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Block 7 Week 4 > Schistosomiasis -Hunter > Flashcards

Schistosomiasis -Hunter Flashcards

1
Q

What is the risk of schistosomiasis (blood fluke)

A

1/6th of worlds pop

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2
Q

What are the major parasites that cause schistosomiasis?

A

Schistosoma mansoni; S. japonicum; S. haematobium

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3
Q

What are the minor parasites that cause schistosomias?

A

S. mekongi, S. intercalatum

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4
Q

S. manson and S. intercalatum is most commonly located in what country?

A

subsaharan Africa and western hemisphere of S. America

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5
Q

S. haematobium is limited to (blank) and is considered the (blank) schistosoma

A

Africa

urinary

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6
Q

S. Japoncium is found where?

A

china, philliapenes

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7
Q

Where do you find S. mekongi?

A

vietnam

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8
Q

Are the life cycles of the schistosomes similiar?

A

yes

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9
Q

Schistosoma is acquired through (blank)

A

wading through water

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10
Q

What is the life cycle of schistosomes?

A

cercariae enter skin-> migrate to lungs then liver-> then to mesentaric veins-> adults develop here -> males and females copulate and make eggs-> enter intestine-> passed in feces

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11
Q

Are schistoma mansoni eggs large?

A

yes

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12
Q

What is the female version of shistosomes and what does it need to survive

A

miracidia-> needs to be in a snail to survive

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13
Q

What am I talking about:

you need snails and a bad sewer system to have this pathogen survive

A

Schistosoma mansoni

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14
Q

The schistosoma egg cannot hatch until it hits (blank)

A

water

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15
Q

Adult schistomsome are (blank) to the immune system, the eggs are not

A

invisible

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16
Q

Since eggs of schistosomes have to erode its way through the blood vessel and into the bowel, eggs release (blank)

A

enzymes (this are crazy immunogenic)

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17
Q

In S. mansoni, what snail do you need for it to survive?

A

biomphalaria

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18
Q

In S. hematobium, what snail do you need for it to survive?

A

Bulinus

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19
Q

In S. Japonicum, what snail do you need for it to survive?

A

oncomelania

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20
Q

cercariae have a head that senses (blank)

A

amino acids

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21
Q

Use the names of schistosomes to describe life cycle:

A

cercariae- shistosomula- miracidia and cecariae

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22
Q

THe males shcistomsoma mansoni have 2 suckers that do what?

A

link them to the mesentaric veins.

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23
Q

How do the worms hide from the immune system?

A

worms have skin or tegument that allows them to acquire host moecules (such as RBC, glycotproeins and MHC molecules) (makes an antigenic disguise)

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24
Q

Cercarial penetration of skin can cause a transient (blank)

A

dermatitis

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25
Q

Migration of (Blank) through lungs can cause (blank) that can be severe in heavy infections

A

schistosomules

pneumonitis

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26
Q

What adult worms do you find in the superior mesentaric veins?

A

mansoni and japonicum

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27
Q

What adult worms do you find in the vesicle plexus of bladder?

A

hematobium (cause no clinical symptoms)

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28
Q

Onset of egg production causes (blank)

A

katayama fever (allergic response)

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29
Q

Intestinal or urinary bladder symptoms are due to eggs passing though tissue to lumen-> which can result in what?

A

severe hemorrhagic cystitis

gastroenteritis

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30
Q

Eggs swept up into portal circulation to liver cause (blank) and a (blank)

A

granulomas

T-cell mediated delayed hypersensitivity reaction to eggs

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31
Q

Blockage of sinusoids by eggs leads to (blank) and (blank)

A

pipestem fibrosis

portal hypertension

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32
Q

What are the cinical and lab findings of schistosomiasis?

A

Hepatosplenomegaly
Eosinophilia
hyperimmunoglobulinemia

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33
Q

With portal hypertension you wil get (blank), so some patients with schistosomiasis will have this.

