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HUBS192 Renal system > renal physiology > Flashcards

renal physiology Flashcards

1
Q

renal blood supply

A
  • 20-25% of cardiac output
  • 1-1.2L/min
  • high flow for filtration rather than metabolism
  • glomerulus has afferent and efferent arterioles
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2
Q

what makes up filtration barrier

A
  1. capillary endothelium (fenestrated, charged)
  2. basement membrane (3 layers, size, charge)
  3. epithelial podocyte (slit diaphragm, size, charge)
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3
Q

what determines glomerular filtration

A
  • pressure gradient between glomerular capillary and Bowman’s capsule
  • permeability of glomerular capillary
  • SA of glomerular capillary
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4
Q

effective filtration pressure

A

= (glomerular hydrostatic pressure + capsular osmotic pressure) - (glomerular osmotic pressure + capsular hydrostatic pressure)

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5
Q

main driving force for filtration

A

blood pressure in glomerular capillaries

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6
Q

forces opposing filtration

A

osmotic pressure in glomerular capillary and fluid pressure in Bowman’s capsule

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7
Q

what is renal clearance (not formula)

A

the rate at which substance S is cleared by the kidneys per unit time

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8
Q

formula for renal clearance

A

Clearance (Cs) = Us x V / Ps (in mL/min)

  • Us = concentration of S in urine (mg/L or mol/L)
  • V = volume of urine produced per unit time (mL/min or L/hour)
  • Ps = concentration of S in plasma (mg/L or mol/L)
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9
Q

what is glomerular filtration rate

A
  • GFR - amount of fluid filtered per unit time
  • Usually around 180L/day
  • tightly regulated
  • varies from person to person, declines from age 30
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10
Q

conditions for a substance to be used as a measure of GFR

A

substance must:

  • not be reabsorbed from the tubule
  • not be secreted into the tubule
  • not be metabolised
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11
Q

substances used to measure GFR

A
  1. inulin - polysaccharide not metabolised by body. Not found in body, must be injected (exogenous)
  2. creatinine - waste product produced by muscles. Already in body so most commonly used
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12
Q

filtered load

A

amount of a particular substance (solute) filtered per minute

filtered load = GFR x solute plasma conc

units are g/min or mol/min

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13
Q

reabsorption

A

movement of substance from renal tubule back into capillaries

some solutes such as glucose, Na+, Cl-, water are only reabsorbed (not secreted)

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14
Q

secretion

A

movement of substance from capillarie into renal tubule (not Bowman’s capsule)

some solutes are only secreted (not reabsorbed) e.g. drugs, organic cations, organic anions

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15
Q

secretion of p-aminohippurate

A
  • organic anion
  • represents secretion of all drugs
  • actively secreted by cascade of basolateral apical transporter
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16
Q

why are some solutes secreted and reabsorbed by renal tubule

A

some solutes e.g. K+, ammonia, H+, urea are regulated according to homeostatic requirements

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17
Q

how is reabsorption across tubular epithelium improved

A

variety of epithelial types

cells held together by TIGHT junctions

microvilli increase surface area!

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18
Q

paracellular pathway

A
  • water and solutes can move between cells without entering
  • leaky - used for bulk reabsorption
  • single barrier
  • connects tubular lumen and lateral interstitial space
  • no requirement for transport proteins, limited selectivity
  • permeability depends on ‘tightness’ of tight junction
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19
Q

transcellular pathway

A
  • water and solutes can move through cells
  • two barriers: apical (mucosal) and basolateral (serosal) membrane
  • connects tubular lumen and LIS or peritubular space
  • tighter control through membrane transport proteins, so selective and energy dependent
  • e.g. hormonal control
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20
Q

what is reabsorbed in proximal tubule

A

most reabsorption occurs here:

  • 66% sodium, water, chloride
  • all of the filtered glucose
  • all of the filtered amino acids
  • most of K+ (90%) , PO43-, Ca2+
  • 80% of the filtered HCO3-
  • half of urea
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21
Q

sodium reabsorption in kidney

A

66% in PCT

25% in TAL

5% in DCT

3% in CCT

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22
Q

reabsorption of solutes in PCT

A

driven by Na+ reabsorption:

