Renal Flashcards
Vasopressin and CAD?
Vasopressin may precipitate myocardial ischemia by vasoconstriction of the coronary arteries.
What do the V1 and V2 receptors for vasopressin do? It dilates and constricts?
V1 receptor activation increases systemic vascular resistance without affecting pulmonary vascular resistance. V2 receptor activation increases blood volume. It can dilate pulmonary and cerebral vascular beds, but can constrict vessels associated with esophageal varices. It can also constrict coronarty arteries.
Vasopressin and VWdz?
Vasopressin increases VWF and factor 8
What is MOST likely responsible for intraoperative oliguria caused by hyperventilation when using positive pressure ventilation?
Increased respirations=increased intrathoracic pressure=increased pressure on IVC=impairment of renal perfusion=oliguria. KIM that the increased intrathoracic pressure increases right heart afterload.
Positive pressure ventilation increases intrathoracic pressure which can decrease urine output through four main effects:
1) Impaired renal perfusion and renal venous drainage
2) Decreased preload and increased right ventricular afterload
3) Stimulation of the sympathetic nervous system
4) Release of inflammatory cytokines
Wassup with calcium levels and people with renal dz?
Hypocalcemia. The kidney loses the ability to reabsorb calcium with decreased function. Additionally, the kidney is responsible for converting 25-hydroxycholecalciferol to 1, 25-hydroxycholecalciferol. 1, 25-hydroxycholecalciferol is responsible for increasing calcium absorption in the gastrointestinal tract.
Blood levels in ESRD? Calcium? K? Mg? Lipids? BP? Phosphate? Parathyroid?
- Anemia
- Hypocalcemia
- Hyperkalemia
- Hypermagnesemia
- Hyperlipidemia
- Hypertension
- Hyperphosphatemia
- Secondary hyperparathyroidism
- Uremic bleeding diathesis
Sodium and renal dz?
Can be either hypo or hyper
Anuria vs oliguria: THERE IS A DIFFERENCE!
Anuria: Less than 50 mL per day
Oliguria: Less than 0.5 mL/kg/hr
FeNa and urine Na in pre-renal vs renal dz
FeNa pre renal: <1 and urine Na pre renal: <20
FeNA renal dz: >2 urine Na: >40
FeNa formula:
FENa = 100 * (Urine Na / Plasma Na) / (Urine Cr / Plasma Cr)
Why is sevoflurane slightly controversial with renal issues?
The only agent that is slightly controversial is sevoflurane. When exposed to CO2 absorbents in the setting of low fresh gas flow, sevoflurane can be degraded to the potentially nephrotoxic compound A.
Normal urine osmolality:
400
glycine and TURP:
can cause transient blindness
distilled water and TURP:
Distilled water is hypotonic and can lead to severe intravascular hemolysis, fluid overload, and dilutional hyponatremia.
Normal saline and TURP:
Normal saline and other balanced salt solutions promote significant current dispersion due to their ionic composition. They are not used in a classic TURP because the ions in the solution cause electric dispersion of the monopolar current. Normal saline does not promote significant hyponatremia or hemolysis.
NS does reduce TURP though, but it’s not used
Sorbitol and Mannitol and TURP: Do they cause current dispersion? What do they both cause? Mannitol is contraindicated for which patient population?
Sorbitol 3.3% / mannitol 5% combination irrigating solutions are widely used owing to slight hyperosmolality or iso-osmolality. They do not cause electrical current dispersion. Sorbitol may cause hyperglycemia if absorbed. Mannitol and sorbitol both cause an osmotic diuresis. Recall that mannitol initially causes intravascular volume expansion and is therefore relatively contraindicated in patients with congestive heart failure.
transient blindness d/t glycemia in TURP is very common T/F
FALSE! ITS RARE. More common is the hypothermia that can result from the solutions
Complications of TURP:
Vision, coagulopathy, ammonia? what can get damaged?
Complications of TURP include hypothermia from room temperature irrigation fluids, transient blindness and hyperammonemia from glycine-containing fluid, intraperitoneal bladder perforation, extraperitoneal prostatic capsular perforation, cardiopulmonary compromise, and coagulopathy from fibrinolysis.
How do you calculate sodium deficit?
Sodium deficit = (140 – serum sodium) x total body water
Total body water = kilograms of body weight x 0.6
what goes n first, glucose or thiamine?
When replacing glucose in a hypoglycemic alcoholic patient, thiamine should be given first. This is because thiamine is used as a cofactor in glucose metabolism. If subclinical thiamine deficiency is present and a significant glucose load is given then thiamine store can become depleted. This depletion of thiamine will result in Wernicke encephalopathy. People with Wernicke encephalopathy have ataxic gait disturbances, altered mental status, and oculomotor dysfunction.
Electrolyte abnormalities in alcoholic patients include:
The 4 hypo’s:Electrolyte abnormalities in alcoholic patients include:
Mac in acute vs chronic alcoholic, Gastric emotying and alcohol, fresh gas flows?
Alcohol has effects on the minimum alveolar concentration (MAC). Acute alcohol intoxication will decrease a patient’s MAC and chronic alcoholism will increase a person’s MAC. Additional effects of acute alcohol intoxication include delayed gastric emptying, which increases the risk of aspiration with induction of anesthesia. Substances exhaled by the patient include alcohol, acetone, carbon monoxide, and methane. Therefore, the use of low fresh gas flows in a circle system is contraindicated in patients who are intoxicated, in uncompensated diabetic states, or who are suffering from carbon monoxide poisoning.
vol status and post-op risk of a fib:
Proper volume management is crucial to help decrease the development of AF. Both hypovolemia and hypervolemia can increase the risk.Hypovolemia causes a decreased venous return to the right atrium which reduces stroke volume and cardiac output. Both of these cause decreased tissue oxygen delivery, which induces catecholamine release – both can increase the risk of AF development. Hypervolemia leads to mechanical stimulation of the right atrium which leads to myocardial stretch and the increase in atrial cell triggeri
Tx of post operative a fib:
Once AF has developed in the postoperative period, treatment is important. Approximately 25% to 80% of patients will have spontaneous conversion within 24 hours. Rate control is a reasonable place to start in patients who do not convert spontaneously, and this includes use of agents that slow atrioventricular nodal conduction such as beta-blockers and calcium channel blockers. These two blocking agents are considered first line by the American Heart Association/American College of Cardiology (AHA/ACC), whereas amiodarone is considered a second-line agent. If a patient is symptomatic or hemodynamically unstable, rhythm control may be needed. Another option is direct current cardioversion. Fluid management is also important to help assure AF does not reoccur following spontaneous, pharmacologic or electrical conversion back to sinus rhythm.
what factors increase risk of post op a fib
male gender, volume status, abdominal or cardiac surgeries, thoracic surgeries
Mannitol and renal transplant
Intraoperative mannitol administration prior to vessel clamp release during renal transplant has been shown to decrease post-transplant kidney injury, but has not been shown to reduce graft rejectio
Why does mannitol help prevent kidney injury?
Maintenance of intravascular volume is the key ingredient in prevention of post-transplant renal injury with no particular fluid being more important than the sheer maintenance of intravascular volume.Administration of mannitol prior to removal of vessel clamps has been shown to decrease the incidence of post-transplant renal injury requiring dialysis, however it has not been proven to prevent graft rejection acutely or chronically
Why is urine Na still high in SIADH?
Antidiuretic hormone acts at the renal distal convoluted tubules and collecting ducts to cause retention of free water without any direct effects on solute reabsorption. Elevated ADH, such as in SIADH, therefore prevents diuresis but still permits natriuresis and excretion of other solutes including uric acid resulting in concentrated urine.
Typical lab findings in SIADH: Urine osm? FeNa? BUN and serum uric acid? sodium and volume status?
1) Urine osmolality >100 mOsm, and often > 200-300 mOsm
2) Fractional excretion of sodium (FENa) > 1%
3) Urine Na+ > 20 mEq/L
4) Low serum uric acid and BUN
5) Dilutional, euvolemic hyponatremia (serum Na+ < 135 mEq/L)
