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AHN 554 > deck_7751389 > Flashcards

deck_7751389 Flashcards

1
Q

Management of the comatose (poisoned) patient

A

A - Airway - maintain by positioning, suction, or insertion of artificial nasal ororopharyngeal airway, perform endotracheal intubation
B - Breathing - assess quality and depth of respirations, use of supplementaloxygen if needed, BVM/ventilator, monitor arterial or venous blood CO2 and/orarterial blood PO2
C - Circulation - measure pulse and BP, estimate tissue perfusion, continuousECG monitoring, insert IV, blood draw for glucose/electrolytes/serumcreatinine/liver tests, quantitative toxicologic testing
D - Drugs

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2
Q

3 Drugs used in management of the comatose (poisoned) patient

A

■ Dextrose and Thiamine - administer 50% dextrose (50-100ml) by IV bolusin all comatose or convulsing patients unless hypoglycemia is ruled out,administer 100 mg IM thiamine (or in IV fluids) in alcoholic ormalnourished patients
■ Opioid Antagonists - Naloxone 0.4-2 mg IV may reverse opioid-inducedrespiratory depression and coma, may repeat up to 5-10mg, short durationof action (2-3 hours) so repeated doses may be needed and continuousobservation for at least 2-4 hours after the last dose is mandatory
■ Flumazenil - Flumazenil 0.2-0.5 mg IV repeated as needed up tomaximum of 3mg may reverse benzodiazepine-induced coma, should notbe given if patient has coingested a potential convulsant drug, is a user ofhigh dose benzodiazepines, or has a seizure disorder

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3
Q

What is Organophosphate

A

Insecticide like Malathion and Parathion

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4
Q

Organophosphate poisoning Subjective findings

A

Nausea, vomiting, cramping, diarrhea, excessive salivation, diaphoresis,headache, blurred vision (miosis), mental confusion, slurred speech,anxiety, drowsiness, urinary incontinence, muscle fasciculations

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5
Q

Organophosphate poisoning physical findings

A

Miosis, seizures, paralysis, coma, bradycardia, conduction defects,respiratory depression/paralysis

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6
Q

Organophosphate poisoning management (6 things)

A

■ Maintain airway and assist ventilation
■ Wash skin thoroughly (wear neoprene or nitrile gloves)
■ Activated charcoal if ingested - given 1 gram/kg PO. Insert OG/NG tubeto facilitate administration.
■ Atropine is drug of choice for organophosphate toxicity - 2 mg (6 mg iflife threatening) in initial dose, then 2 mg IV every 15 min untilatropinization occurs - flushing, dry mouth, dilated pupils, tachycardia
■ Administer pralidoxime 1-2 grams IV over 10 min, then constant infusionof 250-500 mg/hr to reverse nicotinic signs (muscle weakness andrespiratory depression), not recommended for asymptomatic patients orwith known carbamate exposure
■ Place urinary catheter to prevent urinary retention

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7
Q

What are the dangers of tricyclic antidepressants

A

Tricyclic antidepressants are among the most dangerous drugs involved insuicidal overdose. These drugs have anticholinergic and cardiac depressantproperties. Tricyclic antidepressants produce marked membrane depressantcardiotoxic effects. They affect both serotonin and norepinephrine reuptake.

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8
Q

When do TCA symptoms of toxicity occur

A

Signs of severe intoxication may occur abruptly w/out warning within 30-60min after acute overdose

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9
Q

TCA toxicity symptoms

A

-Anticholinergic effects: Dilated pupils, Tachycardia, Dry mouth, flushed skin, Muscle twitching, Decreased peristalsis
-Quinidine-like cardiotoxic effects: QRS interval widening, Ventricular arrhythmias, AV block, Hypotension
Other symptoms: Hallucination, Confusion, Blurred Vision, AMS, Urinary retention, Seizures, Hypothermia, Hyperthermia

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10
Q

When to admit TCA toxicity to ICU

A

Evidence of CNS or cardiac toxicity w/in 6 hours of ingestion

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11
Q

Medical management for TCA toxicity (5 meds)

A
  • Activated Charcoal, 1gm/kg: avoid emesis if risk for seizures; INsert large boreOG/NG tube, to facilitate administration of activated charcoal.
  • Sodium Bicarbonate IV (1-2 mEq/kg); additional boluses every 5 min or 1000 ml D5W with 150 mEq sodium bicarbonate and infuse at 100-150 ml/hr until QRS interval narrows or serum pH exceeds 7.55. (Barkley-Target pH between 7.5-7.55/CMDT pH 7.45-7.5)
  • Benzodiazepine to control seizure ( e.g. diazepam 5-10mg IV PRN
  • Cardiotoxicity in patients with overdoses of lipids-soluble drugs have respondedto IV lipid emulsion (Intralipid), 1.5 ml/kg repeated one or two times if needed.
  • If patient still demonstrates signs of delirium, agitation, and enhanced skeletalmuscle tone or hyperreflexia, cyproheptadine may be used.Seen in moderate Serotonin syndrome
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12
Q

Supportive measures for TCA toxicity

A
  • Supportive measures such as cooling blankets are used to control temperature
  • Patient should be monitored for hypotension and should be treated with vasopressors
  • Prolongation QT interval or Torsades de pointes is usually treated with IV Magnesium or overdrive pacing.
  • Severe hyperthermia should be treated with neuromuscular paralysis and endotracheal intubation in addition to external cooling measures.
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13
Q

Serotonin syndrome symptoms

A

Rigidity, hyperthermia, autonomic instability, myoclonus, confusion, delirium, and coma.

