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RB Y2 Renal > Physiology > Flashcards

Physiology Flashcards

1
Q

define osmolality

A

concentration of osmotically active particles present in a solution

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2
Q

how is osmolality calculated

  • 150mM NaCl
  • 100mM MgCl2
A
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3
Q

what is the normal osmoraltiy of body fluids

A

285-295 mosmol/L

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4
Q

define tonicity

A

the effect a solution has on cell volume

  • Hypotonic solutions have a lower osmolality, and so more water. Cause cell lysis as water diffuses in by osmosis.
  • Isotonic solutions don’t change cell volume
  • Hypertonic solutions have a higher osmolality, cause cells to shrink
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5
Q

what else is tonicity influenced by

A

the ability of a solute to cross the cell membrane

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6
Q

compare total body water of male and female

A

females have less as they have more fat cells which contain little water

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7
Q

which tracer can be used to measure TBW

A

trihydrate

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8
Q

which tracer can be used to measure ECF

A

inulin

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9
Q

which tracer can be used to measure plasma

A

labelled albumin

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10
Q

sensible and insensible losses of fluid

A

insensible are those over which there is no physiological control

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11
Q

average composition of ECF

A
  • Na 140mM
  • Cl 115mM
  • HCO3- 28mM
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12
Q

Average composition of ICF

A

K - 140mM

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13
Q

how are the ECF and ICF separated and compare the osmotic concentrations

A
  • separated by a semi permeable memrbane
  • the osmotic concentrations are the same
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14
Q

how does a gain in NaCl affect the ECF and ICF

A
  • isotonic fluid
  • results in a change in ECF volume only as it does not affect fluid osmolality
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15
Q

where it the majority f sodium lost

A

mainly from urine

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16
Q

what is an importnat role of K

A

establishing membrane potential

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17
Q

compare the body weight of kidneys and the CO they recieve

A
  • 25% CO
  • 0.5% body weight
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18
Q

what is the functional unit of the kidney

A

the nephron

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19
Q

describe the blood supply of the kidney

A
  • cortical - peritubular capillaries
  • juxtamedullary -vasa recta
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20
Q

how many nephrons does one collecting duct recieve input from

A

multiple

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21
Q

what is different about juxtamedullary nephrons

A
  • they have a longer loop of Henle which descends further down into the medulla
  • therefore produce a more concentrated urine as are exposed to more of the multiplying concentration gradient
  • have a single vasa recta instead of multiple peritubular capillaries
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22
Q

function of mesangial cells

A
  • provide support to capillaries
  • regulate blood flow throughthem by controlling contractile status
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23
Q

granular cells - location and function

A
  • modified smooth muscle cells inthe walls of the afferent arteriole
  • secrete and produce renin
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24
Q

macula densa

A
  • Macula densa is an area of closely packed cells lining the wall of the distal tubule
  • senses Sodium concentration as the tubular fluid passes through that region of the nephron
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25
Q

what is urine

A

a modified filtrate of blood

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26
Q

what percentage of plasma entering the glomerulus is filtered

A

20%

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27
Q

define rate of excretion

A
  • Rate of excretion = rate of filtration + rate of secretion – rate of reabsorption
  • Rate of excretion of X is the mass excreted per unit time: [X]urine x Vu
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28
Q

rate of filtration

A
  • mass of X filtered into the Bowman’s capsule per unit time, for a freely filterable substance X: [X]plasma x GFR
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29
Q

what is the outer layer of Bowman’s capsule formed from

A

a single layer of simple squamous epithelium

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30
Q

what does the glomerular capillary enodthelium act as a barrier towards

A

RBCs

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31
Q

describe the basement membrane

A
  • acellular and composed of collagen and glycoprotein
  • net negative charge which repels negatively charged plasma proteins
  • plasma protein barrier
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32
Q

