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First Aid > Heme/Onc 3 > Flashcards

Heme/Onc 3 Flashcards

1
Q

What are 2 classic findings on blood smear in G6PD deficiency?

A

Heinz bodies and bite cells

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2
Q

What test is used to diagnose G6PD deficiency?

A

Fluorescent spot test

Detects generation of NADPH from NADP, positive test if blood spot fails to fluoresce under UV light.

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3
Q

What is the treatment for G6PD deficiency?

A

Avoid triggers

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4
Q

What are spherocytes?

A

Slightly smaller and spherical RBCs that lack central pallor

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5
Q

What is the underlying mechanism of Hereditary Spherocytosis?

A

Abnormal proteins that tie cytoskeleton to RBC membrane, leading to chronic destruction in spleen.

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6
Q

What is the O2 carrying function of spherocytes?

A

Normal

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7
Q

What proteins are commonly involved in Hereditary Spherocytosis?

A

Spectrin, ankyrin

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8
Q

What diagnosis is suggested for a patient from Africa presenting with jaundice, dark urine, anemia, and back pain after an infection?

A

G6PD Deficiency

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9
Q

Hereditary Spherocytosis results in a [low/high] Red Cell distribution Width (RDW). Why?

A

High RDW, due to progressive loss of cell membrane.

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10
Q

What is the MCHC in Hereditary Spherocytosis?

A

High (smaller volume but same amount of hemoglobin)

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11
Q

What is the MCV in Hereditary Spherocytosis?

A

Normal or low (may be normal due to increased reticulocytes)

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12
Q

What is the consequence of loss of membrane flexibility in Hereditary Spherocytosis?

A

More rigid cells and high resistance to blood flow in small vessels (increased viscosity)

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13
Q

Patients with Hereditary Spherocytosis are at risk of aplastic crisis with what infection?

A

Parvovirus B19 (hemolysis is compensated until B19 exposure)

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14
Q

What does the Rule of 3 state regarding RBC count, Hgb, and Hct?

A

Hgb = 3 x Red Blood Cell Count; Hct = 3 x Hgb

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15
Q

What is the suggested diagnosis for a child with infection showing signs of anemia and spherocytes on blood smear?

A

Hereditary Spherocytosis

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16
Q

What test is used to diagnose Hereditary Spherocytosis?

A

Osmotic fragility test

Spherocytes will lyse in hypotonic solution and release Hgb.

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17
Q

What is the treatment for Hereditary Spherocytosis?

A

Splenectomy

Howell-Jolly bodies may appear on blood smear after this treatment.

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18
Q

What are Howell-Jolly bodies?

A

RBCs with nuclear remnants, normally cleared by the spleen

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19
Q

What is hematocrit?

A

Volume % of red cells

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20
Q

What are the 3 components of RBC indices?

A

MVC: Mean corpuscular volume; MCH: Mean corpuscular hemoglobin; MCHC: Mean corpuscular Hgb concentration

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21
Q

How do RBCs in Microcytic Anemias usually appear?

A

Hypochromic (low hemoglobin)

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22
Q

What are the 3 underlying mechanisms of Microcytic Anemias?

A

Loss of iron; Loss of globins; Loss of heme

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23
Q

How is non-heme iron absorbed?

A

Fe3+ is converted to Fe2+ with help of Vitamin C, then absorbed by duodenal epithelial cell.

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24
Q

What is ferroportin?

A

Transports iron out of enterocytes and other cells so it can enter the circulation.

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25
Q

Transferrin levels are [increased/decreased] when iron stores are low.

A

Increased

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26
Q

Where is ferritin stored?

A

Intracellularly in macrophages of liver and bone.

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27
Q

Total Iron binding capacity is the:

A

Amount of transferrin in serum.

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28
Q

Iron deficiency is common in what age group? Why?

A

Babies, iron stores depleted ~6 months.

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29
Q

What can exclusive breast feeding in an infant lead to?

A

Iron deficiency

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30
Q

Malabsorption of iron can result from the loss of:

A

Acid (increases Fe3+)

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31
Q

What must an adult or post-menopausal female with iron deficiency have work-up for?

A

Colon cancer

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32
Q

What are 3 causes of bleeding that can lead to iron deficiency?

A

Menorrhagia; Peptic ulcers; Colon cancer

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33
Q

Prenatal vitamins often contain what?

A

Iron and folate

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34
Q

How to calculate % saturation of transferrin?

A

Iron/transferrin

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35
Q

What is often used to diagnose iron deficiency in pregnancy? Why?

A

Low ferritin

There is an increase in plasma transferrin which leads to a low % saturation.

