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Renal Recap Flashcards

1
Q

Label the Nephron

A
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2
Q

What is the difference between the Principal Cells and Intercalated Cells in the CD?

A

Principal cells have a few mitochondria, mostly function for NaCl reabsorption and K secretion.
Intercalated cells have a lot of mitochondria and function in acid-base regulation. Some IC secrete H+, some secrete HCO3-

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3
Q

What is the structure of the juxtaglomerular apparatus?

A

macula densa of thick ascending LH + extraglomerular mesangial cells + granular cells of afferent arteriole (manufacture, store, and secrete renin)

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4
Q

What is the function of the juxtaglomerular apparatus?

A

sense Na/pressure, involved in autoregulation of renal blood flow, GFR, systemic BP control

Increase in afferent arteriole pressure 🡪 increased glomerular pressure 🡪 increased GFR.
Increased Na/K delivery to macula densa 🡪 decreased renin. And viceversa.

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5
Q

Within what range of systemic BP is the (healthy) kidney able to provide auto-regulation of renal blood flow?

A

80-180 mmHg

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6
Q

What happens to renal blood flow and GFR with dilation of the afferent arteriole?

A

RBF: up
GFR: up

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7
Q

What happens to renal blood flow and GFR with Constriction of the afferent arteriole?

A

RBF: down
GFR: down

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8
Q

What happens to renal blood flow and GFR with Dilation of the efferent arteriole?

A

RBF: up
GFR: down

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9
Q

What happens to renal blood flow and GFR with constriction of the efferent arteriole?

A

RBF: down
GFR: up

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10
Q

Name the 3 main renal transport mechanisms:

A
  1. Passive transport (diffusion)
  2. Active transport
  3. Endocytosis
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11
Q

Describe passive transport (diffusion)

A

Movement down a concentration gradient or electrical gradient.

Includes solvent drag (movement of ions with water even if not with concentration gradient) and Facilitated diffusion (passive, but requires transport protein- uniport, smport, antiport, or secondary active transport)

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12
Q

Describe Active transport

A

coupled directly with energy (ATP)

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13
Q

Describe endocytosis

A

movement by invagination of plasma membrane, does require ATP

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14
Q

Draw and explain the basic mechanisms of electrolyte reabsorption/secretion in the kidneys.
This does not have to be a specific site or electrolyte.

A
  1. Active transport at the basolateral membrane (3Na/2K/ATPase pump) creates a gradient (Na out of cell into interstitium, K into cell)
  2. Passive transcellular transport at the luminal membrane driven by concentration gradient, partially created by the active pump (cotransporters, antitransporters) and partially created due to lower concentration of electrolytes in blood (highly filtered at glomerulus)
  3. Paracellular transport driven by transepithelial (transmembrane) potential difference (electrical charge)- lumen positive or lumen negative
    Paracellular solute drag along with water (aids with reabsorption)
  4. “Sink” effect from rapid tubular flow (aids excretion)
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15
Q

What is the PRIMARY function of the proximal tubule?

A

reabsorption of most water (67%) and solutes (Na, Cl, K, glucose, AA’s) linked to Na/K ATP-ase pump in basolateral membrane

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16
Q

What is the PRIMARY function of the thin descending LH?

A

H20 reabsorption through aquaporins with NO NaCl

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17
Q

What is the PRIMARY function of the thin ascending LH?

A

Na/Cl reabsorbed through passive diffusion, NO H20

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18
Q

What is the PRIMARY function of the Thick ascending LH?

A

Reabsorption of solutes via Na/K/ATPase in basolateral membrane. NO H20. “Diluting segment”- solutes out of tubule, H2O stays in.

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19
Q

What is the PRIMARY function of the distal tubule?

A

“Adjustment” of lytes but impermeable to H20

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20
Q

What is the PRIMARY function of the late distal tubule and the CD?