  • Na+ moves down its concentration gradient
  • Na+/K+ ATP pump keeps conc. Na+ inside the cell low, so Na+ can move into cell
  • this creates sodium gradient on luminal side compared to inside cell
  • transport of many solutes is coupled to Na+ reabsorption via a transporter protein e.g. glucose (through SGLT1 or 2), amino acids
  • once glucose is inside cell, it can move into interstitium via facilitated diffusion through sodium independent GLUT2
  • secondary active transport
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23
Q

how much glucose is reabsorbed

A
  • at normal filtered loads all glucose reabsorbed - none in urine
  • high plasma glucose (e.g. diabetes mellitus) - filtered load exceeds re-absorptive capacity of transporters as they become saturated - glucose in urine (glucosuria)
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24
Q

movement of water

A

sodium absorption in leaky epithelium results in a huge water gradient over the epithelium, which drives trans and paracellular reabsorption of water

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25
Q

water absorption in PCT

A

has leaky epithelium so high water permeability, so paracellular and transcellular (via aquaporin 1) can take place

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26
Q

water absorption in CCT

A

has tight epithelium so has low water permeability so only transcellular absorption can take place through aquaporin 2

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27
Q

role of loop of Henle in reabsorption

A
  • descending limb (tDLH) removes water from filtrate
  • ascending limb (TAL) removes NaCl from filtrate
  • makes interstitium around tubule in medulla hyperosmotic (forms Hyperosmotic medullary gradient HOMG)
  • leaves filtrate inside tubules very dilute
  • more water needs to be reabsorbed in CD (dependent on hydration)
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28
Q

role of DCT and collecting duct

A

fine tune electrolytes, pH and water

  • reabsorb the remaining NaCl (8%) and water (up to 7%)
  • secrete K+ and H+

hormonal control

  • Na+ reabsorption/ K+ secretion by aldosterone
  • water reabsorption by ADH (anti-diuretic hormone)
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29
Q

counter-current multiplier system in loop of Henle

A

tDLH is leaky epithelium, reabsorption of 25% water, which makes urine concentrated

TAL is more tight epithelium so impermeable to water, reabsorption of 25% NaCl. This makes medulla hyperosmotic (very salty) so more water is drawn out of tDLH which makes urine more complicated

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30
Q

distribution of water in body

A

2/3 in ICF and 1/3 in ECF

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31
Q

how much of our body weight is water

A

55-60%

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32
Q

distribution of water in ECF

A

1/5 in plasma

4/5 in interstitial fluid

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33
Q

osmolarity

A

based on number of osmotically active ions (can bind water) or solutes

can be estimated by density of solutions (gravity)

145 mM of NaCl = 290 mosmol/L

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34
Q

osmolarity and tonicity prefixes

A

iso = same

hypo = lower

hyper = higher

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35
Q

tonicity

A

based on effect of a solution on cells

36
Q

osmolarity of ECF/ICF

A

275-295 mosmol/L

37
Q

where is most water lost in body

A

kidneys via urine (urine output is adjusted to maintain balance)

38
Q

water reabsorption in nephron

A

66% in PCT

25% in tDLH (leaky epithelium)

2-8% in CCT (varies based on your hydration)

0.5-7% excreted in urine

39
Q

water reabsorption in PCT

A

driven by Na+ reabsorption

facilitated by aquaporins (transcellular) and via leaky tight junctions (paracellular)

40
Q

what does changing body osmolarity cause

A

fluid shifts between ECF and ICF to equalise osmolarity

41
Q

what effect does changing water content of cells have

A

changes size

changes structure

function = impaired

42
Q

why must be regulate water

A

in order to regulate osmolarity to regulate cell size

43
Q

what effect does no drinking (dehydration) have

A

water lost from ECF

ECF osmolarity increases (more conc than ICF)

water moves from ICF (lower osmolarity) to ECF (higher osmolarity) until osmolarity balances

cells become smaller

44
Q

how is body osmolarity regulated

A
  1. TBW changes alter plasma (ECF) osmolarity
  2. this is detected by osmoreceptors in hypothalamus
  3. this stimulates pituitary gland to secrete more/less ADH
  4. ADH alters permeability of renal collecting duct so water retained/excreted to balance initial change in TBW
45
Q

