High Yield Topics-HemOnc Flashcards

1
Q

Describe order of primary hemostasis (platelet plug formation)

A
  1. Endothelial cell damage/injury
  2. Endothelial cell releases vWF and collagen
  3. vWF binds to platelets via Gplb
  4. Platelets release ADP and Ca+2
  5. ADP binds to platelets via P2Y12 –> platelet aggregation
  6. Fibrinogen binds to platelets via Gpllb/Gpllla –> forms mesh
  • platelet plug is temporary and is unstable –> can easily dislodge
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2
Q

What are the coagulation factors of common pathway for coagulation cascade (secondary hemostasis)?

A

10, 5, 2

*STUDY AID: “COMMON” math problem
2 x 5 = 10

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3
Q

What are the coagulation factors of intrinsic pathway for coagulation cascade (secondary hemostasis)?

A

12, 11, 9, 8 —> 10, 5, 2

  • STUDY AID: write down 12-8 (exclude 10 b/c it’s already used for the common pathway)
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4
Q

What are the coagulation factors of extrinsic pathway for coagulation cascade (secondary hemostasis)?

A

7 –> 10, 5, 2

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5
Q

What test is used to measure intrinsic pathway?

A

PTT

  • STUDY AID: intrinsic pathway has more coagulating factors –> PTT (more letters)
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6
Q

What test is used to measure extrinsic pathway?

A

PT

  • STUDY AID: extrinsic pathway has less coagulating factors –> PT (less letters)
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7
Q

Which coagulation cascade pathway is slower?

A

Intrinsic

  • STUDY AID: intrinsic pathway has more coagulating factors –> takes longer
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8
Q

What lab test is used to measure/monitor the effect of Heparin?

A

PTT

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9
Q

What lab test is used to measure/monitor the effect of Warfarin?

A

PT

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10
Q

What lab test(s) will be elevated when common pathway coagulating factors are deficient?

A

Both PT and PTT

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11
Q

What lab test will be elevated in platelet disorders?

A

Bleeding Time (BT)

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12
Q

Immune-mediated platelet destruction that is usually idiopathic and follows a recent infection; caused by antibodies against GpIIb/IIIa antibodies; it’s a diagnosis of exclusion

A

Idiopathic Thrombocytopenic Purpura (ITP)

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13
Q

Abnormal lab finding for ITP

A

↑ Bleeding Time

Thrombocytopenia

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14
Q

Clinical presentation of ITP

A

Increased bleeding

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15
Q

“BONE MARROW” biopsy finding for ITP

A

Megakaryocytes

  • no schistocytes on PBS
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16
Q

A blood disorder due to deficiency of ADAMTS-13 that typically presents in females

A

Thrombotic Thrombocytopenic Purpura (TTP)

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17
Q

What is the function of ADAMTS-13?

A

A protease that degrades vWF

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18
Q

Describe the pathophysiology of TTP

A

ADAMTS-13 deficiency leads to ↓ degradation of vWF –> larger vWF (attached to endothelial cells) –> ↑ platelet adhesion and aggregation –> obstructed vessels –> destruction of RBCs as they pass through vessels –> intravascular hemolysis

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19
Q

Abnormal lab finding for TTP

A

↑ Bleeding Time

Thrombocytopenia

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20
Q

Clinical presentation of TTP

A
Thrombocytopenia
Anemia (hemolytic; ↓ Hb, schistocytes)
Renal Dysfunction (↑ creatinine)
Fever
Neurologic symptoms (confusion)
  • STUDY AID: TTP
    “ The Terrible Pentad”
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21
Q

Blood smear finding for TTP

A

Schistocytes

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22
Q

Toxin-mediated hemolysis that is caused by Shiga-like toxin from EHEC infection that typically presents in children

A

Hemolytic Uremic Syndrome (HUS)

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23
Q

Abnormal lab finding for HUS

A

↑ Bleeding Time
Thrombocytopenia
↑ Creatinine

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24
Q

Why does HUS present with ↑ Creatinine?