A

Principal cells: reabsorb Na/H2O, secrete K

Intercalated cells:
— α-intercalated cells secrete H+, reabsorb HCO3- and K+
— β-intercalated cells secrete HCO3-, reabsorb H+ and Cl-

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21
Q

Angiotensin II:

Major stimulus:
Nephon site of action:
Effect on transport:

A

Major stimulus: ↑ Renin

Nephon site of action:
Proximal tubule
Thick ascending limb
Distal tubule /Collecting duct

Effect on transport: ↑ NaCl and H2O reabsorption

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22
Q

Aldosterone

Major stimulus:
Nephon site of action:
Effect on transport:

A

Major stimulus: ↑ Angiotensin II
↑ [K+]p

Nephon site of action:
Thick ascending limb
Distal tubule /Collecting duct

Effect on transport: ↑ NaCl and H2O reabsorption

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23
Q

ANP, BNP, urodilatin

Major stimulus:
Nephon site of action:
Effect on transport:

A

Major stimulus: ↑ ECFV

Nephon site of action: Collecting duct

Effect on transport: ↓ H2O and NaCl reabsorption

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24
Q

Uroguanylin, guanylin

Major stimulus:
Nephon site of action:
Effect on transport:

A

Major stimulus: Oral ingestion of Nacl

Nephon site of action:
Proximal tubule
Collecting duct

Effect on transport: ↓ H2O and NaCl reabsorption

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25
Sympathetic nerves Major stimulus: Nephon site of action: Effect on transport:
Major stimulus: ↓ ECFV Nephon site of action: Proximal tubule Thick ascending limb Distal tubule /Collecting duct Effect on transport:↑ NaCl and H2O reabsorption
26
Dopamine Major stimulus: Nephon site of action: Effect on transport:
Major stimulus: ↑ ECFV Nephon site of action: Proximal tubule Effect on transport: ↓ H2O and NaCl reabsorption
27
ADH/AVP Major stimulus: Nephon site of action: Effect on transport:
Major stimulus: ↑ Posm ↓ ECFV Nephon site of action: Distal tubule /Collecting duct (aquaporins) Effect on transport:↑ H2O reabsorption
28
Briefly explain RAAS
- Juxtaglomerular cells in the afferent arterioles synthesize and secrete renin - Renin secretion is stimulated when: -- Perfusion pressure to the kidneys is reduced -- Sympathetic innervation to the kidneys is activated -- NaCl delivery to the macula densa is decreased - Renin converts Angiotensinogen (produced by liver) 🡪 Angiotensin I -- AT I 🡪 AT II by ACE in the kidneys and lungs -- AT II stimulates aldosterone secretion, vasoconstricts arterioles, stimulates ADH + thirst, and enhances NaCl reabsorption by the kidneys
29
What is the primary regulator of K secretion in the kidney?
Aldosterone
30
Define Net endogenous Acid production (NEAP)
The production of non-volatile acid to the body daily. Due to diet, cellular metabolism, and the loss of bicarbonate in the feces.
31
Define Renal Net Acid Secretion
The amount of acid secreted by the kidney per day, typically equal to the NEAP
32
What are the 2 main buffer systems in the kidney that lead to formation of new HCO3?
Phosphate and Ammonia
33
What is the expected compensatory response for metabolic acidosis?
0.7 decrease in pCO2 for every 1mEq decrease in HCO3
34
What is the expected compensatory response for metabolic alkalosis?
0.7 increase in pCO2 for every 1mEq increase in HCO3
35
What is the expected compensatory response for respiratory acidosis?
Acute: 0.15 increase HCO3 for 1mmHg pCO2 Chronic: 0.35 increase HCO3 for 1mmHg pCO2
36
What is the expected compensatory response for respiratory alkalosis?
Acute: 0.25 decrease HCO3 for 1mmHg pCO2 Chronic: 0.55 decrease HCO3 for 1mmHg pCO2
37
What portion(s) of the kidney contain Calcium Sensing Receptors (CaSR’s)?
Thick Ascending LH and Proximal Tubule
38
What is the primary regulator of urinary Calcium excretion? What effect does this hormone have on calcium and phosphorus?
PTH - it increases calcium reabsorption (decreases excretion) and increases phosphorus excretion (inhibits reabsorption)
39
Label the following diagram with the diuretic that acts at each site.
