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VTS ECC 2024 > Renal/Urinary/ECT/RAAS > Flashcards

Renal/Urinary/ECT/RAAS Flashcards

1
Q

Path of Urine Production

A

Afferent/Efferent arterioles → Glomerulus → Bowmans Capsule → PCT → Descending loop of Henle → Ascending loop of Henle → DCT → collecting ducts → minor calyces → major calyces → Renal Pelvis → Ureter → Bladder → Urethra

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2
Q

Afferent vs Efferent capillaries

Where does O2 transfer take place?

A

Afferent: Carry blood into glomerulus

Efferent: Capillaries that surround rest of nephron “peritubular capillaries”; where O2 transfer occurs; solutes return/leave blood stream

Afferent = carried towards
Efferent = carried away

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3
Q

Urinary Output

A

Dependent on GFR and BP

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4
Q

Glomerular Filtration Rate (GFR)

definition; forces affected

A

Volume of fluid filtered from kidneys/glomerular capillaries → Bowmans capsule
–Balance of hydrostatic and colloid osmotic forces
– 3–5 mL/min/kg for dogs
– 2.5–3.5 mL/min/kg for cats

per unit/time

< 80 mmHg = decreased renal blood flow/GFR

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5
Q

Baroreceptors

Regulated by;

A

Stretch receptors are primary regulators of circulating volume
hypotension/volemia; less stretch → reduces activity → activation of SANS and RAAS
Converse also true; ↑ increase of volume = decreased Renal reabsorption = ↑UOP

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6
Q

Antidiuretic Hormone (ADH)
Comes from
stimulated by; lack of ADH =

A

Small peptide secrete by pituitary gland
Stimulated by; ↑ plasma osmolality and ↓ effective circulating volume.
Absence of ADH; renal tubular cells impermeable to H2O
ADH activated V2 receptors to open aquaporin channels to move H2O back into circulation = ↓ UOP

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7
Q

Functions of the Kidneys (#5)

A

1: Blood filtration/reabsorption/secretion
2: Fluid balance regulation
3: Acid-Base regulation
4: Hormone production
5: BP regulation

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8
Q

Micro Anatomy of Kidney

Define 5

A

Nephron: responisble for filtering/reabsorption/secreting
Renal corpuscle: located in cortex (Glomerulus → collection of capillaries; Bowmans capsule → capsule surrounding glomerulus)
PCT: continuation from BC; twisted path that has increased cellular surface area exposed for filtration
Loop of Henle: descending loop similar to PCT then becomes more narrow as it ascends
DCT: continues after ascending LOH
Collecting Ducts: where DCT empties into then carry filtrate to medulla → then calyces → renal pelvis

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9
Q

Renal Nerve Supply

A

Primarily sympathetic portion of ANS → vasoconstriction → temporary ↓ of UOP

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10
Q

Renal Blood Supply

where does O2 transfer take place?

% of BV entering kidneys

A

–25% of blood pump from ♡ goes to kidneys
–TCBV passes thru kidneys q4-5 min
Afferent glom. Art: carry blood TO glom. capillaries
Efferent Glom. Art: network of capillaries surrounding nephron O2 transfer takes places here that EXITS glomerulus
–Subtances reabsorped and secreted

Peritubular caps → venules around nephron → larger veins → Renal vein → exit kidney to join abdominal portion of CVC

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11
Q

Blood Filtration

location; what does it rely on?

A

Occurs in Renal Corpuscle
–Glomerulus caps. RELY on BP to force plasma out into BC
–Large fenestrations in cap. endothelium allow for more fluid to leave
– Lg blood cells and plasma proteins too large to pass thru - unless there is damage to endothelium

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12
Q

Reabsorption

examples of ions absorped

location

A

Movement of substances → tubular lumen → epithelium → peritubular caps
65% occurs in PCT
–80% of H20/Na+/Cl-/HCO3 reabsorped
–100% Glucose/AA

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13
Q

Na+ Reabsorption

location; co-transport; exchanged for

A

Actively “pumped” out in PCT to bloodstream via carrier protein requires energy
–Co-transport of glucose/AA attaches to same protein
–Exchanged for secreted H+/ammonium or K+ ions (influenced by Aldosterone)

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14
Q

K+ Reabsorption

locations;

A

diffuses out of filtrate between epithelium → interstitial fluid → peritubular caps
–Occurs in PCT/ALOH/DCT

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15
Q

Ca++ Reabsorption

location; influenced by

A

–Occurs in ALOH/DCT/Collecting tubules
movement influenced by Vit D/parathryoid hormone/Calcitonin
–PTH blockes phosphate to promote reabsorption

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16
Q

Mg++ Reabsorption

locations; stimulated by;

A

Occurs in PCT/ALOH/collecting ducts
–Increased with PTH release

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17
Q

Cl- Reabsorption

A

Restores neutrality after Na+ reabsorption
Occurs in PCT via passive transport

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18
Q

BUN

A

Urea is passively reabsorbed substance typically excreted but a certain normal amount returns to bloodstream

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19
Q

Renal Threshold of Glucose

normal values K9/Fel

A

Limit to amount of glucose that can be reabsorbed by PCT
–Excessive amounts will end up in urine
–K9: 150 mg/dl
–Fel: 240 mg/dl

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20
Q

Glucosuria

efx on water

A

Glucose in urine will pull water out with it → polyuria due to osmotic diuresis
–excess loss of H2O will cause imbalance and lead to excess drinking (PD)

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21
Q

Secretion

location/flow; examples

A

Waste products/foreign substances (drugs)
–Mostly occurs in DCT
–transfers from perturb caps → interstitial fluid → tubular epithelium → filtrate
–H+/ammonia/K+ most important ions excreted

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22
Q

Pathphys of CKD

A

–Glom. fenestrations become damaged and larger → allows proteins to pass into filtrate →proteinuria
–Progression leads to destruction of nephron
–Kidneys compensate until no long able to filter toxins properly

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23
Q

Clin Path of CKD

A

–Blood proteins lost in urine
–↑ water loss → dilute urine, dehydration
–Accumulation of waste products (BUN/Creat/SDMA)
–Nonregen anemia → ↓ RBC lifespan, ↓ erythropoeitin
–UPC → glomerular dz
–Acidemia

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24
Q

IVF therapy goal for CKD tx

A

fluid therapy should be directed towards normalization of hydration status and improvement in acid-base and electrolyte abnormalities, rather than towards inducing diuresis for the purpose of improving azotemia.

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25
Q

HypoK+ supplemetation wtih CKD

A

if hypokalemia is refractory to aggressive supplementation, additional electrolyte abnormalities (e.g., hypomagnesemia, hypocalcemia) and/or endocrinopathies (e.g., hyperaldosteronemia) should be investigated

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26
Q

Dietary reccomendations for CKD

A

optimized to achieve both optimal caloric and limited protein/phosphorus intake.

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27
Q

consequence of diluting commercial diets for CKD

A

the low sodium content of renal diets can predispose patients to severe hyponatremia and neurologic sequelae if large volumes of water are administered after being blended with the diet

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28
Q

Anemia managment with CKD

A

– patient’s ability to synthesize and secrete endogenous erythropoietin is impaired
– erythropoiesis stimulating agent (ESA) may be indicated
– Darbepoetin α is hyperglycosylated, which prolongs the circulating half-life of the molecule and may reduce immunogenicity
– Adequate iron stores are necessary for an optimal response, and iron administration usually is required

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29
Q

Additional tx considerations for CKD

A

– phosphate binding drug for hyperphosphatemia
– Hypertension can be managed with amlodipine with or without ACE inhibitor

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30
Q

Renal Transplant canidates

A

– cats with stage II to III CKD, without concurrent illness or infection.
– should be considered before end-stage CKD, rather than as an emergency or salvage procedure
– free of other disease conditions including advanced primary cardiomyopathy, feline leukemia virus/feline immunodeficiency virus (FeLV/FIV), recurrent urinary tract infections, uncontrolled hyperthyroidism, and underlying neoplasia.

