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Year 1/2 > Elimination & Detox 2: Nephrotoxins > Flashcards

Elimination & Detox 2: Nephrotoxins Flashcards

1
Q

2 UNIQUE functions of the kidneys?

A
  1. VITAMIN D SYNTHESIS
  2. BP REGULATION
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2
Q

TOXICANTS are more likely to cause RENAL INJURY because… (2)

A
  1. KIDNEY TAKES 25% OF ALL CO, so EXPOSED to a HIGH AMOUNT OF BLOOD FLOW
  2. some toxicants can CONCENTRATE in URINE or TUBULE EPITHELIUM than the rest of the body
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3
Q

give 3 drugs that can ALTER RENAL BLOOD FLOW/GFR

A
  1. NSAIDs
  2. ACE-INHIBITORS
  3. DIURETICS
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4
Q

if AKI develops, what 3 interventions should we administer?

what should we BE WARY OF? how should we handle it? (2)

A
  1. IV fluids
  2. anti-emetics
  3. early NUTRITIONAL support

BEWARE OVERHYDRATION;

  1. patients with AKI can have VARIABLE URINE OUTPUT, so if they become OLIGURIC or ANURIC then MULTIORGAN DAMAGE IS LIKELY
  2. if URINE OUTPUT DECREASES = DECREASE or STOP IV FLUIDS
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5
Q

what is the MOST COMMON TOXICANT in SMALL ANIMAL MEDICINE?

A

NSAIDs!

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6
Q

how do NSAIDs STOP PAIN?

what are the 3 ORGANIS that they can IMPACT? how?

what 2 OTHER THINGS can occur with NSAID OVERDOSE?

A

they INHIBIT COX-1 & COX-2, which then INHIBITS PRODUCTION OF PROSTAGLANDINS, PROSTACYCLIN & THROMBOXANE A2

4 organs?
1. GI TRACT = PROSTAGLANDINS are INHIBITED by NSAIDs, and they help REGULATE PRODUCTION OF GASTRIC ACID, BICARB & MUCOUS
–> NSAIDs can lead to GI ULCERS!

  1. KIDNEYS = PROSTAGLANDINS usually help cause GLOMERULAR VASODILATION, so NSAIDs can cause TUBULAR NECROSIS & AKI
  2. PLATELETS = THROMBOXANE A2 helps PLATELET AGGREGATION, so WITHOUT IT w/ NSAIDs CAN CAUSE GI BLEED/THROMBOPATHIA

ACUTE LIVER INJURY & CNS SIGNS can also occur with NSAID OVERDOSE

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7
Q

DECONTAMINATION in NSAID TOXICITY

we should start with ___ INDUCTION or ___ ___ if appropriate (quickly enough)

what 2 other things should we start with?

if an animal has ingested a LIFE-THREATENING OVERDOSE, consider WHAT intervention? why?

A

we should start with EMESIS INDUCTION or GASTRIC LAVAGE if appropriate (quickly enough)

2 other things?
1. ACTIVATED CHARCOAL to ABSORB WHATEVER IS STILL IN GI TRACT
2. IV LIPID EMULSION = NSAIDs are often LIPID-SOLUBLE, so we can EMULSIFY/BREAK IT DOWN

if LIFE-THREATENING OVERDOSE, consider EXTRACORPOREAL BLOOD PURIFICATION via HEMOPERFUSION or THERAPEUTIC PLASMA EXCHANGE
–> THROWING OUT NSAID & replacing with DONOR PLASMA

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8
Q

NSAID toxicity…

we should monitor WHAT 2 kinds of organ values?

4 other options for MEDICAL TREATMENT? 2 are +/-

A

MONITOR HEPATIC & RENAL VALUES

MEDICAL tx?
1. GASTROPROTECTANTS
–> MISOPROSTOL (PGE analog)
–> ANTACIDS like FAMOTIDINE
–> SUCRALFATE to BIND & PROTECT ulcers

  1. IV FLUIDS to MAINTAIN EUHYDRATION & RENAL PERFUSION, but caution with OVERHYDRATION
  2. +/- HEPATOPROTECTANTS
  3. +/- DIURETICS if OLIGURIA develops
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9
Q

ETHYLENE GLYCOL…

what is the MOST COMMON kind of EXPOSURE?

this substance is ALSO found in what other 4 things?

METABOLISM of ETHYLENE GLYCOL occurs PRIMARILY in the ___ within ___-____ ____ of INGESTION

pathophysiology (4)

the LETHAL DOSE is..

A

MOST COMMON EXPOSURE = ANTIFREEZE

this substance is ALSO FOUND IN…
1. SOLVENTS
2. DEICERS
3. STAINS
4. PHOTOGRAPHY DEVELOPING SOLUTIONS

METABOLISM of ETHYLENE GLYCOL occurs PRIMARILY in the LIVER within 2-4 HOURS of INGESTION

pathophysiology?
1. ETHYLENE GLYCOL gets converted to GLYCOALDEHYDE by ALCOHOL DEHYDROGENASE

  1. eventually, forms OXALIC ACID
  2. OXALIC ACID will COMPLEX WITH CALCIUM to form CALCIUM OXALATE STONES
  3. CALCIUM OXALATE STONES will cause TUBULAR OBSTRUCTION & NEPHROTOXICITY

the LETHAL DOSE is NOT MUCH

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10
Q

CLINICAL STAGES of ETHYLENE GLYCOL POISONING (3)

give TIMING post-ingestion, clinical signs

which stage DOES NOT ALWAYS OCCUR?

A
  1. STAGE 1 = 30 MINS to 12 HOURS POST-INGESTION
    –> V+
    –> PU/PD
    –> CNS depression
    –> ataxia
  2. +/- STAGE 2 = 12 to 24 HOURS POST-INGESTION
    –> CNS signs MIGHT IMPROVE SLIGHTLY
    –> “FALSE RECOVERY” but even though this doesn’t always happen, MORE COMMON IN DOGS
  3. STAGE 3 = 12 to 36 HOURS POST-INGESTION
    –> OLIGURIC to ANURIC AKI
    –> severe DEPRESSION
    –> SWOLLEN & PAINFUL KIDNEYS
    –> ANOREXIA
    –> SEIZURES
    –> COMA/DEATH
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11
Q

what are the BEST 3 DIAGNOSTIC PARAMETERS we can use for ETHYLENE GLYCOL POISONING?

& include WHY we see them

A
  1. HIGH ANION GAP METABOLIC ACIDOSIS = from GLYCOLIC ACID, GLYOXYLIC ACID & OXALIC ACID
    –> noticed at 3 HOURS, PEAKS at 6 HOURS, can stay UP TO 48 HOURS
  2. ISOSTHENURIA, HYPOCALCEMIA & CALCIUM OXALATE CRYSTALLURIA within 3 HOURS post-ingestion
  3. AZOTEMIA around 12-24 HOURS POST-INGESTION
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12
Q

in ETHYLENE GLYCOL POISONING, when does HIGH ANION GAP METABOLIC ACIDOSIS…

BECOME noticeable?

PEAK?

how LONG can it stay increased?

A

NOTICED WITHIN 3 HOURS post-ingestion

PEAKS at 6 HOURS post-ingestion

can REMAIN INCREASED for 48 HOURS

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13
Q

can we use ACTIVATED CHARCOAL for ETHYLENE GLYCOL?

A

NO!

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14
Q

3 TREATMENTS for ETHYLENE GLYCOL POISONING?

include WHEN they’re effective, what they can do

A
  1. FOMEPIZOLE = EFFECTIVE if given WITHIN FIRST 8 HOURS
    –> INHIBITS ALCOHOL DEHYDROGENASE from converting ETHYLENE GLYCOL into GLYCOALDEHYDE
  2. ETHANOL (GRAIN ALCOHOL) = EFFECTIVE if given WITHIN FIRST 8 HOURS
    –> has HIGHER AFFINITY FOR ALCOHOL DEHYDROGENASE than ETHYLENE GLYCOL
    –> EASILY AVAILABLE
  3. HEMODIALYSIS = usually WITHIN HOURS OF EXPOSURE
    –> helps REMOVE EG & METABOLITES to try and PREVENT AKI
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15
Q

why might giving FOMEPIZOLE for ETHYLENE GLYCOL POISONING in a CAT be CONTRAINDICATED? (2)

A
  1. CATS NEED A MUCH HIGHER DOSE > DOGS
  2. EXPENSIVE MEDICATION
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16
Q

GRAPES & RAISINS TOXICITY…

what is the PROPOSED method of action of toxicity?

dose-response relationship?

A

method of action? = TARTARIC ACID causes ACUTE PROXIMAL TUBULAR NECROSIS, CASTS & TUBULAR OBSTRUCTION

NO DEFINITIVE DOSE-RESPONSE RELATIONSHIP

17
Q

if an animal RECOVERS from an AKI, WHAT is likely to REGENERATE?

