Physiology Flashcards
What is osmolarity
Concentration of osmotically active particles present in a solution
What 2 factors do you need to calculate osmolarity
Molar concentration
Number of osmotically active particles
What is the difference between osmolarity and osmolality
The units - osmolality is osmol/kg of water
osmolarity is osmol/l
In weak salt solution the 2 are interchangeable
What is tonicity
The effect a solution has on cell volume
What effect will a isotonic solution have on cell volume
There will be no change to cell volume
Concentrations equal in and out of cell so no gradient
What effect will a hypotonic solution have on cell volume
Will lead to an increase in cell volume
Due to movement of water into the cell - down gradient
Cell may burst
What effect will a hypertonic solution have on cell volume
Decrease in cell volume as there is less water outside the cell
Water moves out of cell down the gradient
RBC are permeable to urea - true or false
TRUE
They have specific transporters for it
This is why it draws water into the cells
Why do women’s total body water make up less of their body weight compared to men
Females have higher % body fat which contain less water
List sources of insensible water loss
This is water loss we have no control over
Through skin by diffusion
Lungs - we breathe out small volumes
List sources of sensible water loss
Sweat
Faeces
Urine
Determined by a variety of regulatory mechanisms
What are the main ions in the ECF
Na+, Cl- and HCO3-
What are the main ions in the ICF
K+, Mg2+ and negatively charged proteins
The ECF has a higher osmotic concentration than the ICF - true or false
False
They are identical
What factors can alter fluid homeostasis
Gain or loss of water
Gain or loss of NaCl
Gain or loss of isotonic fluid
Regulation of ECF volume is important for what
Long term regulation of blood pressure
Why is electrolyte balance important
Total conc can directly affect water balance
The conc of individual electrolytes can affect cell function
Which electrolytes are the biggest contributors to osmotic concentration of ECF and ICF
Na+ for ECF
K+ for ICF
What affect can altered K+ lead to
Muscle weakness then paralysis
Cardiac irregularities that can lead to arrest
What are the functions of the kidneys
Water and salt balance
Maintaining plasma volume and osmolarity
Acid-base balance
Excretion of metabolic waste products and exogenous foreign compounds
Secretion of renin and erythropoietin
Conversion of Vit D to its active form
Describe the lining of the ureter
Lined by smooth muscle – peristaltic movement helps propel urine towards the bladder
At what point is there no more modification of urine
Once it enters the ureter
Describe the progression of blood vessels through the kidneys
Artery > afferent arteriole > glomerular capillary > efferent arteriole > peritubular capillary > venule > vein
What are the peritubular capillaries
They form a network that is closely related to the nephron
They collect anything that is reabsorbed from the nephron tubules
What is the substance found in the nephron called
Tubular fluid
At what point does tubular fluid become urine
As it leaves the collecting duct to the renal pelvis
What are the differences between the cortical and juxtamedullary nephrons
Juxtamedullary has a much longer loop of henle
Cortical has the peritubular capillary network whilst the juxtamedullary has a single vasa recta
What is the juxtaglomerular apparatus
Area of nephron where arterioles form a fork around part of the distal tubule
Afferent arteriole is narrower than the efferent one - true or false
False
It is greater in diameter
What makes up the glomerular membrane
Endothelial cells, basement membrane + podocytes
Where are the macula densa found
In the distal tubule
What is the function of the macula densa
Salt sensitive cells that monitor salt content of tubular fluid
If too salty it releases vasoactive chemicals that cause constriction of the afferent arteriole
What are the 3 processes that contribute to urine production
Glomerular filtration
Tubular reabsorption
Tubular secretion
GFR in a healthy adult is usually kept constant - true or false
True
How do you calculate rate of filtration of substance X
Xplasma x GFR
How do you calculate rate of excretion of substance X
Xurine x urine production rate
How do you calculate rate of reabsorption of substance X
Rate of filtration - rate of excretion
How do you calculate rate of secretion of substance X
rate of excretion of X – rate of filtration of X
Describe the charge of the basement membrane
Basement membrane is negatively charged
Plasma proteins are also negatively charged so should be repelled and remain in the plasma
RBC can normally enter the nephrons and then the urine
RBC are too big to filter through so if blood is present in the urine it means there is damage to the system
Which forces make up net filtration pressure
Glomerular capillary blood pressure - for filtration
Bowman’s capsule hydrostatic pressure - opposes filtration
Capillary oncotic pressure - opposes filtration
Bowman’s oncotic pressure - for filtration
Oncotic pressure refers to what
Gradients created by plasma proteins
Which of the 4 net filtration forces should be 0
Bowman’s capsule oncotic pressure
Glomerular filtration is a passive process - true or false
True
What is GFR
rate at which protein-free plasma is filtered from the glomeruli into the Bowman’s capsule per unit time.
What is the normal GFR in a healthy adult
125ml/min
What extrinsic mechanism regulates GFR
Sympathetic control via baroreceptor reflex
What intrinsic mechanisms regulate GFR
Myogenic - affects vascular smooth muscle
Tubuloglomerular feedback
GFR is relatively unaffected by MAP - true or false
True
This avoids unintentional fluid shifts
If BP drops you still produce enough urine to get rid of waste
What can increase pressure in Bowman’s capsule
Kidney stone causing a blockage that leads to increase in hydrostatic pressure
Will lead to decreased GFR
What increases capillary oncotic pressure
Dehydration (e.g. diarrhoea) means there is higher conc of plasma proteins so increases oncotic pressure
There will be more opposition to filtration
What is plasma clearance
A measure of how effectively the kidneys can ‘clean’ the blood of a substance
Equal to the volume cleared per minute
Clearance of what exogenous substance is equal to GFR
Inulin
Has to be infused so not very practical
Which body substance is used to estimate GFR
Creatinine
Name a substance that is completely reabsorbed by the kidney
Glucose
Should be none in the urine
If clearance of a substance is less than GFR what does it tell us
At least some of it is being reabsorbed
e.g. urea
If clearance of a substance is more than GFR what does it tell us
More of the substance is being secreted into the nephrons and not reabsorbed
e.g. H+
How do you measure renal plasma flow
PAH clearance test
All of it will be excreted
What properties should a clearance marker have
non-toxic
inert
easy to measure
Where in the nephron does the majority of reabsorption occur
Proximal tubule
Which substances are 100% reabsorbed in the kidney
Glucose - exception is poorly controlled diabetes
Amino acids
Is reabsorption specific or non-specific
Specific - relies on specific transport proteins or channels for each substance
Kidneys reabsorbed the majority of salt and fluid that is filtered - true or false
True
99% is reabsorbed
How does the glomerular filtrate differ from blood
It contains the same concentration of ions and solutes but lacks RBC and large proteins
Which substances are reabsorbed in the proximal tubule
Sugars Amino acids Phosphate Sulphate Lactate
which substances are secreted in the proximal tubule
H+
Uric acid
Bile pigments
Drugs and toxins
Describe the steps in transcellular tubular reabsorption
Must cross the apical/luminal membrane of the epithelial cell, cross the cytoplasm, leave via the basal membrane, cross the interstitial membrane and then into the capillary
Describe the process of paracellular reabsorption
Substances pass between the cells - across junctions
Varies depending on how tight the junction is
What is primary active transport
When energy is required to move the substance against its concentration gradient
e.g. Na/K pump
What is secondary active transport
A substance is transported alongside an ion that is moving down its gradient - coupled
What is facilitated diffusion
Passive carrier-mediated transport of a substance down its concentration gradient
Where is the Na/K pump found
Basolateral membrane of tubular cells
Drives reabsorption of salt
Describe how salt is absorbed in the proximal tubule
Sodium enters the epithelial cells down its concentration gradient and then leave the cells via the Na+/K+ pump
This sets up an electrical gradient that causes Cl- to follow
Also creates a osmotic gradient so water follows
How is glucose reabsorbed in the proximal tubule
By secondary active transport
Coupled to the movement of Na+ - co-transport
Why do you get glucosuria in diabetes
Glucose transporters become saturated at a certain level - cannot reabsorb any more
High blood sugar seen in diabetes exceeds the limit and so some is excreted
What is meant by counter current flow in the loop of Henle