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14
Q

What is static pain and what meds should be used?

A

pain regardless of movement like wound pain, use opioids

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15
Q

What is dynamic pain and what meds should be used?

A

pain with movement, like joint pain; use NSAIDS

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16
Q

Adjuvants for WHO analgesic ladder (8)

A

tricyclic antidepressants, SNRIs, anticonvulsants, corticosteroids, muscle relaxers, lidocaine patch, capsaicin, cannabinoids

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17
Q

Step 1 of WHO analgesic ladder

A

mild pain, nonopioid+/- adjuvant, ASA, NSAID, tylenol

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18
Q

Step 2 of WHO analgesic ladder

A

+/- adjuvant, codeine, hydrocodone, tramadol, oxycodone

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19
Q

Step 3 of WHO analgesic ladder

A

+/- adjuvant, morphine, oxycodone, hydromorphone, methadone, fentanyl, toradol

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20
Q

Pain meds for acute pain

A

COX inhibitors (NSAIDS), tylenol, opioids

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21
Q

Ketorolac

A

COX 1; analgesic effect equivalent to morphine; can be nephrotoxic

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22
Q

Celecoxib

A

COX 2

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23
Q

Side effects of COX inhibitors

A

Side effects gastritis, renal dysfunction, bleeding, HTN, cardiac events: MI, stroke, heart failure.Has ceiling effect

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24
Q

When to use PCA pump

A

PCA for post op pain keep plasma concentration of opioid within “therapeutic window”

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25
Q

Gender identity definition

A

a person’s internal sense of gender

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26
Q

Sex definition

A

assigned sex at birth, based on assessment of external genitalia, chromosomes, and gonads.

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27
Q

Predisposing risk factors to breast cancer for lesbian patients

A

Lesbians have an increased prevalence of risk factors for breast cancer→ nulliparity, alcohol use, obesity and smoking

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28
Q

HIV testing for gay women patients

A

Should encourage both partners in a lesbian relationship to have HIV screening prior to sexual contact. Use barrier protection for 6 months until rescreening to determine if they are still negative. If they are monogamous they can then d/c barrier protection

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29
Q

HIV testing for gay men patients

A

men who have sex with men account for 67% of all new HIV cases in US. all sexuallly active MSM should undergo screening with fourth generation HIV antigen/antibody test at least annually, or more often if high risk. Preexposure prophylaxis is recommended for high risk MSM

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30
Q

What is the double effect

A

argues that potential to hasten imminent death is acceptable as known but unintended consequence of a primary intention to provide comfort and relieve suffering.

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31
Q

6 ethical legal principles

A

Truth-telling, Non-maleficence, Beneficence, Autonomy, Confidentiality, Procedural

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32
Q

Definition of palliative care

A
  • To improve quality of life (QOL) for people living w/ serious illness.
  • Addresses and tx’s symptoms, supports patients’ families and loved ones.
  • Helps align patients’ care w/ their preferences and goals.
  • Near the end of life (EOL), palliative care becomes the sole focus of care.
  • Alongside cure-focused “(curative intent)” tx it is beneficial throughout the course of a serious illness, regardless of prognosis.
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33
Q

During palliative care, what is managed

A
  • Physical symptoms: Pain, dyspnea, n/v, constipation, agitation
  • Emotional distress: Depression, anxiety, interpersonal strain-Existential distress: Spiritual crisis
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34
Q

End of life management of dyspnea

A
  • Treat nonspecifically with opioids
  • doses lower than those needed for pain control-Immediate release oral or IV morphine
  • Sustained release morphine for ongoing dyspnea
  • Supplemental oxygen for hypoxic patient
  • Benzos for dyspnea related agitation
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35
Q

End of life management of delirium

A

-Terminal restlessness
-Keep patient oriented with familiar environment, clocks, calendars
Treatment: -Haloperidol, Risperidone → watch because there is increased risk of death with older patients
-Ramelteon → avoid in patients with liver dz
-Delirium refractory to tx may need sedation with midazolam (versed) or barbiturates

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36
Q

Med treatment for opioid addiction in pregnant women

A

Buprenorphine and methadone have both been shown to be safe and effective treatments for opioid use disorder during pregnancyOpioid agonist pharmacotherapy is the recommended therapy and is preferable to medically supervised withdrawal because withdrawal is associated with high relapse rates, which lead to worse outcomes.

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37
Q

1st line treatment for opiate addiction inpatient

A

Buprenorphine or Methadone

Buprenorphine/naloxone is preferred 1st-line treatment initiated in tapering doses

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38
Q

Adjunct tx for opiate addiction inpatient

A
  • Clonidine 0.1 mg bid - tid: minimizes autonomic symptoms (sweating and craving)
  • NSAIDS: for body and muscle aches
  • Anticholinergic: dicyclomine: minimizes GI hyperactivity
  • Nonbenzodiazepine hypnotics, low dose atypical antipsychotics, or low-dose tricyclic antidepressants:effective for promoting adequate sleep
  • Psychosocial support: tailored to the patient, should be offered as an adjunct to medical treatment
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39
Q

Strategies for the practitioner confronting drug seekers (6)

A
  • Risk assessment tool: Opioid Risk Tool to determine how closely to monitor patients who are receiving opioids long term, or whether to offer long-term opioids at all
  • Patient-provider agreements: “pain contracts”-Urine drug testing
  • Dose limitations and avoid tapering too quickly, No more than 120 mg of morphine per day. monthly decrease of 10% of original daily dose
  • Special medication limitations: prescription of Fentanyl and Methadone be limited to specialists. CDC recommends against concurrent prescription of opioids and benzodiazepines
  • Antidotes to overdose: Distribute naloxone and educate patients/families/caregivers of use
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40
Q

