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TXP: Pulm/ Tox. And Rheumatology > Week 6: Toxicology Part II > Flashcards

Week 6: Toxicology Part II Flashcards

1
Q

cannabinoid types

A

compounds that bind to and agonize the cannabinoid receptors
*phytocannabinoids
*synthetic cannabinoids
*endocannabinoids

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2
Q

what is the main component of marijuana that is responsible for the major psychoactive effects

A

THC

*mood elevation, euphoria, relaxation, creative thinking, and increased sensory awareness

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3
Q

cannabinoid receptors

A

CB1: high levels in the brain regions expected from psychoactive effects
*lack of coma and respiratory depression seen w. cannabis use

CB2: high levels expressed in periphery
*expressed on a number of immune cells
*isolated agonism of CB2 receptors has been the target for novel pharmaceutical candiates as anti-inflammatory agents

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4
Q

ex of medical conditions claim to be treated by marijuana

A

anorexia

anxiety

asthma

depression

epilepsy

glaucoma

head injury

insomnia

migraine headaches

multiple sclerosis

muscle spaciity and spasms

nausea and vomiting

neurologic disorders

pain

parkisons disase

tourette syndrome

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5
Q

cannabis plant parts

A

Hemp:
*cbd oil, hemp oil, cannabis oil (made form industrial hemp)
* contains 0.3% THC

Marijuana
*thc oil, marijuana oil, cannabis oil (made from marijuana plant)
contains 10% THC

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6
Q

wanted clinical effects of phytcannabinoids

A

mood elevation

euphoria

relxation

creative thinkning

increased sensory awareness

appetite stimuation

nausea supression

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7
Q

unwanted clinical effects of phytocannabinoids

A

short term memory difficulties

agitation

feeling tense

anxiety

dizziness

lightheadedness

confusion

loss of coodination

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8
Q

synthetic cannabinoids

A

thc is a partial agoinst at cb1 RECEPTOR
*EX: ab-chiminaca
*amb-FUBINACA

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9
Q

differences in cannabinoids

A

thc is a partial agonist at cb1

synthetic cannabinoids are full agoinsts
*higher receptor affinity
*longer half lives

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10
Q

desired clinical effects of synthetic cannabinoids

A

mood elevation

euphoria

relaxation

creative thinking

increased sensory awareness

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11
Q

clinical presenttion of synthetic canabinoid poisoning

SS:

Lab abnormalities

A

SS:
cns depression
disorientation
restlessness/agitation
hallucinations
seizures, generalized
conbativeness
anxiety
mydriasis
tachycardia
vomitingss

lab abnormalities:
*dec. K+
increased blood glucose
inc. creatinine kinase
inc. white bloos cells
inc. creatinine

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12
Q

management of synthetic cannabinoids

A

supportive, symptomatic care
*fluid electrolyte replacement
*antiemetics
*benzos
*ketamine
*intubation

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13
Q

Cannabinoid hyperemesis syndrome

patho

dx

A

patho: dysregulation of endocannabinoid system
*desensitization and downregulation of cb1 receptors that generally have antiemetic effects
*alteration in TRPV1 receptor after chronic cannabinoid use

dx:
hx of reg cannabinoid use
*cyclic N/V
*generalized diffuse abdominal pain
*compulsive hot showers w. symptom imrpovement

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14
Q

phases of CHS

preemetic/prodromal phase

A

pre metic /prodromal phase
*months-years
*diffuse abdom. disocmfort, feelings or agitation or stress, morning nausea, and fear of vomitinf

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15
Q

phases of CHS

hyperemetic phase

A

hyperemtic phase

*24-48 hrs
*cyclic episodes of N/V
*diffuse, severe abdom pain

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16
Q

phases of chs

recovery phase

A

upon total cessation of cannabis
bowel regimens, fluids , electrolyte replacement
full resolution may take ~ 1month

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17
Q

CHS management

A

clnical management;
* hot showers (activate trpv1)
*CAPSAIcin topical cream (activate trpv1
antinausea:
*haloperidol, ondansetron
*HaVOC trial found haloperidol was superior to ondansetron for improvement of N and abdom pain of 120 min
benzos:
*inhibitoy effects on medulary and vestibular nuclei associated w. n/v
supportive care:
*fluids and electrolytes

