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Drug Action I > Block 4: AKI Phys > Flashcards

Block 4: AKI Phys Flashcards

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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
What are causes of prerenal AKI?
1. Decreased blood flow from intravascular volume depletion 2. Decreased effective arterial BV → shock
26
What components regulate renal BF?
1. CO 2. Renal perfusion pressure 3. Glomerular hemodynamic factors 4. Autoregulation (MAP 70-150)
27
How does you body try to compensate for pre renal AKI?
1. RAAS activation → activation of aldosterone 2. SNS activation
28
Clinical manifestations of pre renal AKI?
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)
29
How do you prevent pre renal AKI?
Correction and prevention of hypovolemia
30
What drugs interfere with auto regulation of kidneys?
ACEIs, diuretics, and NSAIDs
31
What are presentations of intrinsic AKI?
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
32
What are the types of intrinsic AKI affect?
1. Vacular 2. Actue intersticial nephritis 3. Acute glomerulonephritis 4. Acute tubular necrosis (ATN) → Ischemia and nephrotoxic
33
What is intrinsic AIN?
Inflammation of interstitial tissue of the kidney usually from medications
34
What are medications that may cause intrinsic AIN?
Penicillin, NSAIS, PPI
35
How do you diagnose AIN?
Renal biopsy Hematuria Eosinophiluria Sterile pyuria
36
What is glomerulephritis?
Glomerular disorders that produce AKI: 1. Acute glomerulonephritis 2. Rapidly progressive glomerulonephritis (RPGN) Inflammation and structural damages to glomerular cells from macrophages and inflammation
37
What is Acute Glomerulonephritis (GN)?
IgA nephropathy most common form Adults age 20-30 years
38
What are the presentations of acute GN?
1. Gross microscopic hematuria 2. Deposition of IgA 3. Formation of crescents 4. Proliferation of macrophages 5. Crescent shaped scar
39
How do you manage milk IgA nephropathy?
BP and HLD medications
40
How does Rapidly Progressive GN (RPGN) differ from GN?
1. Postinfectious GN 2. Caused by good pasture syndrome 3. Extensive necrotic crescent formations
41
How is RPGN diagnosed?
Serologic tests
42
What are the types of acute tubular necrosis (ATN)?
1. Ischemic ATN 2. Nephrotoxic ATN 3. Contrast-induced nephropathy (CIN) 4. Sepsis-induced ATN
43
What is ischemic ATN? MOA?
Prolonged hypo perfusion from sepsis, surgery, or unresolved HF Loss of auto regulation that causes renal vasoconstriction
44
What is nephrotoxic ATN caused by?
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
What is Contrast-induced nephropathy?
IV radiocontrast agents cause increased sCr within 24 hours of administration
46
What contributes to increased mortality during hospitalization and after discharge?
Hospital-acquired CIN
47
What is sepsis-induced ATN?
1. 70% mortality rate 2. Common cause of AKI → Ischemia from hypotension → toxic damage from endotoxins
48
What are endotoxins?
Secreted by G- bacteria → promote activation of inflammatory mediators → systemic response
49
What is miscrovascular ATN?
Injury disrupts microvascular BL and auto regulation of RBFWh a
50
How happens during ATN when tubular epithelia cell injury?
1. Decreased RBF 2. Renal hypoxia 3. Pro inflammatory and vasoactive mediators
51
What is ESRD?
1. Irrecoverable loss of renal function 2. Requires renal replacement therapy 3. AKI → ESRD
52
What are phases of intrinsic AKI?
1. Initial (Changes in UO and sCr) 2. Maintenance (Fluid overload) 3. Recovery (Polyuria and fluid/electrolyte abnormalities)
53
What is the most common and inexpensive method of diagnosing AKI?
Urinalysis (Urine Na+ concentration, urinary fractional excretion of Na+, fractional excretion of urea)
54
What is the difference between pre renal and intrinsic ATN?
Pre: Osmolality increased In: Osmolality decreased
55
What is the Urinary fractional excretion of sodium (FENa)?
Below 1% – suggests prerenal AKI. Above 2% – indicates ATN
56
What Urinary fractional excretion of urea (FEurea)?
Below 35% – indicates prerenal AKI. Above 50% – indicates intrinsic ATN
57
What is post renal
Obstruction of the urinary collecting system
58
Where do obstruction of post renal AKI occur?
1. Kidneys, ureters, urethra 2. Bilateral kidneys or ureters 3. Kidneys
59
How can postrenal AKI occur in pregnancy?
Fetus obstructs urine flow
60
What is the difference between complete and partial obstruction?
C: Anuria P: Flank pain, hematuria, incomplete emptying