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31
Q

Immunosuppressive therapy for Renal transplant

A

– Cyclosporine prevents the activation of a number of transcription factors that regulate cytokine genes with a role in allograft rejection, including interleukin 2 (IL-2), IL-4, interferon γ (IFN-γ), tumor necrosis factor-α (TNF-α), and granulocyte-macrophage colony-stimulating factor (GM-CSF)
– Corticosteroids also inhibit these cytokines

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32
Q

Urine Volume Regulation

Determined by;

A

Determined by amount of H2O contained in tub filtrate @ renal pelvis
ADH (posterior pituitary gland)
Aldosterone (adrenal cortex)

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33
Q

ADH efx on Kidneys

Acts on which locations;
Promotes/Prevents

A

–Acts on DCT/Collecting Ducts
–Promotes H2O reabsorption →prevent H2O loss
–W/o ADH H2O will be lost in urine

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34
Q

Aldosterone efx on Kidneys

Acts on which locations;

A

–↑ reabsorption of Na+ from DCT/collecting ducts into bloodstream
–Osmotic imbalance makes H2O follow Na+ into bloodstream
*must be sufficient ADH present

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35
Q

Kidney BP regulation

vasculature involved;

A

RAAS responds to hypotension
–Afferent glom. art have juxtaglomerular cells = monitor BP
–Macula densa = cells in ALOH monitor NaCl concentration in filtrate → less NaCl will activate Renin

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36
Q

Renin Definition

A

Enzyme that facilitates splitting of Angiotensin I from Angiotensin

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37
Q

ACE Definition

What does it cause/stimulate?

A

Angiotensin -converting-enzyme
–Converts Angiotensin I to Angiontensin II
–Angiontensin II → causes arterial constriction to directly ↑ BP
–Stimulates Aldosterone release

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38
Q

Uremia
Pre
Renal
Post

A

–Pre-renal: ↓ blood flow to kidneys = dehydration/CHF/shock
–Renal Uremia: inability of kidneys to regulate urine production = not enough functional nephrons
–Post-Renal: obstruction preveting urine from being expelled

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39
Q

IRIS Stage 1 CKD

A

Creat: < 1.4/<1.6
SDMA: < 18
UPC: < 0.2
BP: < 140

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40
Q

IRIS Stage 2 CKD

Identifiers;
Tx:

A

Creat: 1.4 - 2.8
SDMA: 18-35
UPC: Border 0.2- 0.5
BP: Pre 140 - 159

Tx; same as stage 1, renal theraputic diet; tx hypoK+ in cats; address nausea/inappetance

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41
Q

IRIS Stage 3 CKD

Identifiers; Tx

A

Creat: 2.9 - 5.0
SDMA: 36 - 54/ 26 - 38
UPC/BP varies on stage

Same as stage 1-2; maintain Phos < 5;
tx acidosis/+/- anemia; SQF

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42
Q

IRIS Stage 4 CKD

identifiers; tx

A

Creat: > 5.0
SDMA: > 54/ >38

same as 1-3; keep Phos < 6; consider feeding tube

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43
Q

Diabetes Insipidus

2 types

A

Excessive urinary electrolyte-free water (free water) loss
–Dilute PU
–Obligate PD
–Central: insufficient or absent circulating arginine vasopressin (AVP)
–Nephrogenic: reduced or absent receptor response to circulating AVP

Central tx: DDAVP Nephrogenic tx: Thiazide diuretics

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44
Q

Effects of Hypertension on Kidneys

A

–exacerbates glomerular capillary hypertension
–contributes to progression of CKD via glomerulosclerosis and tubulointerstitial fibrosis
–Leads to proteinuria

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45
Q

Aquaporin channels

A

Aquaporins are channels that allow water to move from the tubular lumen into the renal tubular cell

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46
Q

Renal managment of Mg++

A

LOH and DCT are the main sites of magnesium reabsorption in the kidney
– kidney is the main regulator of serum magnesium concentration and total body magnesium content
– regulation is achieved by both glomerular filtration and tubular reabsorption

47
Q

Renal production of Bicarb

A

kidney has the ability to excrete large quantities of bicarbonate, such that metabolic alkalosis should be rectified rapidly.
When metabolic alkalosis is persistent, there must be factors limiting renal bicarbonate excretion

48
Q

What process can affect Renal bicarb production?

