Renal

Question 1

Vasopressin and CAD?

Answer 1

Vasopressin may precipitate myocardial ischemia by vasoconstriction of the coronary arteries.

Question 2

What do the V1 and V2 receptors for vasopressin do? It dilates and constricts?

Answer 2

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.

Question 3

Vasopressin and VWdz?

Answer 3

Vasopressin increases VWF and factor 8

Question 4

What is MOST likely responsible for intraoperative oliguria caused by hyperventilation when using positive pressure ventilation?

Answer 4

Increased respirations=increased intrathoracic pressure=increased pressure on IVC=impairment of renal perfusion=oliguria. KIM that the increased intrathoracic pressure increases right heart afterload.

Question 5

Positive pressure ventilation increases intrathoracic pressure which can decrease urine output through four main effects:

Answer 5

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

Question 6

Wassup with calcium levels and people with renal dz?

Answer 6

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.

Question 7

Blood levels in ESRD? 
Calcium? 
K?
Mg? 
Lipids? 
BP? 
Phosphate? 
Parathyroid?

Answer 7

• Anemia
• Hypocalcemia
• Hyperkalemia
• Hypermagnesemia
• Hyperlipidemia
• Hypertension
• Hyperphosphatemia
• Secondary hyperparathyroidism
• Uremic bleeding diathesis

Question 8

Sodium and renal dz?

Answer 8

Can be either hypo or hyper

Question 9

Anuria vs oliguria: THERE IS A DIFFERENCE!

Answer 9

Anuria: Less than 50 mL per day
Oliguria: Less than 0.5 mL/kg/hr

Question 10

FeNa and urine Na in pre-renal vs renal dz

Answer 10

FeNa pre renal: <1 and urine Na pre renal: <20

FeNA renal dz: >2 urine Na: >40

Question 11

FeNa formula:

Answer 11

FENa = 100 * (Urine Na / Plasma Na) / (Urine Cr / Plasma Cr)

Question 12

Why is sevoflurane slightly controversial with renal issues?

Answer 12

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.

Question 13

Normal urine osmolality:

Answer 13

400

Question 14

glycine and TURP:

Answer 14

can cause transient blindness

Question 15

distilled water and TURP:

Answer 15

Distilled water is hypotonic and can lead to severe intravascular hemolysis, fluid overload, and dilutional hyponatremia.

Question 16

Normal saline and TURP:

Answer 16

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

Question 17

Sorbitol and Mannitol and TURP: Do they cause current dispersion? What do they both cause? Mannitol is contraindicated for which patient population?

Answer 17

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.

Question 18

transient blindness d/t glycemia in TURP is very common T/F

Answer 18

FALSE! ITS RARE. More common is the hypothermia that can result from the solutions

Question 19

Complications of TURP:

Vision, coagulopathy, ammonia? what can get damaged?

Answer 19

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.

Question 20

How do you calculate sodium deficit?

Answer 20

Sodium deficit = (140 – serum sodium) x total body water

Total body water = kilograms of body weight x 0.6

Question 21

what goes n first, glucose or thiamine?

Answer 21

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.

Question 22

Electrolyte abnormalities in alcoholic patients include:

Answer 22

The 4 hypo’s:Electrolyte abnormalities in alcoholic patients include:

Question 23

Mac in acute vs chronic alcoholic, Gastric emotying and alcohol, fresh gas flows?

Answer 23

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.

Question 24

vol status and post-op risk of a fib:

Answer 24

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

Question 25

Tx of post operative a fib:

Answer 25

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.

Question 26

what factors increase risk of post op a fib

Answer 26

male gender, volume status, abdominal or cardiac surgeries, thoracic surgeries

Question 27

Mannitol and renal transplant

Answer 27

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

Question 28

Why does mannitol help prevent kidney injury?

Answer 28

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

Question 29

Why is urine Na still high in SIADH?

Answer 29

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.

