Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

SMP - Renal > Lecture 15 - Renal Failure > Flashcards

Lecture 15 - Renal Failure Flashcards

1
Q

What are the 2 types of dialyses? Is one better?

A
  1. Hemodialysis: dialysis machine hook up to a surgically made fistula between an artery and a vein in the arm, 3 x /week for 4 hours (to remove 2 days of fluid intake) => uses hydrostatic pressure, clearance is due to passive diffusion from plasma to dialysate
  2. Peritoneal dialysis: underused, more life independence => uses oncotic pressure

About the same outcomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Purpose of dialysis?

A
  1. Control volume via ultrafiltration
  2. Clearance
  3. Acid base balance to correct acidosis, hyperkalemia, and low Ca++
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What issue cannot be corrected via dialysis?

A

Phosphate accumulate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Dietary management of renal failure?

A
  1. Limit dietary salt to limit volume accumulation and regulate BP
  2. Limit dietary K+, since excess in ECF can cause depolarization of muscles and death
  3. Limit dietary phosphate with drugs that bind phosphate in the gut to inhibit it from being absorbed
  4. Vitamin D supplement needed since kidneys can no longer product the active form, which causes issues with Ca++ absorption and PTH regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Can failed kidneys still secrete renin/stimulate the SNS?

A

YUP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why do patients with renal disease have anemia? Treatment?

A

Because the kidneys make erythropoietin

Treatment: erythropoietic agents, iron as needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the physiologic response of acute renal failure.

A

Loss of HALF THE RENAL FUNCTION:

  1. GFR is suddenly cut in half, since of the kidneys is no longer working
  2. Serum creatinine doubles over a certain period of time (increases exponentially) => positive balance until new steady state is reached
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Normal production creatinine rate?

A

10-20 mg/kg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List the concentration changes due to renal failure (from highest to lowest)

A

INCREASES:

  1. Non protein nitrogen
  2. K+
  3. H2O
  4. Na+
  5. H+
  6. Phenols
  7. HPO4–/SO4–

DECREASES:
1. HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 3 types of acute renal failure?

A
  1. Block perfusion = pre-renal
  2. Damage/kill nephrons = intrarenal
  3. Block urinary drainage = post-renal (or intra-renal in all collecting ducts, still considered post though)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Examples of causes of damaged/dead nephrons?

A
  1. Sepsis with inflammatory mediators
  2. Nephrotoxic injury
  3. Inflammation due to allergies => interstitial nephritis
  4. Ischemic tubular necrosis
  5. Transplant rejection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

4 clinical examples of pre-renal acute renal failure?

A
  1. Volume depletion
  2. Hemorrhage
  3. Decompensated CHF
  4. Arterial-arteriolar occlusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Physiology of pre-renal acute renal failure?

A

Decreased afferent perfusion/pressure => Ang II-dependent effort to maintain GFR via efferent vasoconstriction + afferent vasodilation with opposing effects of NO and prostaglandins
=> high filtration fraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Consequence of increase filtration fraction?

A

Increased peritubular oncotic pressure => increased proximal and distal tubular reabsorption => salt-avid kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe plasma urea and creatinine in pre-renal acute renal failure.

A

Decrease in urea clearance exceeds the decrease in creatinine clearance (so higher plasma urea) because urea can be reabsorbed but not secreted and creatinine can be secreted but not reabsorbed => high plasma BUN/creatinine ratio (>20)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe urine concentration and solute avidity in pre-renal acute renal failure.

A
  1. Urine concentration > 500 mOsm/L
  2. Increase in urine creatinine
  3. Decrease in fractional excretion of Na+ (<1%)
  4. Decrease in fractional excretion of urea (<35%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Normal BUN/creatinine plasma ratio?

A

10:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe plasma urea and creatinine in intra-renal acute renal failure.

A

Normal BUN/creatinine (unless production changed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe urine concentration and solute avidity in intra-renal acute renal failure.

A

Impaired tubular function, which varies with the predominant site of damage

  1. Acidemia
  2. Impaired urine concentration/dilution => isosthenuria (same osmolarity of plasma)
  3. Low urine creatinine
  4. Salt wasting, with an increase in excretion fraction of Na+ (>2%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Consequence of post-renal acute renal failure?

A

Transmission of pressures back along the nephron leading to a stop in filtration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where is tubular dysfunction more severe in post-renal acute renal failure?

A

Distal nephron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe plasma urea and creatinine in post-renal acute renal failure.

A

High BUN/creatinine due to stasis in tubule causing increase urea reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe urine concentration and solute avidity in post-renal acute renal failure.

A
  1. Decrease in fractional excretion of Na+ (<1%)
  2. Hyperkalemia
  3. Acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the intact nephron hypothesis?