Drug interactions of anxiolytics and warfarin

A
  • Decreased prothrombin time
  • examples of anxiolytics: Alprazolam (Xanax), Clonazepam (Klonopin, Rivotril), Clorazepate (Tranxene), Diazepam (Valium), Lorazepam (Ativan)
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41
Q

What underlying medical issues to rule out before diagnosing with anxiety

A

Cardiac dz like arrhythmias
Pulmonary dz like COPD
Hyperthyroidism
Hypoglycemia
Substance abuse → cocaine, amphetamines, and PCP
Substance withdrawal → alcohol and benzos
Other anxiety disorders or mood disorders

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42
Q

Benzodiazepines mechanism of action

A

enhance the effect of the neurotransmitter gamma-aminobutyric acid (GABA) at the GABAA receptor, resulting in sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties.

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43
Q

First line treatment for GAD

A
  • Antidepressants→ SSRIs and SNRI for long term management
    1. low risk of dependence
    2. Start with a benzodiazepine→ benzo starts working immediately, antidepressants take a while to work
    3. SNRIs: venlafaxine and duloxetine
    4. SSRIs: escitalopram, paroxetine5. TCAs and MAOs are 2nd and 3rd line because of their side effects and numerous drug interactions
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44
Q

Patients at risk for suicide

A

Men over age 50
Patients with cancer, respiratory illnesses, AIDS
Patients on dialysis
Increased alcohol use
Those with major acute situational problems like breakup or public humiliation
Those with severe depression and schizophrenia
Those with a previous attempt of suicide

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45
Q

Management following attempted suicide

A

If hospitalization not indicated, plan must be made
Make referral
Dispense medications in small amounts→ TCA overdose common
Remove guns and other medications from home, hold on driving

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46
Q

Criteria for bipolar 1

A

Bipolar 1: manic episode

  • Distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal oriented activity or energy lasting 1 week (less if hospitalized)
  • Accompanied by 3 of the following (4 if only irritable): inflated self esteem/grandiosity, decreased need for sleep, pressured speech, racing thoughts, distractibility, increased involvement in goal directed activity, psychomotor agitation, excessive involvement in pleasurable activities with high potential for painful consequences.
  • Symptoms don’t meet criteria for mixed episode
  • Disturbance should be severe enough to cause marked impairment in social or occupational functioning, require hospitalization, or have psychotic features
  • Symptoms not due to direct physiologic effect of med use or substance abuse
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47
Q

Criteria for Bipolar 2

A

Bipolar 2: Hypomanic episode

  • Distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently elevated activity or energy lasting at least 4 consecutive days
  • Accompanied by 3 of the following (4 if only irritable): inflated self esteem/grandiosity, decreased need for sleep, pressured speech, racing thoughts, distractibility, increased involvement in goal directed activity, psychomotor agitation, excessive involvement in pleasurable activities with high potential for painful consequences.
  • Hypomanic episodes must be clearly different from the person’s usual non depressed mood and there must be clear change in functioning that is not characteristic of the person’s usual functioning
  • Changes in mood and functioning must be observable by others. In contrast to manic episodes, a hypomanic episode is NOT severe enough to cause marked impairment in social or occupational functioning, DOES NOT require hospitalization, and DOES NOT have psychotic features-Symptoms not due to direct physiologic effect of med use or substance abuse
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48
Q

Manic DSM criteria

A

a distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal
-directed activity or energy.

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49
Q

Medications that are appropriate for acute inpatient treatment for mania

A
  • 2nd generation antipsychotics: Olanzapine, Risperidone, aripiprazole
  • Valproic acid→ best for patients with AIDS or patients with dehydration/malnutrition problems which would affect lithium level
  • Lithium
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50
Q

4 hallmarks for clinical evaluation of depression

A
  1. depressed mood
  2. Anhedonia→ loss of interest in usual activities/interests
  3. Physical symptoms→ sleep disturbance, appetite change, fatigue, psychomotor changes
  4. Psychological changes→ difficulty concentrating, indecisiveness, guilt, worthlessness, suicidal ideation
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51
Q

4 Types of psychotherapy and definitions

A
  1. Cognitive psychotherapy: identify and correct negative patterns of thinking
  2. Interpersonal psychotherapy: identify and work through role transitions or interpersonal losses, conflicts, or deficits
  3. Problem solving therapy: Identify and prioritize situational problems; plan and implement strategies to deal with top priority problems
  4. Psychodynamic psychotherapy: use therapeutic relationship to maximize use of the healthiest defense mechanisms and coping strategies
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52
Q

ECT indications

A

severe refractory depression, mania and psychosis during pregnancy (since they can’t take certain meds), chronic schizophrenic disorder, extreme suicidality

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53
Q

Depression Time frame to assess response

A
  • Response is seen as early as 2 wks & among pts showing little to no response the odds of response decrease the longer pts remain unimproved.
  • Monitor tx Q 1-2 wks
  • Assess response on week 6 & week 12
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54
Q

Depression Time frame for follow up

A

Therapy should be continued for 4-9 mos after full remission of symptoms.