#4

A
  1. Decreased effective circulating volume
  2. hypochloremia can both limit renal bicarbonate excretion.
  3. Hypokalemia and
  4. aldosterone excess further impair renal bicarbonate excretion
49
Q

Renal conservation of water and sodium is stimulated by:

A

Hypovolemia stimulates baroreceptors that cause the hypothalamic-pituitary-adrenal axis to produce and release ADH, aldosterone, renin, and cortisol

50
Q

Renal water and sodium excretion is stimulated by:

A

overexpansion of the cardiovascular system causes stretch of the atria and release of atrial natriuretic peptide = increase in renal water/Na+ excretion
— RAAS countermeasures

51
Q

Acute kidney injury (AKI)

A

wide spectrum of disease ranging from clinically undetectable, subcellular damage to fulminant, excretory failure that leads to retention of uremic toxins and dysregulation of fluid, electrolyte, and acid-base balance
– typically multifactorial: overlapping ischemic, inflammatory, toxic, and septic components.

52
Q

Acute Kidney Injury Staging Scheme for Dogs: Stage 1

A

Nonazotemic AKI:
1. Creat = < 1.6
1. Documented AKI
1. nonazotemic increase in serum creatinine ≥0.3 mg/dl w/i 48 hrs
1. Measured oliguria (<1 ml/kg/hr) or anuria over 6 hours

53
Q

Acute Kidney Injury Staging Scheme for Dogs: Stage 2

A

Mild AKI:
1. Creat = 1.6–2.5
1. Documented AKI and static or progressive azotemia
1. azotemic increase in serum creatinine ≥0.3 mg/dl (≥26.4 μmol/L) within 48 hours,
1. Measured oliguria (< 1 ml/kg/hr) or anuria over 6 hours

54
Q

Acute Kidney Injury Staging Scheme for Dogs: Stage 3

A

Moderate to Severe AKI:
1. Creat = 2.6–5.0
1. Documented AKI and increasing severities of azotemia and functional failure

55
Q

Acute Kidney Injury Staging Scheme for Dogs: Stage 4 and 5

A

Stage 4 = Creat = 5.0–10.0
Stage 5 = Creat > 10

56
Q

AKI characterization

A

hemodynamic (prerenal),
renal parenchymal (intrinsic), postrenal causes.

57
Q

AKI: PreRenal

A

Hemodynamic causes include decreases in renal perfusion or excessive vasoconstriction and are characterized as rapidly reversible if the inciting cause is eliminated. However, prolonged ischemia can contribute to renal parenchymal injury

58
Q

AKI: Renal

A

intrinsic causes of AKI include infectious diseases, toxins, or systemic diseases with renal manifestations.

59
Q

AKI: Post Renal

A

due to obstruction or diversion of urine flow, including urethral obstruction, bilateral ureteral obstruction, unilateral obstruction with a nonfunctional contralateral kidney, or rupture of any portion of the urinary tract.
–prolonged obstruction of urine flow may lead to renal parenchymal injury

60
Q

AKI: UA findings

A

USG = isosthenuric (1.007 to 1.015)
– urine pH is usually acidic, unless there is a concurrent bacterial urinary tract infection (caused by a urease-producing organism)
– urine sediment may disclose dysmorphic red blood cells (suggestive of glomerular disease), pyuria, or casts (most frequently granular)

61
Q

AKI: ClinPath findings

A

– hematocrit may be increased from hemoconcentration or decreased from gastrointestinal blood loss or hemolysis
– suspect infectious with leukocytosis
– severity of azotemia depends on the cause and duration
– anion gap is usually high secondary to retained organic and inorganic acids that the injured kidney is unable to excrete

62
Q

Acid-base abnormalities with AKI

A

– with tubular function compromised, the ability to reabsorb bicarbonate and excrete hydrogen ions is diminished.
– Lactic acidosis secondary to compromised tissue perfusion also may contribute to altered blood pH.

63
Q

ECT Definition

A

modalities in which blood is removed from patient circulation and processed before being returned to the patient.
During processing, blood can be cleared of endogenous and exogenous substances, and beneficial substances can be added to the blood.

