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LSS 2- Life Support System 2 > Urinary System > Flashcards

Urinary System Flashcards

1
Q

What does the urinary system comprise of?

A

Kidneys
Ureters
Urinary bladder
Urethra

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2
Q

Describe the anatomy of the kidneys

A

Retroperitoneal in upper abdomen

Highly vascularised

Surrounded by dense fibrous capsule
Outside this is a fascial pouch (renal fascia) containing the peri-renal adipose tissue
Posteriorly overlapped by the diaphragm and pleural cavity superiorly

Multilobar

Suprarenal glands (adrenal) sit on top of superior poles

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3
Q

Which kidney is slightly lower?

A

Right kidney is usually slightly lower than the left

Superior pole of the R kidney lies at the level of the 11th intercostal space and that of the L at the 11th rib

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4
Q

Where does the hilum of the kidney lie?

A

About the level of L2

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5
Q

What are the posterior relations of the kidneys?

A

Overlapped by diaphragm (at top)

Psoas major muscle (medial)
Quadratus lumborum muscle
Transversus abdominis muscle (lateral)

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6
Q

What is the kidney surrounded by?

A

Surrounded by dense fibrous capsule
Outside this is a fascial pouch (renal fascia) containing the peri-renal adipose tissue (perinephric fact)
Paranephric fat is outside the renal fascia

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7
Q

What are the anterior relations of the kidney?

A

Right= liver, hepatic flexure and hilus lies behind second part of duodenum

Left= stomach, pancreas, spleen and splenic flexure

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8
Q

What is the blood supply to the kidneys?

A

Abundant blood supply via renal arteries
- Short direct branches from abdominal aorta

Blood pressure drives ultrafiltration by glomerular capillaries

Renal veins drain into the IVC

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9
Q

Describe the external surface of the kidney

A 
From top:
Suprarenal gland (adrenal)
Superior pole
Anterior surface (with lateral margin)
Inferior pole

Renal arter/vein/pelvis connected
Renal pelvis-> ureter

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10
Q

How does drainage from the kidneys work?

A

Each lobe drains through its own papilla and calyx

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11
Q

What do the cortex and medulla of the cortex look like and why?

A

Cortex= granular-looking
Because of random organisation

Medulla= striated
Because of radial arrangement of tubules and micro-vessels
Houses nephrons

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12
Q

What are the minor and major calyxes?

A

Calyx= chamber of the kidney where urine passes through

Renal pyramid into minor calyx (through renal papilla)
Minor calyxes-> major calyx
Major calyxes-> renal pelvis-> ureter

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13
Q

How are renal pyramids and minor calyxes separated from neighbouring ones?

A

Renal pyramids separated by renal columns

Renal minor calyxes separated by renal sinus (under column)

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14
Q

What are the ureters?

A

Ducts by which urine passes from the kidney to the bladder

Run vertically down posterior abdominal wall in the plane of the tips of the transverse processes of the lumbar vertebrae

Cross the pelvic brim anterior to the sacro-iliac joint and bifurcation of the common iliac arteries

Descend anteromedially to enter bladder at the level of the ischial spine (open obliquely through bladder wall)

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15
Q

How is urine transported in ureters?

A

By peristalsis in ureter smooth muscle walls

Ureters open obliquely through bladder wall

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16
Q

What are the 3 sites of ureteric constriction? What can cause sites of renal colic?

A
  1. Pelviureteric junction
  2. Where ureter crosses pelvic brim
  3. Where ureter traverses bladder wall

Sites of renal colic caused by kidney stones attempting to pass

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17
Q

What is the bladder?

A

Hollow muscular pelvic organ (triangular pyramid with apex pointing anteriorly and base posteriorly)

Collects urine from the kidneys before disposal by urination

Very distensible (up to 600ml urine can be held)

Lined by urothelium (transitional epithelium)

3-layered epithelium with very slow cell turnover

Large luminal cells have highly specialised low-permeability luminal membrane

Prevents dissipation of urine-plasma gradients

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18
Q

How many ml can the bladder hold?

A

The bladder is a distensible organ- can hold up to 600 mL of urine

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19
Q

What are the surfaces of the urinary bladder and how do they connect?

A

Superior surface (triangle between ureters and median umbilical ligament)

  • Joins ureters at fundus (base)
  • Joins median umbilical ligament (apex)

Inferolateral
- Neck underneath-> urethra

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20
Q

What are the urinary sphincters?

A

INTERNAL URETHRAL ORIFICE
Other names= sphincter visicae / internal sphincter
Location= Neck of bladder (bottom)
Musculature= Smooth
Opening= Reflex
Stimulus= Bladder wall tension (i.e. distension- filling)
Control= Parasympathetic

EXTERNAL URETHRAL ORIFICE
Other names=sphincter urethrae / external sphincter
Location= Perineum (outside opening)
Musculature= Striated
Opening= Voluntary
Stimulus= Urge to urinate (continence)
Control= Voluntary inhibition (somatic- pudendal nerve)

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21
Q

What does it mean ‘the external urethral orifice is under control by voluntary inhibition’?

A

Tone is maintained by the nerves, on urination you are inhibiting these messages (i.e. relaxing the sphincter) rather than engaging anything

Somatic control- pudendal nerve

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22
Q

Outline reflex and voluntary control in opening of the bladder sphincters

A 
REFLEX
Bladder fills
-> + stretch receptors (in bladder wall)
-> + parasympathetic nerve
-> + bladder
-> bladder contracts
-> internal urethral sphincter mechanically opens when bladder contracts

Bladder fills

  • >
    • stretch receptors (in bladder wall)
  • >
    • motor neuron
  • > external urethral sphincter opens when motor neurone is inhibited

VOLUNTARY CONTROL
Cerebral cortex
-> + motor neuron
-> external urethral sphincter remains closed when motor neurone is stimulated

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23
Q

How are urethra different in males and females?

A

FEMALE
Very short urethra (hence why women are more prone to UTIs)

MALE
Length is variable

Four major areas of the male urethra:

  1. Pre-prostatic
    - Internal urethral orifice (bladder neck, bladder outlet)
  2. Prostatic
  3. Membranous
  4. Spongy
    - Bulbar urethra
    - Penile urethra
  • Navicular Fossa
  • External urethral meatus
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24
Q

Outline the passage of urine

A

Kidney-> ureter-> bladder-> urethra

Urine is made in the kidneys (within each nephron)
It drains through each collecting duct into the renal pelvis (via the minor and major calices)
Travels down the ureters via peristalsis
Enters the bladder
Passes through internal urethral orifice
Travels down the urethra
Opening of the external urethral orifice results in urination

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25
Q

What type of muscle lines ureters?

A

Smooth muscle

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26
Q

How does food and drink become faeces, exhalation, urine and sweat?

A

Food and drink-> BODY and faeces (undigested residue)

BODY
Regulation of osmolarity, [Na+], [K+], pH, nitrogen etc.
Controls body fluid volume
-> Exhalation (H2O, CO2)
-> Urine (H2O, Na, K, H, urea)
-> Sweat (H20, Na)
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27
Q

What is the function of the kidneys?

A

Production of urine:

  • Filtration of blood plasma
  • Selective reabsorption of contents to be retained
  • Tubular secretion of some components
  • Concentration of urine as necessary

Filtration and excretion of waste produces
- Control of osmolarity and composition of blood and urine

Electrolyte homeostasis
- Control of osmolarity of blood

BP control

  • Control of volume of blood
  • Responds to various blood pressure states to maintain homeostasis

Acid-base homeostasis

Endocrine function
- Signals to rest of body (hormones include renin, erythropoietin, 1,25-OH vitamin D)

Sensitive to body needs via hormones, nerves

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28
Q

How is urine produced in the kidney?

A

FILTRATION (glomerulus)
Blood passing through glomerulus is filtered
Filtrate consists of all components

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29
Q

What is a renal corpuscle?

A

A renal corpuscle is the initial blood-filtering component of a nephron

Consists of two structures: a glomerulus and a Bowman’s capsule

Also, podocytes associated with glomerulus

FOR FILTRATION

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30
Q

What is the blood supply of the renal corpuscle?

A

At vascular pole
From afferent arteriole
Exit through efferent arteriole

Glomerular capillaries at high pressure

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31
Q

What does the filtration barrier of the renal corpuscle consist of?

A

Fenestrae (“windows”) in capillary endothelium

Specialised basal lamina

Filtration slits between foot processes of podocytes

Allows passage of ions and molecules

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32
Q

How is filtrate drained from the renal corpuscle?

A

At urinary pole of corpuscle

Drains to proximal convoluted tubule

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33
Q

What are the functions of the proximal convoluted tubule?

A

FOR REABSORPTION

Reabsorption of 70% of glomerular filtrate
Na+ uptake by basolateral Na+ pump
Water and anions follow Na+
Glucose uptake by Na+/glucose co-transporter
Amino acids by Na+/amino acid co-transporter
Protein uptake by endocytosis

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34
Q

What are the structural features of the proximal convoluted tubule?

A

Cuboidal epithelium

Sealed with (fairly water-permeable) tight junctions

Membrane area increased to maximise rate of resorption

  • Brush border at apical surface
  • Interdigitations of lateral membrane

Contains aquaporins
- Mediate transcellular water diffusion

Prominent mitochondria reflect high energy requirement

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35
Q

What is the function of the loop of Henle and vasa recta?

A

Creation of hyper-osmotic fluid

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36
Q

Describe the Loop of Henle (concurrent mechanism)

A

DESCENDING THIN TUBULE
Passive osmotic equilibrium (aquaporins present)
Simple squamous epithelium

ASCENDING THICK LIMB
Na+ and Cl- actively pumped out of tubular fluid
Very water-impermeable tight junctions
Membranes lack aquaporins - low permeability to water
Results in hypo-osmotic tubular fluid, hyper-osmotic extracellular fluid
Cuboidal epithelium, few microvilli
High energy requirement - prominent mitochondria

VASA RECTA
Blood vessels also arranged in loop
Blood in rapid equilibrium with extracellular fluid
Loop structure stabilises hyper-osmotic [Na+]

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37
Q

What cell types are in the PCT, DCT, ascending and descending limbs of the loop of Henle?

A

PCT= cuboidal epithelium

Descending= simple squamous epithelium

Ascending= cuboidal epithelium, few microvilli

DCT= cuboidal epithelium, few microvilli

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38
Q

What is the difference in permeability of the ascending and descending limbs of the loop of Henle?

A

Descending= low/no permeability to ions (Na and Cl), moderate permeability to urea, highly permeable to water

Ascending= impermeable to water, pumps out NaCl

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39
Q

Why is the loop of Henle described as ‘countercurrent’?

A

Fluid flows in opposite direction through two adjacent parallel sections of a nephron loop (ascending and descending)

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40
Q

What is the function of the distal convoluted tubule (and cortical collecting duct)?

A

ADJUSTMENT OF ION CONTENT IN URINE

Site of osmotic re-equilibration (control by vasopressin)
Adjustment of Na+/K+/H+/NH4+ (control by aldosterone)
Cuboidal epithelium, few microvilli
Complex lateral membrane interdigitations with Na+ pumps
Numerous large mitochondria
Specialisation at macula densa, part of juxtaglomerular apparatus

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41
Q

What is the function of the (medullary) collecting duct?

A

CONCENTRATION OF URINE

Passes through medulla with its hyper-osmotic extracellular fluid

Water moves down osmotic gradient to concentrate urine

Rate of water movement depends on aquaporin-2 in apical membrane
- Content varied by exo-/endocytosis mechanism
Under control from the pituitary - hormone vasopressin

Basolateral membrane has aquaporin-3, not under control

Duct has simple cuboidal epithelium

Cell boundaries don’t interdigitate

Little active pumping so fewer mitochondria

Drains into minor calyx at papilla of medullary pyramid
Minor and major calyces and pelvis have urinary epithelium

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42
Q

What does the juxtaglomerular apparatus do?

A

Endocrine specialisation
Secretes renin to control blood pressure via angiotensin
Senses stretch in arteriole wall and [Cl-] in tubule

Cellular components are

  • Macula densa of distal convoluted tubule
  • Juxtaglomerular cells of afferent arteriole
  • Mesangial cells
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43
Q

What is ‘correction’ in the kidneys?

A

Ascending limb= major site of correction

Minute changes enable ions to cross back into the blood to regulate urine concentration

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44
Q

Outline the role of the different parts of the nephron

A

AFFERENT ARTERIOLE
Blood to nephron
Controls perfusion

GLOMERULUS
Ball of capillaries-> filtration
Alter perfusion (respond to signals)

BOWMAN’S CAPSULE
Hollow tubular epithelium surrounding glomerulus

PCT
Major site of reabsorption (H2O, K, Na, HCO3, AAs)

DESCENDING LIMB
Major site of concentration (of urine)
Highly permeable to ions not water

DCT
Fine tuning site
Sensitive to ADH and thiazide diuretics

COLLECTING DUCT
Small amount of reuptake

EFFERENT ARTERIOLE
Takes filtered blood away away from nephron
Constriction controls GFR (assisting in ultrafiltration of the blood)

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45
Q

In terms of the kidney, what is reabsorption?

A

What goes back into the blood

So at the glomerulus, everything goes in and then throughout the nephron composition of the urine is altered depending on the body’s requirements

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46
Q

Outline the role of the juxtaglomerulus

A

The JGA has three cellular components

  1. Macula Densa cells ([Na+] sensor)

Columnar epithelium
Located in the DCT
Senses high NaCl delivery and secretes ATP causing afferent vasoconstriction

  1. Granular cells (responds to PNS and SNS changes in tone)

Present throughout JGA but most dense in afferent arteriole
Senses changes caused by PNS and SNS
β-adrenergic stimulation
Reduced renal perfusion pressure
Reduced [Na+]
Secretes renin in response to decreased perfusion

Mesangial cells (produce EPO)
Extra-glomerular cells
Form part of the supportive matrix

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47
Q

What is glomerular filtration?

A

Formation of an ultra-filtrate of plasma in the glomerulus

Passive process: fluid is ‘driven’ through the semipermeable (fenestrated) walls of the glomerular capillaries into the Bowmans capsule space by the hydrostatic pressure of heart

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48
Q

What is renal failure?

A

An abrupt fall in glomerular filtration

Abnormalities in renal circulation-> reduced glomerular filtration i.e. renal failure

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49
Q

What is the glomerular filtration barrier permeable to?

A

Fenestrated endothelium of capillaries and semipermeable Bowman’s capsule

Highly permeable to:
Fluids
Small solutes (freely-filtered- sam concentration in filtrate and plasma)

Impermeable to:
Cells
Proteins
Drugs etc. carried bound to protein

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50
Q

What is produced by glomerular filtration?

A

A clear fluid (ultrafiltrate), completely free from blood and proteins, is produced containing electrolytes and small solutes

This is ‘primary urine’

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51
Q

Describe the movement of filtrate in glomerulus

A

From capillary lumen through fenestra into basement membrane

Through filtration slits between foot processes (podocyte) into capsular space

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52
Q

What is the blood flow to the glomerulus?

A

Renal input= renal artery

Renal output= renal vein and ureter

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53
Q

How can the amount excreted be described in terms of amount filtered, secreted and absorbed?

A

Amount excreted = amount filtered + amount secreted - amount absorbed

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54
Q

What is the driving force of glomerular filtration?

A

Hydrostatic pressure in glomerular capillaries (due to blood pressure) (Pgc)
- The force of the body circulating the blood to the renal artery

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55
Q

What are the pressures the oppose the driving force in glomerular filtration?

A

Hydrostatic pressure of tubule (Pt)
- The opposing force from the tubule against the glomerulus

Osmotic pressure of plasma proteins in glomerular capillaries (πgc)
- Protein (mainly albumin) exerts a pressure pulling water back

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56
Q

What determines the net ultrafiltration pressure (Puf)?

A

DRIVING FORCE:
Hydrostatic pressure in glomerular capillaries (due to blood pressure) (Pgc)

OPPOSING PRESSURES:
Hydrostatic pressure of tubule (Pt)
Ssmotic pressure of plasma proteins in glomerular capillaries (πgc)

Puf= Pgc - Pt - πgc

Ultimately there is a net ultrafiltration pressure of 10-20mmHg

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57
Q

What is the usual net ultrafiltration pressure?

A

10-20mmHg

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58
Q

What is the glomerular filtration rate?

A

GFR = Puf x Kf

The amount of fluid filtered from the glomeruli into the Bowmans capsule per unit of time (mL/min)

Sum of the filtration rate of ALL functioning nephrons

Index of kidney function

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59
Q

What happens to GFR when there is a loss of nephrons?

A

E.g. in kidney disease, may reduce number of functioning glomeruli so reduced surface area and reduced Kf

Loss of nephrons-> loss of surface area-> fall in Kf-> fall in GFR

Any changes in Kf-» GFR imbalances

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60
Q

What is Kf?

A

An ultrafiltration coefficient,

Accounts for

  • Membrane permeability
  • Nephrons available for filtration

Any changes in Kf-» GFR imbalances

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61
Q

How can Kf be reduced or increased?

A

Kidney diseases may reduce number of functioning glomeruli = reduced surface area = reduced Kf

Dilation of glomerular arterioles by drugs/ hormones will increase Kf

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62
Q

What is the formula for GFR?

A

GFR = Puf x Kf

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63
Q

What does renal flow deliver?

A

Oxygen, nutrients and substances for excretion

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64
Q

How is GFR affected by Puf and Kf?

A

Puf= overall pressure of the filtrate, influenced by

  • HP of the glomerular capillary
  • Opposing HP of the tubule
  • COP of the plasma proteins in the glomerulus

Kf = ultrafiltrate coefficient, accounts for

  • Membrane permeability
  • Nephrons available for filtration

SO….
GFR depends of Pgc, πgc, Pt and Kf

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65
Q

How is renal blood flow calculated?

A

Renal blood flow (RBF) = approx 1L/min (1/5 of cardiac output)

Renal plasma flow (RPF) = approx 0.6L/min

Filtration fraction (FF) = 0.2 (ratio between RPF and amount of filtrate filtered by glomerulus, which is normally 20%)

Glomerular filtration rate (GFR) = RPF x FF
= Approx 120ml/min (volume of filtrate formed in 1 minute)

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66
Q

How is GFR regulated?

A

GFR is not a fixed value but is subject to physiological regulation

Achieved by neural or hormonal input to the afferent/efferent arteriole resulting in changes in Puf

Mechanisms of autoregulation

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67
Q

What is autoregulation of the GFR?

A

Autoregulation ensures fluid and solute excretion remain reasonably constant (otherwise varying pressure will vary urine production and cause loss of important ions)

To decrease GFR

  • Constrict afferent arteriole
  • > Decreased Pgc
  • > Decreased GFR
  • Dilate efferent arteriole

To increase GFR

  • Constrict efferent arteriole
  • > Increased Pgc
  • > Increased GFR
  • Dilate afferent arteriole

Mechanisms to do this

  • Myogenic mechanisms
  • Tubuloglomerular feedback
  • RAAS
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68
Q

How do myogenic mechanisms in autoregulation work to regulate GFR?

A

Vascular smooth muscle constricts when stretched-> Keeps GFR constant when blood pressure rises

Arterial pressure rises -> afferent arteriole stretches -> arteriole contracts -> (vessel resistance increases)-> blood flow reduces and GFR remains constant

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69
Q

How does tubuloglomerular feedback work in autoregulation to regulate GFR?

A

NaCl concentration in fluid sensed by macula densa in juxtaglomerular apparatus

Macula densa signals afferent arteriole and changes its resistance and so GFR

Increased NaCl-> ATP released by macula densa-> vasoconstrict afferent arteriole-> decreased filtration-> NEGATIVE FEEDBACK

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70
Q

What happens to GFR is there is a severe haemorrhage, obstruction in nephron tubule, reduced plasma protein concentration or small increase in blood pressure?

A

Severe haemorrhage= decrease GFR

Obstruction in nephron tubule= decrease

Reduced plasma protein concentration= increase GFR

Small increase in blood pressure= no effect

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71
Q

Why and how does a severe haemorrhage cause GFR to decrease?

A

Need to drop GFR to maintain volume

Haemorrhage-> blood pressure drop (MAP drop detected by carotid baroreceptors)

Sympathetic nervous system overides renal regulation
-> Innervates afferent arteriole and constricts it

GFR decreased (to maintain volume)

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72
Q

Why does a drop in oncotic plasma proteins increase GFR?

A

Increased Puf -> increased GFR

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73
Q

Why does a small increase in blood pressure not change GFR?

A

Regulated by renal autoregulation and constriction

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74
Q

What is renal clearance?

A

As substances in blood pass through the kidney they are filtered to different degrees

The extent of filtering a substance undergoes and litres of plasma produced per unit time

Urinary excretion rate over plasma concentration

Cs= (Us x V)/ Ps

Substance s

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75
Q

What is the formula for renal clearance?

A

C= (U x V)/ P

U = concentration of substance in urine
P = concentration of substance in plasma
V = rate of urine production
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76
Q

How is GFR estimated using clearance?

A

If a molecule is freely filtered and neither reabsorbed nor secreted in the nephron then the amount filtered equals amount excreted

Use INULIN
(Gives clearance value of 120ml/min)
Needs to be transfused

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77
Q

Why could inulin be used to estimate GFR using clearance?

A

Gold standard but not used (have to transfuse)

A plant polysaccharide
Freely filtered and neither reabsorbed nor secreted
Not toxic
Measureable in urine and plasma

Gives a clearance value of 120ml/min which is GFR for average adult

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78
Q

Why is creatinine used to estimate GFR using clearance?

A

Endogenous (unlike inulin) so don’t need to infuse it

Waste product from creatine in muscle metabolism
Amount of creatinine released is fairly constant
If renal function stable, amount creatinine in urine is stable

Low values of creatinine clearance may indicate renal failure
High plasma creatinine may indicate renal failure

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79
Q

How can creatinine indicate renal failure?

A

Low values of creatinine clearance may indicate renal failure

High plasma creatinine may indicate renal failure

i.e. Creatinine plasma concentration goes up

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80
Q

How is renal plasma flow (RPF) measured?

A

By PAH (Para aminohippurate) clearance= 625ml/min

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81
Q

Why is PAH used to measure RPF?

A

Filtered and actively secreted in one pass of the kidney

I.e. all PAH is removed from the plasma passing through the kidney so its clearance equals the renal plasma flow

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82
Q

What do most solutes, inulin/creatinine and PAH do in the kidneys?

A

Most solutes= controlled excretion, reabsorption

Inulin/creatine= GFR, no reabsorption or secretion

PAH= RPF, secretion

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83
Q

What diagnostic features show renal disease?

A

Fall in GFR (-> excretory products build up in plasma)
Raised plasma concentration of creatinine

Excretion of some substances may be impaired in renal failure (including some drugs) so need to take into account when calculating drug doses

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84
Q

What is tubular function?

A

Need to go from 180L of filtrate a day to the 0.6-2.5L of urine

On average day, consume more water and salt than we need-> need to lose this with other waste products (e.g. urea)

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85
Q

How is waste removed while keeping necessary components?

A

Controlled reabsorption and secretion

  • Need to reabsorb 99% of the ultra filtrate
  • Need to maintain solute balance, plasma concentration and pH

Different parts of the nephron are specialise to perform specific tasks

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86
Q

What is osmolarity?

A

A measure of the osmotic pressure exerted by a solution across a perfect semi-permeable membrane

All the concentrations of the different solutes (measured in mmol/l) added together
- Each ion is “counted” separately

Osmolarity is dependent on the number of particles in a solution and NOT the nature of the particles

E.g. 1mmol/L of Na2HPO4 is the equivalent of 3 mosmoles/L
This is made up from 1 mosmol/L HPO42- and 2 mosmol/L of Na+

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87
Q

What effect does a solute present at equal concentrations either side of a semi-permeable membrane have on water movement?

A

Any solute present at equal concentrations either side of a semi-permeable membrane can have no net effect on water movement

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88
Q

How do solutes travel between the peritubular capillary (blood) and tubular fluid?

A

REABSORPTION
Tubular fluid-> peritubular capillary
- Transcellular
- Paracellular

SECRETION
Peritubular capillary -> and tubular fluid
- Transcellular
- Paralcellular

Through the renal tubular wall
- Tight junctions throughout, very tight in some places-> don’t let water through at all (depends on function)

89
Q

What types of transport are there in the tubules?

A

Osmosis

  • From low osmolarity to high osmolarity
  • Via tight junctions of aquaporin

Active transport

  • Directly coupled to ATP hydrolysis
  • Indirectly coupled to ATP hydrolysis

Passive transport

  • Protein independent transport (lipophilic molecules)
  • Protein dependent transport (hydrophilic molecules)

Co-transport

Movement down electrical gradient

90
Q

How is a passive uptake system regulated?

A

More or less channels

In low capacity state, few channels in membrane (many stored in cell)-> slow rate

In high capacity state, more channels in membrane-> faster rate

91
Q

How are proteins reabsorbed in the tubule?

A

Proteins are too big but need to be reabsorbed

Bound to low affinity but high variability receptors (which sit on membrane surface)

Invaginate membrane and internalise protein

Dissociate protein that is reabsorbed from protein

Recycle receptor

92
Q

What is a transport maxima?

A

How much of a substance can be resorbed

Don’t just apply to individual cells
Applies to whole system

Can vary dependent on circumstance

E.g. glucose: as plasma glucose goes up, more filtered (still filtering same proportion but actual amount increases) and then it is resorbed
Protein dependent so reaches a maximum (transport systems are saturated) and then rest is excreted
(In DM)

93
Q

How are small molecules (e.g. ions, glucose and AAs) reabsorbed from the filtrate?

A

Specialised proteins called transporters are located on the membranes of the various cells of the nephron

These transporters trap the molecules as they flow by them

  • Each transporter traps only one or two types of molecule
  • For example glucose is reabsorbed by a transporter that also traps sodium

Water gets reabsorbed passively by osmosis in response to build up of Na in intercellular spaces

Some transporters require energy, usually in the form of ATP (active transport), while others do not (passive transport)

Transporters are located in different parts of the nephron

Most of the Na transporters are located in the proximal tubule, while fewer are spread out through other segments

94
Q

How is the tubule involved in secretion?