A

No matter where you injure the nephron, the entire nephron will be injured

25
What happens during the shift from acute renal failure to chronic kidney disease?
Decrease in number of nephrons => hypertrophy and vasodilation of surviving nephrons + increase in arterial pressure => increase in glomerular pressure and filtration => glomerular sclerosis => further decrease in number of nephrons
26
Why is the sensitivity of plasma creatinine low to detect GFR decrease?
Because plasma creatinine is low and because there is tubular secretion
27
Which happens first during renal failure: high plasma creatinine or phosphate accumulation/acidosis?
Phosphate accumulation/acidosis
28
How is plasma osmoregulation (and K+, Na+, and Cl-) affected by renal failure?
Preserved into advanced CKD because they are mostly being reabsorbed by the kidneys normally so low GFR doesn't affect the plasma levels much, PLUS thirst still works even when dilution/concentration by the kidney fails
29
What is the staging of CKD dependent on?
Estimated GFR normalized to body surface area
30
Describe the 5 stages of CKD and their necessary action.
1. Normal GFR but indication of renal failure (e.g. albuminuria) => manage CVD risks and avoid nephrotoxic drugs 2. Mild GFR decrease = 60-89 3. Moderate GFR decrease = 30-59 4. Severe GFR decrease = 15-29 5. Kidney failure: GFR < 15 => replacement if uremia present
31
At what CKD stage is it noticeable? Why?
Stage 3 because of lab values
32
At what CKD stage is there an ABSOLUTE need for replacement therapy (transplant or dialysis) in an otherwise healthy person? What does this mean?
GFR = 4-5 mL/min With artful medical management, the first 95% of kidney function is the safety margin
33
Why does the specific gravity of urine decrease as number of nephrons decrease? What to note?
Hypertrophy and vasodilation of surviving nephrons => flow through residual nephrons increases => inability to maintain medullary concentration or to reabsorb water => ability to maximally concentrate/dilute urine falls => isosthenuria => make more urine to excrete the same amount of waste => bladder capacity exceeds overnight
34
Prevalence of HT in patients with CKD?
80-100%
35
What is HT with CKD due to?
1. Primarily to increased volume | 2. Also due to vasoconstriction due to SNS and RAAS
36
2 consequences of HT with CKD?
1. Accelerates loss of renal function | 2. Worsens proteinuria
37
What do most patients with CKD die of?
CVD more than end stage renal disease
38
What vessels are use to create a fistula in the arm for hemodialysis? Purpose?
Radial or brachial vessels => loop of of high flow/low resistance causing vein to arteriolize
39
How does hemodialysis work?
Pump before hemodialyzer pushing blood into the hemodialyzer (artificial glomerulus), in which it is pressurized => water and waste products leave and blood is pressured back out => back into vein
40
How does peritoneal dialysis work?
Catheter inserted into peritoneal cavity and patient learns sterile technique to hook it up to sterile dialysis fluid (2L) => ultrafilter into the fluid (contains glucose as an osmotic agent) => drain 3 L out
41
Clearance of hemodialysis? What does this mean? Average urea clearance?
200 mL/min => 156 hours/week w/o clearance Average urea clearance = 14mL/min
42
Clearance in peritoneal dialysis? How does this compare to HD?
5.5 mL/min (lower than HD)
43
Which dialysis method has better volume control?
PD
44
What is uremia?
Syndrome due to retention of toxic wastes in the blood: multiple toxins but urea is used as a marker
45
Does a low BUN dialytic clearance in patient with renal failure a good sign?
Could be, but could also mean that the dialysis is inadequate leading to uremia
46
Symptoms of uremia?
Decreased appetite, overlap with anemia symptoms, malnutrition
47
What is uremic acidosis?
Nephron loss => impaired renal ammoniagenesis => sulfate/phosphate retention => mild bicarbonate wasting + mild increase in anion gap
48
How to control acidosis of renal failure patients? What to note?
1. Oral Na+HCO3- (or citrate) => problem with increased volume caused 2. HCO3- in HD (but engineering issue because substances can bubble away) 3. Lactate in PD
49
Describe K+ excretion in renal failure?
Without a tubular defect, normal until ESRD
50
Describe the removal of K+ in patients in renal failure.
Either dialysis or GIT removal
51
What is K+ removal limited by?
Redistristribution to intracellular compartment, which happens fast
52
When does low vitamin D and increasing PTH occur in CKD? Consequence?
Very early on => renal metabolic bone disease => increased osteoclastic bone reabsorption due to calcium insufficiency + calcium mobilization from bone due to acidosis
53
Phosphate concentration during dialysis? Implication?
Falls rapidly during but rebounds within hours because of redistribution => inefficient => instead we use phosphate binds in GIT
54
When does metabolic bone disease start?
Stage 2
55
Why do you have to be careful with VD supplement?
Too much can cause a different bone disease
56
Prevalence of dialysis patients?
1/2 M
57
Incidence of ESRD patients?
115 K
58
Number of kidney transplants/year?
17 K

SMP - Renal (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions