Brainscape's Knowledge GenomeTM

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


See full index

IHO Week 3 > Malaria Module -Krafts/Regal > Flashcards

Malaria Module -Krafts/Regal Flashcards

1
Q

How was the organism discovered?

A

Infected RBC containing parasite forms hemozoin that is pigmented. Laveran found pigment

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

What transmits malaria?

A

Anopheles mosquito

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

Organism that causes malaria?

A

Plasmodium (Protazoa)

–it is a parasite in the blood

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

Plasmodium vivax, P. ovale, P. malariae

A

low parasite burden
mild anemia
relapses (in P. vivax and P. ovale)

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

Plasmodium falciparum

A
  • infects any stage of RBC
  • high parasite burden
  • severe anemia
  • cerebral and multi-organ symptoms
  • high fatality rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Most common?
Most deadly?
Relapses?

A

Most common = P. vivax, P. falciparum

Most deadly = P. falciparum

Relapses = P. vivax and P. ovale

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

Infection cycle?

A
  1. Sporozoite gets into hepatic cell
  2. Replication of little baby particles in cell == hepatic schizonts
  3. Get released and are called Merozoites that infect RBC
  4. Ring form in RBC becomes trophozoite
  5. Trophozoite –> schizont —->Merozoites get released from RBC —>become gametes that will infect another mosquito
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Characteristics of P. falciparum life cycle?

A

Lots of rings in torphozoite stage

Crescent or sickle shaped gametocytes!

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

Characteristics of P. malariae life cycle?

A

“rosette” arrangement of merozoites

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

Characteristics of P. ovale and P. vivax life cycle?

A

enlarged red cells

Schuffner’s dots in trophozoites

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

Why is P. faciparum so much worse?

A
  1. Able to infect RBC at ANY age.
  2. Causes RBC pathology:
    • “rosettes” -cells clump around infected cell
    • abnormal binding to endothelium - has “knobs” to help bind
    • blood flow impeded
  3. Stimulates high production of cytokines: causes fever, tissue damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Main cause of death in children with P. falciparum?

A

Cerebral ischemia

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

Clinical symptoms:

A
  1. Enlarged spleen: fibrosis, grayish color
    • Where infected RBCs are getting destroyed
  2. Liver enlarged and pigmented
  3. Brain vessels get plugged
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Incubation?
Prodrome?
Symptoms?

A

Incubation: 1-2 weeks

Prodrome: flu-like illness

Paroxysms (episodic): fever/chills, sweating, myalgia

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

Paroxysms of:

P.falciparum:
P. vivax or ovale:
P. malariae:

A

P.falciparum: Quotidian (daily)
P. vivax or ovale: Tertian (every 48 hrs)
P. malariae: Quartan (every 72 hrs)

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

Host resistances to malaria:

Inherieted and immune mediated

A

Inherited: hemoglobinopathies, thalassemias, G6PD def, RBC antigens

Partial immune mediated: develops over time, reduces severity,

**P. falciparum uses antigenic variation to get around this (PfEMP proteins that stick out change)

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

Diagnosis:

A

Gold standard: blood smear (regular and thick)

Rapid immunochromatographic tests if no one is trained to do/read blood smears.

Clinical symptoms

18
Q

Considerations in tx:

A

What area is visited? Resistance? previous use of antimalarials?

Probability of persistent hepatic forms?

Clinical status of disease–Severe?

19
Q

Radical cure?

A

For hepatic forms: P. vivax and P. ovale that can cause relapse.

Primaquine

20
Q

Primaquine

A
  • Radical cure
  • MOA-unknown (maybe generates reactive O2 species?)

gets rid of hyponozoite forms dormant in liver

Unexpected effects: GI distress, nausea, headache, pruritis, leukopenia

**Hemolytic anemin in G6PD def pts

21
Q

1st and 2nd choices for prophylaxis

A
  1. Chloroquine

2. Atoqaquone/proguanil

22
Q

1st and 2nd prophylaxis drugs if chloroquine resistant area?

A
  1. Atovaquone/proguanil

2. Doxycycline or Mefloquine

23
Q

Chloroquine selectivity

A

Parasitized RBC concentrates the drug at least 25 fold more than unparasitized RBC

-drug accumulated in acid pH of the food vacuole

24
Q

Chloroquine MOA:

A

Malaria digests host Hbg –> FPIX (toxic)
Malaria enzyme heme polymerase crystalizes it to Hemozoin (non toxic)

Chloroquine keeps it in toxic form (CQ-FPIX)

25
Q

Chloroquine adverse effects at acute attack doses?

A

dizziness, headache, itching, vomiting, skin rashes. difficulty in visual accommodation

Large doses for prolonged periods = severe EYE DAMAGE and even BLINDNESS

26
Q

Quinine and Quinidine

A
  • More toxic than chloro but no resistance to it

- MOA probs the same

27
Q

Cinchonism = Adverse effects of quinine

A
  • Tinnitus, blurred vision, nausea
  • headache, decreased hearing acuity
  • permanent damage to vision, balance, and hearing can result
28
Q

Quinidine:
MOA:
AE:

A

Blocks Na and K currents
-give IV for severe malaria

AE: cardiac problems

29
Q

Mefloquine

This drug is as serious as Mifflin party in Madison!

A

MOA: same as chloroquine
AE: same as chloroquine

-only used for tx and prevent of chloroquine resistant P.falciparum

**possible neuropsychiatric reaction (hallucinations, depression, disorientation)

30
Q

Atovaquone: MOA

A

Given with Proguanil

Depolarizes parasitic mitochondria and inhibits their electron transport –>selective for parasites :)

31
Q

Proguanil MOA

A

Given with Atovaquone to enhance the MT toxicity and reduce resistance to Ato

inhibits DHFR
Selective for plasmodial enzyme :)

concentrated in erythrocytes

32
Q

Atovaquone-Proguanil

A

Slow onset

GI disturbances :(

33
Q

Artemisinins Combos

A

Artensunate + mefloquine

Artemether + lumefantrine

34
Q

Artemisinins

MOA

A
  • *Produces free radicals that damage parasite proteins
  • inhibit a calcium ion ATPase in P.falciparum

RAPID and potent against MDR organisms

DO NOT USE ALONE –we don’t want to select resistant organisms dude.

35
Q

Lumefantrine

Give with what else?

A

give with Artemether

Rapid initial reduction in parasite biomass :)

36
Q

I’m going to a place with Chloroquine resistant P. falciparum. What should I do, Doc?

A
  1. Quinine + doxycycline

2. Attovaquone/proguanil or Artemether/lumefantrine or Mefloquine

37
Q

Similarities between Chloroquine, Mefloquine, Quinine, and Quinidine?

A

Vision problems as A.E.’s

All probably have similar mechanism to Chloroquine (block FPIX—>hemozoin)

38
Q

What drug might give me pysch problems?

Maybe don’t prescribe this to people with depression…

A

Mefloquine

Serious as Mifflin

39
Q

What gives me GI problems?

A

Atovaquone/Proguanil

40
Q

Doxycycline

A

Inhibits Protein synthesis

IHO Week 3 (11 decks)

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