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18
Q

Sympathomimetic

A

inhibtion of norepineprine and dopamine reuptake, or increased release of neurotransmitters

“uppers”

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19
Q

adrenorecptor activation effects

A

a1:
*vasoconstriction
*inc peripheral resistance
*mydriasis
*inc closure of internal bladder sphincter

a2:
inhibitoin of norepinephrine relase
*inhibition of catecholamine release
*inhibition of insulin release

b1:
*tachycardia
*increased lipolysis
*increased myocardial contractility
*increased release of renin

b2:
*vasodilation
*decreased peripheral resistance
*bronchodilation
*increased muscle and liver glycogenolysis
*increased release of glucagon
*relaxed uterine smooth muscle

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20
Q

sympathomimetic toxidrome

A

inc vitals (bp, hr, rr, temp)
mental sttaus: agitated, hyperalert
pupil size: increases
bowel sounds: increased
diaphoresis: increased
other: tremor, seizures

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21
Q

general management of sympathomimetic toxirome

A

SUPPORTIVE CARE!

elmimination strategies (i.e activated charcoal)

benzos
anti-hypertensives
fluids
antipsychotics
electrolyte management
ice baths
sodium bicarb

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22
Q

substances that can cause sympathimometic toxidromes

A

cocaine
amphetamines
bath salts
pseudoephedrine
nootropics
buproprion
psuedoephedrine

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23
Q

cocaine

A

toxic dose: typical line=20-30 mg
*ingestion of 1 g is likely to be ftal

SS: euphoria, seizures, dysrhthmias, htn
CORNOARY ARTERY SPASM/mi

adulterants (laced w.)
*levimasole (antiparasitic agent): can cause neutropenia, vasculitis, urpura

management:
*benzos, supportive care

notes:
*be aware of body packers.

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24
Q

amphetamines

A

moa:release catecholamines

SS: adrenergic: similar to cocaine though longer lasting
*agitation, seizures, hyperhermia, htn, delerium

management: benzos,barbiturates, anti-HTN
*supportive care

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25
Q

Bath Salts

A

synthetic cathinones
ex: cathinone, methcathinone, mephedrome, methylone, MDPV

SS:
agitation, tachycardia, insomnia, paranoia, seizures, violen unpredictable behavior

Management: supportive care

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26
Q

buproprion and pseudoephedrien

A

have similar chemicalstructure to epinephrine or amphetamines, so when overdosed, can exibit sympathomimetic toxidromes

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27
Q

supportive care for sympathomimetic toxidrome

A

clinical effects: benzos
airway protection: intubation
hyperthermia: ice packs, cool fluids, antipyretics, benzos
dysrhythmias: sodium bicarb, lidocaine
rhabdomyolysis: fluids

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28
Q

where can salicylates be found

A

aspirin

methyl salicylate (oil of wintergreen)

topical salicylates

bismuth subsalicylate (peptobismol)
1ml=8.7 mg of Salicylic acid

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29
Q

epidemiology of salicylate exposure

A

ranked first amoung pharmaceuticals most frequently reported in human exposure

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30
Q

PK of aspirin

A

A: rapidly bsorped in non ionized form due to acidic ph

D: small Vd (-0.2L/kg) and highly protein bound

M: metabolized by liver. hydrolized to salicylic acid

E: excretes renally
t1/2 at low doses (antiplatelet effects)=2-3 hrs
t1/2 at high doses (anti-inflammatory)= 12 hours

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31
Q

toxicokinetics of aspirin

A

delayed absorption due to pylorospasm and bezoar formation in the stomach (immediate release stomach)

peak ocnc may not be seen until 24-36 hrs after ingestion w. enteric coated products

decreased protein binding and larger vd
*higher conc and low pH
*larger amounts of free drugs reach the tissue

prolonges t1/2 due to hepatic metabolism saturation saturation
*elmimnatino changes from irstorder kinetics tozero order kinetics

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32
Q

patho of SA overdose

A

serum ph faks and SA acid shifts to a nonioned state than can readily cross lipid bilayers and cell membranes effecting s variety of organs

krebs cycle inhibition impairs cellular respiration and uncoupling of oxidative phosphorylation leading to accumulation of pyurivc and lactic acid release of energy as heat

Acid base disturbances
*depend on time from exposure
*anion gap metabolic acidosis from presence of SA, production of lactate, ketones, and inorganic acids

neurologic; neuronal dysfunction causing cerebral edema
*discordance btw serum and cfs glucose

ototoxicity and tinnitus

hematologic
*plaelet dysfunction and hypoprothombinemia

pulmonary
*stimualte resp. driving causing hyperpnea and tachypnea
*acutre resp. distress syndrome (ARDS)

GI
*N/V

Renal
*prerenal AKi due to volume losses
8excrete large quantities of bicard, Na, and K

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33
Q

Acute toxicity of SA Signs and symptoms

A

n/v
gi irritation
tinnitus
tachypnea,hyperpnea
resp alkalosis or resp acidosiss
metabolic acidosis(anion gap or non-anion gap)
altered mental status/halucinations
coma
seizures
hyperglycemia or hypoglycemia (neuroglycopenia)
pulmonary edema
hepatic injury

HUGE CONSEQUENCES
*coagulopathy
*cerebral edema
*acure resp distress syndrome (ARDS)
*hyperthermia

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34
Q

acid base abnormality stages of ASA overdose

A

early: primary resp alkalosis, alkalemia, alkauria

intermediate: mixed resp alkalosis and anion gap metabolic acidosis, alkalemia, and aciduria

late: metabolic acidosis w. either a resp alkalosis or resp acidossi, acidemia, and aciduria

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35
Q

chronic toxicity of ASA

A

non specific and often misiagnosed

severe toxicity is associated w. serum conc.>60 mg/dl, altered mental sttaus, and acid base disturbances

cerbral edema and acutelung injury may be present

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36
Q

Acute vs chronic ASA toxicity

A

acute:
*younger
*intentional
*early dx
*suicial ideation
*severely elevated serum conc
*death is uncommen

chornic
*older
*Iatrogenic/unintentional
*underrecognized as a dx
*intermediate elevation in serum conc
*death is more common due to delayed recognition

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37
Q

evaluation and dx of asa testing

A
  1. serum salicylate level
    *toxiicty associated w. conc >30 mg/dL
    *THEREPEUTIC RANGE (INFLAMMATORY CONDITIONS(15-30g/dL)
    *therepeutic range for analgesia (5-10 mg/dL)

acute toxicity
*mild symptoms seen in 150-200 mg/kg or 6.5 g of spirin
*severe symptoms>300-500 mg/kg

chronic toxicity>100 mg/kg/day for several days

  1. blood gas and anion gapto classify acid-base disorder
38
Q

general treatment of ASA toxicity

A

no true antidote:

tratment based on supportive therapies
1. GI decontamination
2. IV fluids
3. glucose amdinisistration

39
Q

Supportive therapies for asa toxicity

A
  1. multiple-dose activated charcoal(MDAC)
    *prevents absoprtion of salicyates, can consider if pharmcobezoar or XR preparation suspected

2.hypovolemia should be corrected w. iv crystalloids

3.0.5-1g/kg of dextrose followed by additional bolus doses or continuous infusion for severe salicylate toxicity

40
Q

Serum and Urine Alkalization

A

cornerstone of management for ASA toxicity.
shifts ASA out of brain and intro the serum to promote renal elimination

ion trapping of salicylate into serum and urine by alkalination. promotes excretion once ionized.

iv sodium bicarb is recommended for all symptomatic pts
*bolus dose: 1-2mEq/kg
continuous in fusion: 150mEq sodium biacrb in 1000mL of 5% dextrose at a rate of 1.5-2x maintenance rate
*goal urine pH 7.5-8
maintain normal K+ levels (due to shifts of K+ into intracellular space by admin of sodium bicarb)

41
Q

hemodialysis in sa toxicity

A

can be considerd in severe toxicity and is recommended in the following ocnditions

*serum salicylate level >100 mg/dL
*serum salicylate level>90 w. impaired renal function OR failure of supportive therapies

serum salicylate level >80 w. imapired renal function AND failure of supportive therapies

supplemental o2 required due to altered mental status form hypoxemia

d/c HD when serum salicylate level is <19 mg/dL and pt is clinically improving

42
Q

monitoring during treatment of SA

A

serum salicylate conc q2-4 hrs until pt is improving clinically

urine pH

serum pH

more frequent monitoring may be needed in critically ill patients

43
Q

epedemiology of alcohol poisoning

A

methanol containing consumer products
*windshield wiper fuid (>60% of cases)

ethylene glycol
*engine coolant (antifreeze) in car radiators. it has sweet taste, but bittering agents have been added

isopropanol
*rubbing alcohol
*solvent used in household products, cosmetics, and topical pharmaceuticals

