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ACVIM GENERAL MY OWN > Renal urinary > Flashcards

Renal urinary Flashcards

1
Q

What are the three main functions of the kidneys?

A

1) excretion
2) endocrine organ
3) homeostasis

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2
Q

The kidney excretes products that need to be retained, and waste products to be discarted. Why take this approach and not just eliminate the waste product?

A

Two reasonds;
1) Speed; dumping everything out and then taking back what is needed is fast, and toxins can be eliminated in as little as 30 min
2) selectivity; it is more efficient to have a limited number of receptors to reabsorb the limited amount of things you need to retain, rather than have an near infinite nuber of receptors to excrete the near infinite number of toxins/metabolites etc that need to be waisted

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3
Q

What is the total energy use of the kidneys and why is it so low?

A

~10% of daily total body energy consumption (heart is ~7%). This is so low, because the kidneys use osmotic gradients to control water retention/excretion which do not require ATP

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4
Q

What occurs in the cortex and the medulla of the kidney ?

A

Cortex contains the glomeruli where blood filtration occurs. The medulla contains the nephrons which are responsive for re-absorbtion of products.

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5
Q

What is acute interstitial nephritis?

A

Inflammatory condition affecting the renal interstitium.
Symptoms may include an acute rise in plasma creatinine levels and
proteinuria (protein in urine), both reflecting a general renal dysfunction.

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5
Q

What are causes of acute interstitial nephritis? Is this reversible?

A

AIN usually results from drug exposure, -lactam antibiotics (e.g., penicil-
lin and methicillin) being the most common offenders. 1 Kidneys typically
recover normal function after discontinuing drug use.

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6
Q

What is polycystic kidney disease?

A

inherited disorder characterized by the presence of
innumerable fluid-filled cysts within the kidneys and, to a lesser degree,
the liver and pancreas. The cysts form within the nephron and progres-
sively enlarge and compress the surrounding tissues, preventing fl uid
flow through the tubules.

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7
Q

Symptoms associated with polycystic kidney disease?

A

many patients remain asymptomatic,
others may begin to show symptoms of impaired renal function such as
hypertension. Elevation in crea and BUN can result in innapetence, nausea and weight loss.

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8
Q

What is the treatment for polycystic kidney disease?

A

There is no treatment

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9
Q

What is the difference in tissue osmolarity between the different regions of the kidney and why the difference?

A

The cortex has an osmolality that approximates that of plasma, but the osmolality
of the inner medulla is increased severalfold. This osmotic gradient is essential to normal kidney function because it is used to recover virtually all of the water that is filtered from the vasculature each day

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10
Q

Which vascular networks are responsible for blod filtration and reabsorbtion

A

1) filtration; Glomerular capillary network
2) peritubular capillary network

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11
Q

Describe the glomerular capillary network of the kidney

A

Blood enters the glomerulus via an interlobular artery. Blood passes down at high pressue (~60mmHg) into the afferent arteriole that pases this into a tuft of specialised glomerular arteries. The glomerular arteries are porous, and anastamose to one another to maximise the filtration surface area. Spaces between the capillaris are filled with mesangial cells, an epithelial cell that can contracts and relaxes as a way of controlling glomerular capillary surface area and filtration rate. Blood leaves the glomerular capillariers through an efferent arteriole the leads back into an a peritubular capillary network that runds along the ascending limb of the tubule. These will then anaestamose into the peritubular veins that lead into the interlobular vein.

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12
Q

Where can the peritubular network be found and what are its roles?

A

This originates from the afferent arteriole and closely follows the renal tubule in the kidney eventulaly merging into the peritubular venous netwok
Roles include
1) providing O2 and nutrients to the tubule
2) carries away fluid and solutes that have been reabsorbed from the tubule lumen
3) prompt solute removal allows the concentration gradient to be maintained between the tubule and blood

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13
Q

What are the segments of the tubule (in order) ?

A

1) glomerulus
2) Proximal convoluted tubule (PCT)
3) proximal straight tubule (PST)
4) Descending thin limb
5) ascending thin limb
6) loop of henle
7) Ascending thick limb
8) distal convoluted tubule
9) cortical collecting duct
10) outer medullary collecting dusct
11) inner medulalry colelecting duct

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14
Q

Do juctamedullary and superficial nephrons interact ?