A

ascites

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34
Q

In schistosoma mansoni, Eggs will cause fibrotic liver which will cause (blank)

A

pulmonary hypertension

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35
Q

What do the schistosoma mansoni eggs look like

A

like a chicken head with a beak

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36
Q

Schistosoma hematobium are distinguished in a H and E by…

A

have a spine at the ends of their egg

37
Q

If you see blood/burning in the urine then you should think of what schistoma?

A

schistosoma hematobium

38
Q

Schistosoma hematbium is acquired in (blan)

A

africa

39
Q

What do the eggs of schistosoma japonicum?

A

small, no lateral spine and a tiny penis looking thing

40
Q

How do you treat schistomas?

A

praziquantel

41
Q

How can the immune system kill a schistocyte?

A

if the schistocyte has an IgG switch to IgE and immune system recognizes and attacks via granule release

42
Q

Wht are the four malarial parasites?

A

Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
Plasmodium falciparum

43
Q

What is this:

sporocytes enter the skin and go straight to the liver and will rupture the hepatocyte and flood into the blood

A

Malaria

44
Q

The leading cause of sepsis and septic shock is (blank)

A

malaria

45
Q

What is the life cycle of plasmodium?

A

sporozites are injected into skin via mosquito-> merozites enter bloodstrem-> goes to liver-> ruptures heptocytes which releases merozoites->enters blood

46
Q

(blank) form of plasmodium is what infects RBCS-> binds to target receptors of RBC and can get into it without rupture the RBC.

A

merozoite

47
Q

Malaria is a (Blank) disease with many clinical manifestatins caused by proinflamatory and pyrogenic cytokines such as (blank)

A

systemic inflammatory disease

TNF-alpha

48
Q

Where do you classical fever paroxysm?

A 
malaria
P-falciparum-daily 
P. Vivax- every other day
P. Ovale- every other day
P. Malaria-> every third day
49
Q

What are important clinical and laboratory findings of malaria?

A

hepatosplenomegaly, anemia, hyperimmunoglobulinemia

50
Q

What is the disease sequellae of malaria?

A

glomerulonephritis, nephrosis, cerebral malaria (most organ systems affected)

51
Q

(blank) malarias relapse due to liver hypnozites that restablish infection

A

Vivax and Ovale

52
Q

(blank) do not relapse but they can recrudesce (subclinical infection becomes active clinical disease)

A

Falciparum and malariae

53
Q

Explain how malaria works

A

It is an intracellular amoebae which grows within the RBC by consuming the globin portion of hemoglobin leaving behind a black pigement-> eventually the RBC ruputre and the produced merocyte go out and infect other RBCs.

54
Q

What is happening when you have rigors in malaria?

A

RBC are rupturing

55
Q

What are the stages of malaria

A

Cold stage-> hot stage-> diaphoresis

56
Q

What are the relapsing malarias?

A

P. vivax and P ovale

57
Q

What are the recrudescing malaria?

A

p. falciparum and p malariae

58
Q

A patient with plasmodium falciparium is the most common cause of (blank) and (Blank) in the world

A

sepsis and septic shock

59
Q

Malaria loves the (blank) so kills fetuses :(

A

placenta

60
Q

All malarias can cause immune complex disease which can cause (blank) …. worst in p malariae

A

glomerulonephritis

61
Q

Treat falciparum malaria like (blank0

A

sepsis

62
Q

IF you see a patient who is acutely febrile nad has traveled then think (blank)

A

malaria

63
Q

In the ICU if you suspect malaria check blood (blank)

A

glucose

64
Q

How should you treat a Falciparum malaria patient

A

Ensure correct fluid, electrolyte, and acid-base balance. Control fluid replacement to prevent circulatory overload and pulmonary edema. Anticipate renal and respiratory failure
(dont give steroids, heparin, epi)

65
Q

What will you see in the kidney with malarai?

