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Pathophysiology Test 3 > renal function > Flashcards

renal function Flashcards

1
Q

what are the functions of the kidney?

A
  1. maintain a stable internal environment (homeostasis)
  2. endocrine functions (secrete hormones)
  3. gluconeogenesis
  4. form urine
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2
Q

what is maintained in homeostasis within the functions of the kidney?

A

solutes + water
acids + base
nutrients
waste

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3
Q

what hormones are secreted within the functions of the kidney?

A

renin
EPO
vitamin d3 (calcium metabolism)

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4
Q

what is gluconeogensis?

A

create glucose from things such as amino acids

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5
Q

what is contained in the kidney function of forming urine?

A

filtration
reabsorption
secretion
storage
removal (waste)

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6
Q

what force favors filtration?

A

capillary hydrostatic pressure
BHP, CHP

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7
Q

how much do the kidneys filter in a healthy individual?

A

120mL/minute

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8
Q

in a healthy individual, how much of the content that os filtered is reabsorbed and returned to the body by the tubules?

A

99%

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9
Q

what effect does vasoconstriction of the afferent renal arteriole have on GFR and body fluid conservation?

A

GFR decreases
BFC increases

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10
Q

what effect does vasoconstriction of the efferent renal arteriole have on GFR and body fluid conservation?

A

GFR increases
BFC decreases

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11
Q

what effect does severe malnutrition (without dehydration) have on GFR and body fluid conservation?

A

GFR decreases
BFC increases

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12
Q

what effect does obstruction to the outflow of urine have on GFR and body fluid conservation?

A

GFR decreases
BFC increases

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13
Q

what does the PCT reabsorb?

A

glucose
sodium
H2O

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14
Q

what does the DCT reabsorb?

A

H2O directly stimulated by ADH

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15
Q

Which hormone leads to increased reabsorption of Na?

A

aldosterone

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16
Q

How does tubular secretion occur in the nephron?

A

-Movement of substances from the peritubular capillaries to the tubular lumen
-Proximal tubule and CD receive secretions of H +
-Distal tubule and CD receive secretions of K + (aldosterone)

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17
Q

what ways do we access renal function?

A

urine output
plasma creatine-PCR
blood urea nitrogen-BUN

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18
Q

How do PCR levels help to access renal function?

A

Creatinine is a product of muscle metabolism (breakdown of macromolecules), and is filtered by the glomerulus

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19
Q

How do BUN levels help to access renal function?

A

Urea is filtered by the glomerulus

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20
Q

what is urea?

A

The molecule urea is formed from protein and amino acid degradation

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21
Q

when GFR is low, what happens to PCR and BUN?

A

they are high

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22
Q

when protein malnuturton occurs, what happens to PCR and BUN?

A

they are decreased INITIALLY

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23
Q

how do we classify kidney disfunction?

A

acute or chronic
reversible or irreversible

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24
Q

how is considered decreased renal reserve?

A

less than 25% kidney function
-require increased demands of kidneys

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25
Q

what are the BUN and PCR levels during decreased renal function?

A

increased

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26
Q

how does increased fluid intake effect decreased renal function?

A

the kidneys unable to keep up with urine production
– fluid overload
-can affect heart function and BP

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27
Q

how does insuffienct fluid or fluid loss effect decreased renal function?

A

-Urine not concentrated properly - risk of fluid deficit
-Kidneys trying to hold on to as much as possible

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28
Q

what is considered renal insufficiency?

A

25-10% of normal kidney function

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29
Q

what are the manifestations of renal insufficiency?

A

polyuria
nocturia

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30
Q

what is polyuria?

A

increased urine output
-appears with the loss in the concentrating ability (lack of water reabsorption)

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31
Q

what is nocturia?

A

Increase of urine output at night
-Normally, the kidneys are more efficient at reabsorption at night - that way you don’t have to get up and pee in the middle of the night

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32
Q

what is considered end-stage renal failure?

A

less then 10% of renal function

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33
Q

what does end-stage renal failure lead to in the body?