44
Q

toxic alcohols =not intended for ingestion

A

primary alcohols
*methanol
*ethylene glycol

secondary alcohols
*isopropanol

45
Q

toxicokinetics of toxic alcohols

A

A:
ingestion: rapidly absorpbed. F=92-100%
inhalation: occupational or intentional inhalation of methanol (huffing)
athylene glycol inhalation does not cause poisoning
transdermal: isopropanol and methanol penetrate skin better than EG

D: rapidly to total body water
0.5-0.77L/kg

Metab and elminiation:
(alcohol dehydrogenous and/or aledhyde dehydgrogenase (ALDH) couples to the reduction of NAD+ to NADH
*EG is eliminated via kidney unchanged
*methanol eliminated as vapor in expired air

46
Q

toxic metabokites of toxic alcohols

A

methanol: formic acid formed by conversion by alcohol dehydrogenase and then aldehyde dehydrogenase
*formic acid causes metabolic acidosis w. minimally elevated latate

EG: metabolized by alcohol and then aldehyde dehygrognse.
toxic metab is glyoxilic acid

Isopropanol: acetone is toxic metabolite whihc is formed by alcohol dehydrogenase

47
Q

clinical manifestations of toxic alcohol

A

cns
*iINEBRIATION is dependenton dose and mlecular-weight
*absense of inebriation doe snot include ingestion

metabolic acidosis
*toxic alcohols are metabolized to toxic organic acids [methanol->formic acid; EG->glycolic acid] which cause high anion gap metabolic acidosis
*exception: isopropanol’s metabolite acetone does not cause metabolic acidoses. it causes ketosis w.o an acidosis

48
Q

methanol clinical manifestations

A

retinl toxicity
*blurry vision to complete blindness which can be asymptomatic

neurotixicity
*basal ganglia lesions bilaterally which can lead to parkinsonism

AKI

pancreatitis

49
Q

ethylene glycol tox. clinical maninfestations

A

neurotoxicity
*oxalic acid+calcium=calcium oxalate monohydrate crystals which deposit renal tubules
*this precipitation can cause hypocalcemia

50
Q

isopropanol clinincal mainfestations

A

hemorrhagic gastritis

51
Q

dx testing for toxic alcohol poisonings

A

serum conc.
*results may not e availbale in timely manner
*prolonged time from ingestion?formate levels may be helpful

serum and urine oxalate conc are usually not clinically relevant

handle samples w. care (put in airtight container to prevent evaporation (isopropanol and ethanol)

toxic conc of methanol and eg>25 mg/dL

obtain electrolytes, Ca, BUN, Cr, UA, VBG or ABG, lactate, measured serum osmolality and serum ethanol concentration

52
Q

anion gap and osmol gap and time of ingestion

A

! ANION GAP AND OSMOL GAP CAN BE USED TO INITIATE TREATMENT WHILE AWAITING RESULTS ON SERUM CONCENTRATION!

high anin gap metabolkic acidosis of unkown etiology
*lack of high anion gap metabolic acidosis can be seen with recent ingestion of toxic

alcohol

extrememly elevated osmal gap (>50 mOsm/L)
*normal osmol gap ranges from -14+10 mOsm/L

**a baseline osm gap is needed to compare current value as results maybe within normal range, but abnormal for the pt (i,e osmol gap=12, currentlyosmol gap=+6)

serum ethanol conc can prevent metbaolism to the organic acid and is consider protective

elevated lactate leves can be seen wih methanol and ethylene glycol poisoning

53
Q

management of toxic alcohol poisoings

for antidotes
a: moa
b:dosing:
c:target conc:
d:AE:

A

resucitation

inhibition of ADH: cornerstone of therpy
*indicated for methanol and EG toxicity
1)IV ETOH10%continous infusion (rarely used in US)
*serum conc
*many complication s including hypotension, respiratory depression, cns depression and inebriation, flushing, hypoglycemia, hyponatreia, pancreatitis and gastrititis

