Renal and Urinary Review Flashcards

1
Q

What are the functions of the kidneys?

A

Excretory, regulatory, Endocrine

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2
Q

What are the excretory functions of the kidneys?

A

Nitrogenous waste, phosphorus, potassium, medications

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3
Q

Regulatory functions of the kidneys

A

Fluids, electrolytes, acid -base, minerals, blood pressure

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4
Q

Endocrine functions of the kidney

A

Erythropoietin, vitamin D, RAAS

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5
Q

What is the most metabolically active part of the nephron?

A

Cortex

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6
Q

What % of cardiac output goes to the kidneys?

A

20%

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7
Q

Flow of blood through kidneys

A

Renal artery -> segmental arteries -> interlobar arteries -> arcuate arteries -> interlobular arteries -> afferent arteries -> NEPHRON (glomerulus -> efferent arteriole -> peritubular capillaries) -> venules -> interlobular veins -> arcuate veins -> interlobar veins -> renal vein

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8
Q

Autonomic innervation of kidneys

A

Entirely sympathetic

NE and dopamine releases cause vasoconstricton, Na+ reabsorption on PCT, stimulation of renin release in JGA

Afferent fibers: baroreceptors and chemoreceptor impulses

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9
Q

Explain endocrine function of kidneys

A

1) Renin is produced from JGA in kidneys.

Renin released is simulated by
-decreased renal perfusion or extracellular fluid volume sensed by granular cells in afferent arteriole
-sympathetic stimulation- systemic hypotension is detected by cardiac and arterial baroreceptors -> increased concentrations of circulating catecholamines -> stimulation of beta1 adrenergic receptors on granular cells -> renin released
-decreased Cl- delivery to macula densa

2) PCT converts 25-hydroxyvitamin D to 1,25- dihydroxyvitamin D (calcitriol)

3) Fibroblasts-like cells in the interstitium of cortex and outer medulla secrete EPO

4) Prostaglandins, kinins

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10
Q

Glomerular filtration

A

Glomerular filtration decreases drastically with kidney disease

Grams of urea/GFR (L) = BUN concentration in plasma (mg/dL)

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11
Q

Functions of nephrons

A

Reabsorption and section of ions, carbohydrates, amino acid, H2O, etc

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12
Q

Types of nephrons

A

-cortical 85%
-juxtamedullary - close to medulla, loop of Henle extends deep into pyramids

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13
Q

Functions of proximal tubule

A

1) Reabsorption of 65-70% of filtered H2O and NaCl (is osmotic), 90% of filtered HCO3-, and 100% of filtered glucose and amino acids, K+, PO4-, Ca2+, Mg2+, urea, urate

2) secretion of organic anions and cations

3) Production of NH3 (major site)

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14
Q

What part of the nephron do carbonic anhydrase inhibitors work on?

A

PCT

They block the action of CA4 on the luminal membrane -> decreases the excretion H+ -> increased loss of Na+ -> diuresis

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15
Q

What is Fanconi’s Syndrome?

A

-Defect of the proximal tubule
-Inherited or acquired
-Caused by toxins (aminoglycosides, jerky treats) or neoplastic
-Causses increased excretion of amino acids, glucose, phosphate, Na+, K+, HCO3-, uric acid

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16
Q

What affect does angiotensin II have on the kidneys?

A
  • Stimulates luminal Na/H+ antiporter (NHE3) which causes increased proximal tubular reabsorption of Na+
  • Stimulated aldosterone secretion which causes increased Na+ reabsorption and K+ excretion
  • Causes alterations in glomerular hemodynamics to enhance Na+ and H2O reabsorption which causes decreased peritubular capillary hydrostatic pressure and increased peritubular oncotic pressure
  • Increased Na+ and H2O reabsorption -> volume expansion
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17
Q

Renal replacement therapies

A

-A form of artificial blood purification
-Primarily restores homeostasis in AKI
-Removes nitrogen waste and corrects acid-base, electrolytes, and fluid imbalance

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18
Q

What does the loop of Henle do?

A

-The loop of Henle is the countercurrent multiplier
-reabsorption of 15-25% of filtered NaCl and 20% K+
-active regulation of Mg2+ excretion

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19
Q

Renal Replacement Therapy Modalities

A
  • Intermittent hemodialysis: highly effective, PRN (2-3x/wk)
  • Continuous RRT: less effective, continuous treatment
  • Peritoneal dialysis: least effective, instill and drain dialysate from peritoneal space
20
Q

Indications for Hemodialysis (AKI)

A
  • Anuria, severe oluguria
  • Failure of conventional medical therapy to initiate adequate diuresis and go control azotemia
  • Life-threatening: fluid overload, electrolyte disturbances, acid-base disturbances
  • Severe azotemia
21
Q

Indications for Hemodialysis (CKD)

A

Indefinite intermittent RRT​

Support for acute decompensation of CKD​

Finite RRT for client transition to irreversible disease status​

Bridge to and/or from staged surgery (e.g. ureteral obstruction, renal transplantation)

22
Q

Indications for Hemodialysis/Other ECT​
(Miscellaneous)

A

Severe overhydration, pulmonary edema, CHF​

Acute poisoning/drug overdose​

Endogenous intoxicants (i.e. liver failure) ​

Immune-mediated disease such as ​
-Myasthenia gravis​
-Polymyositis​
-Polyneuropathy​
-IMHA​
-ITP​
-rapidly progressing GN​

Hyperproteinemia (TPE) such as in multiple myeloma

23
Q

Components of dialysate

A

-Purified water​
-Acid concentrate​
-Bicarbonate

Dialysate composition determines blood composition​

Patient exposed to 120-200 liters dialysate per tx

24
Q

What electrolytes can we modify in dialysate?

A

K+ (0 vs. 3 mEq/L)​

Na+​

Ca2+​

Phosphorus

25
Solute exchange and removal in IHD occurs by:
-Diffusion​ -Ultrafiltration​ -Convection​ -Adsorption Magnitude of solute transfer depends on​: -Forces across membrane​ -Chemical and physical characteristics of solute​ -Structural properties of porous membrane
26
Diffusion
Clearance dependent on:​ -Molecular weight​ -Concentration gradient​ -Membrane permeability/pore size​ -Blood flow (Qb)​ -Dialysate flow (Qd)​ -Duration​ IHD, CRRT (hemodiafiltration)
27
Convection
Clearance dependent on:​ -Transmembrane pressure gradient​ -Ultrafiltration coefficient​ -Membrane surface area​ -Duration​ IHD with hemofiltration, CRRT (hemofiltration, hemodiafiltration)
28
Adsorption
Clearance dependent on:​ -Solute size​ -Affinity to sorbent​ -Ability to penetrate membrane​ Charcoal hemoperfusion
29
IHD Prescription What patient factors do we need to consider?
Degree of azotemia​ Hemodynamic stability​ Hematocrit​ Electrolyte and acid-base status​ Coagulation assessment
30
IHD prescription What treatment factors do we need to consider?
Catheter selection​ Characteristics of dialyzer​ Blood flow rate (Qb)​ Dialysis time (Td)​ Ultrafiltration rate (UFR)​ Dialysate composition​ Dialysate flow rate (Qd)​ Anticoagulation​ Ancillary treatments/additives
31
Dialysis Disequlibrium Syndrome​
IHD -> removal of undesired solutes​ Solutes distributed throughout body compartments​ Only removed from intravascular space in IHD​ Solutes move down concentration gradient​ Fluids move in opposite direction
32
Initial treatments (rapid solute removal)​ -Higher initial BUN​ -Coagulation disorders (thrombocytopathia, DIC)​ -Pre/coexisting neuro signs (Uremic encephalopathy, uncontrolled hypertension)​ -Electroyte abnormalities​ -Acid base disorders​ Small cats and dogs Paradoxical cerebral acidosis
33
Why is paradoxical CNS acidosis so bad and what is this concept called?
Results of rapid correction of severe metabolic​ acidosis​ - Rapid increase in pH may results in hypoventilation and​ increase in CO2​ - CO2 diffuses readily into the CSF​ - Bicarbonate diffusion into the brain is slower​ - Lower CSF pH The Monro-Kellie hypothesis (MKH) states that volume changes in any intracranial component (blood, brain tissue, cerebrospinal fluid) should be counterbalanced by a co-occurring opposite change to maintain intracranial pressure within the fixed volume of the cranium.
34
Ultrafiltration​
Rate of fluid removal = ultrafiltration​ Depends on:​ -Degree of overhydration​ -Rate of fluid shift between body compartments​ Must assess for each patient​ Usually no more than 10 ml/kg/hr​ Reassessed throughout tx​ -Clinical assessment​ -Blood volume/saturation – i.e. if using CritLine​ -Heart rate​ -Blood pressure
35
Toxins removed with hemodialysis
Ethylene-glycol​ Baclofen​ Ethanol​ Phenobarb
36
Toxins removed with charcoal hemoperfusion
Ibuprofen​ Meloxicam​ Methotrexate​ Phenobarbital​ Cyclosporine
37
Toxins removed with TPE
Meloxicam​ Ibuprofen​ Carprofen​ Naproxen​ Calcitriol
38
TPE mechanism of action
Removal of large-molecular weight substances​ -Pathologic antibodies​ -Immune complexes​ -Cryoglobulins​ -Myeloma light chains​ -Endotoxin​ -Cholesterol-containing lipoproteins​ -Cytokines​ -Toxins
39
TPE indications
One or more of the following:​ -Substance MW > 15,000 D​ -Prolonged half-life​ -Acutely toxic, resistant to conventional therapy​ AND​ Small volume of distribution (Vd)
40
Mechanism of plasma removal
1) Filtration- devices that separate the plasma from the cellular components based on size 2) Centrifugation- devices that separate the plasma from cellular components based on density or specific gravity
41
What else is removed with TPE?
Declines in factor V, VII, IX, X and vWF​ VII, IX and vWF return to normal after 4 hours​ Other factors may take up to 24 hours​ Fibrinogen reaches 66% pre-apharesis levels by 72 hours​ Other Abs -> false (-) results
42
43
Antibiotics that cause UTIs
-E.coli -Staph, strep, enterococcus -Klebsiella, proteus -Pasteurella, enterobacter
44
Empysematous cystitis
-E.coli -Clostridium spp -Klebsiella, Proteus
45
Pyelonephritis
-E.coli -Strep, staph -Enterococcus -Proteus, Klebsiella, Pseudomonas -Anaerobes