A

Moves substances from peritubular capillaries into tubular lumen

Like filtration, this constitutes a pathway into the tubule

Can occur by diffusion or by transcellular mediated transport

The most important substances secreted are H+ and K+

Choline, creatinine (very small amount), penicillin and other drugs also secreted

Active secretion from blood side into tubular cell (via basolateral membrane) and from cell into lumen (via luminal membrane)

95
Q

How much of what goes into kidney goes into tubular system?

A

About 20% of what goes into kidney goes into tubular system (rest goes around kidney and around body)

Significant proportion of filtrate is reabsorbed

Some will be secreted

Net effect

96
Q

Is reabsorption uniform?

A

No- there is regional specificity

PCT
60-70% of all solute
100% glucose (if below transport maximum)
65% Na
90% bicarb
Water and anions follow Na+ (osmolarity is maintained)

LOOP OF HENLE
Concentration of urine
25% Na

DCT
8% Na

COLLECTING DUCT
Variable absorption regulated by aldosterone and vasopressin

97
Q

Does the PCT have many mitochondria or villi?

A

Many mitochondria

High metabolic demand
Pumps sodium out all the time (into blood) so it has low IC Na concentration
So it can use that concentration gradient to bring other solutes

Brush border= large surface area for resorption

98
Q

Does the descending Loop of Henle have many mitochondria or villi?

A

Not many
Not much metabolic activity
Not much resorption so not many villi

99
Q

Does the ascending Loop of Henle have many mitochondria or villi?

A

Lots of mitochondria

Resorption but not as much as PCT (so less ciliated brush border)

100
Q

Does the DCT have many mitochondria or villi?

A

Similar to LoH
Need mitochondria
Ciliated surface (some resorption, not as much as PCT)

101
Q

Does the collecting tubule have many mitochondria or villi?

A

Just modulating system
Few mitochondria
Less ciliated surface

102
Q

How does the PCT lead to reabsorption?

A

Resorbs most things

Na very important (because of co-transporters/exchangers)

Na/K ATPase-> generates Na concentration gradient (keeps low inside so molecules can be brought in)

Used to bring in glucose and AAs from tubular fluid (-> higher in cell so then diffuse out through transporter on other side into blood)

Sodium also used to reabsorb bicarbonate and excrete protons
- Exchange one sodium for one proton
- Buffer bicarbonate by excreting proton
- Carbonic anhydrase activity leads to Na+ re-absorption and increased urinary acidity
(breaks down bicarbonate to H2O and CO2 which can enter cell and then generate bicarbonate in cell with carbonic anhydrase)

103
Q

What happens in the PCT overall?

A

PASSIVE REABSORPTION
Urea and water

ACTIVE REABSORPTION (i.e. require ATP and carriers):
Glucose
Amino-acids
Sodium
Potassium
Calcium
Vitamin C
Uric acid

Reabsorption of all solutes/water is sensitive to metabolic poisons

104
Q

Why is net secretion important?

A

Some substances have net secretion from the plasma into the proximal tubular fluid

IMPORTANT BECAUSE…
Some drugs and other substances are excreted in this way
Some drugs enter the tubular fluid and act further down the nephron

105
Q

What happens in the Loop of Henle regarding reabsorption?

A

DESCENDING LIMB
Water passively reabsorbed; squamous epithelium
Draws in Na and K

ASCENDING LIMB
Cl actively reabsorbed (up conc gradient)
Na passively reabsorbed with it (pulled in through same transporter as Cl)
Bicarbonate reabsorbed
Impermeable to water

By now 85% water and 90% Na and K have been reabsorbed

Tubular fluid leaving the loop of Henle is hypo-osmolar with respect to plasma

Driven by triple transporter
Na out of cell, K in
K leaks out taking Cl with it
Gradient allows Na, Cl comes in and so does K

106
Q

What happens in the proximal part of the DCT regarding reabsorption?

A

PROXIMAL PART OF DISTAL CONVOLUTED TUBULE
Complex lateral membrane interdigitations with Na+ pumps

Na+ and Cl- co-transporter linked to Ca2+ reabsorption

Na+ and chloride are reabsorbed by a channel sensitive to thiazides (Blocked by thiazide drugs -> rise in plasma Ca2+)

SPECIALISATION AT MACULA DENSA (at juxtaglomerular apparatus)
Detects changes in Na concentration of filtrate

107
Q

What happens in the distal part of the DCT and cortical collecting duct regarding reabsorption?

A

‘Fine’ tuning of the filtrate to maintain homeostasis

Distal part of DCT= Sodium reabsorbed
(dependent on aldosterone)

Collecting duct= Sodium reabsorbed
(dependent on aldosterone)

Adjustment of Na+/K+/H+/NH4+

Water reabsorbed under control of ADH

Distal part of nephron is impermeable to water without ADH

108
Q

What cells are important in reabsorption in the distal part of the DCT and cortical collecting duct?

A

Principal Cell: important in sodium, potassium and water balance (mediated via Na/K ATP pump)

Intercalated Cell: important in acid-base balance (mediate via H-ATP pump)

Very tight epithelium
-> Very little paracellular transport so tight regulation of water

109
Q

What single gene defects affect tubular function?

A

Renal tubule acidosis
Bartter syndrome
Fanconi syndrome
(Dent’s disease)

110
Q

What is renal tubular acidosis?

A

Hyperchloremic metabolic acidosis-> problems excreting acid
Impaired growth
Hypokalemia (can be sufficient to cause temporary paralysis)

Inability to secrete protons (or extra proton leaks back)
Affects bicarbonate
Can’t get rid of acid

111
Q

What is Bartter syndrome?

A

Excessive electrolyte secretion

Antenatal Bartter syndrome

  • Premature birth, polyhydramnios
  • Severe salt loss
  • Moderate metabolic alkalosis
  • Hypokalaemia
  • Renin and aldosterone hypersecretion

Mutation in mechanism to reabsorb salt (Na/K pump)

112
Q

What is Fanconi Syndrome?

A

Increased excretion of uric acid, glucose, phosphate, bicarbonate

Increased excretion of low molecular weight protein

Disease of the proximal tubules associated with

Seen in renal tubular acidosis (type 1)

  • Protein pulled into endosome
  • Requires proton pump (acidify-> dissociate protein from transporter) so proteins pumped into endosome but run out of transporter
  • Let 1 proton out, 2 Cl in
  • Endosome becomes positively charged, can’t recycle protein capturing receptors back to surface
113
Q

What happens when kidneys stop working?

A

Loss of excretory function
- Accumulation of waste products

Loss of homeostatic function

  • Disturbance of electrolyte balance
  • Loss of acid-base control
  • Inability to control volume homeostasis

Loss of endocrine function

  • Loss of erythropoeitin production
  • Failure to 1 alpha hydroxylase vitamin D

Abnormality of glucose homeostasis
- Decreased gluconeogenesis

Clinical features determined by rate of deterioration

114
Q

In advanced kidney failure, what are blood results likely to show? What will arterial blood gases show?

A 
Sodium= little low
Potassium= very high (homeostatic mechanism should keep EC potassium in tight)
Urea= very high (don’t use much)
Creatine= very high 
Haemoglobin= anaemic

ABG shows METABOLIC ACIDOSIS

115
Q

What are common clinical findings in end stage kidney disease?

A

Symptoms of extreme lethargy, weakness and anorexia

Clinically volume depleted resulting in severe hypotension

Elevated plasma urea and creatinine make diagnosis of renal failure

This is complicated by 
- Hyperkalaemia 
- Hyponatraemia
- Metabolic acidosis 
anaemia

ULTRASOUND shows 2 small shrunken kidneys

116
Q

Why are lethargy and anorexia caused by kidney failure?

A

Accumulation of nitrogenous waste products (don’t know which ones specifically), hormones, peptides and other ‘middle-sized’ molecules (Mol Wt 2-5000)

Acidosis

Hyponatraemia

Volume depletion (low blood pressure)

Anaemia

Chronic neurological damage – peripheral neuropathy

117
Q

What causes imbalanced salt and water in renal failure?

A

WHEN SODIUM CAN’T BE EXCRETED (low Na loss)
It is more usual for patients with renal dysfunction to have difficulty in excreting salt and water

Global kidney dysfunction-> lose GFR-> hard to get rid of Na and water

This leads to a tendency to retain sodium

  • > Hypertension
  • > Oedema
  • > Pulmonary oedema

Salt and water loss can be found in patients with tubulointerstitial disorders in which the concentrating mechanisms have been damaged

WHEN SODIUM IS DEPLETED (high Na loss)
Inability to decrease sodium excretion (i.e. increase sodium reabsorption) when sodium depleted

Osmotic diuresis - caused by high concentration small MW waste substances, e.g., urea

This inappropriately high loss of salt and water results in volume depletion which causes the low blood pressure

DO NOT CONFUSE SERUM SODIUM LEVELS WITH TOTAL BODY SODIUM – CKD AND AKI ARE OFTEN ASSOCIATED WITH HYPONATRAEMIA

118
Q

What are the implications of acidosis because of renal failure?

