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HDT 2.1 > renal physiology > Flashcards

renal physiology Flashcards

1
Q

Where are the kidneys located?

A
  • located retroperitoneally in the flanks or mid-back region.
    -under the lower part of the ribcage either side
    of the vertebral column.
    Right kidney is slightly lower due to the liver.
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2
Q

what are the major functions of the kidney?

A
  1. Filtration
  2. Production
  3. Regulation
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3
Q

how nitrogenous waste like ammonia produced and what can it be converted into?

A

produced from protein catabolism
- it is toxic and soluble in water

can be converted to urea which is due to amino acids being broken down
can also be converted to uric acid and this is due to nucleotides being broken down

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4
Q

how can you detect the kidneys are not working?

A

if the serum creatinine is too high

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5
Q

what is the kidney involved in the production of?

A
  • renin
  • prostoglandins
  • vitamin D
  • erythropoietin - EPO
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6
Q

what is renin?

A

an enzyme produced by juxtaglomerular cells that allow BP to be maintained

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7
Q

how do the kidneys regulate the body fluid?

A

they have help from the adrenal glands; aldosterone release and the brain which releases ADH

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8
Q

how much of the body volume is water?

A

around 40-45L is H2O

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9
Q

what does kidney do if there’s too much or too little water in the body?

A

if there’s too much H2O -> remove the water; dilute urine
- this also means that sodium ion levels will increase

if there’s too little H2O -> conserve the water; concentrated urine

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10
Q

what’s the normal osmolality of the body?

A

285 mOsm/kg H2O

can be from 275-295

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11
Q

what are cells usually surrounded by?

A

interstitial fluid

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12
Q

what is meant by hypotonic and hypertonic?

A

hypotonic is when there is more solutes inside the cell than in the EC region
hypertonic is when there is less solutes inside the cell than in the EC region

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13
Q

how do RBC act in isotonic, hypertonic and hypotonic solutions?

A

RBC in isotonic do not change volume
RBC in hypertonic solution so h2o will diffuse out causing it to shrivel
RBC in hypotonic solution will swell as h2o will diffuse into them

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14
Q

how is exchange and mixing of body fluids regulated?

A

by the hydrostatic and osmotic pressure

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15
Q

what are starlings forces and what do they do?

A

allows h2o and electrolytes to freely move across the capillaries and the IF
occurs by diffusion
the changes in hydrostatic pressure leads to fluid movement across the capillaries

(mmHg)

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16
Q

what is meant by oncotic and hydrostatic pressure?

A

hydrostatic pressure is the pressure of fluids against their barrier. plasma in capillaries have a +ve pressure while IF usually have -ve IF
- from the pumping of the heart

oncotic pressure is the pressure created by the presence of solutes. as capillaries are not plasma protein permeable there is a higher conc of solutes in the plasma than the IF creating the gradient
- from plasma proteins

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17
Q

how is asymmetric distribution of K+ and Na+ maintained across plasma membrane?

A

this is due to the Na+K+ATPase in the plasma membrane which removes Na+ in exchange for the K+

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18
Q

what does the nephron contain?

A

the glomerular capsules, the glomerulus, the collecting ducts, the proximal and distal tubule, the loop of henle

collecting duct opens into ureter
nephrons are closed at proximal end and open at the distal end

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19
Q

what enters and leaves the nephron?

A

the fluid called filtrate will enter the nephron and uric will flow out of the other
this fluid is modified by cells that line the nephron

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20
Q

what is stage 1 of glomerular filtration?

A

this is the urine formation

  1. blood enters glomerulus and sit inside the Bowmans capsule
  2. Plasma will filter out of the capillaries in glomerulus into the Bowmans capsule
  3. blood cells and protein do not pass but any other molecule does
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21
Q

what are the three layers plasma passes through in the filtration barrier?

A
  1. endothelial cells; they line the capillaries; have large pores to let fluid enter; has high hydrostatic pressure so lot plasma can be forced through pores
  2. basement membrane; is very thick and excludes proteins due to size and -ve charge; it has -ve charged proteoglycans on it
  3. podocytes; epithelial cells of bowman capsule visceral layer and cover capillaries
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22
Q

how are molecules filtered in the basement membrane?