A

The connect tohether at the Cortical collecting duct of via the connecting tubule that lins the aformentioned with the distal convoluted tubule of the superficial nephron

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15
Q

what is the renal corpuscle and where is it located?

A

Glomerulus + bowmans capsule. Located in the cortex of the kidney

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16
Q

What is the bowmans space?

A

Filtrate from the glomerular capillaries filters into the bowmans space, which then enters the proximal tubule

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17
Q

Draw the layout of the nephron throughout the kidney layers

A
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18
Q

What are the differences between superficial and juxtaglomerular nephrons?

A

Superficial;
- receive 90% of renal blood supply
- reabsorb the majority of the filtrate
- glmeruli are in the cortex and they have short nephrons
- loops dip into the outer medulla but not medulla

Juxtaglomerular:
- receive 10% of blood
- glomeruli located in th einner cortex
- long nephron loops that dive into the inner medulla.
- have a specialised peritubular network
- juxtamedullary neprons plus the capillaries that follow dive deep into the medulla and form the vasa recta
- juxtamedullary nephrons are designed to concentrate urine

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19
Q

In the kidney what are the forces hat promote fluid filtration and retention?

A

1) filtration - capillary hydrostatic pressure (Pgc)
2) Colloing osmotic pressure (πgc)

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20
Q

what happens if capillary hydrostatic pressure increases?

A

increased urine production up until the point where we have hypertensive damage

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21
Q

What is the force that governs fluid movement accross the glomerular capillary wall and what is the formula?

A

Starling equation
GFR= Kf[(Pgc-Pbs)-(πgc-πbs)]

Kf= glomerular filtration coeficient
Pbs and πbs; are hydrostatic and colloid osmotic pressure of fluid in the bowmans space)

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22
Q

What is Kf in the starling equation ?

A

Filtration coeficient. Representation of the filtration ability of the filtrate barrier. It is a measure of glomerular permeability and the surface area

23
Q

What is the filtrate barrier and what layers is it made of?

A

There are 3 layers, which create a 3 step molecular filter which produces protein and cell free plasma ultrafiltate. The three layers are;
1) Capillary endothelial membrane
2) Thick glomerular basement membrane
3) filtration slit diaphram

24
Q

Describe the glomerular capillary endothelial membrane (of the filtrate barrier) structure and function?

A

Layer 1; Dense endothelial layer with fenestrations (pores of ~70nm) which allow free passage of water, solutes and proteins. Cells cannot pass and are trapped in the vasculature.

25
Q

Describe the thick glomerular basement membrane structure and role (Filtration barrier)

A

Comprised of 3 layers (inner->outer)
1) lamina rara interna
2) lamina densa
3) lamina rara externa

The lamina rara externa if fused to podocytes.
The basement membrane has a net negative chare that repels proteins (also carry a negative charge) and reflects them back into the vasculature.

26
Q

Draw a diagram of the 3 layers of the filtration barrier and its constituents

A
27
Q

What is the filtration slit diaphragm?
Describe it

A

Layer 3 of the filtration barrier.
Glomerular capillaries are ensheathed in tentacle like processes from the podocytes. The podocyte tentacles, and “toes” that come off them form gaps in which a gelatinous filtration slit diaphragm lives. This filtration slit diaphram prevents proteins entering the bowmans space

28
Q

Define the shifts in colloid oncotic pressure along the renal capillary network

A

πgc is ~25mmHg when it enters the glomerulus. This is the same as in the rest of the circulation. As water and solutes pass through into the bowmans space, protein is left behind. Blood looses 15-20% of its total volume to filtrate during passage through the capillary netweork increasing the colloid oncotic pressure to the point that this ~35mmHg when it enters the efferent arteriole

29
Q

What is the colloid oncotic pressure of the bowmans space?

A

πbs In healthy individuals it should be 0 as proteins are prevented from entering the BS by the basement membrane and filtration diaphragm

30
Q

What is the hydrostatic pressure of the bowmans space?

