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Autopsy pathology > IVDU & its complications > Flashcards

IVDU & its complications Flashcards

3.1 - health and safety at autopsy 3.2 - pathology of IVDU 3.3 - infective endocarditis 3.4 - valvular heart disease 3.5 - thromboembolic disease 3.6 - PM toxicology

1
Q

Define a hazard (3.1)

A

a source or situation that has the potential to cause harm

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2
Q

Define a risk (3.1)

A

the chance of a negative event occurring

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3
Q

List some hazards from the body during autopsy.

3.1

A 
sharp injuries from body
aerosols 
infection
radioactivity
implanted cardiac devices
chemical exposure
moving injury
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4
Q

What is the infectious disease hazard group classification?

3.1

A

infectious disease hazard groups are organised by likelihood of acquisition, severity of resulting disease, availability & efficacy of treatment and risk of transmission from staff to general public.

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5
Q

Hazard Group 1

3.1

A

unlikely to cause human disease

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6
Q

Hazard Group 2

3.1

A

can cause disease and may affect employees, UNLIKELY to spread to community and treatment available.

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7
Q

Hazard Group 3

3.1

A

Causes severe human disease and may cause serious harm to employees, MAY spread to community BUT effective treatment available

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8
Q

Hazard Group 4

3.1

A

Causes severe human disease and may be serious harm to employees, LIKELY TO SPREAD to community and effective treatment NOT available.

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9
Q

Which hazard group is TB in and list any precautions that should be taken during autopsy.

A

HG3
separate/isolated room w/ limited staff
N95 masks or suits with HEPA filters worn
bulb syringe used for body fluids
staff get yearly TB tests and should be vaccinated

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10
Q

Give examples of HG2 agents.

A

zika virus (Reclassified from 3)
adenovirus
HPV
staph and strep infections typically causing common respiratory infections

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11
Q

give examples of HG4 agents.

A

viral haemorrhage fevers - ebola, lassa, crimean-congo

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12
Q

Give examples of HG3 agents.

A

yellow fever, TB, Hep B-E, E coli 0157, HIV

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13
Q

What precautions would you take when performing autopsy on CJD body?
3.1

A

use waterproof gown, HEPA filters, disposable equipment where possible
keep reusable equipment wet
have dedicated equipment for Transmissible spongiform encephalopathy (TSEs)
take care when removing and fixing brain - place it and cover it immediately in a pre-weighted container.

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14
Q

HBV is more infectious than HCV but there is no vaccine against it.
T/F?
3.1

A

HBV is highly infectious but there is a vaccine against it.

HCV is less infectious but has no vaccine.

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15
Q

What increases the risk of acquiring HIV from an infected body?
3.1

A

AIDS, high viral load or a deep injury with visible blood

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16
Q

Describe the groups of drugs of misuse.

A

Stimulants - cocaine, amphetamine, methamphetamine, and amphetamine derivatives like XTC
Opioids & opiates - heroin, morphine, pethidine, fentanyl, methadone, oxycodone, dihydrocodeine.
Sedatives - benzodiazepam & related drugs.
Miscellaneous - ket & cannabis.

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17
Q

Describe the GENERAL stigmata of drug use seen on external examination.

A 
malnourished
recent injury/self-harm
signs of resus
bright red hypostasis 
scars and homemade tattoos
abnormal patterns of hypostasis
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18
Q

What are the main pathological skin features from drug use?

A

track marks w/ puckered scarring, hyperpigmentation & chronic sinuses.
skin popping scars (ovoid)
haemosiderin forms at injection site 2-3 days post-injection
granulomatous inflammation if foreign material also injected

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19
Q

What are the main cardiovascular features of drug use?

A

COCAINE & AMPHETAMINES - enlarged heart w/ interstitial & perivascular fibrosis (due to catecholamine effect). Accelerated atherosclerosis coronary & aortic dissection, coronary thrombus in young. Contraction band necrosis, cardiomyopathy, increased chance of MI

HEROIN - infective endocarditis but no fibrosis. may have myocarditis & cardiomyopathy due to HIV infection (needles)

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20
Q

What are the main respiratory features of drug use?

A

Crack lung
barotrauma and emphysematous lung disease
oedema (cardiogenic)

HEROIN
pulmonary oedema - mushroom plume
aspiration

CANNABIS
pneumonia/pneumonitis 
pneumopericardium/thorax
bullous disease 
desquamative interstitial pneumonitis
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21
Q

What are the main GI features of drug use?

A

COCAINE - gastro-duodenal perf., accelerated atherosclerotic disease - ischaemic colitis & colonic perforation.

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22
Q

List some signs of liver failure - external exam.

A

ABDO + CHEST: Spider nave, caput medusa, haemorrhoids & abdominal distention
FACE: jaundice
HANDS: palmar erythema, Dupytren’s contractures

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23
Q

Necrosis of the nasal tip would indicate ?

A

infective endocarditis in PWID

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24
Q

Mushroom plume is a sign of what?

A

pulmonary oedema occurred due to drug use - common with opiate overdose.

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25
Q

poor dental hygiene and tooth damage is common with which drug use?

A

cocaine esp.

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26
Q

Describe crack lung.

A 
Alveolar haemorrhage
Haemosiderin laden macrophages 
Pneumonitis 
Interstitial fibrosis 
Carbon laden macrophages (black)
Small artery medial hypertrophy
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27
Q

What is cardiogenic oedema.

A

seen in cocaine use; low protein count, doesn’t foam as much as opiates

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28
Q

As aspiration pneumonia suggests use of which drug group?

A

opiates>stimulants

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29
Q

desquamated epithelial cells, gastric contents, clumps of bacteria, alveolar haemorrhage - describes?

A

aspiration pneumonia/pneumonitis

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30
Q

Describe the histology of desquamated interstitial pneumonitis.

A 
goblet cell hyperplasia
squamous metaplasia 
nucelar atypia, BM thickening
sub epithelial inflammation
brown pigment macrophages
fibrosis & atelectasis
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31
Q

Which drug can cause cystitis?

A

ketamine

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32
Q

Which drugs can impair spermatogenesis?

A

cocaine and cannabis

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33
Q

Which drug can cause urinary retention (distended bladder)?

A

amphetamines

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34
Q

Which drugs can cause rhabdomyolysis independent of muscle compression?

A

cocaine, heroine, XTC

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35
Q

General lung pathology due to drug misuse?

A

gastric contents w/o subsequent inflammation
intravascular granulomatous disease - injecting talc/lactose/crushed tablets
septic emboli/mycotic aneurism
TB
If HIV+ - bacterial & pneumocytic pneumonia

36
Q

what are the main causes of liver pathology in drug use?

A

ethanol

hep b and c

37
Q

describe triaditis

A

due to hep b and c - lymphocytic infiltration w/ few plasma cells & neutrophils

38
Q

when is steatosis seen?

A

IVDU Hep C - a mixed macro micro vesicular pattern.

39
Q

Describe the 2 forms of liver damage seen with XTC use.

A
  1. steatosis, sinusoidal dilatation & hepato-necrosis - patients due from hyperpyrexia.
  2. hepatitis & fulminant liver failure - direct toxicity of drug, all seen in MDMA use.
40
Q

which organisms are most commonly implicated in IE?

A

most common microbes in Europe - S. aureus, Viridans group strep (VGS), coagulase negative staph (CoNS), enterococcus sp., s. bovis

41
Q

Explain the differences between native, prosthetic and IVDU endocarditis

A

Native - due to some form of heart disease incl. RHD, congenital, mitral valve prolapses and degenerative heart disease.
Prosthetic - presents after valve replacement surgery and aortic valve infection is particularly assoc. with local abscesses, fistula formation, and valvular dehiscence.
IVDU - 2/3rd of patients have no previous Hx of heart disease or murmured on admission.

42
Q

Which organisms are most commonly implicated in prosthetic valve IE?

A

CoNS/S. aureus
VGS
enterococcus
s. bovis

43
Q

which organisms are most commonly implicated HIV+ IE patients?

A

s. aureus
e. faecalis
CoNS
VGS
pseudomonas sp.

44
Q

What factors predispose patients to nosocomial/healthcare-associated IE?

