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Unit 8 > Renal physiology Lecture > Flashcards

Renal physiology Lecture Flashcards

1
Q

What is paracellular transport?

A

Transport between cells (through the gaps between cells) does not pass into the cytoplasm of any cells

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2
Q

Roughly what percentage of circulating blood goes to the kidneys?

A

25%

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3
Q

What section of the kidney are the nephrons found?

A

THe renal pyramids

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4
Q

How does osmolality related to water potential?

A

As the osmolality increases (more solute per solvent) the water potential decreases

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5
Q

What is the term for the blood vessek that surrounds the loop of Henle what does it originate from?

A

The vasa recta
Branch from the efferent arteriole.
VAsa recta wil branch into peritubular vessels

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6
Q

What are the three categories that renal function can be seperated into?

A

Homoeostatic function - BP, urine output, salt and water balance (osmolality)
Hormonal influence - renin, EPO, vitamin D
Protein catabolism and gluconeogenesis

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7
Q

Why did the kidney develop evolutionary?

A

Transition from water to land
As a mechansim to conserve salt and water

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8
Q

What is important to remember about the rate of filtration and reabsorption in the nephron?

A

Almost all of the content that is filtered out of the blood in the glomerula filtrate is reasborbed - particularly glucose, water and bicarbonate
Only 50% of urea is absorbed

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9
Q

What is the basic function of the glomerulus?

A

Filtration

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10
Q

What is the basic function of the proximal convoluted tubulule?

A

Reabsorbs the majority of NaCl and water
Reabsorbs HCO3-
Produces NH3
Secrete organinc anions and cations
Rebsorbs most of the filtrate - ions, urea, glucose and aminio acids

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11
Q

What is the basic role of the loop of henle?

A

Maintain the countercurrent multiplier
Reabsorbs some NaCL
Activate the regulation of magnesium excretion

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12
Q

What is the basic role of the distal convoluted tubule?

A

Small amount of NaCL reabsorded
Active regulation of Calcium ion excretion

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13
Q

What is the basic role of the connecting segment and the cortical collecting duct?

A

Aldosterone mediated potassium excretion
H+ ion secretion
Potassium reabsorption
ADH mediated water reabsorption

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14
Q

What is the basic role of the medullary collecting duct?

A

Potassium absorption or secretion
Final NaCL reabsorptions
ADH mediated water and urea reabsoprtion
H+ and NH3 secretion

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15
Q

What forces control filtration rate in the glomerulus?

A

Starling forces - oncotic and hydrostatic

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16
Q

What is important to remember about the arterioles that supply and drain the glomerulus?

A

Supplied by the afferent arteriole
Drained by the efferent arteriole
These are able to constrict and dilate independently of each other due to external and internal factors.
This allows them to influence glomerular flow and pressure hence filtration

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17
Q

What has a larger diameter the afferent or efferent arteriole of the glomerulus?
Why is this important?

A

The afferent has a larger diameter
This means the diamater of the blood vessel decreases in the glomerulus, this will increase the pressure of the vessel aiding ultrafiltration

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18
Q

What forces drives movement of fluid through the nephron?

A

The pressure within the bowmans space (continuous with the urinary space in the rest of the nephron)

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19
Q

How do the afferent and efferent arteriole protect the kidney?

A

Control the volume and pressure of blood flow in the glomerulus
Hence can maintain the glomerular filtration rate

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20
Q

If the blood pressure is too low explain how the afferent and efferent arteriole will respond in the glomerulus?

A

The afferent would dilate to increase blood flow
The efferent would constrict to maintain flow and pressure within the glomerulus

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21
Q

How does renal blood flow relate to systemic blood pressure?

A

Blood pressure within a normal range should not influence renal blood flow
This is becuase of renal autoregulation where the afferent and efferent arterioles can act indepently of systemic trends to control renal blood flow hence GFR

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22
Q

What are the intrinsic factors that can control the afferent and efferent arteriole?

A

Renal autoregulation
-arteriole myogenic mechanism
- tubuloglomerular feedback

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23
Q

What are the extrinsic factors that regulate the afferent and efferent arterioles?

A

Sympathetic vasoconstriction
Activation of RAAS

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24
Q

What is the typically system blood pressure regulation range where real autoregulation is effective?

A

90-180mmHg

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25
Q

Describe the impact of RAAS activation on the afferent and efferent arteriole?

A

RAAS = try to increase blood pressure
Causes constriction of the afferent and efferent arteriole
However the efferent is more sensitive the RAAS to constrict more, this limits the amount of blood that can leave the glomerulus so increases GFR

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26
Q

Describe the impact of ACEinhbitors and ARB on the afferent and efferent arteriole in the glomerulus?

A

Aims to decrease systemic blood flow
Causes vasodilation of the afferent and efferent arteriole
However the efferent arteriole is more sensitive to its effects so dilates more, so more blood can leave the glomerulus than is entering decreasing GFR

27
Q

What is the impact of NSAIDS on renal blood flow and the GFR?

A

NSAIDs - anti-inflammatory so cause vasconstriction
This decreases renal blood flow
The afferent arteriole will constrict more so decreases GFR

28
Q

What is the impact of CCB and alpha blockade on the renal blood flow and glomerular filtration?

A

INhibits the affects of the sympathetic nervous system
Therefore promotes vasodilation in the periphery
More vasodilation in the afferent arteriole so increases renal blood flow and increases GFR.

29
Q

Give a detailed description of the RAAS system in relation to the kidney?

A

Decreased blood pressure means there is decreased renal perfusion
This is detected by the juxtaglomerulus cells which releases renin.
Angiotensinogen is released from the liver
Angiotensinogen is converted to angiotensin 1 by renin
In the lungs angiotensin 1 is converted to angiotensin 2 by ACE enzymes
Angiotensin two will bind to AT1 and AT2 receptors
- increase sympathetic activity - decrease renal blood flow by constriction
- efferent more effected so increase GFR
-Adrenal cortex secrete aldoesterone to increase Na+ (ion) reabsorption and water retention
Pituitary gland will secrete ADH to increase water reabsoprtion.

30
Q

What is the mechanism of tubuloglomerular feedback?

A

Decreased sodium delivery to the macular densa - due to low BP
Causes RAAS activation by the release of renin from juxtalomerular cells
Increase blood flow to the afferent arteriole
Vasconstriction of efferent arteriole
This increases intraglomerular hydrostatic pressure
This will increase sodium and water reabsorption downstream

31
Q

What are the layers of the glomerular filter?

A

Podocytes of the visceral layer of the bowmans capusle
Fused basmenet membranes of the endothelial cells and visceral bowmans capsule
Fenestrated capillary endothelial cells

Mesangium - filter tissue that anchors the above structures in space (is not a layer itself)

32
Q

Explain what substances can and can’t undergo glomerular filtration.

A

Water is freely filtered
Small charged particles are freelt filtered (ions and glucose)
Large particles are not filtered e.g red blood cells and protein
Minimal filtration of negatively charged particles e.g albumin as repelled by barrier

33
Q

What happens if intraglomerular pressure is too high?

A

The glomerular filter will breakdwon
Leaking of large molecules into the filtrate across the barrier causing haematuria and proteinuria

34
Q

What happens if intraglomerular pressure is too low?

A

Not enough flow to the glomerulus
Fall in filtrate and GFR
Chronic kidney disease as nephrons die
Risk of blood poisoning if waste kept in blood for too long

35
Q

What drugs can be used to preserve the health of the glomerulus why?

A

Aim to decrease glomerular pressure
ACE inhibitors and ARB
This prevents constriction of the afferent and prevents stronger contraction of the efferent
This promotes vasodilation of the afferent and efferent leading to a lower glomerular pressure
This leads to an acute decrease in GFR but is better for a long term preservation of GFR.

36
Q

How do we measure GFR?

A

Creatinine is excreted in urine
Creatinine is a product of creatine muscle metabolism
We estimate how much creatinine that person is likley to produce based on age, gender and muscle mass
Measure the amount of creatinine in urine to estimate the GFR.

37
Q

What is the water potential of the blood like compared to the water potenial of the filtrated in the distal convoluted tubule?

A

The same

38
Q

What porpotion of reabsorbtion occurs in the PCT?

A

60% of filtrate
90-100% of glucose and amino acids

39
Q

How is glucose reabsorbed in the PCT?

A

By co-transport with sodium
Secondary active transport - Na+ conc gradient maintained by Na+K+ pump in basolateral membrane
Sodium diffuses in and carries glucose with it
In early PCT occurs by SGLT2 sodium glucose cotransporter the out of apical membrane by GLUT2
In distal PCT occurs by SGLT1 sodium glucose cotransporter then out of apical membrane by GLUT1

40
Q

How does the function of SGLT1 anf SGLT2 vary in the PCT?

A

SGLT2 - more active in the proximal PCT, has a low affinity but a high capacity for glucose, transports the majority
SGLT1 - more active in the distal PCT, has a higher affinity for glucose, picks up the smaller remaining amounts of glucose.

41
Q

What would the effects of an SGLT2 inhibitor be on urine volume and content?

A

INhibits glucose reabosprtion
More glucose and sodium would be present in the urine
Hence less water would be absorbed
So larger volumes of urine, will decrease BP

42
Q

Explain the link between glycosuria and diuresis and diabetes?

A

Blood glucose levels are higher
Glucose freeely filtered into glomerulus filtrate - high conc than normal
SGLT1/2 are fully saturated
More glucose in urine
Osmotically active so reduces water reabsorption
Leading to increased urine production

43
Q

What does diuresis mean?