A

Toxin mainly affects the KIDNEY (glomerulus) by formation of platelet microthrombi (which causes obstruction and schistocytes)

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25
Clinical presentation of HUS
Kidney failure, BLOODY diarrhea
26
Blood smear finding for HUS
Schistocytes
27
What E. coli serotype causes HUS?
O157:H7
28
A blood disorder caused by widespread clotting factor activation; caused by many factors (sepsis, snake venom, trauma, transfusion)
Disseminated Intravascular Coagulation (DIC)
29
Describe the pathophysiology of DIC
Sepsis/venom/trauma --> widespread clotting factor activation --> ↓ clotting factors, anticoagulant factors (protein C, protein S, antithrombin), platelets, and fibrinogen --> ↑ bleeding state * STUDY AID: DIC " Damn I'm Clotting"
30
Abnormal lab finding for DIC
↑ Bleeding Time ↑ PT/PTT ↑ D-Dimer Thrombocytopenia ↓ Fibrinogen
31
Clinical presentation of DIC
↑ Bleeding, sepsis
32
Blood smear finding for DIC
Schistocytes
33
A blood disorder caused by vWF deficiency; most common inherited bleeding disorder that can present with heavy menstrual bleeding and prolonged bleeding after tooth extraction
Von Willebrand Disease (VWD)
34
Inheritance pattern for Von Willebrand Disease (VWD)
Autosomal Dominant * remember that it is most common type of inherited bleeding disorder!
35
Describe the pathophysiology of Von Willebrand Disease (VWD)
↓ vWF --> ↓ factor VIII activity & ↓ platelet adhesion to vWF --> ↑ PTT (can be normal) & ↑ BT
36
What coagulating factor is carried and protected by vWF?
Factor VIII
37
Tx for VWD
Desmopressin
38
MOA of Desmopressin in treating vWD
Desmopressin ↑ vWF release from endothelium
39
A bleeding disorder caused by GpIb deficiency
Bernard-Soulier Syndrome
40
What activity of platelet is defective in Bernard-Soulier Syndrome?
Platelet adhesion to vWF
41
Abnormal lab finding for Bernard-Soulier Syndrome
↑ Bleeding Time | Thrombocytopenia
42
Blood smear finding for Bernard-Soulier Syndrome
Large platelets * same size as RBCs!
43
A bleeding disorder caused by GpIIb/GpIIIa deficiency
Glanzmann Thrombasthenia
44
What activity of platelet is defective in Glanzmann Thrombasthenia?
Platelet to platelet aggregation due to lack of fibrinogen mesh formation
45
Abnormal lab finding for Glanzmann Thrombasthenia
↑ Bleeding Time
46
Blood smear finding for Glanzmann Thrombasthenia
No platelet clumping
47
A bleeding disorder caused by factor VIII deficiency
Hemophilia A
48
A bleeding disorder caused by factor IX deficiency
Hemophilia B
49
A bleeding disorder caused by factor XI deficiency
Hemophilia C
50
Inheritance pattern for each type of Hemophilia
Hemophilia A: x-linked recessive Hemophilia B: x-linked recessive Hemophilia C: AR
51
Abnormal lab finding for all three types of Hemophilia
↑ PTT * remember factors 8, 9, 11 are all intrinsic pathway coagulating factors!
52
A bleeding disorder caused by ↓ activity of factors II, VII, IX, X, protein C, protein S
Vitamin K deficiency
53
Abnormal lab finding for Vitamin K deficiency
↑ PTT | ↑ PT
54
Conversion of fibrinogen to fibrin requires
Thrombin (factor IIa)
55
Aggregation of fibrin monomers to form fibrin mesh (fibrin polymer) requires
Factor XIIIa
56
Conversion of factor XIII to XIIIa requires
Thrombin (factor IIa) * thrombin activates both fibrinogen and XIII
57
Protein C and S are regulatory ANTIcoagulant proteins that inhibit
Factors VIIIa and Va
58
A hyper-coagulability disorder caused by production of mutant factor V that is RESISTANT to degradation by protein C; presents with ↑ coagulating symptoms (DVT, pregnancy loss)
Factor V Leiden
59
MCV < 80 is ____ anemia
Microcytic
60
MCV=80-99 is ____ anemia
Normocytic
61
MCV > 80 is ____ anemia
Macrocytic
62
Anemia caused by low iron level
Iron deficiency anemia
63
Iron deficiency anemia is considered (micro/macro/normocytic) anemia
Microcytic
