cell.
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Angiotensin II -- The Master Effector

ONAngiotensin I passes through pulmonary capillaries > ACE cleaves it to Angiotensin II

EFFECTMultiple coordinated actions: (1) systemic vasoconstriction > raises BP; (2) preferential efferent arteriole constriction > maintains GFR when BP is low; (3) stimulates aldosterone release (zona glomerulosa); (4) stimulates ADH (posterior pituitary); (5) stimulates thirst (hypothalamus); (6) increases PCT Na+ reabsorption

OFFACE inhibitors (lisinopril, enalapril) block conversion; ARBs (losartan, valsartan) block AT1 receptor

LINKDraw Ang II in the center with SIX arrows fanning out to its targets. One hormone, six coordinated effects, all aimed at raising BP and conserving Na+/water.
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Aldosterone -- Principal Cell Action

ONReleased from zona glomerulosa (adrenal cortex) in response to: Ang II, high plasma K+ (direct stimulation), ACTH (minor)

EFFECTEnters principal cells > binds intracellular mineralocorticoid receptor > gene transcription > upregulates ENaC (apical), ROMK (apical), Na/K ATPase (basolateral) > Na+ retention, K+ secretion, water follows Na+

OFFLow Ang II, low plasma K+, ANP directly suppresses aldosterone release; spironolactone blocks the mineralocorticoid receptor

LINKSlow onset (hours), long duration (gene transcription). Clinical: primary hyperaldosteronism = hypertension + hypokalemia. Addison disease = opposite (low aldosterone > hyperkalemia, hyponatremia, low BP).

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ADH Release -- Posterior Pituitary

ONPrimary: plasma osmolarity above ~280 mOsm (hypothalamic osmoreceptors). Secondary: decreased blood volume (atrial/carotid baroreceptors, needs ~10% volume loss). Also Ang II, nausea, pain, stress.

EFFECTADH binds V2 receptor on principal cells > cAMP > AQP2 inserted into apical membrane > water flows DOWN the osmotic gradient from lumen to hyperosmotic interstitium > concentrated urine

OFFLow osmolarity, high blood volume, alcohol (directly inhibits release), caffeine. Leads to AQP2 endocytosis > dilute urine.

LINKOsmoreceptors are exquisitely sensitive (detect 1% change in osmolarity). Baroreceptors are less sensitive but more powerful when activated. Draw both inputs converging on hypothalamus > posterior pituitary.
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Clinical: DI vs SIADH

EFFECTDiabetes insipidus (DI): no ADH (central) or no V2 response (nephrogenic) > dilute, high-volume urine, hypernatremia, intense thirst. SIADH: too much ADH > concentrated, low-volume urine, hyponatremia, water retention.

LINKTest: water deprivation + desmopressin. If urine concentrates with desmopressin = central DI (kidney works, no ADH). If no concentration = nephrogenic DI (ADH present, kidney doesn't respond).

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ANP / BNP -- The Volume Dump Hormone

ONAtrial stretch (ANP from atria) or ventricular stretch (BNP from ventricles) from high blood volume, hypertension, or heart failure

EFFECT(1) Dilates afferent arteriole + constricts efferent > INCREASES GFR and filtration fraction; (2) Inhibits Na+ reabsorption in collecting duct; (3) Suppresses renin, aldosterone, ADH; (4) Systemic vasodilation. Net: natriuresis + diuresis + lower BP.

OFFVolume normalizes > atrial stretch stops > ANP drops

LINKDraw ANP and RAAS as opposing seesaw. High volume > ANP up, RAAS down. Low volume > RAAS up, ANP down. BNP is clinically measured to diagnose heart failure.

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New HCO3- Generation (Alpha Intercalated Cells)

ONAcidemia (low blood pH); low luminal HCO3- arriving at collecting duct

EFFECTAlpha cells secrete H+ via H+-ATPase and H+/K+-ATPase; intracellular CO2 + H2O forms new H2CO3 > new HCO3- generated > exits basolateral via AE1 (Cl-/HCO3- exchanger) to blood. Net: acid excreted, new base added to blood.

OFFAlkalemia > beta intercalated cells take over (pendrin apical secretes HCO3-, H+-ATPase basolateral reabsorbs H+)

LINKKey distinction: PCT RECOVERS old HCO3-; intercalated cells MAKE new HCO3-. This is how kidneys correct chronic acidosis over days to weeks.
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Urinary Buffers

ONSecreted H+ must be buffered to keep urine pH above ~4.5 (limit of H+ gradient); two main buffers: phosphate (HPO4^2-) and ammonia (NH3)

EFFECTTitratable acidity: H+ + HPO4^2- > H2PO4-. Ammonia buffer: PCT generates NH3 from glutamine metabolism > NH3 + H+ > NH4+ (trapped in lumen)

LINKAmmonia is the MAJOR adaptive buffer (can upregulate x10 during chronic acidosis). Each H+ trapped on NH3 = one new HCO3- added to blood.

