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Year 2 (&1) NSF Urinary > Yr1 Regulation GFR, K+ and BP > Flashcards

Yr1 Regulation GFR, K+ and BP Flashcards

1
Q

What is GFR

A

Glomerular filtration rate - volume of fluid filtered from the glomerular capillaries into bowman’s space per minute mls/min IT IS A RATE

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2
Q

Why is the regulation of GFR important?

What if too hgih or low?

A
  1. don’t want the GFR to change whenever blood pressure does as would mean whenever do any exercise change filtration NOT GOOD
  2. Too high GFR - Too much filtrate, and increased urine production (diuresis). Needed substances pass too quickly thro tubules, insufficient reabsorption = lost in urine
  3. Too low GFR - too little filtrate. Reduced flow of filtrate. Certain waste substances may not be excreted
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3
Q

What is autoregulation?

A
  1. Maintains GFR during short term and moderate variations in mean arterial pressure by changing resistance of the afferent arteriole
  2. All about changing the resistance of the afferent arteriole by 2 mechanisms:
  • Tubuloglomerular feedback
  • Myogenic response
  1. afferent arteriole constricts = GFR decreases
  2. afferent arteriole dilates = GFR increases
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4
Q

What is the JUXTAMEDULLARY apparatus?

main function

A
  1. The ascending LOH (google says DCT) runs between afferent and efferent blood vessels
  2. Adjacent cells of the juxtaglomerular cells (arteriole cells) and macula densa (tubule cells) form the J apparatus
  3. main function is to regulate blood pressure and the filtration rate of the glomerulus.
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5
Q

What are the 2 mechanisms whereby autoregulation occurs?

A
  1. Tubuloglomerular feedback - measures amount of filtration occuring
  2. Myogenic response – blood pressure changes in AA
  3. Both mechanisms respond to changes in BP
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6
Q

Tubuloglomerular feedback
What cells detect flow?
What happens if detech inc GFR and dec?

A
  • Macula densa cells in LOH, at angle between A and E arterioles, detect flow rate
  • if detect increase in GFR - paracrine (local) signal to neighbouring AA to constrict - reduces filtration rate
  • Detect decreased GFR - vasodilation in AA to increase GFR
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7
Q

Myogenic response

A

blood pressure changes in AA
• Contraction of vascular myocytes in afferent arteriole: vasoconstriction
• Relaxation of vascular myocytes in afferent arteriole that follows a reduction in pressure: vasodilation

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8
Q

Talk about K+ homeostasis

A

 K+ not stored in the body
 Major component of intracellular fluid in all animals and plants
 Urine concentration of K+ is greater than ECF
 Concentration of K+ in ECF is relatively low
 More potassium may be excreted than was originally filtered
 Regulation of secretion is more important than regulation of reabsorption
1. Secretion in DCT
 Principle cells in DCT
1. Asymmetric, large amount Na+ and K+ ATPASE driving Na+ gradient
2. Leaky channels on apical side (tubular), allow Na+ and K+ to move down conc gradients
3. Difference to cells in PCT, in DCT  regulated by hormone aldosterone

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9
Q

Adrenal Gland

A

 Paired = lie cranial medially in bod
 Adrenal gland produces whole range of hormones
3. has distinct functional zones: Medulla, cortex
4. MEdulla secretes hormones like adrenaline and noradrenaline
5. Zona glomerulus (outermost part of cortex) secretes aldosterone

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10
Q

Aldosterone and K+ conc

A
  1. negative feedback mechanism
  2. If [K+] in plasma goes UP = adrenal gland empties ALDOSTERONE into blood stream, binds to receptos n principle cells DCT, take more K+ into cell, flows down conc gradient and into urine
  3. ALDOSTERONE is released in response to HIGH K+
  4. If K+ conc goes down in blood, less is released
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11
Q

How is systemic blood pressure controlled?