podocytes

A
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33
Q

is filtration passive or active

A

entirely passive

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34
Q

outline the Starling forces involved in filtration

A

NFP = 10mmHg

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35
Q

what is the oncotic pressure of Bowman’s capsule

A

0, no plasma proteins

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36
Q

define GFR

A
  • The rate at which protein-free plasma is filtered into Bowman’s capsule per unit time
  • = Kf x NFP
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37
Q

what is Kf

A

the filtration coefficient - how holey the glomerulus is

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38
Q

which straling force is the major determinant of GFR

A
  • The BPGC ­is the major determinant of GFR, as it is the largest in terms of magnitude
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39
Q

extrinsic regulation of GFR - sympathetic control via baroreceptor reflex

A
  • In situations of falling blood volume, carotid and aortic baroreceptors stop firing, allowing uninhibited sympathetic activity. Respond to stretching (increased blood pressure and volume) by inhibiting sympathetic activity.
  • Adrenaline from the adrenal medulla acting on alpha 1 receptors causes vasoconstriction of afferent arterioles (smooth muscle in walls)
  • This decreases the blood flow into the glomerulus, decreasing BPGC, and decreasing NFP, and GFR. Results in a decrease in urine volume.
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40
Q

how is GFR protected from short term changes in MABP

A
  • autoregulation - intrinsic control (no hormones)
  • helps eg maintain water and salt balances in exercise - MABP inc but want to retain fluid
  • myogenic: If vascular smooth muscle of afferent arteriole is stretched by increased arterial pressure it responds by contracting, thus constricting the arteriole
  • Tubuloglomerular feedback:
    • If GFR rises, more NaCl flows through the tubule leading to constriction of the afferent arterioles
    • Increased Sodium in the tubular fluid is sensed by the macula densa causes the release of adenosine, which causes vasoconstriction
    • This is a negative feedback mechanism
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41
Q

how does diarrhoea affected COP of the glomerular capilllary

A

increases it - decreased GFR

(lost water so plasma proteins are now in greater concentation)

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42
Q

causes for decreased COP of the glomerular capillary

A
  • burns - loss of plasma proteins from site of injury
  • increased GFR
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43
Q

how does a kidney stone effect GFR

A

increased hydrostatic pressure of Bowman’s capsule - dec GFR

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44
Q

define plasma clearance

A
  • a measure of how effectively the kidneys can clean the blood of a substance
  • Clearance of substance X = rate of excretion of X ([X]urine x Vu) / plasma concentration of X
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45
Q

inulin

A
  • neither secreted or reabsorbed in the tubules - measure of GFR
  • not conveient though as patient must be hooked up to IV line as it is exogenous substance
46
Q

calculate GFR from inulin

A
47
Q

what is now used to measure GFR

A

creatinine - endogenous substance

48
Q

production of creatinine

A
  • produced at a constant rate
  • slight tubular secretion - approx GFR
49
Q

name 2 problems with creatinine

A
  • creatinine is not sensitive to changes in GFR until it is quite low, at which point most patients swill already have presented for clinical reasons
  • muscle mass and diet are proxies for age, sex and ethnicity - influenced by amount of urine creatinine and volume of urine
    • marker of skeletal muscle breakdown
50
Q

eGFR

A
  • estimated GFR, calculated on patient’s age, sex, race and serum creatinine
  • better
51
Q

shortfall of eGFR

A

not very accutate >60ml/min - anything above this is reported as just that

52
Q
A
53
Q

glucose

A
  • Filtered, completely reabsorbed and not secreted
54
Q

urea

A
  • Filtered, partially reabsorbed and not secreted - clearance<gfr>
    </gfr><li>not produced at a constant rate </li>