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K+ Reabsorption Along the Nephron

ONK+ filtered at glomerulus then ~65% reabsorbed PCT (paracellular with water), ~25% TAL (via NKCC2 + ROMK recycling)

EFFECTBy time filtrate reaches DCT, most K+ has already been reabsorbed. Net urinary K+ = principal cell secretion minus any intercalated reabsorption.

LINKThis is why "potassium balance" is really "potassium SECRETION control" in the late DCT and collecting duct.
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K+ Secretion by Principal Cells

ONHigh serum K+ > direct aldosterone release; high Na+ delivery to late DCT; high distal flow; alkalosis

EFFECTPrincipal cells upregulate Na/K ATPase (pumps K+ in basolateral) and ROMK (secretes K+ to lumen apical); ENaC brings Na+ in, creates lumen-negative voltage that pulls K+ out

OFFLow K+ intake, low Na+ delivery (e.g., volume depletion), acidosis (H+ competes with K+ for secretion)

LINKDraw the principal cell: ENaC in apical (Na+ in), ROMK in apical (K+ out), Na/K ATPase basolateral. The electrical coupling is the key: Na+ absorption DRIVES K+ secretion.

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Storage Phase (Sympathetic Dominant)

ONBladder filling below threshold; sympathetic nerves (T11-L2, hypogastric) dominant

EFFECTBeta-3 receptors > detrusor relaxes (accommodates filling); alpha-1 receptors > internal urethral sphincter contracts. Pudendal nerve keeps external sphincter tone up (voluntary).
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Voiding Phase (Parasympathetic Dominant)

ONBladder volume ~300-400 mL > stretch receptors fire > afferents via pelvic splanchnic nerves (S2-S4) > spinal reflex and cortical processing

EFFECTParasympathetic efferents > M3 receptors > detrusor contracts; internal sphincter relaxes (smooth, involuntary). Voluntary relaxation of external sphincter (pudendal nerve releases its hold) allows voiding.

OFFVoluntary override via cortex can inhibit the reflex until appropriate location reached (pontine micturition center coordinates)

LINKInfants lack cortical control (spinal reflex only). Spinal cord injury above S2: reflex bladder (no voluntary control). Below S2 or cauda equina: flaccid bladder (no reflex, overflow incontinence).

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Tubuloglomerular Feedback Loop

MAP ITDraw at the JGA: high GFR > high NaCl at macula densa > adenosine > afferent arteriole constricts > GFR drops back. A tiny circle with + and - arrows around the JGA.
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Full RAAS Cascade Map

MAP ITLow BP > JG cells release renin > angiotensinogen (liver) > Ang I > ACE (lungs) > Ang II > [vasoconstriction + efferent constriction + aldosterone + ADH + thirst + PCT Na+ reabsorption]. Draw as a linear cascade with Ang II fanning out to six targets.
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ADH-Osmolarity Loop

MAP ITHigh plasma osmolarity > hypothalamic osmoreceptors > posterior pituitary > ADH > V2 on principal cells > AQP2 inserted > water reabsorbed > osmolarity drops > ADH stops. A closed circle with the hypothalamus as the sensor and principal cell as the effector.
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ANP-RAAS Opposing Seesaw

MAP ITDraw a balance beam. Left: HIGH volume > ANP up, RAAS suppressed. Right: LOW volume > RAAS up, ANP low. Use "+" and "-" arrows from each hormone to Na+/water retention.
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Acid-Base Compensation Loop

MAP ITAcidemia > alpha intercalated cell H+ secretion up > NH3 buffer up > H+ excretion as NH4+ > NEW HCO3- returned to blood > pH rises. A compact loop drawn at the collecting duct.
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Countercurrent + ADH Integration

MAP ITLoop of Henle creates medullary gradient (300 > 1200 mOsm) > ADH opens AQP2 in collecting duct > water flows down gradient into interstitium > concentrated urine. The loop is the engine; ADH is the switch. Draw both on the same map.
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K+ Secretion Coupling

MAP ITAldosterone > principal cell: ENaC (Na+ in) + ROMK (K+ out) + Na/K ATPase basolateral. Na+ entry creates lumen-negative charge that drives K+ out. Draw the one cell with all three pumps labeled.

Physiology Map Tips: Tiny labeled arrows are enough, no paragraphs needed. A small circle with "+" and "-" communicates a feedback loop perfectly. Use a different ink color for physiology annotations so they stand out from anatomy labels. If you are a BIO 004 anatomy student, this panel is optional context; if you are in A&P or taking BIO 431 next semester, these loops are the scaffolding you will build on.

🔍 Urinary System Lab Identification List

Rubric | 50 pts Total

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