64
Q

Uses for ECT

A
  1. acute kidney injury (AKI)
  2. treatment of intoxications and poisonings
  3. rarely for fluid removal in refractory congestive heart failure.
65
Q

Types of renal replacement therapies

A
  1. intermittent hemodialysis (IHD)
  2. continuous renal replacement therapy (CRRT),
  3. prolonged intermittent renal replacement therapy
66
Q

intermittent RRT

A

hybrid therapy where hemodialysis is performed over prolonged periods of time (6 to 12 hours), rather than shorter periods in IHD or continuously as with CRRT.
– safely provide solute removal and decrease the risk for hemodynamic instability and other complications that can occur with more rapid treatment, while allowing a veterinary hospital to provide care without overburdening the veterinary team

67
Q

Peritoneal dialysis (PD)

A

uses the large peritoneal surface area as a natural “dialysis membrane” and is not an extracorporeal therapy because blood is never outside the patient’s body.
– PD can be performed without a dialysis machine.
– relies on solute removal via diffusion and convection
– dialysate in the peritoneal cavity equilibrates with the blood compartment through the peritoneal membrane and peritoneal capillaries

68
Q

Dialysis definition

A

the movement of solutes between two aqueous solutions separated by a semipermeable membrane.
– two major factors that contribute to solute movement are diffusion and convection

69
Q

ECT

What does diffusion of solutes depend on?

A

depends on the concentration gradient between the two compartments, the solute charge and molecular weight, and the surface area and permeability of the membrane
– BUN and Creat are low molecular weight molecules that freely diffuse across dialysis membrane

Diffusion utlized by IHD treatment

70
Q

ECT

Convective solute removal

A

solutes are dragged with plasma water across the dialysis membrane as a result of an osmotic or hydrostatic pressure gradients (solvent drag).
– Convection allows for effective removal of middle molecular weight solutes and small amounts of large molecular weight solutes during dialysis, if membrane pores are of sufficient size

CRRT utilizes conective solute removal

71
Q

ECT

Rate of solute removal

A

dictated by amount of water movement across the membrane, the membrane pore size, and the membrane surface area.

72
Q

ECT

Ultrafiltration

A

Fluid movement driven by hydrostatic pressure gradients prescribed to treat hypervolemia
– Fluid removal from a patient to correct fluid overload; solutes will be removed; however,
– pressure gradient results from either positive or negative osmotic pressure caused by non‐permeable solutes. This leads to the removal of “plasma water” from the blood and produces a fluid referred to as the ultrafiltrate (UF)
ultrafiltration is prescribed for the purpose of treating fluid overload

73
Q

ECT

Convection

A

Bulk flow of solutes dragged across a semipermeable membrane with water movement by hydrostatic or osmotic pressure gradients
– Removal of small, medium, and large MW solutes
– Convection is the movement of solutes with water flow

CRRT example

74
Q

ECT

Diffusion

A

Diffusive movement of solutes from a region of high concentration to a region of lower concentration across a semipermeable membrane
– Removal of small and some middle molecular weight (MW) solutes

IHD example

75
Q

Contraindications for Dialysis

A

– Severe hypotension,
– Severe preexisting coagulopathies
– peritonitis, recent abdominal or thoracic surgery, hypoalbuminemia, and severe hypercatabolic states

76
Q

ECT

Dialysis disequilibrium syndrome

A

– Rapid removal of osmotically active solutes (primarily BUN) from the blood compartment creates temporary acute osmotic pressure gradients between the blood, extravascular, and intracellular compartments.
– gradient can allow plasma water to shift from the vascular compartment and into the intracellular compartments. When this phenomenon occurs in brain tissue, secondary swelling occurs, and this can lead to irreversible neurologic damage or death
– initial treatments are prescribed to achieve slow solute removal, with lower rates of urea reduction; this allows redistribution of osmotically active solutes between fluid compartments to occur before large osmotic pressure gradients develop.

77
Q

Potential complications of Hemodialysis

A
  1. hypotension,
  2. hemorrhage secondary to systemic heparinization (which can occur internally such as in the lungs or GI tract and not be readily visible),
  3. hypocalcemia or alkalemia from regional citrate anticoagulation,
  4. dialysis disequilibrium syndrome,
  5. air embolism,
  6. dialyzer membrane reaction,
  7. blood loss through clotting of the extracorporeal circuit,
  8. catheter occlusion.
78
Q

ECT

Apheresis

A

ECT in which blood is removed from patient circulation, the blood is separated into its components, and one or more of the components is removed or processed before the blood is returned to the patient.

Example TPE

79
Q

ECT

therapeutic plasma exchange (TPE)

A

apheresis treatment in which the plasma component of blood is removed and replaced with a replacement solution such as a colloid solution or a combination of crystalloid and colloid solutions before being returned to the patient
– combinations of saline, hetastarch, and fresh-frozen plasma are used for replacement

80
Q

ECT

category I condition for apheresis

A

First-line therapy
acute, short-term therapy for moderate to severe myasthenia gravis (MG) or hyperviscosity from hypergammaglobulinemia.

81
Q

ECT

category II condition for apheresis

A

second-line therapy (e.g., severe immune-mediated hemolytic anemia [IMHA])

82
Q

ECT

category III condition for apheresis

A

immune thrombocytopenia or sepsis with multiorgan failure) is one where controlled trials are limited or results are inconclusive

83
Q

category IV condition for apheresis

A

condition where apheresis is considered ineffective or harmful.

84
Q

ECT

Success of TPE treatment depends on:

A

prescribed apheresis treatment plans. The ability to remove a substance successfully during TPE depends on the distribution of the substance within the body (the volume of distribution), the rapidity with which the substance equilibrates between body compartments, and the ability to remove adequate amounts of the pathologic substance
– most successful treatments are achieved with substances that have a small volume of distribution (and are located primarily in the intravascular space) because removal is occurring directly from the intravascular space.

85
Q

What does TPE remove?

A

pathologic substances such as:
antibodies,
immune complexes,
cytokines,
and by these means, can alleviate or improve manifestations of some immune-mediated diseases

86
Q

TPE for toxicities

A

drug overdoses and toxicities, particularly nonsteroidal antiinflammatory drug (NSAID) overdoses, where the drug is largely protein bound and therefore distributed largely in the intravascular space

87
Q

TPE for IMHA

A

– has been shown to decrease antibody, immunoglobulin concentrations
– dogs that have not responded to 4 or more days of appropriate immunosuppressive therapy or incompatible to crossmatches
–

88
Q

TPE for Myasenthia Gravis

A

– cases refractory to medical management or in patients with rapidly progressive, severe disease, TPE might improve outcomes.

89
Q

Other applications for TPE

A

– severe signs of hepatic encephalopathy
– severe hyperbilirubinemia, and neurologic signs suspected to be secondary to severe hyperbilirubinemia

90
Q

ECT

Selection of blood purification treatment depends on:

A
  1. Volume of toxin distribution
  2. degree toxin is protein bound
  3. molecular weight of toxin
91
Q

Hemodialysis treatment

A
  1. blood flows through the extracorporeal circuit and across a hemodialyzer.
  2. dialyzer is composed of thousands of semipermeable straws.
  3. patient’s blood passes through the hemodialyzer straws, while a contrived dialysate solution passes in a countercurrent direction.
  4. dialysate solution may be augmented depending on the intoxication to either prevent the development of electrolyte disturbances or prevent ongoing metabolism of the toxin.
92
Q

Hemofiltration or Hemodiafiltration treatment

A

primary method of clearance is via convection.
– solvent is removed by augmenting the transmembrane pressure across the dialyzer. As the solvent is removed, solute clearance occurs via solvent drag

93
Q

Hemoperfusion treatment

A

Achieves Adsorptive clearance
– more effective at removing larger molecules
– blood is perfused across a charcoal or adsorbent polymer cartridge
– toxin will reversibly bind and be removed from circulation

94
Q

What is the purpose of blood priming with dialysis machines?

A

– purpose of a blood prime is to prevent hemodilution and maintain adequate tissue oxygenation during the initial stages of treatment.
– Priming with packed red blood cells is most typically used in anemic patients or in cats and small dogs because of their smaller blood volume

95
Q

Recirculation phase

A

– purpose of this step is to remove any substances that may remain in the tubing. The flow during this stage is quite rapid and this will also help remove air from the circuit.
– At the end of the recirculation stage, the prescribed treatment rates are set and the patient is connected to the dialyzer for the treatment stage