</gfr>

55
Q

H ions in the tubules

A
  • Filtered, secreted and not reabsorbed
  • Clearance > GFR = secreted
56
Q

what is used to calculate renal plasma flow

A
  • para-amino hippuric acid
  • PAH is freely filtered at the glomerulus, secreted into the tubule from the capillary and completely cleared from the plasma (e.g. all the PAH that escapes filtration is secreted from the peritubular capillaries)
  • RPF is usually around 650 ml/min
57
Q

define renal plasma flow

A
  • volume of blood plasma delivered to the kidneys per unit time
58
Q

osmolality of fluid in filtrate and proximal tubule

A

the same - there is no change in osmolality between the start and end of PT as water and salt are absorbed in equal proportions

59
Q

what is reabsorbed in the PT

A
  • Sugars -100%
  • Amino acids – 100%
  • Phosphate
  • Sulphate
  • Lactate
  • Urea
60
Q

what is the wall of the tubule formed by

A

single layer of epithelial cells

61
Q

define facilitated diffusion

A

passive carrier mediated transport of a substance down its concentration gradient

62
Q

sodium reabsorption in the PT

A
  • Na+ reabsorption is driven by the Na+ K+ ATPase pump at the basolateral membrane. This pump is exclusively expressed here
  • Sodium drives the secretion of hydrogen ions across the apical membrane
  • The net movement of sodium sets up an electrochemical gradient for the net reabsorption of chloride ions across the paracellular route
  • This sets up an osmotic gradient, down which water follows paracellularly
  • The plasma proteins in the capillary (which are in greater concentration as the capillary has 20% less volume due to glomerular filtration) exert an oncotic drag which pulls the fluid into the peritubular capillary
63
Q

howb much glucose does each transporter reabsorb

A
  • 90% through SLGT2 in S1
  • the rest through SGLT1 in S3
64
Q

glucose reabsorption in PT

A
  • Normally, 100% of glucose is reabsorbed in the proximal tubule
  • It crosses the apical membrane by a secondary active transporter (SGLT1 and 2), and then crosses the basolateral membrane down its concentration gradient by facilitated diffusion
  • The movement of glucose sets up an osmotic gradient for water to follow paracellularly
65
Q

transport maximum for glucose

A

2mmol/min

66
Q

what is the function of the loop of Henle

A

to generate a cortic-medullary solute concentration gradient which enables the formation of hypertonic urine in the presence of ADH

67
Q

what is the name for the opposing flow int he two limbs of loop of Henel

A

countercurrent flow

68
Q

how is NaCL reabsorbed inthe thick and think ascending loop

A
  • active in the thick
  • passive in the thin
69
Q

compare the osmolality of fluid leaving the LoH to that entering it

A

osmolality decreases

70
Q

Na transport in the thick ascending loop of Henle

A
  • TALH triple cotransporter pumps ions out of the lumen of the loop of Henle
  • 2 Cl ions, 1 Na and 1 K. This creates an electroneutral transporter
  • K+ recycling at apical and basolateral membrane allows for NaCl to be reabsorbed into the interstitial fluid
71
Q

urea cycle in the kidney

A

The urea cycle also contributes to approximately half of the medullary osmolality. The distal tubule is not permeable to urea. The collecting duct absorbs around 50% of urea, which diffuses passively into the loop of Henle. Urea adds solid to the interstitium.

two solute hypothesis

72
Q

what forms a counter current system

A

The vasa recta act as a countercurrent exchanger, and together, the loop of Henle and vasa recta form a countercurrent system.

73
Q

how do JM nephrons minimise the problem of blood flow washing away NaCl and urea

A
  • Following hairpin loops
  • Freely permeable to NaCl and water
  • Low blood flow in comparison to the flow in the renal cortex

this preserves the CM gradient as blood equilibrates at each layer, as well an ensuring that solute is not washed away

74
Q

in summary what makes the medullary osmotic gradient, and what preserves it

A
  • The countercurrent multiplier and the urea cycle create the medullary osmotic gradient
  • The countercurrent exchanger preserves that gradient
75
Q

synthesis of ADH

A

An octapeptide that is synthesised in the hypothalamus in neuron cell bodies. It is transported down neuron axons to nerve terminals in the posterior pituitary gland, where it is stored in granules.

76
Q

what is the most important stimulus for ADH release

A

hypothalamic osmoreceptors

77
Q

halflife of ADH

A

peptide hormone - 10-15 minutes

78
Q

ADH mechanism

A
  • acts on vasopressin receptors 2
  • inserts new aquaporin channels into the luminal membrane
  • water moves down its concentration gradient into the medullary interstital fluid, enabling the formation of hypertonic urine
  • acts on the distal tubule and collecting duct
79
Q

ADH on vasopressin receptor 2: when will water stop moving across

A

Water continues to be reabsorbed along its osmotic gradient until osmotic equilibrium is restored.

80
Q

what happens in the distal tubule in the presence of minimal ADH

A

In the presence of minimal ADH concentration in the plasma, the AQP have become internalized and the distal tubule and collecting ducts are no longer permeable to water.

81
Q

ADH vasoconstrictor effect

A

ADH binds to V1 on vascular smooth muscle to cause vasoconstriction, which increases arterial pressure.

82
Q

role of ADH in severe hypovolemic shock

A
  • In cases of e.g. severe hypovolemic shock, ADH release is very high and contributes to the compensatory increase in systemic vascular resistance
  • Hypovolemia results in a decrease in atrial pressure, which is sensed by specialized stretch receptors within the atrial walls and large veins (cardiopulmonary baroreceptors) entering the atria decrease their firing rate when there is a fall in atrial pressure
  • Atrial receptor firing normally inhibits the release of ADH, this leads to increased ADH release.
83
Q

name another system that release ADH

A
  • Increase in angiotensin II stimulates ADH release (RAAS)
84
Q

nicotine, alcohol and ecstacy effect on ADH release

A
  • Nicotine stimulates ADH release
  • Alcohol and ecstasy inhibit ADH release
    • this is why you can get dehydrated cos you are not concentrating your urine (people can die from drinking too much water when on ecstacy)??
85
Q

ADH in heart failure

A
  • Heart failure is associated with a paradoxical increase in ADH, increased blood volume and atrial pressure should decrease ADH secretion, but they do not
  • this may be due to an abnormal increase in RAAS due to decreased CO and BP
86
Q

what effect does decrease renal blood flow have on EPO release and kidney function

A
  • EPO is released in the kidney in response to hypoxia (decreased renal blood flow), it stimulates RBC production in bone marrow
  • dec urine output conserve PV
87
Q

where is aldosterone secreted from

A

This is a steroid hormone secreted by outer zona glomerulosa of the adrenal cortex.

88
Q

effect of decrease in plasma sodium and potassium concentration on aldosterone

A
  • A decrease in plasma concentration of Sodium activates the RAAS system, which causes aldosterone secretion.
  • An increase in plasma concentration of Potassium stimulates the cells of the adrenal cortex directly to increase aldosterone secretion.
  • aldosterone acts to stimulate sodium reabsorption and potassium secretion
89
Q

how much potassium is normally excreted in the urine

A

none

90
Q

name 3 things which cause renin release

A
  • reduced pressure in the afferent arteriole is sensed by the granular cells
  • decreased NaCl in the distal tubule is sensed by the macula densa which stimulates the granular cells to release renin
  • Increased sympathetic activity as a result of reduced arterial blood pressure
    • Granular cells are directly innervated by the sympathetic nervous system and cause renin release
91
Q

how does aldosterone increase Na reabsorption

A
  • Aldosterone increases Sodium reabsorption in the distal and collecting tubule by increasing expression of NaK pump at the basolateral membrane, and apical Sodium channels.
92
Q

does AGT II constrict the afferent or efferent arteriole more

A

efferent

93
Q

where is ANP found and what generally does it do

A
  • Synthesised, stored and released by atrial myocytes
  • It is released when these cells are mechanically stretched due to an increase in circulating plasma volume
  • Therefore, elevated levels are found during hypervolaemic states.
94
Q

where is BNP produced and what is it a marker of

A
  • ventricles - and brain
    • secreted by ventricles in response to stretch
  • diagnostic marker of heart failure
95
Q

