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A complete set of 150 English question-and-answer flashcards covering Chapter 11 (Burns and Scalds) from Knight’s Forensic Pathology, suitable for exam revision.
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What causes the characteristic cherry-pink discoloration seen in many fire victims?
Carboxyhaemoglobin formed from carbon-monoxide inhalation.
Which cerebellar cells are typically damaged in fatal heat-stroke?
Purkinje cells.
Which burn type shows a precise outline that matches the heated object?
Contact burn.
Which autopsy feature indicates antemortem burning?
A red inflammatory line (line of redness) around the burn margin.
In forced-immersion scalds, what typical pattern appears on the buttocks of children?
Doughnut burns (central sparing with peripheral burn).
Which burn-depth category destroys full skin thickness and is usually painless?
Third-degree (full-thickness) burn.
What heat-related posture results from muscular contraction and produces a ‘boxer-like’ stance?
Pugilistic attitude.
A well-demarcated scald without splash marks in a child most strongly suggests what?
Intentional immersion (non-accidental injury).
Which toxic gas is the most frequent cause of death in fire victims?
Carbon monoxide.
Which combustion product can cause almost instantaneous death before burns develop?
Hydrogen cyanide.
What burn distribution is typical of a flash explosion?
Superficial, wide burns that spare areas covered by clothing.
What gross brain change is often noted at autopsy in heat-stroke cases?
Cerebral oedema with flattened gyri.
Which microscopic feature distinguishes antemortem burns?
Early neutrophilic infiltration at the burn edge.
Which blood finding is characteristic in a victim who inhaled fire smoke while alive?
Elevated carboxyhaemoglobin level.
What clinical feature is classical of heat-stroke in elderly patients?
Anhidrosis (absence of sweating).
Which clothing material carries the greatest risk of deep burns because it melts?
Synthetic fabrics.
Define the ‘wick effect’ sometimes mislabelled as spontaneous combustion.
Body fat melts and, like candle wax, sustains a localized flame that slowly consumes tissue.
How can skull heat fractures be differentiated from traumatic fractures?
Heat fractures have irregular, often bevelled edges and lack associated bleeding.
Heat haematomas usually collect in which intracranial location?
The frontal or temporal extradural (epidural) space.
For what purpose is Wallace’s Rule of Nines primarily used?
Rapid estimation of the percentage of total body surface area (TBSA) burned.
What is the primary mechanism of tissue destruction in thermal burns?
Protein denaturation and coagulative necrosis.
Which skin area offers the greatest natural resistance to heat damage?
Palmar (thick) skin of the hands.
Which burn degree is typically associated with painful blisters?
Second-degree (partial-thickness) burn.
Which chart is most accurate for estimating burn surface area in children?
Lund and Browder chart.
A full-thickness burn often appears how on gross inspection?
Leathery and insensate (painless).
Burns associated with ignition of clothing are classified as what type?
Flame burns.
Why are burns over >30 % TBSA particularly dangerous?
They cause burn shock from massive plasma loss.
Loss of the skin barrier in large burns chiefly predisposes to what complication?
Systemic infection/sepsis.
Forced sitting in hot water usually produces which burn pattern?
Doughnut burns on buttocks and perineum.
What liquid is responsible for the majority of scald injuries?
Hot water.
Which key feature characterises immersion scalds on the body?
A sharp upper border with uniform depth below it.
Uniform burns without splash marks are highly suspicious for what?
Non-accidental (intentional) injury or abuse.
Give an example of a classic dry-heat source that causes contact burns.
A hot iron (or any heated metal surface).
Flash burns commonly spare which areas?
Regions protected by clothing or hair.
Burning plastics often liberate which lethal gas?
Hydrogen cyanide.
What immediate physical process produces pugilistic attitude in a body exposed to fire?
Heat-induced coagulation and shortening of muscle proteins and tendons.
Which finding suggests a burn occurred post-mortem?
Clear, air-filled blisters with no inflammatory base.
What single autopsy observation most strongly proves the victim breathed during the fire?
Carbon soot deposition in the trachea and bronchi.
Heat haematomas are most frequently located where?
Frontal extradural (epidural) region of the skull.
What burn-related skin split may mimic an incised wound?
A thermal fissure (heat tear).
What colour change of tissues is typical in carbon-monoxide poisoning?
Bright cherry-pink discolouration.
Which burn type often reproduces the exact outline of the causative object?
