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HEME Micro & Immuno > Malaria and Other infections > Flashcards

Malaria and Other infections Flashcards

1
Q

causes of malaria

A
  • P. vivax
  • P. falciparum
  • P. malariae
  • P. ovale
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2
Q

Genus Plasmodium:
Sporozoa–> Reproduce 1) in RBCs of vertebrate host;
Reproduce 2) in gut of mosquito

A

1) Asexually

2) sexually

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3
Q

Malaria transmitted by:

A

Anopheles mosquitoes

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4
Q

malaria manifestation in host

A

Periodic fever and anemia

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5
Q

3 features aid in identification on staining of RBCs:

A
  • Red nuclear chromatin
  • Blue cytoplasm
  • Brownish-black pigment = hemozoin
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6
Q

what is HEMOZOIN

A

Brownish-black pigment seen on staining; helps ID RBCs in malaria;
They are Protein from degradation of hemoglobin in acidic food vacuoles

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7
Q

Seen In RBCs infected by P. vivax and P. ovale

A

Schuffner’s dots or granules

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8
Q

Morphology of infected RBC

Elongated and irregular in shape or fimbriated

A

P. ovale

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9
Q

Morphology of infected RBC
P. malariae
Trophozoites seen as: 1)
Mereozoites seen as: 2)

A

1) band forms

2) rosettes around central pigment

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10
Q

Morphology of infected RBC

Rings = very small and may contain 2 chromatin dots

A

P. falciparum

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11
Q

Morphology of infected RBC

Parasites lying along margin of cell

A

P. falciparum

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12
Q

Morphology of infected RBC

Gametocytes = large, banana-shaped

A

P. falciparum

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13
Q

Morphology of infected RBC
Schizonts and merozoites not seen in peripheral blood;
Often more than 1 parasite per cell

A

P. falciparum

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14
Q

P. vivax and P. ovale invades what subpopulation of RBCs?

A

immature cells/reticulocytes

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15
Q

P. malariae invades what subpopulation of RBCs?

A

senescent cells

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16
Q

P. falciparum invades what subpopulation of RBCs

A

does not discriminate

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17
Q

P. vivax binds to what type of antigen?

A

Duffy blood group antigens

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18
Q

P. falciparum binds to what type of antigen?

A

glycoprotein A; found on all RBCs, which is why P. falciparum does not discriminate subpopulation of RBCs

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19
Q

1) what condition limits intensity of parasitemia

A

Hemoglobin S associated with sickle cell

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20
Q

Parasite growth retarded under conditions of low oxygen tension

A

Reason why sickle cell limits malaria

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21
Q

Malaria Affected by RBC abnormalities; ID

A

Hemoglobin S associated with sickle cell;
Thalassemias;
Glucose-6-phosphate dehydrogenase deficiencies

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22
Q

Thalassemias

• 1) retards maturation of parasite

A

1) Fetal hemoglobin

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23
Q

Malarial Parasites induce changes in RBC membrane:

  • Alterations in 1)
  • Modification of 2)
  • Incorporation of parasite neoantigens e.g 3) produces a high molecular weight adhesive protein that binds receptors on endothelium leading to obstruction and microinfarcts
A

1) lipid content
2) osmotic properties
3) P. falciparum

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24
Q

Malarial Parasites induce changes in RBC membrane:

how does P. falciparum cause microinfarcts?

A

produces a high molecular weight adhesive protein that binds receptors on endothelium leading to obstruction and microinfarcts

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25
Q

Malarial Parasites generate energy by 1)

A

1) anaerobic metabolism of glucose

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26
Q

Protein from degradation of hemoglobin in acidic food vacuoles

A

hemozoin; helps ID RBC infected by malaria;

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27
Q

Synthesize folate de novo

A

Malaria parasties

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28
Q

Life cycle of malarial parasite:

In mosquito, 1) ruptures and 2) from saliva of mosquito penetrate salivary gland of human; travel to 3) where they undergo SCHIZOGONY producing 4)

A

In mosquito, OOCYST ruptures and SPOROZOITES from saliva of mosquito penetrate salivary gland of human; travel to LIVER where sporozoites undergo SCHIZOGONY producing merozoites;

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29
Q

Life cycle of malarial parasite:

1) are released from hepatocytes, penetrate RBC and becomes 2);

A

MEROZOITES are released from hepatocytes, penetrate RBC and becomes TROPHOZOITE;

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30
Q

Life cycle of malarial parasite:

MEROZOITES are released from hepatocytes, penetrate RBC and becomes TROPHOZOITE;