A

large molecules are excluded due to spatial restriction.
intermediate-sized molecules are restricted due to their charge and size

+ve molecules attracted to the BM and uncharged molecules can pass through into the filtrate.
-ve charged anions are excluded
all small molecules can pass through despite charge but repulsive forces can reduce rate of movement

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23
Q

what does starling forces allow to happen?

A

this means fluid movement will occur out of capillaries into Bowmans capsule; due to hydrostatic pressure of 50mmHg and oncotic pressure of BC of 0mmHg; the wider afferent arteriole allows this

this also means fluid movement into the capillaries from BC will occur; due to hydrostatic pressure of filtrate in BC of 15mmHg and oncotic pressure of capillaries of 25mmHg; proteins draw fluid back to them causing oncotic pressure and the fluid entering the full nephron allows plasma to get pushed back into capillaries

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24
Q

why is albumin not in the filtrate?

A

it is not filtered due to its negative charge which is repelled by the basement membrane

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25
Q

what is proteinuria and what are the major causes?

A

it is when there is protein in the urine due to disruption of the filtration barrier and so protein leaks into the BC

causes:

  • diabetes mellitus; excessive plasma glucose damages filter
  • hypertension; high hydrostatic pressure damages filter
  • glomeruluonephritis; inflammatory damage due to immunological attack
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26
Q

when you have damaged kidney filters what does this mean for proteins and starling forces?

A

this means that there is a decrease in plasma proteins which lowers the plasma oncotic pressure
more fluid is coming out of arteriole vessel but proteins are unable to draw fluid back in for the venule vessels
so decreased plasma protein levels

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27
Q

what are symptoms of oedema?

A
  • bubbly or frothy urine
  • swollen around eyes
  • swollen hands or feet
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28
Q

what is the normal GFR? what is GFR?

A

should be 125ml/min or 180 L/day
this should be maintained

the glomerular filtration rate is the volume of fluid filtered from the renal capillaries into the BC during a certain period of time

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29
Q

what happens if the GFR is too high/low?

A

if the GFR is too high this means the needed substances cant be reabsorbed quickly enough and are lost in urine
if GFR is too low then everything will be absorbed included toxic or nitrogenous wastes than needed to be disposed of

GFR is dependant on hydrostatic pressure

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30
Q

What are the four basic renal processes?

A
  1. Glomerular filtration; glomerular capillaries
  2. Tubular reabsorption; PCT
  3. Tubular secretion; PCT
  4. Excretion; collecting ducts
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31
Q

what occurs in the PCT?

A

this is where most active (uses ATP) and passive (e.g. osmosis ) reabsorption takes place
has a large SA for reabsorption -> brush border on tubular cells

  • ions
  • h2o
  • glucose
  • AA and vitamins
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32
Q

what is meant by clearance and excretion?

A 
clearance = volume of blood cleared of drug over a period of time 
excretion= amount of drug excreted over period of time by kidneys
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33
Q

what does clearance depend on?

A

clearance depends on the GFR, drug structure, age, whether drug has been filtered/secreted or reabsorbed

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34
Q

how is dosage determined from clearance and GFR?

A

drugs have different clearance rates and this determines the dosage
the higher clearance = higher dosage needed to maintain the plasma conc.
low clearance- inefficient excretion
if GFR is low a lower dose is needed; drug isn’t being removed quickly so lower dose needed

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35
Q

how is PCT structured to help with kidney function?

A

it has many organelles such as mitochondria and it has a brush border
the mitochondria creates ATP to be used in AT reabsorption
the brush border allows a higher absorption capacity and increases SA of each cell

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36
Q

where is the apical side and the basolateral side?

A

apical is side of the tubule lumen containing the brush border
basolateral side is the opposite side of the PT cells

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37
Q

what pathways are there in the PCT?

A

there is transcellular pathway- through the cell across apical membrane and basolateral membrane; through interstitium and into capillaries

there is paracellular which moves across the leaky junctions in between the cells

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38
Q

how are peri-tubular capillaries structured to allow quick diffusion to occur?

A

they are porous and have low BP and so allow material to diffuse back into them

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39
Q

in the PCT what does the Na+K+ATPase channel allow?

A

it allows an ionic gradient across tubular cell membrane to be established
Na+ out of intracellular area of cell which provides driving force for Na+ reabsorption from filtrate to tubular cell and then out into blood
The Na+ entry allows other solute entry by secondary AT alongside the reabsorbed Na+

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40
Q

why is energy for Na+ reabsorption needed?

A

when Na+ is reabsorbed then the other solutes and water can be reabsorbed also
H20 can move by osmosis with Na+

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41
Q

what is the process of reabsorption of Na+ in peri-tubular capillaries?

A

there is an Na+K+ATPase channel on the basolateral membrane of PT cell.
3 Na+ will be pumped out of the tubular cell by this channel in exchange for 2 K+. the Na+, high conc., will then diffuse into blood in PTC
at the same time, high Na+ will enter tubular cells through Na+ channels and move down an electrochemical gradient to be pumped into interstitium by Na+K+ATPase channel

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42
Q

how does Na+ reabsorption allow glucose uptake to occur?

A
  1. at the Na+K+ATPase channel on basolateral
  2. membrane, Na+ is pumped out and K+ in. When Na+ moves into tubular cells down EC gradient it pulls glove with it into cell due to SGLT1 and SGLT2 co-transporter channels
  3. glucose diffuses out of basolateral membrane through GLUT2 channels while Na+ is pumped out through Na+K+ATPase
  4. glucose and Na+ reabsorbed
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43
Q

how HCO3- uptake occur with Na+ reabsorption?t

A
  1. Na+ down its EC gradient and is exchanged for H+ via a NA+/H+ anti-porter. Na+ is pumped out the Na+K+ATPase
  2. secreted H+ combines with filtered with HCO3- to give rise to water and CO2
    - > need carbonic anhydrase which is located on the apical brush border of PCT tubular cells
  3. CO2 diffuses into to cell and recombines with H20 to produce HCO3- and H+
  4. the H+ will then be removed from the cell through the Na+/H+ anti-porter and the HCO3- exits the cell into interstitium and diffuses into the blood
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44
Q

how does water reabsorption in the PCT occur?

A
  1. the paracellular route; between cells

2. transcellular route; through aquaporins in cells

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45
Q

how does H20 and solutes reabsorption occur with Na+ reabsorption?

A
  1. Na+ moves down gradient due to Na+K+ATPase and exits into interstitium (primary active)
  2. many substances are transported into tubular cell with Na+ ( secondary active; no ATP)
  3. H20 is reabsorbed by osmosis - as it follows Na+
  4. the conc. of the remaining solutes increasing in filtrates and so move down gradient by diffusion
  5. Lipids move transcellularly through interstitium into blood; passive diffusion
  6. the ions move down gradient paracellularly into capillaries; passive diffusion
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46
Q

what is the loop of henle and what occurs here?

A

this is a looped region
has a countercurrent flow
filtrate contains h20 and solutes that change in conc through the loop
ensures as much h20 is reabsorbed as possible but mainly from CD and DCT
absorbed h20 is taken up by vasa recta (blood vessels)

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47
Q

what is corticomedullary or corticopapillary osmotic gradient?

A

it is when moving from outer renal cortex -> inner renal medulla the interstitium of medullary region becomes MORE CONCENTRATED

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48
Q

what happens at the thick ascending LoH?

A
  • actively extrudes solutes into interstitium- makes filtrate hypo osmotic as solute conc. goes lower
  • interstitial osmolality increases (intersitium hyper osmotic)
  • lots of Na+K+ATPase channels on tubular cells due to removal of Na+/Cl; requires a lot of energy
  • no H20 removed as ascending loop is only permeable to solutes so H20 stays in filtrate
    there are no water pores and cells are packed tightly together
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49
Q

what is the role of the thin descending loop of henle?

A

this is when h20 is extruded from the LoH
the medullary interstitium reabsorbs h20 and then is picked up by vasa recta
not obligatory h20 reabsorption
in descending it is impermeable to solutes and only permeable to h20 so solute stays in filtrate
has aquaporins for h20 to be extruded

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50
Q

how does the cortico-medullary interstitial gradient occur?

A

the extrusion of Na+/Cl- from the ascending and the reabsorption of water from the descending creates an increasing vertical hyper osmotic gradient in the medullary interstitium
- the interstitium is very concentrated

the outer cortex is less hyper osmotic (more hypo) and so inner medulla is more hyper osmotic
this creates the corticomedullary gradient

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51
Q

why is the interstitial fluid made only 200mOsm/kg H2O more concentrated than the filtrate in ascending limb at levels?

