Urinary System Pt. 2 Flashcards

1
Q

What is reabsorption in the kidney?

A

Return of filtered water and solutes to blood. Most occurs in PCT. Essential because filtered volume exceeds plasma volume.

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2
Q

What substances are reabsorbed?

A

Glucose, amino acids, small proteins, ions (Na⁺, K⁺, Ca²⁺, Cl⁻, HCO₃⁻, HPO₄²⁻).

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3
Q

What is secretion in the kidney?

A

Transfer of materials from blood/tubule cells into filtrate. Helps manage pH. Eliminates toxins and foreign substances.

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4
Q

What substances are secreted?

A

H⁺, K⁺, NH₄⁺, creatinine, certain drugs (e.g., penicillin).

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5
Q

Where does most reabsorption occur?

A

Primarily in PCT (Proximal Convoluted Tubule). Continues along nephron loop. Variable amounts in DCT and collecting duct.

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6
Q

Why is reabsorption necessary?

A

Volume entering PCT in 30 minutes > total plasma volume. Must return fluid to maintain blood volume. Preserves essential nutrients and ions.

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7
Q

What are the functions of secretion?

A

pH regulation (H⁺ secretion), elimination of toxins, removal of foreign substances, enables substance testing via urinalysis.

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8
Q

How is secretion useful clinically?

A

Enables urinalysis testing, helps monitor drug levels, indicates kidney function, shows presence of toxins.

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9
Q

What makes reabsorption and secretion different?

A

Reabsorption: movement from tubule to blood. Secretion: movement from blood to tubule. Different substances involved, different purposes.

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10
Q

What are the two main routes for reabsorption?

A

Paracellular (between cells)
Transcellular (through cells)

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11
Q

What is paracellular reabsorption?

A

• Passive fluid leakage between cells • Through leaky tight junctions • Accounts for ~50% of ion reabsorption • No energy required

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12
Q

What substances typically use the paracellular route?

A

• Water • Some ions (Na⁺, Ca²⁺) • Small molecules that can fit through tight junctions

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13
Q

What is transcellular reabsorption?

A

• Movement directly through tubule cells • Three steps:

Enter through apical membrane
Cross cytosol
Exit through basolateral membrane

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14
Q

Compare energy requirements of both routes:

A

• Paracellular: Passive (no energy needed) • Transcellular: Often requires energy (active transport)

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15
Q

What are tight junctions?

A

• Connections between adjacent cells • Can be ‘leaky’ (PCT) or ‘tight’ (later segments) • Control paracellular transport • Act like seals between cells

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16
Q

Why do kidneys use two routes for reabsorption?

A

• Increased efficiency • Energy conservation • Better control • Backup system if one route fails

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17
Q

What are the key components of transcellular transport?

A

• Apical membrane (faces urine) • Cell cytosol • Basolateral membrane (faces blood) • Specific transporters on each membrane

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18
Q

What determines if tight junctions are ‘leaky’ or ‘tight’?

A

• Location in nephron • PCT has leaky junctions • Later segments have tight junctions • Affects amount of paracellular transport

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19
Q

How does the PCT differ from later segments in terms of reabsorption?

A

• PCT has leakier tight junctions • More paracellular transport possible • Higher overall reabsorption rate • Less selective reabsorption

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20
Q

What is the key difference between paracellular and transcellular reabsorption?

A

• Paracellular: Movement between cells
• Transcellular: Movement through cells

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21
Q

List characteristics of paracellular reabsorption:

A

• Occurs between cells
• Uses leaky tight junctions
• Passive process (no energy needed)
• Accounts for ~50% of ion reabsorption

Like water seeping between bricks

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22
Q

List characteristics of transcellular reabsorption:

A

• Through cells (3 steps)

Enter through apical membrane
Cross cytosol
Exit through basolateral membrane
• Often requires energy
• Highly selective

Like going through security

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23
Q

What substances typically use paracellular transport?

A

• Water
• Na⁺ ions
• Ca²⁺ ions
• Other small ions

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24
Q

What substances typically use transcellular transport?

A

• Glucose
• Amino acids
• Proteins
• Specific ions requiring transporters

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25
Q

Compare advantages of both routes:

A

Paracellular:
• Energy efficient
• Rapid
• High capacity

Transcellular:
• Precise control
• Selective transport
• Can concentrate substances

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26
Q

What role do tight junctions play?