Then Trophozoite–>____-> ____

gametocytes produced through ASEXUAL reproduction from MEROZOITES

A

Then Trophozoite–>SCHIZONT–> microgametocyte and macrogametocyte

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31
Q

Life cycle of malarial parasite:

1) taken into mosquito stomach with BLOOD meal;
2) undergo fertilization in the mosquito to form OOKINETE which then forms an OOCYST;

Cycle Repeats

A

1) Gametocytes

2) Macro and MICROgametocyte

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32
Q

Pathogenesis of Fever in malaria;

  • Initiated by RBC rupture and release of 1)
  • May result from release of parasite pyrogens
  • May result from release of 2) from 3) involved in ingestion of parasitic or erythrocytic debris
A

1) merozoites
2) IL-1 and/or TNF-α
3) macrophages

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33
Q

Early in malaria, RBCs infected with parasites at different stages of development manifested as: 1)
Later, sporulation is synchronized = 2)

A

1) irregular FEVER

2) fever at 48h intervals

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34
Q

Intravascular hemolysis may occur in 1)

A

1) P. falciparum malaria

35
Q

Circulatory changes in malaria:
1) (type of parasite): adhesion of infected RBCs to endothelium and can impair microcirculation, precipitate tissue hypoxia, lactic acidosis, and hypoglycemia

A

P. falciparum

36
Q

Significant vasodilation leads to decrease in circulating blood volume and hypotension
Brain most intensely affected

A

Circulatory changes in malaria:

37
Q

Cytokines in malaria:
Elevated levels of 1) – modulate effects of endothelial cells, macrophages, monocytes, and neutrophils to destroy parasite

A

1) IL-1 and TNF-α

38
Q

Cytokines in malaria:

High concentrations of TNF-α precipitate 1) by increasing sequesteration of parasitized RBCs in the 2)

A

1) cerebral malaria

2) cerebral vascular endothelium

39
Q

what is premunition?

A

malaria immunity:

Initial immune response by limits parasite multiplication, but does not eliminate infection

40
Q

Malaria:
Prolonged recovery marked by 1) and numbers of parasites;
Recovery requires 2) lymphocytes

A

1) recurrent exacerbation in symptoms

2) both T and B

41
Q

Malaria lengh of infection:
P. falciparum –> 1)
P. malariae has persistent form in 2)
P. vivax and P. ovale has latency in infected hepatocytes (3)

A

1) does not exceed 1 year;
2) SPLEEN;
3) 3-5 years

42
Q

Different stages of the malaria life cycle combatted differently in host:

LIVER stage: 2)

A

Cytotoxic T-cells;

Inflammatory cytokines such as TNF; IFN-alpha; IL-1

43
Q

Different stages of the malaria life cycle combatted differently in host:
asexual erythrocyte stage: 1)

A

antibodies,
ROS
reactive N2 species
TNF-alpha.

44
Q

Clinical signs of malaria:

Hallmark is malarial paroxysm;

1) for 20-60 minutes;
2) for 3-8 hours due to vasodilation;
3) = decrease in fever and profuse sweating

A

Cold stage for 20-60 minutes;
Hot stage for 3-8 hours due to vasodilation;
Wet stage = decrease in fever and profuse sweating

45
Q

Malarial paroxysm occur when?

A

2nd or 3rd week of fever

46
Q

1)
First attack often severe and may last for weeks in untreated;
Become less regular, less frequent, and less severe as parasite disappears from blood

A

1) Malarial paroxysm:

47
Q

Complications of malaria:
1)
Splanchnic capillaries involved = 2)
3) and renal failure in severe disease

A

1) Cerebral malaria
Splanchnic capillaries involved = vomiting, abdominal pain, diarrhea with or without bloody stools
Jaundice and renal failure in severe disease

48
Q

How to diagnose Malaria:

A

thick or thin stained blood smears from capillary or vein;

49
Q

How to diagnose Malaria:
1) of centrifuged parasites in quantitative buffy coat tubes with visualization on a 2)
Less reliable, but rapid and easy

A

1) Acridine orange staining

2) fluorescence microscope

50
Q

Card antigen detection tests

1) = detects protein excreted by P. falciparum

A

ParaSight F

51
Q

Distinguishes between P. falciparum and P. vivax

A

OptiMAL Card antigen detection tests

52
Q

detects parasite lactate dehydrogenase

A

OptiMAL Card antigen detection tests

53
Q

Complete treatment of malaria requires elimination of 3 parasitic forms:
Erythocytic schizont = 1)
• Hepatic schizont =2)
• Erythrocytic gametocyte = 3)