Contact burn.
Overall, what is the leading mechanism of death in fires?
Carbon-monoxide poisoning rather than the thermal injury itself.
Which posture produced by heat exposure resembles a boxer guarding himself?
Pugilistic attitude.
What is the dominant macroscopic brain finding in fatal heat-stroke?
Diffuse cerebral oedema (flattened gyri, narrowed sulci).
What renal tubular finding is typical in heat-stroke victims?
Albumin (protein) casts within renal tubules.
How does hydrogen cyanide cause cellular death?
By blocking cytochrome oxidase and producing cellular asphyxiation.
State the hallmark triad of malignant hyperthermia.
Rapid hyperthermia, generalized muscle rigidity, and metabolic acidosis/raised CK.
What major clinical difference separates classical from exertional heat-stroke?
Classical heat-stroke features absence of sweating; exertional may still have sweating.
Which heat-related artifact can resemble an extradural haemorrhage on CT or autopsy?
Heat haematoma.
In the wick effect, what bodily substance actually fuels the fire?
Liquefied body fat acting as combustible fuel.
Describe the appearance of post-mortem burned skin.
Dry, parchment-like, yellow-brown surface with no vital reaction.
Approximately what blood carboxyhaemoglobin level is usually fatal?
About 50 % saturation or higher.
Which white blood cell predominates in early vital reaction to a burn?
Neutrophils.
Why are synthetic fabrics hazardous during flame exposure?
They melt and adhere to skin, causing deeper contact burns.
What common hepatic lesion is encountered in severe heat-stroke?
Centrilobular (zone 3) hepatic necrosis.
Identify a moist-heat burn type.
Scald burn from hot liquid or steam.
What pulmonary change is frequently observed after intense heat inhalation?
Frothy, often blood-tinged fluid in airways (pulmonary oedema).
Which CNS neuronal population is first to show necrosis in hyperthermia?
Cerebellar Purkinje cells.
Benign environmental hyperthermia is chiefly caused by what?
Exogenous heat exposure without underlying pathology.
List four major systemic complications that follow extensive burns.
Hypovolaemic shock, electrolyte imbalance, acute renal failure, and sepsis/MODS.
Contrast heat-contact burns with immersion scalds in forensic terms.
Contact burns are localised with object imprint; immersion scalds are symmetrical with sharp waterline, suggesting possible abuse.
Why does airway soot deposition conclusively indicate vitality during fire exposure?
Soot can reach the tracheobronchial tree only if the victim was actively breathing.
Give three histological differences between antemortem and post-mortem burns.
Antemortem burns show vascular congestion, oedema, and neutrophil influx; post-mortem burns lack inflammation and vital reaction.
Define heat tears and state their forensic importance.
Post-mortem splits in charred skin from dehydration; may mimic sharp trauma and must be distinguished histologically.
Enumerate the forensic implications of the pugilistic attitude.
Indicates heat exposure, rules out defensive posture, aids reconstruction of body position during burning.
How can one separate traumatic extradural haemorrhage from a heat haematoma?
Traumatic bleeds are clotted, often unilateral, and linked to skull fracture; heat haematomas are gelatinous, bilateral, and fracture-free.
Name three toxic agents in smoke and specify their effects.
CO (hypoxia), HCN (cellular asphyxia), aldehydes/irritants (airway oedema and chemical injury).
Summarise the Rule of Nines for burn assessment.
Head 9 %, each arm 9 %, each leg 18 %, anterior trunk 18 %, posterior trunk 18 %, perineum 1 % — for rapid TBSA calculation.
How do synthetic fibres alter burn pattern interpretation?
They melt, adhere, and may imprint fabric weave, helping confirm clothing worn at ignition.
List three burn-pattern clues that differentiate accidental scalds from abuse.
Irregular splash marks imply accident; sharp upper demarcation and doughnut pattern suggest forced immersion (abuse).
Explain the forensic significance of delayed medical management in burns.
Lack of treatment may indicate neglect, increases infection, and provides timeline clues through varied healing stages.
Differentiate thermal fissures from knife wounds.
Thermal fissures are irregular, dry, bloodless splits; knife wounds have sharp, regular edges and vital bleeding.
How do flash burns differ from flame burns regarding depth and distribution?
Flash burns are superficial and widespread, sparing clothed skin; flame burns are deeper and often localised to ignition points on clothing.
Describe the fatal pathophysiological cascade of heat-stroke.
