Renal Pathophysiology I Flashcards

Prep for the test

1
Q

What are the 5 components of renal functions that can go awry and result in renal disease?

A

Fluid balance

Electrolyte balance

Acid-base balance

Waste removal

Hormonal release

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2
Q

What are some ways to decrease potassium levels in a hyperkalemic patient?

A
  • Insulin + glucose
  • Oral kaexylate (removes K+ from bloodstream via binding); also decreases H+ in blood (K+ goes into cell as H+ comes out of cell to compensate)
  • These are just temporary measures though b/c pts still need dialysis to decrease total body K+
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3
Q

Describe how ADH works?

A

Hypothalamic osmol receptors stimulate release of ADH from the posterior pituitary

  • ADH works in distal tubules and collecting ducts to open up water channels and promote water reabsorption in distal parts of nephrons (increases kidney permeability)
  • ADH triggers thirst in the brain
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4
Q

Why are renal patients often in a chronic metabolic acidotic state?

A

Kidneys are responsible for removal of H+ and retention of HCO3-.

In disease state, these functions are decreased, leading to chronic metabolic acidosis.

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5
Q

A pt with ESRD and HTN for 10 years suddenly begins to exhibit stable normal blood pressures. If this change is renally related, what would you suspect has happened?

A

Renal pts that progress to complete renal failure may lose their HTN and exhibit normal pressures (nephrons unable to produce any renin to activate the RAA system)

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6
Q

At what GFR would a renal pt usually require dialysis?

A

<10 mL/min

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7
Q

What is the ratio of cortical to medullary nephrons in the kidney?

A

7:1

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8
Q

Difference in function between cortical and medullary nephrons?

A

Cortical nephrons are shorter nephrons. Medullary nephrons are longer and deeper + have more major role in urinary composition.

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9
Q

What are a few methods by which RBF can be disrupted?

A
  • Abrupt drop in perfusion for any reason
  • Arterial tumors
  • AS
  • Inflammation/infection of nephron tubules can lead to sludge (shedding off of tubule endothelial cells) which can obstruct nephral lumen
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10
Q

What are the 3 subtypes of renal failure? What do they refer to in terms of the source of the problem.

A
  1. Prerenal (lower blood flow to kidneys)
  2. Intrarenal pathology (uncommon but possible, dysfunction originates from kidneys themselves)
    • AKI / Acute renal failure is not a permanent state (Recovery is possible)
  3. Postrenal (backup of filtered fluids)
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11
Q

What are common causes of the 3 subtypes of renal failure?

A
  1. Prerenal (lower blood flow to kidneys): low CO, hypotension, renal artery obstruction, dehydration, etc.. (common)
    • Primary reason for low UO intra op = hypovolemia and induction-related hypotension
  2. Intrarenal pathology (uncommon but possible)
    • AKI / Acute renal failure is not a permanent state (Recovery is possible)
  3. Postrenal (backup of filtered fluids): kinked foleys, UTI, calcium deposits causing sludge-like urine, obstructer uretal
    • Not uncommon
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12
Q

What is the difference between oliguric and anuric renal failure?

A
  • Oliguric/non-anuric renal failure : kidney still making urine, but unable to regulate the composition of urine normally
    - “Stupid urine”; glomeruli still filtering but nephrons dysfunctional
  • Anuric renal failure : no urine is being made at all (despite absence of post/prerenal issues)
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13
Q

What are some causes of chronic kidney failure?

A

Chronic kidney failure mechanisms:

- AS 
- Inflammatory damage (glomerular nephritis) at the glomerulus
	- Caused by antigens (antibiotics) and infections
- Tubule damage leading to casts (sloughed up cells that clump together in tubules) 
	- Can be eventually repaired in oliguric kidney failure
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14
Q

What are some concerns with giving blood to renal patients?

A

Hyperkalemia.

Giving PRBCs will increase potassium levels. The older the blood, the more potassium will be in the blood.

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15
Q

What are some concerns with our IV drugs in renal patients?

A

If they are acidemic, it can change the way our drugs work by interfering with protein binding, allowing more of our IV drugs to stay in the serum and exert a longer effect*.

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16
Q

What are severe symptoms of uremia?

A

When your BUN gets high enough, it can cause altered mental status and eventually coma.