A

this is because although there are millions of Na+K+ATPases, energy is still used to pump Na+ and Cl- out of these cells
they can only do so much

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52
Q

what is the role of the LoH as a countercurrent multiplier?

A

it creates an osmotic gradient (300-1200 mOsm) from renal cortex to medulla

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53
Q

how do Low and CD reabsorb H2O and concentrate urine?

A

the extruded Na+ and Cl- in the interstitium creates a gradient
this gradient is used to reabsorb H2O and concentrate urine

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54
Q

what is the LoH known as and why?

A

it is called the countercurrent multiplier

the countercurrent flow of the LoH enlarges the hyperosmolar medullary interstitium into a large vertical gradient

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55
Q

at the base of the LoH what is the osmolality of filtrate?

A

the filtrate osmolality increases to 1200mOsm/kg H2O

it is hyperosmostic

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56
Q

what substances can increase the medullary osmotic gradient?

A

by the extrusion of urea
the corticomedullary gradient can be made more hyper osmotic by this extrusion
the urea presence contributes hard of the osmotic gradient
it is mainly excreted through CD in urine as it is a metabolic waste product
some is absorbed in the interstitium

57
Q

what is urea recycling?

A

urea is reabsorbed passively from the inner medullary region of the CD
accumulates in medullary interstitium
when H2O is absorbed in CD, urea conc. increases so it can move out of the urea permeable areas of the nephron by diffusion

58
Q

what is the process of loop diuretics?

A
  • the Na+ and K+ channels in ascending LoH are blocked
  • this means no reabsorption of these ions and so they stay in the medullary interstitium
  • no portico-medullary gradient is produced
  • no hypertonic interstitium surrounding LoH, DCT and CDs
  • increased urine is produced for less fluid in the body
  • less Na+ reabsorption as more Na+ excretion occurs at Asc
  • decreased blood volume -> decreased BP
59
Q

where does blood supply arrive at the kidney?

A

arrives through there renal artery and then branches into some smaller arteries

60
Q

does the efferent or afferent artery have a smaller diameter and why is this important?

A

the efferent has a smaller diameter
this maintains hydrostatic pressure in the capillaries and allows plasma to be filtered in the BS
BP can be controlled by changing the diameters of the AA and EA

61
Q

what do the PTC surround?

A

they surround the renal tubules

these tubules become the vasa recta and then the renal venous system

62
Q

what do peritubular capillaries do?

A

the PTC start as EA and surround PCT

  • provides nutrients to epithelial and interstitial cells
  • the capillaries also supply the blood for reabsorption and secretion in the PCTs
63
Q

what is the vasa recta and what does it do?

A

long hairpin shaped vessels that run alongside LoH
there is descending and ascending

  • provide nutrients to the cells in this region
  • main function as countercurrent exchangers which contribute to the urine conc. by the CD to reabsorb that water
64
Q

how is the GFR regulated

A

it has an external and intrinsic mechanism

65
Q

what is the external mechanism for controlling GFR?

A

it is controlled by the CVS or the ANS

sympathetic and hormonal mechanisms

66
Q

what is the intrinsic mechanism for controlling GFR?

A

controlled by kidney
autoregulation; alters diameter of afferent/efferent arterioles = myogenic control mechanisms
also by a tubuloglomerular feedback mechanism

67
Q

what systems are activated when the BP drops?

A
  1. the CV system
  2. the renal system
  3. the neuroendocrine system
68
Q

how does the CV system respond to drop in BP?

A

the baroreceptors detect the drop and activate the SNS

69
Q

how does the renal system respond to drop in BP?

A

release of renin from JGA (juxtaglomerular apparatus)

aldosterone from adrenal cortex

70
Q

how does the neuroendocrine system respond to drop in BP?

A

release of ADH from pituitary gland

71
Q

if afferent arteriole dilates or constricts what happens to renal blood flow, GFR and hydrostatic pressure and filtration?