2)fomepizole
*competitive inhibition of ADH
*intial boud: 15mg/kg IV piggyback over 30 in
*maintnenance dose: 10mg/kg iv piggyback q12 hours x4 doses hours then increase dose to 15mg/kg iv piggyback q 12 hours(induced its own metabolism after ~48hrs)
*continue until serum toxic alcohol conc is <20mg/dL+ asymptomatic w. normal serum pH
AE: hypotension and bradycardia

hemodyalisys preffered over renal replacement therapy

54
Q

adjunctie therapy for methanol toxicities

A

methanol:
folic acid: enhances formate elmination
*methylprednisolone 1 g(high dose) q24 hrs for 3 days may improve the amount o vision loss experienced
*sodium bicarb continuous infusion: shifts formic acid to formate and causes ion trapping in the urine
Goal serum pH:>7.2

55
Q

adjunctive therapies for ethylene glycol toxicities

A

thiamine: promotes coversion of EG to ketodipate

pyridoxine: promotes conversion of glycine to hippuric acid

sodium bicarb continuous infusion can be administered in pts w. ph <7.15

56
Q

Examples of TCAs

A

imipramine (1st approved)
desipramine
amitriptalyine
nortriptyline
doxepine
trimipramine
protriptyline

57
Q

epidemiology of tca overdoes

A

higher incidence of hospitalization and fatality in comparison to SSRI’s

58
Q

pharmacoloy of TCA’s

A

classified at tertiary or secondary amines

inhibit reutake of NE and seretonin, incrasing amount at cns receptors

competitive antags of muscuranic ach receptots

peripheral a1 receptor antsgonists

inhibit periheral and central postsynaptic histaminr receptos

interfere w. chloride conductance

59
Q

PK of tcas

A

A: completely and rapidly absorbed i gi tract
d: 10-40L/kg and variable
lipophillic
rapidly distribute to other organs

M:demtyhlat

E: 7-58 hrs

60
Q

toxicokinetics

A

delayed absoprtion due to decreased gastric motility

severe overdoses leas to low blood ph increasing amount of free drug

saturable metabolisms prolong t1/2

clinicaltoxiicty is rapid and unpredictale: therepeutic dose: 2-4 mg/kg/day; conc. 50-300 ng/mL
NARROW therepeutic index

Acute ingestino causing cardiotoxicity and cns toxicity
dose: 10-20 mg/kg; conc 300-1000ng/mL

61
Q

PAtho of tca toxiity

A

EEG findings
*prolonged qrs complex
*ight bundle branch bloc pattern

Sinus bradycardia
*antimuscarinic, vasodilatory, and sympathomimetic effects

Hypotnsino
*dirct myocardial depression from alterations in sodium channels
*alpha 1 blockade cuasing peripheral vaso dilation

binding to na channels occurs in ionized state
*tcas weak bases and become increasingly ionized in acidic environment

agitation, delerium, and depressed sensorium

seizures
*increases conc of monoamines, muscarinic antagonism, na channel alterations, and gaba inhibiton

62
Q

acute clinical maniestatins of tca tox

A

cv
*hypotension and ventricular dysrythmias
*prolonges pr interval, qrs and qt interval

cns
*delerium, agitatoin, psychotic behaviors w. hallucinations, seizures lethargy, and ocma

other
*anticholinergic: dilated pupils minimally responseive to light, dry moutg, drug flushed skin, urinary retention and ileus
*ARDS aspiration oneumonitis, and multisympton organ fialure

63
Q

chronic toxiity of tca

A

not life threatening

sedation and sinus tachycardia

64
Q

dx testing for tca toxiicty

A

ECG

TCA conc : limited utility early after ingestion

electrolytes

glucose

venous or arrterial blood gas

65
Q

tca overdose management

A

GI decom.
*actiated charcoal given to pts within 2 hrs and pt must have normal mental status and protected airway

serum alkanalization: membrane stbailization effect
*sodium stabilizing effect

control arrthmias, hypotension and seizures

IV lipid emulsion (ILE)
salavge therapy when cv therapy is refractory standard therapues
*only effective for lipophillic drugs (amitriptylie and clopiramine
8AE: ARDS and pancreatitis

