• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/38

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

38 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
What are the steps involved in C-diff diarrhea:
1. C.diff causes production of toxins A & B that lead to production of ______ & ________. What is the effect of these (4)?
Then, local production of hydrolytic enzymes leads to what (3)?
C. Diff causes production of toxins A & B that lead to production of TNF-a and pro-inflammatory IL's that:
- increase vascular perm
- recruite PMN's & monocytes
- open epithelial junctions
- cause epithelial apoptosis
Finally local production of Hlytic enzymes leads to:
- CT breakdown (=colitis)
- pseudomembranes
- watery diarrhea
Marked neutropenia and mucositis usually develops ~ 1 week after starting chemo. When does fever occur?

When do CVC infections occur?

When do lung infections occur?
Fever usually develops 1 week later (when bacteremia mostly occurs)
CVC infection signs & symptoms usually appear during the 3rd week after starting chemo
Lung infections tend to occur a few days later, often being recognized only after 5-6days of fever
Hospitalized pt's have are at a greater risk of getting what 5 infections?
1. C.diff
2. UTI's
3. MRSA/VRE
4. Surgical site infections
5. Bacteremia (usually d/t venous catheters)
Complement deficiency states are rare, the only apparently improtant infection risk is for what type of infection (in what type of deficiency?)
Late component compliment deficiency (C5-9) is the most important & the most common type of C-deficiency.
It is associated with a significant increase in meningococcal disease, especially later in life (~17yrs) than in the general populations (3-5yrs). THerefore these ppl should receive the tetravalent vaccine.
What are 3 types of neutrophil dysfunction?
1. presentation in babies?
2. what is the defect? what effect does it have?
3. what is the defect? What is the effect?
1. Leukocyte adhesion deficiency: babies who have high WBC's but develop abscesses with little pus

2. Hyper IgE: defective chemotaxins causes recurrent "cold" abscesses, otitis media & sinusitis

3. Chronic Granulomatous Disease: aka Job's disease - defective intracellular killing d/t abnormal oxidases. Usually produces focal infection from microflora
What infection occurs almost uniformly in pt's recovering from prolonged chemo-induce febrile Np?
*hint*

How/why does this occur?

What 2 things would you expect to find in biopsy?
Hepatosplenic Candidiasis!

During the course of their Np the pt was candidemic at some point. The candida seede the liver and spleen asymptomatically. When neut's recover you get a robust reaction and granuloma formation

Granuloma's & negative tissue sample - this is b/c the disease isn't coming from candida but from the PMN response!!
Not in the lungs!!
Some antiviral drugs are pro-drugs. What do they require in order to become active?

How can this lead to resistance?
Some antiviral drugs need to be P-lated into active agents in the body. P-lation is done a variable # of times and can be done by either host or viral enzymes (therefore can get resistance if virus mutates P-lating enzymes!)
Most antiviral drugs act at what phase of viral replication?

What phase of viral replications currently has not been targeted by any drugs?
Most antiviral drugs act at the TRANSCRIPTION phase of viral replication.

We currently have NO drugs to target the regulation phase of the viral life cycle
What type of mutation produces resistance to Acyclovir?
Viruses can become resistant to acyclovir by having:
- altered thymidine Kinase (P-lating enzyme)
- absent TK
- altered DNA polymerase (less common)
What type of mutation produces resistance to Gancyclovir?

When is this drug used and under what circumstances do viruses become resistant to it?
Virus can mutate it's DNA polymerase gene
(drug is used to treat CMV eye infections in HIV pt's, resistance in seen when they get lots of the drug)
What type of mutation produces resistance to Amantidine?
Mutations in the matrix MS protein such that the drug can no longer prevent viral uncoating
What are the following drugs used for:
- Acyclovir
- Ganciclovir & Foscaranet
Acyclovir
- HSV and varicella zooster (must be given in 1st 72hrs & will only shorten duration by 24hrs)

Ganciclovir / Foscaranet:
- serious CMV infections in ppl with AIDS or Tplants
For what diseases are the following antivirals used?
Amantidine (1)
Ribavirin (1)
Interferon (3)
Amantidine
- influenza A (prevention & tx)

Ribavirin:
- RSV

Interferon:
- HPV, Kapsoi's sarcoma, chronic Hep C
What is the difference between an intermediate host and a definitive host?
An intermediate host is where development of a parasite occurs but not to maturity
A definitive host is where sexual maturity & reproduction occurs
Define each of the following:
Cestode, Nematode, Trematode
Cestode is a segmented flat worm
Nematode is a round worm
Trematode is an unsegmented flat worm
What is the only worm that kills it's human host when it multiplies? (it's found in Canad - eek!)
Strongyloides stercoralis
Who is the definitive host of malaria and who is the intermediate host?
What (in general terms) is the life cycle? From mosquito --> human --> mosquito
Definitive host = the mosquito
Intermediat host = the human
Life cycle:
Mosquito bites --> goes into liver (asymptomatic)
Into the RBC's where they mature and are released (causing RBC lysis)
male & female gametocytes float around in the blood waiting to be picked up by a mosquito so they can get it on!
What are the main differences between protozoa & helminths with regards to their:
- stages of life cycle
- # of cells
- whether or not they multiply
- eosinophilia
- life span
- stages of life cycle
P: trphozoite --> cyst
H: egg --> larvae --> worm

- # of cells
P: single
H: multi

- whether or not they multiply
P: multiply in host
H: don't (except for strongyloides!!)

- eosinophilia
P: no!
H: yes!

- life span
P: indefinite
H: definite
What 2 things does the parasite burden determine?