96
Q

Toxicities using ECT treatments

list as many

A
  1. ethylene glycol
  2. propylene glycol
  3. barbiturates
  4. cannabinoids
  5. methotrexate
  6. NSAID
  7. aspirin
  8. alcohols
  9. theophyllines
  10. antianxiety medications
97
Q

mean renal arterial pressure

A

100 mmHg, for both dogs and cats

98
Q

pressure within the glomerular capillary

A

55 mmHg in dogs and 59 mmHg in cats
– pressure within the glomerular capillary is substantially higher than the pressure within Bowman’s space, thus leading to a difference in hydrostatic pressure of 35 mmHg = rapid filtration

99
Q

Loop of Henle reabsorption

A

– continues to reabsorb sodium and chloride as well as calcium and magnesium after PCT
– requires an active transport mechanism
– Very little water is reabsorbed in the loop of Henle as the cells are relatively impermeable to water
– reabsorption of sodium, without reabsorption of water, causes a dilution of the filtrate and a hyposmotic fluid

100
Q

Proximal Convaluted tubule reabsorption

A

65% occurs in PCT
–80% of H20/Na+/Cl-/HCO3 reabsorped
–100% Glucose/AA
uses active transport
– while water moves passively along the concentration gradient as solutes move out of the tubule lumen and into the tubular cells

101
Q

Distal convuluted tubule

A

– relatively impermeable to water but continues to reabsorb sodium and chloride.
– Parathyroid hormone acts on the distal tubules to regulate calcium and Mg++ reabsorption

102
Q

Urine osmolality

A

fluid reaching the collecting duct is hyposmotic to plasma with an osmolality of approximately 100 mOsm/kg
– antidiuretic hormone (ADH), released from the posterior pituitary, influences the collecting ducts begin to reabsorb water
– Without ADH, the collecting ducts are relatively impermeable to water.

103
Q

Renal autoregulation

A

an animal that can maintain (MAPs) of 80–100 mmHg, the kidney can maintain a constant RBF and GFR that varies less than 10%
– resulting in constriction or dilation of the afferent or efferent arterioles in response to varying mean arterial pressures

104
Q

Renin‐Angiotensin‐Aldosterone System

A
105
Q

Azotemia

A

abnormal concentration of urea nitrogen and creatinine in the blood.
related to a diminished capacity of the kidney to remove these substances, but equally as common, it can be related to conditions that affect the volume of blood reaching the kidneys, or impaired outflow of urine

Pre, Renal, Post

106
Q

Prerenal Azotemia

A

– failure of blood supply to reach the glomerulus and subsequent reduction of solutes that move through the nephron.
– conditions affecting intravascular volume such as
1. hypovolemic shock
2. third space losses
3. decreased cardiac output,
4. high‐protein diet,
5. gastrointestinal bleeding
– Prolonged ischemia may result in damage to the renal parenchyma, thus causing intrinsic kidney injury

107
Q

Postrenal Azotemia

A

impediment to the flow of urine out of the body, or redirection of urine flow.
– urethral obstruction in the male cat; other examples include ruptured or herniated bladder, ruptured urethra, urinary blockage from neoplasia of the urethra, bladder, or surrounding tissues, prostatic disease, and ureteroliths

108
Q

Feline Urethral Obstruction

A

– feline interstitial cystitis, crystaluria, urolithiasis, neoplasia, stricture, and, uncommonly, urinary tract infection
– relieve obstruction, treat hypovolemia/shock, electrolyte and pH abnormalities,

109
Q

Postobstructive diuresis

A

– extreme polyuria following relief of obstruction
– high IVF rates may be needed to prevent dehydration until kidneys can regulate again

110
Q

catheter‐associated urinary tract infection (CAUTI)

A

CAUTI can arise via either intraluminal (through the inside of the catheter) or extraluminal (along the outside of the catheter) means

111
Q

Central venous pressure (CVP)

A

measurement of the hydrostatic pressure in the intrathoracic vena cava, and estimates right atrial pressure (RAP)

euvolemic patients is approximately 0–5 cmH2O

112
Q

Lyme Nephritis

A

Exposure to the spirochete Borrelia burgdorferi from deer tick Ixodes scapularis
– suspected in Lyme-seropositive PLN cases (Lyme+PLN) in endemic regions

113
Q
A

VTS ECC 2024 (17 decks)

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