ALL ABOUT KIDNEYS <3 Flashcards
What are the 3 main components of the filtration barrier?
- Endothelial cells- fenestrations
- Basement membrane- shape, size and charge
- Epithelial cells (podocytes)- slit pores
What are the main determinants of filtration?
- Permeability of B.M
- Physical forces driving filtration
- Mass
- Charge
What is Starling’s equation?
GFR= Kf(Pcap+ONCbc) - (Pbc+ONCcap)
What are the average figures for each component of Starling’s equation?
Pcap= 60mmHg
ONCbc= 0
Pbc=20mmHg
ONCcap=30mmHg
What happens in autoregulation?
Arterial b.p fluctuates in the range 80-200mmHg
Afferent arteriole constriction/relaxation
Effects the resistance in the afferent arteriole
Counteracts any changes in the GFR caused by the change in b.p
What are the 2 main hypotheses explaining autoregulation?
1.Myogenic theory Stretch receptors 2.Tubuloglomerular feedback theory rate of flow of tubular fluid macula densa cells- vasoactive chemicals
What is osmolality and how is it calculated?
Osmolality is the measure of concentration of a solution. Units are Osm/kg H2O
Concentration x number of particles it dissociates into
Describe counter current multiplication
It is the process of creating differing osmotic gradients in order to reabsorb water from the tubular fluid and produce concentrated urine.
It relies on differing permeabilities in the loop of Henle and collecting ducts.
Discuss the difference in handling of Na,CL, Urea and H20 in CCM
Thin DL- permeable to water, little solute movement inner medulla- urea enters tubular fluid Thin AL- impermeable to water very permeable to Cl and Na Thick AL- impermeable to water permeable to solute CD- very permeable to water impermeable to solute- apart from inner medullary CDS- reabsorption of urea
Transport proteins and diseases
Bartters syndrome ROMK,NKCC2,CLCK, Barttin subunit stops reabsorption of Na and Cl in TAL Diabetes insipidus AQ-2/ Vasopressin *UT-B mutation- washing out of urea in IF- effects counter current exchange
What are the normal pH ranges?
7.35-7.45
Explain the davenport diagram
metabolic acidosis- H+ high/ HCO3- low pH down metabolic alkalosis- HCO3- high pH high resp. acidosis- CO2 high H+ high resp alkalosis- CO2 low H+ low (to make more CO2) pH high
Peripheral chemoreceptors main stimulus
Hypoxia
What nerves do the Glomus cells signal to
Vagus, sinus and glossopharyngeal nerves
What changes causes an increase in sensitivity of peripheral chemoreceptors?
high pCO2
low pH
low O2
Central chemoreceptors main stimulus
Hypercapnia
Where are the 2 main locations of the central chemoreceptors
Brain parenchyma
Ventrolateral medulla and other brainstem nuclei
What are the properties of the BBB
Separates the blood and brain extracellular fluid (BEF)
Poor ion permeability
CO2 moves across easily
What is the buffering power like in the BEF?
Reduced bicarb buffering power
As a result- larger fall in pH in BEF
chronic acid/base disturbance- HCO3- moves across (small qtys) from blood to BEF
With a change in plasma pH- what are the differences in response in metabolic and respiratory disorders
Met disorder- small change in BEF pH due to H+ and HCO3- poor ion permeability of BBB
Resp disorder- larger change in BEF pH due to CO2 being freely permeable across the BBB
What is the integrated chemoreceptor response to respiratory acidosis?
Central chemoreceptors more important- tonic drive for breathing
However peripheral receptors respond faster
What is the integrated chemoreceptor response to metabolic acidosis?
If severe- hyperventilation
Peripheral receptors involved in short term response
Central receptors- longer term
3 main renal mechanisms involved in balancing acids and bases
- HCO3- handling (net reabsorption of bicarbonate)
- Urine acidification (binding H+ with buffers)
- Ammonia synthesis
What causes respiratory acidosis?
lung disease-
emphysema, chronic bronchitis
What causes respiratory alkalosis?
hyperventilation-
due to stress,fear, pain
What causes metabolic acidosis?
ingestion of acid
loss of alkaline fluid- diarrhoea, cholera
What causes metabolic alkalosis?
ingestion of alkaline fluid
loss of acid- vomiting
Symptoms of Liddles syndrome
Hypertension
Hypokalaemia
Metabolic alkalosis
What causes Liddle’s syndrome and how is it treated
Gain of function mutation- deletion of proline rich motif (on beta or gamma subunit) which means the protein is no longer degraded correctly
Too much Enac in apical membrane of principal cells
Amiloride is used as treatment
Types of diabetes insipidus
Central- impaired AVP production
Nephrogenic- impaired AVP effect
Gestational- AVP metabolised
Causes of central and nephrogenic DI?
Central
acquired= head trauma, surgery, infection
congenital= 67 diff mutations associated- impaired transport of AVP from hypothalamus to posterior pituitary
Nephrogenic
acquired= lithium, some antibiotics, acute and chronic renal failure
congenital= mutations in AVPR2 gene/ AQP2 gene
Treatments of DI
Central- desmopressin
Nephrogenic- modulatory drugs
pharmacological chaperones