A

if it dilates; more blood enters capillaries so increased blood flow, GFR will increase when BP decreases and pressure and filtration increases
if it constricts; less blood enters so decreased blood flow and decreased GFR with decreased BP so decreased pressure and filtration

72
Q

if efferent arteriole dilates or constricts what happens to renal blood flow, GFR and hydrostatic pressure and filtration?

A

if the efferent dilates, blood leaves capillaries quicker and so pressure decreases; this means GFR decreases if BP increased
if the efferent constricts; blood stays in capillaries longer so increased GFR and increased pressure and filtration

73
Q

when blood pressure drops why is efferent arteriole constriction useful?

A

it causes vasoconstriction and allows hydrostatic pressure to increase causing more blood to be filtered and GFR increases
this increases blood volume and BP

74
Q

how does prostaglandins work?

A

they counteract vasoconstrictors effects on other blood vessels and dilates them
decreasing BP

75
Q

what are some prostaglandins and what are their importance and roles?

A

you have PGE2 and PGI2 - major prostanoids in the kidney

  • modulate the renal microvascular response to a drop in BP
  • prostaglandins will protect the renal hemodynamics against vasoconstrictors e.g. Ang II
  • cause vasodilation
76
Q

what is the effect of NSAIDs on PG synthesis?

A

NSAIDs can decrease renal function and insufficiency of renal blood flow for patients who have vasoconstrictor stimuli to kidney (hypertensive patients)

77
Q

why is perfusion of kidney important to regulate

A

to retain filtration function

glomerulus hydrostatic pressure is balanced by changing vascular tone of EA and AA

78
Q

what is the myogenic mechanism?

A

when the EA or AA constrict/dilate
so if BP is high the AA constrict to maintain normal GFR; ensures high BP doesn’t effect capillaries
if BP is low then the AA dilate and EA constrict to produce high glomerular pressure and maintain GFR

79
Q

what is the tubuloglomerular feedback mechanism?

A

flow-dependant mechanism
directed by macula densa cells in DCT
if GFR increases the filtrate flow increases in tubule so less time for NaCl to be reabsorbed; high conc in DCT macula densa cells which feedback to AA and EA to decrease GFR

80
Q

what are vasa recta?

A

they take reabsorbed H2O away from interstitium to maintain its hyper osmotic level
they are countercurrent loops ; blood flows slowly in opposite directions
freely permeable to solutes and water

81
Q

why are vasa recta looped?

A

prevent high conc. of solutes in the medullary interstitium being washed away
maintains portico-medullary solute gradient

82
Q

how does water and solutes move between interstitium and the descending vasa recta and why?

A

water will leave the vasa recta into the interstitium as there is a higher osmolality outside
solutes enter the vasa recta as there is lower osmolality inside
this occurs till plasma equilibrates with interstitium

83
Q

how does water and solutes move between interstitium and the ascending vasa recta and why?

A

water enters vasa recta due to higher osmolality inside
and solutes leave vasa recta due to higher osmolality outside
this occurs at each level until plasma and interstitum equilibrate

84
Q

how do solutes and water enter and leave the vasa recta?

A

solutes leave and enter by diffusion - high to low solute conc.
water enters and leaves by osmosis - low to high solute conc.

85
Q

what are the 3 main roles of the vasa recta?

A
  1. provide oxygenated blood to medullary region and take away toxins
  2. preserve the portico-medullary gradient ; prevents rapid salt removal from the interstitium
  3. remove reabsorbed H2O; water entering ascending vasa recta either from descending vasa recta or reabsorbed from descending LoH and CD
86
Q

how is vasa recta and LoH set up?

A

anti-parallel

87
Q

how is concentrated urine produced?

A

produced by reabsorbing water from :

  1. PCT - obligatory with Na+ reabsorption
  2. descending LoH
  3. DCT - need gradient and ADH
  4. CD - need gradient and ADH
88
Q

what happens to body fluids and so the urine when you drink too much water?

A

there is an increased water intake that is absorbed into the blood
body fluids become hypo-osmolar
so kidneys need to pass out more urine so large volume of dilute urine is produced; excess water can dilute the body fluids

89
Q

what happens to body fluids and so the urine when you drink too little water?

A

when you drink too little or lose fluid - your body fluids become hyper-osmolar
- insufficient water can concentrate the body fluids so kidney needs to pass out less water -> small volume of conc. urine

waste products produced dont change!!