55
Q

Depression treatment

A
  • 1st line is SSRI
  • The SSRIs include fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram and escitalopram.
  • Non refractory pts should be switched to another SSRI or another class such as Bupropion
  • There is no benefit to combining meds as first line tx
56
Q

Depression Classification/diagnostic criteria

A 
-Dx Criteria - 5 out 9 criteria be present for 2 weeks - Anhedonia
Sleep Disturbance
Appetite Loss/gain or Weight loss/gain
Fatigue
Psychomotor 
Retardation
Agitation
Difficulty Concentrating/Indecisiveness
Feelings of guilt or worthlessness
Recurrent thoughts of death of suicide
57
Q

First degree burn

A
  • (superficial) burns
  • penetrate epidermis only (minimal barrier loss)
  • Very painful, intact, erythematous skin with minimal to no edema and no blistering.
  • Involves epidermis only-Infection barrier not destroyed, minimal barrier loss
58
Q

Superficial Second degree burn

A
  • Partial thickness, papillary dermis
  • Moist, very painful skin with edema and blistering/blebs
  • Extends beyond epidermis to part of dermis
  • Mild to moderate edema-cherry red with two-point discrimination intact, incredibly painful
  • Infection barrier destroyed
59
Q

Third degree burn

A
  • Full thickness
  • Not painful b/c nerve supply destroyed
  • Dry, leathery, black/white, pearly, waxy, may be eschar. The skin is dry, charred, pale, painless, and leathery. Charred vessels may be visible beneath, little or no pain, and hair pulls out easily.
  • Entire epidermis to dermis are affected, extending to underlying tissues, fat, muscle, and bone with destruction of hair follicles and sweat glands.
60
Q

Deep Second degree burn

A
  • Partial thickness, retinal dermis
  • Moist, very painful skin with edema and blistering/blebs
  • Extends beyond epidermis to part of dermis
  • Mild to moderate edema
  • mottled white and cherry red; only the sensation of pressure is intact in these areas
  • Infection barrier destroyed
61
Q

6 “Cs” of care for burn victims

A
  1. Clothing - remove hot or burned clothing
  2. Cooling - cool for 10-30 mins under faucet or compress at approximately 54 degrees F to reduce edema/pain by conducting heat away from the skin. Not recommended for extensive burns. NO ICE PACKS. 3. Cleaning - wash gently with mild alcohol-free soap then normal saline daily, remove ointment and loose skin, blot dry.
  3. Chemoprophylaxis - Tetanus immunization (all deep 2nd and 3rd degree burns) and treated with topical antimicrobial agent - silver sulfadiazine, bacitracin, bismuth-impregnated vaseline gauze or silver-impregnated synthetic dressing. Routine skin cultures and routine prophylactic systemic antibiotics are NOT recommended.
  4. Covering - 2nd and 3rd degree burns should be covered with sterile dressing
  5. Comfort - analgesics - Tylenol, NSAIDS, and/or opioids, give rescue analgesics prior to dressing changes and physical activity
62
Q

Which burns can be treated outpatient

A

only 1st degree and 2nd/3rd degree with limited TBSA should be treated outpatient

63
Q

How to treat 1st degree burn outpatient

A

-If pruritic: cool compresses (no ice), emollients, and antihistamines can be trialed; dressing is not required for 1st degree and antibiotic cream is NOT recommended; limit sun exposure for 1 year

64
Q

How to treat 2nd degree superficial burn outpatient

A

Leave blisters intact, if blisters have cloudy fluid or have not reabsorbed after several weeks they can be unroofed; antimicrobial (bacitracin) or A&D ointment with nonadherent dressing BID OR biosynthetic dressings with silver as antimicrobial; limit sun exposure for 1 year

65
Q

How to treat 2nd degree deep burn and localized 3rd degree burn outpatient

A

Dressing: Silver sulfadiazine 1%: broader spectrum, better penetration of necrotic tissue than bacitracin, but inhibits epithelialization. Must stop use once exudates and eschar have separated from wound. Alternative: enzymatic debrider (e.g., Santyl or Accuzyme)—chemically debrides devitalized tissue without harming healthy tissue. Referral: Burn specialist for consultation regarding need for excision and grafting.

66
Q

American Burn Association criteria for transport to burn center (10)

A
  1. Partial thickness burns greater than 10% total body surface area (TBSA).
  2. Burns that involve the face, hands, feet, genitalia, perineum, or major joints.
  3. Third degree burns in any age group.
  4. Electrical burns, including lightning injury.
  5. Chemical burns.
  6. Inhalation injury.
  7. Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality.
  8. Any patient with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk of morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center before being transferred to a burn unit. Physician judgment will be necessary in such situations and should be in concert with the regional medical control plan and triage protocols.
  9. Burned children in hospitals without qualified personnel or equipment for the care of children.
  10. Burn injury in patients who will require special social, emotional, or rehabilitative intervention.
67
Q

Initial physiological response to thermal injury, myoglobinuria

A
  • Generalized capillary leak with burn comprises >20% TBSA
  • For Moderate to Severe burns: Obtain a urinalysis, urine myoglobin, and CPK levels if concern for rhabdomyolysis or electrical burn
  • If there is severe lactic acidosis, consider checking cyanide level
  • If smoke inhalation expected, obtain serial ABG carboxyhemoglobin and continuous EKG, CBC, electrolytes, BUN, creatinine, glucose, liver function test, venous blood gas, blood coagulation, and type and screen in anticipation of blood transfusion
68
Q

Rule of 9’s Adults

A 
torso (front) total: 18%
torso (back) total: 18%
each leg total: 18% (remember to split for front and back)
each arm: 9%
head: 9%
perineum/genitals: 1%
69
Q

Parkland formula

A

Parkland: 4 cc x weight (kg) x %TBSA burned = volume of Lactated Ringer’s solution per 24 hrs-

  • Use crystalloid fluids (Lactated Ringers preferred as it treats hypovolemia and extracellular sodium deficits c/b burn injury); NO colloids
70
Q

