Renal 2 Flashcards
(27 cards)
What are the main stages of urine formation?
- Glomerular Filtration: Occurs in the glomerulus.
- Tubular Reabsorption: In the proximal tubule, loop of Henle, distal tubule, and collecting duct.
- Tubular Secretion: In proximal and distal tubules.
What is the normal urine osmolarity?
24-hour urine: 500-800 mOsm/kg
Random: 300-900 mOsm/kg
After 12-14 hrs restriction: >850 mOsm/kg
What is urine specific gravity assessment
Urine specific gravity is another assessment method:
Normal specific gravity: 1.005-1.030
Dehydration specific gravity: ≥ 1.035
Specific gravity > 1.015 indicates hypovolemia
What are the 3 main mechanisms that contribute to urine formation and concentration
Countercurrent Multiplier: Involves the interaction between the descending and ascending limbs of the loop of Henle.
Urea Recycling: Urea helps maintain the medullary interstitium.
Hormonal Effects (ADH): Antidiuretic hormone (ADH) regulates water reabsorption.
What is the effect of ADH on urine concentration?
ADH increases water reabsorption in the collecting ducts by inserting aquaporins, making urine more concentrated (~1200 mOsm).
What happens to ADH secretion during dehydration?
It increases ADH release from posterior pituitary leading to water reabsorption and concentrated urine.
What happens to ADH secretion during Overhydration
Overhydration leads to decreased ADH from the posterior pituitary, resulting in hypoosmotic urine (~100 mOsm).
What is ADH’s effect on the collecting duct
Osmoreceptors in the hypothalamus detect increased blood osmotic pressure, triggering ADH release from pituitary gland.
ADH binds to V2R receptor on basolateral side. This receptor activates Adenyl cyclase which increases cAMP which activates pkA which translocates more aquaporins to the apical membrane. Increases water permeability in the collecting ducts by promoting aquaporin insertion.
Plasma half-life of ADH is 10-15 minutes, removed by the liver and kidneys.
What is the countercurrent multiplier and how does it work?
The ascending limb pumps out Na⁺ to keep a 200 mOsm difference with the interstitial fluid (e.g., interstitial fluid becomes 400 mOsm). The descending limb then loses water to match the interstitial fluid’s osmolarity. This cycle repeats deeper into the medulla, progressively concentrating the interstitial fluid and producing urine with less water
What is the role of urea recycling in urine concentration?
Urea is reabsorbed through the loop of Henle and concentrated in the collecting duct.
Urea transporters facilitate the reabsorption of urea, which drags water by osmosis.
This reduces water secretion.
What is the micturition reflex initiated by and when does it become voluntary
Integrated in the spinal cord in infants and in the brainstem in adults.
Becomes voluntary at ages 2-3 years.
Which CNS areas control micturition?
- Sacral micturition center: Bladder and sphincter coordination.
- Pontine micturition center: Storage/voiding mode.
- Cerebral cortex: Conscious control.
What are key words in micturition
Dysuria: Painful urination.
Urges: Strong, sudden need to urinate.
Pollakisuria: Increased frequency of urination.
What happens in microturition when the bladder is empty
Aδ and C sensory fibres in the bladder wall are quiet — they send signals to the brain:
👉 “Bladder is empty. It’s okay to store urine.”
Brain & Brainstem response:
Release acetylcholine (ACh)
ACh binds to nicotinic receptors → causes norepinephrine (NA) release
What NA does:
Binds to β3 receptors on bladder muscle → relaxes the detrusor muscle so bladder can expand
Binds to α1 receptors on internal sphincter → constricts the sphincter to keep urine in
Voluntary control:
You can hold your pee using external sphincter
Controlled by spinal cord → releases ACh, which binds to M3 receptors on the external sphincter, keeping it tight
What happens in microturition when bladder is full
Bladder stretches → Aδ and C fibres send a strong message to brain:
👉 “Bladder is full. Time to empty.”