A

Caused by decreased excretion of H+ ions and by retention of acid bases

Buffered by H+ ions passing into cells in exchange for K+ ions – therefore aggravates tendency to hyperkalaemia

Another compensation mechanism is increasing CO2 loss through the lungs - Kussmahl respiration (air hunger)

Exacerbates anorexia and increases muscle catabolism (central and local mechanisms)

119
Q

What are the implications of hyperkalaemia because of renal failure?

A

Caused by failure of DCT to secrete K

Exacerbated by acidosis - causes shift of potassium from intracellular to extracellular space

Can cause cardiac arrhythmias (usually initial loss of p waves and also bradycardia) and arrest
- Because increased plasma K+ will lead to membrane depolarisation

Can affect neural and muscular activity

Clinical features depend on the chronicity of the hyperkalaemia

120
Q

How can chronic renal failure lead to hyperparathyroidism?

A

Chronic renal failure
-> Phosphate retention
-> Low levels of calcitriol
THESE -> hypocalcaemia-> hyperparathyroidism

Phosphate retention and low levels of calcitriol can also -> hyperparathyroidism directly

Phosphate retention also
-> low levels of calcitriol

121
Q

How does renal failure affect the kidney as a metabolic organ?

A

Decreased erythropoietin production in renal failure results in anaemia

Low 1-25 Vit D levels result in poor intestinal calcium absorption, hypocalcaemia (short term) and hyperparathyroidism (longer term)

Increased cardiovascular risk

122
Q

What is chronic kidney disease likely to cause?

A

Major predictor of ESRF (end stage renal failure)
BUT
Major outcome is CV disease (kidney increases risk of CVD despite age)

123
Q

How does chronic kidney disease increase CV risk?

A

Kidney increases risk of CVD despite age

Hypertension
Secondary cardiac effects
Endothelial effects
Lipid abnormalities

124
Q

What are the differences in symptoms between acute and chronic loss of function?

A 
ACUTE
Anaemia
Acidosis
Tendency to Hyperkalaemia
Hypocalcaemia
* Renal size unchanged
Tendency to hyponatraemia
Volume usually overloaded
-> Oedema, hypertension
* Previously normal creatinine
CHRONIC
Anaemia
Acidosis
Tendency to Hyperkalaemia
Renal osteodystrophy
* Renal size often reduced
* Chronic uraemic symptoms
Tendency to hyponatraemia
Volume usually overloaded
-> Oedema, hypertension
* Previously abnormal creatinine
125
Q

What is the initial management of a patient with kidney disease (acute)?

A

Intravenous normal saline to correct fluid depletion
Intravenous sodium bicarbonate to correct acidosis
Intravenous insulin and dextrose to lower plasma potassium (by driving K+ ions back into cells)
Dialysis

126
Q

What is the outcome of treatment for kidney disease?

A

Patient felt better

Urine output initially 100 ml/day (no longer has osmotic diuresis)

After 2 weeks, urine output increases to 300 - 400 ml/day and pre-dialysis creatinine stabilises at 400 - 450 umol/L

If not enough residual renal function, have to continue on dialysis

127
Q

How can GFR be assessed?

A

UREA
Poor indicator
Confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function etc

CREATININE
Affected by muscle mass, age, race, sex etc.
Need to look at the patient when interpreting the result

CREATININE CLEARANCE
Difficult for elderly patients to collect an accurate sample
Overestimates GFR at low GFR (as a small amount of creatinine is also secreted into urine)

INULIN CLEARANCE
Laborious (involves transfusion) used for research purposes only

RADIONUCLIDE STUDIES
EDTA clearance etc
Reliable but expensive

ESTIMATED GFR
Equation which automatically calculates an estimated GFR from serum creatinine
Result presented ml/min per 1.732 (normalised for BSA)
Easiest equation uses age and ethnicity (MDRD equation)
Newer equations are being introduced
Alternatives can include weight, albumin etc
Generally unreliable once GFR >60ml/min
Generally unreliable in very obese or very thin patients

128
Q

What long term management is given to patients with kidney disease?

A

GFR regularly measured
Haemodialysis (e.g.) 4 hours, 3x a week)
Low potassium diet and fluid restriction
Erythropoietin injections to correct anaemia
1, 25 Vitamin D supplements to prevent hyperparathyroid bone disease

129
Q

How are water and salt balance inter-related?

A

VARIABLE OSMOLARITY
Increased salt and decreased water
-> Increased osmolarity

Decreased salt and increased water
-> Decreased osmolarity

CONSTANT OSMOLARITY
Increased salt have to increase water
-> Increased volume (-> increased BP)

Decreased salt have to decrease water
-> Decreased volume (-> decreased BP)

130
Q

How much more water/salt is consumed than was lost and needs replacing?

A

On an average day we consume 20-25% more water and salt than we need to replace that lost

131
Q

Why does water and salt need to be regulated?

A

Must get rid of the excess volume
-> Or will become oedematous and blood pressure will increase

Must get rid of any excess water
-> Or will dilute the salt in your body
Cells will swell

Must get rid of any excess salt
-> Or will have too high a level of salt
Cells will shrink

132
Q

What is normal plasma composition?

A 
Sodium= 140 mmol/l
Chloride= 105 mmol/l
Bicarbonate= 24 mmol/l
Potassium= 4 mmol/l
Glucose= 3-8 mmol/l
Calcium= 2 mmol/l
Protein= 1 mmol/l

Sodium is most abundant salt in plasma and ECF
Water is most abundant component in plasma and ECF

133
Q

What is normal plasma osmolarity?

A

285-295 mosmol/l

134
Q

What is used to regulate plasma osmolarity?

A

Water balance is used to regulate plasma osmolarity

135
Q

What determines the ECF volume?

A

The level of salt

136
Q

How much water is in the whole body?

A

INTRACELLULAR FLUID
65%= 25L

EXTRACELLULAR FLUID
35%= 15L
Interstitial fluid (most abundant) 28%
Plasma 5%
Transcellular fluid (CSF) 1%
137
Q

How do people get rid of water?

A

Skin and sweat: variable but uncontrollable
Normally about 450 mls/day
- Fever, climate, activity affect this

Faeces: uncontrollable
Normally about 100 ml/day
- With diarrhoea up to 20L/day

Respiration: uncontrollable
350ml/day
- Activity

Urine output: variable and controllable
1500 mls/day

URINE ONLY ONE THAT CAN BE CONTROLLED

138
Q

How does the colour of urine reflect dehydration?

A

Target range= clear, pale yellow

Dehydration= bright yellow

Severe dehydration= orange, green

139
Q

Where is water controlled in the kidney?

A

PCT= getting rid of water

Descending limb and collecting duct= reabsorbing water

DCT= get rid of some water

140
Q

What fraction of filtered load reaches different points in the nephron?

A

GLOMERULUS
125mls/min
180L/day

PCT
Reabsorb about 60-70% of solute in PCT, so reabsorb same amount of water
(Also reabsorb about 100% of glucose and amino acids and 90 % of K+, Bicarb, Ca2+, Uric acid)

LOH
So osmolarity entering LoH is about the same as it is in plasma

In LOH, reabsorb
(Less water than salt)-> hypo-osmolar urine compared to plasma

30%
40mls/min
60L/day

DCT
20%

COLLECTING DUCT
0.7-1.4mls/min
1-2L/day

What is produced at end is very variable
Get rid of between 1 and 10% of what we filter (depending on what balance at the time)

141
Q

How can you concentrate urine above normal plasma osmolarity?

A

Not much water reabsorbed in loop of Henle

Water moves by osmosis

Need to produce a region of ‘hyperosmolar’ interstitial fluid (put more salt in that water in)

Need gradient of osmolarity from plasma to much higher than plasma through the medulla
(Can’t pump water so must have a gradient)

142
Q

How is the gradient to concentrate urine generated?

A

Countercurrent mechanism

  • Lose water in descending limb (inert cells, not many mitochondria or villi)
  • Lose salt in ascending limb (highly metabolically active cells pumping a lot of salt)
143
Q

How is the gradient to concentrate urine amplified?

