Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Dunedin RACP Study Course > ID - Transplant > Flashcards

ID - Transplant Flashcards

1
Q

Immune defects associated with these malignancy (and their therapies)

  • AML, MDS
  • Aplastic anaemia
  • CLL and MM
  • Lymphoma
A
  • AML, MDS
    – Qualitative/quantitative neutropenia
  • Aplastic anaemia
    – Severe, prolonged neutropenia
  • CLL and MM
    – Hypogammaglobulinemia
  • Lymphoma
    – Functional asplenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Consequence of chemo impacting neutrophils?

A

Cytotoxic agents
–> bacterial, fungal infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cancer drugs -> T cells impact ?

Consequences?

A

Purine analogues – Fludarabine, cladribine

Antithymoctye globulin

CD4+ T cell dysfunction:
* Herpes viruses
* Hep B reactivation
* PJP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does s. pneumonia look like in microscopy

A

diplococci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Classic presentation of S Viridans in HIV patient

A

fevers, rash and stomatitis (think where it lives)

Associated with Viridans Group Strep (VGS) shock syndrome
– about 24-48 hr in 1/3 of cases
– Can have ARDS in ¼ of cases (like TSS)

  • Endocarditis rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

RFs S Viridans in HIV

A

neutropenia, mucositis, high-dose cytarabine– use of Cipro (Cipro barely gets above MIC to be effective Gram Positive abx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Neutropenic Enterocolitis (Typhlitis)

A
  • Necrotizing inflammation with transmural infection of damaged bowel wall
  • Mixed infection – GN, GP, anaerobic
  • Can be accompanied by bacteremia
  • Medical Management (less often surgical)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mgmt Neutropenic Enterocolitis

A

Medical Management (less often surgical)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Skin lesion caused by pseudomonas aeriginosa?

A

erythema gangrenosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Timing of fungal infections in neutropaenia

A

yeasts early (candida), mould later (aspergillus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Difference between yeasts and moulds?

(and examples of each)

A

moulds: multicellular hyphae
- e.g. aspergillus, fusarium

Yeasts: single celled forms that reproduce by budding
- e.g. candida, cryptococcus,

Dimorphic exist also (Yeast in blood, but grow as mould in room temperatures)
- e.g. histoplasma, penicillium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How to anti-fungals usually work?

A

usually act on cell wall,
- exception if 5-FC which is converted to 5-FU and inhibits DNA synthesis (pyramidine analogue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Anti-fungal for prophylaxis in high/ intermediate risk haem amlignancy/ HSCT?

A

Posaconazole in high risk

Fluconazole in Intermediate risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the most rapidly cidal agent for Candida?

A

Caspofungin (the penicillin of anti-fungals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Anti-fungal agent ineffective in cryptococcus?

A

Caspofungin

Cryptococcus (Zygomycetes) lack significant beta-glucan in their cell walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Anti-fungal agent that covers everything?

A

posaconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Anti-fungal agent ineffective in moulds?

A

fluconazole (also flucytosine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Important non-medical management candidaemia

A

MUST REMOVE IV LINES, dilated Eye exam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the most rapidly cidal agent for Aspergillus?

A

Voriconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Agents for cryptococcus

A

Flucytosine with Ampho

21
Q

Hepatosplenic Candidiasis Syndrome

A
  • Inflammatory response to fungi invaded by portal vasculature
  • Presents after engraftment (Return of ANC)
  • Abdominal pain, increased LFTs, prolonged fever
  • Differential – bacteria, lymphoma, fungus
  • C albicans most common

Lots of little abscesses in spleen/ liver after white cells returned and body sees all the things again

22
Q

When to think invasive molds

A
  • With profound neutropenia < 100 cells/mm 3 and >10-15 days)
  • Most common AML – 20 x > than seen with lymphoma/
  • Evidence of Sinusitis
    or
  • Radiographic evidence of Evidence of Pulmonary disease
  • If patient has received Fluconazole prophylaxis before.
23
Q

Diagnosis of invasive moulds

A
  • We rarely make diagnosis now by culture – usually inferred through molecular tests AND CT scan findings:
  • (1–3)-beta-D-glucan test – Candida/Aspergillus/Fusarium (NOT Crypto/Zygomycetes)
    – 60-90% sensitive
  • Galactomannan assay – only picks up aspergillus/penicillium –may have a role in BAL fluid in high risk patients – better sensitivity then culture (80 vs 50%)
  • they both have a poor NPV
  • PCR of BAL + GM diagnosis of proven/probable IPA were 90.2% and 96.4%.
24
Q