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36
Q

What are 2 rare causes of iron deficiency?

A

Hookworms: Ancylostoma duodenale, Necator americanus; Plummer-Vinson syndrome

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37
Q

What is the clinical triad seen in Plummer-Vinson syndrome?

A

Iron deficiency anemia, beef red tongue, esophageal webs

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38
Q

What type of anemia does Iron Deficiency Anemia cause?

A

Initially may be normocytic → microcytic, hypochromic anemia

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39
Q

What is the MCV, MCH, and MCHC in Iron Deficiency Anemia?

A

All decreased

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40
Q

Red Cell Distribution Width is often wider in what 3 deficiencies?

A

Iron, B12, folate

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41
Q

Heme is made of what 2 components?

A

Iron + protoporphyrin

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42
Q

Erythrocyte protoporphyrin level will be [increased/decreased] in iron deficiency.

A

Increased (No Fe for protoporphyrin to bind with)

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43
Q

Erythrocyte protoporphyrin level is elevated in what 2 conditions?

A

Lead poisoning, iron deficiency

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44
Q

What is used to screen for iron deficiency and lead poisoning?

A

Erythrocyte protoporphyrin level

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45
Q

What is the treatment for iron deficiency?

A

Iron supplementation

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46
Q

Symptoms from anemia in Anemia of Chronic disease are [common/rare].

A

Rare

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47
Q

What is the mechanism of Anemia of Chronic Disease?

A

Triggered by cytokines: decrease in RBC survival, inadequate EPO level/response, lack of availability of iron (trapped in storage form).

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48
Q

What is Hepcidin? How does it affect iron metabolism?

A

Acute phase reactant produced in the liver; Binds to ferroportin in enterocytes and macrophages → Iron trapped in cells as ferritin.

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49
Q

What is a key lab finding in Anemia of Chronic Disease?

A

↑ ferritin

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50
Q

Can iron supplementation be used to treat Anemia of Chronic Disease?

A

No

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51
Q

What type of anemia does Anemia of Chronic Disease produce?

A

Usually normocytic, 25% microcytic

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52
Q

What is the treatment for Anemia of Chronic Disease?

A

Treat underlying disease

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53
Q

What are the iron studies in Anemia of Chronic Disease?

A

Serum iron: low; Ferritin: high; Transferrin: decreased; % sat: normal

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54
Q

What is a common lead exposure in adults/children?

A

Adults: Inhalation from industrial work (battery factory); Children: Eating lead paint (old house)

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55
Q

Lead inhibits what 2 enzymes in heme synthesis?

A

Delta-aminolevulinic acid dehydratase (δ-ALAD) and Ferrochelatase

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56
Q

Lead poisoning leads to what type of anemia?

A

Microcytic, hypochromic

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57
Q

What can a patient with microcytic, hypochromic anemia and normal iron studies suggest?

A

Beta thalassemia or Lead poisoning

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58
Q

What are the iron studies in Lead poisoning?

A

Normal or low

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59
Q

What is the rate limiting step in heme synthesis?

A

ALA Synthase

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60
Q

What does lead poisoning lead to a buildup of?

A

δ-ALA, Protoporphyrin

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61
Q

What does low levels of heme increase the activity of?

A

ALA Synthase

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62
Q

What are 3 lab findings seen in Lead poisoning?

A

Plasma lead level; ↑δ-ALA; ↑ erythrocyte protoporphyrin

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63
Q

What is seen in a Lead poisoning blood smear?

A

Basophilic stippling

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64
Q

Besides δ-ALAD dehydratase and Ferrochelatase, what else does Lead poisoning inhibit?

A

Pyrimidine 5’ nucleotidase (leads to basophilic stippling)

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65
Q

What are symptoms seen in lead poisoning?

A

Abdominal pain (“lead colic”); Constipation; ‘Lead lines’: Blue pigment at gum-tooth line; Nephropathy: Fanconi-type syndrome, glucose, amino acids, and phosphate wasting; Neuropathy: drop wrist and foot, children may have behavioral issues/developmental delay.

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66
Q

What is Fanconi-type syndrome?

A

Injury to proximal tubules; Results in excess glucose, bicarbonate, phosphates, amino acid, etc loss.

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67
Q

What is the treatment for Lead poisoning?

A

Removal of exposure to lead; Chelation therapy

68
Q

What are 3 chelating agents used in Lead poisoning?

A

Dimercaprol; Calcium disodium EDTA; DMSA

69
Q

What are ‘lead lines’?

A

Blue pigment at gum-tooth line

70
Q

What are Ring sideroblasts?

