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Patho/Pharm 2 > Renal > Flashcards

Renal Flashcards

1
Q

What is AKI (definition)

A

acute kidney injury - sudden decline in kidney function with or without oliguria

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2
Q

what is the criteria for AKI

A

increased serum creatinine (SCr) by 50% in 7 days or >0.3mg/dL in 48 hrs
Likely also increased serum BUN, K, uremia, and fluid/electrolyte imbalances

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3
Q

what is uremia

A

build up of toxins in the blood (BUN & Cr) that manifests as symptoms in multiple body systems

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4
Q

what are the four phases of AKI

A

initiation, extension, maintenance, and recovery/polyurea

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5
Q

what is the initiation phase of AKI

A

hypoperfusion/toxicity leading to acute cell injury and dysfunction; characterized by:
1. increased SCr
2. increased BUN
3. oliguria

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6
Q

what is extension phase of AKI

A

progressive ischemia and inflammation

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7
Q

what is the maintenance phase of AKI

A

established kidney injury after initial event, body unable to excrete waste

–>changes in urine output, fluid & electrolyte imbalance, uremia

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8
Q

what is the recovery phase

A

osmotic diuresis from high urea concentration in the glomerular filtrate & inability of tubules to concentrate urine (due to damage) –> causes polyurea which may lead to loss of Na, K & water

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9
Q

what is the cause of pre-renal AKI

A

renal hypoperfusion (due to hypovolemia, reduced cardiac output, increased vascular resistance, shunting, vasodilation); if prolonged leads to acute tubular necrosis

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10
Q

what labs would be elevated in pre-renal AKI

A

serum urea and serum creatinine (not being filtered due to low pressure), low urine Na (Na & water retention due to RAAS)

*tubules are still intact and can reabsorb urea and excrete creatinine further leading to serum urea +++

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11
Q

what are the clinical manifestations of pre-renal AKI

A

oliguria (30cc/hr or less), salt and water retention, low urine Na, high urine osmolality, high BUN/Plasma creatinine ratio (20:1)

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12
Q

what is the cause of intra-renal AKI

A

intrinsic disorders involving renal parenchymal or interstitial tissue damage (vascular infarctions, HTN/preeclampsia, glomerulonephritis, drug toxicity, or tubulointerstitium causes like ATN or rhabdo)

necrotic cells block tubules and cause them to become dysfunctional (cannot reabsorb urea or excrete creatinine)

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13
Q

what labs are elevated in intra-renal AKI

A

plasma urea and plasma creatinine +++, high urine sodium

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14
Q

what is the most common type of intra renal AKI

A

acute tubular necrosis (ATN)

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15
Q

what are the clinical manifestations of intra-renal AKI

A

nonoliguria, high urine Na, casts (muddy brown), dilute urine (low osmolality)

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16
Q

what is the cause of post-renal aki

A

obstructions - causes increase in hydrostatic pressure upstream and gradually decreases GFR

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17
Q

what are the clinical manifestations of post-renal AKI

A

anuria, flank pain, followed by polyurea

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18
Q

what is glomerulonephritis

A

inflammation of the glomerulus caused by primary injury (infection, ischemia, drugs/toxins, vascular disorder) or secondary injury (systemic disease: DM, CHF, HIV)

*epithelial or podocyte layer to glomerular capillary membrane is disturbed, changing it’s permeability so some proteins can escape into the urine

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19
Q

what is nephrotic syndrome

A

glomerular injury leads to increased permeability leading to protein (esp albumin) to escape in the urine –> 3.5g more more per day (more than glomerulonephritis)

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20
Q

what is creatinine

A

a waste product that comes from energy production in the muscle - normally filtered by glomerulus and excreted by kidneys

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21
Q

how is creatinine clearance altered in pre-renal AKI

A

less Cr filtered due to low perfusion pressure - tubular excretion remains intact

–> serum Cr slightly elevated

22
Q

what is tubular Cr excretion

A

moving Cr from plasma directly into renal tubules for excretion into the urine

23
Q

how is Cr clearance altered in intra-renal AKI

A

less Cr filtered at clomerulus AND tubular secretion impaired

–>serum Cr ++ elevated

24
Q

what is eGFR

A

estimated glomerular filtration rate

25
Q

what is the eGFR and serum Cr in kidney injury

A

reduced eGFR and elevated SCr

26
Q

what are the stages of kidney disease

A
  1. GFR normal >90ml/min, no CM
  2. GFR 60-89, mild HTN, increasing SCr & urea
  3. GFR 30-59, same as 2
  4. GFR 15-29, worsening as above, EPO deficiency anemia, hyperphosphatemia, metabolic acidosis, hyperkalemia
  5. ESKD GFR<15, as 4
27
Q

what is the goal of treatment for AKI

A

prevent progression of injury, resolve any complications (hemodynamics, fluid/electrolytes etc)

