Module 6: Forensic: Sexual Assault, Sexual Child, Lead, Carbon Monoxide, Ethanol Flashcards

(39 cards)

1
Q

First starting off sexual assault we are going to discuss sexual assault. what is it?

A

Unwanted sexual contact that causes discomfort, fright or intimidation

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2
Q

How do you approach the patient in a sexual assault case?

A

Private Room ASAP: remain in clothing
–no urinating, defecating, drinking, eating or smoking
–social support and offer to contact law enforcement
–informed consent for examination
72 hour rule: STD and pregnancy prophylaxis, collecting evidence and documenting injuries

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3
Q

How do you get a history and physical in a sexual abuse patient?

A

Patients own words and document affect

  • -document physical signs of trauma (genital and non genital)
  • -tears (tenderness), redness, abrasions, contusions, swelling
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4
Q

Does absence of injury rule out assault?

A

nope!

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5
Q

What evidence should be collected in a sexual assault case?

A

Sexual assault evidence collection kit
—proper collection and presentation; chain of custody
Drug Facilitated sexual assault (GHB, hallucinogens, sedative-hypnotics, opioids)
–Toluding Blue Dye (normal skin surface has anucleated cells but trauma exposes deeper nucleated cells)

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6
Q

Moving on to sexual abuse of a child, what is the definition of this?

A

Engaging of a child in sexual activities when child is developmentally unprepared or violates social and legal taboos
–oral-genital, genital, anal, non touching

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7
Q

What is high index of suspicion in sexual abuse of a child?

A

Coerced into secrecy and general behavioral problems (sleep, enuresis)

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8
Q

What are specific signs and symptoms as well as patient history for sexual abuse of children?

A

Signs: rectal/genital pain, bleeding, infections, STDs, precocious sexual behavior
History: quite environment and caring attitude
–interview all sources and get a comprehensive medical history

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9
Q

How is a physical exam of a sexually abused child performed?

A

Have a trusted supportive adult present
–slow and complete
–consider general anesthesia
A normal genital/anal exam does not rule out abuse

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10
Q

Explain diagnosis and follow up procedures for a sexual abuse child case

A

Dx: careful documentation and discuss with caregivers and child while remaining neutral
Follow up: asses adequacy of healing, document changes, repeated tests for STDs, assess coping skills
Most common findings in sexually abused children is a norma exam (b.c perpetrator does not want to hurt the child)

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11
Q

What are normal findings in a non abused child?

A

Common: Erythema, pigmentation, congestion, anal fissures (Associated with constipation)
Anal dilation: constipation, prone position, neurological disease, post mortem
Normal variants: midline wedge-shaped smooth areas (diastasis ani), midline anal skin tags, folds and failure of midline fusion

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12
Q

Moving on to lead, what are sources?

A

Air, Soil, water, dust, ceramics, food/soft drinks, moonshine, toys, batteries and ammunition

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13
Q

What is the absorption and distribution of lead?

A

Adults ingest 100-500mg daily (10% absorbed)
–kids ingest less but 50% absorbed
–enhanced with mineral (calcium/iron/zinc) deficiencies
Distribution: bone and teeth (85% — lead lines), blood (5-10%) and soft tissues

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14
Q

What are the biochemical effects of lead?

A

Inhibits iron corporation into heme
competes with calcium
inhibits membrane associated enzymes
impairs production of active vit D — calcium deficiency
Fatal lead poisoning due to cardioresp arrest and cerebral edema
Tx with chelation therapy

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15
Q

Moving on to Carbon Monoxide, what is this/

A

Colorless, odorless gas thats a byproduct of combustion (gas, oil, coal, wood, natural gas and cigarette smoke)
–cause of half of all fire deaths

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16
Q

What is the pathogenesis for carbon monoxide poisoning?

A

CO has 230-300 times the affinity for Hb as oxygen – cherry red discoloration of skin

  • -impairs release of oxygen from Hb
  • -direct toxic cellular effect
  • -greater degree of hypoxemia than an equivalent degree of anemia
17
Q

Moving onto ethanol it is the most widely used/abused. What are acute effects and mechanism?

A

Acute effects: CNS depressant, fatty liver

  • -asymptomatic, acute and reversible
  • -mechanism: increased catabolism of peripheral fat, increased NADH stimulates lipid synthesis, decreased fatty acid oxidation, decreased transport lipoproteins from liver
18
Q

What are the chronic effects (systemic, vitamin deficiencies) of ethanol on the GI system?

A

GI: liver cirrhosis, steatohepatitis, pancreatitis, gastritis, ulceration, varices, oral/esophageal cancer

19
Q

What are the chronic effects of ethanol on the nervous system?