Question 30

``` Typical lab findings in SIADH: Urine osm? FeNa? BUN and serum uric acid? sodium and volume status? ```

Answer 30

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)

Question 31

Why would hemostasis be difficult in someone that has not been dialyzed in 4 days? AT 3 in ESRD?-

Answer 31

Uremia interferes with platelet activation and aggregation (primarily via effects on vWF and GPIIb-IIIa) and leads to increased production of platelet inhibitors (e.g. prostacyclin and nitric oxide). AT3 is usually reduced in ESRD

Question 32

Damage to kidney cells results in decreased ability to reabsorb ? What does this mean?

Answer 32

sodium :) | Therefore, sodium is lost in the urine and is typically >40 mmol/dL.

Question 33

Most affected sites of ATN in the kidney: Pathophys of ATN: ATN is caused by:

Answer 33

The straight segment of the proximal tubule and the medullary portion of the thick ascending limb are the most often affected sites in the kidney.Damage to the endothelial cells leads to a decrease in vasodilators (nitric oxide, PGI-2) and an increase in vasoconstrictors (endothelin) which ultimately decreases the glomerular filtration rate. Damage to the tubular cells and their basement membranes can lead to sloughing of cells and obstruction. ATN is typically caused by either renal ischemia or nephrotoxins.

Question 34

What is the gold standard for distinction between pre-renal disease and ATN? What about serum Cr? Persistent AKI despite adequate fluid repletion

Answer 34

Before discussing lab findings, it should be pointed out that response to fluid repletion is the gold standard for the distinction between prerenal disease and ATN.The serum Cr should return to baseline within 1-3 days in the setting of prerenal disease if volume repletion is adequate. Persistent AKI despite adequate repletion represents ATN.

Question 35

FENa in ATN:

Answer 35

The fractional excretion of sodium (FENa) in ATN is typically >1%.

Question 36

When would you use FeUrea? | Values of FeUrea?

Answer 36

In moments of diuretic use Fractional excretion of urea has been used in the setting of diuretic use. FEUrea < 35% is suggestive of prerenal disease, whereas >50% may indicate ATN.

Question 37

In prerenal disease, UNa is typically

Answer 37

In prerenal disease, UNa is typically < 20 mEq

Question 38

BUN: Cr ratio in ATN:

Answer 38

The BUN to Cr ratio is most often normal (10:1 – 15:1) in ATN

Question 39

Specific gravity is a marker for what? Uosm in ATN: Uosm in Pre-renal dz:

Answer 39

Specific gravity is a surrogate marker for urine osmolality (Uosm). Loss of concentrating ability in ATN typically results in Uosm < 350 mOsm/kg. Prerenal disease is associated with a Uosm >500 mOsm/kg. Unfortunately, the same conditions that alter the specific gravity alter the Uosm which makes this test clinically inadequate from distinguishing between pre-renal disease and ATN.

Question 40

ATN and Pre-renal chart in photos

Answer 40

Okay

Question 41

The use of regional anesthesia for TURP (mostly spinal, except in high-risk patients where caudal may be a consideration) has three main advantages compared to general anesthesia

Answer 41

1) Allows for detection of prostatic capsule or bladder perforation, as long as the patient is not deeply sedated and the spinal level is not higher than T10. 2) It decreases blood loss. This is believed to be due to a decrease in central venous pressure. 3) It decreases the incidence of deep vein thrombosis. TURP procedures are prone to causing deep vein thrombosis. The beneficial effect of regional anesthesia is believed to be due to modulation of the neuroendocrine response to tissue injury.

Question 42

M Turp vs b turp and L turp:

Answer 42

M-TURP is being replaced by bipolar TURP (B-TURP) which has the advantage of using normal saline as irrigating fluid, thus avoiding some of the complications of hypotonic irrigation. Also, laser TURP (L-TURP) is replacing both forms of conventional TURP because of being faster, having less bleeding, and having less fluid absorption. Thus with L-TURP, general anesthesia is an acceptable alternative.

Question 43

Normal anion gap: | How do you calculate anion gap?

Answer 43

8-12 | Anion gap = serum sodium – (serum chloride + serum bicarbonate).

Question 44

Can TPN cause increased chloride with normal anion gap?

Answer 44

Yes

Question 45

Non anion gap metabolic acidosis:

Answer 45

