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Path4 My Cards > Hematopoietic and Lymphoid System > Flashcards

Hematopoietic and Lymphoid System Flashcards

1
Q

Anemias of increased RBC destruction:

-4 types

A
  1. hereditary spherocytosis
  2. Sickle Cell Anemia
  3. G6PD Deficiency
  4. Thalassemia

*Anything that deforms cells basically

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2
Q

hereditary spherocytosis

  • causes
  • how to remember
A

spherocytosis = “sphere shaped” RBCs

Causes:

  • Intrinsic
  • 75% Autosomal Dominant
  • 25% Autosomal recessive
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3
Q

hereditary spherocytosis

-pathophysiology

A
  • Mutation makes hard for RBCs to keep doughnut shape
  • RBCs are less stable, so lose membrane fragments and adopt simpler sphere shape
  • Sphere shape not as flexible so RBCs get stuck in spleen and lysed more often
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4
Q

hereditary spherocytosis

-Clinical

A
  • Jaundice*
  • Hemosiderosis*
  • Pigment Stones*
  • Splenomegally

*Due to increased hemoglobin degradation

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5
Q

Sickle Cell Anemia

-What is it?

A

Doughnut is also the optimal shape for malaria

As a defensive mechanism, RBCs adopt another shape: sickle shape

(HbS for Sickle Shaped)

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6
Q

Sickle Cell Anemia

-Pathophysiology

A
  • HbS polymerize and stick together when deoxygenated
  • Sickling initially reversible
  • Repeated sickling leads to membrane damage and irreversible sickling
  • Stick in spleen more easily and are destroyed
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7
Q

Sickle Cell Anemia

-Clinical

A
  • Chronic hemolytic anemia
  • increased number of immature RBCs*
  • Hyperbilirubinemia*
  • Prone to infection
  • Splenomegally as adult
  • VASO-OCCLUSIVE PAIN CRISES:
  • ->hypoxic injury to bone marrow
  • ->increased stroke risk
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8
Q

G6PD Deficiency

  • What is normal function?
  • How to remember
A

G6PD: normal function is to recycle reduced glutathione “G for Glutathione”
-Reduced Glutathione is needed to protect cells from oxidative stress

“G6PD…Glutathione…Stress…Bites…Beans”

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9
Q

G6PD Deficiency

-Pathophysiology

A

-Without G6PD not enough reduced glutathione and oxidative stress “bites” membranes of cells creating “bite cells” (think called schistocytes)

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10
Q

G6PD Deficiency

-Symptoms may occur after ingesting:

A
  • FAVA beans
  • MOTH balls
  • Antimalarials
  • Sulfonamides
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11
Q

Thalassemia

-What is it?

A

-Deficient globin synthesis of the a- or B-globin chains

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12
Q

Thalassemia

-Pathogenesis

A

Target cells:

  • cells with unbalanced ratios of globin chains
  • these cells are more likely to be lysed
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13
Q

Thalassemia

-Clinical

A
  • Bone marrow has to work harder to churn out cells
  • Iron overload leading to severe hemosideris
  • NEW BONE FORMATION DUE TO MARROW HYPERPLASIA RESULTS IN DISTINCTIVE “CREW CUT” APPEARANCE OF THE SKULL IN X-RAY
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14
Q

Anemias of diminished erythropoiesis

-Two kinds

A
  1. Iron Deficiency Anemia

2. Pernicious Anemia

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15
Q

Iron Deficiency Anemia

-Causes

A
  • Chronic blood loss
  • dietary deficiency
  • inadequate iron absorption (celiac disease, decreased stomach acid production)
  • Increased iron demands (Pregnancy, Lactation, Infancy*)

*Pregnant women and infants have higher demands in general hehe

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16
Q

Iron Deficiency Anemia

  • Histopathology
  • Clinical
A

Histopathology:

  • Anisocytosis (cigar-shaped cells)
  • microcytic-hyperchromic anemia

Clinical: everything related to iron is low
-low bone marrow iron stores
-low serum iron
-low serum ferritin levels
EXCEPT: total iron binding capacity is increased

17
Q

Pernicious Anemia

  • What is it
  • How to remember
  • Causes
A

-Anemia caused by impaired DNA synthesis and maturation of RBC precursors in Bone Marrow

“No other anemias start with P. P looks like B and F”

Causes:

  • B12 deficiency* (not enough Intrinsic Factor)
  • Inadequate Folate (malnutrition, alcoholism, pregnancy)

