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NRP511 > Renal pathophysiology > Flashcards

Renal pathophysiology Flashcards

1
Q

The kidneys receive __________ percent of total cardiac output

A

15 to 25%
95% of this blood is directed to the renal cortex
5% is directed to the medulla

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2
Q

The amount of blood through the renal arteries is

A

1-1.25 L/min

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3
Q

Renal medullary papillae are more vulnerable to

A

ischemic insults

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4
Q

Kidneys successfully autoregulate their blood flow between

A

60-160 mmHg mean arterial pressures

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5
Q

Since it is intrinsic,

A

autoregulation is intact even in the denervated kidneys

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6
Q

Autoregulation is

A

an INTRINSIC MECHANISM that causes vasodilation & vasoconstriction of renal afferent arterioles to regulate renal blood flow

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7
Q

The capillaries are lined with

A

endothelial cells known as PODOCYTES

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8
Q

The glomerular filtration rate is

A

the rate at which blood is filtered through all of the glomeruli measure overall kidney function

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9
Q

The resistance in the efferent arterioles creates

A

HYDROSTATIC PRESSURE within the glomerulus to provide force for ultrafiltration

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10
Q

The glomerulus separates the

A

afferent (brings blood) arterioles from the efferent (takes it away) arterioles

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11
Q

SNS activation will

A

reduce renal blood flow ****
Shunts blood to more important places in times of stress

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12
Q

SNS activation reduces renal blood flow by

A

shunting to skeletal muscle during exercise
surgical stimulation can increase vascular resistance
stimulates the adrenal medulla–> catecholamine release
If BP decreases- SNS will also stimulate RAAS

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13
Q

Anesthetics that decrease renal blood flow include

A

Propofol
PPV
retractors
among many other things

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14
Q

Perioperative causes of ADH release include**:

A 
hemorrhage
positive pressure ventilation
upright position
nausea
medications
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15
Q

The half-life of antidiuretic hormone is

A

16-24 minutes

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16
Q

2 primary functions of ADH include

A

increases reabsorption of sodium & water in the kidneys

causes vasoconstriction and PVR to increase blood pressure

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17
Q

Antidiuretic hormone is synthesized in the

A

hypothalamus & is released from the posterior pituitary

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18
Q

Antidiuretic hormone is released in response to

A

DECREASED stretch receptors in the atrial & arterial wall (low fluid in system means decreased volume and decreased stretch)

INCREASED osmolality of the plasma (monitored by hypothalamus)

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19
Q

Renin is an enzyme secreted by the kidneys that

A

hydrolyzes angiotensin to angiotensin I

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20
Q

Renin is released from the

A

juxtaglomerular cells located near the afferent arterioles in response to
a decreased arterial blood pressure
a decrease in NA load delivered to the distal tubules
& SNS (beta 1 receptors)

