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PHA6131, 6133 3RD SHIFT > (LEC) Toxic Response of the Kidney > Flashcards

(LEC) Toxic Response of the Kidney Flashcards

1
Q

The kidney releases _________ and ______________

A

Renin, Erythropoietin

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2
Q

Principal role: Excretion of
metabolic wastes

A

Kidney

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3
Q

(T/F) The kidney metabolizes VIT A into 1,25 dihydroxyvitamin D

A

False. it metabolizes VITAMIN D3

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4
Q

(T/F) The kidney plays a role on acid-base balance and electrolyte composition

A

True

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5
Q

(T/F) The kidneys ensure the regulation of extracellular fluid volume

A

True

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6
Q

Anatomical areas of the kidney (CMP)

A
  • Cortex (90%)
  • Medulla (~6-10%),
  • Papilla (1-2%)
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7
Q

Functional units of the kidney

NVGT

A
  • Nephron
  • Vascular element
  • Glomerulus
  • Tubular element
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8
Q

A complex, specialized capillary bed composed primarily of endothelial cells.

A

Glomerulus

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9
Q

Interlobar, arcuate, interlobular arteries and afferent arterioles that supply the glomerulus

A

Renal artery

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10
Q

(T/F) BOTH afferent and efferent arterioles control glomerular capillary pressure and glomerular plasma flow rate.

A

True

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11
Q

Carry the blood away from the glomerulus

A

Afferent arteriole

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12
Q

Deliver the blood to the glomerulus

A

Efferent arteriole

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13
Q

The glomerulus is a complex, specialized capillary bed composed primarily of __________________ cells.

A

Endothelial

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14
Q

Three discrete segments of the proximal tubule

CTR 123

A

S1 (pars convolute)
S2 (transition between pars convolute and pars recta)
S3 (pars recta)

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15
Q

Workhorse of the nephron that reabsorbs 60-80% of solute and water filtered at the glomerulus

A

Proximal tubule

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16
Q

(T/F) The proximal tubule reabsorbs virtually all the filtered high MW proteins by specific exocytotic protein reabsorption processes.

A

False. It reabsorbs virtually all the filtered LOW MW proteins by specific ENDOCYTOTIC protein reabsorption processes.

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17
Q

This is characterized by an attenuated and fenestrated cytoplasm & visceral epithelial cells

A

Renal Vasculature/Glomerulus

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18
Q

Reabsorbs 25% Na and K and 20% of filtered water

A

Loop of Henle

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19
Q

Iso-osmotic to the renal interstitium (water is freely permeable)

A

Tubular fluid entering the Thin descending limb

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20
Q

Impermeable to water, and electrolytes are reabsorbed by the active Na+/K+/2Cl- cotransport mechanism

A

Thin ascending limb

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21
Q

________ distal tubule reabsorbs most of the remaining impermeable to water.

A

Early distal tubule

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22
Q

(T/F) The late distal tubule, cortical collecting tubule, and medullary collecting duct perform the final regulation and finetuning of urinary volume and composition.

A

True

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23
Q

Build up of Nitrogenous waste in blood caused by decrease in GFR (AKI)

A

Azotemia

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24
Q

Abrupt decline in GFR with resulting azotemia

A

Acute Kidney Injury

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25
Q

A complex disorder that comprises multiple causative factors with clinical manifestations ranging from minimal elevation in serum creatinine to anuric renal failure.

A

Acute Kidney Injury

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26
Q

Decline in GFR result from?

A

Prerenal, postrenal, intrarenal factors

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27
Q

Cause of GFR decline

renal vasoconstriction, intravascular volume depletion, insufficient cardiac output

A

Prerenal factors

Afferent arteriolar constriction so dec. blood flow

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28
Q

Cause of GFR decline

ureteral or bladder obstruction

A

Postrenal factors

Obstruction inc. tubular pressure = dec. GFR

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29
Q

Cause of GFR decline

glomerulonephritis, tubular cell injury, death and loss resulting in back leak

A

Intrarenal

Back leak in intracellular space/bloodstream

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30
Q

Mechanisms of chemically-induced acute kidney injury

NSAID, Radiocontrast agents, Cyclosporine, Ampho B, Tacrolimus

A

Vasoconstriction

Never Run Cats After tacos (NRCAT)

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31
Q

Mechanisms of chemically-induced acute kidney injury

Sulfonamides, Methotrexate, Acyclovir, Triamterene, Ethylene glycol, Protease inhibitors