A

Pbs, is ~15mmHg due to the large veolume of fluid that enters this space from the higher driving hydrostatic pressure in the capillaries of the glomerulus (~60mmHg)

31
Q

Is the hydrostatic pressure of the glomerular capillaries comparable to other capillary beds?

A

No, it is higher. Glomerullar Pgc is ~60mmHg, which is ~25mmHg higher than other capillary beds.

32
Q

How may mesangial cells affect glomerular filtration?

A

Through
changes in glomerular capillary surface area, which
affects K f. The role of mesangial cells is minor com-
pared with that of glomerular arterioles, however

33
Q

What are the main factors that regulate GFR?

A

Pgc, which is determined by the aortic pressure, renal arterial pressure and by changes in afferent and efferent vascular resistance

34
Q

How does vasocontriction/dilation of the afferent arteriole affect GFR and ultrafiltrate pressure (Puf) ?

A

It reduces GFR and Puf. This is because contriction decreases glomerular blood flow. Dilation is the opposite

35
Q

How does efferent arteriolar constriction/dilation affect GFR/Puf?

A

Constriction increaseds vascular resistance and increases pressure of the glomerular blood increasing GFR and Puf. Dilation reduces pressure and allows blood to flow out of the network faster reducing GFR and Puf.

36
Q

What are the two main mechanisms that regulate renal blood flow (RBF) and GFR ?

A

1) Local vascular autoregulation; maintain RBF and optimise GFR
2) Central homeostatic control; Occurs through the atonomic nervous system can overide the local control and it will do so to adjust vlood volume and blood pressure.

37
Q

What are the regulatory systems in the kidney and what are their roles;

A

1) Autoregulation;
2) Myogenic response
3) Tubuloglomerular
4) Paracrine
5) Central

38
Q

what is the pathophysiology of disease behind glomerular disease?

A

Glomerular disease damages the filtration barrier and
increases Kf, thereby allowing cells and proteins to pass into the tubule.

39
Q

What are the two main subtupes of glomerular disease and what heps distinguish these?

A

Glomerular disease can be divided into two broad and overlapping syndromes based on the characteristics of proteins and cellular debris contained within urine (urine sediments) and the associated symptoms: nephritic syndrome and nephrotic syndrome

40
Q

What is nephric syndrome and describe the pathophysilogy?

A

associated with diseases that cause inflammation of the glomerular capillaries, mesangial cells, or podocytes (glomerulonephritis). Inflammation creates localized breaches in the filtration barrier and allows cells and modest amounts of protein to escape into the tubule and appear in urine (proteinuria). Red cells typically collect and aggregate in the distal convoluted tubule and then appear in urine as tubular red cell casts

41
Q

How can you identify nephrotic syndrome clinically

A

Nephrotic syndrome refers to a set of clinical findings that include heavy proteinuria (>3.5 g/day), ipiduria, edema, and hyperlipidemia. Cell casts, which are characteristic of an inflammatory process, are
absent

42
Q

What is the pathophysiology behind nephrotic syndrome?

A

Nephrotic syndrome reflects a general deterioration of the renal tubule (nephrosis) that includes degradation of glomerular barrier function and is a frequent cause of mortality in patients with diabetes mellitus. Loss of plasma proteins in urine causes plasma oncotic pressure to fall and accounts for the generalized edema associated with nephrotic
syndrome. Hyperlipidemia reflects increased lipid synthesis that helps compensate for loss of lipids in urine.

43
Q

How is RBF and GFR regulated by the renal tubule?

A

The loop of Henle comes into direct contact with the afferent and efferent arterioles after returning from the medulla. The TAL wall is modified at the contact site to form a specialized sensory region called the macula densa.
The macula densa monitors Na and Cl concentrations within the tubule lumen, which, in turn, reflect RBF and GFR. Na and Cl permeate macula densa cells via a Na-K-2Cl cotransporter located in the apical membrane. Cl immediately exitsvia a basolateral Cl channel, causing a membrane depolarization whose magnitude is a direct reflection of tubule fluid NaCl
concentration.

44
Q

How are mesangial cells involved in renal autoregulation ?

