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Drug Action I > Block 4: AKI Phys > Flashcards

Block 4: AKI Phys Flashcards

1
Q

What are the normal kidney functions?

A
  1. Regulation of body fluids and electrolytes
  2. Excretion of waste products
  3. COntrol BP
  4. Regulation of acid-base balance

→ Perfusion to nephrons

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2
Q

Describe the mechanism of the nephron and how it affects electrolytes?

A
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3
Q

What are the characteristics of AKI?

A
  1. Quickly noted
  2. Occurs on a continuum
  3. Often reversible
  4. Progress to CKD if untreated
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4
Q

What are the characteristics of CKD?

A
  1. Silent for many years
  2. Systmemic changes
  3. Long term damage from disease
  4. Can controlled
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5
Q

What is the difference between AKI and CKD

A

AKI: Absence of neuropathy and short onset

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6
Q

What is a common cause of AKI?

A

acute tubular necrosis (ATN)

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7
Q

What is AKI?

A

Abrupt reduction of kidney function → reversible

Characterized by azotemia

AKA acute renal failure

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8
Q

What is azotemia?

A
  1. Accumulation of nitrogenous wastes
  2. Elevated sCr and BUN
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9
Q

What are the classifications of AKI?

A
  1. Risk → Injury → Failure → Loss → End-Stage Renal Disease (RIFLE)
  2. Acute Kidney Injury Network (AKIN) criteria
  3. Kidney Disease Improving Global Outcomes (KDIGO)
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10
Q

What is the purpose of AKI classification systems?

A
  1. Better ID
  2. Standardize diagnosis and treatment
  3. Established and accurate definitions
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11
Q

What are the classes of AKI?

A
  1. Prerenal
  2. Intrinsic
  3. Postrenal
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12
Q

Where does AKI occur?

A
  1. Vascular supply
  2. Glomerular
  3. Tubular
  4. Interstitial disease
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13
Q

What is RIFLE?

A

Risk → Injury → Failure → Loss → End-Stage Renal Disease

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14
Q

What are the criteria AKI classifications to determine the extent of kidney damage?

A
  1. sCr
  2. UO
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15
Q

What is excessive or abnormally large production or passage of urine?

A

polyuria

Greater than 2.5 or 3 L

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16
Q

What is reduced UO?

A

Oliguria

400-500 mL/day

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17
Q

What is non passage of urine?

A

Anuria

<100mL

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18
Q

What is the difference between pyruria and hematuria?

A

P: WBC or puss → UTI
H: Blood

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19
Q

What is GFR?

A

Estimate of kidney function by collecting blood and urine samples

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20
Q

What is sCr?

A

Product of muscle creatine metabolism that is filtered by kidneys but not reabsorbed

Used to measure GFR

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21
Q

What is clearance?

A

the amount that is completely cleared by the kidneys in 1 minute

C = UV/P

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22
Q

What is normal CrCl?

A

125 mL/min

Needs to account for BSA
Age related decline

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23
Q

Normal sCr values?

A

Healthy women – ~0.7 mg/dL of blood.
Healthy men – ~1.0 mg/dL of blood.
Muscular men – ~1.5 mg/dL of blood.

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24
Q

What is sCr used for?

A

Estimate the functional capacity of the kidneys

sCr 2x → 50% loss of renal function.
sCr 3x → 75% loss of renal function.
If values are ≥10 mg/mL → 90% loss of renal function.

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25
Q

What are causes of prerenal AKI?

A
  1. Decreased blood flow from intravascular volume depletion
  2. Decreased effective arterial BV → shock
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26
Q

What components regulate renal BF?

A
  1. CO
  2. Renal perfusion pressure
  3. Glomerular hemodynamic factors
  4. Autoregulation (MAP 70-150)
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27
Q

How does you body try to compensate for pre renal AKI?

A
  1. RAAS activation → activation of aldosterone
  2. SNS activation
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28
Q

Clinical manifestations of pre renal AKI?

A
  1. Decreased urine Na+ (<20 mmol/L)
  2. Decreased fractional excretion of Na+ (<1%)
  3. Decreased fractional excretion of urea (<35%)
  4. Increased urine osmolality
  5. Increased urine specific gravity
  6. Decreased urine output (oliguria)
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29
Q

How do you prevent pre renal AKI?

A

Correction and prevention of hypovolemia

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30
Q

What drugs interfere with auto regulation of kidneys?

A

ACEIs, diuretics, and NSAIDs

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31
Q

What are presentations of intrinsic AKI?

A
  1. Doesn’t always result in prompt return of kidney function
  2. BUN and sCr levels increase
  3. Renal anatomy diseases
  4. Rash fever, eosinophillia
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32
Q

What are the types of intrinsic AKI affect?

A
  1. Vacular
  2. Actue intersticial nephritis
  3. Acute glomerulonephritis
  4. Acute tubular necrosis (ATN) → Ischemia and nephrotoxic
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33
Q

What is intrinsic AIN?

A

Inflammation of interstitial tissue of the kidney usually from medications

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34
Q

What are medications that may cause intrinsic AIN?

A

Penicillin, NSAIS, PPI

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35
Q

How do you diagnose AIN?

A

Renal biopsy

Hematuria
Eosinophiluria
Sterile pyuria

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36
Q

What is glomerulephritis?

A

Glomerular disorders that produce AKI:
1. Acute glomerulonephritis
2. Rapidly progressive glomerulonephritis (RPGN)

Inflammation and structural damages to glomerular cells from macrophages and inflammation

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37
Q

What is Acute Glomerulonephritis (GN)?

A

IgA nephropathy most common form
Adults age 20-30 years

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38
Q

What are the presentations of acute GN?

A
  1. Gross microscopic hematuria
  2. Deposition of IgA
  3. Formation of crescents
  4. Proliferation of macrophages
  5. Crescent shaped scar
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39
Q

How do you manage milk IgA nephropathy?

A

BP and HLD medications

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40
Q

How does Rapidly Progressive GN (RPGN) differ from GN?

A
  1. Postinfectious GN
  2. Caused by good pasture syndrome
  3. Extensive necrotic crescent formations
41
Q

How is RPGN diagnosed?

A

Serologic tests

42
Q

What are the types of acute tubular necrosis (ATN)?

A
  1. Ischemic ATN
  2. Nephrotoxic ATN
  3. Contrast-induced nephropathy (CIN)
  4. Sepsis-induced ATN
43
Q

What is ischemic ATN? MOA?

A

Prolonged hypo perfusion from sepsis, surgery, or unresolved HF

Loss of auto regulation that causes renal vasoconstriction

44
Q

What is nephrotoxic ATN caused by?

A
  1. Direct toxic damage to renal tubule from meds or massive hemolysis
  2. Nephrotoxic agents accumulate in the kidney cortex → damage to PCT and brown urine casts
45
Q

What is Contrast-induced nephropathy?

A

IV radiocontrast agents cause increased sCr within 24 hours of administration

46
Q

What contributes to increased mortality during hospitalization and after discharge?

A

Hospital-acquired CIN

47
Q

What is sepsis-induced ATN?

A
  1. 70% mortality rate
  2. Common cause of AKI → Ischemia from hypotension → toxic damage from endotoxins
48
Q

What are endotoxins?

A

Secreted by G- bacteria → promote activation of inflammatory mediators → systemic response

49
Q

What is miscrovascular ATN?

A

Injury disrupts microvascular BL and auto regulation of RBFWh a

50
Q

How happens during ATN when tubular epithelia cell injury?

A
  1. Decreased RBF
  2. Renal hypoxia
  3. Pro inflammatory and vasoactive mediators
51
Q

What is ESRD?

A
  1. Irrecoverable loss of renal function
  2. Requires renal replacement therapy
  3. AKI → ESRD
52
Q

What are phases of intrinsic AKI?

A
  1. Initial (Changes in UO and sCr)
  2. Maintenance (Fluid overload)
  3. Recovery (Polyuria and fluid/electrolyte abnormalities)
53
Q

What is the most common and inexpensive method of diagnosing AKI?

A

Urinalysis (Urine Na+ concentration, urinary fractional excretion of Na+, fractional excretion of urea)

54
Q

What is the difference between pre renal and intrinsic ATN?

A

Pre: Osmolality increased
In: Osmolality decreased

55
Q

What is the Urinary fractional excretion of sodium (FENa)?

A

Below 1% – suggests prerenal AKI.
Above 2% – indicates ATN

56
Q

What Urinary fractional excretion of urea (FEurea)?

A

Below 35% – indicates prerenal AKI.

Above 50% – indicates intrinsic ATN

57
Q

What is post renal

A

Obstruction of the urinary collecting system

58
Q

Where do obstruction of post renal AKI occur?

A
  1. Kidneys, ureters, urethra
  2. Bilateral kidneys or ureters
  3. Kidneys
59
Q

How can postrenal AKI occur in pregnancy?

A

Fetus obstructs urine flow

60
Q

What is the difference between complete and partial obstruction?

A

C: Anuria
P: Flank pain, hematuria, incomplete emptying

61
Q

What is the definition of CKD?

A

Defined as kidney damage or GFR <60 for 3 months or more

62
Q

How is CKD assessed?

A

Pathologic abnormalities or markers of damage in blood or urine tests

63
Q

What population has a higher incidence of CKD?

A

AA and Native americans

64
Q

How many dialysis patients die within the first year of treatment?

A

25%

65
Q

What are complications regarding decreased kidney functions?

A
  1. Anemia
  2. Uremia
  3. Derangements of bone and mineral metabolism
  4. CVD
  5. Progression of ESRD
66
Q

How do you limit the progressions of ESRD?

A

Management of risk factors

67
Q

What are modifiable (clinical) risk facotors of CKD?

A
  1. DM
  2. HTN
  3. DLD
  4. Obesity
  5. AKI

Frequent screening and education required

68
Q

What are the nonmodifiable (sociodemographic) risk facotrs?

A
  1. Age
  2. Premature birth
  3. Heredity
  4. Ethnicity
  5. Low socioeconomic level
69
Q

How do you detect CKD early?