A

1) terminates clinical attack
2) prevents relapse
3) breaks cycle of transmission

54
Q

breaks cycle of transmission of malaria

A

elimination of Erythrocytic gametocyte

55
Q

Babesia microti Transmission

A

via bite of Ixodes tick

56
Q

Intraerythrocytic parasite

A

Babesia microti

57
Q

which pts do Babesia affect more severely

A

asplenic patients

58
Q

Babesia microti Often co-infection with 1)

A

1) Borrelia burgdorferi

59
Q

Northeastern US coasts

A

Babesia microti

60
Q

Manifestations of Babesia:
• Influenza-like symptoms that progress to 1)
• May be thrombocytopenia and leukopenia

A

1) hepatosplenomegaly and hemolytic anemia

61
Q

Diagnosis of Babesia:

A

Maltese cross formation – tetrad of protozoa

62
Q

Giemsa-stained blood smears of Babesia appearance

A

Intraerythrocytic ring-shaped parasites on Giemsa-stained blood smears

63
Q

Hookworms Parasitology:
• Worm with head curved in opposite direction of the body so it appears 1)
•2) structures or cutting plates allow to attach to mucosa of small intestine and suck blood
• Live in 3) for 2-14 years

A

1) hooked
2) Tooth-like
3) intestines

64
Q

ID types of hookworms that cause anemia

A

Necator americanus

Ancylostoma duodenale

65
Q

Manifestations of hookworm:
• 1) at site of skin penetration
• Epigastric pain and abnormal peristalsis
• 2) and hypoalbuninemia

A

1) Pruritus

2) Iron-deficiency anemia

66
Q

Diagnosis of hookworm:

A

Examination of stool for eggs

67
Q

Leishmania donovani

i. Parasitology

A

Obligate intracellular, flagellated parasite

68
Q

Leishmania donovani Transmitted:

A

by phlebotomine sandflies

69
Q

Tropics and subtropics except Australia

A

Leishmania donovani

70
Q

kala azar or Leishmaniasis (disseminated visceral disease) caused by: 1)
it is lethal in many cases;

A

Leishmania donovani

71
Q
  • Majority asymptomatic
  • Fever persistent for 2-8 weeks with reappearance at irregular intervals
  • Anemia with pallor and tachycardia in advanced cases
  • Thrombocytopenia with mucosal bleeding
  • Immune complex glomerulonephritis
A

Manifestations of L. donovani

72
Q

Pathogenesis of L. donovani
• Dissemination from bloodstram to 1) of spleen, liver, bone marrow, lymph nodes, skin, and small intestine
• Proliferation leads to organ enlargement with atrophy of normal tissue

A

macrophages

73
Q

Bartonella bacilliformis

i. Bacteriology

A

Fastidious, facultative intracellular gram-negative rods

74
Q

Endemic to Andes valleys of Peru, Ecuador, and Colombia;

Mortality as high as 40% without treatment

A

Bartonella bacilliformis

75
Q

Bartonella bacilliformis transmission:

A

Transmitted by Lutzomyia verrucarum (phlebotomine sandfly)

76
Q

Bartonella bacilliformis

  • Febrile illness without or without severe hemolytic anemia and hepatomegaly
  • Vascular collapse
A

Carrion´s disease or Oroya fever (acute phase of infection)

77
Q 
Verruga peruana (chronic phase of infection) by Bartonella bacilliformis:
• 1) vascular lesions
• May be mucosal and internal lesions
A

1) Red, hemangioma-like, cutaneous

78
Q

Pathogenesis of Bartonella bacilliformis:

  • Invasion of and proliferation in 1)
  • Re-entry to blood vessels allows for invasion of RBCs leading to hemolysis and severe anemia
A

1) endothelial lining of blood vessels

79
Q

Parvovirus

i. Virology

A

• Icosahedral, non-enveloped DNA virus

80
Q

Parvovirus B19 targets 1)

A

erythroid progenitors

81
Q
  • Respiratory transmission
  • Common in childhood
  • 60% of all adults and 90% of elderly people are seropositive
A

Parvovirus

82
Q

Transient Aplastic Crisis caused by: 1) in conditions such as:
• Patients with sickle cell disease, thalassemias, and acquired hemolytic anemias in adults
• Following bone marrow transplantation

A

Parvovirus

83
Q

Pathogenesis of Parvovirus:

Viral replication leads to 1) halting red cell production

A

1) erythroid progenitor death

HEME Micro & Immuno (11 decks)

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