Nonanion gap metabolic acidosis (where the anion gap is normal at 8-12 mEq/L) is typically caused by chloride-containing acid administration, increased HCO3- loss or loss of HCO3- precursors, or decreased renal acid excretion. Increased HCO3- loss is usually via the gastrointestinal (GI) tract or the kidneys. Causes of increased GI losses include diarrhea, GI fistulas (e.g. pancreatic, biliary, bowel), high ostomy output, or use of bile or phosphorus binding drugs. Renal losses can be caused by use of carbonic anhydrase inhibitors (e.g. acetazolamide) or type 2 (proximal) renal tubular acidosis (RTA).

Question 46

ACCRUED and FUSEDCARS:

Answer 46

Decreased acid excretion is due to hypoaldosteronism or renal causes including acute and/or chronic renal failure or type 1 (distal) RTA. Several mnemonics exist to remember causes of nonanion gap acidosis. Examples include: ACCRUED: Acid infusion, Compensation for respiratory alkalosis, Carbonic anhydrase inhibitors, Renal tubular acidosis, Ureteral diversion, Extra alimentation, Diarrhea. FUSEDCARS: Fistula, Ureteroenterostomy, Saline administration, Endocrine (hyperparathyroidism), Diarrhea, Carbonic anhydrase inhibitors, Ammonium chloride, Renal tubular acidosis, Spironolactone.

Question 47

When do you see a widened QRS?

Answer 47

Widened QRS is typically seen with hyperkalemia and hypermagnesemia.

Question 48

When do you see U waves?

Answer 48

U waves are seen with severe hypokalemia

Question 49

What can help you to get electrolytes and EKG changes down?

Answer 49

hyPeR hyperkalemia/calcemia/magnesemia leads to PRolongation of the PR interval. The opposite tends to occur with the QT interval for each electrolyte.

Question 50

What does hypocalcemia do to the QT?

Answer 50

prolong it.

Question 51

How is waste removed in dialysis?

Answer 51

Waste is removed by dialysis through a process of passive diffusion with solutes moving down a concentration gradient to equilibrate at the dialysate concentration (or at least that is the goal).

Question 52

Are people on dialysis frequently anemic? If so-why?

Answer 52

Due to lack of erythropoietin production by the kidney, anemia is common and patients are often on periodic erythropoietin injections to maintain hemoglobin concentration of 11-12 g/dL.

Question 53

PTT and dialysis patients:

Answer 53

Elevation in PTT may be seen preoperatively due to the use of heparin for anticoagulation during dialysis depending on the time between therapy and surgery. These patients may also have platelet dysfunction which compounds the risk of increased bleeding.

Question 54

Why can you frequently see hypokalemia in patients who were recently dialyzed?

Answer 54

Hypokalemia is often seen in the early post-dialysis period due to inadequate time for equilibration of intracellular potassium into the intravascular space.

Question 55

Neostigmine and poor kidney function:

Answer 55

Poor kidney function prolongs the duration of neostigmine and can reduce the likelihood of recurarization. Meaning-give neostigmine to patients with renal issues and they'll have it around longer.

Question 56

Explain why we give neostigmine and glyco/atropine for reversal:

Answer 56

Neostigmine increases the concentration of acetylcholine, which competes with muscle relaxants for the nicotinic receptors. However, the acetylcholine also binds to the muscarinic receptors as well. Acetylcholine binding to the muscarinic receptor is the source of most side-effects of neostigmine. These include bradycardia, prolongation of QT interval, stimulation of salivary glands, bronchoconstriction, miosis, and increased intestinal activity. The side-effects are reduced by giving an anticholinergic drug that blocks the muscarinic receptors, such as, glycopyrrolate or atropine.

Question 57

What is the best way to detemine imminent acute renal failure?

Answer 57

Creatinine clearance (CCr) is the best way to determine imminent acute renal failure. CCr = (Urine creatinine * Urine volume) / Plasma creatinine A 24-hour urine collection to measure creatinine clearance is the ideal test to determine acute renal failure, but in the acute perioperative setting, it is reasonable to proceed with a 2-hour urine collection.

Question 58

Formula for TBW:

Answer 58

(Total body water ≈ body weight (in kg) * 0.6)

Question 59

Guidelines for reducing the incidence of TURP

Answer 59

Guidelines for reducing the incidence of TURP syndrome include (1) suspending irrigating fluid bag ≤30 cm above the patient, (2) draining the bladder regularly to avoid increases in bladder pressures, (3) limiting resection time to < 1 hour, (4) avoiding hypotonic IV fluids, and (5) using vasopressors to treat hypotension resulting from regional anesthesia. Regional anesthesia may reduce venous pressures and increase absorption of irrigating fluid.

Question 60

What is central pontine myelinosis and how can you avoid that?

Answer 60