A

STEP 1a- ASCENDING LIMB (NaCl actively from ascending limb-> interstitial)

The active salt pump in the thick ascending limb transports NaCl out of the lumen until the surrounding interstitial fluid is 200 mOsm/l more concentrated than the tubular fluid in this limb

The medullary interstitial fluid becomes hypertonic

Passive diffusion of sodium chloride from the thin ascending limb (impermeable to water) also adds to the increased solute concentration

STEP 1b- DESCENDING LIMB
(Water passively from descending limb-> interstitial)

Descending limb is highly permeable to water so there is net diffusion of water by osmosis from descending limb into the more concentrated interstitial fluid

Passive movement of water continues until the osmolarities of the fluid in the descending limb and interstitial fluid become equilibrated

STEP 1c- DESCENDING LIMB (2)
(Desc LOH becomes more concentrated)

Tubular fluid entering the loop of Henle immediately starts to become more concentrated as it loses water

At equilibrium, the osmolarity of the ascending limb fluid is 200 mOsm/L and the osmolarities of the interstitial fluid and descending limb fluid are equal at 400 mOsm/liter

STEP 2- LOH FROM PCT/TO DCT
200 mOsm/L fluid exits from the top of the ascending limb into the DCT

New mass of isotonic fluid at 300 mOsm/L enters the top of the descending limb from the PCT

At the bottom of the loop, mass of 400 mOsm/L fluid from the descending limb moves forward around the tip into the ascending limb

The 200 mOsm/L concentration difference has been lost at both the top and the bottom of the loop

STEP 3
The ascending limb pumps NaCl out again while water passively leaves the descending limb until a 200 mOsm/liter difference is re-established (between the ascending limb and both the interstitial fluid and descending limb at each horizontal level)

The concentration of tubular fluid is progressively increasing in the descending limb and progressively decreasing in the ascending limb

STEP 4 (like step 2 but higher mOsm/L)
As the tubular fluid advances still further, the 200 mOsm/L concentration gradient is disrupted once again at all horizontal levels
STEP 5 (like step 3 but higher mOsm/L)
Again active extrusion of NaCl from the ascending limb coupled with the net diffusion of water out of the descending limb re-establishes the 200 mOsm/L gradient at each horizontal level

STEP 6
Tubular fluid flows slightly forward again and the stepwise process continues

Fluid in the descending limb becomes progressively more hypertonic until it reaches a maximum concentration of 1,200 mOsm/L at the bottom of the loop

144
Q

How does the rest of the gradient get generated (countercurrent mechanism only generates a proportion of the gradient)?

A

Countercurrent mechanism only generates a proportion of the gradient

To generate very high interstitial osmolarity relies on permeability to urea (bottom of LOH and collecting duct)

As water is removed in the early collecting duct, concentration of urea increases

As urea concentration goes up it becomes higher in collecting duct than in interstitium so goes out into interstitium

-> Higher urea concentration in interstitium than in bottom of LOH so urea enters bottom of LOH

Continuous cycle of circulating urea around region (important for gradient)

145
Q

What urea transporters are there?

A

SLC14A family of urea transporters controls movement of urea

UT-A2 in bottom of LOH (thin descending limb)
UT-A3 and UTA2 and 1 in collecting duct

UT-B1 in vasa recta

146
Q

What is needed for urea?

A

Urea transporters

LOH creating osmolarity gradient in medullary insterstitium

Collecting duct traversing medulla (-> urine concentrated by osmotic water removal when duct wall is made permeable to ADH)

Very tight cell junctions in collecting duct (regulate permeability to urea and water)

147
Q

What happens to the loop of Henle in desert animals?

A

Loop of Henle bigger in desert animals

Need to conserve more water

148
Q

Why doesn’t medullary blood flow eliminate the countercurrent gradient?

A

Vasa Recta

Permeable to water and solutes
Water diffuses out of descending limb and solutes diffuse into descending limb
In the ascending limb the reverse happens
Thus oxygen and nutrients are delivered without loss of gradient

149
Q

Once the loop of Henle has generated a hyperosmolar environment, where does variability of urine come from?

A

Vasopressin/ADH

Peptide hormone (9 AAs)
Synthesised in the hypothalamus
Packaged into granules
Secreted from the posterior pituitary (neurohypophysis)
Binds to specific receptors on basolateral membrane of principal cells in the collecting ducts

Keeps ECF osmolarity in tight range by controlling water reabsorption

  • Determines urine output and water balance
  • Doesn’t determine ECF volume
150
Q

How does ADH regulate passive uptake of water?

A

Causes insertion of water channels (aquaporins) into the cells membranes (stored inside cell)

-> Increased water permeability (predominantly AQP2 into the luminal membrane)

Also stimulates urea transport from innermedullary component of the collecting duct (IMCD) into thin ascending limb of loop of Henle and interstitial tissue by increasing the membrane localisation of UTA1 and UTA3 in the CCD

Keeps ECF osmolarity in tight range by controlling water reabsorption

  • Determines urine output and water balance
  • Doesn’t determine ECF volume
151
Q

What triggers ADH release?

A

Plasma osmolarity is normally 285 - 295mosmol/L

ADH release regulated by osmoreceptors in the hypothalamus (if osmolarity rises above 300mOs = triggers release)

Also stimulated by a marked fall in blood volume or pressure (monitered via baroreceptors or stretch receptors)

Ethanol inhibits ADH release, which leads to dehydration as urine volume increases

152
Q

Outline water permeability in the nephron

A 
PCT= permeable
Descending limb of LOH= permeable
Ascending limb of LOH= permeable
DCT= impermeable
Collecting duct= ADH-dependent (region of regulation)
153
Q

How does water load affect water permeability of the collecting duct?

A

Decreased fluid loss-> decreased plasma osmolarity

Hypothalamic osmoreceptors-> decreased ADH release

Collecting duct water permeability decreases

Urine flow rate increases

(Increased fluid loss will raise plasma osmolarity so opposite effect)

154
Q

What happens when there is low ADH (water diuresis)?

A

E.g. water load-> Large volume of dilute urine

Solute reabsorption without water reabsorption can lower urine osmolarity to 50 mosmol/l

155
Q

How does dehydration cause low urine flow rate?

A

Plasma osmolarity increases-> increased thirst (due to hypothalamic osmoreceptors)

(Increased water intake will tend to lower plasma osmolarity)

Plasma osmolarity increases-> increased ADH release (due to hypothalamic osmoreceptors)

Collecting duct water permeability increases

Urine flow rate decreases

(Decreased fluid loss will tend to lower plasma osmolarity)

156
Q

What happens when there is high ADH (maximal anti diuresis)?

A

E.g. dehydration-> a small volume of concentrated urine

Osmotic equilibration in cortex and medulla leads to high urine osmolarity

157
Q

What are disorders of water balance?

A

No / insufficient production of ADH

No detection of ADH (mutant ADH receptor)

No response to ADH sgnal (mutant aquaporin)

Excretion of large amounts of watery urine (as much as 30 litres each day)

Unremitting thirst

DIABETES INSIPIDUS

158
Q

How is volume of ECF determined by number of mosmoles in ECF?

A

2900 mosmoles in ECF= 10L of ECF

3190 mosmoles in ECF= 11L of ECF

2610 mosmoles in ECF= 9L of ECF

BECAUSE CONCENTRATION IS 290mosm/L

159
Q

How does sodium affect body weight?

A

More sodium-> increased body weight
Lots of salt-> retain water (1L water weighs a kg)
Positive balance by osmolarity

When off a high sodium diet, go into negative balance and lose water

160
Q

How does sodium affect blood volume and pressure?

A

INCREASED DIETARY SODIUM

  • > increased osmolarity (body can’t let this happen)
  • > increased ECF volume
  • > increased blood volume and pressure

DECREASED DIETARY SODIUM

  • > decreased osmolarity (body can’t let this happen)
  • > decreased ECF volume
  • > decreased blood volume and pressure
161
Q

Where is sodium reabsorbed?

A

PCT= 65%

LOH (ascending limb)= 25% of filtered load (MORE THAN THE WATER REABSORBED IN ASCENDING LIMB-> HYPEROSMOTIC INTERSTITIAL FLUID)

DCT= 8%

Collecting ducts- up to 2%

162
Q

What happens to sodium reabsorption in GFR is altered?

A

Increased GFR-> increased Na reabsorption

Decreased GFR-> decreased Na reabsorption

163
Q

How can sodium excretion be reduced?

A

When there are big changes to make (i.e. not so constant so not just fine tuning)

Reduce sodium excretion by not putting Na into tubular system
Keep more in blood

So reduce GFR by increased sympathetic activity

  • Vasoconstriction of kidney tubular blood vessels (predominantly afferent arteriole, because more than efferent-> reduced GFR)
  • Increase activity of Na uptake mechanisms in PCT
  • Stimulates juxtaglomerulus apparatus to release renin and produce angiotensin II
164
Q

How does angiotensin II reduce sodium excretion?

A

STIMULATED WHEN:
- Sympathetic activity stimulates juxtaglomerular apparatus -> renin-> …angiotensin II
Low tubular sodium-> stimulates juxtaglomerular cells -> renin-> …angiotensin II

ACTIONS:
PCT= stimulates Na reabsorption

DCT and collecting duct= stimulates production of aldosterone to stimulate Na reabsorption

165
Q

How does ANP have the opposite effect of angiotensin II?

