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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
poor dental hygiene and tooth damage is common with which drug use?
cocaine esp.
26
Describe crack lung.
``` Alveolar haemorrhage Haemosiderin laden macrophages Pneumonitis Interstitial fibrosis Carbon laden macrophages (black) Small artery medial hypertrophy ```
27
What is cardiogenic oedema.
seen in cocaine use; low protein count, doesn't foam as much as opiates
28
As aspiration pneumonia suggests use of which drug group?
opiates>stimulants
29
desquamated epithelial cells, gastric contents, clumps of bacteria, alveolar haemorrhage - describes?
aspiration pneumonia/pneumonitis
30
Describe the histology of desquamated interstitial pneumonitis.
``` goblet cell hyperplasia squamous metaplasia nucelar atypia, BM thickening sub epithelial inflammation brown pigment macrophages fibrosis & atelectasis ```
31
Which drug can cause cystitis?
ketamine
32
Which drugs can impair spermatogenesis?
cocaine and cannabis
33
Which drug can cause urinary retention (distended bladder)?
amphetamines
34
Which drugs can cause rhabdomyolysis independent of muscle compression?
cocaine, heroine, XTC
35
General lung pathology due to drug misuse?
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
what are the main causes of liver pathology in drug use?
ethanol | hep b and c
37
describe triaditis
due to hep b and c - lymphocytic infiltration w/ few plasma cells & neutrophils
38
when is steatosis seen?
IVDU Hep C - a mixed macro micro vesicular pattern.
39
Describe the 2 forms of liver damage seen with XTC use.
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
which organisms are most commonly implicated in IE?
most common microbes in Europe - S. aureus, Viridans group strep (VGS), coagulase negative staph (CoNS), enterococcus sp., s. bovis
41
Explain the differences between native, prosthetic and IVDU endocarditis
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
Which organisms are most commonly implicated in prosthetic valve IE?
CoNS/S. aureus VGS enterococcus s. bovis
43
which organisms are most commonly implicated HIV+ IE patients?
s. aureus e. faecalis CoNS VGS pseudomonas sp.
44
What factors predispose patients to nosocomial/healthcare-associated IE?
significant comorbidities more advanced age predominant infection with s. aureus new therapeutic modalities involving intravascular devices
45
In which patients would you find fungal endocarditis?
IV drug users and ICU patients who have received broad-spec antibiotics
46
What is the most significant risk factor for IE?
residual valvular damage caused by a previous episode of endocarditis
47
Describe the difference between acute and subacute native valve endocarditis.
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
Describe early prosthetic valve endocarditis.
occurs within 60 days of valve implantation | due to CoNS, gram -ve bacilli, candida sp.
49
Describe late prosthetic valve endocarditis.
occurs 60 days or more after valve implantation | due to Staph., alpha-haemolytic strep., & enterococci
50
What is the main causative organism for both early and late PVE?
staph. aureus
51
What is the most commonly involved valve and causative organism or IVDU endocarditis?
tricuspid (50%) and s. aureus most common PC = right-sided endocarditis 70%
52
List signs/symptoms of right-sided endocarditis.
``` murmur - not always heard fever pleuritic chest pain dyspnoea non-productive cough ```
53
Describe the location of bacteria and fibrin-platelet thrombi in the context of mitral & aortic insufficiency, according to the Venturi effect.
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
Describe the initial development of pacemaker IE.
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
What are some complications of IE?
glomerulonephritis if it includes glomerular antigen-antibody complex deposition. sepsis, arrhythmias and systemic embolisation fatal if untreated
56
What are some previously common manifestations which have now been eradicated by earlier diagnosis and effective treatment of IE?
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
When might you see a ring abscess in the context of IE?
if the vegetations have eroded into the myocardium
58
Vegetations from subacute endocarditis are assoc. with more valvular destruction than those of acute endocarditis. T/F?
FALSE | vegetations from subacute endocarditis are assoc. with LESS valvular destruction than those of acute endocarditis
59
Describe the histological differences between acute and subacute vegetations.
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
Which heart valve is more susceptible to perivascular abscesses?
aortic valve and its adjacent annulus
61
How can IE lead to sudden cardiac death?
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
Natural Hx and mechanism of death of IE?
Heart failure Infection-induced valvular damage & insufficiency (fatigue, SOB) Perivascular abscesses - can lead to heart block Septic emboli - can lead to acute MI
63
what causes the first heart sound?
closure of AV valves during systole
64
what causes 2nd heart sound?
closure of semilunar valves (aortic + pulmonary) during diastole
65
what makes up the functional unit of the AV valves?
valve leaflet (cusp) + chordae tendineae + papillary muscles
66
Both AV valves are microscopically similar - what is the key difference between them?
mitral has 2 (valve) leaflets and 2 papillary muscles | tricuspid has 3 of each.
67
Describe the annulus of a valve - histology
collagenous crown-shaped structure where the valve leaflets attach to the myocardium
68
what are the 4 layers of elastic and collagenous tissue called in the Av valves?
atrialis, lamina spongiosa, lamina fibrosa, ventricularis
69
Describe the endothelial lining in the semi-lunar valves.
smooth on ventricular side and ridged on arterial side (transfers stress to aortic wall)
70
What are the 3 distinct layers of connective tissue in the semilunar valves?
lamina radialis, spongiosa and fibrosa.
71
Main causes of aortic stenosis?
calcification of valve leaflets - due to repeated endothelial injury bicuspid aortic valves - more prone to stenosis RHD - predisposes to calcification
72
Main causes of mitral stenosis?
``` chronic RHD following rheumatic fever mitral annular calcification carcinoid syndrome serotonergic drugs SLE amyloidosis ```
73
Describe how acute rheumatic fever can lead to R-sided heart failure.
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
"fish mouth" appearance of valve leaflets
mitral stenosis - fusion of and thickening of leaflet and commissures
75
which pathogen causes rheumatic heart disease
RHD classically occurs 2-3 weeks following group A streptococcal pharyngitis (strep pyogenes)
76
How can carcinoid syndrome affect the heart valves?
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
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.
carcinoid heart disease - neuroendocrine tumours
78
what are the 2 disorders within the non-infective endocarditis category?
non-bacterial thrombotic endocarditis (NBTE) endocarditis of SLE (Liebman-Sacks endocarditis)
79
What might you suspect if you saw small bland thrombi on valve leaflets with no underlying structural damage or inflammatory response?
NBTE
80
which patients get NBTE?
patients in hypercoagulable states - underlying malignancy, sepsis, endocardial trauma.
81
What would you suspect if you saw significant valvulitis with sterile vegetations formed from fibrin and immune complexes?
endocarditis of SLE (Liebman sacks)
82
List causes of acute mitral regurgitation.
IE, ischaemic damages to papillary muscles rupture, acute rheumatic fever
83
List causes of chronic mitral insufficiency.
mitral valve prolapse, myxomatous degeneration of mitral valve, mitral annular calcification
84
aortic regurgitation is the result of?
abnormalities of the valve leaflets or aortic root dilation
85
What are the pros and cons of bio-prosthetic valves?
PROS - no anticoagulation needed, can be inserted transcather CONS - only last 10-15 years so will need replacement surgery
86
What are the pros and cons of mechanical valves?
PROS - typically long-lasting CONS - requires life-long anticoagulation with warfarin; some designs have audible clicking sound
87
What are the complications of valve replacements?
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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