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Week 2 Flashcards

Introduction to Hemolytic Anemia Continued, Extrinsic Non-Immune Defects Leading to HA

1
Q

What conditions cause physical or mechanical injury to red blood cells (RBCs) in non-immune hemolytic anemia?

A

Non-immune hemolytic anemia can result from physical or mechanical injury to RBCs due to:

Abnormalities in microvasculature, the heart, or large blood vessels
Infectious agents
Chemicals
Drugs
Venoms
Extensive burns

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2
Q

What is Microangiopathic Hemolytic Anemia (MAHA)?

A

MAHA is characterized by red blood cell (RBC) fragmentation and thrombocytopenia. The fragmentation occurs intravascularly due to mechanical shearing of RBC membranes as they pass partially blocked microthrombi. The spleen clears the fragments.

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3
Q

What are the classic lab findings in hemolytic anemia?

A

Decreased hemoglobin level
Increased reticulocyte count
Increased serum unconjugated bilirubin
Decreased serum haptoglobin
Increased urine urobilinogen

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4
Q

What can severe RBC fragmentation result in?

A

Severe fragmentation can lead to hemoglobinemia, hemoglobinuria, and marked decreases in serum haptoglobin.

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5
Q

What peripheral blood smear (PBS) findings are associated with MAHA?

A

RBC fragments
Possible helmet cells & microspherocytes
Polychromasia
nRBCs
Thrombocytopenia

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6
Q

What are the four main types of MAHA?

A

Thrombotic Thrombocytopenic Purpura (TTP)
Hemolytic Uremic Syndrome (HUS)
HELLP Syndrome
Disseminated Intravascular Coagulation (DIC)

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7
Q

What is the cause of Thrombotic Thrombocytopenic Purpura (TTP)?

A

TTP is caused by a deficiency of ADAMTS13, leading to the accumulation of ultralong von Willebrand factor (VWF) multimers that bind and activate platelets. This results in severe thrombocytopenia, ischemia (especially in the brain), and hemolytic anemia due to RBC rupture through microthrombi.

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8
Q

What are the three types of TTP?

A

Idiopathic
Secondary
Inherited form

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9
Q

What are the lab findings in TTP?

A

Severe thrombocytopenia
Increased WBC (immature granulocytes)
Decreased hemoglobin
Schistocytes
Polychromasia/nRBCs
Hemoglobinuria
Urinary casts (protein, RBCs)
Increased LDH
Increased serum unconjugated bilirubin
Decreased serum haptoglobin
Normal PT/PTT
Markedly decreased ADAMTS13

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10
Q

What are the main clinical features of TTP?

A

Severe thrombocytopenia
Ischemia, particularly in the brain
Hemolytic anemia (RBC rupture as they pass through microthrombi)

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11
Q

What is the primary treatment for Idiopathic TTP?

A

Plasma exchange
Corticosteroids
Rituximab

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12
Q

How is secondary TTP managed?

A

Treat the primary disease
Support the patient
Poor prognosis in many cases

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13
Q

What is the treatment for inherited TTP?

A

Fresh frozen plasma (FFP)

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14
Q

What are the main therapeutic strategies for TTP?

A

Replacement therapy:

  1. Plasma exchange
    Recombinant ADAMTS13
  2. Immunomodulation:

Rituximab
Glucocorticoids
Splenectomy
Eculizumab, Bortezomib, Cyclosporine

  1. Inhibition of von Willebrand factor binding to platelets:

Caplacizumab
N-acetylcysteine

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15
Q

What causes Hemolytic Uremia Syndrome (HUS)?

A

HUS is caused by bacteria that produce Shiga toxin, often preceded by acute gastroenteritis with bloody diarrhea. The most common cause is ingestion of improperly cooked meat, especially in children.

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16
Q

How does Shiga toxin contribute to HUS?

A

Shiga toxin binds to endothelial cells, particularly in the glomerulus, leading to cell apoptosis. This causes narrowing of small blood vessels, worsened by the activation of platelets and the formation of platelet-fibrin thrombi, resulting in blockages in the microvasculature of the glomeruli and leading to acute renal failure.

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17
Q

What is the outcome of endothelial damage in HUS?