90
Q

what occurs in the collecting duct and how?

A

final dilution or concentration of urine occurs here and
more H2O reabsorption occurs here
- fine tunes electrolyte and water conc. in urine and so the plasma

  • ADH is major factor
  • > if ADH sends message to CD, for conc urine to be produced water is reabsorbed through PTC and vasa recta
91
Q

what happens when you drink too much water?

A
  • upsets electrolyte balance
  • dilution of Na+ (hyponatremia) occurs in ECF
  • water moves into cells by osmosis ; ECF -> ICF
  • electrolyte imbalance can cause irregular heartbeat and allow fluid to enter lungs
  • pressure on brain and nerves causing alcoholic behaviours
  • causes seizures and death
92
Q

how can you help a dehydrated patient?

A

put them on a saline drip solution with high conc. of salt in it
- hypertonic saline solution

93
Q

when is ADH secreted?

A

from the pituitary gland into the blood in response to hypovolemia and plasma hyperosmolality

94
Q

when ADH is present what occurs?

A

H2O reabsorption from the CD

95
Q

how does ADH affect collecting ducts?

A

it makes the DCT and CD more water permeable
so water comes out due to gradient and is picked up by a blood vessel
ADH also makes CD making them urea permeable -> urea re-cycling as more urea can be added to medullary interstitium and increase osmotic gradient -> more h20 pulled out of CD by osmosis

96
Q

what is the urine volume and osmolality with maximal ADH?

A

urine osmolality; 1400mOsm/kg H20

urine volume; 300-400ml/day

97
Q

what is the urine volume and urine osmolality with no ADH?

A

urine osmolality; 60mOsm/kg H2O
same as filtrate osmolality before CD ; diabetes mellitus

urine volume; 25L/day
- low conc., high volume ; central diabetes insipidus
CDI- cant produce ADH so pee frequently as no reabsorption!

98
Q

what is desmopressin and what is it used for?

A
  • it reduces the volume of urine released from the kidneys
  • synthetic version of ADH ; more powerful
  • stops kidneys producing urine

too much or too much whilst drinking loads of water; water retention so:

  • > headaches and dizziness
  • > feeling bloated
  • > hyponatremia
99
Q

which organs IF compartment has varying osmolality?

A

the loop of Henle so therefore the kidney

100
Q

how does regulation of body fluid osmolality occur?

A
  1. STIMULUS - change in osmolality
  2. RECEPTOR; sensor - osmoreceptors in hypothalamus
  3. CONTROL CENTRE - ADH release from pituitary
  4. EFFECTOR - change in the water permeability of DCT and CD
101
Q

what are the hypothalamic osmoreceptors?

A

they are receptors that detect changes in plasma osmolality

  • very sensitive to changes
  • regulate release of ADH (vasopressin)
  • modulates water retention or loss - no solute effect
102
Q

what is ADH?

A

anti-diuretic hormone

  • produced by hypothalamus and stored in pituitary
  • only released into blood when plasma osmolarity increases
  • kidneys conserve h20 by stimulating passive reabsorption of water ; inserts aquaporins in CD
  • increase CD permeability to water
  • increases urine conc and so urine osmolarity
103
Q

how is plasma osmolality increase detected and what happens?

A

its detected by osmoreceptors in hypothalamus

  • causes increase in ADH release
  • ADH travels in blood to kidney
  • CD more permeable to water
  • more water reabsorbed into blood
  • decrease volume of conc. urine
  • water in blood reduces plasma osmolality
104
Q

how is decrease in plasma osmolality detected and what happens?

A

its detected by osmoreceptors in hypothalamus

  • causes decrease in ADH release
  • less ADH travels in blood to kidney
  • CD less or not permeable to water
  • less water reabsorbed into blood
  • increase volume of dilute urine
  • water in blood increases plasma osmolality
105
Q

why is drinking sea water beneficial?

A

sea water has an osmolality of 2000mOsm/kg H2O
urine osmolality can reach 1400 mOsm/kg H2O
to clear 1Kg (1L) of sea water will require:
2000/1400 = 1.4L of water to clear

drinking sea water will cause

  1. dehydration
  2. muscle cramps, dry mouth => thirst
106
Q

what happens when you ingest NaCl?