A

-accumulation of nitrogenous waste products in the body
-uremia

34
Q

Both azotemia and uremia involve the accumulation of —–?

A

nitrogenous waste products in the blood

35
Q

what is uremia?

A

-Syndrome of renal failure - past renal insufficiency, already renal failure. Farther along
-Elevated blood urea and creatinine levels

36
Q

what are the manifestations of uremia?

A

Fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes

37
Q

hat does uremia lead to?

A

Retention of toxic wastes, deficiency states, electrolyte disorders, and proinflammatory state

38
Q

what is azotemia?

A

buildup of nitrogenous waste products - urea, creatinine. Earlier in the disease process
-Increased serum urea levels and frequently increased creatinine levels

39
Q

what are the manifestations of azotemia?

A

May not be showing symptoms from the increased nitrogen

40
Q

what is acute kidney injury (failure)?

A

Sudden decline in kidney function with a decrease in GFR and accumulation of nitrogenous waste products in the blood

41
Q

what would BUN and PCR in acute kidney injury (failure)?

A

it would be increased

42
Q

what is oliguria?

A

severe reduction in urine output

43
Q

what causes pre renal acute injury (failure)?

A

renal hypoperfusion: decreased circulation of blood to the kidneys

44
Q

what happens to the GFR in pre renal acute injury (failure)?

A

it decreases

45
Q

what could cause decreased blood to the kidneys?

A

-Left sided heart failure
-Atherosclerosis
-Hypovolemia
-Hypotension
-Lack of blood flow or oxygen

46
Q

what is intrarenal acute injury (failure)?

A

intrinsic-problem within the kidney

47
Q

what can causes infrarenal acute injury (failure)?

A

-Acute glomerulonephritis
-Acute tubular necrosis (ATN)

48
Q

what is glomerular nephritis?

A

inflammation and damage to the glomerulus
-primary or secondary

49
Q

what is primary glomerular nephritis caused by?

A

some sort of injury that trigger inflammatory response
-Allergic reactions
-Trauma
-Infections
-Ischemic injuries
-Free radical damage

50
Q

what is secondary glomerular nephritis caused by?

A

this is a consequence of systemic diseases such as diabetes mellitus, lupus, and others

51
Q

what are the steps in acute glomerular nephritis?

A
  1. Immune complexes (antigen-antibody) deposited in the glomerulus
  2. The antibodies cross react with the glomerular cells
  3. Activation of the complement
  4. Recruitment and activation of immune/inflamm cells and immune/inflamm mediators
52
Q

following acute glomerular nephritis, what initial effect does activation of the immune/inflammatory response have on the capillaries and capillary forces inside the glomerulus?

A

-Vasodilation
-increased vascular permeability
-COP decreases. (fewer proteins because of the increased vascular permeability)

53
Q

what are the manifestations of acute glomerular nephritis?

A

-Hematuria (blood in the urine, smoky, brown-tinged urine)
-Proteinuria exceeding 3 to 5 g/day (Albumin excreted from the plasma)
- possibly edema
-Inflammatory response causes glomerular cells to proliferate, and can block the glomeruli
-oliguria

54
Q

what would happen in a response to glomerular cells blocking the glomeruli

A

-GFR decreases
-glomerular perfusion decreases
-BHP increases (due to body fluid retention)
-edema, HTN, heart problems

55
Q

what would BUN and PCR be in acute glomerular nephritis?

A

BUN, PCR would increase and cause azotema

56
Q

what is nephrotic syndrome caused by?

A

acute glomerulonephritis along with other diseases

57
Q

what is nephrotic syndrome?

A

-Excretion of 3.0 g or more of protein in urine
-Protein excretion as a result of glomerular injury
-less Vitamin D is transported to the liver and kidneys by proteins in the blood to become active
-less Activated Vitamin D is required for absorption of calcium from the small intestine

58
Q

What happens to allow the proteins to leave the capillaries in nephrotic syndrome?

A

Increased capillary permeability from the inflammatory response

59
Q

What happens following the loss of these proteins in nephrotic syndrome?

A

-Decreased BOP
-initial increase in GFR

60
Q

What does the smaller amounts of vitamin D mean for calcium in nephrotic syndrome?

A

-Calcium lost if there is less activated vitamin D
-get calcium from the bones (weak bones, osteomalacia)

61
Q

what are the causes of acute tubular necrosis (ATN)?

A

Damage caused by renal ischemia, hypertension, and renal poisons (like antifreeze)

62
Q

what is the result of acute tubular necrosis?

A

-Causes necrosis of the epithelial cells that form the renal tubules
-These cells slough off and block the renal tubules
—-Bowman’s capsule pressure is affected. BHP and Bowmans pressures are opposing each other
—-GFR is decreased

63
Q

what is post-renal acute injury caused by?

A

Results from conditions that arise after the nephrons
-Urinary tract obstructions (Kidney stone, enlarged prostate)

64
Q

what happens in the initiation phase of acute kidney injury?

A

-occurs during the injury itself
-reduced perfusion or toxicity

65
Q

what happens during the matienance or oliguric phase of acute kidney injury?

A

-Decrease GFR
-Increase plasma nitrogen
-Increase water and Na
-Edema can develop, hypertension
-Metabolic acidosis (not getting rid of H+, it is building up in the body)
-This phase could last week or months

66
Q

what happens in the recovery phase of acute kidney injury?

A

-Renal injury is repaired
-Normal renal function is reestablished
-GFR is increasing
-Tubules have trouble concentrating the filtrate
-Diuresis
-Nitrogen decreasing from body
-Na+, K+, H2O decreasing
-Return to normal may take 3-12 months

67
Q

what are the the treatments for acute kidney injury?

A

-Hemodialysis
-Correct fluid and electrolyte disturbances
-BP balance
-Prevent and treat infections
-Maintain nutrition

68
Q

at would your bp be in the maintenance and recovery phase of acute kidney injury?

A

hypertension

69
Q

What kind of diet might be important to minimize elevation of BUN?

A

low protein (less amino acids)

70
Q

what is chronic kidney disease?

A

-Progressive loss of renal function associated with systemic diseases
-GFR less than 60 mL/min/1.73 m 2 for 3 months or more, irrespective of cause

71
Q

what are the clinical manifestations of chronic kidney disease?

A

Do not occur until renal function declines to less than 25% of normal

72
Q

what are the causes of chronic kidney disease?

A

-Chronic glomerulonephritis
-Diabetic nephropathy
-Renal vascular disease
-Recurrent pyelonephritis
-Benign nephrosclerosis

73
Q

how does chronic glomerular nephritis lead to chronic kidney disease?

A

Glomeruli are replaced with scar tissue

74
Q

how does diabetic nephropathy lead to chronic kidney disease?

A

Hyperglycemia damages the nephrons

75
Q

how do renal vascular diseases lead to chronic kidney disease?

A

Atherosclerosis of the renal vessels results in progressive loss of nephrons

76
Q

how does recurrent pyelonephritis lead to chronic kidney disease?

A

kidney infection

77
Q

how does begin nephrosclerosis lead to chronic kidney disease?

A

(Result of aging) Small arteries in the kidneys become thickened and narrowed over time

78
Q

what is chronic glomerular nephritis?

A

-Slow, progressive destruction of the glomeruli
-Many glomeruli are completely replaced by fibrous tissue leading to loss of nephron function

79
Q

is chronic GN reversible?

A

no

80
Q

what is chronic GN caused by?

A

-recurrent streptococcal infections
-more commonly: an autoimmune condition

81
Q

what are the manifestations of chronic GN?

A

-Proteinuria - inflammation causes proteins to leak out because of increased vascular permeability
-HTN - body compensating
-Azotemia - GFR decreases, you are holding on to nitrogen
-Uremia - azotemia further along

82
Q

what are the treatments for chronic GN?

A

-Dialysis
-Transplantation

Pathophysiology Test 3 (4 decks)

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