A

Nucleated red cell precursors that have iron-loaded mitochondria and perinuclear ring of blue granules.

71
Q

Sideroblastic anemia usually causes what type of anemia?

A

Microcytic

72
Q

What are the 2 underlying mechanisms of Sideroblastic anemia?

A

Acquired: Failure to make protoporphyrin usually secondary to a toxin (alcohol, Vitamin B deficiency); X-linked: Inherited deficiency of ALA synthase.

73
Q

X linked Sideroblastic anemia often responds to what treatment?

A

Vitamin B6

74
Q

What are the iron studies in Sideroblastic anemia?

A

Serum iron: increased; Ferritin: increased; Transferrin: decreased

75
Q

What are 2 lab findings seen in Sideroblastic anemia?

A

Iron overload; Low erythrocyte protoporphyrin levels

76
Q

What is thalassemia?

A

Decreased or absent production of globin chains (alpha or beta)

77
Q

All Hgb has two ____ globins.

A

Alpha

78
Q

What is an important diagnostic technique used to evaluate hemoglobinopathies?

A

Hgb Electrophoresis (Different hemoglobin move different distances)

79
Q

How many genes code for alpha chains? Where are they located?

A

4 genes, 2 on each copy of chromosome 16

80
Q

Alpha thalassemia commonly results from what type of mutation?

A

Gene deletion

81
Q

What is Alpha Thalassemia Minima? Clinical presentation?

A

1/4 alpha globin genes mutated; Normal red cells, no symptoms/carrier state.

82
Q

What is Alpha Thalassemia Minor? Clinical presentation?

A

2/4 alpha globin genes mutated; Sometimes mild anemia with ↓ MCV/MCH/MCHC.

83
Q

Alpha Thalassemia Minor is common among what demographic?

A

Asians: cis (αα/–) type more common; Africans: trans (α-/α-) more common.

84
Q

Which type of Alpha Thalassemia Minor is more risk to offspring?

A

Cis (αα/–)

85
Q

What is HbH disease? What does this lead to?

A

3/4 alpha globin gene deletions; Leads to excess beta globin → HbH forms (4 beta chains) which are easily damaged and useless for O2 delivery.

86
Q

HbH disease can lead to what type of hemolysis?

A

Extravascular hemolysis due to RBC deformity; HbH easily oxidized → intravascular hemolysis.

87
Q

How can you diagnose HbH disease?

A

DNA testing (Electrophoresis insensitive)

88
Q

What type of hemoglobin is formed in Hgb Barts? What is the consequence of this?

A

Four gamma globin chains form in utero; Cannot release O2 to tissues → hydrops fetalis → death.

89
Q

How many genes code for β globin chains? Where are they located?

A

2 genes, one on each copy of chromosome 11

90
Q

What is the clinical presentation of Beta Thalassemia Minor?

A

Asymptomatic; May see mild anemia on routine blood work.

91
Q

How to diagnose Beta Thalassemia Minor? What result will you see?

A

↑ HgbA2 (no beta chains) on Electrophoresis.

92
Q

Beta Thalassemia Major is also called?

A

Cooley’s Anemia

93
Q

When does anemia begin in Beta Thalassemia Major? Why?

A

1st year of life, HgbF(α2γ2) production wanes.

94
Q

Beta Thalassemia Major leads to the formation of ______. Clinical manifestations?

A

Alpha chain tetramers → precipitate and cause RBC damage → cleared by the spleen → splenomegaly.

95
Q

What are 3 key features of Beta Thalassemia Major?

A

Abnormal red blood cell shapes; Erythroid hyperplasia; Extramedullary hematopoiesis.

96
Q

What types of RBC abnormalities are seen in Beta Thalassemia Major?

A

Microcytosis; Hypochromia; Anisocytosis: Increased RDW; Poikilocytosis (abnormal shapes); Basophilic stippling; Nucleated RBCs; Target cells.

97
Q

What is Basophilic Stippling? Is seen in what 2 conditions?

A

Residual RNA in red cells, seen in: Lead poisoning; Beta Thalassemia.

98
Q

What are target cells? What conditions can this be seen?

A

Small dark area in center of cell due to ↑ surface area-to-volume ratio; Decreased cell volume: Thalassemia and iron deficiency.

99
Q

What is Basophilic Stippling?

A

Residual RNA in red cells, seen in lead poisoning and beta thalassemia.

100
Q

What are target cells?

A

Small dark area in center of cell due to ↑ surface area-to-volume ratio. Decreased cell volume seen in Thalassemia and iron deficiency; Increased cell membrane seen in liver disease and splenic dysfunction.

101
Q

What is Erythroid Hyperplasia?

A

↑↑ EPO without normal response → massive expansion of bone marrow. Consequence of severe anemia in beta major disease.

102
Q

What symptoms can Erythroid Hyperplasia lead to?

A

Abnormalities of skull and facial bones: ‘Chipmunk facies’, Crew cut appearance of skull on x-ray, delayed skeletal maturation, widening of marrow spaces → osteoporosis.

103
Q

What physical exam finding is associated with Extramedullary hematopoiesis?

A

Hepatosplenomegaly.

104
Q

What virus can cause an aplastic crisis in Beta thalassemia patients?

A

Parvovirus B19.

105
Q

How do you diagnose Beta Thalassemia Major?

A

Electrophoresis: increased HbA2 and HbF, decreased or absent HbA.

106
Q

What is the treatment for Beta Thalassemia Major?

A

Blood transfusion. Complication: iron overload.

107
Q

What is Beta Thalassemia Intermedia?

A

Symptomatic beta thalassemia that does not require transfusions.

108
Q

What do Alpha and beta thalassemia protect against?

A

Malaria (↓ growth of plasmodium falciparum in RBC).

109
Q

How can Red Cell Distribution Width be used?

A

To distinguish iron deficiency and mild thalassemia (normal RDW).

110
Q

What is the inheritance pattern of Sickle Cell Anemia?

A

Autosomal recessive disorder.

111
Q

What is the underlying mechanism of Sickle Cell Anemia?

A

Single base substitution of β gene → substitution of valine (hydrophobic) for glutamate (hydrophilic) → Abnormal beta chains (HbS).

112
Q

What is the problem with HbS?

A

Deoxygenated HbS is poorly soluble and leads to polymerization when O2 low, also in dehydration and acidosis.

113
Q

What RBC appearance is associated with Sickle Cell Anemia?

A

Crescent/sickle shaped.

114
Q

What effect does Sickle Cell Anemia have on ESR?

A

Decreases.

115
Q

What are the two major problems that result from sickle cells?

A

Hemolytic anemia and vaso-occlusion of small blood vessels.

116
Q

What type of hemolysis does Sickle Cell Anemia cause?

A

Mostly extravascular due to continuous sickling/de-sickling leading to RBC membrane damage.

117
Q

What are clinical features of Sickle Cell Anemia?

A

Erythroid Hyperplasia, swollen hands (‘dactylitis’), acute pain crises, spleen failure, splenic sequestration crisis, avascular necrosis, acute chest syndrome, renal dysfunction.

118
Q

What is the treatment for Acute pain crises in Sickle Cell Anemia?

A

Hydration and pain medication.

119
Q

What is a common initial symptom of Sickle Cell Anemia among children?

A

Dactylitis, fingers may look like ‘sausage’ digits.

120
Q

Infection with Parvovirus B19 may lead to aplastic anemia in what conditions?

A

Sickle cell anemia, spherocytosis, thalassemia.

121
Q

What bacteria should Sickle Cell Anemia patients be vaccinated against?

A

Strep pneumoniae and H influenza.

122
Q

What is the common pathogen responsible for osteomyelitis in Sickle Cell Anemia?

A

Salmonella species.

123
Q

What is the leading cause of death in adults with Sickle Cell Disease?

A

Acute chest syndrome.

124
Q

How does Acute chest syndrome present in Sickle Cell Disease?

A

Chest pain and SOB, infiltrates on CXR (looks like pneumonia).

125
Q

What is the treatment for Acute chest syndrome in Sickle Cell Disease?

A

Fluids and pain medication, antibiotics, oxygen, bronchodilators, transfusions as needed.

126
Q

What are four treatments for Sickle Cell Anemia?

A

Immunizations, hydroxyurea (raises amount of HbF), transfusion, bone marrow transplant (curative).

127
Q

What is the Sickle Cell trait?

A

Only 1 mutated beta globin gene, usually no sickling present. Renal medulla may have loss of concentrating ability and ↑ risk of renal medullary carcinoma.

128
Q

How to diagnose Sickle Cell Disease or trait?

A

Electrophoresis: presence of HbS and sickling test.

129
Q

How is the Sickling test performed?

A

Blood sample + Sodium metabisulphite → HbS becomes insoluble and is easily visualized.

130
Q

What is the protective effect of Sickle trait?

A

Protective against Plasmodium falciparum, infection tends to be milder.

131
Q

What is Hemoglobin C?

A

Mutation of beta gene → Glutamic acid replaced by lysine.

132
Q

What do heterozygotes with Hemoglobin C present with?

A

Mild anemia (extravascular hemolysis).

133
Q

What are two key findings in Hemoglobin C?

A

Presence of HbC crystals on smear and ↑ MCHC.

134
Q

What is Hemoglobin SC?

A

One HbS gene plus one HbC gene, same complications as sickle cell disease but at a lower frequency.

135
Q

What are the three underlying mechanisms of Non-hemolytic normocytic anemia?

A

Low iron, low EPO, abnormal marrow.

136
Q

Where is Erythropoietin synthesized?

A

Interstitial cells of the peritubular capillary, in the cortex of the kidney.

137
Q

What type of anemia results from low EPO?

A

Normocytic.

138
Q

What are two EPO injections given to patients with severe anemia of chronic kidney disease?

A

Darbepoetin alfa (Aranesp) and Epoetin alfa (Epogen).

139
Q

What is aplastic anemia?

A

Defective stem cells → Loss of hematopoietic precursors in bone marrow → acellular/hypocellular bone marrow, results in pancytopenia.

140
Q

What is ‘Myelophthisis’?

A

Displacement of bone-marrow tissue.

141
Q

What is the hallmark of Aplastic anemia in bone marrow biopsy?

A

Acellular or hypocellular bone marrow + replacement with fat.

142
Q

What are the symptoms of Aplastic anemia?

A

Anemia → Fatigue, pallor; Thrombocytopenia → Bleeding; Leukopenia → Infections.

143
Q

What is the most common cause of Aplastic anemia?

A

Idiopathic.

144
Q

What are five possible causes of Aplastic anemia?

A

Idiopathic, radiation, chemicals, drugs, viruses, inherited (Fanconi anemia).

145
Q

What is the suggested mechanism of Idiopathic Aplastic anemia?

A

T-cell mediated destruction of stem cells.

146
Q

What are the two treatments for Idiopathic Aplastic anemia?

A

Anti-thymocyte globulin and cyclosporine (both immunosuppressants).

147
Q

What chemical can cause aplastic anemia?

A

Benzene, found in rubber factor and shoe repair shops.

148
Q

What are four drugs that can cause aplastic anemia?

A

Chloramphenicol, methimazole, propylthiouracil (PTU), phenylbutazone.

149
Q

What are five viruses that can cause aplastic anemia?

A

Parvovirus B19, acute viral hepatitis, HIV, EBV, CMV.

150
Q

What is Fanconi Anemia?

A

Inherited aplastic anemia.

151
Q

When does Fanconi anemia usually present?

A

In children <16 y/o.

152
Q

What physical deformities are associated with Fanconi anemia?

A

Short stature, cafe-au-lait spots, malformed thumbs, etc.

153
Q

What mutations are commonly involved in Fanconi anemia?

A

Mutations in DNA repair enzymes, leading to hypersensitivity to DNA damage.

154
Q

What malignancies are associated with Fanconi anemia?

A

Myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), squamous cell carcinoma of head, neck or vulva.

155
Q

What are five treatments for Aplastic anemia?

A

Stop offending agent, transfusions (red cells, platelets), bone marrow stimulation (EPO, GM-CSF, G-CSF), immunosuppression (antithymocyte globulin, cyclosporine), bone marrow transplant.

156
Q

What is Pure Red Cell Aplasia?

A

Absence of erythroid precursors in bone marrow, usually idiopathic.

157
Q

What condition is Pure Red Cell Aplasia associated with?

A

Thymoma.

158
Q

What is Megaloblastic anemia?

A

Red blood cell precursors grow but cannot divide leading to large size, results from abnormal DNA synthesis.

159
Q

What are two findings in Megaloblastic anemia?

A

Large RBCs (↑MCV) and hypersegmented neutrophils (>5 lobes).

160
Q

What are five causes of Megaloblastic Anemias?

A

Folate deficiency, B12 deficiency, orotic aciduria, drugs (MTX, 5-FU, hydroxyurea), zidovudine (HIV NRTIs).

161
Q

What are three causes of Non-megaloblastic Macrocytic anemia?

A

Liver disease, alcoholism, reticulocytosis.

162
Q

What type of antibodies are A and B antibodies?

A

IgM, cannot cross the placenta.

163
Q

What are the antigens part of the Rh system?

A

All transmembrane proteins.

164
Q

Which Rh antigen is highly immunogenic?

A

D antigen.

165
Q

What does ‘Rh positive’ mean?

A

‘Rh positive’ has D antigen; ‘Rh negative’ lacks D antigen.

166
Q

When may a Rh negative individual develop anti-D antibodies?

A

During pregnancy.

First Aid (18 decks)

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