A

• Connect adjacent cells
• Control paracellular movement
• “Leaky” in PCT
• Act as barriers between cells

Like cement between bricks

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27
Q

What are clinical concerns with these pathways?

A

• Tight junction problems can cause:

Excess fluid loss
Electrolyte imbalances
• Can be affected by medications
• Important for drug transport

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28
Q

What drives paracellular transport?

A

• Concentration gradients
• Osmotic pressure
• No energy required
• Natural movement from high to low concentration

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29
Q

What drives transcellular transport?

A

• Active transport mechanisms
• ATP energy
• Specific transporters
• Can move against concentration gradients

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30
Q

What is the main function of sodium-potassium pumps in renal tubules?

A

• Move Na⁺ out of tubule cells into interstitial fluid
• Create and maintain low intracellular Na⁺ levels
• Enable continued Na⁺ reabsorption from filtrate

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31
Q

Why is it important to maintain low Na⁺ levels inside tubule cells?

A

• Creates concentration gradient
• Drives Na⁺ reabsorption from tubular fluid
• Enables continuous movement of Na⁺ into cells
• Maintains reabsorption efficiency

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32
Q

How do sodium-potassium pumps work?

A

• Use ATP energy (active transport)
• Move Na⁺ against concentration gradient
• Transport Na⁺ from lower to higher concentration
• Located in basolateral membrane

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33
Q

What drives Na⁺ entry through the apical membrane?

A

• Low intracellular Na⁺ concentration
• Concentration gradient from lumen to cell
• Maintained by Na⁺/K⁺ pump activity
• Passive movement down concentration gradient

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34
Q

What is the sequence of Na⁺ reabsorption via transcellular route?

A

Na⁺ enters cell through apical membrane
Crosses cytosol
Pumped out through basolateral membrane
Enters interstitial fluid
Absorbed into peritubular capillary

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35
Q

What is the overall importance of this mechanism?

A

• Regulates fluid balance
• Controls blood pressure
• Maintains electrolyte levels
• Ensures efficient Na⁺ reabsorption

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36
Q

How does this process relate to homeostasis?

A

• Helps maintain blood volume
• Regulates blood pressure
• Controls Na⁺ balance
• Supports fluid/electrolyte balance

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37
Q

Where are Na⁺/K⁺ pumps located in renal cells?

A

• Basolateral membrane
• Side facing interstitial fluid
• Away from tubule lumen
• Near peritubular capillaries

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38
Q

What happens if Na⁺/K⁺ pumps malfunction?

A

• Reduced Na⁺ reabsorption
• Disrupted concentration gradients
• Impaired kidney function
• Potential fluid/electrolyte imbalances

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39
Q

What are the two main types of active transport?

A

Primary active transport (uses ATP directly)
Secondary active transport (uses ion gradients)

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40
Q

What is primary active transport?

A

• Directly uses ATP energy • Moves substances against concentration gradients

Example: Na⁺/K⁺ pumps • Uses 6% of body’s ATP at rest

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41
Q

What is secondary active transport?

A

• Uses ion gradients created by primary transport • No direct ATP use

Couples movement of multiple substances • Uses energy stored in electrochemical gradients

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42
Q

What is a symporter?

A

• Type of secondary active transport • Moves multiple substances in same direction

Example: Na⁺-glucose co-transport • Also called co-transporter

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43
Q

What is an antiporter?

A

• Type of secondary active transport • Moves substances in opposite directions

Example: Na⁺-H⁺ exchange • Also called exchanger

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44
Q

Why are transport proteins one-directional?

A

• Ensures controlled movement of substances • Prevents backward flow

Maintains concentration gradients • Increases transport efficiency

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45
Q

How does coupling work in secondary transport?

A

• Links movement of two substances • One substance moves down gradient

Energy released moves second substance • Saves ATP by using existing gradients

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46
Q

Where are different transport proteins located?

A

• Different proteins in different membrane regions • Specific to apical or basolateral membrane

Location determines transport direction • Arranged for efficient reabsorption/secretion

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47
Q

Why is the Na⁺/K⁺ pump important?

A

• Creates Na⁺ gradient for secondary transport • Maintains cell volume

Essential for reabsorption • Uses significant ATP (6% of body’s total)

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48
Q

What drives water reabsorption in kidneys?

A

• Solute reabsorption
• Osmosis
• Movement from low to high solute concentration
• Follows solute movement

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49
Q

Define osmosis in kidney function:

A

• Movement of water from:
Low solute concentration areas
To high solute concentration areas
• Passive process
• Follows concentration gradients

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50
Q

What is obligatory water reabsorption?

A

• 90% of water reabsorption
• Automatically follows solute movement
• Occurs in PCT and descending limb
• Not regulated by hormones

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51
Q

What is facultative water reabsorption?

A

• 10% of water reabsorption
• Regulated by ADH
• Occurs mainly in collecting duct
• Adaptable to body’s needs

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52
Q

Compare obligatory vs facultative reabsorption:

A

Obligatory:
• Automatic
• 90% of total
• PCT and descending limb
• No hormone control

Facultative:
• Controlled
• 10% of total
• Collecting duct
• ADH regulated

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53
Q

Where does water reabsorption occur?

A

Obligatory:
• PCT
• Descending limb of loop

Facultative:
• Collecting duct

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54
Q

How does ADH affect water reabsorption?

A

• Controls facultative reabsorption
• Increases collecting duct permeability
• Allows more water reabsorption
• Responds to body’s hydration needs

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55
Q

Why is water reabsorption important?

A

• Maintains fluid balance
• Prevents dehydration
• Conserves water
• Supports homeostasis

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56
Q

What happens if water reabsorption fails?

A

• Dehydration risk
• Fluid imbalance
• Electrolyte disorders
• Increased urine output

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57
Q

What determines how much water is reabsorbed?

A

• Amount of solute reabsorption
• ADH levels
• Osmotic gradients
• Body’s hydration status

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58
Q

Where are essential substances reabsorbed in the nephron?

A

• First half of PCT
• Via Na⁺-transporters (symporters)
• Complete reabsorption

Examples: glucose, amino acids, vitamins

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59
Q

What is a symporter?

A

• Transport protein that moves multiple substances
• Moves substances in same direction
• Uses Na⁺ gradient as energy source

Example: Na⁺-glucose symporter

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60
Q

How does the Na⁺-glucose symporter work?

A

Na⁺ and glucose bind to symporter
Na⁺ gradient pulls both molecules into cell
Glucose exits via facilitated diffusion
Enters peritubular capillaries

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61
Q

What creates the Na⁺ gradient for symporters?

A

• Na⁺/K⁺ pumps (active transport)
• Uses ATP energy
• Pumps Na⁺ out of cell
• Creates low intracellular Na⁺

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62
Q

What substances use symporters?

A

• Glucose
• Amino acids
• Phosphate ions
• Sulfate ions
• Lactate
• Water-soluble vitamins

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63
Q

Why is symporter transport important?

A

• Prevents loss of essential nutrients
• Energy efficient
• Selective transport
• Maintains homeostasis

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64
Q

How does glucose exit PCT cells?

A

• Via facilitated diffusion
• Through specific transporters
• Through basolateral membrane
• Into peritubular capillaries

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65
Q

Why use Na⁺ for co-transport?

A

• Strong concentration gradient exists
• Gradient maintained by active transport
• Provides energy for transport
• No additional ATP needed

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66
Q

Where are symporters located?

A

• Apical membrane
• Faces tubular fluid
• First half of PCT
• Luminal side of cells

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67
Q

What happens if symporters malfunction?

A

• Loss of essential nutrients
• Increased urinary excretion
• Potential deficiencies
• Metabolic imbalances

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68
Q

What is an Na⁺-H⁺ antiporter?

A

• Transport protein moving Na⁺ and H⁺
• Moves ions in opposite directions
• Na⁺ enters cell
• H⁺ secreted into tubule

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69
Q

What drives the Na⁺-H⁺ antiporter?

A

• Na⁺ concentration gradient
• Created by Na⁺/K⁺ pump
• Secondary active transport
• No direct ATP use

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70
Q

How is H⁺ generated for the antiporter?

A

• CO₂ + H₂O → H₂CO₃
• Carbonic anhydrase catalyzes
• H₂CO₃ → H⁺ + HCO₃⁻
• CO₂ from blood/metabolism

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71
Q

What are the outcomes of antiporter function?

A

• Na⁺ reabsorption
• H⁺ secretion
• HCO₃⁻ reabsorption
• pH regulation

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72
Q

Why is this process important?

A

• Maintains acid-base balance
• Regulates blood pH
• Conserves bicarbonate
• Controls sodium levels

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73
Q

Where does CO₂ come from?

A

• Peritubular capillaries
• Tubular fluid
• Cell metabolism
• Diffuses freely across membranes

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74
Q

What role does carbonic anhydrase play?