A

Routine lab tests or Cr and GFR

70
Q

What is Kidney Disease Outcomes Quality Initiative (KDOQI)?

A

Guidelines that aim to improve identification, prevention, and treatment of CKD

Define CKD and classify stages of disorders

71
Q

CKD presentation is older adults? Children?

A

Reduced GFR

UTI

72
Q

What are the main etiologies of CKD?

A

1, Diabetic neuropathy
2. HTN nephrosclerosis
3. Chronic glomerulonephritis
4. Polycystic kidney disease

73
Q

What is the most common cause of CKD in ESRD?

A

Diabetic nephropathy

74
Q

What are the presentations of diabetic neuropathy?

A

Moderate albuminuria → early indicator

Basement membrane thickening, mesangial expansion, increased glomerular permeability, reduced GFR

Hypertension, severely increased albuminuria, high risk of CVD

75
Q

What is hypertensive nephrosclerosis?

A

In T2D, HTN increase with DM and obesity

Initiates RAAS and increase ESRD risk, Impaired renal autoregulation

Pregnancy and pre-eclampsia

76
Q

What is the pathology of HTN nephorsclerosis?

A
  1. Increased pressure in the glomerulus → damage of glomerular cells → glomerulosclerosis (scarring)
  2. Damage of small vessels (arteries and arterioles) in kidney → decreasing BF
  3. Compensatory hyperfiltration by undamaged nephrons → thickening of vessels
77
Q

What is chronic glomerulonephritis?

A

Direct inflammation of glomerulus for antibody deposition → glomerular and tubulointerstitial fibrosis and nephron is destroyed over time

Similar to diabetic nephropathy

78
Q

What are the patterns of glomerular disease? How is it diagnosed?

A
  1. Nephritic pattern
  2. Nephrotic pattern

Renal biospy

79
Q

What is nephritic pattern?

A
  1. Associated w/ inflammation
  2. Produces active urine sediment
  3. Proteinuria
80
Q

What is nephrotic pattern?

A
  1. Proteinuria
  2. Inactive urine sediment
81
Q

What causes polycystic kidney disease?

A

Mutation of the PKD1 gene and begin at 30

HTN development

Cysts usually develop from nephron collecting duct → encroaching normal renal tissue

82
Q

What are complications of CKD?

A
  1. Chronic kidney disease-mineral and bone disorder (CKD-MBD)
  2. Anemia
  3. Cardiovascular disease
  4. Hypertension
  5. Dyslipidemia
  6. Metabolic acidosis
  7. Hyperkalemia
  8. Hypervolemia
  9. Uremia
83
Q

What is CKD-MBD?

A

Mineral and hormonal changes that is apparent in stage 3

84
Q

What are the complications and outcomes of CKD-MBD?

A

Com: Bone pain, deformities, and fractures
O: Abnormal bone turnover, hypocalcaemia, hyperphospatemia, and hyperparathyroidism

85
Q

How does CKD-MD lead to hypocalcemia?

A

PTH is initially produced to remove calcium from bone to maintain normal levels

Secondary hyperparathyroidism → phosphorus binding to calcium → increased PTH levels

Diminished kidney function causes retained phosphorus to bind with calcium → inhibited calcitriol synthesis → hypocalcemia.

86
Q

How does CKD-MBD affect the bones?

A

PTH and bone become less responsive when phosphorous-calcium complexes cause soft tissue and vascular calcifications

87
Q

What is anemia?

A

Decreased EPO production that stimulated RBC production → Increased Cardiac

88
Q

What are Hb levels for anemia?

A

<12.5 mg/dL in females
13.5 mg/dL in males

89
Q

What causes anemia?

A
  1. Cardiac modeling (LV hypertrophy and dilation) and stroke
90
Q

What is the most common cause of CKD?

A

CVD

91
Q

How CKD cause HTN?

A

Poorly controlled → decreased GFR

92
Q

How can CKD cause DLD?

A

Proteinuria potentiates dyslipidemia

93
Q

How can CKD cause metabolic acidosis?

A

Kidneys retain H+ ions → acid-base imbalance → Increased renal excretion of ammonia and retention of H+ ions and Decreased resorption of sodium bicarbonate → muscle degradation

Especially prominent in stages 4 and 5.

94
Q

How can CKD cause Hyperkalemia?

A
  1. Increased K+ → Oliguria
  2. Decreased aldosterone secretion and decreased excretion of potassium
  3. Hemodynamic instability and arrhythmias
95
Q

How can CKD cause hypervolemia?

A
  1. Renal excretion of sodium and water decreases → hemodynamic instability and arrhythmias
    Meds: diuretics and sodium restriction
96
Q

How can CKD → Uremia?

A

Waste product accumulation → Increase urea in blood

97
Q

What are indications of uremia?

A

Fatigue, nausea, vomitting, HA

  1. GI disturbances
  2. CNS
  3. Edema
  4. Skin changes (yellow)
  5. Metabolic acidosis → severe
98
Q

What are clinical procedures used to treat CKD?

A
  1. Hemodialysis
  2. Peritoneal dialysis
  3. Kidney transplantation

Drug Action I (32 decks)

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