64
Iron Studies (Serum Iron, Ferritin, TIBC/Transferrin) for Iron deficiency anemia
Serum Iron: ↓ Ferritin: ↓ TIBC/Transferrin: ↑
65
Unique clinical presentations associated with Iron deficiency anemia
Pica and Koilonychia (nail spooning)
66
What disorder presents with a triad of esophageal webs, iron deficiency, and Dsyphagia?
Plummer-Vinson Syndrome * STUDY AID: "call Plumber When I Diarrhea" - W: Webs (esophageal) - I: Iron Deficiency - D: Dysphagia
67
Anemia caused by defective heme synthesis (porphyrin pathway), which leads to iron overload/accumulation in mitochondria
Sideroblastic Anemia
68
Genetic cause of Sideroblastic Anemia
ALA synthase deficiency
69
Acquired causes of Sideroblastic Anemia (2)
1. Isoniazid (B6 deficiency) | 2. Lead poisoning (inhibits ferrochelatase and ALA dehydratase)
70
Sideroblastic Anemia is considered (micro/macro/normocytic) anemia
Microcytic
71
Iron Studies (Serum Iron, Ferritin, TIBC/Transferrin) for Sideroblastic Anemia
Serum Iron: ↑ Ferritin: ↑ TIBC/Transferrin: ↓
72
Blood smear finding for Sideroblastic Anemia
ringed sideroblasts (basophilic stippling of iron granules in mitochondria of bone marrow cells)
73
Ringed sideroblasts are only visible by using what stain
Prussian blue stain (stain iron)
74
Anemia caused by defective hemoglobin production
Thalassemia
75
Anemia caused by defective synthesis of ALPHA subunit(s) of hemoglobin
α Thalassemia
76
Anemia caused by defective synthesis of BETA subunit(s) of hemoglobin
β Thalassemia
77
Normal Hb subunits
α2β2 * αα | ββ
78
__ (#) gene(s) deletion of alpha subunit of hemoglobin causes no anemia
1 * αα | α\
79
__ (#) gene(s) deletion of alpha subunit of hemoglobin causes mild anemia
2 * αα | \\ (cis) * α\ | α\ (trans)
80
__ (#) gene(s) deletion of alpha subunit of hemoglobin causes severe anemia
3 * α\ | \\
81
__ (#) gene(s) deletion of alpha subunit of hemoglobin causes hydrops fetalis (can't survive)
4 * \\ | \\
82
(trans/cis) deletion of 2 alpha subunit genes in α Thalassemia is more common in Asians
Cis
83
(trans/cis) deletion of 2 alpha subunit genes in α Thalassemia is more common in African Americans
Trans
84
__ (#) gene(s) deletion of beta subunit of hemoglobin causes no anemia
1 * β Thalassemia Minor
85
__ (#) gene(s) deletion of beta subunit of hemoglobin causes severe anemia
2 * β Thalassemia Major
86
β Thalassemia is more prevalent in what ethnicty?
mediterranean descents
87
Unique clinical feature of β Thalassemia Major
Chipmunk facies (due to increased hematopoiesis in other bones)
88
What Hemoglobin type will be present in infants with β Thalassemia Major?
HbF (αα | γγ) * they will be asymptomatic until HbF is depleted
89
What Hemoglobin type will be present in adults with β Thalassemia Major?
HbA2 (αα | δδ) * they will be symptomatic
90
Thalassemia is considered (micro/macro/normocytic) anemia
Microcytic
91
Blood smear finding for Thalassemia
Target Cells
92
Anemia caused by chronic inflammation/infection
Anemia of Chronic Disease
93
What peptide hormone is produced in Anemia of Chronic Disease to decrease gut absorption of iron and to stimulate iron storage?
Hepcidin
94
Where is Hepcidin made?
Liver
95
What chronic disorders are associated with Anemia of Chronic Disease?
Kidney Disease Autoimmune Disease Rheumatologic Disease * STUDY AID: "listen to CD in KAR" - CD: anemia of Chronic Disease - K: Kidney Disease - A: Autoimmune Disease - R: Rheumatologic Disease
96
Anemia of Chronic Disease is considered (micro/macro/normocytic) anemia
Normocytic
97
Iron Studies (Serum Iron, Ferritin, TIBC/Transferrin) for Anemia of Chronic Disease
Serum Iron: ↓ Ferritin: ↑ TIBC/Transferrin: ↓
98
An intrinsic hemolytic anemia that presents with high hemoglobin level in urine due to a gene mutation
Paroxysmal Nocturnal Hemoglobinuria (PNH)
99
Paroxysmal Nocturnal Hemoglobinuria (PNH) is caused by mutation in what gene?
PIGA
100
Describe pathophysiology of Paroxysmal Nocturnal Hemoglobinuria (PNH)
PIGA gene mutation --> ↓ DAF (CD55) and ↓ MIRL (CD59) on RBCs --> RBCs are susceptible to MAC (membrane attack complex) lysis --> hemolysis --> hemoglobinuria esp. at night
101
Lab findings of Paroxysmal Nocturnal Hemoglobinuria (PNH)
Pancytopenia Negative Coombs Test * STUDY AID: PNH - Pancytopenia - Negative Coombs Test - Hibernating (occurs at night)
102
Paroxysmal Nocturnal Hemoglobinuria (PNH) is considered (micro/macro/normocytic) anemia
Normocytic
103
An intrinsic hemolytic anemia that is caused by G6PD deficiency
G6PD Deficiency Anemia
104
G6PD Deficiency Anemia is usually symptomatic after
oxidative stress
105
What are the most common causes of G6PD Deficiency Anemia that increase oxidative stress?
- Dapsone - Sulfa Drugs - Primaquine (malaria tx) - Fava beans
106
What is the function of G6PD?
G6PD converts NADP to NADPH
107
Describe pathophysiology of G6PD Deficiency Anemia
↓ G6PD --> ↓NADPH (necessary to reduce glutathione) --> ↓ reduced glutathione --> ↑ free radicals --> oxidative damage --> denatured hemoglobin
108
G6PD Deficiency Anemia is considered (micro/macro/normocytic) anemia
Normocytic
109
Blood smear finding for G6PD Deficiency Anemia
1. Heinz bodies (denatured hemoglobin) | 2. Bite cells (RBCs bitten by macrophages to remove heinz bodies)
110
Inheritance pattern of G6PD Deficiency Anemia
X-linked recessive
111
An intrinsic hemolytic anemia that is caused by defective RBC cytoskeleton proteins, leading to the loss of biconcave shape of RBCs
Hereditary Spherocytosis
112
What cytoskeleton proteins are defective in Hereditary Spherocytosis?
Spectrin Ankyrin Bands
113
Hereditary Spherocytosis is considered (micro/macro/normocytic) anemia
Normocytic
114
Lab findings of Hereditary Spherocytosis * Know this cold!
↑ MCHC (dense RBCs) | ↑ osmotic fragility (diagnostic test)
115
Clinical presentations of Hereditary Spherocytosis
- Splenomegaly (RBCs can't easily pass through spleen due to its shape) - Negative Coombs test - Jaundice
116
Blood smear finding for Hereditary Spherocytosis
- Spherocytes | - Howell-Jolly bodies (nuclear remnants)
117
How do you distinguish howell-jolly bodies from heinz bodies?
- Heinz bodies are denatured hemoglobin so they contain iron --> needs special stain to be visualized - Howell-Jolly bodies are nuclear remnants so they do NOT contain iron
118
Anemia caused by B12 or folate deficiency, leading to ↓ DNA synthesis
Megaloblastic Anemia
119
What are the three common causes of B12 deficiency?
1. Pernicious Anemia 2. GI surgery (bariatric surgery, ileum resection) 3. Malabsorption (crohn disease, celiac) * B12 storage is big, and therefore B12 deficiency due to malnutrition is rare and can take a long time to develop!
120
What autoimmune disorder is caused by antibodies against gastric parietal cells or Intrinsic Factor?
Pernicious Anemia
121
B12 deficiency is considered (micro/macro/normocytic) anemia
Macrocytic
122
Lab findings of B12 deficiency anemia
↑ Homocysteine | ↑ MMA
123
What clinical symptom is only present in B12 deficiency anemia and not in folate deficiency anemia?
Neurological symptoms (due to lack of B12 needed to synthesize myelin sheath) * STUDY AID: think of dirty medicine's MMA (knocking off ileum and the head)
124
B12 absorption requires
Intrinsic Factor (IF)
125
What cell produces Intrinsic Factor (IF)?
Gastric parietal cells
126
B12 absorption occurs in what part of GI tract?
Ileum
127
What are the two common causes of folate deficiency?
1. Malnutrition | 2. Drugs (Methotrexate)
128
Folate deficiency is considered (micro/macro/normocytic) anemia
Macrocytic
129
Lab findings of folate deficiency anemia
↑ Homocysteine * normal MMA
130
Blood smear finding for Megaloblastic Anemia (both types)
Hyper-segmented neutrophils
131
How do you distinguish Von Willebrand disease from Bernard-Soulier since they both increase BT (affect primary hemostasis)?
Von Williebrand disease have normal platelet count and is the most common inherited bleeding disorder
132
How do you distinguish ITP from Glanzmann thrombathenia since they are both caused by defective GpIIb/GpIIIa?
ITP: thrombocytopenia, normal PBS | Glanzmann Thrombasthenia: normal platelet count; no platelet clumping on PBS
133
What intrinsic hemolytic anemias (2) are caused by a mutation in B-globin gene?
1. Sickle Cell Anemia | 2. HbC disease
134
What single amino acid substitution occurs in sickle cell anemia?
Glutamic Acid --> Valine * missense mutation
135
Mutant HbA in sickle cell anemia is called
HbS
136
Describe pathogenesis of sickle cell crisis
1. O2 unloading state (low O2 state, high altitude, acidosis, ↓2,3-BPG) 2. Sickling (HbS polymerization/agglutination) 3. Anemia, vaso-occlusion, pain
137
Treatment for sickle cell crisis
- Hydroxyurea (↑HbF) - Hydration - Gardos channel blockers (↓polymerization of HbS)
138
How can sickling of RBCs in sickle cell anemia patients affect spleen?
Sickle cells can sequester in the spleen due to their abnormal shape and cause splenic infarction * functional asplenia
139
Sickle cell anemia patients are at increased risk for what organisms?
Encapsulated organisms (strep. pneumo, H. flu, Neisseria meningitis, Salmonella)
140
What is transient arrest of erythropoiesis due to bone marrow failure
Aplastic crisis
141
Sickle cell anemia patients are prone to "aplastic crisis" due to infection by
Parvovirus B19
142
Blood smear finding for Sickle Cell Anemia
Sickle cells
143
X-ray finding for Sickle Cell Anemia
Crew cut on skull (due to marrow expansion from increased erythropoiesis)
144
Heterozygotes (only one B-chain is affected) for sickle cell anemia
Sickle Cell Trait
145
Patients with sickle cell trait have resistance against
malaria
146
Hematologic lab findings for sickle cell trait
NORMAL hematologic values as general population
147
What single amino acid substitution occurs in HbC disease?
Glutamic Acid --> Lysine * missense mutation
148
Blood smear finding for HbC disease
Target cells
149
What are the substrates/intermediates of Heme synthesis pathway?
``` Glycine Succinyl CoA Aminolevulinic Acid (ALA) Porphobilinogen Hydroxymethylbilane Uroporphyrinogen III Coproporphyrinogen III Protoporphyrin Heme ``` *STUDY AID: Get Some Additional Points Having Understood the Correct Pathway for Heme
150
What is the rate limiting step of heme synthesis pathway, enzyme, and required cofactor?
Glycine + Succinyl CoA ---> Aminolevulinic Acid (ALA) * Enzyme: ALA Synthase * Cofactor: B6
151
What heme intermediate is produced in the mitochondria and gets transported out into cytosol?
Aminolevulinic Acid (ALA) * STUDY AID: going "a la" cytosol
152
What heme intermediate is produced in the cytosol and gets transported back into mitochondria?
Coproporphyrinogen III * STUDY AID: "Cop" me some mitochondria
153
What is the last step of heme synthesis pathway, enzyme, and required cofactor?
Protoporphyrin ---> Heme * Enzyme: Ferrochelatase * Cofactor: Fe+2
154
What enzyme converts Aminolevulinic Acid (ALA) to Porphobilinogen?
ALA Dehydratase
155
What enzyme converts Porphobilinogen to Hydroxymethylbilane?
Porphobilinogen Deaminase
156
What enzyme converts Uroporphyrinogen III to Coproporphyrinogen III?
Uroporphyrinogen Decarboxylase
157
Congenital sideroblastic anemia is caused by
ALA synthase deficiency
158
Acquired sideroblastic anemia is caused by lead poisoning inhibiting what two enzymes?
1. ALA dehydratase | 2. Ferrochelatase
159
Children are exposed to lead via
lead paint
160
Adults are exposed to lead via
batteries, ammunition
161
X-ray finding for Lead poisoning
Lead lines (deposition) on Metaphysis on long bones
162
