Path Lab Trauma Flashcards

1
Q

Discuss the pathology and symptoms behind an abrasion (no…I’m actually not kidding)

A

patho: loss of the superficial (epidermis) surface by frictional forces when the skin is rubbed against a hard surface or by compressional forces.
sx: Superficial = minimal hemorrhage and readily form a thin scab; heal without significant scarring.

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2
Q

Under abrasions we have two specific fun categories of road rash and pattern abrasions. What do these dumb terms mean?

A

Pattern abrasions -skin imprints formed by offending objects (e.g., grid marks on the body of someone hit head-on by a Mack truck).

Road rash - large abrasion caused by contact with pavement.

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3
Q

Injuries to the body can lead to contusions, unlike injuries to the skin which lead to abrasions. What morphological symptoms do we see for contusions and what will it look like to us?

A

sx: rupture of blood vessels, causing extravasation of blood into surrounding tissue (e.g., skin, heart, liver, or brain), hematoma may form.
cause: soft tissue injury that doesn’t break the skin

Small or barely noticeable contusions on the skin may be the only clues signifying significant internal bleeding.

Large skin contusions may only affect the superficial levels of tissue (e.g., dermis or subcutaneous tissue).

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4
Q

Remember neuro injuries? Remind me the difference between coup and contrecoup injuries

A

Brain coup and contrecoup: injury to brain seen on side of impact and 180* opposite

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5
Q

Closed head injuries can be fatal in what circumstance?

A

“closed head” injury = results in diffuse axonal injury to the brain = can be fatal

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6
Q

What’s so special about the morphological change in blunt trauma compared to other things like contusions or abrasions?

A

Blunt trauma- leaves behind fibrous strands or “tissue bridges”(not sufficient to sever the blood vessels or nerves)

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7
Q

Definition for laceration. Also, discuss its specific morphology (for BKR, this is very important)

A

cause: Injuries that cause the tissue to tear apart when it is crushed, stretched, or avulsed

sx: ragged edges; can have abrasions and contusions along the edges of the laceration.
.

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8
Q

When discussing an incision wound, there are three categories we use. Discuss what an incision wound is and what these three subtypes are

A

cause: sharp force injury produced by a sharp edge (e.g., knife, surgical scalpel)
sx: tears vessels/nerves (no tissue bridging)
sx: incision is longer, wider than it is deep; superficial in depth compared to puncture wounds; clean linear margins without tissue bridging

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9
Q

Discuss what hesitation marks are

A

A. HESITATION MARKS – Usually self-inflicted with non-fatal superficial wounds produced during the contemplation or successful attempt of suicide. It is common to see healed hesitation marks in same areas as fresh ones.

Occasionally, these hesitation marks can occur during homicidal acts when the victim is trying to escape from the assailant. Classically, multiple parallel incised wounds are adjacent to a deeper, fatal wound on the arm or neck.

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10
Q

Discuss defensive incised wounds

A

B. DEFENSIVE INCISED WOUNDS - An injury produced during the act of warding off an attack by an assailant. Characteristic locations include the palms or back of the hands, forearms and arms. Usually these injuries are non-fatal, unless vital organs (e.g., heart, lung) are punctured elsewhere.

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11
Q

What the fuck are chop wounds?

A

C. CHOP WOUNDS- Axes, cleavers, shovels, machetes and vehicle propellers are examples. These incised wounds are associated with a wedged cut into underlying bone. Dull weapons may produce a wound that is more consistent with a laceration than an incised wound.

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12
Q

Characterize puncture wounds and what the wound entails.

A

cause: Sharp force injury produced by an instrument with a point (e.g., ice pick or syringe).
sx: wound is deeper than it is wide. small pinpoint lesion on the skin
classified: perforating (entrance and exit wounds) or penetrating (entrance wound, but no exit).

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13
Q

When do we consider a wound “patterned”?

A

An injury that indicates the nature of the instrument that produced it (e.g., dinner fork)

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14
Q

Why do we go into shock with a thermal burn?

A

Shock: Shift of body fluids into interstitial compartment (due to systemic inflammatory response syndrome)

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15
Q

What type of infection do we see with thermal burns?

A

Infection→ most common organism=*Pseudomonas aeruginosa, MRSA, Candida. With compromised blood flow to burn site preventing proper immune response, infection is very common.

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16
Q

What happens to our metabolism with thermal injury?

A

Hypermetabolic state→ heat loss and need for nutritional support.

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17
Q

What happens to our vasculature integrity with a thermal injury?

A

Pulmonary and generalized edema→ Vascular leakiness

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18
Q

Airway after a thermal burn injury?

A

Airway and lung injury from inhalation → complete or partial airway obstruction
Severity of injury depends on: depth of burn, % of body affected, internal injuries from inhalation, effectiveness of tx

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19
Q

How do we characterize burns?

