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Renal Flashcards

1
Q

Renal Blood flow equation

A
  • (MAP- Vascular Pressure) x Vascular resistance
  • directly proportional to pressure gradient between the renal artery and renal vein
  • inversely proportional to resistance of renal vasculature
  • Q= (change of P)/ R -> Ohm’s Law
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2
Q

Renal Autoregulation

A

The kidney autoregulation.:It is anatomically arranged to allow fluid in the DISTAL TUBULE to alter afferent and efferent arteriole tone, and regulate GFR
-RBF will remain constant at 1200 ml/min as long as MAP remains between 50-180 mm/Hg

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3
Q

Neural autoregulation of the kidney

A
  • Decreased GFR-> Increased Na+ and Cl- reabsorption in ascending limb of loop of Henle -> Decreased Na/Cl ions in distal tubule at macula densa
  • Afferent arterioles DILATE in response & increase GFR
  • Sympathetic response is to cause JG cells to release RENIN
  • Angiotensin II: vasoconstriction & constriction of EFFERENT arteriole -> Increased glomerular pressure and increased GFR
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4
Q

What physiologic factors determine GFR?

A
  • The pressure inside the glomerular capillaries
  • The pressure in the Bowman capsule
  • The colloid osmotic pressure of the plasma proteins
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5
Q

Proximal Tubule

A

Primary function: Active transport of Na+

  • 60-70% of solutes reabsorbed here
  • H2O & most ions are cotransported with Na+
  • Osmotic force of Na+: Passive diffusion of H2O out of proximal tubule and into peritubular capillary
  • Glucose, proteins, amino acids, acetoacetate ions, and vitamins almost COMPLETELY reaborbed
  • Cl- ions passively transported to maintain electroneutrality
  • H+ ions are SECRETED into proximal tubule in exchange for Na+ ions SECRETORY TRANSPORT
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6
Q

Complications of Transurethral Resection of the Prostate (TURP syndrome)

A 
hypervolemia*****
hyponatremia*****
bladder perforation*****
hemorrhage
glycine toxicity
ammonia toxicity
electrical hazards
hypothermia
bacteremia.
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7
Q

Counter Current Exchange

A

-occurs in the Loop of Henle and Vasa Recta
-Concentration gradient causes fluid to be exchanged across parallel pathways
- essential for concentration and dilution of urine
- Thin descending limb
Permeable to H2O and small solutes (NaCL, urea)
Tubular fluid becomes progressively hyperosmotic
Thick ascending limb
Permeable to NaCl but impermeable to H2O
Tubular fluid becomes progressively hyposmotic
as it flows up the ascending limb
Descending limb= increased osmolarity (300-> 1200)
ascending limb= decreased osmolarity (1200-> 300)

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8
Q

Loop of Henle

A
  • Primary function: Establish a hyperosmotic state within renal medulla for the purpose of water and salt conservation
  • Water conservation produces concentrated urine
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9
Q

Thick Ascending Limb

A

-Impermeable to water: “the diluting segment”
- Na+-K+-2Cl- cotransporter
- Site of action for loop diuretics
-At physiologic pH, attach to the Cl- binding site of
the Na+-K+-2Cl- cotransporter, disabling it, and
inhibiting NaCl reabsorption

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10
Q

Distal Tubule

A
  • Sodium, under the influence of aldosterone, is reabsorbed
  • Potassium is secreted into the lumen in exchange for sodium (electroneutrality)
  • Aldosterone influence is the MAIN regulator of K+ in the extracellular fluid
    H+ is secreted by the late distal tubule against a concentration gradient
    Acid –Base balance
    Final step of urine acidification
    Reabsorbs 10% of Water BUT ONLY PERMEABLE
    under the influence of ADH
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11
Q

Aldosterone

A
  • Acts directly on principal cells to increase Na+ reabsorption
  • Secreted by the zona glomerulosa of the adrenal cortex
  • It increases more luminal membrane sodium channels, = bring more sodium into the cell and increasing the activity of the ATPASE pump on the basel membrane
    = Increases the number of luminal K+ channels which increases secretion of potassium
  • sodium absorption and potassium excretion
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12
Q

Collecting Duct

A

Permeability of the collecting duct to H2O is controlled by ADH
Water is absorbed OUT of collecting duct INTO the interstium
Urine is concentrated

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13
Q

ADH regulation

A

Osmotic Concentration of ECF:

  • Osmoreceptors located near hypothalamus sense increased osmotic concentration and release ADH
  • Stretching of atrial baroreceptors INHIBITS ADH
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14
Q

Renin

A

Protein enzyme released by kidney
Released by:
Beta adrenergic stimulation
Decreased perfusion to afferent arteriole
Decreased Na+ delivery to distal tubule
Acts on hepatic angiotensinogen-> Angiotensin I ->ACE in Lung ->Angiotensin II