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21
Q

Angiotensin I is converted in the lungs by

A

angiotensin-converting enzyme into angiotensin II

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22
Q

Angiotensin II is a

A

potent vasoconstrictor & stimulates the hypothalamus to secrete ADH

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23
Q

Aldosterone is a

A

mineralocorticoid hormone released from the adrenal gland

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24
Q

The plasma half-life of aldosterone is

A

20 minutes

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25
Aldosterone stimulates epithelial cells in the distal tubule & collecting ducts to
REABSORB SODIUM & WATER | -exchanges potassium to maintain electroneutrality
26
Aldosterone is the complete opposite of
atrial natriuretic hormone function
27
Spironolactone is a
potassium sparing diuretic that blocks the aldosterone receptors
28
Acute kidney injury is the
sudden inability of the kidneys to vary urine volume & content appropriately develops rapidly but may resolve
29
AKI has a ______ mortality rate
50%
30
Causes of AKI include
pre-renal intrinsic-renal post-renal
31
Pre-renal AKI is a result of
hemodynamic or endocrine factors that impair perfusion | hypoperfusion or hypovolemia
32
Factors that can cause hypoperfusion or hypovolemia in pre-renal AKI include
``` skin loss (e.g. burns) fluid loss hemorrhage sequestration vascular occlusion (e.g. thrombosis, aortic, or renal artery clamping) ```
33
Pre-renal AKI will activate
mechanism to conserve salt & water | -RAAS, ADH, low urine sodium with high osmolality)
34
Pre-renal AKI can progress to
permanent parenchymal damage
35
Renal or acute tubular necrosis is the result of
tissue damage from - prolonged ischemia - nephrotoxic injury (e.g. antibiotics, chemotherapeutics, & contrast dye) - glomerulonephritis
36
Patients with parenchymal disease will have trouble
concentrating urine | -high urine Na & low osmolality
37
Nephrotoxic drugs include
aminoglycosides, amphotericin B, chemotherapeutic drugs, cyclosporine modified, NSAIDs, penicillin antibiotics (when used in combo with other nephrotoxic drugs), & radiocontrast dye
38
Post-renal AKI is a result of
obstruction (e.g. calculi, blood clots, & neoplasm) surgical ligation edema
39
Oliguric is described as
<0.5 mL/kg/hr
40
Non-oliguric
also known as anuric is an ominous sign
41
Polyuric is defined as
>2.5 L/day of non-concentrated urine
42
Risk factors for acute renal failure/injury include:
``` increasing age preexisting renal dysfunction certain surgical procedures- mainly cardiac sepsis use of nephrotoxic agents diabetes, HTN ```
43
For each year after age 50, creatinine clearance
decreases by 1.5 mLs and renal plasma flow by 8 mL
44
Surgical procedures that increase risk for AKI include
``` cardiac bypass >2 hours aortic aneurysms (supra-renal aortic clamping) ventricular dysfunctions ```
45
Sepsis can contribute to AKI because of
hypovolemia, hemolysis, DIC, infections, & acidosis
46
_________ of renal insult is far more successful than management
Prevention
47
The 3rd most common cause of hospital acquired AKI include
contrast induced nephropathy 1st- renal hypoperfusion 2nd- postoperative renal injury
48
Contrast induced nephropathy results from
administration of iodinated contrast media | it is a transient & reversible form of acute renal failure
49
Treatment of contrast induced nephropathy is
mainly supportive, consisting of careful fluid & electrolyte management, although dialysis may be required in some cases (dialysis does not remove contrast)
50
In regards to CIN treatment,
treatment is only supportive prevention is important! the benefit for CM-based diagnostic studies or interventional procedures should always be weighed against the risk of CIN
51
Contrast induced nephropathy is worsened by
hypoxia & hypoperfusion
52
Direct toxicity of contrast media could be related to
harmful effects of free radicals & oxidative stress | - thought that activation of cytokine-induced inflammatory mediators by reactive free radicals is responsible
53
In the renal tubules, the excreted contrast media
generates osmotic force causing marked increase in sodium & water excretion
54
The diuresis as a result of contrast media will
increase intratubular pressure, which will reduce the GFR & contribute to the pathogenesis of acute renal failure
55
The incidence of CIN is low in patients with
normal renal function
56
CIN is as high as
50% in patients with diabetic nephropathy
57
Oliguria is often a sign of
inadequate systemic perfusion
58
Rapid recognition and treatment of oliguria in the OR can help
prevent renal insult intraoperatively
59
Monitors used to assess fluid status intraoperatively include
``` urinary catheter TEE CVP Blood pressure SVV ```
60
Treatment of oliguria includes
assume prerenal oliguria is related to FLUID until proven otherwise blood? diuretics- do not give in the setting of intravascular hypovolemia- furosemide & mannitol selective dopamine DA1 receptor agonists-causes renal arteriolar vasodilation- low dose dopamine
61
______ are more likely to suffer from CKD
disadvantaged populations; such as African Americans, American Indian, Hispanics, Asian, & aboriginal populations are more likely to suffer from higher rates of DM & HTN which are leading causes of CKD
62
____ have a 1.5 times greater risk for developing kidney failure
Hispanic Americans
63
ESRD rates are nearly 4-fold higher among_______
African Americans as compared to US whites despite similar prevalence rate of early CKD
64
_______ are about 1.8 times more likely to be diagnosed with kidney failure
Native Americans- | diabetes is the leading cause of kidney failure among this population
65
What increases the risk of developing kidney disease & limit access to preventive measures & treatment in communities with socioeconomic & cultural differences?
``` language barriers education & literacy levels low income unemployment lack of adequate health insurance certain culture-specific health beliefs & practices ```
66
For most Low Middle income countries, transplantation is rare due to
lack of infrastructure, & survival can be complicated by the affordability of immunosuppressive drugs, malnutrition and infectious disease, in particular tuberculosis
67
Chronic renal failure is a
slow, progressive, irreversible disease decreased functioning nephrons, decreased renal blood flow decreased GFR, tubular function & reabsorptive capacity
68
Common causes of chronic renal failure include
glomerulonephritis- inflammation of glomerulus (e.g. autoimmune) pyelonephritis- kidney inflammation (e.g. UTI 70-80% are due to E. Coli) diabetes vascular or hypertensive insults congenital defects
69
States of chronic renal failure include ******
decreased renal reserve renal insufficiency End-stage renal failure or uremia
70
Describe the chronic renal failure phase of decreased renal reserve
asymptomatic until <40% of normal nephron remain
71
Describe the chronic renal failure phase of renal insufficiency
10-40% of functioning nephrons remain | compensated, little renal reserve
72
Describe the chronic renal failure phase of end-stage renal failure or uremia.
>95% of nephrons are nonfunctioning GFR is <5-10% of normal severely compromised electrolyte, hematologic, & acid-base balances uremia (urine in the blood) is eventually lethal dialysis dependent
73
Chronic renal failure manifests as
``` hypervolemia acidemia hyperkalemia cardiorespiratory dysfunction anemia & bleeding disturbances ```
74
Treatment of chronic renal failure includes
hemodialysis peritoneal dialysis kidney transplant

NRP511 (23 decks)

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