A

Endothelial damage causes narrowing of small blood vessels, formation of platelet-fibrin thrombi, and blockages in the microvasculature of the glomeruli, resulting in acute renal failure.

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18
Q

What is the typical treatment for HUS?

A

There is no specific treatment for HUS. Patients are provided supportive care as needed.

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19
Q

What are the hematologic findings in HUS?

A

Decreased hemoglobin
Decreased platelets
Increased reticulocyte count

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20
Q

What are the peripheral blood film findings in HUS?

A

Schistocytes
Polychromasia
Nucleated red blood cells (severe cases)

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21
Q

What are the biochemical findings in HUS?

A

Markedly increased lactate dehydrogenase (LDH) activity
Increased serum total and indirect bilirubin
Decreased serum haptoglobin
Hemoglobinemia
Hemoglobinuria
Proteinuria, hematuria, and urinary casts

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22
Q

What does HELLP syndrome stand for?

A

HELLP stands for Hemolysis, Elevated Liver enzymes, and Low Platelet count.

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23
Q

What is HELLP syndrome, and why is it a severe complication?

A

HELLP syndrome is a severe complication of pregnancy, often associated with preeclampsia. It results from placental vascular insufficiency and endothelial cell dysfunction, leading to hemolysis, elevated liver enzymes, and low platelet count.

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24
Q

What causes endothelial dysfunction in HELLP syndrome?

A

Endothelial dysfunction in HELLP syndrome is caused by abnormalities in the development of placental vasculature, leading to the release of anti-angiogenic proteins. These proteins inactivate placental and endothelial growth factors, causing vascular insufficiency and promoting fibrin deposition, especially in the liver.

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25
Q

What are the characteristic lab findings of HELLP syndrome?

A

Anemia
Biochemical evidence of hemolysis
Schistocytes on peripheral blood smear (PBS)
Low platelet count
Increased serum lactate dehydrogenase (LD)
Increased aspartate aminotransferase (AST)
PT/PTT within reference intervals

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26
Q

What treatments are typically used for HELLP syndrome?

A

Blood transfusion (for anemia)
Bedrest
Continuous monitoring of mother and baby
Magnesium sulfate (to prevent seizures)
Blood pressure medications
Corticosteroids (to aid fetal lung development)

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27
Q

What is Disseminated Intravascular Coagulation (DIC)?

A

DIC is characterized by the systemic activation of the hemostatic system, resulting in fibrin thrombi formation throughout the microvasculature, leading to organ damage and eventually bleeding.

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28
Q

What are the key laboratory findings in DIC?

A

Prolonged PT/PTT
Decreased fibrinogen level
Increased D-dimer
Anemia and thrombocytopenia on CBC
Fragments and possible polychromasia on peripheral blood smear (PBS)

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29
Q

How does DIC relate to Microangiopathic Hemolytic Anemia (MAHA)?

A

DIC shares similar laboratory findings to other MAHAs, including biochemical signs of intravascular hemolysis, anemia, thrombocytopenia, and RBC fragments on the peripheral blood smear.

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30
Q

What causes Traumatic Cardiac Hemolytic Anemia?

A

Prosthetic cardiac valves can cause hemolysis due to turbulent blood flow passing through and around the implanted devices, leading to mechanical fragmentation of red blood cells (RBCs).

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31
Q

How severe is the hemolysis in Traumatic Cardiac Hemolytic Anemia?

A

The hemolysis is usually mild and compensated by the bone marrow, but severe cases may occur, potentially requiring surgical replacement of the prosthesis and blood transfusions.

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32
Q

What are the characteristic laboratory findings in Traumatic Cardiac Hemolytic Anemia?

A

Increased reticulocytes
Normal platelet count
Increased serum unconjugated bilirubin
Increased plasma hemoglobin
Decreased serum haptoglobin
Hemoglobinuria
Hemosiderinuria & decreased serum ferritin (with chronic hemoglobinuria)

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33
Q

What peripheral blood smear (PBS) findings are characteristic of Traumatic Cardiac Hemolytic Anemia?

A

Fragments of RBCs are characteristic on the PBS due to mechanical fragmentation caused by turbulent blood flow.