A
  1. Neural regulation BP:
    - Baroreceptor reflex = regulated SV, HR, TPR via tone of vasculature
  2. Hormonal regulation BP:
    - angiotensin 2= long term regulation, regulates stroke volume, regulates TPR via tone of the vasculature
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12
Q

Mean arterial pressure =

A

Pa = CO x TPR

Mean arterial pressure = CO X total peripheral resistance

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13
Q

Kidney and the CV system

A

• Kidney  25% blood volume

  1. HUUUGE effect on peripheral resistance and CO
  2. Also massively affected by large changes in BP
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14
Q

Renin and Kidney

A
  1. RENIN is released from Juxtaglomerulat cells (in AA)
  2. Angiotensinogen manufactured in LIVER, released in blood
  3. Renin in blood stream converts angiotensinogen to angeiotensin 1 in plasma, once in lungs, enzyme in lungs convert to Angiotensin 2!
  4. Sooooo lot of renin means lots of Ag2
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15
Q

Physiological effects of angiotensin 2

A

It is released in response to decreased blood pressure over time
Systemic effects:
• Arterioles vasoconstrict
• Total Peripheral Resistance

  • CV control system in Medulla O reflexes to inc BP
  • Increases CO and TPR this increases BP
  • hypothalamus, ADH secretion and inc thirst
  • adrenal cortex secreted aldosterone (more K+ in urine)
  • proximal tubule

Effects on GFR:
Overall decreases as decreases blood flow in afferent arteriole but GFR is preserved to a degree as constriction of efferent arteriole helps preserve hydrostatic pressure

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16
Q

What is angiotensin 2’s affect on the adrenal cortex

A
  1. SO important
  2. Ag2 in blood binds to receptors on adrenal cortex causing release of aldosterone
  3. Aldosterone directly controls K+ concentration
  4. By stimulating principle cells in CD to secrete more K+ and reabsorb more Na+ and Cl-
  5. Water follows Na+ so increases blood volume, therefore pressure
  6. a significant drop in BP causes activation RAAS: renin whihc activates angiotensin which causes aldosterone to be released from adrenal gland cortex
17
Q

So what are the types of regulation aldosterone has?

A

2 types
1. K+
2. BP
Inc plasma [K+]
= adrenal gland empties ALDOSTERONE into blood stream, binds to receptors in principle cells DCT, take more K+ into cell, flows down conc gradient and into urine
Decreased BP activates RAAS:
By stimulating principle cells in CD to secrete more K+ and reabsorb more Na+ and Cl-
5. Water follows Na+ so increases blood volume, therefore pressure

18
Q

Systemic vasoconstriction and angiotensin causes which arteriole to constrict more?

A

EFFERENT
becuase reduces blood flow
increases hydrostatic pressure in glomerular caps which helps preserve the
glomerular filtration rate!
therefore maintaining filtration pressure:)
LIMITS damaging affect of vasoconstriction
This overrides autoregulation!

19
Q

normal fluid intake?

A
  1. 2ml/kg/hr
  2. roughly 50ml/kg/day should be
  3. get this through ingestion of liquids, moist foods, metabollic synthesis of water
20
Q

Normal fluid loss?

A

1ml/kg/hr

21
Q

Types of fluid loss

A
  1. Sensible - what you are aware off e.g. kidneys adn peeing

2. insensible - not aware of e.g. exhalation from lungs, evaporation skin, faeces

22
Q

When is angiotensin 2 released

A

in response to a fall in BP

23
Q

Systemic effect of decrease BP

A
  1. Arterioles vasoconstrict
  2. adrenal cortex secretes aldosterone - stimulates principal cells in CD to secrete more K+ and to reabsorb more Na+ and Cl-. osmotic consequence more Na+ and Cl= is that more water is reabsorbed which increases blood volume thus venous return and SV, i.e aldosterone increases blood pressure
  3. Hypothalamus ADH secreted and inc thirst
  4. Medulla oblongate refelxes to inc BP
24
Q

Dec in BP effects on GFR

A
  1. dec overall as dec blood flow in afferent arteriole and GFR
  2. GFR preserved to a degree as constriction of efferent arteriole helps preserve hydrostatic pressure
25
Q

What happens is BP increases

A

o Natriuretic peptides DECREASE blood pressure  inc GFR

26
Q

Systemic effects of inc BP

A
  1. Afferent arteriole vasodilates
  2. adrenal cortex dec aldosterone secretion
  3. hypothalamus dec ADH secretion
  4. Medulla oblongata reflexes to dec BP
  5. increases GFR
27
Q

Does urine composition change between bladder and collecting duct?