28
Q

what is the treatment goal for CKD

A

dialysis, renal transplant, slow progression

29
Q

what is the treatment for AKI

A

-lab evaluation (SCr & urea, lytes, CBC, LFTs, glucose, bone profile, urinalysis, renal US, chest x-ray

-manage hemodynamics & electrolytes, prevent infection, correct metabolic acidosis, maintain nutrition and glucose control, avoid nephrotoxic agents, renal replacement therapy

-no pharm

30
Q

what is management of CKD

A

early screening/detection: lab tests (eGFR, SCr, BUN, urinalysis) and imaging (CT, xray, US, biopsy)

nutrition (adequate calories & vit D, restriction of protein, Na, K, and Ph)

manage dyslipidemia (CV risk) HTN, and glucose control

31
Q

what is the MOA of thiazide diuretics

A

block reabsorption of Na and Cl in the DISTAL convoluted tubule to promote excretion fo Na, CL, K, and water –> leads to mild diuresis

32
Q

what are indications for thiazide diuretics

A

HTN, edema, postmenopausal osteoporosis

–> first line in community “go to” diuretic

33
Q

what is the MOA for Loop diuretics

A

blocks reabsorption of Na and CL in the ascending LOOP of Henle to prevent reabsorption of water–> substantial diuresis (most effective)

34
Q

what is an example of a loop diuretic

A

furosemide/Lasix

35
Q

what is the black box for loop diuretics

A

profound diuresis with water and electrolyte depletion

36
Q

what is a side effect unique to loop diuretics

A

ototoxicity, transient deafness with furosemide

37
Q

what is an indication for loop diuretics

A

urgent diuresis needed, pulmonary edema related to CHF, uncontrolled HTN, not used in primary care often

38
Q

MOA for K-sparing diuretics

A

promotes mild excretion of Na and water while decreasing K excretion, some directly inhibit aldosterone while others work in distal nephron

39
Q

what are Black Box warnings for K-sparing diuretics

A

spironolactone = tumorigenic in rats

triamterene = hyperK

40
Q

indications for K-sparing diuretics

A

combo use with thiazide or loop to prevent hypoK

41
Q

what is azotemia

A

elevation of SCr adn BUN as a result of decreased renal filtration

42
Q

what are the three most common clinical manifestations of AKI

A
  1. anemia (EPO deficiency)
  2. neurological (confusion, drowsiness, seizures)
  3. derm (pruritis, inflammation)
43
Q

prerenal azotemia is associated with: (3 things)

A
  1. decreased excretion of Na
  2. increased salf & water retention
  3. oliguria
44
Q

which medications are associated with PRErenal AKI

A
  1. ACEi, ARBs, epi, dopamine –> cause efferent arteriole vasodilation
  2. NSAID - cause afferent arteriole vasoconstriction

both lead to hypoperfusion

45
Q

are pre-renal AKIs reversible?

A

yes, but can progress to intra-renal if not corrected

46
Q

what are the two main causes of ATN

A

ischemia & nephrotoxins

47
Q

what is the pathology of AKI

A

hypovolemia and decreased renal blood flow stimulates release of renin, which triggers RAAS, leads to constriction of afferent arteriole and decrease in glomerular pressure, further decreasing GFR

ischemia damages tubules, which leads to necrosis

necrotic cells build up within tubules and cause obstructions, and glomerular filtrate leads into the blood

ultimately leads to oliguria

48
Q

when can AKI be reversed?

A

when ischemia is not prolonged, basement membrane not destroyed, tubular epithelium regenerates

49
Q

what are the most common causes of post-renal AKI (5)

A
  1. prostatic hyperplasia
  2. prostate cancer
  3. renal calculi (kidney stones)
  4. trauma
  5. extrarenal tumors
50
Q

what kind of renal injury are associated with casts?

A

intra-renal

51
Q

what is the best indicator of kidney function

A

GFR - provides an approximate measurement of number of functional nephrons

Patho/Pharm 2 (7 decks)

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