A

significant comorbidities
more advanced age
predominant infection with s. aureus
new therapeutic modalities involving intravascular devices

45
Q

In which patients would you find fungal endocarditis?

A

IV drug users and ICU patients who have received broad-spec antibiotics

46
Q

What is the most significant risk factor for IE?

A

residual valvular damage caused by a previous episode of endocarditis

47
Q

Describe the difference between acute and subacute native valve endocarditis.

A

Acute - normal valves, aggressive course, rapidly progressive, caused by virulent organisms e.g. s. aureus & group B strep., may not have underlying structural valve disease

subacute - abnormal valves only, indolent course, alpha-haemolytic strep/enterococci

48
Q

Describe early prosthetic valve endocarditis.

A

occurs within 60 days of valve implantation

due to CoNS, gram -ve bacilli, candida sp.

49
Q

Describe late prosthetic valve endocarditis.

A

occurs 60 days or more after valve implantation

due to Staph., alpha-haemolytic strep., & enterococci

50
Q

What is the main causative organism for both early and late PVE?

A

staph. aureus

51
Q

What is the most commonly involved valve and causative organism or IVDU endocarditis?

A

tricuspid (50%) and s. aureus

most common PC = right-sided endocarditis 70%

52
Q

List signs/symptoms of right-sided endocarditis.

A 
murmur - not always heard
fever
pleuritic chest pain
dyspnoea
non-productive cough
53
Q

Describe the location of bacteria and fibrin-platelet thrombi in the context of mitral & aortic insufficiency, according to the Venturi effect.

A

Venturi effect = bacteria and thrombi are deposited on the sides of the low-pressure sink that lies just beyond a narrowing or stenosis.
In mitral insufficiency: bacteria & thrombus are found on atrial surface of the valve (low pressure sink).
In atrial insufficiency they are found on the ventricular side.

54
Q

Describe the initial development of pacemaker IE.

A

Implantation –> fibrin-platelet thrombus develops involving the generator box + conducting leads.
After 1 week –> connective tissue proliferates and leads are partially embedded into wall of endocardium = partial protection from bacteraemia.
Bacteraemia infects the sterile fibrin-platelet vegetation.
Microorganisms (from various invasive procedures) establish themselves on surface of vegetation -> platelet aggregation & fibrin deposition, multiplication of bacteria etc.

55
Q

What are some complications of IE?

A

glomerulonephritis if it includes glomerular antigen-antibody complex deposition.
sepsis, arrhythmias and systemic embolisation
fatal if untreated

56
Q

What are some previously common manifestations which have now been eradicated by earlier diagnosis and effective treatment of IE?

A

Micro-thromboemboli - splinter or sublingual haemorrhages
erythematous/haemorrhagic non-tender lesions on plams/soles - Janeway lesions
Subcut nodules in pulp of digits (Osler nodes)
Retinal haemorrhages in eyes (Roth spots)

57
Q

When might you see a ring abscess in the context of IE?

A

if the vegetations have eroded into the myocardium

58
Q

Vegetations from subacute endocarditis are assoc. with more valvular destruction than those of acute endocarditis.
T/F?

A

FALSE

vegetations from subacute endocarditis are assoc. with LESS valvular destruction than those of acute endocarditis

59
Q

Describe the histological differences between acute and subacute vegetations.

A

acute - no fibroblasts = no repair. Large amounts of polymorphonuclear leukocyte expanding area of necrosis + rapid spontaneous rupture of leaflets, papillary muscles and chord tendineae.

subacute - granulation tissue at bases = healing. fibrosis > calcification > development of chronic inflammatory infiltrate.

60
Q

Which heart valve is more susceptible to perivascular abscesses?

A

aortic valve and its adjacent annulus

61
Q

How can IE lead to sudden cardiac death?

A

Involvement of conduction system in the setting of aortic valve infection, esp. when there is involvement of the valve ring between the right and non-coronary cusp.
Overlies IV septum that contains the proximal ventricular conduction system -> heart block -> sudden cardiac death.

62
Q

Natural Hx and mechanism of death of IE?

A

Heart failure
Infection-induced valvular damage & insufficiency (fatigue, SOB)
Perivascular abscesses - can lead to heart block
Septic emboli - can lead to acute MI

63
Q

what causes the first heart sound?

