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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
What is GFR?
Volume of plasma filtered across glomerulus per unit of time
26
What do we use to calculate CrCl?
Cockcroft-Gault
27
What are examples of qualitative diagnostics for CKD?
1. KUB (size) 2. IV urogram 3. CT 4. US 5. MRI 6. Biopsy
28
What is the indication of BUN <20 vs >20?
Intrinsic vs Prerenal
29
What is AKI? How does it effect sCr?
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
30
How do we classify AKI?
KDIGO
31
Functional and structural criteria of CKD?
GFR <60 for >3 months, Kid damage >3 minth
32
What are the causes of AKI?
1. Hospital and community acquired 2. Sepsis, shock, drugs, major surgery, comorbidities
33
What are the functional criteria of NDK?
GFR >60, Stable sCr, no damage
34
What are the treatment goals of pre renal?
Restore and ↑ RBF
35
Causes of pre renal injury?
1. Reduced IV volume (hemorrhage, GI losses, burns, diuretics) 2. Reduced effectivecirulatory BV (↓ CO, vasodilation)
36
How does the body compensate for prerenal? Why is that bad?
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
37
What are the types of pre renal injury?
1. Cardiorenal syndrome 2. Hepatorenal syndrome 3. Nephrotic syndrome
38
How do you treat cardio renal?
Fluid overload → give loops
39
How do you treat hepatorenal?
↑ oncotic pressure → spiranolactone
40
How do you treat nephrotic syndrome?
↑ fluid → loop diuretic
41
What is the most common infrarenal injury?
Tubules (renal ischemia or nephrotoxins) Interstitial (acute interstitial nephritis) from nephrotoxins
42
What are the phases of IRA-ATN?
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
What can cause obstruction of post renal injury?
1. BPH, cancer, infection in prostate 2. Improperly placed catheter 3. Neprolithiasis 4. Blood clots
44
What is intra vs post renal?
Intra: structural damge within kidney Post: Obstruction in collecting system
45
Clinical presentation of AKI?
1. Changes in urinary character 2. Presence of edema 3. Sudden weight gain 4. Severe abdominal and/or flank pain
46
How do you calculate extraction of Na (FENa)?
(Urine Na x Scr x100) / (Urine Cr x Serum Na)
47
Compare FeNa in pre renal and intrisic?
Prerenal: <1% Intrinsic: >1% Unreliable if on diuretics
48
Compare BUN:sCr ratio?
Prerenal: >20:1 Intrisic and Postrenal: 10-15:1
49
What is KUB, BT, or US used for?
1. Small/shrunken kidneys indicates chronic disease 2. Identify presence of obstruction or hydronephrosis
50
How don't we use renal biopsy?
Invasive only for cancer → ↑ bleeding risk
51
What is type a and b DIKD?
A: Dose dependent (reduce dose) B: Unpredictable (DC drug)
52
What are the time courses of DIKD?
Acute – 1-7 days Subacute – 8-90 days Chronic - >90 daysWha
53
What are the phenotypes of DIKD?
1. AKI 2. Glomerular disorder 3. Tubular dysfunction 4. Mephrolithiasis/crystalluria
54
What are the drugs that can worsen AKI?
1. NSAIDS 2. Constrast dyes (IV fluids before to prevent KI) 3. Antibiotics (Vanc, AMinoglycosides, Amphotericin)
55
Mechanism of AKI?
A or B
56
Mechanism of Glomerular disorder?
Type A or B
57
Mechanism of nephrolithiasis?
Type A
58
Mechanism of tubular dysfunction?
Type A
59
Subtype of tubular dysfunction?
SIADH
60
Drugs that can worsen nephrolithiasis?
Acyclovir
61
Drugs that can worsen tubular dysfunction?
Lithium
62
What are the aminoglycosides?
Gentamicin, tobramycin , amikacin
63
What are the risk factors of DIKD?
