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Therapeutics I > Block 4: AKI and CKD > Flashcards

Block 4: AKI and CKD Flashcards

1
Q

What are the excretory functions?

A
  1. Glomerular filtration
  2. Secretion
  3. Reabsorption
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2
Q

What occurs during glomerular filtration?

A

Passive process: water and small MW ion and molecule cross membrane in Bowman’s capsule and get secreted in the PT

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3
Q

What occurs during secretion?

A

Active process that utilize transporters → eliminates compounds from renal circulation to tubular lumen

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4
Q

What occurs during reabsorption?

A

Active and passive: Water and solutes reabsorbed throughout the nephron

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5
Q

What are the endocrine functions of kidneys?

A
  1. Renin secretion
  2. Production and metabolism of PG and kinins
  3. EPO production
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6
Q

What are the metabolic functions of the kidneys?

A
  1. Activation of vitamin D
  2. Gluconeogenesis
  3. Metabolism of insulin and endogenous steroids
  4. Enzymatic processes
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7
Q

How do we evaluate kidney functions? When do we use each component? Which is the best?

A
  1. Proteinuria (CKD and increased mortality and ESRD risk)
  2. GFR (Best)
  3. Urine albumin:Cr ratio (Severe CKD and progression monitoring)
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8
Q

How often do you evaluate kidney function? What do you evaluate?

A

Yearly
1. sCr and electrolyes
2. Urine albumin (cr, pH, specific gravity, sediment)
3. Renal ultrasound

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9
Q

What is the presentations of early vs late CKD?

A

e: No distress
L: edema

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10
Q

Signs and symptoms of Early CKD?

A

N/A

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11
Q

Lab tests for early CKD?

A
  1. Microalbuminuria
  2. Mildly elevated sCr and BUN
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12
Q

Lab tests for late CKD?

A
  1. Persistent proteinuria
  2. Reduced GFR or CrCl
  3. Abnormal urinalysis
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13
Q

Normal pH? Elevation?

A

4.5-7.8

Bacteria

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14
Q

Heme lab of CKD?

A

Indicates presence of hemoglobin or myoglobin

Risk factor for worsening CKD or death

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15
Q

Protein in urine?

A

Amount of protein/Albumin used to assess severity and progression of CKD

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16
Q

What is the specific gravity indicate?

A

1.003-1.03

Urine vs serum osmolarity

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17
Q

What does ketones in urine mean?

A

Normal is none

Excreted in DKA and starving/fasting

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18
Q

Indications of nitrates in urine?

A

Bacterial infection

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19
Q

What is proteinuria?

A

Protein loss → nephron injury

Persistant = 3x over period of 3-6 months

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20
Q

What are the cut offs of albuminuria?

A

A1 → <30 mg normal
A2 → 30-300 microalbuminuria
A3 → >300 macroalbuminuria

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21
Q

What is the normal sCr/BUN ratio? Decreased effective circulating volume?

A

Normal: 5-15
Dysfunction: >20

Water and urea get absorbed but not creatine

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22
Q

What does sCr measure?

A

Balance of creatine production (muscle) and renal excretion

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23
Q

What is normal sCr?

A

0.5-1.5 mg/dL

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24
Q

How is UCr eliminated?

A

Glomerular filtration

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25
Q

What is GFR?

A

Volume of plasma filtered across glomerulus per unit of time

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26
Q

What do we use to calculate CrCl?

A

Cockcroft-Gault

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27
Q

What are examples of qualitative diagnostics for CKD?

A
  1. KUB (size)
  2. IV urogram
  3. CT
  4. US
  5. MRI
  6. Biopsy
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28
Q

What is the indication of BUN <20 vs >20?

A

Intrinsic vs Prerenal

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29
Q

What is AKI? How does it effect sCr?

A

Abrupt reduction in kidney function shown in sCr, BUN, UOP

Change in sCr 50% in 7 days or 0.3mg/dL in 24-48 hrs

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30
Q

How do we classify AKI?

A

KDIGO

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31
Q

Functional and structural criteria of CKD?

A

GFR <60 for >3 months, Kid damage >3 minth

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32
Q

What are the causes of AKI?

A
  1. Hospital and community acquired
  2. Sepsis, shock, drugs, major surgery, comorbidities
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33
Q

What are the functional criteria of NDK?

A

GFR >60, Stable sCr, no damage

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34
Q

What are the treatment goals of pre renal?

A

Restore and ↑ RBF

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35
Q

Causes of pre renal injury?

A
  1. Reduced IV volume (hemorrhage, GI losses, burns, diuretics)
  2. Reduced effectivecirulatory BV (↓ CO, vasodilation)
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36
Q

How does the body compensate for prerenal? Why is that bad?

A

SNS, RAAS, ADH increase H2O and Na retention
PG, kinins, NO dilate afferent arteriole
Ang II contract efferent arterioles

Prolongation of compensatory mechanism → overwhelms the kidneys

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37
Q

What are the types of pre renal injury?

A
  1. Cardiorenal syndrome
  2. Hepatorenal syndrome
  3. Nephrotic syndrome
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38
Q

How do you treat cardio renal?

A

Fluid overload → give loops

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39
Q

How do you treat hepatorenal?

A

↑ oncotic pressure → spiranolactone

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40
Q

How do you treat nephrotic syndrome?

A

↑ fluid → loop diuretic

41
Q

What is the most common infrarenal injury?

A

Tubules (renal ischemia or nephrotoxins)

Interstitial (acute interstitial nephritis) from nephrotoxins

42
Q

What are the phases of IRA-ATN?

A

Initiation: renal tubular epithelial cell injury
Extension: inflammatory response in outer medullary region
Maintenance: sCr peaks and cellular repair initiated
Recovery: new tubule cells generated

43
Q

What can cause obstruction of post renal injury?

A
  1. BPH, cancer, infection in prostate
  2. Improperly placed catheter
  3. Neprolithiasis
  4. Blood clots
44
Q

What is intra vs post renal?

A

Intra: structural damge within kidney
Post: Obstruction in collecting system

45
Q

Clinical presentation of AKI?

A
  1. Changes in urinary character
  2. Presence of edema
  3. Sudden weight gain
  4. Severe abdominal and/or flank pain
46
Q

How do you calculate extraction of Na (FENa)?

A

(Urine Na x Scr x100) / (Urine Cr x Serum Na)

47
Q

Compare FeNa in pre renal and intrisic?

A

Prerenal: <1%
Intrinsic: >1%

Unreliable if on diuretics

48
Q

Compare BUN:sCr ratio?

A

Prerenal: >20:1
Intrisic and Postrenal: 10-15:1

49
Q

What is KUB, BT, or US used for?

A
  1. Small/shrunken kidneys indicates chronic disease
  2. Identify presence of obstruction or hydronephrosis
50
Q

How don’t we use renal biopsy?

A

Invasive only for cancer → ↑ bleeding risk

51
Q

What is type a and b DIKD?

A

A: Dose dependent (reduce dose)
B: Unpredictable (DC drug)

52
Q

What are the time courses of DIKD?

A

Acute – 1-7 days
Subacute – 8-90 days
Chronic - >90 daysWha

53
Q

What are the phenotypes of DIKD?

A
  1. AKI
  2. Glomerular disorder
  3. Tubular dysfunction
  4. Mephrolithiasis/crystalluria
54
Q

What are the drugs that can worsen AKI?

A
  1. NSAIDS
  2. Constrast dyes (IV fluids before to prevent KI)
  3. Antibiotics (Vanc, AMinoglycosides, Amphotericin)
55
Q

Mechanism of AKI?

A

A or B

56
Q

Mechanism of Glomerular disorder?

A

Type A or B

57
Q

Mechanism of nephrolithiasis?

A

Type A

58
Q

Mechanism of tubular dysfunction?

A

Type A

59
Q

Subtype of tubular dysfunction?

A

SIADH

60
Q

Drugs that can worsen nephrolithiasis?

A

Acyclovir

61
Q

Drugs that can worsen tubular dysfunction?

A

Lithium

62
Q

What are the aminoglycosides?

A

Gentamicin, tobramycin , amikacin

63
Q

What are the risk factors of DIKD?

A
  1. Cormobidiites
  2. > 75YO
  3. ACUTE ILLNESS
  4. Polypharmacy
    5: Triple whammy: NSAID (constrict afferent), ACEI (dilate efferent), Diuretics (↓ plasma volume)
64
Q

What are the complication of AKI?

A
  1. Electrolyte derangement
  2. Volume overload
  3. Metabolic acidosis
  4. Uremic encephalopathy
  5. Development of CKD
  6. Need for RRT
  7. Increased mortality
65
Q

How do you prevent AKI?

A
  1. Avoid/ limit potential toxins
  2. Dosing adjustment
  3. Adequate hydration
  4. Optimize hemodynamics
66
Q

What pharm do we use to prevent AKI?

A
  1. IV fluid (↑ volume and perfusion) → crystalloids
  2. Ascorbic acid: antioxidants
67
Q

Treatment for pre renal?