Invasive aspergillosis treatment

A

– Voriconazole – PREFERRED
* Follow levels (>2 mg/L favourable response)
* Response is decrease Aspergillus galactomannan level
– No role for combination anti-fungals

– Reduce immunosuppression if possible

– Treatment duration

N Engl J Med, Vol. 347, No. 6

  • 6-12 weeks
  • Until immune recovery
  • Until resolution of disease

– Secondary prophylaxis for further intense immunosuppression

25
Q

AE/ Issues with amphotericin

A
  • Renal failure - ~40-80%
  • RTA1 – acidosis, Hypokalaemia
  • Intense rigors with infusion
  • Cost – newer lipid formulation to combat above

– do work – however cost $$$

  • No Oral options
26
Q

Donor recipient stauts -> highest CMV re-activation risk (in HSCT)

A

Highest in BMT D-/R+ (CMV in their body )
– DIFFERENT THAN SOT!!! (D+/R-)

27
Q

CMV Infection versus CMV disease

A

CMV Infection = illness, versus CMV disease = seropositivity

28
Q

CMV on lung biopsy

A

gold std “Owls’ eyes” in lung bx, now BAL DNA

29
Q

CMV on colitis histology

A

(inclusion bodies) PCR of tissue

30
Q

Manifestiations of GVHD

A

Acute (early ) w/I 100 day
* Fever/rash, GI tract manifestation (hepatitis)
(Herpes viruses/Hepatitis B)

Chronic – late
* Skin – lichen planus, scleroderma
* Hepatic – cholestasis
* Keratoconjunctivitis
* GI
* Pulmonary syndromes

31
Q

What is this on modified acid stain?

A

Nocardia

branching acid fast bacilli indicates nocardiosis,

32
Q

Complications of nocardia in immunocompromised patients

A

branching acid fast bacilli indicates nocardiosis,

Often have concomitant pneumonia (Cavitary)

33
Q

Treatment Nocardia

A

Trimethoprim-sulfamethoxazole

34
Q

CMV prophylaxis in solid organ transplant patients

A

Valganiciclovir
3-6 months after transplant

35
Q

PTLD

A

Post transplant lymphoproliferative disorder

36
Q

Virus related to PTLD

A

EBV

37
Q

Risk factors for PTLD

A

history of organ transplantation and immunosuppression (mandatory to have)

D +, R – 20%

Receipt of organ rich in lymphoid tissue
Intestine (up to 30%) > lung > Heart> Liver (up to 10%) > Kidney(up to 1%)

Antilymphocytic ab use

38
Q

Management of PTLD?

A

Decreasing immunosuppression + RITUXIMAB + Chemo

39
Q

Timing of transplant and PTLD?

A

Biphasic pattern
- 20% cases 1 styr post txplt
- Second peak 7-10 years post txplt

40
Q

Test for BK virus renal failure?

A

BK inclusion in renal tubular epithelium on renal biopsy.

BKV DNA is detected in the urine, followed by detection in the plasma (sensitive but not specific)
Remember rejection could present same way – thus RENAL BX GOLD STD for diagnosis

41
Q

Treatment for BK virus renal failure

A

Decrease immunosuppression most effective

No specific anti-viral treatment has consistently worked

42
Q

PML

A

Progressive Multifocal Leukoencephalopathy\

Rare demyelinating disease of the central nervous system that

results from reactivation of latent JC polyoma virus

43
Q

Agents that -> PML

A

Natalizumab (α4-integrin)

TNF-alpha inhibitors

Rituximab

44
Q

Presentation of PML

A

Insidious onset and steady progression of focal symptoms that include behavioural, speech, cognitive, motor (eg, head tremor), and visual impairment

45
Q

Prescreening transplant

A
46
Q

Strongyloides stercoralis

A

a soil transmitted helminth mainly diffused in tropical and subtropical regions

47
Q

Strongyloides hyperinfection

A

when immunosuppression -> decrease of ususal immune surveillance,

  • triggering an augmentation of the normal life cycle of the parasite and causing massive increases in the reproductive cycle of larvae.
  • Larvae proliferate dramatically in the duodenum, migrate through the bowel wall, and then travel through the venous system to the lungs and back to the small bowel
48
Q

Strongyloides hyperinfection

A

when immunosuppression -> decrease of usual immune surveillance,

  • triggering an augmentation of the normal life cycle of the parasite and causing massive increases in the reproductive cycle of larvae.
  • Larvae proliferate dramatically in the duodenum, migrate through the bowel wall, and then travel through the venous system to the lungs and back to the small bowel
  • Gram Negative meningitis as worms migrate bowel wall
49
Q

Treatment for strongyloides?

A

ivermectin

Dunedin RACP Study Course (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions