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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
Q

Aldosterone stimulates epithelial cells in the distal tubule & collecting ducts to

A

REABSORB SODIUM & WATER

-exchanges potassium to maintain electroneutrality

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26
Q

Aldosterone is the complete opposite of

A

atrial natriuretic hormone function

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27
Q

Spironolactone is a

A

potassium sparing diuretic that blocks the aldosterone receptors

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28
Q

Acute kidney injury is the

A

sudden inability of the kidneys to vary urine volume & content appropriately
develops rapidly but may resolve

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29
Q

AKI has a ______ mortality rate

A

50%

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30
Q

Causes of AKI include

A

pre-renal
intrinsic-renal
post-renal

31
Q

Pre-renal AKI is a result of

A

hemodynamic or endocrine factors that impair perfusion

hypoperfusion or hypovolemia

32
Q

Factors that can cause hypoperfusion or hypovolemia in pre-renal AKI include

A 
skin loss (e.g. burns)
fluid loss
hemorrhage
sequestration
vascular occlusion (e.g. thrombosis, aortic, or renal artery clamping)
33
Q

Pre-renal AKI will activate

A

mechanism to conserve salt & water

-RAAS, ADH, low urine sodium with high osmolality)

34
Q

Pre-renal AKI can progress to

A

permanent parenchymal damage

35
Q

Renal or acute tubular necrosis is the result of

A

tissue damage from

  • prolonged ischemia
  • nephrotoxic injury (e.g. antibiotics, chemotherapeutics, & contrast dye)
  • glomerulonephritis
36
Q

Patients with parenchymal disease will have trouble

A

concentrating urine

-high urine Na & low osmolality

37
Q

Nephrotoxic drugs include

A

aminoglycosides, amphotericin B, chemotherapeutic drugs, cyclosporine modified, NSAIDs, penicillin antibiotics (when used in combo with other nephrotoxic drugs), & radiocontrast dye

38
Q

Post-renal AKI is a result of

A

obstruction (e.g. calculi, blood clots, & neoplasm)
surgical ligation
edema

39
Q

Oliguric is described as

A

<0.5 mL/kg/hr

40
Q

Non-oliguric

A

also known as anuric is an ominous sign

41
Q

Polyuric is defined as

A

> 2.5 L/day of non-concentrated urine

42
Q

Risk factors for acute renal failure/injury include:

A 
increasing age
preexisting renal dysfunction
certain surgical procedures- mainly cardiac
sepsis
use of nephrotoxic agents
diabetes, HTN
43
Q

For each year after age 50, creatinine clearance

A

decreases by 1.5 mLs and renal plasma flow by 8 mL

44
Q

Surgical procedures that increase risk for AKI include

A 
cardiac bypass >2 hours
aortic aneurysms (supra-renal aortic clamping)
ventricular dysfunctions
45
Q

Sepsis can contribute to AKI because of

A

hypovolemia, hemolysis, DIC, infections, & acidosis

46
Q

_________ of renal insult is far more successful than management

A

Prevention

47
Q

The 3rd most common cause of hospital acquired AKI include

A

contrast induced nephropathy
1st- renal hypoperfusion
2nd- postoperative renal injury

48
Q

Contrast induced nephropathy results from

A

administration of iodinated contrast media

it is a transient & reversible form of acute renal failure

49
Q

Treatment of contrast induced nephropathy is

A

mainly supportive, consisting of careful fluid & electrolyte management, although dialysis may be required in some cases (dialysis does not remove contrast)

50
Q

In regards to CIN treatment,

A

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
Q

Contrast induced nephropathy is worsened by

A

hypoxia & hypoperfusion

52
Q

Direct toxicity of contrast media could be related to

A

harmful effects of free radicals & oxidative stress

- thought that activation of cytokine-induced inflammatory mediators by reactive free radicals is responsible

53
Q

In the renal tubules, the excreted contrast media

A

generates osmotic force causing marked increase in sodium & water excretion

54
Q

The diuresis as a result of contrast media will

A

increase intratubular pressure, which will reduce the GFR & contribute to the pathogenesis of acute renal failure

55
Q

The incidence of CIN is low in patients with

A

normal renal function

56
Q

CIN is as high as

A

50% in patients with diabetic nephropathy

57
Q

Oliguria is often a sign of

A

inadequate systemic perfusion

58
Q

Rapid recognition and treatment of oliguria in the OR can help

A

prevent renal insult intraoperatively

59
Q

Monitors used to assess fluid status intraoperatively include

A 
urinary catheter
TEE
CVP
Blood pressure
SVV
60
Q

Treatment of oliguria includes

A

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
Q

______ are more likely to suffer from CKD

A

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
Q

____ have a 1.5 times greater risk for developing kidney failure

A

Hispanic Americans

63
Q

ESRD rates are nearly 4-fold higher among_______

A

African Americans as compared to US whites despite similar prevalence rate of early CKD

64
Q

_______ are about 1.8 times more likely to be diagnosed with kidney failure

A

Native Americans-

diabetes is the leading cause of kidney failure among this population

65
Q

What increases the risk of developing kidney disease & limit access to preventive measures & treatment in communities with socioeconomic & cultural differences?

A 
language barriers
education & literacy levels
low income
unemployment
lack of adequate health insurance
certain culture-specific health beliefs & practices
66
Q

For most Low Middle income countries, transplantation is rare due to

A

lack of infrastructure, & survival can be complicated by the affordability of immunosuppressive drugs, malnutrition and infectious disease, in particular tuberculosis

67
Q

Chronic renal failure is a

A

slow, progressive, irreversible disease
decreased functioning nephrons, decreased renal blood flow
decreased GFR, tubular function & reabsorptive capacity

68
Q

Common causes of chronic renal failure include

A

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
Q

States of chronic renal failure include ****

A

decreased renal reserve
renal insufficiency
End-stage renal failure or uremia

70
Q

Describe the chronic renal failure phase of decreased renal reserve

A

asymptomatic until <40% of normal nephron remain

71
Q

Describe the chronic renal failure phase of renal insufficiency

A

10-40% of functioning nephrons remain

compensated, little renal reserve

72
Q

Describe the chronic renal failure phase of end-stage renal failure or uremia.

A

> 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
Q

Chronic renal failure manifests as

A 
hypervolemia
acidemia
hyperkalemia
cardiorespiratory dysfunction
anemia
& bleeding disturbances
74
Q

Treatment of chronic renal failure includes

A

hemodialysis
peritoneal dialysis
kidney transplant

NRP511 (23 decks)

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