There is opposing flow in the two limbs (ascending and descending)
Generates a concentration gradient between the cortex and medulla
What is reabsorbed in the ascending loop of Henle
Na+ and Cl-
Impermeable to water
What is reabsorbed in the descending loop of Henle
Water
Impermeable to salt
Describe the osmolarity of the tubular fluid, and interstitial fluid as they leave the loop of Henle
Tubular fluid has low osmolarity - lower than plasma
Interstitial fluid in the cortex is 300
Describe the changes in interstitial fluid osmolarity as the collecting duct passes down through the medulla
Progressively increases
Hormones affect which parts of the nephron
Hormones only affect the distal tubule and collecting duct – only have influence in the later parts
List the hormones that affect ion and water balance in the kidneys
ADH - water reabsorption
Aldosterone - increases Na reabsorption and H/K secretion
Atrial natriuretic hormone - decreases Na+ reabsorption
parathyroid hormone - increased Ca reabsorption and decreased phosphate
Describe water reabsorption in the distal tubule
It isn’t permeable to water
However, ADH release can change this by recruiting water channels
Where is ADH released from
It is synthesised by nerve cells in the hypothalamus
Stored as granules in the posterior pituitary
How does ADH work
Hormone binds to receptor that triggers an intracellular increase in cAMP (secondary messenger)
This stimulates insertion of aquaporin channels into the tubular cells – allows more water to move
ADH has a long half life - true or false
False
Very short = 10/15 mins
What stimulates ADH release
Dehydration
By releasing ADH you reabsorb more water
Also stimulated by nicotine
What happens in the distal tubule when there is little or no ADH
Low ADH = fewer aquaporin channels so little or no water reabsorption
Does ADH have any influence on salt reabsorption
NO
solute conc remains constant regardless of ADH level
What are the 2 types of diabetes insipidus
Central – unable to produce or secrete ADH
Nephrogenic – ADH is secreted but it cannot act on the target cells (e.g. defective receptor)
What are the symptoms of diabetes insipidus
Constant thirst
Producing large volumes of dilute urine
What inhibits ADH release
Alcohol
Where is aldosterone secreted from
Adrenal cortex
When is aldosterone secreted
In response to rising [K+] or falling [Na+] in the blood
Or activation of the renin-angiotensin system
What does aldosterone do
Stimulates Na+ reabsorption and K+ secretion
What triggers renin release form the juxtaglomerular apparatus
Reduced pressure in afferent arterioles
Reduced NaCl - detected by the macula densa cells
Increased sympathetic activity
Defects in the RAAS can lead to what
|Hypertension
Fluid retention - congestive heart failure
When is ANP released
Released from the walls of the atria when they are mechanically stretched
- e.g. when blood volume is higher
What is the function of ANP
Promotes excretion of Na+ and diuresis so will decrease plasma volume
What controls emptying of the bladder
Micturition reflex - stretch receptor
Voluntary control of the external sphincter
Venous blood is more alkaline than arterial - true or false
False
More acidic due to higher CO2 content
What is defined as acidosis
pH below 7.35
What is defined as alkalosis
pH above 7.45
What can acidosis lead to
Depression of the CNS
This can lead on to coma and death in severe cases
What can alkalosis cause
Over-excitability of the nervous system and later the CNS
Get pins and needles and muscle spasms
Severe cases include spasms of the respiratory muscles
How is H+ added to the blood
Continually due to metabolic reactions such as:
Carbonic acid formation
Inorganic acids from breakdown of nutrients
Organic acids from metabolism
Which type of acids dissociate completely in solution
Strong acids