A

• Catalyzes CO₂ + H₂O reaction
• Forms carbonic acid
• Speeds up H⁺ production
• Essential for antiporter function

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75
Q

What happens to HCO₃⁻?

A

• Reabsorbed into blood
• Exits via basolateral membrane
• Maintains blood buffering
• One HCO₃⁻ saved per H⁺ secreted

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76
Q

What maintains the Na⁺ gradient?

A

• Na⁺/K⁺ pump
• Uses ATP
• Located on basolateral membrane
• Keeps intracellular Na⁺ low

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77
Q

What drives passive reabsorption in late PCT?

A

• Solute reabsorption
• Osmotic gradients
• Electrochemical gradients
• Water following solutes

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78
Q

What is Aquaporin-1?

A

• Water channel protein
• Located in PCT cells
• Enables rapid water movement
• Present in descending limb

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79
Q

Which solutes are reabsorbed passively?

A

• Chloride (Cl⁻)
• Potassium (K⁺)
• Calcium (Ca²⁺)
• Magnesium (Mg²⁺)
• Urea

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80
Q

How does Cl⁻ reabsorption affect other ions?

A

• Creates negative charge
• Attracts positive ions
• Promotes cation reabsorption
• Uses paracellular pathway

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81
Q

What happens when water is reabsorbed?

A

• Increases solute concentration
• Creates new gradients
• Promotes more reabsorption
• Maintains homeostasis

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82
Q

What are the pathways for solute reabsorption?

A
  • Paracellular (between cells)
  • Transcellular (through cells)
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83
Q

What creates the osmotic gradient?

A

• Initial solute reabsorption
• Concentration differences
• Movement into interstitial fluid
• Differential membrane permeability

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84
Q

Where does reabsorbed water go?

A

• Leaves tubular fluid
• Enters interstitial fluid
• Enters peritubular capillaries
• Returns to bloodstream

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85
Q

What role do electrochemical gradients play?

A

• Drive ion movement
• Create charge differences
• Promote passive transport
• Aid solute reabsorption

86
Q

What is the osmolarity of fluid entering the nephron loop?

A

Similar to blood osmolarity
• Due to PCT osmosis
• Balanced solute/water reabsorption
• Isotonic to blood

87
Q

What happens in the descending limb?

A

Water permeable
• Some water reabsorption
• Driven by osmosis
• Fluid becomes concentrated

88
Q

Describe the ascending limb characteristics:

A

Impermeable to water
• Active solute reabsorption
• Little obligatory water movement
• Fluid becomes dilute

89
Q

What happens to tubular fluid osmolarity in ascending limb?

A

Progressively decreases
• Due to solute reabsorption
• No water follows
• Becomes hypotonic

90
Q

Compare descending vs ascending limb:

A

Descending:
• Water permeable
• Concentrates fluid

Ascending:
• Water impermeable
• Dilutes fluid

91
Q

What ions are reabsorbed in ascending limb?

A

Sodium (Na⁺)
• Chloride (Cl⁻)
• Potassium (K⁺)
• Calcium (Ca²⁺)
• Magnesium (Mg²⁺)

92
Q

Why is little obligatory water reabsorption important?

A

Allows flexible water handling
• Enables concentration/dilution
• Supports homeostasis
• Adapts to body needs

93
Q

What creates osmotic gradients in nephron loop?

A

Active solute transport, Selective water permeability, Ion reabsorption, Concentration differences

94
Q

What is the overall function of the nephron loop?

A
  • Regulates fluid volume
  • Controls osmolarity
  • Prepares for further adjustment
  • Maintains homeostasis
95
Q

What is a Na⁺-K⁺-2Cl⁻ symporter?

A

• Transport protein • Moves 1 Na⁺, 1 K⁺, 2 Cl⁻ • Located in ascending limb • Moves ions from filtrate to cells

96
Q

How is Na⁺ handled after entering the cell?

A

• Actively pumped out • Via Na⁺/K⁺ ATPase • Into interstitial fluid • Then into vasa recta

97
Q

What happens to K⁺ after transport?

A

• Leaks back to lumen • Through K⁺ channels • Maintains gradient • Supports continued transport

98
Q

How does Cl⁻ exit the cell?

A

• Through Cl⁻ channels • On basolateral side • Into interstitial fluid • Maintains ion balance

99
Q

What drives the symporter?