1. Cormobidiites 2. >75YO 3. ACUTE ILLNESS 4. Polypharmacy 5: Triple whammy: NSAID (constrict afferent), ACEI (dilate efferent), Diuretics (↓ plasma volume)
64
What are the complication of AKI?
1. Electrolyte derangement 2. Volume overload 3. Metabolic acidosis 4. Uremic encephalopathy 5. Development of CKD 6. Need for RRT 7. Increased mortality
65
How do you prevent AKI?
1. Avoid/ limit potential toxins 2. Dosing adjustment 3. Adequate hydration 4. Optimize hemodynamics
66
What pharm do we use to prevent AKI?
1. IV fluid (↑ volume and perfusion) → crystalloids 2. Ascorbic acid: antioxidants
67
Treatment for pre renal?
1. Hydration → crystalloids to restore volume → ↑ peerfusion (UOP>0.5 mL/kg/h) 2. Diuresis → CHF or edema
68
Treatment for intrisic?
adjust or DC offenders
69
Treatment for post renal?
Removal of obstruction
70
Last resort treatment for AKI?
Dialysis when life threatening Remove waste/toxins to maintain fluid, electrolyte, and acid/base balance AEIOUs
71
What are the roles of loop diuretics in AKI?
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
What are the indications of acute dialysis?
A: Acid/base disturbances E: electrolyte imbalances I: intoxications O: overload of fluid U: uremia
73
What is the definition of CKD?
eGFR< 60 mL/min > 3 months
74
Leading cause of CKD?
DM followed by HTN
75
How do you prevent amino glycosides from causing ATN?
1. Preform TDM 2. Use extended interval dosing 3. Avoid concomitant nephrotoxins
76
How does NSAIDS cause pre renal AKI
1. ↓ PG → afferent arteriolar vasoconstriction and reduced glomerular BF
77
How do you prevent NSAIDs from causing pre renal AKI?
Avoid use in patients with ACEI/ARBs and/or diuretics
78
How does ACE/ARBS cause pre renal AKI?
Vasodilation of efferent arteriole
79
What are the presentations of drug induced pre renal AKI?
Reduction of GFR
80
How do you prevent ACE/ARB pre renal AKI?
Hold it the day of surgical procedures
81
How does amphotericin B cause ATN?
Direct proximal and distal tubular toxicity and afferent arteriole vasodilation
82
Presentation of amphotericin B induced ATN?
1. Tubular injury resulting in electrolyte wasting (hypokalemia, magnesia, natremia) 2. Metabolic acidosis
83
How do you prevent amphotericin B from causing ATN?
Limit daily dose
84
How does vanc cause ATN and AIN? Prevention?
Direct proximal tubular toxicity Perform TDM: target trough <20 mg/L
85
What causes CKD?
Loss of nephron mass → remaining nephrons compensate → secretion renin and kinin→ Intraglomerular HTN → progressing CKD → proteinuria → direct cellular damage → speeds up nephron loss
86
What CKD stages are sympotmatice mostly? What symptoms?
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
How is CKD classified?
1. Cause 2. GFR 3. Albuminuria
88
Describe the staging of GFR?
89
Describe the staging of albuminuria?
A2: micro A3: macro
90
What is the non pharm management of CKD?
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
How cormobidities do you need to manage?
1. Porteinuria 2. HTN 3. Diabetes: gola A1c <7%
92
What are treatment goals of CKD?
Slow progression
93
What are the pharms for CKD?
1. ACE/ARB 2. SGLT2I 3. Statins
94
How is ACE/ARB used for CKD?
Delay progression by lowering intraglomerular pressure and proteinuria 1st line for proteinuria if A2 Start with low dose
95
ACEI/ARB ADR?
AKI, hyperkalemia, cough with ACEIs
96
What is the role of SGLT2I?
Reduce glomerular hyper filtration by reducing glucose and sodium reabsorption in proximal tubule
97
What is the role of statins?
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
What are the complications of CKD?
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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