Weak acids only dissociate partly
What happens if acid is added to the acid dissociation equation
The free A- mops up the excess protons to form more HA
This stops the pH falling
What happens if base is added to the acid dissociation equation
The excess base is taken up with combining with H+ so more HA dissociates
Prevents rise in pH
Which organ controls HCO3 levels
Kidney
Which organ controls CO2 levels
Lungs
How does the kidney affect HCO3 levels
They regulate reabsorption by varying how much is reabsorbed
They can add new HCO3 to the blood
All dependent on H+ secretion
Describe how HCO3 is reabsorbed in the proximal tubule
Carbonic anhydrase forms carbonic acid in the epithelial cell
H+ is released from this and enters the tubular fluid in exchange for Na
Filtered bicarbonate combines with the secreted H+ to form carbonic acid again
This is broken down into CO2 and water by carbonic anhydrase
The products can enter the epithelial cell where it is reabsorbed as bicarb by sodium co-transport
How does the kidney form new HCO3
When HCO3 is low, the secreted H+ combines with phosphate instead
As the H+ leaves the epithelial cell, it allows Na to move in
This Na is used to pump HCO3 created in the cell back into the blood
What is the titratable acid
The measure of the amount of H+ excreted as H2PO4
Max is 40mmol/day
How do you measure titratable acid
Record the amount of NaOH needed to get urine pH back to 7.4
Doesn’t determine amount of ammonium
High ammonium in the urine is caused by what
Acidosis
If the maximum amount of titratable acid has been produced but you are still acidotic, the excess H+ combined with ammonia from broken down glutamine to form ammonium which is then excreted
What range of HCO3 and PCO2 is considered normal
HCO3 - 23-27 mmol/l
Arterial PCO2 - 35-45mmHG
What is the difference between compensation and correction
Compenstaion comes first and is the restoration of pH, regardless of levels of CO2 or HCO3
Correction occurs after and is when pH is restored and HCO3 and CO2 return to normal
What buffers exist in the blood
Hb
HCO3
First line of defence in acid-base balance
What causes of respiratory acidosis
Retention of CO2
E.g. chronic bronchitis or emphysema, airway restriction, chest injury
How do we compensate for respiratory acidosis
H+ secretion in the urine via the renal system
It increases excretion of titratable acid and ammonium (gets rid of H+)
Generates more HCO3 to balance pH
How do we correct respiratory acidosis
After renal system compensates you need to correct by lowering CO2 by restoring normal ventilation
What causes respiratory alkalosis
Excessive CO2 removal
Low inspired PO2 - altitude
Hyperventilation
How do you compensate for respiratory alkalosis
Renal system
The H+ secretion isn’t enough to reabsorb all the HCO3 (even though bicarb is normal)
So some HCO3 is excreted in the urine
Also no TA or ammonium is formed so no new HCO3 is made
How do we correct respiratory alkalosis
Need to restore normal ventilation
What causes metabolic acidosis
Excess H+ from any source other than CO2
Excessive metabolic production - exercise or DKA
Excessive loss of base - diarrhoea
How do we compensate for metabolic acidosis
Respiratory system compensates by increasing ventilation and more CO2 is blown off
How do we correct after metabolic acidosis
Renal system kicks in later to increase H+ secretion and generate more HCO3
Ventilation can then return to normal
What causes metabolic alkalosis
Excessive loss of H+
Vomiting, alkali ingestion, aldosterone hypersecretion
How do we compensate for metabolic alkalosis
respiratory system compensates - slows ventilation
CO2 is retained so pH lowers
How is metabolic alkalosis corrected
H+ cannot drive the reabsorption as HCO3 conc is too high so HCO3 is excreted in the urine
No new HCO3 is generated either