Blood smear finding for sideroblastic anemia caused by lead poisoning or ALA synthase deficiency
Basophilic stippling or ringed sideroblasts
163
Porphyria (heme synthesis disorder) caused by Porphobilinogen Deaminase dysfunction
Acute Intermittent Porphyria
164
Clinical presentations of Acute Intermittent Porphyria
- Port wine colored urine - Painful abdomen - Polyneuropathy - P450 inducers - Psychological symptoms * STUDY AID: The 5 P's
165
Porphyria (heme synthesis disorder) caused by Uroporphyrinogen Decarboxylase dysfunction
Porphyria Cutanea Tarda
166
What are the acquired cause of Uroporphyrinogen Decarboxylase dysfunction?
Hep C
167
Clinical presentations of Porphyria Cutanea Tarda
Blistering hyperpigmentation | Photosensitivity
168
Porphyria Cutanea Tarda is exacerabated by
Alcohol consumption
169
The most common type or porphyria
Porphyria Cutanea Tarda * this means it's higher yield!
170
Lymphoid or myeloid neoplasm with widespread involvement of bone marrow; tumor cells are usually found in peripheral blood
Leukemia
171
Describe Dirty Medicine's spectrum for "Leukemias"
ALL CML AML CLL * ALL and CLL for "lateral" sides of the spectrum * CML and AML for "medial" sides of the spectrum
172
Describe Dirty Medicine's way of distinguishing b/w LYMPHOID vs. MYELOID leukemias on CBC w/ diff
Lymphoid Leukemia: ↑ lymphocytes (T-cells, B-cells) Myeloid Leukemia: ↑ Neutrophils
173
Describe Dirty Medicine's way of distinguishing b/w ACUTE vs. CHRONIC leukemias
Acute leukemia: Immature cells Chronic leukemia: Mature cells
174
Describe Dirty Medicine's spectrum for the most affected age group for each "Leukemia" type
ALL CML AML CLL 10 40 50 80
175
Which leukemia is + for TdT marker?
ALL
176
Which leukemia has Philadelphia chromosome (t: 9:22)?
CML
177
Which leukemia is + for myeloperoxidase stain?
AML
178
Which leukemia has Auer rods visible on blood smear?
AML
179
Tx for ALL
Cytarabine (aka. ARA-C)
180
Tx for CML
Bcr-abl tyrosine kinase inhibitors | - Imatinib
181
Tx for AML
All-trans retinoic acid (ATRA) aka. Vitamin A
182
B cell, T cell, and NK cells all arise from
lymphoid stem cell
183
Erythrocyte, platelet, granulocytes, and macrophage all arise from
myeloid stem cell
184
Which leukemia is associated with Down syndrome?
ALL
185
Polycythemia vera is a disorder of ↑ RBCs due to acquired mutation of
JAK2
186
Clinical presentations of Polycythemia vera
- Aquagenic pruritus (itching after shower) | - Erythromelalgia (severe, burning pain and red/blue coloration of extremities)
187
Lab finding of Polycythemia vera
↑ RBCs | ↓ EPO (erythropoietin)
188
How do you distinguish b/w primary vs. secondary polycythemia vera?
Primary: ↑ RBCs and ↓ EPO Secondary: ↑ RBCs and ↑ EPO * secondary polycythemia vera is caused by ↑ EPO
189
Tx for polycythemia vera
Phlebotomy | Ruxolitinib (JAK 1/2 inhibitior)
190
Uncontrolled proliferation and bone marrow infiltration by malignant PLASMA cells
Multiple Myeloma
191
Clinical presentation of Multiple Myeloma
- hyperCalcemia - Renal involvement - Anemia - Back Pain * STUDY AID: CRAB
192
Describe how multiple myeloma can cause anemia
Bone marrow infiltration by malignant PLASMA cells → suppression of hematopoiesis → leukopenia, thrombocytopenia, anemia
193
Describe how multiple myeloma can cause renal dysfunction
Overproduction of monoclonal immunoglobulin and/or light chains --> ↑ excretion --> kidney damage
194
Which type of immunoglobulin is overproduced in multiple myeloma?
IgG > IgA * IgG in 55% of cases!
195
X-ray finding for Multiple Myeloma
"Punched out" holes (bone lytic lesions) in the skull
196
Blood smear finding for Multiple Myeloma
Rouleaux formation * RBCs are stacked in a row
197
Bone marrow biopsy finding for Multiple Myeloma
> 10% monoclonal plasma cells with clock-face chromatin
198
CML can progress into what other type of leukemia?
AML *20% chance of CML to become AML!