What is the natural Hx of parasitic infections?
Tissue pathology and morbidity

Natural Hx of parasitic infections is to resolve
What type of TH response mediates the host immune response to intracellular parasites?
What 3 cytokines are involved? What cytokine would allow disease progression?
TH1 is the primary response for intracellular parasites. TH1 cells release:
- IL 2
- TNF
- IFN y
which activate Mphages & resolve the disease

IL4 leads to no Mphage activation and subsequent disease progression
What type of TH response mediates the host immune response to extracellular parasites?
TH2 kills extracellular protozoa with Ab's to complement lyse them, opsonize & neutralize them.
How does the immune system kill tissue helminths?
Tissue helminths are killed with Ab-mediated cytotoxicity:
Ab's coat the worm and attract eosinophils which then bind and degranulate, releasing a whole bunch of things that kill/burn the worm!!
Define the following types of immunity:\
concomitant
premunition
Concomitant - means that you have an adult parasite but are immune to new infections of the same parasite (ie can kill babies only)

Premunition - means that you need constant stimulation of your immune system by a viable parasite, to maintain your immunity (ie need persistent exposure)
What 6 mechanisms do parasites use to evade the immune system?
* hint available *
1. Ag variation (triggering multiple rounds of Ab production)
Malaria

2. Intracellular resistance to phagosome - lysosome fusion
toxoplasmosis

3. Intracellular - resistance to lysosomal enzymes
Leishmaniasis (divides in phagosome)

4. Production of soluble Ag's to soak-up Ab's and prevent them from binding the bug
Typanosomiasis

5. Extracellular mechanical barriers
toxoplasmosis

6. Coating with host Ag (this is how you get concominant immunity - adults are alive but babies/new infections are killed)
Schistosomiasis

7. Immunodepression
Av
r-F
r-Le
sA
MB
CHA
Id
How is each of the following infections contained?
1. Intracellular protozoa
2. Extracellular protozoa
3. Helminths
1. Intracellular protozoa = Cell-mediated immunity (TH1)
2. Extracellular protozoa = Ab +- complement
3. Helminths = Ab-dependant cytotoxicity
The immunocompromised host is MOST susceptible to what type of infection?
IC hosts are most susceptible to intracellular parasites (protozoa) & strongyloides!
What are 5 acquired causes of Ig deficiency?
*hint*
1. Nephrotic Syndrome - renal losses
2. Malabsorption from the gut
3. Protein losing enteropathy
4. Cirrhosis (reduced production)
5. Chronic Lymphocytic Leukemia (CLL)
N s
M
Pl
C
C_ _
Who is more likely to get an infection (both are instances of low flow) a person with cirrhosis or lymphadenopathy (edema d/t Lnode removal)?
Why?
Ppl with ascities are at higher risk, not only does this fluid not have flow but it also has a very low [Ig] and the leakiness of the vessels allows bacteria to escape into the gut.
What does the presence of Howell-Jolly & Heinz bodies indicate?
A pt who has these is at risk for what?
Asplenia!! (the bodies represent functional asplenia as in the case of sickle cell disease - but you can also get surgical asplenia)
Asplenic pt's are at risk for overwhelming infection (d/t P.pneumo & N. meningitidis
Viral load and CD4 count are useful parameters to guide what (respectively)?
Viral load is useful for initiating and monitoring treatment of HIV (but it is not useful with regards to Dx)
CD4 count is inversely correlated to the risk of developing an opportunistic infection
What opportunistic infections are people with HIV prone to:
1. Viral (4)
2. Bacterial (2)
3. Fungi (3)
4. Protozoa(2)
Viral: HSV, HPV, reactivation/cancer, community acquired (flu)

Bacterial: TB, MAI

Fungi: Candidiasis, PCP, dimorphic fungi

Protozoa: Toxoplasmosa & intestinal protozoa
If a person has had long-term immunosuppression with steroids, what type of protozoal infection are they at risk for?
Strongyloides!
Before stem cell transplantation, a pt undergoes "conditioning". What is the effect of this process on the patient?
Neutropenia
Defects in:
phagocytosis
humoral, and
CMI
varying degrees of mucositis
In general what are the 3 phases (ie types of infections seen) of H stem cell transplant pt's?

1. Pre-Engraftment
2. Engraftment (30-100days post)
3. Post-Engraftment
1. Pre-engraftment:
Similar to Febrile Np (infectious mostly caused by NF) or HSV (aspergillus comes later!)

2. Engraftment:
reduced CMI - the extent of this depends on the presence/severity of GVHD and subsequent I-suppression
- pulmonary/GI CMV
-EBV
- Aspergillus & pneumocysits occur later

3. Post-Engraftment (Late phase)
>100days later. Still the scope of disease depends on the presence/severity of GVHD and subsequent I-suppression.
(CMI - deficient = viral infections
Humoral - deficient = bacterial)
Polyoma viruses are DNA viruses (with latency) that are acquired in childhood.
- where is BK virus found? What disease does it cause when reactivated?
- where is JK virus found? What disease does it cause?
BK virus lives (latent) in the UG tract and cause Hemorrhagic Cystitis
(in renal Tplant receipients, it can cause renal graft failure d/t BK Npathy)

JK virus lives latent in the CNS and can cause Progressive Multifocal Leukoencephalopathy when reactivated
CMV infections cause serious illness and we have few treatment options. Under which donor-recepient (infection) states is there the greatest risk of acquiring post-transplant CMV?
If the recipient has no anti-CMV Ab's but the donor does, there is ~30% risk of infection.
What are the common/frequent infections for each of the following solid organ transplants:
- lung
- liver
- renal
Lung: pneumonia d/t MDR normal flora, anatomical dysfunction/intubation, or from host

Liver: infections at Sx anatamoses

Renal: pyelonephritis
Eosinophilia is only associated with what type of parasite? Its degree depends on what?
Eosinophilia is only associated with HELMINTH infections and its degree depends on the extent of tissue invasion.