ADH synthesis

A
  1. in cell body of central neurons (hypothalamus)
  2. axonal transport to posterior pituitary
46
Q

2 major stimuli for ADH release

A
  1. increased ECF osmolarity
  2. decreased blood volume
47
Q

effects of ADH in nephron

A
  1. inserts water channels (aquaporins) in luminal membrane of CD
  2. increases H2O reabsorption in the collecting duct
48
Q

method of action of ADH

A
  1. ADH (vasopressin) binds to the receptor on the basolateral side of the principal cell in the collecting duct
  2. this via a cascade of events increases the insertion of vesicles containing AQP2 into the apical membrane
  3. this increases water permeability of the apical membrane
49
Q
A
50
Q

without ADH:

A

collecting duct is relatively impermeable to water

majority of water remains in CD and is not reabsorbed

increased water loss in urine

large volume of dilute (low osmolarity) urine

51
Q

with ADH:

A

collecting duct more permeable to water

water reabsorbed from CD (“down” HOMG)

decreased water loss in urine

small volume of concentrated (high osmolarity) urine!

52
Q

osmotic regulation of ECF

A

fast, controlled by ADH

53
Q

regulation of ECF by volume

A

slow, when you drink isotonic liquid, corrected by sodium excretion/retention

54
Q

iso-osmotic water and salt losses due to diarrhoea, vomiting etc

A

ECF volume decreases

no change in osmolarity since both water and salt is lost so no difference in osmolarity between ECF and ICF so no gradient for water to move out of cells

so cells are ok but circulating volume decreases

corrected via sodium excretion/retention (slow)

55
Q

iso-osmotic water and salt gains due to renal failure, excess IV fluids

A

ECF volume increases

no change in osmolarity

cells are ok but circulating volume increases

corrected via sodium excretion/retention (slow)

56
Q

gains/losses of just water

A

excess intake/not drinking

spread over both compartments (ECF and ICF)

problems with cell size and function

corrected via ADH mechanism (fast)

57
Q

hypo-volaemia

A

decreased blood volume

increased pulse

decreased blood pressure

increased urine concentration

58
Q

hyper-volaemia

A

increased blood volume

shortness of breath

hypertension

59
Q

3 detectors of changes in ECF

A

high pressure baroreceptors (aorta, carotid)

low pressure baroreceptors (vena cava, right atrium)

intra-renal baroreceptors and macula densa (juxtaglomerular apparatus)

60
Q

high pressure baroreceptors

A

(pressure sensors)

in carotid sinus and aortic arch

signals to brainstem CVS centres

inputs to brainstem –> renal nerve activity (sympathetic)

61
Q

low pressure baroreceptors

A

(volume sensors)

in atria, vena cava, pulmonary blood vessels

signals to brainstem cardiovascular centres

62
Q

response to high blood volume

A

atria release atrial natriuretic peptide (ANP) in response to signal from low pressure receptors. This increases filtered load of Na+, decreases Na+ reabsorption, and decreases renin secretion. This causes less water to be reabsorbed, so more is excreted

63
Q

afferent arteriole intra-renal sensor

A
  • juxtaglomerular cells
  • mechanoreceptors
  • sense BP
  • fall BP falls, renin is released which stimulates angiotenin II formation
64
Q

macula densa intra-renal sensor

A

chemoreceptors

sense NaCl concentrations

can stimulate afferent arteriole to alter glomerular filtration and renin release

65
Q

renin-angiotensin-aldosterone system

A

renin enzyme secreted by juxtaglomerular apparatus (JGA) when BP is low

renin cleaves angiotensinogen into angiotensin I

angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE)

angiotensin II is the active form, a potent vasoconstrictor, stimulated tubular Na+ reabsorption and stimulates aldosterone release, which causes BP to increase

66
Q

how is renal blood supply regulated so that filtration is relatively constant despite variations in blood pressure

A
  1. intrinsic (autoregulation) by myogenic vascular smooth muscle in afferent arteriole and tubuloglomerular feedback via JGA
  2. extrinsic by sympathetic vasoconstrictor nerves and angiotensin II
67
Q

content of normal urine

A

95-98% water

Creatinine

Urea, uric acid

H+, NH3

Na+, K+

Drugs (anti-viral, diuretics)

Toxins

pH 4.8-7.2

68
Q

content of pathological urine

A

Glucose (glucosuria, diabetes)

Protein (proteinurea)

Blood (erythrocytes, haematuria)

Haemoglobin (haemoglobinurea)

Leukocytes

Bacteria (infection)

69
Q

functions of kidneys

A

Filters blood

Water homeostasis (hydration, BP)

Salt / ion homeostasis (Na+, K+, Ca2+, BP)

Hormone production (EPO - RBC production)

Excretion of drugs, endogenous metabolites, toxins etc.

Re-absorption of nutrients (amino acids, glucose etc.)

pH regulation

Metabolism

Gluconeogenesis

70
Q

importance of salt/ion homeostasis

A

K+ is vital for resting membrane potential in all cells, action potentials and signalling in neurons, rhythm generation in pacemaker cardiomyocytes

Kidney failure can result in hyperkalaemia which is too much potassium

71
Q

what is filtration

A

process by which certain substances and fluid is filtered from the blood (in glomerular capillaries), through the filtration barrier, to the Bowman’s space, and into the tubular system

produces a ‘plasma-like’ filtrate of the blood

rate of 125mL/min or 180L/day

72
Q

secretion

A

adds additional wastes from the blood, to the filtrate

some substances such as drugs need to be completely secreted (are not filtered)

73
Q

reabsorption

A

removes useful solutes from the filtrate and returns them to the blood

some substances need to be partly (Na+, K+)/entirely (glucose) re-absorbed

74
Q

factors affecting renal filtration

A

renal blood flow

filtration barrier

driving forces/gradient between glomerular capillary and bowman’s space

permeability of glomerular capillary

surface area of glomerular capillary

75
Q

what makes up filtration barrier

A

Fenestrated capillary endothelium, shared basement membrane, epithelial podocyte (pedicels and filtration slits)

76
Q

what is filtered and not filtered through filtration barrier

A

Small substances (low molecular mass) are freely filtered - e.g. Na+, K+, Cl-, water, urea and glucose

Large substances (high molecular mass) are not filtered - e.g. Hb, Serum albumin

77
Q

how much urine is produced per day

A

1.5L

78
Q

renal blood supply

A

20-25% of cardiac output

1-1.2L/min

high flow for filtration rather than metabolism

mostly goes to glomerular capillaries

79
Q

forces for filtration

A

Glomerular hydrostatic pressure (60mmHg)

  • BP in glomerulus
  • Pressure exerted by fluid in glomerulus
  • Main driving force for filtration

Capsular osmotic pressure

  • Negligible bc its nearly isosmotic
80
Q

forces against filtration (into glomerulus)

A

Glomerular osmotic pressure

  • Largely determined by albumin and other larger plasma proteins - high osmotic drive

Capsular hydrostatic pressure

  • Pressure exerted by filtrate (fluid in Bowman’s space)
81
Q

glomerular filtration rate

A

Amount of fluid filtered by the kidneys per unit time

Normally around 180L/ day (125mL/ minute)

cannot be readily measured - must estimate using substances that are only filtered e.g. inulin or creatinine

82
Q

filtration fraction

A

how much of the blood reaching kidney is being filtered

FF = GFR/RPF

RPF - renal plasma flow (1/2 of renal blood flow)

83
Q

solutes that are only reabsorbed

A

Glucose

Water

Na+

Cl-, PO4- and Ca2+

84
Q

solutes that are only secreted

A

Organic cations such as histamine or morphine

Organic ions such as bile salts, penicillin or PAH

85
Q

solutes that are both reabsorbed and secreted

A

K+

NH3

H+

HCO3-

Urea

86
Q
A
87
Q

stimuli for RAAS system

A

Reduce renal perfusion pressure (BP) in afferent arteriole

Decreased delivery of NaCl to macula densa

Renal sympathetic nerves (activated by baroreceptors)

Low plasma volume → increases renin production

HUBS192 Renal system (3 decks)

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