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Residency > Kidney Review > Flashcards

Kidney 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?

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

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

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
Q

Solute exchange and removal in IHD occurs by:

A

-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
Q

Diffusion

A

Clearance dependent on:​

-Molecular weight​
-Concentration gradient​
-Membrane permeability/pore size​
-Blood flow (Qb)​
-Dialysate flow (Qd)​
-Duration​

IHD, CRRT (hemodiafiltration)

27
Q

Convection

A

Clearance dependent on:​

-Transmembrane pressure gradient​
-Ultrafiltration coefficient​
-Membrane surface area​
-Duration​

IHD with hemofiltration, CRRT (hemofiltration, hemodiafiltration)

28
Q

Adsorption

A

Clearance dependent on:​

-Solute size​
-Affinity to sorbent​
-Ability to penetrate membrane​

Charcoal hemoperfusion

29
Q

IHD Prescription

What patient factors do we need to consider?

A

Degree of azotemia​

Hemodynamic stability​

Hematocrit​

Electrolyte and acid-base status​

Coagulation assessment

30
Q

IHD prescription
What treatment factors do we need to consider?

A

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
Q

Dialysis Disequlibrium Syndrome​

A

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
Q
A

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
Q

Why is paradoxical CNS acidosis so bad and what is this concept called?

A

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
Q

Ultrafiltration​

A

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
Q

Toxins removed with hemodialysis

A

Ethylene-glycol​

Baclofen​

Ethanol​

Phenobarb

36
Q

Toxins removed with charcoal hemoperfusion

A

Ibuprofen​

Meloxicam​

Methotrexate​

Phenobarbital​

Cyclosporine

37
Q

Toxins removed with TPE

A

Meloxicam​

Ibuprofen​

Carprofen​

Naproxen​

Calcitriol

38
Q

TPE mechanism of action

A

Removal of large-molecular weight substances​

-Pathologic antibodies​
-Immune complexes​
-Cryoglobulins​
-Myeloma light chains​
-Endotoxin​
-Cholesterol-containing lipoproteins​
-Cytokines​
-Toxins

39
Q

TPE indications

A

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
Q

Mechanism of plasma removal

A

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
Q

What else is removed with TPE?

A

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
Q
A

Residency (13 decks)

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