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PHAR 123 > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

True or false: You can feel pain in your kidney

A

False- Only in the ureters

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2
Q

How many nephrons can we lose before we start to see kidney decline?

A

1 million out of 2 million

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3
Q

How much glomerular filtrate enters?

A

100-120ml/min

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4
Q

What size of particles are able to bypass glomerulus filter?

A

under 70 kDa

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5
Q

What does the proximal tubule do?

A

substantial resorb and secrete
resorb 60-70% of Na most of K, Glucose

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6
Q

How ,much filtrate enters loop of Henle?

A

30ml/min

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7
Q

What does the descending part of loop resorb?

A

Water

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8
Q

What does the ascending loop resorb?

A

Na

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9
Q

What amount of filtrate enters distal?

A

5-10 ml/min

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10
Q

What does vasopressin do?

A

antidiuretic= resorb water NO na

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11
Q

What does aldosterone do?

A

Na resorb and K excrete

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12
Q

How much filtrate leaves the kidney?

A

1-2 ml/min

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13
Q

What are NCC channels and what drugs effect them?

A

These are thiazide sensitive channels NaCl cotransporter

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14
Q

What is ENaC?

A

This is amiloride sensitive channels, moves Na

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15
Q

What are the normal levels of Creatinine?

A

0.9-1.3

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16
Q

Why is creatinine a good marker for kidney function?

A

lots produced by muscles easily filtered in a normally functioning kidney. if rising levels this means that GFR is reduced

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17
Q

What is the Cockroft-Gault formula? (CrCl)

A

CrCl= (140-age)(IBW)/(0.814 x Scr(microM). x 0.85 if female

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18
Q

How to estimate IBW?

A

5 foot tall man= 50kg women= 45kg
add 2.3 kg for every inch

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19
Q

What is the MDRD equation?

A

GFR= 175 x Scr^-1.154 x age^-0.203 x 0.742(if female) x (1.212 if black)

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20
Q

Are drugs more likely to be filtered if they are mostly protein bound?

A

NO

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21
Q

Give me the stages of CKD and their corresponding GFR

A

1= >90
2= 89-60
3a=59-45
3b= 45-30
4= 30-15
5=<15 OR dialysis

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22
Q

What are the stages of Albuminuria?

A

1= <30
2=30-300
3=>300

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23
Q

WHat is the size of albumin?

A

67kDa

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24
Q

Spec gravity normal values

A

1.005-1.029

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25
Q

When can you diagnose AKI?

A

if Sir rises by 25microM in 2 days or decrease of urine to less than 0.5 ml/kg/hr for 6 hrs

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26
Q

Symptoms of AKI

A

low urine output
fatigue
swellling
confusion

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27
Q

What are the causes of AKI

A

pre renal azotemia
Intrinsic renal parenchyma disease
post renal obstruction

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28
Q

What is pre renal azotemia

A

increase of blood urea due to reduced glomerular pressure
NO signs of damage to tubules
reversible before damage
due to low BP, low CO, medications ie) NSAIDS

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29
Q

What conditions can cause pre renal azotemia

A

atherosclerosis, hypovolemia, NSAIDS

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30
Q

How does NSAIDS cause AKI

A

1-reduce flow to kidney
2-direct injury= nephritis

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31
Q

How does Glomerulus usually get injured?

A

HTN, diabetes, immune due to auto or antigens getting stuck there,

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32
Q

T/F Glomerular injury is reversible

A

False

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33
Q

How do tubular systems get damaged

A

Necrosis due to ROS from toxins, direct toxicity, rhabdomyolysis

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34
Q

How does Cisplatin cause damage to tubules?

A

accumulates in proximal tubule, direct toxicity, more hydration lowers toxicity

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35
Q

How does rhabdomyolysis effect tubules?

A

myoglobin from muscle injury can precipitate and halt flow

36
Q

What symptom of rhabdomyolysis is indicative of kidney issues?

A

DARK urine

37
Q

What drug can cause rhabdomyolysis

A

STATINS

38
Q

What drug can cause rhabdomyolysis

A

STATINS

39
Q

What causes interstitial nephritis?

A

Inflammation of interstitial space
usually caused by sensitivity to drugs like penicillins, NSAIDS

40
Q

Why does ischema affect the kidneys so much?

A

because the kidneys use up a lot of oxygen and blood
hypoxic region of kidney very sensitive to O2 levels

41
Q

What part of the kidney operates at hypoxic levels

A

Medulla

42
Q

What conditions increase kidney damage?

A

atherosclerosis, ischemia,

43
Q

T/F Necrosis of tubules is reversible

A

True

44
Q

What is the only way to confirm intra renal damage?

A

biopsy

45
Q

True or false Kidney stones are directly related to calcium intake

A

False

46
Q

What increases your risk of kidney stones?