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15
Q

Angiotensin II

A

Potent vasoconstrictor

Stimulates release of Aldosterone from Adrenal Cortex

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16
Q

ANF

A

Atrial Natriuretic Factor
– Peptide hormone synthesized, stored, and secreted by atria ( activated by atrial distention, stretch, and pressure)
- Increases urine flow
- Increases Na+ excretion
- Inhibits BOTH release AND end organ effects of:
Renin
Aldosterone
ADH
Can produce dose dependent decrease in BP
VERY POTENT DIURETIC

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17
Q

Volatiles and Renal disease

A 
Temporary depression of 
Renal blood flow
GFR
Urine flow
Electrolyte excretion
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18
Q

Diagnostic criteria for AKI

A

Diagnostic Criteria

  • Absolute increase in serum Creatinine of 0.3 mg/dL OR
  • Percentage increase in serum creatinine of 50 % AND
  • Urine output less than 0.5ml/kg/hr
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19
Q

ATN

A

Acute Tubular Necrosis
Factors that interfere with GFR OR tubular reabsorption of urea, Na+, and H2O are all impaired
In AKI, these functions are maintained

20
Q

Labs for AKI

A

Patients with parenchymal disease cannot concentrate urine
Urine Na+ levels are HIGH
Urine Osmolality is LOW
Progressive rise in serum creatinine, uric acid, and polypeptide levels
Serum K+ increases
Serum Na+, Ca2+, and albumin levels decrease

21
Q

KEY factors for development of AKI in septic patients

A

Hypovolemia, decreases pulmonary function, and acidosis

22
Q

Anesthetic considerations for AKI

A

Prevention of AKI is more successful than management

  • Most common cause of AKI is prolonged hypoperfusion
  • Duration and magnitude of initial insult determine severity
  • A key strategy is limiting the duration and severity of renal ischemia
  • Identify high risk patients
  • Correct fluid losses & Prevent hypovolemia
  • Fluids and inotropes
  • Adequate hydration BEFORE anesthetic induction minimizes secretion of ADH and renin-angiotensin-aldosterone system
  • Saline vs. solutions low in sodium can help prevent aldosterone secretion, hyponatremia and oliguria
  • Maintain cardiac output and renal perfusion
23
Q

Chronic Kidney Disease

A

Slow and progressive
Decreased function of nephrons
Decreased renal blood flow, GFR, tubular function and reabsorption ability
GFR less than 60ml/min/1.73m2

24
Q

Stages of CKD

A

Stage I: Kidney damage with normal or increased GFR
Stage 2: GFR 60-89 ml/min/1.73m2 with kidney damage
Stage 3: GFR 30-59 ml/min/1.73m2
Stage 4: GFR 15-29 ml/min/1.73m2
Stage 5: ESRD with GFR less than 15/ml/min