66
Q

membrane stabilizing effect in tca overdose treatment

A

in presence of tcas na channel is altered slowing the rate of rise of action potentioal

increase in sodium gradient 9by giving sodium bicarb) speeds rate of rise of action potential

drug induced effects are counteracted
increasing ph removes tcas from binding to sodium channels

67
Q

serum alkalination and sodium loading

A

effective for wide comples dysrthrimas (qrs compex duraion>100ms) w. ocnduction delays and hypotenion

sodium bicarb preffered
*BOLUS OR RPAID INFUSION OVER SEVERAL MINUTE 1-2 MEQ/KG
*ADDITIONAL BOLUSES Q 3-5 MIN UNTIL QRS DURATION NARROWS AND HYPOTENSION IMPROVES, THEN consider initiatinf continuous infusion to maintain ph
target ph: 7.5-7.55
monitor K and ionized calcium

alternative: hypertonic saline 1-2 meq/kg bolus
only used with alkanization when sodium bicarb admin is not possible or ci

68
Q

ANTIDYSRHThmic therapy for tca overdose

A

if pt not responsive to sodium bicarb therapy

Lidocaine:
*Class 1b
*for pts who not responsive to sodium bicarb therapy

Magnesium sulfate:
consider after alkalinzation, sodium loading and trial of lidocaine fails

69
Q

CI antidysthrmics in pts w. tca overdose

A

class 1a: (procainamide-similar pharm action to tcas
class 1c: (flecainide-similar pharm action to tcas)
class III: amiodarone and sotalo prolongn qtc

70
Q

hypotension treatment in tca overdose

A

*0.9% NaCl or sodium bicarab bolus doses

if hyotension continues dispite volume resucitation
*norepinephrine
vasopression

Extracorporeal membrane oxygenation

71
Q

seizures

A

first line: benzos

second line:propofol or barbiturate

72
Q

CI agents in tca overdose in pts being treated for seizures

A

phenytoin
*fails to temrinate seizures
*enhances cv toxicity

flumezanil
*induces seizures

physostigmine
*induces seizures

73
Q

digoxin-specific antibody fragments indication

A

indictated when exposed to digoxin or digitoxins including cardioacive steroids
ex: lilly of the valley

74
Q

epidemiology of digoxin toxiitcty

A

causes most cases of pharm induced cardioacctive steroid toxicity (CAS)

more ocmmonly seen in pts at extremes of age or with ckd

75
Q

pk of digoxin

A

onset of action
*po: 1.5-6 hrs
IV: 5-30 min

max effect:
po:4-6 hrs
iv: 1.5-3 hrs

intestinal absorption : 40-90%

plasma protein binding: 25%

Vd:
*adults:5-7 days
*4-5

route of elimination :60-80% w. limited hepatic metabolism

enterohepatic circulation: 7%

76
Q

toxicokinetics of digoxin tox

A

elevated serum conc result in greater renal cl before distribution to tissues , dec. t1/2

hypokalemia and hypomagnesemia enhances efffects on myocardim leading to toxicity at lower serum conc

tox can be seen w. changes in liver, kidney, or heart function, aong w. drgu-drug interactions including quinidine, verapamil,carvedilol, amiodarone and spirinolactone

77
Q

digoxin moa of effects on heart

A

in presence of dgoxin, sodium-K ATP-ASE is inhibited, causing increase in intracellular sodium conc, preventing antiporter calcium and enhanced inotropy

excessive elevations in calcium inc resting potential, leading to dysrhtmias

78
Q

electrophysilogical effects of cardioactive steroids on myocardium

A

increase excitability

increase automaticity

decrease conduction velocity

decrease refractory time

toxiciy causes increased dysryhtmias and mocardial irritability

79
Q

acute ss of CAS toxiicity

A

asymptomatic period of min -sev hours

n/v, abdominal pain, lethargy, confusion , and weakness

80
Q

chornic ss of CAS tox

A

difficult to dx
loss of appetite, weakness, anoriexia, n/v abdominal pain, weightloss, delerium, confusion, drowsiness, headache, visual disturbances, andrarely seizures

81
Q

other ss of cas

A

electrolyte abnormalities (hyperkaemia)

cardiac abnormalities includuing ventricular tachy dys. or brady dys , a flutter, a fib w. av block, etc.