A

• Na⁺ gradient • Created by Na⁺/K⁺ pump • Secondary active transport • Electrochemical gradient

100
Q

How does Cl - moving into interstitial fluid VIA leaky channels affect other cations?

A
  • Creates positive charge in lumen * Promotes paracellular transport * Affects Ca²⁺ and Mg²⁺ * Enables passive reabsorption
101
Q

Where are these symporters located?

A

• Thick ascending limb • Apical membrane • Facing tubular lumen • Multiple per cell

102
Q

What’s the overall effect on tubular fluid in the ascending limb?

A
  • Becomes more dilute * Solutes removed * No water follows * Osmolarity decreases
103
Q

Why is K⁺ recycling important?

A

• Maintains gradient • Supports continued transport • Creates positive charge • Enables cation movement

104
Q

What percentage of filtered water is reabsorbed before DCT?

A

• 80% already reabsorbed
• Additional 10-15% in early DCT
• Total ~90-95%
• Reduced flow rate

105
Q

What ions are reabsorbed in early DCT?

A

• Sodium (Na⁺)
• Chloride (Cl⁻)
• Calcium (Ca²⁺)
• ~5% of filtered Na⁺/Cl⁻

106
Q

How do Na⁺-Cl⁻ symporters work?

A

• Located on apical membrane
• Move Na⁺ and Cl⁻ together
• Into tubule cells
• From tubular fluid

107
Q

What’s on the basolateral membrane?

A

• Na⁺-K⁺ pumps
• Cl⁻ leakage channels
• Move ions to blood
• Via peritubular capillaries

108
Q

What’s PTH’s role in the DCT?

A

• Stimulates Ca²⁺ reabsorption
• Inhibits PO₄³⁻ reabsorption
• Regulates Ca²⁺ balance
• Affects PCT phosphate handling

109
Q

What enters the early DCT?

A

• Partially processed filtrate
• ~25 mL/min flow rate
• More concentrated fluid
• 20% of original water

110
Q

What are the key functions of early DCT?

A

• Fine-tunes ion balance
• Regulates water reabsorption
• Controls Ca²⁺ levels
• Responds to hormones

111
Q

How does PTH affect phosphate?

A

• Inhibits reabsorption in PCT
• Increases excretion
• Balances with calcium
• Maintains mineral homeostasis

112
Q

What happens to reabsorbed ions?

A

• Enter tubule cells
• Pass through basolateral membrane
• Enter peritubular capillaries
• Return to bloodstream

113
Q

Why is early DCT important?

A

• Further refines filtrate
• Hormone-responsive
• Fine-tunes electrolytes
• Prepares for final processing

114
Q

What percentage of filtrate is processed before late DCT?

A

• 90-95% of water reabsorbed
• 90-95% of solutes reabsorbed
• Only 5-10% remains
• Final adjustments occur here

115
Q

What are the two main cell types?

A

Principal Cells:
• Na⁺/K⁺ regulation
• Hormone responsive
Intercalated Cells:
• pH regulation
• K⁺/HCO₃⁻ handling

116
Q

What do principal cells do?

A

• Reabsorb Na⁺
• Secrete K⁺
• Respond to aldosterone
• Respond to ADH
• Have aquaporin-2

117
Q

What do intercalated cells do?

A

• Reabsorb K⁺
• Reabsorb HCO₃⁻
• Secrete H⁺
• Regulate pH
• Help maintain acid-base balance

118
Q

How is Na⁺ reabsorbed?

A

Enters through leakage channels
Pumped out by Na⁺-K⁺ pumps
Moves to interstitial fluid
Enters peritubular capillaries

119
Q

How is K⁺ secreted?

A

• Enters cells via Na⁺-K⁺ pumps
• Exits through leakage channels
• Amount varies with needs
• Present in both membranes

120
Q

What hormones affect these processes?

A

Aldosterone:
• ↑ Na⁺ reabsorption
• ↑ K⁺ secretion
ADH:
• ↑ water reabsorption
• Controls aquaporin-2

121
Q

What are aquaporin-2 proteins?

A

• Water channels
• ADH controlled
• In principal cells
• Enable water reabsorption

122
Q

What determines water reabsorption?

A

• ADH levels
• Aquaporin-2 presence
• Osmotic gradients
• Body’s hydration needs

123
Q

What triggers RAAS activation?