A

Crystalluria

Silly Monkeys Are Trying Extra Potions (SMATEP)

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32
Q

Mechanisms of chemically-induced acute kidney injury

Cyclosporine, Mitomycin C, Tacrolimus, Cocaine, Conjugated estrogens, Quinine

A

Endothelial Injury

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33
Q

Mechanisms of chemically-induced acute kidney injury

Gold, Penicillamine, NSAID

A

Glomerulopathy

Gold Pigs Nibble (GPN)

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34
Q

Mechanisms of chemically-induced acute kidney injury

Antibiotics, NSAID, Diuretics

A

Interstitial Nephritis

Anti Naughty Dog (AND)

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35
Q

Mechanisms of chemically-induced acute kidney injury

Aminoglyco, Cisplatin, Vancomycin, Pentamidine, Radioconstrast agents, Heavy metals, Halo-alkane

A

Tubular Toxicity

36
Q

Mechanisms of chemically-induced acute kidney injury

Diuretics, ARa, ACEi, Anti-htn

A

Prerenal

Something to do with htn + diuretics

37
Q

Nephrotoxic Insult

Path of Uninjured Cells

A

Compensatory hypertrophy, Cellular adaptation, Cellular proliferation

38
Q

Nephrotoxic Insult

Path of Injured Cells

A

Cellular repair, Cell death

39
Q

Nephrotoxic Insult

_________________> Re-epithelialization > Differentiation

A

Cellular proliferation

40
Q

Endpoint after toxic insult

A

Structural and functional recovery of nephron

41
Q

Chemicals that induce renal deterioration

A

Analgesics, Lithium, Cyclosporine (ALC)

42
Q

Progressive deterioration of renal function may occur with longterm exposure to various chemicals

A

Chronic Kidney Disease

longterm exposure = chronic

43
Q

Leads to tubular atrophy and interstitial fibrosis

A

CKD

44
Q

(T/F) A nontoxic concentration of a chemical in the plasma may reach toxic concentrations in the kidney and its tubules.

A

True

45
Q

The kidneys receive ____% to ____% of resting cardiac output

A

20% to 25%

46
Q

NSAID toxicity mechanism

A

prostaglandin synthesis suppressor → ↓renal blood flow → AKI

47
Q

ACEi toxicity mechanism

A

block vasoconstriction → precipitous decline in filtration pressure and AKI

48
Q

Site selective injury can be attributed to:

A
  • site-specific differences in blood flow
  • transport and accumulation of chemicals
  • physicochemical properties of the epithelium
  • reactivity of cellular/ molecular targets
  • balance of bioactivation/ detoxification reactions
  • cellular energetics
  • regenerative/ repair mechanisms
49
Q

Initial site of chemical exposure within the nephron

A

Glomerulus

50
Q

Glomerular Injury

Impair glomerular ultrafiltration without significant loss of structural integrity and decrease GFR

Drugs

A

Cyclosporine, Amphotericin B, Gentamicin

51
Q

Glomerular injury

↓GFR by renal vasoconstriction and ↓glomerular capillary ultrafiltration coefficient (Kf)

Specific Drug

A

Amphotericin B

52
Q

Glomerular injury

interacts with anionic sites on the endothelial cells → ↓GFR and Kf

Specific Drug

A

Gentamicin

53
Q

Glomerular injury

Renal vasoconstriction and vascular damage, injurious to the glomerular endothelial cell

Specific drug

A

Cyclosporine

54
Q

Proximal Tubular Injury

Most common site of toxicant-induced
renal injury

A

Proximal tubule

55
Q

Proximal Tubular Injury

(T/F) The proximal tubule has a tight epithelium, favoring the outflow of compounds outside proximal tubular cells

A

False. The proximal tubule has a leaky epithelium, favoring the flux of compounds into proximal tubular cells

56
Q

Proximal Tubular Injury

Localized primarily in proximal tubule

A

Organic anions, cations, low MW proteins and peptides, GSH conjugates, and heavy metals

57
Q

Loop of Henle / Distal Tubule / Collecting Duct Injury

These drugs induce an ADH resistant polyuria occurs at the level of the medullary thick ascending limb and /or the collecting duct.

A

Amphotericin B, Cisplatin, Methoxyflurane

58
Q

Loop of Henle / Distal Tubule / Collecting Duct Injury

Manifestation of functional abnormalities in distal nephron sites

A

Impaired concentrating ability and/or acidification defects

59
Q

Papillary injury

Susceptible to the chronic injurious effects of abusive consumption of analgesics

A

Renal papilla

60
Q

Papillary injury

Initial target of abusive consumption of analgesics

A

Medullary interstitial cells > Degenerative changes in capillary > Loops of Henle > Collecting ducts

61
Q

Site specific biomarkers

Thrombotic microangiopathy

A

Glomerulus/Kidney

62
Q

Site specific biomarkers

Collagen IV, Cystatin C, Total protein

A

Glomerular markers

63
Q

Site specific biomarkers

Calbindin d28, RPA-1

A

Collecting duct markers

64
Q

Site specific biomarkers

NHE3, Osteopontin

A

Loop of Henle markers

65
Q

Site specific biomarkers

Clusterin, H-FABP, NGAL, Osteopontin, pi-GST

A

Distal tubule markers

66
Q

Specific Nephrotoxicants

Heavy metals

A

Mercury, Cadmium

67
Q

Specific Nephrotoxicants

Characterized by proximal tubular necrosis and AKI within 24 to 48 hours after administration.

A

Mercury

HgCl2

68
Q

Specific Nephrotoxicants

Induce proximal tubule dysfunction (S1 and S2 segments) and injury that may progress to chronic interstitial nephritis

A

Cadmium

69
Q

Specific Nephrotoxicants

Proteinuria, glucosuria, ↑BUN levels

Inc. BUN = Chloroform induced nephrotoxicity

A

Chloroform

70
Q

Specific nephrotoxicants

Primary cellular target of chloroform

A

Proximal tubule

71
Q

Specific Nephrotoxicants

The products of the reaction are ammonia, pyruvate, and a reactive thiol that is capable of binding covalently to cellular macromolecules, causing cellular damage.

A

Tetrafluoroethylene

72
Q

Specific Nephrotoxicants

Penultimate nephrotoxicant (under TFE)

A

Cysteine S-conjugate

73
Q

Specific Nephrotoxicants

(T/F) Chloroform poses no primary damage to the glomerulus or distal tubule.

A

True

74
Q

Specific Nephrotoxicants

(T/F) Biotransformation of bromobenzene and other halogenated benzenes is critical for their nephrotoxicity.

A

True

75
Q

Specific Nephrotoxicants

Metabolizes bromobenzene and conjugates it to glutathione

A

Hepatic cytochrome P450

It is released it as a form that can cause nephrotoxicity

76
Q

Specific Nephrotoxicants

1000-fold more potent than bromobenzene

A

diglutathione conjugate of the hydroquinone

77
Q

Specific Nephrotoxicants

(T/F) Mycotoxins are products of bacteria and fungi

A

False. Molds and fungi.

Mycotoxins produce nephrotoxicity.

78
Q

Specific Nephrotoxicants

↓urine osmolality, GFR and RBF, glycosuria, ↑urinary enzyme exretion

A

Citrinin nephrotox

79
Q

Specific Nephrotoxicants

  • Found on corn and corn products
  • Nephrotoxicity in rats and rabbits (↑ urine volume, ↓osmolality, ↑ low and high MW proteins)
A

Fumonisins B1 and B2

80
Q

Specific Nephrotoxicants

Aristolachia and I genera

A

Aristolochic acids and aristolactams

(tubular dysfunction, proteinuria, interstitial fibrosis)

81
Q

Specific Nephrotoxicants

Upon a large dose of (answer), AKI may occur within hours; but reversible on withdrawal

Chronic consumption >3 years – irreversible nephrotoxicity (Analge

A

NSAIDs

such as Aspirin, Ibuprofen, Naproxen, Indomethacin,
celecoxib

82
Q

Specific Nephrotoxicants

Proximal tubular necrosis with increases in BUN and plasma creatinine, ↓ GFR, and clearance of para-aminohippurate

A

Acetaminophen

83
Q

Specific Nephrotoxicants

Characterized by non oliguric renal failure with ↓ GFR, ↑serum creatinine, and proteinuria

A

Aminoglycosides

84
Q

(T/F) The process that concentrates urine also serves to concentrate potential toxicants in the tubular fluid.

A

True

85
Q

(T/F) Toxicants may also cause mitochondrial dysfunction via compromised respiration and ATP prod; leading to apoptosis or necrosis

A

True

PHA6131, 6133 3RD SHIFT (7 decks)

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