A

Atrial naturietic peptide
Small peptide made in the atria (also make BNP)
Released in response to atrial stretch (i.e. high blood pressure)

Dilates blood vessels

PCT= reduces Na reabsorption
JGA= reduces stimulation
DCT and collecting duct= reduces Na reabsorption

Vasodilatation of renal (and other systemic) blood vessels
Inhibition of Na reabsorption in proximal tubule and in the collecting ducts
Inhibits release of renin and aldosterone
Reduces blood pressure

166
Q

What are the cellular components of the juxtaglomerulus apparatus?

A

Macula densa cells (Na+ concentration sensor)- secretes ATP

Granular cells (responds to PNS and SNS changes in tone)- secretes renin

Mesangial cells (produce EPO)

167
Q

How does the structure of the JGA look?

A

Afferent and efferent arteriole are over-laid by the macular densa which are cells of the distal tubule

JGA apparatus is just outside renal corpuscle

168
Q

How does the renin-angiotensin-aldosterone system increase blood pressure?

A

Changes in perfusion sensed by granular cells

Renin (enzyme, granular cells) released from granular cells, converting angiotensinogen (inactive peptide, liver) to angiotensin I (no intrinsic activity)

ACE (lungs) converts Ang-I -> Ang-II (active peptide, end function to increase BP)

Ang-II works on AT1/2 receptors:

  • AT1 = systemic constriction (increase BP); efferent arteriole (increase GFR); PCT Na/H exchange; ADH release; Aldosterone release
  • AT2 = vasodilation, NO release and reduced proliferation

ACTIONS OF ANGIOTENSIN II

169
Q

Where are renin and angiotensinogen released?

A

Renin released from JGA of kidney

Angiotensinogen released by liver

170
Q

What does angiotensin II affect?

A

VASOCONSTRICTION
Vascular system-> vasoconstriction-> increased BP
- In kidney= vasoconstriction in efferent arteriole (AT1 Rs)

ALDOSTERONE
Adrenal gland-> aldosterone synthesis
- Ang-II stimulates aldosterone release (zona glomerulosa, adrenals) (AT1 receptors)
- Aldosterone binds to MR in kidneys

SODIUM
Proximal tubule-> increased Na uptake-> increased water reabsorption-> increased ECF-> increased BP
- Aldosterone increases sodium retention -> water retention-> increased blood volume-> increased BP
- Stimulates epithelial sodium channels (ENaC) at DCT
- Stimulates Na/K exchanger at basal site

ADH
Also stimulates ADH release from pituitary (-> thirst -> water retention)

171
Q

What is aldosterone?

A

Steroid hormone

Synthesised and released from the adrenal cortex

Released in response to Angiotensin ll

  • Decrease in blood pressure (via baroreceptors)
  • Decreased osmolarity of ultrafiltrate
STIMULATES
Stimulates:
Increased Na reabsorption (controls reabsorption of 35g Na/day)
Increased K secretion
Increased hydrogen ion secretion

ALDOSTERONE EXCESS
Leads to hyokalaemic alkalosis

172
Q

How does aldosterone work?

A

Steroid hormones enter cells and binds to steroid hormone receptors which sit in the cytoplasm (bound to inhibitor protein which is released upon binding)

Steroid hormone receptor dimerises and translocates into the nucleus and drives transcription

Aldosterone

  • Increases expression of Na/K/ATPase-> increased expression of Na channel on apical side
  • Activates transport machinery expression so channels are located appropriately
  • Increases expression of regulators

So more Na reabsorbed (can pump more out and bring more in)

173
Q

What are the diseases of aldosterone secretion?

A

Hypoaldosteronism:

Hyperaldosteronism:

Liddle’s Syndrome

174
Q

What is hypoaldosteronism?

A

Reabsorption of sodium in the distal nephron is reduced
Increased urinary loss of sodium
ECF volume falls
Increased renin, Ang II and ADH

ECF falling and increased RAAS-> dizziness, low BP, salt craving, palpitations

175
Q

What is hyperaldosteronism?

A 
Reabsorption of sodium in the distal nephron is increased
Reduced urinary loss of sodium
ECF volume increases (hypertension)
Reduced renin, Ang II and ADH
Increased ANP and BNP

High BP, muscle weakness, polyuria, thirst

176
Q

What is Liddle’s syndrome?

A

An inherited disease of high blood pressure

Mutation in the aldosterone activated sodium channel

  • > Channel is always ‘on
  • > Results in sodium retention, leading to hypertension
177
Q

Where are baroreceptors in the low pressure and high pressure sides of the system?

A

LOW
Heart= atria, right ventricle
Vascular system= pulmonary vasculature

HIGH
Vascular system= carotid sinus, aortic arch, juxtaglomerular apparatus

178
Q

What is the effect of increased/decreased ECF volume and BP?

A

Baroreceptor activity
Low pressure= volume expansion
High pressure= volume contraction

LOW PRESSURE SIDE
Low pressure-> signal through afferent fibres to brainstem-> sympathetic activity and ADH release

High pressure-> atrial stretch-> ANP, BNP released

HIGH PRESSURE SIDE
Low pressure-> signal through afferent fibres to brainstem-> sympathetic activity and ADH release
OR
Low pressure-> JGA cells-> renin released

REDUCING ECF VOLUME REDUCES BLOOD PRESSURE

179
Q

What effects does reducing Na reabsorption have on Na levels, ECF volume and BP?

A

Reducing Na+ reabsorption reduces total Na+ levels, ECF volume and BP

180
Q

Why do ACE inhibitors lower blood pressure?

A

Prevent angiotensin I-> II

Angiotensin II increases blood pressure (e.g. through vasoconstriction and Na reabsorption)

181
Q

List diuretic drugs

A

Osmotic Diuretics: glucose (as in diabetes mellitus) also mannitol

Carbonic anhydrase inhibitors
(Carbonic anhydrase activity-> Na reabsorption and increased urinary acidity)

Loop Diuretics: furosemide (blocks triple co-transporter) (on ascending LOH)

Thiazides: block Na/Cl co-transport (on DCT)

K+ sparing diuretics:

  • Amiloride- block Na channels
  • Spironolactone- aldosterone antagonist
182
Q

Why does potassium need to be regulated?

A

Potassium is the main intracellular ion (150 mmol/l), extracellular [K+] = 3-5 mmol/l

Extracellular K+ has effects on excitable membranes (of nerve and muscle)

High K+-> depolarises membranes - APs, heart arrhythmias.
Low K+ -> heart arrhythmias (asystole)

183
Q

How is potassium regulated by the kidneys?

A

Potassium handling is under influence of aldosterone

Regulated by the kidney

Regulation is a balance between loss and intake

  • Intake (RDA) = 80 mmol
  • Loss – through colonic fluid, sweat and urine

Potassium reabsorption occurs mainly in pct
Na/K ATPase (principle cells) maintains high [K+] by K+ diffusing out from the lumen

Urinary losses of potassium are dependent on:

  • Availability of Na
  • Amount of H and K in distal tubule
  • Aldosterone

K+ is secreted in the medullary connecting duct by intercalated cells

  • Dependent on active Na reabsorption in principle cells and H+ concentration
  • K+ is linked with H+
Potassium depletion results in
K shift to ECF
- Extracellular alkalosis
- Acidic urine 
- High plasma bicarbonate
184
Q

Where is potassium reabsorbed in the kidneys?

A

30% in descending limb of LOH
10% in DCT

Variable urine output 1-80%

185
Q

What is potassium secretion stimulated by?

A

Increased plasma K concentration
Increased aldosterone
Increased tubular flow rate
Increased plasma pH

186
Q

What are the disorders of potassium handling?

A

Hypokalaemia

Hyperkalaemia

187
Q

What is hypokalaemia?

A

Loss of body [K+] – GI (vomiting, diarrhoea, surgical fistula) and kidney (diuretics, renal disease, Cushing’s, increased aldosterone)

There is a shift of K+ from ECF into cells
-> Primary alkalosis
(H+ leaves cells to correct this therefore K+ shifts in exchange)
Insulin – drives glucose in and K+ out

Symptoms of low K
Tetany
Weakness
ECG changes (ST depression, flat T wave, arrythmia)

188
Q

What is hyperkalaemia?

A

False hyperkalaemia
- Common due to incorrect sampling, haemolysis, lab error, familiar pseudohyperkalaemia (rare)

True hyperkalaemia
Due to:
- Increased intake
- Renal disease
- Inhibition of Na transport
- Metabolic acidosis (K/H exchange)
- Cellular damage
- Insulin deficiency
- Drugs
  • Increased body [K+]
  • There is a shift from cells to ECF
189
Q

What is hyponatraemia?

A

Low EC [Na+]

Usually caused by water overload

Causes of sodium loss

  • Vomiting/Diarrhoea
  • GI fistula
  • Burns
  • Kidney tubule dysfunction

Results in over-hydration

190
Q

What is hypernatraemia?