A

Classification: no longer using 1st-4th degree

1* Superficial: confined to epidermis,

2* Partial thickness burns: injury to top of dermis, wet and pink
Deep partial thickness: through all dermis, dry and red

3* Full-thickness: extension to subcutaneous tissue, white/brown and leathery, no pain

4* into muscle tissue or bone, black charred

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20
Q

What are some late complications of thermal burns?

A

Complications: shock, sepsis and respiratory insufficiency, pneumonia

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21
Q

Heat cramps vs heat exhaustion

A

Heat cramps: from loss of electrolytes from sweating. A/w vigorous exercise

Heat exhaustion: most common. From failure of cardiovascular system to compensate for hypovolemia caused by dehydration. Onset is sudden with prostration and collapse

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22
Q

Discuss what we see with heat stroke and who is at risk for this

A

Heat stroke: Body temp>40C→ multiorgan dysfunction.

Sustained contractions of skeletal muscle → muscle necrosis and rhabdo; Generalized vasodilation→ peripheral blood pooling and ineffective circulation; hyperkalemia, tachycardia, arrhythmias.

A/w high temp, high humidity and exertion.

At risk: older people, people undergoing physical stress, people with CV dz

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23
Q

Discuss heat stroke as it relates to RYR1 nitrosylation

A

RYR1 nitrosylation: responsible for regulating Ca2+ release in sarcoplasm in skeletal muscle.
Heat stroke causes RYR1 dysfunction allowing Ca2+ to leak into cytoplasm, stimulating muscle contraction.

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24
Q

What is malignant hyperthermia?

A

Malignant hyperthermia: Inherited mutation in RYR1. Rise in body temp in response to anesthetics

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25
Q

Presentation of hypothermia

A

Less than 90 F, loss of consciousness and bradycardia and afib at lower temps

26
Q

Trench foot and gangrene are examples of what kind of hypothermia?

A

Slow chilling: vasodilation and increased vascular permeability→ edema and hypoxia. Ex: Trench Foot + gangrene

27
Q

Compare rapid vs slow chilling?

A

Slow chilling: vasodilation and increased vascular permeability→ edema and hypoxia. Ex: Trench Foot + gangrene

Rapid chilling: vasodilation and increased blood viscosity → local ischemic injury and peripheral nerve degeneration. Gangrene can be seen. Vascular injury and edema seen as temp returns to normal.

28
Q

Discuss low voltage vs high voltage electrical injuries

A

Low voltage (120 or 220v): home or workplace. With low resistance (wet skin) can cause ventricular fibrillation. Sustained current (caused by alternating current leading to tetanic muscle spasm→ prolonged grasp of wire) can cause burns (entry/exit sites and internal)

High voltage: high-power lines or lightning Injury. Same mechanism as above but stronger. more likely to cause paralysis of medullary centers and extensive burns.

29
Q

Discuss the injuries we see with different forms of radiation

A

UV → skin

infrared → thermal

ionizing → cellular changes

30
Q

Non ionizing vs ionizing radiation

A

Nonionizing: UV, infrared light, microwave, sound→ can cause atoms in molecule to vibrate but can’t displace electrons

Ionizing: X-ray, gamma rays, high-energy neutrons, alpha particles (2p+ 2n), beta particles (e-)→ can remove bound electrons. Electrons hitting other molecules releases more electrons→ known as ionization

31
Q

Discuss the oxygen effects we see with radiation

A

Oxygen effects/hypoxia: Radiolysis of H2O→ free radical production→ ROS formation → DNA damage. Tissue with poor oxygen supply (center of rapidly growing tumors) are less susceptible to effects of radiation.

32
Q

Discuss the vascular injury we see with radiation

A

Vascular damage: endothelial cells sensitive to radiation→ occlusion of vessels → impaired healing, fibrosis, chronic ischemic atrophy

33
Q

Symptoms of ionizing radiation

A

Sx: teratogenesis, sterility, depression of hematopoiesis, pulmonary edema, GI mucosal injury and ulceration and skin erythema

34
Q

What happens to us with masive total-body radiation

A

massive-total body radiation (5000cGy) = cerebral syndrome → death in hours

35
Q

Late symptoms of radiation

A

Later changes include skin dyspigmentation and atrophy, scarring, adhesions, keloid formation, Fibrosis, mutagenesis, carcinogenesis

36
Q

Structure and source for Anthrax

A

Large Gm (+) rods in boxcar chains

encapsulated (made of protein poly-D-glutamate, not polysaccharides), obligate aerobe, spore forming (environmentally durable)
source: inhaled spores, skin infection, eating infected meat

37
Q

Toxins we see with anthrax and how they present

A

Exotoxins: must have both to cause sx

Lethal factor (LF): exotoxin that acts like a protease and cleaves map kinase (controls cells growth) → tissue necrosis (black eschar)

Edema factor (EF): acts like adenylate cyclase that inc cAMP → fluid buildup in extracellular space → edema → prevents phagocytosis and host defenses

38
Q

Symptoms of anthrax

A

sx: Lungs: wool sorter’s disease from spores present in the wool. Sx: dry cough (cold sx → rapidly progresses to pulmonary hemorrhage→ hemorrhagic mediastinitis (widened mediastinum on CXR) → 100% death

Skin: black eschar, spread to lymph noes

GI: n/v, fever

39
Q

How do we treat anthrax?