82
Q

dx tests for cas toxiity

A

gi decomtam:
AC 1g/kg q2-4 hrs up to 4 doses

electrolyte therapy
(hypo/hyperkalemi)
*do not admin calcium, could exagerate cardiac effects

hypomag:
*mg sulfate 2g iv over 20 min followed by 1-2 grams/hrs if needed

dig-specific antibody fragments
CORNERSTONE

83
Q

indications for dic-specific antibody fragment

A

lifethreatenning dysrthmias regardless of digoxin serum conc

K+ more than 5meq in setting of acute digoxin tocitiy

chornic levls of serum dig w. dysrhtmias, gi symptoms, and ams

serum digoxin conc
at anytime:>15
6hrs after injestion>10

acute ingestion of 10mg of digoxin in an adult

84
Q

moa of digifab

A

antigen binding fragments binds to free digoxin in iv and interstitial space

*movement of free intracellular and dissociated digoxin into II or IV space due to concentration gradient which is established

immediate decl.ien in free digoxin

massive increase in serum dig conc(clinically unimportant)

increases renal cl

dec serum potassium conc

85
Q

dosing of digifab

A

emperic
if dig serum conc unknown:
give 3-6 vials for chrnoic toxicity
give 10 vials for acute “

dig-secific fab dosing
*if serum conc known
[serum dig conc (ng/mL)x pt weight (kg)]/100=# of vials

*known amount ingested
[amount ingested mg/0.5 mg/vial]x 80% bioavailability=# of vials
ROUND U TO A WHOLE VIAL

86
Q

other cardiac therpaied for digoxin tox

A

atropine:early bradydysryhtmias
05 mg iv push q5min

phenytoin and lidocaine:ventricular tachydysrythmias

pacemaker

cardioverison

87
Q

clinical manifestatatins of bb tox

A

hypotension

bradyardia

dysryhtmias

hypoglycemia

seizures

resp depression and apnea

coma

88
Q

ccb overdose SS

A

halmark SS:hypotension and bradycardia

lack of perfusion to cns can cause fatigue, dizziness, lighthededness

hyperglycemia

severe overdose can cause syncope, coma, sudden death, ARDS

89
Q

dx testing for bb or ccb testing

A

ecg

cardiac and hemodynamic miint=oting

chest xray and o2 sat

digoxin level

thyroid function

cardiac enyzymes

lactate

90
Q

mgt of ccb/bb tox

A

gi decom: ac!!, mdac, whole bowel irrigation

hypotensive: crystalloid fluid

bradycardia: atropine 0.5-1mg IV titrate

in severe posioning, wont respond to above therapies, need to move on to these next therapies

calcium:
calcium chloride 10% : increase extracellular calcium and leading to improvements in hypotensino and reverses impairs inotropy and conduction

glucagon
*3-5 mg iv over 1-2 min; may repeat with 4-10 mg after 1-2 minutes; may repeat with 4-10 mg after 5 min w. no improvement in hemodynamics
(glucagon has ionotrpoic and chronotropic effects bypassing adrenergic receptors)

IN CCB overdose: calcium should be given beforegglucagon

BB overdose: glucagon before calcium

REMEMBER: do not use calcium if digoxin tox is suspected or confirmed due to stone heart phenomena

IV lipid emulsion-salvage therapy. only done if above therapies failed

91
Q

mgt of ccb/bb -HIGH DOSE INSULIN

A

trt of choice

HDI impairs sodium calcium antiporter resulting in an increase of intracellular calcium which increases calcium in sarcoplasmic reticulum increasing cardiac contractility

delayed onset of action 15-40 min

bolus:
1 u/kg iv push w. 0.5g/kg of dextrose infusion at 0.5 /kg/hr

continuous infusion
1u/kg/hr titrated to effect in combo w. dextrose infusion at 0.5g/kg/hr
monitor bg q 30 min for the first 4 hours and then every hr
monitor more frequently of bloog glucose if pt has renal failure

adverse reactions” hypoglycemia and kyopkalemia

92
Q

adjunctive hemodynamic support

A

inotropes and vasopressors

cardiac pacing

intraaortic balloon pump

extracorpeal membrane oxygenation

TXP: Pulm/ Tox. And Rheumatology (7 decks)

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