25
Labs for CKD
Evaluate GFR and renal tubular function GFR: BUN 10-20 mg/dL/Serum Creatinine (0.7-1.5mg/dl) Renal Tubular Function Urine specific gravity (1.003-1.030) Urine Osmolality (65-1400 mOsm/L) Urine Na+ Concentration (130-260 mEq/Day) Better indicator of uremic symptoms vs. GFR less than 8 mg/dL: overhydration or underproduction of urea 20-40 mg/dl: dehydration, High Nitrogen, Low GFR BUN > 50 mg/dl: decreased GFR BUN Elevated with normal creatinine : nonrenal
26
Creatinine Clearance
Creatinine Clearance: MOST specific test for GFR and MOST reliable test of renal function Normal Range 95-150 ml/min - Mild Renal Dysfunction: 50-80 ml/min - Moderate Renal dysfunction: less than 25 ml/min - ESRD : less than 10 ml/min--> Anephric & Require dialysis
27
CV and CKD
Combination of HTN, anemia, hypoalbuminemia and circulatory overload lead to Peripheral Edema Pulmonary edema CHF Ischemic heart disease is the MOST common cause of death in patients with CKD…ASSUME it is PRESENT Fibrous carditis in 50% of patients with severe uremia (pain on inspiration, frictional rub) Enlarged cardiac silhouette: pericardial effusion
28
Hematologic Changes in CKD
Normochromic, normocytic anemia HCT levels 20%-30% and parallel azotemia (Elevation of serum creatinine and BUN) Decreased production of erythropoietin Decreased life span of erythrocyte secondary to hemolysis Patients with uremia bleed excessively due to decrease in platelet FUNCTION
29
Cause of uremic coagulopathy in renal failure:
defective platelets
30
Side effects Associated with Extracorporeal Shock Wave Lithotripsy:
``` Hypothermia hyperthermia cardiac dysrhythmias**** hemorrhagic blisters of skin renal edema***** renal hematoma lung injury flank pain hypertension/hypotension autonomic hyperreflexia N/V ```
31
Considerations for CKD
- Increased GI bleeds - increased risk for infection - increased neuro symptoms (mirrors stages of azotemia) - Autonomic neuropathy-> delayed gastric emptying - seizure d/t hypertensive encephalopathy - Hyperparathyroidism in response to hypocalcemia - Adrenal insufficiency secondary to exogenous steroid therapy - “uremic lung” : Bilateral butterfly infiltrates indicative of pulmonary edema
32
Acid- Base Balance with CKD
- Impaired excretion of H+ ions - Metabolic acidosis - Symptoms of N/V, lethargy common to uremic patients may also indicate acidosis - Impaired Na+ absorption and excretion Sodium wasting early renal insufficiency Sodium and H2O retention late stages with volume overload, HTN, edema, and CHF
33
Potassium and CKD
Hyperkalemia Inability of distal nephron to secrete K+ in exchange for Ca2+ Acidosis: K+ shift from ICF to ECF Fatal Dysrhythmias : K+ 7-8 meq/L Unexpected hyperkalemia can occur RAPIDLY so check K+ even within 6-8 hours of dialysis
34
Calcium and CKD
Hypocalcemia Impaired ability to hydroxalate Vitamin D Elevated blood levels of PTH and Calcitonin Presence of osteodystrophy and predisposition to bone fractures
35
Nonrenal Surgery and transplant pts
1.) Management involves maintenance of adequate volume status, avoiding nephrotoxic medicines such as nonsteroidal antiinflammatory drugs (NSAIDs) or contrast dyes, and proper dosing of immunosuppressive drugs. 2.) Whenever possible, immunosuppressive drugs should be given by the enteral route. 3.) A simple way to dose IV steroids is to prescribe the same milligram-for-milligram dose of IV methylprednisolone as the maintenance prednisone dose; supplemental stress-dose hydrocortisone is then prescribed separately. 4,) IV cyclosporine should be prescribed in slow-infusion form at one third of the total daily oral dose, and intravenous tacrolimus should be at one fifth of the total daily dose
36
Precautions for Renal Transplant patients
- Caution with radio contrast - Maintain hydration. - Avoid nephrotoxic antibiotics and analgesic. - Stress-dose” steroids: not always necessary. - Monitor allograft function, plasma potassium, and acid-base balance daily. - Consider wound-healing impairment.
37
Anesthesia for robotic surgeries
- increased risk of VTE d/t long surgeries in trend position - maximize protection of pressure spots and eyes - neuropathies, (2) CVP elevation (3) intraocular/intracranial pressure elevation (4) increased pulmonary venous pressure, (5) decreased pulmonary compliance, (6) reduced functional residual capacity (FRC), (7) swelling of the face, eyelids, conjunctivae, and tongue. Facial swelling requires careful airway assessment prior to extubation.
38
Severe Turp Syndrome interventions
``` - Terminate the surgery ASAP. • Administer 20mg of IV Lasix. • Order the following labs: HcT -Electrolytes and glucose - Creatinine and serum osmolality levels - ABG - Ekg • Continue or start normal saline. - Hypertonic saline (3% or 5%) may be administered (at a rate less than rate 100 mL/hour) if Na is less than100 mEq/L, ``` Administer IV midazolam in1mg incremental doses to treat twitching or seizure
39
IV fluids and Renal Insufficiency
•Patients with normal or mildly compromised renal function should receive balanced salt solutions at 3 to 5 mL/kg/hr. - A bolus of 500 mL ought to improve output related to hypovolemia. - Use of mannitol or furosemide to increase output may further exacerbate volume depletion. - No potassium-containing solutions (lactated Ringer’s) should be administered to anuric patients
40
How do the afferent and efferent arterioles help regulate RBF?
changing diameters is the main way the kidneys regulate renal blood flow - efferent are smaller and have a greater resistance
41
Pharmacokinetics with ESRD
- depends on VOD, protein binding, low pH, and drugs that are dependent on renal excretion. 1. ) patients will have decreased proteins d/t hypoalbumenia, (more free drug) 2. ) Anemia causes increased cardiac output and enhanced delivery to the brain. Also uremia makes the BBB more permeable --> increased sensitivity to IV anesthetics. (Shorter DOA for proposal d/t increased CO) 3. ) Acidic state causes more drug to be in the unionized form and less protein binding= more free drug 4. ) Increased VOD---> proposal requires increased dose
42
Which NMBAs are good for renal patients?
Good: sux is renal excreted, but okay for renal patients as long as K+ is less than 5.5. Cis and Roc are best choices. Atra causes histamine release. Roc will have increased DOA and recovery time in ESRD.
43
Which NMBAs should be avoided for renal patients?
Bad: pancuronium is 80% renal excreted--> prolonged excretion vec is 30% renal excretion, recommended low dose.
44
Opiods/ Sedatives and ESRD
Benzos, Precedex (cleared by the liver), sufentanil, and proposal are all good choices. Fentanyl is okay but has exaggerated effect. Avoid Morphine and Demerol due to active metabolites that are renal excreted. (can't dialyze out) caution with diluadid--> active metabolites but can be dialyzed. Ketamine may be deleterious d/t increased HR and BP and dependent on renal excretion
45
Laproscopic urology disadvantages (5)
1. ) CO2 extravastion 2. ) post-op airway compromise (sub Q emphysema can occur and extend to head an neck) 3. ) increased acidosis (d/t increased CO2) 4. ) increased incidence of oliguria (SNS stimulation and activation of RAS) intrathoracic pressures greater than 10= increased SVR, decreased CO 5. ) longer DOA

Renal- Nagelhout (1 decks)

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