A

• Decreased blood pressure
• Decreased blood volume
• Less stretch of afferent arterioles
• Juxtaglomerular cells release renin

124
Q

What’s the sequence of RAAS activation?

A

Renin release
Angiotensin I formation
ACE converts to angiotensin II
Effects begin

125
Q

What does angiotensin II do to GFR?

A
  • Causes vasoconstriction of afferent arterioles
  • Decreases filtration
  • Conserves water/solutes
126
Q

How does RAAS affect sodium handling?

A

• Stimulates Na⁺-H⁺ antiporters
• Enhances Na⁺ reabsorption
• Increases water reabsorption
• In PCT

127
Q

What’s aldosterone’s role in RAAS?

A

• Released by adrenal cortex
• Increases Na⁺ reabsorption
• Increases K⁺ secretion
• Promotes water retention

128
Q

What organs are involved in RAAS?

A

• Kidneys (renin)
• Lungs (ACE)
• Adrenal cortex (aldosterone)
• Blood vessels

129
Q

What’s the main purpose of RAAS?

A

• Maintain blood pressure
• Regulate blood volume
• Control fluid balance
• Adjust kidney function

130
Q

What hormones are part of RAAS?

A

• Renin (enzyme)
• Angiotensin I
• Angiotensin II
• Aldosterone

131
Q

What’s the end result of RAAS?

A

• Increased blood pressure
• Increased blood volume
• Restored fluid balance
• Normalized kidney function

132
Q

Where is ADH released from?

A

• Posterior pituitary gland
• Also called vasopressin
• Released in response to dehydration
• Controls water balance

133
Q

What’s facultative water reabsorption?

A
  • Optional water reabsorption
  • Controlled by ADH
  • Occurs in late DCT, and collecting duct
134
Q

How does ADH affect water permeability?

A

• Increases water permeability
• In principal cells
• Via aquaporin-2 insertion
• In apical membrane

135
Q

What triggers ADH release?

A

• Increased plasma osmolarity
• Decreased blood volume
• Dehydration
• Low blood pressure

136
Q

How does the negative feedback work?

A

High osmolarity detected
ADH released
Water reabsorbed
Osmolarity normalized
ADH release decreases

137
Q

What are aquaporin-2 proteins?

A

• Water channels
• Inserted into membrane
• Allow water passage
• ADH controlled

138
Q

What happens without ADH?

A

• Low water permeability
• High urine output
• Dilute urine
• Risk of dehydration

139
Q

What’s Diabetes Insipidus?

A

• ADH deficiency/resistance
• Extreme water loss
• Up to 20L urine daily
• Severe dehydration risk

140
Q

Where does ADH act?

A

• Late DCT
• Collecting duct
• Principal cells
• Apical membrane

141
Q

What’s the end result of ADH action?

A

• Increased water reabsorption
• Concentrated urine
• Restored blood volume
• Normalized osmolarity

142
Q

How does high fluid intake affect urine?

A

• Higher urine volume
• More dilute urine
• Less water reabsorption
• Maintains balance

143
Q

How does low fluid intake affect urine?

A

• Lower urine volume
• More concentrated urine
• More water reabsorption
• Conserves water

144
Q

What’s the starting osmolarity?

A

• Blood: 300 mOsm/L
• Filtrate: 300 mOsm/L
• Initially isotonic
• Changes in tubules

145
Q

How does osmolarity change in descending limb?

A

• Increases
• Water reabsorbed
• Due to medulla gradient
• Becomes concentrated

146
Q

How does osmolarity change in ascending limb?

A

• Decreases
• Solutes removed
• Water impermeable
• Becomes dilute

147
Q

How does ADH affect urine concentration?

A

High ADH:
• More water reabsorbed
• Concentrated urine
Low ADH:
• Less water reabsorbed
• Dilute urine

148
Q

What happens in the descending limb?

A

• Medulla has high osmolarity
• Water leaves by osmosis
• Fluid becomes concentrated
• Osmolarity increases

149
Q

What happens in thick ascending limb?

A

• Na⁺, K⁺, Cl⁻ actively reabsorbed
• Water can’t follow (impermeable)
• Solutes leave, water stays
• Osmolarity decreases

150
Q

What happens without ADH?

A

• Low water permeability
• Less water reabsorbed
• More dilute urine
• Larger urine volume

151
Q

How does osmolarity change in descending limb?

A

• Starts at ~300 mOsm/L
• Increases to ~1200 mOsm/L
• Due to water loss
• Into medulla

152
Q

How does osmolarity change in ascending limb?

