Physiology Flashcards
Osmolarity
Number of solute particles per litre
Osmolarity of body fluids
300mosmol/L
Specific gravity
Weight of particles
Total body water exists as 2 major compartments
ECF
ICF
ECF includes:
Plasma
IF
Lymph and transcellular fluid
How are fluid compartments measured?
Tracers
Useful tracers
TBW: water
ECF: Inulin
Plasma: albumin
How to calculate volume
V = Dose/Concentration
Main ions in ECF
Na
Cl
HCO3-
Main ions in ICF
K
Mg
Negatively charged proteins
Changes in ICF/ECF during gain/loss of water
Similar changes (both increase or decrease)
Changes in ICF/ECF during gain/loss of NaCl
Opposite changes (one increases and other decreases)
What happens in gain/loss of isotonic fluid?
No change in fluid osmolarity, change in ECF only
Electrolyte
Any substance that dissolves to form free ions
What ion plays a role in establishing membrane potential?
K
Effects of hypokalaemia
Paralysis
Cardiac arrest
How is salt imbalance manifested?
Changes in ECF volume
2 types of nephron
Juxtamedullary
Cortical
Juxtamedullary nephrons
Long loop of henle
Vasa recta
Concentrated urine
Cortical nephrons
Short loop of henle
Peritubular capillaries
Function of macula densa
Modified tubular cells
Sense NaCl content
Granular/juxtamedullar cells
Secrete renin
What % of plasma that enters glomerulus is filtered?
20%
Rate of filtration
[X]plasma x GFR
Rate of excretion
[X]urine x urine flow rate (Vu)
Rate of reabsorption
Rate of filtration - Rate of excretion
Filtration > Excretion
Rate of secretion
Rate of excretion - Rate of filtration
Filtration
3 layers of filtration barrier/glomerular membrane
Glomerular capillary endothelium
Basement membrane
Slit processes of podocytes
Forces comprising net filtration pressure
Glomerular capillary hydrostatic pressure (55) BPgc
Bowman’s capsule hydrostatic pressure (15) HPgc
Glomerular Capillary oncotic pressure (30) COPgc
Bowman’s capsule oncotic pressure (0) COPbc
Net filtration pressure
10mmHg
Major determinant of net filtration pressure
Glomerular capillary hydrostatic pressure (BPgc)
Constant along capillary (due to back pressure, smaller efferent)
GFR
Rate at which protein free plasma is filtered
Kf x net filtration pressure
What happens to urine if GFR increases/decreases?
GFR increases = more urine
GFR decreases = less urine
Extrinsic regulation of GFR
Sympathetic control - baroreceptor reflex
BPgc controlled by vasoconstriction/dilation
Intrinsic autoregulation of GFR
Myogenic mechanism
Tubuloglomerular feedback
Effect of vasoconstriction on GFR
Less blood flow = decreased BPgc = decreased GFR
Effect of vasodilation on GFR
More blood flow = increased BPgc = increased GFR
Autoregulation
Stops short term changes in BP affecting GFR
Myogenic mechanism of autoregulation
Increased BP = vascular smooth muscle stretched = vasoconstriction of afferent
Tubuloglomerular feedback mechanism of autoregulation
If GFR rises = more NaCl detected by JGA = vasoconstriction of afferent
Which type of control can override?
Extrinsic control, e.g. in haemorrhage
What pathology increases HPbc
Kidney stone
Decreased GFR
What pathology increases COPgc
Diarrhoea
Decreased GFR
What pathology decreases COPgc
Burns
Increased GFR
What pathology decreases Kf
Physical damage
Decreased GFR
Plasma clearance
Measure of how effectively plasma cleared of a substance ml/min
How to calculate clearance
Rate of excretion/Plasma concentration
Inulin and creatinine clearance
= GFR
Filtered, not reasorbed or secreted
Glucose clearance
= 0
Filtered, completely reabsorbed
Urea clearance
less than GFR, reabsorbed
H+ clearance
> GFR
Filtered, secreted, not reabsorbed
What do you use to calculate RPF
PAH (filtered, secreted completely, not reabsorbed, completely cleared from plasma)
RPF
650ml/min
RBF
1200ml/min
Fluid reabsorbed in PCT is ________ with filtrate
Iso-osmotic
What is reabsorbed in PCT?
Sugars 100% Amino acids 100% Phosphate Sulphate Lactate Na 67%
What is secreted in PCT?
H+ Hippurates NTs Bile pigments Uric acid Drugs Toxins
Barriers to transcellular reabsorption
Apical membrane, tubular cell, basolateral membrane, interstitial fluid, capillary endothelium
Primary active transport
Energy directly required (hydrolysis of ATP) to move substance against concentration gradient, e.g. Na/K
Secondary active transport
Carrier molecule transported coupled to ion concentration gradient (Na) e.g. Na/glucose
Symport
Secondary AT in same direction
Antiport
Secondary AT in opposite directions
What is essential for Na reabsorption?
Na/K on basolateral membrane
Water is reabsorbed via what route?
Paracellular route - follows Cl
After glucose transporters are saturated, what happens?
Glucose excretion
Transport maximum for glucose
2mmol/min
Tubular fluid is ________ when it leaves PCT
Iso-osmotic 300mosmol/L
Function of LOH
Generates concentration gradient to allow formation of concentrated urine
Opposing flow in 2 limbs of LOH is termed:
Countercurrent flow
The LOH and vasa recta establish a __________ medullary IF
Hyperosmotic
NaCl reabsorption in thin ascending limb
Passive
NaCl reabsorption in thick ascending limb
Active transport
Fluid entering ascending LOH is:
Hypertonic
Fluid leaving LOH and entering DCT is:
Hypotonic 100mosmol/L
What else contributes to medullary osmolarity?
Urea cycle
Where is urea recycled?
Between CD and ascending LOH
2 solute hypothesis contributing to medullary gradient
NaCl
Urea
Range of urine production
0.3-25ml/min
What is the countercurrent exchanger?
Vasa recta
ANP functions
Decreases Na reabsorption
Vasodilation of afferent arteriole
Decreases BP
Decreases symp activity
PTH functions
Na reabsorption
Phosphate excretion
Early DCT
Na/K/2Cl
Late DCT
Ca reabsorption
Na reabsorption
K reabsorption
H secretion
Where is ADH receptor?
Basolateral membrane of DCT and CD
Functions of ADH
Increases aquaporins at apical membrane
In presence and absence of ADH where is impermeable to water?
Absence: ascending LOH, DCT, CD
Presence: ascending LOH
At what bladder volume do stretch receptors initiate micturition reflex?
250-400ml
Stimuli for ADH release?
Hypothalamic osmoreceptors
Left atrial stretch receptors
Upper GIT = feedforward inhibition
Nicotine stimulates ADH, alcohol inhibits ADH
Stimuli for aldosterone release?
Increase in plasma K directly stimulates adrenal cortex
Decrease in plasma Na = JGA = RAAS
Stimuli for renin release?
Reduced pressure in afferent arteriole
Reduced Na detected by macula densa
Reduced BP = increased symp activity = granular cells stimulated
Treatment for HF
Low Na diet
Loop diuretic
ACEI
Where is ANP produced?
Heart
Stimuli for ANP release
Stretch receptors in heart due to increased BP
Acidosis can lead to:
Depression of CNS
Alkalosis can lead to:
Overexcitability of PNS then CNS
Strong acids dissociate __________ in solution
Completely
The most important physiolgical buffer is:
CO2/HCO3-
What drives bicarbonate reabsorption?
H+ secretion
What drives H+ secretion?
CO2 retention
What happens when bicarbonate in tubular fluid is low?
Secreted H+ combines with phosphate = acid phosphate excreted (H2PO4)
Amount of H+ secreted as acid phosphate can be measured as:
titratable acid
What rids the body of buffer stores?
TA and ammonia
Compensation
Restoration of pH irrespective of what happens to bicarb and CO2
Correction
Resoration of pH and bicarb and CO2
Examples of respiratory acidosis
COPD - chronic bronchitis, chronic epmhysema, asthma, tumour
Respiratory acidosis on Davenport diagram
Left and up of normal
How is respiratory acidosis compensated?
Bicarb reabsorbed, H+ secreted as TA and ammonia
New bicarb added to blood
Why does bicarb rise in respiratory acidosis?
As a result of the disease (equation to right)
As a result of renal compensation (excreting acid, adding new bicarb)
How do you correct resiratory acidosis?
Restoring normal ventilation
Causes of respiratory alkalosis
Hyperventilation, fever, altitude
Respiratory alkalosis on Davenport diagram
Right and down of normal
Compensation in respiratory alkalosis
Excess removal of CO2 = decreased H+ secretion = can’t reabsorb bicarb = bicarb excreted in urine
No TA or ammonia formed = no new bicarb
Renal compensation further lowers bicarb
How do you correct respiratory alkalosis?
Restore normal ventilation
Causes of metabolic acidosis
Excess H+ from sources other than CO2
Ingestion of acids, DKA, lactic acidosis during exercise
Excess loss of base (diarrhoea)
Why is bicarb depleted in metabolic acidosis?
Buffers excess H+
Loss of bicarb (diarrhoea)
Respiratory compensation in metabolic acidosis
Decrease pH stimulates peripheral chemoreceptors = ventilation increases = CO2 blown off
H+ and bicarb lowered
Metabolic acidosis on Davenport diagram
Left and down of normal
Correction for metabolic acidosis
H+ secretion = TA and ammonia formed to generate more bicarb
Acid load excreted
Metabolic alkalosis
Excess loss of H+ from the body
Causes of metabolic alkalosis
Vomiting, ingestion of alkali, aldosterone hypersecretion
Metabolic alkalosis on Davenport diagram
Right and up from normal
Respiratory compensation for metabolic alkalosis
Increased pH slows ventilation (peripheral chemoreceptors)
CO2 retained = H+ rises, bicarb rises
Correction for metabolic alkalosis
Not all filtered bicarb reabsorbed
No TA or ammonia = bicarb excreted