Session 2 Flashcards
Normal plasma glucose conc
2.5-5.5 mol/L
Virtually all filtered glucose is reabsorbed in the
Proximal convoluted tubule
Glucose Reabsorption by
Secondary active transport, driven by energy released from transport of sodium down its conc grad
What is Tm
Maximum tubular resorptive capacity for a solute
Limited number of Na+/glucose carriers
Why is glycosuria
When plasma glucose rises above 10mmol/L as in diabetes
Common in pregnancy as Tm for glucose falls and glucose is excreted in urine
Plasma conc of amino acids
2.5-2.5 mmol/L
Reabsorbtion and filtration of amino acids
Filter easily through glomerulus
Reabsorbed by proximal convoluted tubule by secondary active transport
Reabsorption by proximal convoluted tubule of amino acids
Symport with Na+, driven by Na+/K+ ATPase as with glucose
Tm limited process
5 different transport systems coupled with amino acid reabsorption
Sodium reabsorption in proximal convoluted tubule
Basolateral 3Na-2K-ATPase
Apical- Na H exchange, Co transport with glucose, AA, carboxyl is acids, phosphate
Aquaporin 1
Summary of proximal convoluted tubule
Reabsorption is isosmotic, responsible for bulk reabsorption of many solutes, very metabolically active, high conc of mitochondria, provide energy for Na/K ATPase
Beyond the loop of henle water permeability
Water permeability of early DCT is fairly low
Active Na+ reabsorption results in further tubular dilation- stimulated by aldosterone
Water permeability is variable depending on
ADH- low bp stimulated ADH increases water reuptake by aquaporin channels
Impaired ADH synthesis or secretion by hypothalamus can be due to
Brain injury, tumour, sarcoidosis or tuberculosis, aneurysm, encephalitis or meningitis
Not enough ADH can lead to
Not enough water reabsorbed from collecting ducts so a large quantity of urine is produced
Central diabetes insipidus - treat by ADH administration,
What is nephrogenic diabetes insipidus
Acquired insensitivity of the kidney to ADH
Water is inadequately reabsorbed from collecting ducts so a large quantity of urine is produced
Clinical management of nephrogenic diabetes insipidus
Low salt and protein diet reduces urine output
Causes of nephrogenic diabetes insipidus
Mutations in gene coding for V2 receptors, chronic pyelonephritis, Poly cystic kidneys, drugs such as lithium
What is too much ADH called
SIADH
Syndrome of inappropriate anti diuretic hormone secretion
Too much ADH released from PP gland or anther source
SIADH characterised by
Dilutional hyponatremia, plasma sodium conc lowered, total body fluid increased
2 mechanisms involved in auto regulation
Myogenic mechanism and tubuloglomerular feedback
Why is it important that the hydrostatic pressure within the glomerulus remains relatively constant
Doesn’t overload transporters
Maintains perfusion- stops kidney damage
Features of acute tubular necrosis
Reversible if quickly dealt with
Reduced oxygen and glucose getting to cells
Cells die, obstruction, back leak and tubular injury
Explain myogenic mechanism
Arterial smooth muscle responds to increases and decreases in vascular wall tension
it is a property predominant of the preglomerular resistance vessels
Myogenic mechanism at afferent arteriole
Vasoconstriction if increased BP
Prevents transmission of high BP to glomerular capillary
Maintains normal glomerular capillary pressure
Myogenic mechanism at efferent arteriole
vasoconstriction if decreased BP
Increased GFR
Tubuloglomerular feedback mechanism in high tubular flow
macula densa cells of DCT detect osmolality (rate of Na+ or Cl-)
higher flow of filtrate = higher Na+ conc in cells
Signal sent by Juxtaglomerular cells, due to increase in NaCl conc, ATP released
What happens when ATP is released in the Tubuloglomerular feedback mechanism in high bp
ATP converted to adenosine, binds with A1 receptor on afferent arteriole
Further vasoconstriction of smooth muscle of adjacent afferent arterioles, Decreased renal perfusion pressure, decreased glomerular filtration rate
Renin synthesis inhibited
Tubuloglomerular feedback mechanisms in low bp
Release of prostaglandins- stop constriction of afferent arteriole
renin released by juxtaglomerular cells
3 stimuli responsible for renin release by juxtaglomerular cells
Sympathetic nerve stimulation
Decreased stretch of afferent arteriole
Signals generated by macula densa cells in response to decreased NaCl delivery
What does systemic vasoconstriction do to renal blood flow
Reduces
What is the action of renin
Angiotensin 1 -> A2 -> Constriction of efferent arterioles -> Increased GFR
Renin key points
Enzyme that is synthesised and stored in JGA in kidneys. Fall in plasma Na+ leads to fall in ECF volume, causing release of renin
What do prostaglandins do
Acts on granular cells to release renin
things that cause release of renin
granular cells of JGA innervated by sympathetic system
Wall tension in afferent arterioles falls
Decreased Na+ to macula densa
What does Angiotensin 2 do
Directly vasoconstricts efferent arterioles within glomerulus
Released ADH
Stimulate thirst
Stimulates zona glomerulosa of adrenal cortex to release aldosterone (directly increases Na+ reabsorption from DCT)
Other factors affecting Na+ resorption in low blood pressure
Decrease in effective circulating volume= cortical prostaglandin synthesis. Occurs in kidney in cortex, medullary interstitial cells, collecting ducts epithelial cells
Results in vasodilators and renin release
A significant reduction in BP may result in
Acute tubular necrosis
What adaptation do simple columnar cells have to help with resorption
Brush border- lots of villi
What adaptation do simple cuboidal epithelial cells have which helps to distinguish them from PCT cells
A wide lumen, no brush borders
What structure is formed from the merging of the collecting ducts and acts as the gateway to the cavity known as wider calyx
Papillary ducts of Bellini- open sieve like at area cribosa
Cavity of minor calyx is lined with
Transitional epithelium
Which region of the nephron is this from and what cells are these
Proximal convoluted tubule
Brush border- simple cuboidal
Where is this and what are the cells
Descending limb of loop of henle
Simple squamous epithelial
Where is this and what cells
Ascending limb of loop of Henle
Simple cuboidal epithelial cells
Where is this and what Cells
Collecting duct
Simple cuboidal epithelial cell
Clearance =
(Urine conc x urine flow rate) / Plasma conc
Secretion=
Excretion - filtration
Filtration rate =
Plasma conc x GFR
Excretion rate =
urine conc x urine flow
Excretion =
Filtration - (reabsorption + secretion)
What can be used as GFR
Clearance rate in something like inulin where it is not secreted or absorbed
What forces control capillary movement of plasma
Hydrostatic pressure in capillary
Hydrostatic pressure in the Bowman’s capsule
Oncotic pressure difference between capillary and tubular lumen
Starlings forces
Hydrostatic pressure and colloid osmotic (oncotic) pressure due to
Water and then protein