Parkland formula definition and rules

A
  • Used to calculate fluid resuscitation for critical burn pts.
  • Used specifically for pts who have sustained large deep partial thickness or full-thickness burns >20% TBSA in adults, and >10% in children/elderly
  • Also useful for pts w/ smaller burns who sustained oral or inhalation injuries and are unable to tolerate fluids by mouth
  • Begin ASAP (in the field, not just when patient gets to hospital. Requirements calculated from time of injury)
  • General rule: HALF of all fluids required during first 24 hrs are administered within the first 8 hrs of injury, with remaining fluid given over next 16 hrs. (½ in 1st 8 hrs, ¼ in next 8 hrs, ¼ in remaining 8 hrs). After 24 hrs, switch from LR to D5 ½ NS at maintenance rate.
71
Q

What labs to monitor in burn patients

A
  • Urinary output goal: 30-50 mL/hr, formulas used to calculate fluid requirements. if pt isn’t putting out enough urine, fluid should be adjusted
  • Monitor for Metabolic Acidosis (expected during early resuscitation phase

)-Monitor for HYPERKALEMIA during first 24-48 hrs after burn injury, and then HYPOKALEMIA after fluid resuscitation/diuresis around 3 days post-burn

72
Q

Meds for burn pain

A

After stabilization, IV agents (Morphine is most common) and anxiolytics in small doses. Never use IM or SQ routes d/t uncertain absorption.

73
Q

Rule of 9s in infants

A 
Head 18%
Posterior torso 18%
Anterior torso 18%
Each arm 9%
Each leg 14%
74
Q

Alcohol poisoning tx algorithm

A
  1. Airway management and fluids for hypotension
  2. Get chem panel, osmols, calcium, magnesium, ABG, UA (look for crystals), ethanol levels, toxic alcohol levels, salicylate and acetaminophen levels
  3. If Anion gap acidemia or osmol gap >10 then confirm with stat tox alcohol level, ecg and start tx
  4. If toxic alcohol level >20 start tx
  5. If none of the test are positive check for other possible diagnoses and psych eval
75
Q

Alcohol poisoning tx

A
  • ADH blockade with ethanol or fomepizole
  • Sodium bicarb for severe acidosis pH < 7.2
  • Consult toxicology
  • Consult nephrology for possible hemodialysis
  • Cofactor supplement with thiamine, pyrodoxine, nd folate
  • ADMIT
76
Q

CAGE questioning for alcohol screening

A
  • feeling need to Cut down, Annoyed by criticism, Guilty about drinking, and need for an Eye opener in the morning
  • The most popular screening test in the primary care.
  • A positive response should lead to further questioning.
77
Q

TWEAK scale for alcohol screening

A
  • Tolerance, Worry, Eye-opener, Amnesia, K-cut down
  • Designed to screen pregnant women for alcohol misuse.
  • They detect lower levels of alcohol consumption that may pose risks during pregnancy.
78
Q

CRAFFT for alcohol screening

A
  • Riding in Car with someone who was drinking, using alcohol to Relax, using alcohol while Alone, Forgetfulness, criticism from Friends and Family, Trouble.
  • useful for adolescents
79
Q

Expected labs for alcoholic

A
  • lab tests alone do not accurately detect alcohol problems but can identify medical complications related to alcohol use, such as pancreatitis
  • MOST DEFINITIVE biologic marker of ETOH Abuse: carbohydrate deficient transferrin
  • Gamma-glutamyltransferase (GGTP), generally elevated (>30 = heavy drinking
  • Liver transaminase ALT, AST often elevated, may be normal or low in advanced liver disease
  • Low albumin level, hypophosphatemia, hypomagnesemia from malnutrition
  • CBC reveals elevated mean corpuscular volume (MCV > 95-100) from toxic effect of alcohol on erythrocyte development in nutritional deficiencies.
  • Stool for occult blood may be positive as a result of gastritis or variceal bleeding
  • RBC folate, vit B12 level, B6, B1 deficiencies
  • Increased uric acid, triglycerides
80
Q

Mineral abnormalities of alcoholics

A
  • Decreased RBC folate, vitamin B12 level, vitamin B6, vitamin B1 level.
  • Low albumin level, hypophosphatemia, hypomagnesemia from malnutrition.
  • Thiamine deficiency
  • Hypokalemia and Hypo or hypernatremia.
81
Q

Differential diagnosis for alcohol related seizures

A
  • Withdrawal (alcohol or drugs)
  • Exacerbation of idiopathic or posttraumatic seizures
  • Acute intoxication (amphetamines, anticholinergics, cocaine, isoniazid, organophosphates, phenothiazines, tricyclic antidepressants, salicylates, lithium).
  • Metabolic (hypoglycemia, hyponatremia, hypernatremia, hypocalcemia, hepatic failure)
  • Infection (meningitis, encephalitis, brain abscess)
  • Trauma (ICH)
  • CVA
  • Sleep deprivation
  • Noncompliance with anticonvulsants
82
Q

When do alcoholic seizures occur

A

Time interval usually occurs 7 to 30 hrs after cessation of drinking, with a peak incidence between 13-24 hrs.

83
Q

Manifestations and diagnostic work up for alcoholics during seizures

A
  • Generalized convulsions with loss of consciousness, focal signs are usually absent
  • Consider further investigation with CT scan of head and electroencephalography if clearly indicated (presence of focal neurologic deficits, prolonged postictal confusion state).
  • In addition, in a febrile patient who is having a seizure or altered mental state, a lumbar puncture is necessary.
84
Q

Medication tx for alcoholic with seizures

A
  • Diazepam 2.5mg/min IV until seizure is controlled (check for respiratory depression or hypotension)
  • May be beneficial for prolonged seizure activity, IV lorazepam 1-2 mg q2h can be used in place of diazepam.
  • Withdrawal seizures generally are self-limited and treatment is not required, the use of phenytoin or other anticonvulsants for short term treatment of alcohol withdrawal seizures is not recommended.
  • Thiamine 100mg IV followed by IV dextrose should be administered.
  • Electrolyte imbalances (increased Mg, decreased K, increased or decrease Na, decreased PO4) that may exacerbate seizure should be corrected.
85
Q

How often to do vitals

A
  • Tremulous state - vital signs every 4 hours with seizure precautions
  • DTs - vital signs every 30 mins and neurologic signs if necessary
86
Q

CIWA scoring

A
  • CIWA-Ar can be used to measure the severity of alcohol withdrawal using 10 items: nausea, tremor, autonomic hyperactivity, anxiety, agitation, tactile, visual, and auditory disturbances, headaches and disorientation.
  • CIWA-Ar score 16-20 moderate withdrawal - continuous pulse oximetry and cardiac monitoring should be considered
  • CIWA-Ar score greater than 21 severe withdrawal - continuous pulse oximetry and close observance of the patient’s respiratory status is required
87
Q

Peak incidence of delirium tremens (DTs)

A

DTs is the most severe form of alcohol withdrawal. It is an acute organic psychosis that usually manifests 48-72 hours after the last drink but may occur up to 7-10 days later. It is characterized by extreme mental confusion, agitation, tremor, diaphoresis, sensory hyperacuity, visual hallucinations (often snakes, bugs, etc).

88
Q

Alcohol withdrawal symptoms

A

There is a wide spectrum of manifestations of alcohol withdrawal, ranging from anxiety, decreased cognition, and tremulousness, through increasing irritability and hyperactivity to full-blown delirium tremens (DTs).

89
Q

Mild alcohol withdrawal time frame

A

Mild withdrawal: Symptoms including tremor, anxiety, tachycardia, nausea, vomiting, and insomnia begin within 6 hours after the last drink, often before the blood alcohol levels drop to zero, and usually have passed by day #2

90
Q

Severe or major withdrawal time frame

A

Severe or major withdrawal occurs 48- 96 hours after the last drink and is usually preceded by prolonged heavy alcohol use. Symptoms include disorientation, agitation, diaphoresis, whole body tremor, vomiting, hypertension, and hallucinations (visual> tactile>auditory).

91
Q

Salicylate overdose ABG findings

A
  • Salicylate is found in Aspirin, Methyl Salicylate, Bismuth Subsalicylate and more.
  • respiratory alkalosis with metabolic acidosis
92
Q

Calcium channel blocker -Med associated with fatalities

A

Verapamil and Diltiazem

93
Q

Extrapyramidal side effects:

A

-acute dyskinesias and dystonic reactions
tardive dyskinesia - rapid, repetitive movements of jaw, lips, tongue, trunk, and limbs

  • seen with long-term use of antipsychotic medication…particularly 1st generation antipsychotics (Haloperidol)
  • Parkinsonism
  • akinesia - loss or impairment of voluntary movement
  • akathisia - uncomfortable restlessness
  • neuroleptic malignant syndrome - life threatening - s/s of high fever, confusion, muscle rigidity, variable BP, diaphoresis, tachycardia
94
Q

COHb level in carbon monoxide exposure

A
  • measured by CO-oximetry on arterial or venous blood
  • COHb level >3% in nonsmokers confirms exposure.
  • Heavy smokers may have baseline levels of up to 10%.
  • Levels may be low if the patient has already received supplemental oxygen or if delays occur between exposure and testing.
95
Q

Use of Pulse oximetry and arterial blood gas (ABG) for carbon monoxide exposure

A
  • May be falsely normal because neither measures oxygen saturation of hemoglobin directly.
  • Pulse oximetry is inaccurate because of the similar absorption characteristics of oxyhemoglobin and COHb.
  • An ABG is inaccurate because it measures oxygen dissolved in plasma (which is not affected by CO) and then calculates oxygen saturation of hemoglobin.
96
Q

nonrebreather mask or endotracheal tube use for carbon monoxide exposure

A

-100% oxygen by nonrebreather mask or endotracheal tube (decreases half-life of COHb from 4 to 6 hr (room air) to 60 to 90 min) until COHb level is <10% and patient is asymptomatic.

97
Q

Hyperbaric oxygen use for carbon monoxide exposure

A

Decreases half-life of COHb to 20 to 30 min; increases amount of oxygen dissolved in plasma. It also reduces CO binding to other heme-containing proteins.

98
Q

Who to use hyperbaric oxygen on

A

Consider for:
1. Severe intoxication (COHb >25%, history of loss of consciousness, neurologic
symptoms or signs, cardiovascular compromise, severe metabolic acidosis)
2. Pregnant women with COHb >20% or signs of fetal distress. CO elimination is
slower in fetus than mother, fetal Hgb has greater affinity for CO than adult Hgb
3. Should be instituted quickly if deemed necessary

• Consider concomitant poisoning with other toxic/irritant gases that may be present in smoke (e.g., cyanide) or thermal injury to airway. Toxic effects of CO and cyanide are synergistic.