A

Nervous system: peripheral neuropathy, wernicke-korsakoff, cerebral atrophy and cerebellar degeneration

20
Q

What are the chronic effects of ethanol on the cardiovascular system/

A

Toxic effects: HTN and dilated cardiomyopathy

Protective effects: increased HDL and decreased platelet aggregation

21
Q

What are the chronic effects of ethanol on the reproductive system?

A

Fetal alcohol syndrome (most common preventable cause of mental retardation)

  • -microcephaly
  • -short palpebral fissures
  • -flat midface
  • -thin upper lip
  • -epicanthal folds
  • -low nasal bridge
  • -short nose
22
Q

What is the pharmacology of ethanol?

A

Absorption: stomach and small intestine
Metabolism: 9gm/her and 90% metabolized to acetaldehyde and acetic acid in gastric mucosa and liver
Elimination: 10% excreted unchanged in urine, sweat and breath

23
Q

Moving on to Ethylene Glycol, what is it?

A

Colorless, odorless, sweet alcohol in antifreeze, deicing and industrial solvents
fatal dose= 100-200mL

24
Q

What are the stages of ethylene glycol poisoning?

A

Neurologic: 0.5-12 Hrs: nausea/vomiting, inebriation/euphoria and CNS depression and seizures
Cardiopulmonary: 12-24 hrs: compensatory hyperventilation and heart failure
Renal: 24-72 hours: acute tubular necrosis

25
How is a dx of ethylene glycol poisoning made?
Intoxication to come with severe metabolic acidosis, seizures to acute renal failure and death - -high anion gap: greater than 18mEq/L - -Urine microscopy: sodium fluorescein and calcium oxalate crystals
26
Moving on to Methanol (Wood Alcohol), what is it?
Colorless, clear alcohol found in antifreeze, pain and varnish solvent, methylated spirits and alternative energy --fatal dose: 15-500mL
27
What are the stages of methanol (Wood alcohol) poisoning?
Early: transient euphoria, inebriation, drowsy Latent: 6-30 hrs: blurred vision, abd pain, vomiting, metabolized to formic acid and formaldehyde Delayed: systemic effects of metabolic acidosis (high anion gap) CNS: mild/moderate: HA and severe: parkinson like syndrome Ocular: blurred vision to blindness GI: abd pain Cardio: resp arrest and shock
28
Moving on to drug abuse, what are therapeutic drugs?
Adverse drug reaction: ---undesired response at therapeutic doses --predictable or idiopathic/idiosyncratic Prescription drug abuse
29
What are risk factors for drug abuse?
``` Family history Male Psychiatric disorders Ethanol abuse Access and peer pressure ```
30
What are the top drugs of abuse?
Marijuana Pain relievers Cocaine
31
Moving on to opioid analgesics, what does this include?
Heroin Oxycodone Methadone Morphine
32
What are acute effects of opioid analgesics?
Anxiolytic, sedation, mood changes, nausea, resp depression | Convulsion: cardioresp arrest, death
33
What are chronic effects of opioid analgesics?
Tolerance and dependence | Infectious complications of IVDA: cellulitis, endocarditis, viral hep and pneumonia
34
In regards to heroin (diacetylmorphine), what are some features?
Source = poppy plant Cutting agents: talc, quinine Routes: IV or SQ injection, smoking and snorting Effects: euphoria, hallucinations, sedation Adverse effects from: heroin and/or cutting agents, HSR, injection
35
What are the toxic effects of heroin (Diacetylmorphine)?
Sudden death: profound resp depression, arrhythmia, pul edema Pulmonary: edema, septic emboli, abscess Skin: abscess, cellulitis, ulceration, vein thrombosis and scarring/hyperpigmentation Infection: endocarditis, hep and AIDS
36
Finally cocaine, what are some features/
Source: leaves of erythroxylon coca Forms: cocaine HCL + cutting agent (talc and lactose) or crack cocaine Routes: snorted, smoked, ingested and injected Mechanism: blocks reuptake of DA, E and NE
37
What are the effects of cocaine?
Fast acting stimulant of short duration - -rush: pleasure, strength, power, and excitement - -high: increased alertness, confidence, disinhibition - -side effects: weight loss, insomnia and fatigue
38
What are the toxic effects of cocaine?
``` Toxic effects: CNS: hyperpyrexia, seizure Cardio: increased BP and HR Pulmonary dysfunction Pregnancy: abruption Other: perforated nasal septum ```
39
In regards to cocaine what is fatal excited delirium syndrome (acute onset)?
Delirium (transient disturbance in consciousness and cognition and hallucinations) Violent behavior Sudden cardiac death History of chronic stimulant abuse Fatal Arrhythmia precipitated by ischemia ---accelerated atherosclerosis and thrombosis