1. Diuretic: Furosemide (loop) 2. Diuretic: Thiazides 3. Diuretic: K sparing 4. Diuretic: Osmotic (Mannitol)
40
Explain the net effect of Furosemide (inhibition, stimulation, electrolyte changes in the patient).
- Loop diuretic - Net effect: inhibits Na/K/2Cl cotransporter, leading to increased loss of Na/K/Cl in urine 🡪 increased water loss. - **MOST POTENT- loop of henle is the main site of creation of the urine concentration gradient**
41
Explain the net effect of Thiazides (inhibition, stimulation, electrolyte changes in the patient).
- Net effect: inhibits Na/Cl cotransporter leading to increased Na/Cl and water loss in the urine. - Less potent because the DCT is mostly for fine tuning (not large volume of electrolyte movement).
42
Explain the net effect of K sparing diuretics (inhibition, stimulation, electrolyte changes in the patient).
- Net effect: block Na channels in the CD (ENaC- amilioride, triamterene) , so less Na reabsorption. - Aldosterone antagonists (like spironolactone) antagonize the effect of aldosterone on these channels. - Loss of Na and water, but not K.
43
Explain the net effect of osmotic diuretics (mannitol) (inhibition, stimulation, electrolyte changes in the patient).
Net effect: inability to reabsorb H20 due to osmotic pull into tubule
44
What are the 4 methods of solute/water movement across the dialysis membrane?
Ultrafiltration Diffusion Convection Adsorption
45
Describe Ultrafiltration
movement of water only (either pressure or osmotic)
46
Describe diffusion
solute moves down concentration gradient, small molecules
47
Describe convection
solute moves with drag due to water flow, medium molecules
48
Describe adsoprtion
solute binds to the membrane itself, larger molecules
49
List the indications for renal replacement therapy
Azotemia not responsive to traditional therapy Severe uremic symptoms Severe hyperkalemia Oliguria Volume overload Diffusible toxins
50
What is dialysis disequilibrium syndrome?
- Rapid changes in osmolarity (drop in BUN) can lead to fluid shifts into the brain 🡪 cerebral edema, neurologic symptoms, death - Need to drop BUN slowly at first - Can prophylactically give mannitol in high-risk patients (BUN >150, < 5kg) - Can use “sodium profiling” with initially high-sodium dialysate
51
Label the diagram with the 4 different modes of CRRT/hemodialysis.
SCUF - CVVH CVVHD - CVVHDF
52
Describe SCUF.
= slow continuous ultrafiltration - No dialysate or replacement fluids - Just fluid removal (ie CHF)
53
Discuss CVVH.
= continuous veno-venous hemofiltration - Removal of solutes via convection (also ultrafiltration) - Needs replacement fluid, no dialysate
54
Discuss CVVHD.
=continuous veno-venous hemodialysis (also ultrafiltration) - Removal of solutes via diffusion, no convection - Dialysate only, no replacement fluids
55
Discuss CVVHDF.
= continuous veno-venous hemodiafiltration - Removal of solutes by diffusion, convection, ultrafiltration - Dialysate and replacement fluid
56
What are the possible treatment options for obstructive ureteral disease?
- Medical management: IVF, osmotic diuretics, smooth muscle dilators, renal replacement therapy - Nephrostomy tube (short term) - Ureterotomy - Ureteral re-implantation - Ureteral stenting - Subcutaneous ureteral bypass - Renal transplant
57
What percentage of cats with urethral obstruction due to idiopathic causes will reobstruct ever in their lifetime?
33-50% depending on study
58
Debate: is a uroabdomen a surgical emergency?
Yes: can cause significant chemical peritonitis, could be a septic peritonitis (if other internal injuries or if urine was infected), hyperkalemia can be life threatening No: can divert urine with combination of abdominal and urinary catheter to get patient more stable
59
What are the 4 phases of AKI?
1. Initiation phase 2. Extension phase 3. Maintenance phase 4. Recovery phase
60
Discuss the initiation phase of an AKI
- Intervention may prevent progression to more severe injury. - Injury is at subcellular level and may not be biochemically evident.
61
Discuss the extension phase of an AKI
- Cellular injury progresses to cell death - Biochemical derangements and clinical manifestations of disease manifest