A
  1. Hydration → crystalloids to restore volume → ↑ peerfusion (UOP>0.5 mL/kg/h)
  2. Diuresis → CHF or edema
68
Q

Treatment for intrisic?

A

adjust or DC offenders

69
Q

Treatment for post renal?

A

Removal of obstruction

70
Q

Last resort treatment for AKI?

A

Dialysis when life threatening

Remove waste/toxins to maintain fluid, electrolyte, and acid/base balance

AEIOUs

71
Q

What are the roles of loop diuretics in AKI?

A

Loops if fluid overload

  1. ↑ UOP
  2. Inhibit Na/K/Cl cotransporters reducing O2 demand and risk for ischemic injury
  3. ↑ RBF from increased availability of renal prostaglandins
72
Q

What are the indications of acute dialysis?

A

A: Acid/base disturbances
E: electrolyte imbalances
I: intoxications
O: overload of fluid
U: uremia

73
Q

What is the definition of CKD?

A

eGFR< 60 mL/min > 3 months

74
Q

Leading cause of CKD?

A

DM followed by HTN

75
Q

How do you prevent amino glycosides from causing ATN?

A
  1. Preform TDM
  2. Use extended interval dosing
  3. Avoid concomitant nephrotoxins
76
Q

How does NSAIDS cause pre renal AKI

A
  1. ↓ PG → afferent arteriolar vasoconstriction and reduced glomerular BF
77
Q

How do you prevent NSAIDs from causing pre renal AKI?

A

Avoid use in patients with ACEI/ARBs and/or diuretics

78
Q

How does ACE/ARBS cause pre renal AKI?

A

Vasodilation of efferent arteriole

79
Q

What are the presentations of drug induced pre renal AKI?

A

Reduction of GFR

80
Q

How do you prevent ACE/ARB pre renal AKI?

A

Hold it the day of surgical procedures

81
Q

How does amphotericin B cause ATN?

A

Direct proximal and distal tubular toxicity and afferent arteriole vasodilation

82
Q

Presentation of amphotericin B induced ATN?

A
  1. Tubular injury resulting in electrolyte wasting (hypokalemia, magnesia, natremia)
  2. Metabolic acidosis
83
Q

How do you prevent amphotericin B from causing ATN?

A

Limit daily dose

84
Q

How does vanc cause ATN and AIN? Prevention?

A

Direct proximal tubular toxicity

Perform TDM: target trough <20 mg/L

85
Q

What causes CKD?

A

Loss of nephron mass → remaining nephrons compensate → secretion renin and kinin→ Intraglomerular HTN → progressing CKD → proteinuria → direct cellular damage → speeds up nephron loss

86
Q

What CKD stages are sympotmatice mostly? What symptoms?

A

4-5

  1. ↓ UO
  2. Muscle cramping and edema
  3. Anemia and mineral bone disorder
  4. Depression or decreased sexual dysfunction
  5. Decreased appetite → weight loss
87
Q

How is CKD classified?

A
  1. Cause
  2. GFR
  3. Albuminuria
88
Q

Describe the staging of GFR?

A
89
Q

Describe the staging of albuminuria?

A

A2: micro
A3: macro

90
Q

What is the non pharm management of CKD?

A
  1. Exercise at least 30 min, 5 x per week
  2. BMI goal 20-25
  3. Smoking cessation
  4. Reduced protein intake for CKD4+
  5. Sodium < 2 g/day
  6. Dialysis
91
Q

How cormobidities do you need to manage?

A
  1. Porteinuria
  2. HTN
  3. Diabetes: gola A1c <7%
92
Q

What are treatment goals of CKD?

A

Slow progression

93
Q

What are the pharms for CKD?

A
  1. ACE/ARB
  2. SGLT2I
  3. Statins
94
Q

How is ACE/ARB used for CKD?

A

Delay progression by lowering intraglomerular pressure and proteinuria

1st line for proteinuria if A2

Start with low dose

95
Q

ACEI/ARB ADR?

A

AKI, hyperkalemia, cough with ACEIs

96
Q

What is the role of SGLT2I?

A

Reduce glomerular hyper filtration by reducing glucose and sodium reabsorption in proximal tubule

97
Q

What is the role of statins?

A
  1. Ages 18-49 with CKD (non-dialysis): Indicated if CAD, DM, prior ischemic stroke, or >10% CV risk
  2. Ages >50 with non-dialysis CKD
  3. Not indicated in dialysis patients
98
Q

What are the complications of CKD?

A
  1. Electrolyte disorders
  2. Alterations in sodium and water balance
  3. Metabolic acidosis
  4. Anemia
  5. CKD-related mineral and bone disorder
  6. Progression to ESRD

Therapeutics I (32 decks)

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