Loss of thermoregulation → hyperthermia → vasodilation & hypotension → enzymatic failure → multi-organ dysfunction and death.
List three gross pulmonary findings in heat-stroke and state their significance.
Pulmonary oedema, congestion, and frothy airway fluid indicate respiratory compromise contributing to death.
Contrast skull heat fractures with blunt-force fractures.
Heat fractures are irregular, non-radiating, and bloodless; blunt-force fractures radiate from impact and show haemorrhage.
Name four external post-mortem features commonly seen in burned bodies.
Charred/leathery skin, bullae, singed hair, pugilistic attitude.
Outline brain changes found at autopsy in heat-stroke.
Diffuse oedema, flattened gyri, petechial haemorrhages, and selective neuronal death (Purkinje/cortical).
List four methods used to identify severely burned bodies.
Dental records, DNA profiling, medical implants/serial numbers, and personal effects correlation.
Why are elevated CK and aldolase informative in heat deaths?
They indicate rhabdomyolysis from muscle breakdown, common in exertional and malignant hyperthermia.
Define malignant hyperthermia and its anaesthetic triggers.
An inherited skeletal-muscle disorder triggered by agents such as halothane or succinylcholine, causing fulminant hyperthermia and rigidity.
How does soot distribution assist in estimating survival time during a fire?
Soot deep in bronchi/alveoli suggests several breaths; superficial only suggests brief survival; absence indicates post-mortem burning.
State two crucial scene observations that refute claims of spontaneous combustion.
Presence of an ignition source (e.g., cigarette/heater) and limited fire damage beyond the body (supports wick effect).
What forensic value does cherry-pink skin carry in burned bodies?
Signals high carboxyhaemoglobin, proving the victim inhaled CO while alive.
Give two ways post-mortem skin changes can mimic trauma in burn victims.
Heat fissures look like cuts and bullae can resemble blunt contusions, potentially misleading investigation.
Explain the forensic relevance of rhabdomyolysis in hyperthermic deaths.
Muscle breakdown releases myoglobin, causing renal failure and confirming exertional or malignant hyperthermia as cause.
How can flame-burn patterns help reconstruct body position during the fire?
Areas shielded by clothing or pressed to the floor remain less burned, indicating orientation and possible restraint.
List four clues suggesting a burn victim was unconscious before the fire began.
Uniform burns, absence of defended areas, no airway soot, and minimal vital inflammatory reaction at burn edges.
Enumerate the classic clinical signs of classical (non-exertional) heat-stroke.
Core temperature >40.5 °C, anhidrosis, altered mental status/coma, hot dry skin, tachypnoea/tachycardia.
Summarise systemic physiological responses to extensive burns.
Capillary leak and hypovolaemia, electrolyte shifts, renal failure risk, immunosuppression, and systemic inflammatory response syndrome.
List four principal thermal burn types with distinguishing features.
Flame (deep), contact (object outline), flash (superficial wide), scald (moist, gravity run-off).
Describe four autopsy criteria used to confirm immersion scald abuse.
Symmetric gloves/socks pattern, sharp waterline, doughnut buttock burns, absence of splash marks/inconsistent history.
Contrast antemortem versus post-mortem burn features at autopsy.
Antemortem burns show redness, blisters with proteinaceous fluid, neutrophils, soot in airway; post-mortem burns are dry, bloodless, with no inflammatory cells.
Discuss the role of airway soot in confirming vitality during fires.
Its presence proves respiration during fire; absence favours post-mortem burning or rapid incapacitation before flames.
Detail gross and microscopic characteristics of heat haematomas.
Soft, gelatinous dark collections in extradural space without skull fracture; microscopically show thermal coagulation rather than arterial rupture.
Explain why pugilistic attitude is not evidence of a struggle.
It results from heat-induced muscle contraction post-mortem, not from voluntary defensive action.
State five utilities of the Rule of Nines in forensic practice.
TBSA estimation, prognosis, evaluating survivability, fluid resuscitation guidance, and assessing feasibility of self-rescue.
List common toxicological findings in fire deaths and their interpretations.
COHb >50 % (CO poisoning), blood cyanide (HCN inhalation), irritant aldehydes (airway injury), helping determine cause of death.
Define the wick effect and list two key scene clues that support it.
Body fat sustains a candle-like flame; clues include minimal surrounding fire damage and presence of ignition source such as a dropped cigarette.