62
Discuss the Maintenance phase of an AKI.
- Both cell death and regeneration occur simultaneously - The potential for and length of recovery may be determined by the balance b/w these processes. - Removal of inciting cause does not alter existing damage but may allow for balance to shift in favor of parenchymal regeneration.
63
Discuss the recovery phase of an AKI.
- Characterized by improvement of GFR and tubular function - May last weeks to months.
64
Do fluids fix kidneys? Explain your answer.
Yes: Dehydration and poor perfusion are detrimental to the kidneys. Fluid therapy once re-hydrated and hemodynamically stable can help to replace losses (higher losses if polyuric + insensible losses) to prevent future development of dehydration. Appropriate amounts of fluids are helpful. No: Fluid overload has been found to be more harmful to the kidneys than being mildly dehydrated. Renal edema worsens urine output. Edema of other organs is also very harmful (ie GI edema- nausea/ileus, cerebral edema, pulmonary edema). More fluids are not better.
65
Explain the basic concept/utility of staging systems for acute kidney injury and name them.
- These are a way to track/identify renal injury in hospitalized patients and aid in prognosis - Based on single Creat or rise in creat + urine output - Studies have shown that any rise in creat, even if still within reference range, increases risk of death! - RIFLE/AKIN (human), VAKI (Veterinary)
66
Why do patients with CKD become anemic? Based on this, what would be ways to treat it?
- Inadequate EPO production, blood loss (uremic ulceration, iatrogenic from sampling), decreased RBC lifespan due to uremic damage, anemia of chronic disease (illness/inflammation related bone marrow suppression, iron deficiency) - Minimize uremia, antacids, minimize blood draws, hormone supplementation (Darbo preferred to EPO- less anti-EPO-antibody formation)
67
What 3 criteria are used to determine IRIS stage for CKD?
- Degree of azotemia (determined by STABLE Creat) - Proteinuria - Hypertension
68
BRIEFLY name/explain the 3 main theories for perpetuation of kidney injury (from canine remnant kidney model)
1. Intact nephron hypothesis: If 1 part of a nephron is damaged, remaining parts degenerate so whole nephron is lost. Remaining intact nephrons hypertrophy to compensate for the increased load (hyperfiltration) which damages them. 2. Hyperfiltration theory: Remaining nephrons are hyperperfused, have hyperfiltration, and glomerular hypertension + glomerular inflammation 🡪 Proteinuria 🡪 nephron damage. 3.Trade-off hypothesis: Phosphorus build up, ionized hypocalcemia 🡪 high PTH levels, low calcidiol/calcitriol levels, high FGF-23 levels 🡪 faster progression of CKD
69
Explain the pathogenesis of renal secondary hyperparathyroidism.
- Loss of nephron mass from chronic disease increase in serum Phos 🡪 increased FGF-23 (which binds to receptor only with the help of his friend Klotho which is present in kidneys and parathyroid gland) - Phos initially is kept in normal range - FGF-23 and progressive renal disease both cause decreased calcitriol/calcidiol production 🡪 low iCa 🡪 PTH secretion - Normalizes iCa but also increases serum Phos (and PTH is now increased) - Worsening GFR/hyperphosphatemia 🡪 further increase in FGF-23 and further decreases in calcitriol/calcidiol 🡪 worsening hypocalcemia, continual increase in PTH, Phos also gets much worse because FGF-23 stops working (not enough tubules, not enough receptors) - Chronic bone reabsorption 🡪 loss of bone mass - This whole process speeds up progression of CKD
70
List the most effective ways to slow the progression of CKD
- Renal diet (phosphorus limited + fatty acids/antioxidants, also low protein which is less important) - Phosphate binders if not controlled enough with diet - Calcitriol supplementation - Mimimize proteinuria and glomerular hypertension (ACE inhibitors) - Control systemic hypertension - All of these are most effective earlier, rather than later
71

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