A

High EC [Na+]

Usually caused by water deficit

Causes of sodium excess

  • Inappropriate aldosterone
  • Endocrine syndromes
  • Organ failures
  • Results in dehydration
191
Q

Summarise sodium reabsorption

A 
PCT
Reabsorption controlled by:
- Semipermeable membrane 
- Mitochondria 
- Brush border 
- Ion pumps

Tight junctions prevent the passage of cations

Transporters

  • Na/K ATPase
  • ENaC
  • Na/H Transporter
  • Co-transport
  • Osmotic gradient

LOOP OF HENLE
Sodium is absorbed via a co-transporter NKCC2

DCT
Transport is via
- Basolateral Na/K pump
- NCC

Regulation is mainly via aldoesterone

Non-aldosterone regulation

  • Changes to GFR (low GFR, increases Na abs)
  • Changes to RBF (low flow increases reabs)
  • Changes to oncotic pressure

COLLECTING DUCT
Principle cells of the collecting ducts contain ENa

Aldosterone binds to MR which upregulates ENa

192
Q

What diseases are caused by an inability to secrete excess water?

A

SIADH – syndrome of inappropriate ADH secretion

Polydipsia – inappropriate ingestion of water

193
Q

What diseases are caused by renal salt retention with secondary water retention?

A

Renal failure
Heart failure
Liver failure

194
Q

Acid base homeostasis: What happens when there is a change in lung function (HYPERVENTILATION)?

A

Change in lung volume

  • Increased ventilation
  • CO2 ‘blown off’
  • Increased pH (and decreased H+)

RESPIRATORY ALKALOSIS

Compensatory change in renal function

  • H+ gain and HCO3 loss
  • Decreased pH (and increased H+)
195
Q

Acid base homeostasis: What happens when there is a change in lung function (HYPOVENTILATION)?

A

Change in lung volume

  • Decreased ventilation
  • CO2 retention
  • Decreased pH (and increased H+)

RESPIRATORY ACIDOSIS

Compensatory change in renal function

  • H+ loss and HCO3 gain
  • Increased pH (and decreased H+)
196
Q

Acid base homeostasis: What happens when there is a change in GI/renal (metabolic) function (PROTON GAIN)?

A

Change in GI/renal function

  • H+ gain and HCO3 loss
  • Decreased pH (and increased H+)

METABOLIC ACIDOSIS

Compensatory change in lung function

  • Increased ventilation
  • CO2 ‘blown off’
  • Increased pH (and decreased H+)
197
Q

Acid base homeostasis: What happens when there is a change in GI/renal (metabolic) function (PROTON LOSS)?

A

Change in GI/renal function

  • H+ loss and HCO3 gain
  • Increased pH (and decreased H+)

METABOLIC ALKALOSIS

Compensatory change in lung function

  • Decreased ventilation
  • CO2 retention
  • Decreased pH (and increased H+)
198
Q

What is the normal blood pH?

A

7.35-7.45

Tightly regulated

199
Q

What is the normal urine pH?

A

7-7.75
Large range because it is the pH regulator (controlling pH)

Buffer takes hours/days depending on extent of disturbance

200
Q

How much volatile acid is excreted by the lungs?

A

99%

13000 mmols/d

201
Q

How much non-volatile acid is excreted by the kidneys?

A

1%

100 mmols/d

202
Q

What is the concentration of H+ in plasma?

A

40nmol/L

203
Q

What is the normal arterial bicarbonate?

A

22-26 mEg/L

204
Q

What must happen to acids in the body?

A

Buffered, transported away from cells and eliminated from the body

205
Q

What are the most important buffers?

A

Phosphate

  • Important renal tubular buffer
  • HPO4- + H+ H2PO4

Ammonia

  • Important renal tubular buffer
  • NH3 + H+ NH4-

Proteins

  • Important intracellular and plasma buffers
  • H+ Hb HHb

Bicarbonate

  • Most important extracellular buffer
  • Important renal tubular buffer
  • H2O + CO2 H2CO3 H+ + HCO3
206
Q

How does renal buffering occur?

A

The renal buffer system uses bicarbonate, phosphate and ammonium

In the kidneys, the bicarbonate buffer may increase plasma pH in three ways

  • Secrete H+
  • “Reabsorb” bicarbonate
  • Produce new bicarbonate

H+ secretion occurs mostly in the proximal tubule by the carbonic anhydrase reaction

In acidic conditions, CO2 diffuses inside tubular cells and is converted to carbonic acid-> dissociates to yield a H+ which is secreted into the lumen by the Na+/H+ shuttle

207
Q

What is alkalosis?

A

Arterial blood pH rises above 7.45

208
Q

What is acidosis?

A

Arterial blood pH drops below 7.35

209
Q

How does compensation happen?

A

Lungs (only if not a respiratory cause)

  • Low pH-> more ventilation
  • High ph-> less ventilation (to trap CO2)

Kidneys

  • Low pH-> intercalated cells secrete more acid into tubular lumen and make NEW bicarbonate (more base)
  • High pH-> PCTs don’t reabsorb filtered bicarbonate (base) and eliminate it from body
210
Q

What causes metabolic acidosis?

A

Bicarbonate levels below normal (22 mEq/L)

Diarrhea (loss of intestinal bicarbonate)
Ingestion, infusion or production of more acids (alcohol)
Salicylate overdose (aspirin)
Accumulation of lactic acid in severe Diabetic ketoacidosis
Starvation

211
Q

What causes metabolic alkalosis?

A

Bicarbonate levels higher than normal (26 mEq/L)

Excessive loss of acids due to loss of gastric juice during vomiting
Excessive bases due to ingestion, infusion, or renal reabsorption of bases
Intake of stomach antacids
Diuretic abuse (loss of H+ ions)
Severe potassium depletion
Steroid therapy

212
Q

What is the pneumonic ROME?

A

R – Respiratory
O – Opposite
M - Metabolic
E – Equal

If your CO2 opposes the pH -> Respiratory
If your HCO3- follows the pH -> Metabolic

213
Q

What is bicarbonate?

A

HCO3- is an important
high capacity chemical buffer

Can respond rapidly to changes in metabolic acid
Can be produced from volatile respiratory acid

214
Q

Where is bicarbonate reabsorbed?

A

PCT= 80%
Ascending limb= 10%
DCT= 6%
Collecting duct= 4%

215
Q

How can you apply the Henderson-Hasselback equation to acid-base regulation?

A

pH=pK+ log10 ([HCO3]/[CO2])
pH= 6.1 + log10 (24mmol/L / 1.2mmol/L)

pH= 7.4

216
Q

How is HCO3- reabsorbed?

A

In the cuboidal epithelial cells of the PCT
From filtrate into the interstitium (to go back into the blood)
Almost 100% bicarbonate reabsorbed

Bicarbonate can’t fuse across into cuboidal epithelial cells and no specific transporters

Protons pumped (requires ATP) from in cell to filtrate

Proton will combine with bicarbonate in presence of carbonic anhydrase (CA)-> CO2 and H2O

CO2 and H2O enter cell (diffuse across membrane) and then form H+ and bicarbonate (with CA) which will then dissociate inside the cell

HCO3 transported into interstitium via:

  • Chloride bicarbonate exchanger (HCO3 into capillary, Cl- into cell)
  • Sodium bicarbonate co-transporter (3HCO3 into capillary, Na+ also into capillary)
  • Na/K/ATPase (3Na into capillary, 2K into cell)-> important for co-transporter
217
Q

What is the difference between an acid-secreting cell and a bicarbonate secreting cell of the collecting duct?

A

Intercalating cells of collecting duct

ACID-SECRETING (want to save bicarbonate)

  • H+/ATPase and H/K/ATPase-> protons into filtrate
  • H+ and HCO3- bind (with CA)- H2O and CO2
  • H2O and CO2 with CA-> HCO3- and H+ in cell
  • Chloride bicarbonate exchanger (AE1)-> HCO3- into interstitium and Cl- into cell (usually brings water with it)

BICARBONATE SECRETING

  • H2O and CO2 with CA-> HCO3- and H+ in cell
  • HCO3 goes to apical border to chloride bicarbonate exchanger (HCO3- into filtrate, Cl- into cell)
  • H+ goes to interstitium side (H+ into intersitium with H+ ATPase)
218
Q

How is HCO3- generated by cells in the PCT?

A
  • H2O and CO2 with CA-> HCO3- and H+ in cell
  • H goes to H+/ATPase -> protons into filtrate
  • H+ + HPO4^2 (phosphate in filtrate)
  • HCO3 goes to basal border to chloride bicarbonate exchanger (HCO3- into interstitium, Cl- into cell)

Deamination of glutamine-> 2NH4+ and 2HCO3

  • HCO3 goes to basal border to chloride bicarbonate exchanger (HCO3- into interstitium, Cl- into cell)
  • 3Na+ out (into interstitium) and 2K+ into cell
  • NH4+ goes out cell into apical border (filtrate side) (anti-porter with Na, Na enters cell from filtrate)
  • Glu and Na+ into cell at apical border from filtrate (SGLT-1)

Interested in saving glucose

LSS 2- Life Support System 2 (3 decks)

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