99
Q

HTN management with cocaine use

A

-Usually responds to benzodiazepines, but if this fails:
Phentolamine or nitroglycerin

  • Hydralazine hydrochloride 25 mg IM or IV if diastolic pressure > 120, may repeat every hour
  • Sodium nitroprusside initially at 0.5 mg/kg/min not to exceed 10 mg/kg/min if hypertension is uncontrolled or hypertensive encephalopathy is present
  • Consider arterial line for continuous monitoring
  • BAD: Avoid use of calcium channel blockers (they may potentiate the incidence of seizures and death, especially in body packers)
  • BAD: The use of beta-blockers may exacerbate vasoconstriction and may cause paradoxical hypertension.
100
Q

Phase 1 of cocaine overdose

A
  • CNS: euphoria, agitation, headache, vertigo, twitching, bruxism, unintentional tremor
  • Nausea, vomiting, fever hypertension, tachycardia
101
Q

Phase 2 of cocaine overdose

A

-CNS: lethargy, hyperreactive deep tendon reflexes, seizures (status epilepticus)

-Sympathetic overdrive: tachycardia, hypertension, hyperthermia
Incontinence

102
Q

Phase 2 of cocaine overdose

A
  • CNS: flaccid paralysis, coma, fixed dilated pupils, loss of reflexes
  • Pulmonary edema
  • Cardiopulmonary arrest
103
Q

Normal digoxin level

A

Normal range 0.5-2ng/mL

104
Q

What is digoxin mechanism of action

A

It paralyzes the Na-K- ATP pump (potent vasogenic effect) and enhances calcium dependent contractility and shortens action potential duration

105
Q

Management of acute ingestion of digoxin

A
  • Emergency and supportive
  • Activated charcoal (60-100 g oral or NGT in aqueous slurry)
  • Monitor K, (hyperK in acute and hypoK in chronic) correct either
  • Monitor cardiac rhythm
  • Treat bradycardia INITIALLY w/ atropine, and or pacing
106
Q

Management of significant intoxication of digoxin

A
  • Digoxin-specific antibodies (digoxin immune fab- DigiFab)
  • DigiFab indicated for hemodynamically significant arrhythmias, serum K greater than or = to 5, Mobitz II or 3rd HB, AV block, ingestion of bufadienolide –or cardenolide- containing agents, or renal insufficiency
107
Q

How to calculate antidote dose of digoxin based on the ingested dose

A

number of vials= approximately 1.5-2x ingested dose (mg)

108
Q

How to calculate antidote dose of digoxin based on serum concentration

A
  • Number of vials= serum digoxin x body weight in kg x 10 (to the neg 2 power)
  • after acute overdose, serum levels may be falsely high for several hours D/T tissue distribution, overestimation of DigiFab dose is likely
109
Q

what lab abnormalities would affect digoxin concentration

A
  • Toxicity may occur at a LOWER blood concentration in the presence of: HYPOkalemia, HYPOmagnesemia, HYPERcalcemia
  • Both hypokalemia and hypomagnesemia may be associated with concurrent diuretic Tx
110
Q

Mild and severe symptoms of Theophylline overdose

A
  • Mild: nausea, vomiting, tachycardia, tremulousness, restlessness, agitation, irritability
  • Severe: ventricular and supraventricular tachyarrhythmias, hypotension, and seizures (status epilepticus is common)
  • After acute overdose, patients often present with hypokalemia, hyperglycemia, and metabolic acidosis.
111
Q

Opiate antidote and dosage

A
  • Narcan 0.2-2mg IV
  • Repeat as needed to awaken patient and maintain airway (narcan is only effective to 2-3 hours, repeat doses may be necessary for long acting opioids)
112
Q

Observation period after narcan use

A

Continuous observation for at least 3 hours after the last naloxone dose is mandatory.

113
Q

4 grades of withdrawal for opiate use

A

Grade 0

  • Grade 0: Cravings and anxiety
  • Grade 1: Yawning, lacrimation, rhinorrhea, and perspiration
  • Grade 2: Previous symptoms plus mydriasis, piloerection, anorexia, tremors, and hot and cold flashes with generalized ache
  • Grades 3 and 4: Increased intensity of previous symptoms and signs, with increased temperature, blood pressure, pulse, and respiratory rate and depth

-Withdrawal from the most severe addiction, vomiting, diarrhea, weight loss, hemoconcentration, and spotaneous ejactulation or orgasm commonly occur

114
Q

What is acetaminophen poisoning

A

Acetaminophen (APAP) poisoning is a disorder caused by excessive intake of APAP and is manifested by jaundice, N/V, and potential death from hepatic necrosis if not treated appropriately.

-#1 cause of acute liver failure in the US.

115
Q

Signs and symptoms of acetaminophen poisoning (and time frames)

A
  • 0-24hr- Asymptomatic - N/V, malaise towards in of stage
  • 24-72 hr- Onset of hepatotoxicity- RUQ pain, AST(most sensitive indicator of hepatotoxicity)/ALT increase. Later INR rises and renal fx deteriorates.
  • 72-96 hr- Maximal hepatotoxicity- hepatic encephalopathy, jaundice, coag defects, myocardial abnorms, AST/ALT level peak, INR rises, BUN/Cr rise, pH drops. Death may occur
  • 4 days-2wks- Recovery phase- labs return to normal 5-7 days after overdose (if survive).
116
Q

Labs for acetaminophen poisoning

A
  • Initial lab eval should include an initial plasma APAP level with a second level drawn apprx 4 hr after the initial ingestion.
  • Subsequent levels can be obtained every 2-4hr until the levels stabilize or decline.
  • Transaminases (AST, ALT), serum glucose, bilirubin level, lipase level, prothrombin time (INR), BUN, Cr, EKG, and UA should be initially obtained on all pts.
  • Serum and urine tox screen for other potential toxic substances is also recommended on admission.
  • Screening for infectious hepatitis should be considered.
  • Urine for beta-HCG should be obtained from all women of childbearing age.
117
Q

Standard management of tylenol poisoning

A
  • All pts with confirmed APAP poisoning will require admission, usually to ICU.
  • Nonpharm therapy: Consult Poison Control Center
  • A single toxic dose of APAP usually exceeds 7g or 150mg/kg adults.
  • Provide adequate IV hydration (D5 1/2NS @150ml/hr), If APAP level is nontoxic, N-acetylcysteine may be D/Cd.
118
Q

How much is toxic dose of acetaminophen

A

-A single toxic dose of APAP usually exceeds 7g or 150mg/kg adults.

119
Q

Pharm tx and antidote for acetaminophen poisoning

A
  • Hepatotoxicity is defined as any increase in ALT or AST >1000 and hepatic failure manifests as hepatotoxicity with hepatic encephalophy.
  • ANTIDOTE: N-acetylcysteine should be administered w/o delay to those >12yr and >8hr after ingestion at presentation. This would include anyone with an ingestions of APAP over many days with an APAP level <20 ug/ml (with or w/o ALT elevation) or anyone with undetectable APAP levels with an elevated ALT and hx of excessive APAP intake.
  • Treatment with N-acetylcysteine is most effective if it is started within 8–10 hours after ingestion.
  • Activated charcoal 1g/kg PO if the pt is seen within 1hr of ingestion or the clinician suspects polysubstance ingestion that delays gastric emptying.
  • N-acetylcysteine (NAC) either IV (Acetadote) or PO (Mucomyst). N-acetylcysteine should be started within 24hr of APAP overdose. Total admin time is 72hrs.
120
Q

Advantages and disadvantages of IV antidote for acetaminophen poisoning

A
  • Advantages of IV admin: more reliable absorption, fewer doses, shorter duration of tx
  • Disadvantages: cost, lower hepatic concentrations from first-pass flows as compared to PO
121
Q

When to repeat labs for acetaminophen poisoning

A

-Repeat AST/ALT and APAP levels after 12 -14hr of IV acetylcysteine infusion and continue infusion longer than 16 hr if transaminases are elevated, if APAP concentration is still measurable, or if coag exists (INR>1.5-2.0)

122
Q

Presentation with beta blocker overdose

A
  • Most common PE finding with mild/moderate OD: Hypotension, Bradycardia
  • Subjective findings: Nausea, vomiting, diarrhea
  • Cardiac Depression from severe OD often not responsive to beta stimulants (dopamine and norepi)

-Propranolol and other lipid-soluble cause:
Seizures, coma

123
Q

EKG changes from beta blocker overdose

A

Olol drugs will lead to wide QRS interval

124
Q

Treatment of beta blocker OD

A
  • Atropine and pacemakers are often ineffective
  • Activated charcoal if can be given within first hour of ingestion
  • Glucagon and high dose insulin along with glucose supplements
  • Norepi and dobutamine infusion ; IV milrinone
125
Q

Lithium: acute attack levels and frank toxicity levels

A
  • 1 to 1.5 mEq/L in acute attacks

- Frank toxicity usually occurs at blood levels > 2.

126
Q

Which meds increase lithium level

A

Ace inhibitors, celecoxib, fluoxetine, ibuprofen, indomethacin, potassium sparing diuretics (spirolactone, amiloride, triamterene), thiazide diuretics

127
Q

Which meds increase lithium excretion

A

Osmotic diuretics (urea, mannitol) sodium bicarb, theophylline, aminophylline

128
Q

Which med decreases lithium levels

A

Valproic acid

129
Q

Lithium interaction with methyldopa

A

Rigidity, mutism, fascicular twitching

130
Q

Lithium interaction with succinylcholine

A

increases duration of action of succinylcholine

131
Q

Anticoagulant overdose general management

A
  • Discontinue the drug at the first sign of gross bleeding and determine the PT.
  • The PT is increased w/in 12-24 hours (peak 36-48 hrs) after overdose warfarin or “superwarfarin”.
  • The newer oral anticoagulants do not predictably alter the PT however a normal INR suggest no significant toxicity;
  • If acute overdose administer activated charcoal
132
Q

Treatment of Warfarin overdose

A
  • In case of Warfarin overdose do not treat prophylactically with Vitamin K. Wait for evidence of anticoagulation.
  • Give FFP, Prothrombin complex concentrate or activated factor VII as needed to rapidly correct the coagulation factor deficit if there is serious bleeding.
  • If the patient is chronically anticoagulated and has a strong medication indication for being maintained in the status give much smaller doses of vitamin K, FFP, to titrate to desired Pt level.
  • If patient ingested brodifacoum or a “superwarfarin”: prolonged observation (over weeks) and repeated administration of large doses of Vitamin K may be required.
133
Q

Treatment of Direct acting oral anticoagulants overdose

A
  • No treatment or reversing agent exist for these agents.
  • In case of intentional overdose with PO agents, activated charcoal may be considered.
  • Vitamin K does not reverse the anticoagulant effects of the direct acting oral anticoagulants.
  • Idarucizumab has been approved reversal of the thrombin inhibitor dabigatran.
134
Q

Heparin overdose treatment

A
  • Give protamine sulfate IVPB over 15-30 minutes, 1 mg/100 units heparin; use 0.5mg/100 units heparin if given more than 30 minutes after heparin. Maximum 50mg IVPB, given over 15-30 minutes
  • Monitor s/s of bleeding until activated PTT is normal; must administer slowly to prevent anaphylaxis and hypotension.

AHN 554 (13 decks)

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