Central pontine myelinolysis (a demyelinating CNS lesion), now known as osmotic demyelination syndrome, may result with rapid increase in serum osmolality during hypertonic saline therapy. Typically, 50% of the Na+ deficit is corrected during the first 24 hours, and the rate of hypertonic saline administration should never be higher than 100 ml/hr. Hypertonic saline is typically discontinued once the serum Na+ is >120 mEq/L and/or mental status returns to baseline.

Question 61

So, which fluids do you give in hyponatremia?

Answer 61

Symptomatic patients with serum Na less than 120 mEq/L should have their serum osmolality corrected with 3% hypertonic saline, not normal saline. Serum electrolytes should be assessed regularly and hypertonic saline should be discontinued once symptoms resolve and/or serum Na+ rises above 120 mEq/L.

Question 62

Would you give furosemide in hyponatremia?

Answer 62

Loop diuretics, such as furosemide, are utilized to eliminate excess free water and treat the sodium deficit

Question 63

Which kind of patients would you be worried about having laparoscopic surgery?

Answer 63

Patients at risk for intracranial saccular aneurysms include those with ADPKD, Marfan syndrome, and Ehlers-Danlos syndrome. As well as people with ICP issues

Question 64

What tests does a patient with Marfan syndrome need to undergo?

Answer 64

A patient with Marfan syndrome should undergo echocardiography in addition to cerebrovascular imaging. This is due to the risk of aortic valve and root pathology related to the mutation of the fibrillin 1 gene. Fibrillin 1 normally wraps around the amorphous elastin connective tissue protein, giving it shape and consistency

Question 65

Hyponatremia in inpatients vs outpatients:

Answer 65

In general, hyponatremia in the inpatient population is secondary to increased antidiuretic hormone release while in the outpatient population it is secondary to chronic disease.

Question 66

sugar and sodium-how does that thing work?

Answer 66

Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space. Serum sodium concentration is diluted by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration

Question 67

Plasma osmolality formula:

Answer 67

Posm = 2.0 * [Na] + Glucose/18 + BUN/2.8.

Question 68

Substances removed and kept in dialysis:

Answer 68

Substances that are commonly removed from the patient’s blood include calcium, creatinine, magnesium, phosphate, potassium, urea, and free water. Substances that may be added to, or removed from, the patient’s blood include bicarbonate, chloride, glucose, and sodium. The serum concentrations of these substances may therefore increase or decrease based on predialysis levels.

Question 69

Proteins and dialysis:

Answer 69

Large molecules such as proteins are unable to pass through the semipermeable membranes used for hemodialysis (HD) and are not removed from the body. Since HD often involves ultrafiltration, serum protein concentrations usually increase following HD due to a concentrating effect

Question 70

Who has increased risk of AKI after cardiopulmonary bypass?

Answer 70

Preoperative creatinine greater than 1.2mg/dL, combined valve and bypass procedures, emergency surgery, and preoperative intraaortic balloon pump are risk factors most strongly correlated with post-cardiopulmonary bypass acute kidney injury. Other well-known minor risk factors include: female gender, congestive heart failure, chronic obstructive pulmonary disease, insulin-requiring diabetes, and depressed left ventricular ejection fraction.

Question 71

Does pulsatile flow help prevent kidney failure?

Answer 71

n patients with normal preoperative kidney function, no difference in the rate of acute kidney has been demonstrated between use of non-pulsatile and pulsatile perfusion during cardiopulmonary bypass. Some renal, cardiac, and pulmonary benefit may be gained with the use of pulsatile perfusion in the most critically ill patients; however, quality randomized studies are still lacking on this topic.

Question 72

Reasons for emergent dialysis:

Answer 72

Reasons for emergent dialysis include AEIOU: Acidosis, Electrolytes, Ingestions (toxins), Overload, Uremia.

Question 73

Fluid chart in True learn

Answer 73

Okay

Question 74

RTA: which type of acid base disturbance does it cause?

Answer 74

It causes non-anion gap metabolic acidosis

Question 75

Tell me about RTA type 1:

Answer 75

Sjrogen's syndrome: dysfunction in the alpha cells of the collecting tubule.

Question 76

RTA type 2:

Answer 76

Fanconi syndrome and is caused by defects of the proximal tubule, leading to bicarbonate wasting

Question 77

RTA type 3:

Answer 77

Renal tubular acidosis type 4 is caused by aldosterone deficiency or resistance.