A

dehydration, protein intake, high salt intake(causes Ca excretion)

47
Q

What does RIFLE stand for

A

R=Risk
I=injury
F= failure to function
L=loss of function
E=ESRD

48
Q

What are the GFR and UO Criteria for R of RIFLE

A

increase of Scr 1.5 x baseline, GFR decrease by 25% or <0.5 urine /kg/h for 6 hrs

49
Q

What are the GFR and UO Criteria for I of RIFLE

A

increase of Scr 2 x baseline, GFR decrease by 50% or <0.5 urine /kg/h for 12 hrs

50
Q

What are the GFR and UO Criteria for F of RIFLE

A

increase of Scr 3 x baseline, GFR decrease by 75% or <0.3 urine /kg/h for 24 hrs or no pee for 12 hrs

51
Q

What are the GFR and UO Criteria for L of RIFLE

A

no function for 4 weeks

52
Q

What are the GFR and UO Criteria for E of RIFLE

A

ESRD

53
Q

what are the pros and cons of RIFLE

A

Pros- good accuracy
cons= baseline not known, MDRD only for CKD, using only Scr decreases accuracy

54
Q

What is the criteria to be in stage 1 of AKIN?

A

increase of Scr 1.5-2 x baseline or >0.3 mg/dl in 2 days UO< o.5ml/kg/h for 6 hrs

55
Q

What is the criteria to be in stage 2 of AKIN?

A

Increase of Scr 2-3 x baseline
UO<0.5ml/kg/h for 12 hrs

56
Q

What is the criteria to be in stage 3 of AKIN?

A

Increase of Scr >3 x baseline or >4mg/dl DIALYSIS
or No pee in 12 hrs or <0.3ml/kg for 24 hrs

57
Q

Complications of AKI

A

Pulmonary edema, anemia, weakness, hyperkalemia, acidosis

58
Q

Complications of AKI

A

Pulmonary edema, anemia, weakness, hyperkalemia, acidosis

59
Q

How does pulmonary edema happen

A

Na K ATPase, ENaC and aquaporin down regulated= retain fluid and inflammation

60
Q

How does hyperkalemia happen in AKI

A

Distal tubules damaged= can’t excrete K

61
Q

How does metabolic acidosis happen in AKI

A

loss of bicarbonate= causes nausea and vomitting

62
Q

How can you prevent AKI

A

only reduce risk by living healthy, managing conditions, and being careful with meds

63
Q

How to generally treat AKI

A

treat underlying cause, balance fluids, electrolytes, control K and Ca, dialysis

64
Q

What are the kidney dialysis options?

A

Hemodialysis- blood is removed filtered then returned
peritoneal dialysis-put into cavity the solution absorbs toxins then remove

65
Q

What are the cons of Hemodialysis

A

Need blood thinners, permanent graft need surgery, or

66
Q

T or f Diuretics help with AKI

A

False

67
Q

What are the thiazide diuretics?

A

indapamide, chlorothiazide, hydrochlorothiazide

68
Q

What are the loop diuretics

A

furosemide, torsemide, numetanide

69
Q

Potassium sparing diuretics

A

amiloride, ARA, spironolactone

70
Q

Osmotic diuretics

A

mannitol, glycerine, urea

71
Q

When do we want to use thiazide diuretics

A

HTN

72
Q

What are the side effects of thiazide

A

hypovolemia, hyperglycaemia

73
Q

Where do the loop diuretics act

A

ascending limb= block Na resorb

73
Q

Where do the loop diuretics act

A

ascending limb= block Na resorb

74
Q

Side effects of loop diuretics

A

electrolyte loss, hypotension, cramps, hyperglycaemia

75
Q

Side effects of loop diuretics

A

electrolyte loss, hypotension, cramps, hyperglycaemia

76
Q

Do K sparing diuretics lower blood pressure

A

NO

76
Q

Do K sparing diuretics lower blood pressure

A

NO

77
Q

Adverse effects of K sparing diuretics

A

hyperkalemia= arrythmias
cramp, ab pain

78
Q

Where do osmotic diuretics act

A

proximal tubule,

79
Q

Where do osmotic diuretics act

A

proximal tubule,

80
Q

adverse effects of osmotic diuretics

A

electrolyte loss, headache, dizzy

81
Q

What cancers cause AKI

A

Kidney, liver, bladder, leukaemia

82
Q

What anticancer agents cause AKI

A

Cisplatin, gemcitabine, mabs, PD-1 and PD-l1 inhibitors

83
Q

What anticancer agents cause AKI

A

Cisplatin, gemcitabine, mabs, PD-1 and PD-l1 inhibitors

84
Q

How to treat AKI if they have cancer too

A

very aggressively as prognosis is very poor

PHAR 123 (18 decks)

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