Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal Exam > Renal Toxicology > Flashcards

Renal Toxicology Flashcards

1
Q

why is the kidney so susceptible to toxic injury?

A

*receives 20-25% of the cardiac output, but only <1% of total body mass
*metabolically active
*concentrates xenobiotics
*susceptible to immune-mediated attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

causes of nephrotoxicity

A
  1. toxic syndromes:
    -acute renal failure (prerenal, postrenal, intrinsic [ATN, acute interstitial nephritis])
    -chronic renal failure
    -nephrotic syndrome
  2. functional toxic disorders:
    -renal tubular acidosis
    -nephrogenic diabetes insipidus
    -SIADH
  3. acid base disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

toluene

A

*aromatic hydrocarbon
*inhalant abuse (“sniffing”) - paints, lacquer thinners, glue
*inhalation causes:
-CNS alteration
-cardiac effects
-Type 1 RTA with profound hypokalemia
~typically with chronic abuse
~inability of the distal nephron to lower urine pH
~hyperchloremic metabolic acidosis, hypokalemia, urine pH > 5.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

distal renal tubular acidosis (RTA type 1) - defect

A

*inability of alpha-intercalated cells to secrete H+ → no new HCO3- generated → metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

distal renal tubular acidosis (RTA type 1) - urine pH

A

> 5.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

distal renal tubular acidosis (RTA type 1) - serum K+

A

*DECREASED (hypokalemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

distal renal tubular acidosis (RTA type 1) - causes

A

*amphotericin B toxicity
*analgesic nephropathy
*congenital anomalies (obstruction) of urinary tract
*autoimmune diseases (ex. SLE)
*chronic TOLUENE INHALATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

distal renal tubular acidosis (RTA type 1) - associations

A

*increased risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover related to buffering)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

proximal renal tubular acidosis (RTA type 2) - defect

A

*defect in PCT HCO3- reabsorption → increased excretion of HCO3- in urine → metabolic acidosis
*urine can be acidified by alpha-intercalated cells in collecting duct, but not enough to overcome increased bicarb excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

proximal renal tubular acidosis (RTA type 2) - urine pH

A

< 5.5 when plasma HCO3- below reduced resorption threshold
> 5.5 when filtered HCO3- exceeds resorptive threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

proximal renal tubular acidosis (RTA type 2) - serum K+

A

DECREASED (hypokalemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

proximal renal tubular acidosis (RTA type 2) - causes

A

*Fanconi syndrome
*multiple myeloma
*carbonic anhydrase inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

proximal renal tubular acidosis (RTA type 2) - associations

A

*increased risk for hypophosphatemic rickets (in Fanconi syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

hyperkalemic tubular acidosis (RTA type 4) - defect

A

*hypoaldosteronism or aldosterone resistance
*hyperkalemia → decreased NH3 synthesis in PCT → decreased NH4+ excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hyperkalemic tubular acidosis (RTA type 4) - urine pH

A

< 5.5 (or variable)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

hyperkalemic tubular acidosis (RTA type 4) - serum K+

A

INCREASED (hyperkalemic)

17
Q

hyperkalemic tubular acidosis (RTA type 4) - causes

A

*decreased aldosterone production (diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency)
*aldosterone resistance (K+ sparing diuretics, nephropathy due to obstruction, TMP-SMX)

18
Q

CAT MUDPILES mnemonic for anion gap metabolic acidosis

A

Cyanide or carbon monoxide
Acetaminophen (massive), aspirin, or alcoholic ketoacidosis
Toluene
Methanol, metformin, or massive overdoses
Uremia
Diabetic ketoacidosis
Paraldehyde or propylene glycol
Iron, isoniazid, or ibuprofen (massive)
Lactic acidosis
Ethylene glycol
Salicylates

19
Q

ingestion of antifreeze causes which type of anion gap metabolic acidosis

A

*antifreeze = ethylene glycol

20
Q

toxic alcohols & sources

A

*ethylene glycol (antifreeze)
*methanol (windshield washer fluid)
*diethylene glycol (solvent)
*propylene glycol (solvent)

21
Q

clinical features of toxic alcohols

A

*inebriation / altered levels of consciousness
*profound metabolic acidosis

22
Q

treatment for toxic alcohol ingestion

A

*inhibition of alcohol dehydrogenase (fomepizole)

23
Q

ethylene glycol poisoning

A

*most prominent end-order effect = nephrotoxicity
*oxalic acid metabolite complexes with calcium to form calcium oxalate; precipitates in the renal tubules
*intermediate products of metabolism are directly toxic to renal tubules (ATN) as a secondary mechanism

24
Q

ethylene glycol poisoning - microscopic urinalysis

A

*may reveal crystals:
1. calcium oxalate monohydrate: spindle-shaped
2. calcium oxalate dihydrate: envelope-shaped

25
Q

diethylene glycol

A

*clear, colorless, mildly sweet liquid
*efficient solvent for water-insoluble active ingredients in medications
*poisoning commonly results in acute renal failure (metabolite 2-hydroxyethoxyacetic acid thought to be responsible)

26
Q

salicylate poisoning - acid-base disorder

A

*MIXED respiratory alkalosis with metabolic acidosis
-respiratory alkalosis prominent in early or mild poisoning
-metabolic acidosis: uncoupling of oxidative phosphorylation, ketoacids from fatty acid metabolism, salicylic acid

27
Q

salicylate poisoning - renal effects

A

*loss of prostaglandin-mediated compensatory mechanisms to maintain renal blood flow

28
Q

salicylate poisoning - management

A

*treat based on clinical symptoms, acidosis, and salicylate levels
*serum and urine alkalinization:
-sodium bicarbonate infusion
-urine alkalinization enhances elimination of salicylic acid
-important to monitor potassium during treatment with sodium bicarbonate
*hemodialysis if significant poisoning or renal failure

29
Q

MDMA (molly)

A

*3,4-methylenedioxymethamphetamine
*common street name = ecstasy
*enactogen:
-“touching within”
-euphoria, inner peace, desire to socialize
-ataxia, restlessness, confusion, poor concentration, memory problems

30
Q

MDMA - renal effects

A

*causes an SIADH:
-can cause profound HYPONATREMIA
-increased release of vasopressin (ADH)
-often in association with large free-water intake and sodium loss from physical exertion
-clinical presentation: altered mental status + seizures

31
Q

lithium

A

*used for treatment of bipolar disorder
*eliminated almost entirely by the kidneys:
-handled like sodium
->60% reabsorbed at the proximal tubule
-any condition that makes the kidney sodium-avid increases lithium reabsorption (ex. volume depletion, salt restriction)
-narrow therapeutic index

32
Q

lithium toxicity - clinical manifestations

A

*GI symptoms: nausea, vomiting, diarrhea
*CNS effects: tremor, hyperreflexia, choreathetoid movements, clonus, dysarthria, nystagmus, ataxia
*NEPHROGENIC DIABETES INSIPIDUS:
-most common adverse event of chronic therapy
-causes HYPERNATREMIA

33
Q

lithium toxicity - renal effects

A

*nephrogenic diabetes insipidus:
-lithium enters collecting tubular cells via Na+ channel
-downregulates aquaporin-2 channels
-results in HYPERnatremia

Renal Exam (44 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions