ALL ABOUT KIDNEYS <3 Flashcards

1
Q

What are the 3 main components of the filtration barrier?

A
  1. Endothelial cells- fenestrations
  2. Basement membrane- shape, size and charge
  3. Epithelial cells (podocytes)- slit pores
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2
Q

What are the main determinants of filtration?

A
  1. Permeability of B.M
  2. Physical forces driving filtration
  3. Mass
  4. Charge
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3
Q

What is Starling’s equation?

A

GFR= Kf(Pcap+ONCbc) - (Pbc+ONCcap)

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4
Q

What are the average figures for each component of Starling’s equation?

A

Pcap= 60mmHg
ONCbc= 0
Pbc=20mmHg
ONCcap=30mmHg

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5
Q

What happens in autoregulation?

A

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

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6
Q

What are the 2 main hypotheses explaining autoregulation?

A
1.Myogenic theory
Stretch receptors
2.Tubuloglomerular feedback theory
rate of flow of tubular fluid
macula densa cells- vasoactive chemicals
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7
Q

What is osmolality and how is it calculated?

A

Osmolality is the measure of concentration of a solution. Units are Osm/kg H2O
Concentration x number of particles it dissociates into

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8
Q

Describe counter current multiplication

A

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.

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9
Q

Discuss the difference in handling of Na,CL, Urea and H20 in CCM

A
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
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10
Q

Transport proteins and diseases

A
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
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11
Q

What are the normal pH ranges?

A

7.35-7.45

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12
Q

Explain the davenport diagram

A
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
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13
Q

Peripheral chemoreceptors main stimulus

A

Hypoxia

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14
Q

What nerves do the Glomus cells signal to

A

Vagus, sinus and glossopharyngeal nerves

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15
Q

What changes causes an increase in sensitivity of peripheral chemoreceptors?

A

high pCO2
low pH
low O2

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16
Q

Central chemoreceptors main stimulus

A

Hypercapnia

17
Q

Where are the 2 main locations of the central chemoreceptors

A

Brain parenchyma

Ventrolateral medulla and other brainstem nuclei

18
Q

What are the properties of the BBB

A

Separates the blood and brain extracellular fluid (BEF)
Poor ion permeability
CO2 moves across easily

19
Q

What is the buffering power like in the BEF?

A

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

20
Q

With a change in plasma pH- what are the differences in response in metabolic and respiratory disorders

A

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

21
Q

What is the integrated chemoreceptor response to respiratory acidosis?

A

Central chemoreceptors more important- tonic drive for breathing
However peripheral receptors respond faster

22
Q

What is the integrated chemoreceptor response to metabolic acidosis?

A

If severe- hyperventilation
Peripheral receptors involved in short term response
Central receptors- longer term

23
Q

3 main renal mechanisms involved in balancing acids and bases

A
  1. HCO3- handling (net reabsorption of bicarbonate)
  2. Urine acidification (binding H+ with buffers)
  3. Ammonia synthesis
24
Q

What causes respiratory acidosis?

A

lung disease-

emphysema, chronic bronchitis

25
Q

What causes respiratory alkalosis?

A

hyperventilation-

due to stress,fear, pain

26
Q

What causes metabolic acidosis?

A

ingestion of acid

loss of alkaline fluid- diarrhoea, cholera

27
Q

What causes metabolic alkalosis?

A

ingestion of alkaline fluid

loss of acid- vomiting

28
Q

Symptoms of Liddles syndrome

A

Hypertension
Hypokalaemia
Metabolic alkalosis

29
Q

What causes Liddle’s syndrome and how is it treated

A

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

30
Q

Types of diabetes insipidus

A

Central- impaired AVP production
Nephrogenic- impaired AVP effect
Gestational- AVP metabolised

31
Q

Causes of central and nephrogenic DI?

A

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

32
Q

Treatments of DI

A

Central- desmopressin
Nephrogenic- modulatory drugs
pharmacological chaperones