Blocks previous mechanisms. GABA binds to GABAnergic neurones, induces potassium efflux so reduces ACH released so external sphincter relaxes
Ach releases and binds to M3 causing constriction of the detrusor muscle causing constriction and bladder to release
How does the RAAS system regulate ions blood volume and pressure
Angiotensin II promotes Na+ and Cl- reabsorption and K+ secretion.
Aldosterone increases sodium reabsorption and potassium secretion.
ANP inhibits Na+ reabsorption, promoting excretion of Na+ and water.
What compensation mechanisms are there to regulate acid base balance
Urinary system: Excretion and reabsorption of HCO3- and H+.
Respiratory system: Adjusting respiratory rate and CO2 exhalation.
Plasma buffers: Proteins, phosphate, bicarbonates, and carbonic acid maintain pH.
How do kidneys respond to acidosis?
Excrete H+ and reabsorb HCO3⁻ in both PCT and DCT
Acidosis in the DCT (Type A Cells)
H⁺ and HCO₃⁻ are filtered into the tubule and form H₂CO₃
Luminal carbonic anhydrase IV converts H₂CO₃ → CO₂ + H₂O
CO₂ and H₂O enter cells and are converted back to H⁺ + HCO₃⁻ by CA II
Transport
HCO₃⁻ is reabsorbed into blood via HCO₃⁻/Cl⁻ exchanger
H⁺ is secreted via Na⁺/H⁺ exchanger, H⁺ ATPase, and K⁺/H⁺ ATPase
Clinical Link
In hypokalaemia, kidneys reabsorb K⁺ in exchange for H⁺
Leads to more H⁺ loss in urine → causes alkalosis.
How do the kidneys respond in alkalosis
Alkalosis in the DCT (Type B Cells)
H⁺ and HCO₃⁻ are filtered into the tubule and form H₂CO₃
Luminal carbonic anhydrase IV breaks H₂CO₃ → CO₂ + H₂O
CO₂ and H₂O enter intercalated cells and reform H⁺ + HCO₃⁻ via CA II
Transport
HCO₃⁻ is secreted into the urine via HCO₃⁻/Cl⁻ exchanger
H⁺ is reabsorbed into blood via Na⁺/H⁺ exchanger, H⁺ ATPase, and K⁺/H⁺ ATPase
Clinical Link
In hyperkalaemia, kidneys excrete K⁺ in exchange for reabsorbing H⁺
This leads to increased H⁺ in blood → causing acidosis
What enzymes are involved in renal acid-base control?
Carbonic anhydrase type IV (lumen) and type II (cell cytoplasm).
What are the effects of Angiotensin II and Aldosterone on the kidney?
Angiotensin II promotes Na+ and Cl- reabsorption and K+ secretion.
Aldosterone increases Na+ reabsorption and K+ secretion.
What causes metabolic acidosis in uncontrolled diabetes (DKA), and how does the body compensate?
Problem: Lack of insulin → fat breakdown → ketone production → metabolic acidosis
Blood Effect: ↓pH, ↑[H⁺]
Compensation:
Hyperventilation (↓CO₂ → ↓H₂CO₃ → ↑pH)
Kidneys excrete H⁺ and reabsorb HCO₃⁻
What causes metabolic acidosis in severe exercise, and how is it compensated?
Problem: Anaerobic respiration → lactic acid buildup
Blood Effect: ↓pH, ↑[H⁺]
Compensation:
Hyperventilation to remove CO₂
Kidneys excrete H⁺ and reabsorb HCO₃⁻
What leads to metabolic alkalosis in vomiting or antacid use, and how does the body respond?
Problem: Loss of gastric acid or ingestion of base
Blood Effect: ↑pH, ↑HCO₃⁻, ↓[H⁺]
Compensation:
Hypoventilation to retain CO₂
Kidneys reabsorb H⁺ and excrete HCO₃⁻