A

Tx: fluoroquinolones, tetracyclines (specifically doxycycline) (2’)

40
Q

Discuss the labs for staph aureus and what we see with structure

A

Gm (+) cocci that form clusters
catalase (+), coagulase (+) (contrast to epidermidis) (converts fibrinogen to fibrin, allowing blood to coagulate), beta-hemolytic.

Grows yellow (not pink) on mannitol agar

41
Q

Discuss the virulence factor for staph aureus

A

Protein A (part of bacterial cell wall that binds Fc portion of igG antibody→ prevents opsonization/phagocytosis)

42
Q

1 cause of septic arthritis in adults and osteomyelitis in adults/kids

A

Staph Aureus

43
Q

Talk about the skin and soft tissue changes we see with staph aureus

A

Skin/soft tissue infections: 85-95% of all s. aureus infections. Focal pussy abscesses/boils, and wound infections. Impetigo

44
Q

Heart issues with staph aureus

A

Acute endocarditis esp. in IVDU and diabetes

45
Q

What leads to scalded skin syndrome?

A

Scalded skin syndrome: exfoliative toxin (protease) mediated → scaling of skin

From Staph Aureus

46
Q

Discuss toxic shock syndrome

A

Toxic shock syndrome (tampons!): mediated by toxic shock syndrome toxin (a superantigen) that causes non specific binding of MCHII and T-cells, leading to cytokine storm

47
Q

Discuss GI symptoms we see with Staph Aureus

A

Acute poisoning w/ vomiting>diarrhea. Due to preformed enterotoxin.

48
Q

Discuss the structure for Staph Epidermidis

A

Gm (+) cocci, catalase (+), urease (converts urea to ammonia) (+), novobiocin sensitive, coagulase (-)

49
Q

Discuss who is at risk for staph epidermidis and how it presents

A

At risk: artificial joints, indwelling catheters, mechanical heart valves (endocarditis)

Forms polysaccharide biofilms that protects it from immune system

50
Q

Where do we find staph epidermidis? How do we treat it?

A

Normal skin flora (it’s everywhere!) → can contaminate blood cultures

Vancomycin to treat

51
Q

What does diptheria toxin lead to

A

diphtheria toxin causes myocarditis, nerve damage/demyelination, and pseudomembrane in throat/mucosa

52
Q

Discuss the structure for diptheria and how we transmit it?

A

Gm (+) rods, club shaped
non-motile, non-spore-forming aerobic

form “Chinese letters” or “V/Y”
metachromatic granules (red and blue)

transmission: resp droplets

catalase (+)

53
Q

How do the diptheria toxins work

A

A:B single chain toxin that ADP-ribosylates EF-2 and shuts down protein elongation/synthesis

54
Q

Discussthe culture and treatment for diptheria

A

Cx: tellurite and laeffer’s media
(+) Elek’s test= toxic form

Tx: passive therapy with horse anti-toxin, and abx

55
Q

Discuss the movement and morphology for listeria

A

Gm (+) rod, beta-hemolytic, facultative intracellular, catalase (+)

Intracellular movement: polymerize actin against the bacterial wall→ “actin rockets”

Extracellular movement: tumbling motility

56
Q

What does listeria grow in? (Not a culture question)

A

Grows in near freezing temps (contamination of dairy like milk and soft cheeses)

57
Q

Who is at risk for listeria and how does it present?

A

At risk: pregnant women, vertical transmission

Dz: Meningitis in neonates and elderly >60

58
Q

How do we treat listeria

A

Tx: vancomycin +ceftriaxone +ampicillin

59
Q

Discuss the structure for Nocardia and who is at risk

A

Gm (+) branching rod, partially acid fast, catalase (+), obligate aerobe, urease (+)
Found in the soil, non-spore forming,
At risk: immunocompromised (esp poor cell-mediated immunity), M>F

60
Q

How does Nocardia present?

A

Lung: Pneumonia w/ abscesses
CNS: Brain abscesses
Skin: indurated lesions

61
Q

How do we treat Nocardia

A

Tx: sulfonamides