A

• Starts at ~1200 mOsm/L
• Decreases to ~100 mOsm/L
• Due to solute loss
• Water retained

153
Q

What’s the final urine osmolarity?

A

• 65-70 mOsm/L
• Very dilute
• Large volume
• Low solute concentration

154
Q

What are symporters in ascending limb?

A

• Transport Na⁺
• Transport K⁺
• Transport Cl⁻
• Active reabsorption

155
Q

Why is ascending limb water-impermeable?

A

• Prevents water following solutes
• Helps dilute filtrate
• Essential for concentration gradient
• Creates dilute urine

156
Q

What’s the role of the medulla?

A

• Creates concentration gradient
• Draws water from descending limb
• Receives solutes from ascending limb
• Key for urine concentration

157
Q

What’s the end result?

A

• More solutes reabsorbed
• Less water reabsorbed
• Large urine volume
• Low osmolarity

158
Q

What makes concentrated urine possible?

A

• Osmotic gradient in medulla
• Juxtamedullary nephrons
• Countercurrent multiplier
• ADH action

159
Q

What creates the osmotic gradient?

A

Different permeability in nephron sections
Countercurrent flow
Solute pumping from ascending limb
Water retention in tubules

160
Q

What’s the osmolarity range in kidney?

A

• Cortex: ~300 mOsm/L
• Deep medulla: ~1200 mOsm/L
• Creates concentration gradient
• Drives water reabsorption

161
Q

What happens in descending limb?

A

• Water leaves by osmosis
• Into hypertonic medulla
• Fluid becomes concentrated
• Follows osmotic gradient

162
Q

What happens in ascending limb?

A

• Na⁺-K⁺-2Cl⁻ symporters active
• Pumps solutes out
• Water stays in tubule
• Creates dilute fluid

163
Q

How does urea contribute?

A

• Reabsorbed from collecting duct
• Recycled into medulla
• Increases osmotic gradient
• Requires ADH presence

164
Q

What’s the vasa recta’s role?

A

• Maintains osmotic gradient
• Countercurrent exchange
• Prevents solute washout
• Matches nephron flow

165
Q

What’s the maximum urine concentration?

A

• Up to 1200 mOsm/L
• 4x plasma concentration
• Requires ADH
• Needs medulla gradient

166
Q

What’s countercurrent multiplication?

A

• Opposite flow directions
• Amplifies osmotic gradient
• Occurs in nephron loop
• Essential for concentration

167
Q

What happens when ADH is present?

A

• Collecting ducts become water-permeable
• Tubular fluid concentrates
• Urea moves into medulla
• Increases medullary osmolarity

168
Q

What is countercurrent flow?

A

• Fluids moving in opposite directions
• In parallel tubes

Examples: Descending/ascending limbs, Vasa recta blood flow

169
Q

How do juxtamedullary nephrons help?

A

• Have long loops
• Act as countercurrent multiplier
• Create osmotic gradient
• Allow concentrated urine

170
Q

How does urea contribute?

A

• Moves with water into medulla
• Increases medullary osmolarity
• Gets recycled
• Maintains gradient

171
Q

What happens in ascending limb?

A

• Fluid flows up
• Solutes actively removed
• Water stays in tubule
• Dilutes tubular fluid

172
Q

Why is the gradient important?

A

• Enables water reabsorption
• Allows urine concentration
• Responds to ADH
• Conserves water

173
Q

What’s the purpose of vasa recta?

A

• Maintains osmotic gradient
• Prevents solute washout
• Matches nephron flow
• Enables concentration

174
Q

What’s the end result?

A

• Concentrated urine formed
• Water conserved
• Wastes eliminated
• Homeostasis maintained

175
Q

What’s exchanged in vasa recta?

A

• Solutes (Na⁺, Cl⁻, urea) • Water • Oxygen • Nutrients

176
Q

Why is vasa recta structure important?

A

• Forms loops like nephron • Allows countercurrent flow • Matches medulla gradient • Preserves concentration

177
Q

What happens in descending vasa recta?

A

• Solutes enter blood • Water leaves blood • Blood osmolarity increases • Follows medulla gradient

178
Q

What happens in ascending vasa recta?

A

• Solutes leave blood • Water enters blood • Blood osmolarity decreases • Preserves gradient

179
Q

Why is countercurrent exchange needed?