A

EPITHELIAL CELLS LIKELY TO REGENERATE IF THEY’VE NECROSED

18
Q

4 steps for TREATMENT of GRAPES & RAISINS?

one is +/-

A
  1. EARLY DECONTAMINATION via EMESIS +/- ACTIVATED CHARCOAL (if 8-12 hours post)
  2. IV FLUID THERAPY for MINIMUM of 48 HOURS
  3. SERIALLY MONITOR SERUM CHEM VALUES & URINE OUTPUT for 48 HOURS
  4. +/- DIURETIC if OLIGURIA DEVELOPS, may also need DIALYSIS
19
Q

LILY TOXICITY…

ALL ___ of ____ genera and ____ genera are considered ____ to ____

EVERY ___ of the ____ are ____, even the ____

what do we see on HISTOPATH?

A

ALL SPECIES of LILIUM genera and HEMEROCALIS genera are considered NEPHROTOXIC to CATS

EVERY PART of the LILY are TOXIC, even the POLLEN

on HISTOPATH = WIDESPREAD DEGENERATION & NECROSIS of PROXIMAL TUBULE EPITHELIAL CELLS

20
Q

LILY TOXICITY…

WHEN do clinical signs usually occur?

2 EARLY clinical signs?

what 3 DANGEROUS clinical signs can occur & when?

A

clinical signs usually seen WITHIN 6-12 HOURS AFTER EXPOSURE

2 EARLY clinical signs?
1. V+
2. LETHARGY

3 DANGEROUS clinical signs?
1. AKI usually within 24-48 HOURS, usually first POLYURIC than OLIGURIC/ANURIC

  1. SEIZURES
  2. DEATH can occur 3-7 DAYS POST-INGESTION
21
Q

4 steps for TREATMENT in LILY TOXICITY?

one is +/-

OVERALL, if the patient is NOT ___/there’s NO SIGNS OF ____ by ___-___ ____, they’ll….

A
  1. EARLY DECONTAMINATION via EMESIS +/- ACTIVATED CHARCOAL; BATHE if exposed to POLLEN
  2. IV FLUID THERAPY for MINIMUM 48 HOURS
  3. SERIALLY MONITOR SERUM CHEM VALUES (baseline, 24 & 48 hours) and URINE OUTPUT
  4. +/- DIURETIC if OLIGURIA develops, may need DIALYSIS

OVERALL, if the patient is NOT AZOTEMIC/there’s NO SIGNS OF AKI by 24-48 HOURS, they’ll LIKELY BE OK

22
Q

what is the MOST IMPORTANT intervention we can do to PREVENT AKI from LILY TOXICITY in CATS?

A

EARLY DECONTAMINATION (EMESIS +/- ACTIVATED CHARCOAL) & SUPPORTIVE CARE

23
Q

RED MAPLE LEAF TOXICITY…

aka?

toxicity is reported in what 3 SPECIES?

most commonly occurs WHEN? why?

A

aka = ACER RUBRUM

3 species?
1. HORSES
2. ALPACAS
3. ZEBRAS

most commonly occurs in FALL when LEAVES FALL or LESS FOOD AVAILABLE

24
Q

RED MAPLE LEAF TOXICITY…

pathophysiology? (4)

what 4 other CLINICAL SIGNS can be seen?

A

pathophysiology?
1. LEAVES are METABOLIZED by INTESTINAL BACTERIA & produce TANNINS

  1. TANNINS broken down into GALLIC ACID & PYROGALLOL
  2. these products then cause OXIDATIVE INJURY to RBCs & Hb, causing INTRA/EXTRAVASCULAR HEMOLYSIS & METHEMOGLOBINEMIA
  3. can lead to RENAL HYPOXIA and AKI

what 4 other signs?
1. FEVER
2. GENERALIZED ICTERUS
3. COLIC
4. LAMINITIS

25
Q

5 TREATMENT OPTIONS for RED MAPLE LEAF TOXICITY?

which medication is CONTRAINDICATED?

A
  1. IV FLUID THERAPY
  2. ASCORBIC ACID (vitamin C) for ANTIOXIDANT (prevent OXIDATIVE injury)
  3. NSAIDs to REDUCE INFLAMMATION
  4. ANALGESIA like BUTORPHANOL
  5. LAMINITIS PREVENTION via DIGITAL CRYOTHERAPY

CORTICOSTEROIDS CONTRAINDICATED

26
Q

CHOLECALCIFEROL (VITAMIN D) TOXICITY…

this is found in what 3 items?

what NET EFFECT DOES IT CAUSE & HOW? (4)

A

found in….
1. RODENTICIDES
2. VITAMINS
3. PSORIASIS CREAMS

NET EFFECT = HYPERCALCEMIA & HYPERPHOSPHATEMIA

  1. CHOLECALCIFEROL converted to CALCITRIOL in KIDNEY
  2. CALCITRIOL stimulates ENTEROCYTES to make CALBINDIN
  3. CALBINDIN INCREASES GI ABSORPTION of Ca & P from DIET
  4. increases RENAL Ca & P RESORPTION in DISTAL TUBULES
27
Q

CHOLECALCIFEROL TOXICITY…

when is there a RISK for SOFT TISSUE MINERALIZATION?

A

Ca x Phos > 70

28
Q

6 CLINICAL SIGNS of CHOLECALCIFEROL TOXICITY?

WHEN do clinical signs usually occur? (range)

what is the MOST COMMON CLINICAL SIGN? why?

A

CLINICAL SIGNS?
1. WEAKNESS/DEPRESSION
2. ANOREXIA
3. PU/PD
4. V+
5. D+
6. AKI

clinic signs usually seen WITHIN 12-18 HOURS AFTER EXPOSURE

MOST COMMON clinical sign is PU/PD because CALCIUM fights for ADH RECEPTORS on COLLECTING DUCT & causes MORE DIURESIS

29
Q

WHAT is the most IMPORTANT PREVENTION we can take to PREVENT AKI secondary to CHOLECALCIFEROL TOXICITY?

describe both the BIOCHEMICAL process (2) & WHAT WE DO IN PRACTICE (2)

A

BIOCHEMICALLY?
1. we need to DECREASE SERUM CALCIUM to PREVENT AKI
2. using SALINE, COMPETITION from SODIUM causes REDUCED RENAL CALCIUM RESORPTION & CALCIURESIS

IN PRACTICE?
1. IV FLUID THERAPY via 0.9% NaCl (SALINE)
2. correct DEHYDRATION over 4-6 HOURS

30
Q

what DRUG of choice is best for CHOLECALCIFEROL TOXICITY?

what must be ACHIEVED IN PATIENT FIRST before starting it? why?

what SIMILAR type of medication is CONTRAINDICATED?

A

DRUG of choice = FUROSEMIDE (diuretic)

BEFORE starting diuretics, PATIENT MUST HAVE EUHYDRATION because DEHYDRATION could cause an AKI!

NO THIAZIDE DIURETICS

31
Q

GCCs for CHOLECALCIFEROL TOXICITY…

mechanism of action? (2)

2 SPECIFIC drugs we could give?

when should we NOT use this medication/why?

A

mechanism of action?
1. REDUCES OSTEOCLASTIC BONE RESORPTION & GI ABSORPTION of CALCIUM
2. PROMOTES CALCIURESIS

2 SPECIFIC drugs?
1. DEXAMETHASONE
2. PREDNISONE

we should NOT use GCCs if WORRIED ABOUT LYMPHOMA because it could INHIBIT ITS DIAGNOSIS

32
Q

BISPHOSPHONATE…

used to treat WHAT toxicity?

mechanism of action?

how LONG to TAKE EFFECT? how long does EFFECT LAST?

A

used to treat CHOLECALCIFEROL TOXICITY

mechanism of action? = INHIBITS OSTEOCLASTIC BONE RESORPTION

takes 1-2 DAYS to TAKE EFFECT but CAN LAST UP TO 8 DAYS

33
Q

SYNTHETIC SALMON CALCITONIN…

used to treat WHAT toxicity?

why might this NOT be our first go-to treatment? when IS IT usually used?

A

used to treat CHOLECALCIFEROL TOXICITY

EXPENSIVE & EFFECTS are SHORT-LIVED, but can BE A GOOD OPTION if NOTHING ELSE WORKS

34
Q

CHOLECALCIFEROL TOXICITY

DURATION of…
–> hospital stay?
–> at-home MAINTENANCE therapy? what 2 medications are included? what 1 lifestyle change?

if the patient was HYPER____, what ADDITIONAL medication do they need?

A

DURATION of…
–> hospital stay = DAYS to WEEKS
–> at-home MAINTENANCE therapy = 3-4 WEEKS with ORAL FUROSEMIDE & PREDNISONE with LOW Ca DIET

if patient was HYPERPHOSPHATEMIC, might need ALUMINUM HYDROXIDE (PHOSPHORUS BINDERS)

Year 1/2 (139 decks)

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