NP effect on veins and arteries

A
  • dilate veins, decrease central venous pressure, which reduce CO by decreasing ventricular preload
  • Dilate arteries which decreases systemic vascular resistance and systemic arterial pressure
  • Does this by increasing vascular smooth muscle cGMP, and decreasing sympathetic vascular tone
96
Q

NP effect on the kidneys

A
  • Afferent arteriole vasodilation
  • Increasing GFR which produces natriuresis and diuresis
    • These renal effects are potassium sparing
  • Decrease renin release, thereby decreasing circulating levels of AGT II and aldosterone. This leads to further natriuresis and diuresis
  • = Counter regulatory system for RAAS
97
Q

water diuresis vs osmotic diuresis

A

In water diuresis, there is an increase urine flow but not an increased solute excretion.

In osmotic diuresis, the increased urine flow is as a result of primary increase in salt excretion. E.g. failure of normal Sodium reabsorption causes both increased sodium and water excretion.

Any loss of solute in the urine must be accompanied by water loss (osmotic diuresis), but the reverse is not true (water diuresis is not necessarily accompanied by equivalent solute loss).

98
Q

filtration fraction

A

The fraction of plasma flowing through the glomeruli that is filtered into the tubules.

99
Q

compare the pH of venous and arterial blood

A

venous blood is more acidic as it contains more CO2

100
Q

dissociation of stong and weak acids in solution

A

strong acids dissociate completely, weak acids partly dissociate

101
Q

proton donors and acceptors

A

Acids are proton donors, and bases are proton acceptors

102
Q

Henderson-Hasselbalch equation

A
103
Q

pH equation

A

pH = -log [H+]

104
Q

pKa

A

-log [Ka]

105
Q

what 3 things does H secretion by the tubule do

A
  1. drive bicarbonate reabsorption
  2. form acid phosphate
  3. form ammonium ion
106
Q

H secretion and bicarbonate reabsorption

A
  • Bicarbonate is reabsorbed in the proximal tubule through the action of CA, unorthodox reabsorption at the apical membrane as the same bicarbonate ion that is absorbed does not cross the epithelium - principal buffer
  • An increase in H ion secretion causes an increase in bicarbonate ion reabsorption
  • An increase in CO2 has the same effect
107
Q

H ion secretion forming acid phosphate

A
  • The kidneys can regenerate buffer stores by generating new HCO3- if they are depleted by an acid load:
  • When bicarbonate concentration in the tubular fluid is low, secreted H+ ions combine with phosphate (buffer). Acid is excreted with phosphate, and there is a net gain of 2 bicarbonate ions – ‘new bicarbonate.’
108
Q

measurement of H ions with as acid phosphate

A
  • The amount of H ions secreted as H2PO4- can be measured as titratable acid – the amount of strong base (e.g. NaOH) that must be added to titrate the urine back to pH 7.4 is measured. This titration simply reverses the addition of H ions that has occurred as fluid flows along the tubule.
109
Q

what is the maximum titratable acid that can be excreted

A
  • The maximum amount of titratable acid that can be excreted is around 40mmol/day. If this much titratable acid is added, 40mmol/day of ‘new’ bicarbonate is simultaneously gained by the circulation
110
Q

H secretion forming ammonium ion

A
  • In severe acidosis, when the compensatory mechanisms are overloaded, glutamine from the liver is used as a tubular buffer. It diffuses as a gas into the tubular fluid. Acid is excreted as NH4+ and 2 new bicarbonate ions are generated per molecule
  • can again be measured by titrable acid
111
Q
A

RB Y2 Renal (26 decks)

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