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34
Q

What is the genus of the protozoan parasite that causes malaria?

A

Plasmodium.

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35
Q

Which species of Plasmodium is predominantly found in Asia, South and Central America, and also occurs in Southeast Asia, Oceania, and the Middle East?

A

Plasmodium vivax.

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36
Q

Which Plasmodium species is found mainly in West Africa and India?

A

Plasmodium ovale

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37
Q

Where is Plasmodium malariae most prevalent?

A

East Africa and India.

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38
Q

Which species of Plasmodium is predominant in sub-Saharan Africa, Saudi Arabia, Haiti, and the Dominican Republic?

A

Plasmodium falciparum.

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39
Q

Which Plasmodium species is less common than the others?

A

Plasmodium knowlesi.

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40
Q

How has malaria impacted the human genome?

A

It has influenced the evolution of genetic traits like G6PD deficiency and the Duffy antigen.

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41
Q

How does malaria cause anemia?

A

Malaria causes anemia through direct lysis when merozoites are released from RBCs and by the destruction of both infected and non-infected RBCs in the spleen.

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42
Q

Why is Plasmodium falciparum particularly lethal?

A

Plasmodium falciparum is particularly lethal because infected RBCs adhere to endothelial cells in internal organs, especially the brain, leading to cerebral malaria.

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43
Q

What is the significance of a parasite’s ability to invade RBCs in malaria?

A

The ability of the parasite to invade RBCs affects the extent of parasitemia and the severity of the disease.

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44
Q

Which RBCs do Plasmodium vivax and Plasmodium ovale invade?

A

Plasmodium vivax and Plasmodium ovale only invade reticulocytes.

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45
Q

Which RBCs does Plasmodium malariae invade?

A

Plasmodium malariae only invades older RBCs.

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46
Q

Which RBCs does Plasmodium falciparum invade?

A

Plasmodium falciparum invades RBCs of all ages.

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47
Q

What are some common clinical symptoms of malaria?

A

Cyclic fever and chills, rigors, sweating, headache, muscle pain, nausea, and diarrhea. Severe cases may include jaundice, splenomegaly, hepatomegaly, shock, prostration, bleeding, seizures, or coma.

48
Q

What happens to WBC counts during fevers in malaria patients?

A

The WBC count is normal to slightly increased. However, neutropenia with monocytosis may develop during chills and rigors.

49
Q

What laboratory findings are associated with severe malaria?

A

Metabolic acidosis, decreased serum glucose, increased serum lactate, increased serum creatinine, decreased hemoglobin levels, hemoglobinuria, and hyperparasitemia.

50
Q

What laboratory techniques are used to detect malarial parasites in a peripheral blood smear (PBS)?

A

Two thick smears are used to detect the parasite, and two thin smears are used to speciate the parasite and calculate parasitemia.

51
Q

How many blood specimens are required to confirm malaria?

A

Two specimens are required, taken within 24 hours and at least 8 to 12 hours apart, to confirm negativity.

52
Q

How is parasitemia calculated in malaria cases?

A

Parasitemia is calculated by counting how many red cells have malarial parasites in 500 to 3000 RBCs, and then calculating the percentage of infected RBCs per 100 RBCs.

53
Q

Does Plasmodium vivax show Schüffner’s dots?

A

Yes, fine Schüffner’s dots are present.

54
Q

What is the size of infected RBCs in Plasmodium vivax infections?

A

Enlarged RBCs.

55
Q

How many merozoites are present in the schizont stage of Plasmodium vivax?

A

16-24 merozoites.

56
Q

What is the shape of Plasmodium vivax gametocytes?

A

Round or oval.

57
Q

Does Plasmodium ovale show Schüffner’s dots?

A

Yes, large Schüffner’s dots are present.

58
Q

What is the size of infected RBCs in Plasmodium ovale infections?

A

Enlarged RBCs.

59
Q

How many merozoites are present in the schizont stage of Plasmodium ovale?

A

4-16 merozoites.

60
Q

What is the shape of Plasmodium ovale gametocytes?

A

Round.

61
Q

Does Plasmodium malariae show Schüffner’s dots?

A

No, Schüffner’s dots are absent.

62
Q

What is the size of infected RBCs in Plasmodium malariae infections?

A

Smaller to normal size RBCs.

63
Q

How many merozoites are present in the schizont stage of Plasmodium malariae?

A

6-12 merozoites.

64
Q

What is the shape of Plasmodium malariae gametocytes?

A

Round.

65
Q

Does Plasmodium falciparum show Schüffner’s dots?

A

No, Schüffner’s dots are absent.

66
Q

What is the size of infected RBCs in Plasmodium falciparum infections?

A

Normal size RBCs.

67
Q

How many merozoites are present in the schizont stage of Plasmodium falciparum?

A

8-24 merozoites.

68
Q

What is the shape of Plasmodium falciparum gametocytes?

A

Crescent-shaped.

69
Q

What are some key morphological differences of Plasmodium falciparum in blood smears?

A

Numerous rings, smaller rings, no trophozoites or schizonts, crescent-shaped gametocytes.

70
Q

What are some key morphological differences of Plasmodium vivax in blood smears?

A

Enlarged erythrocyte, Schüffner’s dots, amoeboid trophozoite.

71
Q

What are some key morphological differences of Plasmodium ovale in blood smears?

A

Similar to P. vivax, with compact trophozoite, fewer merozoites in schizont, and elongated erythrocyte.

72
Q

What are some key morphological differences of Plasmodium malariae in blood smears?

A

Compact parasite, merozoites in rosette.

73
Q

What is the BinaxNOW malaria test used for?

A

It is a rapid antigen test that detects Plasmodium antigen.

74
Q

What is the molecular-based test (PCR) used for in malaria diagnosis?

A

PCR is used for the detection and speciation of malarial parasites.

75
Q

What does a serology test detect in malaria diagnosis?

A

It detects antibodies, but may not indicate a current infection.

76
Q

What is the mechanism of action of Artemisinin-based combination therapies (ACTs) in malaria treatment?

A

ACTs combine two or more drugs that target the malaria parasite at all stages of its life cycle.

77
Q

How does chloroquine phosphate work as an antimalarial drug?

A

Chloroquine phosphate prevents the malaria parasite from detoxifying the heme metabolite when metabolizing hemoglobin.

78
Q

What is Babesiosis?

A

A tick-transmitted disease caused by intraerythrocytic protozoan parasites of the genus Babesia.

79
Q

How do humans become infected with Babesia?

A

Humans become incidental hosts after injection of sporozoites during a blood meal by infected ticks.

80
Q

Where is Babesia endemic?

A

Babesia is endemic to the US and Europe.

81
Q

What symptoms are associated with Babesiosis?

A

Fever, non-respiratory flu-like symptoms (chills, headache, sweats, nausea, anorexia, fatigue), and possibly jaundice, splenomegaly, or hepatomegaly.

82
Q

What laboratory findings indicate hemolytic anemia in Babesiosis?

A

↓ Serum haptoglobin
Bilirubinemia
Hemoglobinuria
Proteinuria
Leukopenia
Thrombocytopenia
↓ Hemoglobin
↑ Reticulocytes
Abnormal renal and liver tests

83
Q

What is a distinguishing feature of Babesia morphology compared to Plasmodium falciparum?

A

Babesia may show extracellular merozoites.
Rings are vacuolated and don’t produce pigment.
Formation of merozoite tetrads (Maltese cross formation).

84
Q

What method is used to confirm Babesia species if suspected?

A

PCR-based methods after sending the sample to PHL (Public Health Laboratory) for species identification.

85
Q

What causes filariasis?

A

Filariasis is caused by microscopic, thread-like worms that live in the human lymphatic system.

86
Q

What is the severe manifestation of filariasis called?

A

Elephantiasis.

87
Q

How widespread is lymphatic filariasis?

A

It affects over 120 million people in 72 countries.

88
Q

In which regions is lymphatic filariasis most common?

A

Tropics and sub-tropics of Asia, Africa, the Western Pacific, and parts of the Caribbean and South America.

89
Q

What is the life cycle stage of Brugia malayi when the mosquito takes a blood meal?

A

The mosquito takes in the L3 larvae during a blood meal.

90
Q

Where do adult Brugia malayi worms live in the human body?

A

In the lymphatic system.

91
Q

What happens after the adult Brugia malayi worms produce microfilariae?

A

The microfilariae enter peripheral circulation and are then ingested by a mosquito during a blood meal.

92
Q

How do Brugia malayi microfilariae develop in the mosquito?

A

After ingestion, they shed their sheaths, penetrate the mosquito’s midgut, migrate to the thoracic muscles, and develop into L1 and L3 larvae.

93
Q

Does filariasis cause hemolytic anemia?

A

No, filariasis does not cause hemolytic anemia. Most of the damage is limited to the lymphatic system.

94
Q

Do most people with filariasis show clinical symptoms?

A

No, most people do not show clinical symptoms. However, a few may develop lymphedema and elephantiasis.

95
Q

What is the standard method for diagnosing active filariasis infection?

A

The identification of microfilariae in a blood smear by microscopic examination.

96
Q

When should blood collection for diagnosing filariasis be done?

A

Blood collection should be done at night to coincide with the appearance of microfilariae in circulation.

97
Q

How do microfilariae appear on a blood smear?

A

Microfilariae usually appear at the edge of the smear, have a serpentine (worm-like) shape, and do not stain uniformly due to visible internal structures.

98
Q

What WBC abnormality may be present in filariasis?

A

Absolute eosinophilia.

99
Q

What is the treatment for filariasis?

A

Diethylcarbamazine (DEC), which kills microfilariae and some adult worms.

100
Q

Where is Clostridium perfringens commonly found?

A

In raw meat and poultry. It can cause food poisoning if meat products are not cooked properly.

101
Q

What is a rare complication of Clostridium perfringens infection?

A

Sepsis

102
Q

What does Clostridial sepsis cause in terms of hemolysis and urine/plasma appearance?

A

It causes massive intravascular hemolysis and dark red plasma and urine due to increased plasma hemoglobin and hemoglobinuria.

103
Q

What are some laboratory findings associated with Clostridial sepsis?

A

Significantly decreased hematocrit
Spherocytes and microspherocytes
Toxic changes in neutrophils

104
Q

What is the treatment for Clostridial sepsis?

A

Rapid therapy with transfusions, antibiotics, and fluid management is critical for survival.

105
Q

What is the prognosis for Clostridial sepsis?

A

The prognosis is grave.

106
Q

How can drugs and chemicals cause hemolytic anemia?

A

They cause oxidative denaturation of hemoglobin, leading to the formation of methemoglobin and Heinz bodies.

107
Q

What are the typical laboratory findings in hemolytic anemia caused by drugs and chemicals?

A

↓ Hemoglobin level
↑ Reticulocyte count
↑ Serum indirect bilirubin
↓ Serum haptoglobin level

108
Q

What are the peripheral blood smear (PBS) findings in hemolytic anemia caused by oxidative injury?

A

Heinz bodies (using supravital stain)
Bite and blister cells (Wright stain)

109
Q

How do heavy metals like copper and lead affect red blood cells?

A

They cause shortened red cell survival.
Lead to basophilic stippling in the absence of other RBC abnormalities.
RBCs are usually normocytic/normochromic (N/N).

110
Q

What types of venoms can induce hemolytic anemia in some individuals?

A

Venoms from snakes, spiders, bees, or wasps.

111
Q

What are the mechanisms by which venoms can induce hemolysis?

A

Disruption of the RBC membrane.
Alteration of the RBC membrane leading to complement-mediated lysis.
Initiation of Disseminated Intravascular Coagulation (DIC).

112
Q

What type of injury can cause hemolytic anemia due to extensive burns?

A

Thermal injury (extensive burns).

113
Q

What are the typical laboratory findings in hemolytic anemia caused by thermal injury?

A

Fragments
Spherocytes
Microspherocytes
RBC fragmentation and budding

114
Q

How long does it take for the spleen to clear the damaged RBCs after a burn injury?

A

The spleen clears the damaged RBCs within 24 hours of the burn injury.

115
Q

What other situation can cause a similar morphology to that seen in thermal injury?

A

Overheating of blood in malfunctioning blood warmers prior to transfusion or malfunctioning dialysis machines.

Hematology (6 decks)

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