A

Increased urine production

44
Q

What are some of the symptoms of diabetes?

A

Frequent urinatino
Blurry vision
increased hunger
Pins and needles in the feet
weight loss
Extreme fatigue
Excessive thirst

45
Q

How is water reabsorbed in the PCT?

A

Follows movement of solutes
Glucose and sodium have been reaborbed into interstitium
Decreases water potential
Water moves by osmosis from the filtrate to the cyotplasm of PCT epithelial cells in the instertitium into blood down a wp gradient
Aided by high oncotic pressure in peritubular capillaries from RBCs and protein unable to be filtered out

46
Q

How is bicarbonate reabsorobed in the PCT?

A

Enters the cell from the apical lumen in the form of H+ and CO2, this may be by a sodium hydrogen antiporter
Then within cell reacts with water to form bicarbonate
Leaves the cell
Bicarbonate chloride antiporter

47
Q

Where are the macula dense cells located?

A

At the start of the distal convoluted tubule
Just after the end of the loop of henle

48
Q

How does abosrption of salt and water different in the PCT and DCT?

A

DCT no water
DCT lower amounts NaCl - remaining only

49
Q

How is salt (ions) reabsorbed in the loop of henle?

A

In the thick ascending limb
NKCC2 actively transports one Na+, one K+ and two Cl- into lumen.
K+ is recycled back into lumen by ROMK channel
Cl- exits basolateral membrane to channel protein
Na+ is activly transported into interstitum by sodium potassium pump
Cytoplasm of cell is more negativly charged than the lumen of the DCT, this causes positivly charged ions to leave the lumen and enter the intersitium by paracellular transport down a chemical gradient

50
Q

What is the purpose of the counter-current mechanism in the loop of Henle?

A

Creates a higher concentration of sodium deeper in the medullar
thin limb - more dilute
Thick limb - more concentration
Continuously more Na+ is pumped out of thick limb as replaced by filtrate from thin limb - concentration in medullar increases/is maintained.

51
Q

What drugs can be used in the loop of henle?

A

Loop diuretics - furosemide and bumetanide
INhibits NKCC2 to stop salt reabsorption
Increases osmolality of filtrate so less water being reabsorbed
Increases volume of urine and contains more ions.

52
Q

What is the role of the distal convoluted tubule in water reabsorption?

A

There is no water reabsorption in the DCT

53
Q

How and what is reabsorbed in the DCT?

A

NCCT - active transport of Na+ and Cl- into cytoplasm
Na+/H+ exchanger - Na+ in and H+ out
Cl- HCO3- exchanger - Cl- in and HCO3 out
H+ and HCO3- can react to form H2O and CO2
PTH causes reabsorption of vitamin D

54
Q

How does the concentration of the filtrate change along the DCT?

A

Is impermeable to water and salt is absorbed so becomes more dilute

55
Q

What are the two anatomical division of the collecting ducts?

A

Cortical collecting ducts
Medullary collecting ducts

56
Q

What key exchange happens in the collecting duct?

A

At the apical membrane Na+ are absorbed from the filtrate and K+ are secreted into the filtrate.
At the basal membrane sodium potassium pump - Na+ out and K+ in.
Urea is reabsorped by UT-A1 and UT-A£

57
Q

What hormones influence the collecting duct?

A

Aldosterone and ADH

58
Q

What cells regulate acid and base handling in the collecting ducts?

A

Intercalated cells

59
Q

How is water reabsorbed in the collecting ducts?

A

Tubular (lumen) side is originally impermeable to water
Permeability is increased by ADH influencing aquaporins to be inserted into the tubular membrane
Basolateral surface in permeable to water so is able to move into interstitum by osmosis
The osmotic gradient is set up by the counter current multiplier in the loop of henle.

60
Q

What does aldosterone effect in realtion to the colllecting duct?

A

Increases sodium hence water reabsorption by ENaC (epithelial Sodium Channels).

61
Q

What are the consequences is ENaC are over expressed?

A

Increased reabsorption of sodium into blood
Increased water absorption down a water potential gradient
Increases action of sodium potassium pump leading to hypokalemia
Increased blood pressure
Autosomal dominanat condition called Liddle syndrome

62
Q

What drugs can be used to inhibits ENaCs in the collecting ducts?
What are the consequences of this?

A

Mineralcorticoids antagonist (MRAs) e.g spironolactone
Reduce sodium absorption
Decrease K+ secretion
Low blood pressure and hyperkalemia

63
Q

What are the two types of diabetes insipidus and how are they different?

A

Both cause the body to make too much urine
Nephrogenic - ADH does not respond to V2 receptors
Cranial - not enough ADH is produced
Both lead to decreased aquaporins in the basolateral membrane of the collecting ducts.

Unit 8 (22 decks)

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