61
What is the definition of CKD?
Defined as kidney damage or GFR <60 for 3 months or more
62
How is CKD assessed?
Pathologic abnormalities or markers of damage in blood or urine tests
63
What population has a higher incidence of CKD?
AA and Native americans
64
How many dialysis patients die within the first year of treatment?
25%
65
What are complications regarding decreased kidney functions?
1. Anemia 2. Uremia 3. Derangements of bone and mineral metabolism 4. CVD 5. Progression of ESRD
66
How do you limit the progressions of ESRD?
Management of risk factors
67
What are modifiable (clinical) risk facotors of CKD?
1. DM 2. HTN 3. DLD 4. Obesity 5. AKI Frequent screening and education required
68
What are the nonmodifiable (sociodemographic) risk facotrs?
1. Age 2. Premature birth 3. Heredity 4. Ethnicity 5. Low socioeconomic level
69
How do you detect CKD early?
Routine lab tests or Cr and GFR
70
What is Kidney Disease Outcomes Quality Initiative (KDOQI)?
Guidelines that aim to improve identification, prevention, and treatment of CKD Define CKD and classify stages of disorders
71
CKD presentation is older adults? Children?
Reduced GFR UTI
72
What are the main etiologies of CKD?
1, Diabetic neuropathy 2. HTN nephrosclerosis 3. Chronic glomerulonephritis 4. Polycystic kidney disease
73
What is the most common cause of CKD in ESRD?
Diabetic nephropathy
74
What are the presentations of diabetic neuropathy?
Moderate albuminuria → early indicator Basement membrane thickening, mesangial expansion, increased glomerular permeability, reduced GFR Hypertension, severely increased albuminuria, high risk of CVD
75
What is hypertensive nephrosclerosis?
In T2D, HTN increase with DM and obesity Initiates RAAS and increase ESRD risk, Impaired renal autoregulation Pregnancy and pre-eclampsia
76
What is the pathology of HTN nephorsclerosis?
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
What is chronic glomerulonephritis?
Direct inflammation of glomerulus for antibody deposition → glomerular and tubulointerstitial fibrosis and nephron is destroyed over time Similar to diabetic nephropathy
78
What are the patterns of glomerular disease? How is it diagnosed?
1. Nephritic pattern 2. Nephrotic pattern Renal biospy
79
What is nephritic pattern?
1. Associated w/ inflammation 2. Produces active urine sediment 3. Proteinuria
80
What is nephrotic pattern?
1. Proteinuria 2. Inactive urine sediment
81
What causes polycystic kidney disease?
Mutation of the PKD1 gene and begin at 30 HTN development Cysts usually develop from nephron collecting duct → encroaching normal renal tissue
82
What are complications of CKD?
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
What is CKD-MBD?
Mineral and hormonal changes that is apparent in stage 3
84
What are the complications and outcomes of CKD-MBD?
Com: Bone pain, deformities, and fractures O: Abnormal bone turnover, hypocalcaemia, hyperphospatemia, and hyperparathyroidism
85
How does CKD-MD lead to hypocalcemia?
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
How does CKD-MBD affect the bones?
PTH and bone become less responsive when phosphorous-calcium complexes cause soft tissue and vascular calcifications
87
What is anemia?
Decreased EPO production that stimulated RBC production → Increased Cardiac
88
What are Hb levels for anemia?
<12.5 mg/dL in females 13.5 mg/dL in males
89
What causes anemia?
1. Cardiac modeling (LV hypertrophy and dilation) and stroke
90
What is the most common cause of CKD?
CVD
91
How CKD cause HTN?
Poorly controlled → decreased GFR
92
How can CKD cause DLD?
Proteinuria potentiates dyslipidemia
93
How can CKD cause metabolic acidosis?
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
How can CKD cause Hyperkalemia?
1. Increased K+ → Oliguria 2. Decreased aldosterone secretion and decreased excretion of potassium 3. Hemodynamic instability and arrhythmias
95
How can CKD cause hypervolemia?
1. Renal excretion of sodium and water decreases → hemodynamic instability and arrhythmias Meds: diuretics and sodium restriction
96
How can CKD → Uremia?
Waste product accumulation → Increase urea in blood
97
What are indications of uremia?
Fatigue, nausea, vomitting, HA 1. GI disturbances 2. CNS 4. Edema 5. Skin changes (yellow) 6. Metabolic acidosis → severe
98
What are clinical procedures used to treat CKD?
1. Hemodialysis 2. Peritoneal dialysis 3. Kidney transplantation

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