A

NO except in horses where Glands in the renal pelvis and upper ureter secrete mucus. Equine urine is therefore quite viscous

28
Q

Organisation of excretory passage way innermost to outer

A

• Mucosa: innermost
o Luminal sheet of transitional epithelium : cells in multiple layers, not lined up. In areas that tend to expand (bladder and uretha)
o Lamina propria = connective tissue lies beneath epithelium
• Sub mucosa
o Not particularly large, unusually merged with lamina propria
• Muscularis Externa
o 2-3 layers smooth muscle (involuntary)
o Inner layer longitudinal, middle circular, outer longitudional
• Adventitia or Serosa

29
Q

Male urethra organsiation

A 
•	Mucosa
o	Folded longitudinally
o	Epithelium varies from TE to stratified squamous at urethral orifice
o	Lamina propria
•	Sub-mucosa
o	Usually merged with lamina propria
•	Muscularis Externa
o	2-3 layers of smooth muscle bundles
•	Adventitia or Serosa
30
Q

How is urine outflow controlled?

A

Parasympathetic effect:
1. Contraction of the detrusor (smooth) muscle (outside of bladder, in bladder wall): INVOLUNTARY.
Pelvic nerve, Ach acting on muscarinic receptors

Somatic Motor effect:
2. Inhibition of continuous excitation of External urethral sphincter (striated muscle: VOLUNTARY skeletal)
Pudendal nerve, Via inhibition Ach acting on NICOTINIC receptors
——————————
3. Internal urethral sphincter – smooth muscle: INVOLUNTARY. Reduction in alpha adrenergic tone

31
Q

What nervous system controls bladder?

A

AUTONOMIC NERVOUSSS

32
Q

Talk about Autonomic nervous system of bladder

A

Autonomic nervous system - para and sym
• Parasympathetic: rest and digest: controls detrusor muscles:
1. Parasympathetic contracts detrusor = urination
• Sympathetic nervous system: motor supply: does 2 things (oppos to para) Sympathetic relaxes Detrusor
1. Causes relaxation of D = more urine accomodation in bladder
2. Causes contraction of internal sphincter = holds urine in
3. To do with filling

33
Q

Prevention of bladder emptying nervous

A

Somatic and Sympathetic effects

  1. Somatic motor - pudendal nerve = continuous excitation of external urethral sphincter to keep tightly closed
  2. Via acetylcholine acting on NICOTINIC receptors (NM juction)

Sympathetic effects:
o Hypogastric nerve
- Contraction internal sphincter = Sympathetic motor (thoracolumbar) Via noradrenaline acting on alpha 1 ADRENO-receptors on ISM
-Relaxation detrusor = Sympathetic motor to accommodate filling Via Noradrenaline acting on beta 2 ADRENO-receptors on Detrusor muscle

34
Q

What 3 nerves are important with regards to micturition

A
  1. PELVIC (weeing contracts D Ach on M)
  2. PUDENDAL (external urethral sphincter Ach on N)
  3. HYPOGASTRIC (filling, relaxes D, Nora on B2 AR, and contracts IUS Nora on A1 adreno r)
35
Q

What would occur if pelvic nerve damaged?

A
  • Parasympathetic affected
  • Para controls Detrusor muscle
  • If motor supply to detrusor muscle, animal won’t be able to pee
  • If bladder stretched too much get a pressure necrosis. Need to manually express these animals until improve
36
Q

What would occur if pudendal nerve damaged?

A
  • Somatic supply (conscious supply)
  • Supplying external sphincter
  • If damaged animal CAN pee normally as still got supply to detrusor and sympathetic supply too
  • Might find urinary incontinent as lost inhibition to external sphincter
37
Q

What would happen if spinal damage in sacral (vertebrae over pelvis, distal spinal) section of spinal cord

A
  • Sacral section (vertebrae over pelvis) = tail
  • Often disruption to supply of lots of things as affect lot of reflexes going up and down spinal chord
  • Bladder tends to not properly contract = damage to pelvic nerve
  • Often find sympathetic side is easy to overcome so easier to express than if pelvic nerve damages

Year 2 (&1) NSF Urinary (7 decks)

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