A

Mesangial cells provide a physical pathway for communication between the sensory (macula densa) and effector (arteriole) arms of the TGF system. All cells in
the JGA are interconnected via gap junctions , which
allows for direct chemical communication between the system components.

45
Q

Draw the juxtaglomerular apparatus and its constituents?

A
46
Q

How is the afferent arteriole involved in autoregulation?

A

The afferent arteriole is notable for its adenosine
receptor and for renin-producing granular cells within its walls.

A) Adenosine receptor; A1 receptors are bound to a downregulatory G protein–coupled receptor -> reduces cAMP pathway. cAMP normally inhibits smooth muslce contractily via PKA. Thus when the afferent arteriole binds adenosine it constricts

B) Granular cells; secrotory cells which contain renin granules. Release rening -> RAAS increase -> increase ANGII whuc is vasoactive

47
Q

How are efferent arterioles autoregulated ?

A

These have A2 (adenosine 2 receptors) which bind adenosine -> Gprot -> increase cAMP -> efferent arteriolar dilation

48
Q

What is autoregulation as a regulatory response in the kidneys ?

A
  • Stabilises RBF and GFR during mean arterial pressure (MAP) changes.
  • GFR remains stable with MAPS between ~80-180mmHg)
49
Q

What is the myogenic regulatory response?

A

Myogenic response
- MEchanoreceptors in the smooth muscle of afferent arterioles cause a calcium release during vascular stretching causing vascular constriction
- this myogenic response stabilises GFR and RBF during chnages in posture

50
Q

What is the tubuloglomerular feedback system?

A
  • autoregulatory mechanism mediated by the juxtaglomerular apparatus (JGA)
  • Complex involves the renal tubule, mesangial cells and afferent/efferent arteioled.
  • Adjusts RBF and GFR flow through th etubules
51
Q

What is the role of the paracrine autoregulation ?

A

several hormoes are involved
- Prostaglanding and NOX; dilate glomerular arterioles and increase RBF and GFR. May be released in response to ANGII vasocostriction in shock
- Endothelins; local vasocostrictions released in responde to ANGII or when glomerular flow rates are damagingly high
-ANGII; RAAS is the primary autoregulation system which regulates RPF and GFR. ANGII is the hormonal link between GFR and blood pressure

52
Q

How is RPF and GFR controlled centrally?

A

kidney governs total body water and Na content, which, in turn, determines blood volume and MAP. The kidney also receives 10%
of cardiac output at rest, a significant blood volume that might be used to sustain more critical circulations (e.g., cerebral and coronary
circulations) in the event of circulatory shock Renal
blood flow is, thus, subject to control by the ANS, acting through neural and neuroal and/or endocrine pathways.

53
Q

What are the two central regulatory pathways which affect RBF and GFR?

A

1) Neural
2) endocrine

54
Q

What are neural central controls?

A

Glomerular arterioles are innervated by noradrenergic
sympathetic terminals that activate when MAP falls. Sympathetic activation raises systemic vascular resistance by restrict ing blood flow to all vascular beds, including the kidneys. Mild sympathetic stimulation preferentially constricts the efferent arteriole, which reduces RBF while simultaneously maintaining GFR at sufficiently high levels to ensure continued kidney function. Intense sympathetic stimulation severely curtails blood flow through both glomerular arterioles, and urine formation ceases.
In cases of severe hemorrhage, prolonged occlusion of arteriolar
supply vessels can cause renal ischemia, infarction, and failure

55
Q

What are the centrally controlled endocrine pathways?

A

Hormonal regulation of RBF is mediated principally
by epinephrine and atrial natriuretic peptide (ANP). Epinephrine is released into the circulation following sympathetic activation and stimulates the same pathways as does norepinephrine released from sympathetic nerve terminals. ANP is released from cardiac atria when they are stressed by high blood volumes. The ANP receptor has intrinsic guanylyl cyclase activity that dilates the afferent arteriole and increases RBF. It also relaxes mesan gial cells to increase filtration barrier surface area. The net result is an increase in RBF and GFR and salt and water excretion

56
Q
A

ACVIM GENERAL MY OWN (10 decks)

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