A

• Preserves medulla gradient • Supplies oxygen/nutrients • Prevents solute washout • Supports concentration

180
Q

How does blood osmolarity change?

A

• Enters ~300 mOsm/L • Changes with depth • Returns near starting level • Minimal net change

181
Q

What’s supplied to loop cells?

A
  • Nutrients snd Oxygen
  • From blood supply; Via vasa recta
182
Q

How does this differ from multiplication?

A

• Passive vs active transport • Preserves vs creates gradient • In vasa recta vs nephron loop • Maintains vs builds concentration

183
Q

What’s the end result?

A

• Gradient maintained • Tissues nourished • Concentration preserved • Efficient kidney function

184
Q

What is urinalysis?

A

• Examination of urine properties
• Checks physical/chemical aspects
• Shows metabolism state
• Reveals kidney function

185
Q

What’s normal urine composition?

A

• 95% water
• 5% solutes
• Volume: 1-2 L/day
• Contains waste products

186
Q

What do blood tests measure?

A

• Blood Urea Nitrogen (BUN)
• Plasma creatinine
• Waste product clearance
• Kidney function

187
Q

What’s renal plasma clearance?

A

• Kidney efficiency measure
• Rate of substance removal
• Expressed in mL/min
• Shows filtration ability

188
Q

What are ureter functions?

A

• Transport urine
• Use peristalsis
• Use gravity
• Use hydrostatic pressure

189
Q

How is backflow prevented?

A

• Physiological valve
• Bladder pressure
• Compresses ureter openings
• When bladder full

190
Q

Describe bladder function

A

• Stores urine
• 700-800 mL capacity
• Distensible organ
• Collapses when empty

191
Q

What’s creatinine significance?

A

• From muscle metabolism
• Normal: ~1.5 mg/dL
• Higher = poor function
• Kidney efficiency marker

192
Q

Why check glucose clearance?

A

• Usually zero
• Complete reabsorption
• Abnormal = problem
• Diagnostic tool

193
Q

What is micturition?

A

Discharge of urine
Also called urination
Involves muscle contractions
Both voluntary & involuntary

194
Q

How does micturition control develop?

A

Starts with stretch receptors
Triggers spinal reflex
Control learned in childhood
Involves voluntary muscles

195
Q

What’s the urethra’s role?

A

Carries urine out of body
From internal orifice
To body exterior
Final pathway for urine

196
Q

What is stress incontinence?

A

Weak pelvic floor muscles
Leakage with physical stress
Due to abdominal pressure
During coughing/sneezing

197
Q

What is urge incontinence?

A

Common in older adults
Sudden urge to urinate
Followed by involuntary loss
Unexpected discharge

198
Q

What is overflow incontinence?

A

Due to blockage
Or weak muscle contractions
Affects bladder musculature
Causes incomplete emptying

199
Q

What is functional incontinence?

A

Can’t reach toilet in time
Physical mobility issues
Environmental barriers
Time constraints

200
Q

What causes incontinence?

A

Various muscle weaknesses
Nerve problems
Physical barriers
Age-related changes

201
Q

How are muscles involved in micturition?

A

Voluntary sphincters
Involuntary muscles
Pelvic floor muscles
Bladder muscles

202
Q

What triggers urination?

A

Stretch receptors
Bladder fullness
Spinal reflex
Voluntary control

203
Q

What are kidney stones?

A

• Mineral deposits in kidneys • Caused by concentrated urine • Symptoms: severe pain, blood • Treatment: fluids, lithotripsy

204
Q

What causes UTIs?

A

• Bacterial infection • Poor hygiene • Short urethra (females) • Weak immune system

205
Q

What is glomerular disease?

A

• Affects kidney filters • Types: glomerulonephritis, nephrotic • Shows protein/blood in urine • Causes swelling

206
Q

Describe renal failure types

A

• Acute: sudden, reversible • Chronic: gradual, permanent • Causes: hypertension, diabetes • Needs dialysis/transplant

207
Q

What is polycystic disease?

A

• Genetic disorder • Fluid-filled cysts form • Causes high blood pressure • Can lead to kidney failure

208
Q

Signs of bladder cancer?

A

• Blood in urine • Frequent urination • Painful urination • Risk factor: smoking

209
Q

What is dialysis?

A

• Blood filtering treatment • Types: Hemodialysis (machine), Peritoneal (abdominal) • For kidney failure

210
Q

Renal failure symptoms?

A

• Fatigue • Swelling • Decreased urine • Waste buildup