A

closure of AV valves during systole

64
Q

what causes 2nd heart sound?

A

closure of semilunar valves (aortic + pulmonary) during diastole

65
Q

what makes up the functional unit of the AV valves?

A

valve leaflet (cusp) + chordae tendineae + papillary muscles

66
Q

Both AV valves are microscopically similar - what is the key difference between them?

A

mitral has 2 (valve) leaflets and 2 papillary muscles

tricuspid has 3 of each.

67
Q

Describe the annulus of a valve - histology

A

collagenous crown-shaped structure where the valve leaflets attach to the myocardium

68
Q

what are the 4 layers of elastic and collagenous tissue called in the Av valves?

A

atrialis, lamina spongiosa, lamina fibrosa, ventricularis

69
Q

Describe the endothelial lining in the semi-lunar valves.

A

smooth on ventricular side and ridged on arterial side (transfers stress to aortic wall)

70
Q

What are the 3 distinct layers of connective tissue in the semilunar valves?

A

lamina radialis, spongiosa and fibrosa.

71
Q

Main causes of aortic stenosis?

A

calcification of valve leaflets - due to repeated endothelial injury
bicuspid aortic valves - more prone to stenosis
RHD - predisposes to calcification

72
Q

Main causes of mitral stenosis?

A 
chronic RHD following rheumatic fever 
mitral annular calcification
carcinoid syndrome 
serotonergic drugs
SLE 
amyloidosis
73
Q

Describe how acute rheumatic fever can lead to R-sided heart failure.

A

acute rheumatic fever -> fusion of leaflet commissures + thickening of leaflets -> reduction in flow -> increased LA pressure & decreased LV pressure -> reduced CO + pulmonary HTN -> R-sided HF

74
Q

“fish mouth” appearance of valve leaflets

A

mitral stenosis - fusion of and thickening of leaflet and commissures

75
Q

which pathogen causes rheumatic heart disease

A

RHD classically occurs 2-3 weeks following group A streptococcal pharyngitis (strep pyogenes)

76
Q

How can carcinoid syndrome affect the heart valves?

A

neuroendocrine tumours form in the gut and secrete compounds such as serotonin. when the person has significant liver pathology, these cannot be broken down and are carried to the heart - typically seen in right side of heart since this is the first area to receive blood from the liver.

77
Q

if you saw glistening white plaques on the endocardial surface of the tricuspid valve - what might you suspect?
Histology clue: comprised of extracellular matrix, my-fibroblasts, mast cells and lymphocytes.

A

carcinoid heart disease - neuroendocrine tumours

78
Q

what are the 2 disorders within the non-infective endocarditis category?

A

non-bacterial thrombotic endocarditis (NBTE)

endocarditis of SLE (Liebman-Sacks endocarditis)

79
Q

What might you suspect if you saw small bland thrombi on valve leaflets with no underlying structural damage or inflammatory response?

A

NBTE

80
Q

which patients get NBTE?

A

patients in hypercoagulable states - underlying malignancy, sepsis, endocardial trauma.

81
Q

What would you suspect if you saw significant valvulitis with sterile vegetations formed from fibrin and immune complexes?

A

endocarditis of SLE (Liebman sacks)

82
Q

List causes of acute mitral regurgitation.

A

IE, ischaemic damages to papillary muscles rupture, acute rheumatic fever

83
Q

List causes of chronic mitral insufficiency.

A

mitral valve prolapse, myxomatous degeneration of mitral valve, mitral annular calcification

84
Q

aortic regurgitation is the result of?

A

abnormalities of the valve leaflets or aortic root dilation

85
Q

What are the pros and cons of bio-prosthetic valves?

A

PROS - no anticoagulation needed, can be inserted transcather

CONS - only last 10-15 years so will need replacement surgery

86
Q

What are the pros and cons of mechanical valves?

A

PROS - typically long-lasting

CONS - requires life-long anticoagulation with warfarin; some designs have audible clicking sound

87
Q

What are the complications of valve replacements?

A

thromboembolism
infective endocarditis - increased risk for both types of valve
structural deterioration - in bio-prosthesis
continued valve dysfunction

Autopsy pathology (3 decks)

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