A

lumpy bumpy appearance cuz of immune complex caused by malaria

66
Q

You see (blank) on the outside of malaria infected RBCs

A

Knobs (excretions produced by parasite)

67
Q

How do you know you have plasmodium vivax?

A

stippling on surface, lots of spots more than 12, RBCs get bigger

68
Q

How do you know you have plasmodium ovale

A

Its an ovale… lol

69
Q

How do yo know you have plasmodium malaria?

A

less than 12 dots, stippling, RBCs dont get bigger

70
Q

How do you know you have plasmodium falciparum>

A

can see it sitting on a platelet, you can see the rings, can have multiparasites in one RBCs. can have aplique forms, the gametocyte is crescent moon shaped.
(WHEN YOU SEE RINGS AND BANANAS!!!)

71
Q

Susceptibility to vivax malaria is determined by the presence or absence of (Blank)

A

duffy blood group (parasite receptor)

72
Q

(blank) allele is protective in west africa

A

HLA-B53

73
Q

(blank) is a complex interaction of cell-mediate and humoral immune mechanism; immunity is species, strain and stage specific

A

Acquired immunity

74
Q

Host RBCs dont have MHC on RBC so you dont get an (Blank) when parasites enter them

A

immune response

75
Q

HOw can you get innate and acquired immunity?

A

Duffy blood group
Sickle cell
HLA b53
Antigenic variation and immunosuppresion

76
Q

Is duffy positive or duffy negative helpful to plasmodium vivax

A

helpful, it allows vivax to enter the RBC

77
Q

What are the drugs that kill the erythrocytic froms of malaria?

A

artemisinin (artemisinin combined therapy), chloroquine, doxycycline, halofantrine, quinidine, quinine, mefloquine, proguanil, pyrimethamine-sulfadoxine

78
Q

What are the drugs that kill hepatic forms of erythrocytic forms of malaria and prevents relapses with vivax and ovale?

A

primaquine (contraindicated in G6PD deficiency)

79
Q

Drug resistance in malaria is widespread; particularly (blank) resistance

A

chloroquine

80
Q

(blank) is used for travelers

A

Chemoprophylaxis

81
Q

How do you attempt to get rid of/ prevent malaria?

A

Mosquito control with long-lasting insecticidal nets and residual indoor insecticide sprayin
There is no malaria vaccine

82
Q

What do you use chloroquine (4-aminoquinoline) for?

A

Prophylaxis and Therapy for Blood Stage Parasites (Resistance)

83
Q

What do you use primaquine for (8-aminoquinoline)?

A

Used to Purge Liver Stage Parasites (Hypnozoites of P. vivax and P. ovale)

84
Q

Why didnt eradication of malaria work

A

DDT was bad for people

mosquitos became resistant to DDT and insecticides, lack of funding, lack of community participation

85
Q

Whats the worst malaria?

A

P. falciparum

86
Q

What are the clinical complications of p. malariae?

A

immune complex

glomerulonephritis-leading to nephrotic syndrome

87
Q

What are the clinical complications of p. vivax (p. ovale)?

A

splenic rupture
anemia (mild)
debilitating fevers
higher TNF alpha per parasite

88
Q

What are the clinical complications of p. falciparum?

A 
cerebral coma
anemia
pulmonary edema
renal failure
shock
lactic acidosis
hypoglycemia
tropical splenomegaly
pregnancy (maternal death, stillbirth, low birth weight, anemia)
89
Q

HOw does malaria effect the mosquitos?

A

gametocytes in peripheral blood-> gametocytes are ingested with blood meal-> gamete formation occurs in stomach-> exflagellatio and fertilization occur in stomach-> oocyst formation occurs in wall of stomach-> sporozonite formation and release occur in stomach-> sporozites migrate to salivary gland-> sporozoite are injected into human host when infected mosquito takes second blood meal

Block 7 Week 4 (7 decks)

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