A

ingest NaCl
this increases osmolality and salt goes in ECF but this draws water out of ICF and this increases ICF osmolality
ADH release from pituitary -> increase in CD permeability to water
increase in thirst
increase in water retention
restore osmolality to 285
- osmoregulation disturbs volume!!

107
Q

how is ECV changes detected in the body?

A

detected by the baroreceptors
- baroreceptors detect pressure changes perfusing through them
ECV changes are detected by:
1. systemic arterial baroreceptors in the aortic arch and carotid sinus - send message to ANS which decides how to regulate BP
2. renal glomerular afferent arterioles baroreceptors -hence we detect out water body volume changes

108
Q

what is the juxtaglomerular apparatus?

A

made up of macula densa chemoreceptor cells and baroreceptor and renin releasing releasing JGC of the AA before it enters G

109
Q

what is RAAS?

A

renin-angiotensin-aldosterone system

  • it is a hormone-based system that aims to increase ECV
  • regulates BP and Fluid Volume
110
Q

what happens if the BP/fluid volume within AA is decreased?

A

renin will enter the blood circulation
this makes filtrate flow slower through PCT and so more time to absorb more sodium
so less sodium is in DCT which is sensed by the MD cells
they send paracrine signals to JGC cells that result in more renin release

111
Q

what role does aldosterone play when their is low fluid flow or low Na+ conc. ?

A

aldosterone stimulates Na+ uptake on the apical cell membrane in the DCT and CD

112
Q

where is Ang I converted to Ang II?

A

the renal endothelial cells

113
Q

how can you clinically inhibit the RAAS system?

A
  1. ACE inhibitors- hypertension, congestive heart failure, acute MI, cardiac failure, diabetic nephropathy
  2. Ang II receptor antagonists/blockers - treat hypertension and heart failure
  3. Aldosterone receptor antagonists - used to treat hypertension and oedema associated with heart failure
  4. Renin inhibition
114
Q

what is loss of Na+ and Cl- in urine known as?

A

natriuresis

115
Q

where are aquaporins inserted in the CD and DCT?

A

in the apical membranes of principal cells in the renal collecting ducts

116
Q

what are some sources of H+ ions?

A
  • ingested protein metabolism
  • cell metabolism ; produces CO2 which disturbed acid-bas balance
  • food products
  • medications - aspirin, warfarin, indomethacin
  • metabolic intermediate by-products
  • disease processes
117
Q

what buffer systems are there in the IC fluid, IF and blood?

A

in intracellular fluid there is phosphates which is good at accepting H+ and there’s amino acids
in interstitial fluid there’s the carbonic acid/ bicarbonate buffer system
in the blood there’s haemoglobin which accepts H+ and there’s plasma proteins and there’s H2CO3 /HCO3-

118
Q

how does the carbonic acid/bicarbonate buffer system work?

A
  • HCO3- can bind to H+ to form H2CO3 but the H2CO3 can then be dissociated into CO2 and H2O
  • this means H2CO3 and HCO3- conc can be regulated by lungs and kidneys respectively

CO2+ H2O H2CO3 H+ + HCO3-
CO2 and H2O can alter depth/rate of ventilation = alter arterial PCO2
H+ + HCO3- can allow tubular excretion or reabsorption of these ions

119
Q

what are the three defence mechanisms that buffer/prevent pH changes?

A
  1. chemical buffering - seconds
    e. g. phosphates
  2. respiratory - minutes
  3. renal - days

each compensate for each other if one doesn’t work!

120
Q

what are the 4 ways the kidney regulates acid-base disturbances?

A
  1. reabsorb HCO3- when high H+ and low pH
  2. excrete H+ when high H+ and low pH
  3. generate HCO3- when high H+ and low pH
  4. excrete HCO3- when high HCO3- and high pH
121
Q

how do kidneys deal with acidosis?

A

remove excess H+ using phosphates

remove excess H+ using ammonium

122
Q

what’s the renal phosphate buffer system

A

it generates HCO3-

  • filtered (HPO4)2- can buffer excess H+ in the filtrate
    H2PO4- is excreted in the urine
    in the process of buffering excess H+ with (HPO4)2-, new HCO3- can be generated by the renal tubules
123
Q

how does the renal ammonia buffer system?

A

it generates HCO3-
glutamine in to PCT cell is converted to ammonia which accepts H+ to become NH4+

in kidneys the NH4+ is excreted in urine
in the process of buffering excess H+ with NH3, new HCO3- can be generated by the renal tubules

124
Q

if HCO3- is lost from the body and not reabsorbed in PCT what can occur?

A

acidosis would occur as nothing is there to buffer the H+ produced from metabolic processes
blood buffering capacity is reduced

125
Q

how should you excrete lots of excess H+?

A

filtering free H+ will cause discomfort or burning when peeing and the maximum free H+ you can add is until it gives a urine of pH 4.4
to excrete the excess, you would you need to buffer it in the filtrate in the tubules and then excrete it.
first buffer it with phosphate or with ammonia produced in PCT cells
then it is put in urine as titratable acid or NH4+ \
NH3 is most effective as no need to absorb NH4+ once made so easier to get rid of in the urine

126
Q

how can acid-base imbalance/disturbances occur?

A
  1. respiratory dysfunction - change in PCO2
  2. metabolic dysfunction - change in HCO3-

therefore changes in H+ ions or pH are reflected by changes in the ratio of HCO3- to CO2

127
Q

what is respiratory acidosis?

A

the ph is lower than 7.35
the pCO2 is higher than 45mmHg

it is the accumulation of CO2 in the blood stream and increases H+/HCO3-

128
Q

what are causes of respiratory acidosis?

A

caused by:

  • respiratory patterns
  • holding CO2 in the body
  • lung problem
  • trauma to respiratory centre
  • dysfunction of respiratory muscles
  • overuse of sedatives, narcotics
129
Q

what is the renal compensatory mechanism for respiratory acidosis?

A
  • peripheral chemoreceptors will sense change in pH and change ventilation rate
  • lungs are unresponsive
  • kidneys remove excess H+ in an acidic urine and conserve HCO3-
  • generate HCO3- and blood pH increased
130
Q

what are the causes of respiratory alkalosis?

A
  • respiratory patterns - hyperventilation
  • removing CO2 from body
  • anxiety, fear, pain
  • lung problems
  • aspirin overdose/toxicity
  • over-ventilation
  • ascent to high altitude; not enough o2 so breathe deeper
131
Q

what is respiratory alkalosis?

A

it is the loss of CO2 form blood stream which decreases H+/HCO3-

132
Q

what is the renal compensation for respiratory alkalosis?

A
  • peripheral chemoreceptors detect pH change and change ventilation rate
  • so kidneys retain H+ and excrete HCO3- into uric
  • blood pH decreased closer to 7.4, down isobar and decrease HCO3- helps
  • H+ is sat unbound
133
Q

what are the causes of metabolic acidosis?

A
  • loss of HCO3- due to severe diarrhoea
  • accumulation of acid
  • renal dysfunction -> impaired H+ excretion
  • excess protein consumption
  • ingestion of an acid ; aspirin, ethanol or antifreeze
  • exercise
134
Q

what is metabolic acidosis?

A

the addition of H+ reduces HCO3-

CO2 + H2O H2CO3 decreased HCO3- + increased H+

135
Q

what is the compensatory mechanism for metabolic acidosis?

A
  • peripheral chemoreceptors sense the change in pH and lungs hyperventilate to remove CO2 from body
  • pulmonary compensation
  • this lowers HCO3- even more
  • eventually excess H+ is removed in acidic urine and conserve HCO3-
  • blood pH increased
136
Q

what are the causes of metabolic alkalosis?

A
  • loss of acid due to severe vomiting
  • gastric suction
  • use of diuretics
  • excessive alkaline drug intake - antacids
  • excessive intake of fruits
137
Q

what is metabolic alkalosis?

A

loss of H+, or gain of HCO3-) increases the HCO3-

CO2 + H2O H2CO3 increased HCO3- + decreased H+

138
Q

what is the compensatory mechanism of metabolic alkalosis?

A
  • peripheral chemoreceptors detect pH change
  • hypoventilate the drugs to retain CO2 and increase its levels; lowers pH
  • this raises HCO3-
  • eventually excess HCO3- is removed in urine
  • H+ is conserved and can be reabsorbed back into the body

HDT 2.1 (11 decks)

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