17
Q

Why are renal patients on hemodialysis sometimes coagulapathic?

A

Due to heparin in their AV grafts/fistulas. Highly concentrated heparin prevents them from clotting between dialysis.

18
Q

Explain hemodialysis and peritoneal dialysis.

A

Hemodialysis = AV graft/fistula; blood taken out for semi-permeable membrane filtration process that resembles our countercurrent filtration system

Peritoneal dialysis catheter: catheter placed in belly that sits next to the peritoneum around the bowel; every night dialysis fluids (dialysate) are placed in the abdominal cavity and as blood flows by, it is filtered; fluids are drained every morning

19
Q

What are pros and cons of peritoneal dialysis?

A
  • Nice alternative to hemodialysis, but not for everyone
  • Usually a last resort for pts that have dwindling vascular access
  • Over time, peritoneum lining can get destroyed, infections can occur
20
Q

What is the difference between fistula and graft?

A

Fistula = direct contact btwn artery and vein (vein will grow to match the artery into a fistula, ideal for dialysis access)

Graft = synthetic material used to connect artery and vein
21
Q

Why are parathyroidectomies a common surgery for renal patients?

A

PTH can get really high due to renal failure (no more feedback from kidneys)

-Can remove to prevent build up of PTH from the 4 parathyroid glands and its effects
22
Q

What are the number 1 predictors for a pt needing a renal transplant?

A

DM and HTN

23
Q

Describe the reserve of our kidneys.

A

We have almost 90% reserve in our kidneys (we would still be able to support sufficient filtration if up to 90% of your kidneys are shot)

24
Q

What is the treatment of choice for renal patients?

A

Renal transplantation

25
Q

What are two kinds of kidney harvesting techniques?

A

Kidney harvest:

- Laparoscopic becoming more popular (less traumatic; supine) over thoracoabdominal appraoch
- Retroperitoneal approach common as well
26
Q

How are kidneys implanted?

A
  • Kidneys are anastamosed to the iliac vessels; native renal vessels of the donor kidney attached to iliac vessels of the pt (incision occurs down at the pelvic level)
    • Often time, only 1 kidney is being transplanted b/c only 1 is necessary for sufficient function
27
Q

How soon after kidney implantation is urine produced?

A

Almost immediately

28
Q

What are the main electrolytes that the kidneys regulate?

A

Na+
K+
Ca++
HCO3-

29
Q

What is acute tubular necrosis (ATN)?

A

Type of acute renal failure where tubular cells don’t get enough blood flow/nutrients; they die and slough off; renal failure persistant until the tubular cells reform once their in the recipient

Cadaveric kidneys are more susceptible to this due to metabolism not completely stopped in cells (just slowed down by the preservative)

Hence, pts with cadaveric donor kidneys may have renal failure in the first 2 days to 2 weeks of their kidney transplantation until ATN are resolved

30
Q

What are anesthetic complications for renal transplantation procedures?

A

• IV Access – Potential for Blood Loss

• Pre-Op/Intra-Op Medications
– P.O. Immunosuppression (concern about reaction to donor kidney and blood transfusions)
– I.V. Steroids
– Diuretics

• Monitoring
– CVP for fluids
– ± A-line
– ± PAWP

31
Q

What should we be concerned about with regional anesthesia in renal patients?

A

Plt dysfunction due to renal issues

Heparin in blood (potentially) if pt has AV fistula/graft

32
Q

Where do you want to keep your CVP at for these patients?

A

Normally 10-15 mm Hg, better range is 12-18 mm Hg

33
Q

What should you do right after reperfusion of the transplanted kidney?

A

Immediately diuresis promotion

Vasopressors +/- depending on surgeon preference

34
Q

Effect of Hct in DM on cardiac issues

A

Cardiac complications decrease by 24% if DM pts Hct>30%

35
Q

Why are renal failure patients often anemic?

A

kidneys produce erythropoietin, which stimulates RBC production in the bone marrow

36
Q

Why might the parathyroid need to be removed in ESRD patients?

A

Parathyroid releases PTH, which signals the kidneys to reabsorb Ca++. Since kidneys are no longer able to respond, the Ca++ is leeched from bones instead and patients become osteoporotic. Another important point to remember is that kidneys normally reabsorb Ca++, and dialysis often removes more Ca++ than kidneys normally would.