*Autoimmune attack of gastric mucosa atrophies the fundic glands

18
Q

Polycythemia

  • What is it?
  • Two classification
  • Two types (which i suppose can apply to each class)
A

Polycythemia is an abnormally high RBC count with increased hemoglobin level

Classifications are Primary and Secondary

Types:

  • Absolute: actual increase in RBC mass
  • Relative: increased hemoconcentration due to a decreased plasma volume
19
Q

Primary Polycythemia

A

Primary Polycythemia:

  • More RBCs without an increase in EPO
  • Eg Polycythemia Vera (“True” Polycythemia:)
  • -> EPO independent RBC proliferation cuz of mutations in EPO receptors
20
Q

Secondary Polycythemia
What?
Caused by?

A 
Too much EPO for a variety of reasons
Reasons:
1. Compensation
-Lung Disease
-High altitude
-cyanotic heart disease
2. Paraneoplastic syndromes
-Tumors (eg Renal Cell Carcinoma) can secrete EPO
3. Genetic Disorders
-chuVash (mutated VHL)
-Prolyl hydroxylase mutations
21
Q

Polycythemia

-Clinical (applies to all types of polycythemia)

A
  • Viscous Blood
  • cardiac function and blood flow impaired as a result
  • Skin Dark Red
22
Q

Leukopenia

  • What is it
  • Types of Causes
A

WBC deficiency

Causes:

  • Decreased Production
  • Ineffective Production
  • Increased Destruction
23
Q

Leukopenia

-Things that lead to Decreased WBC Production

A
  1. Irradiation
  2. Drugs
  3. Viral infections
24
Q

Leukopenia

-Things that lead to ineffective production

A

megaloblastic anemia

25
Q

Leukopenia

-Things that lead to increased destruction

A
  1. autoimmune related

2. idiopathic infections

26
Q

Leukopenia

  • Bone Marrow Responses
  • Clinical
A

Bone Marrow Responses:

  1. Marrow hypercellularity
    - response to excessive destruction (more cells cuz pumping out more WBC progenitors
  2. Marrow Hypocellularity
    - Drugs suppress or are toxic to WBC/RBC production so there are less RBC/WBC progenitor cells

Clinical:
-Vulnerable to infections (duh)

27
Q

Types of Leukemia

A
  1. Acute Promyelocytic Leukemia (APML)
  2. Chronic Myelogenous Leukemia (CML)
  3. Acute Lymphoblastic Leukemia (ALL)

All leukemias have to do with the bone marrow, contrasting to lymphomas which originate in lymph nodes

28
Q

acute promyelocytic leukemia (APML)

  • mutation
  • Tx
A

mutations in genes encoding TFs required for normal myeloid cell differentiation
mutation:
-In the fusion protein PML/RARA (a TRANS-cription gene)
-This blocks differentiation at the ProMyelocytic* stage, increasing cell survival

Tx:
-TRANS-cription gene so Tx with all-TRANS retinoic acid

*aPMl so remember blocks differentiation at the ProMyelocytic stage

29
Q

Chronic Myelogenous Leukemia (CML)

-how to remember

A

myelogenous. ..myeloproliferative disorder…hyperproliferation…hyperproliferation of neoplastic myeloid progenitors
* Unlike APML, CML has the ability to differentiate terminally

30
Q

chronic myelogenous leukemia (CML)

  • Causes
  • What is required to Dx
A

Causes:

  • philadelphia chromosome and or demonstration of BCR/ABL fusion gene*
  • This leads to activation of mutations in tyrosine kinase GF receptors causing increased growth and survival

*philadelphia chromosome and or demonstration of BCR/ABL fusion gene (caused by philadelphia translocation) required to diagnose

31
Q

Acute Lymphoblastic Leukemia (ALL)

A

ALL: second L for Lymphoblasts
-specifically immature B lymphoblasts
Immature=childhood
-this is the most common childhood leukemia (what Steve Davis had)

32
Q

Mature B Cell Lymphomas

A
  1. Diffuse Large B-Cell Lymphoma (Large BCL)
  2. Burkitt Lymphoma
  3. Hodgkin Lymphoma
  4. Multiple Myeloma
33
Q

Diffuse Large B-Cell Lymphoma (Large BCL)

how to remember:

  • who it affects
  • histopathology
  • Gene rearrangements
A

Large=Older
-most common lymphoma in adults

Histopathology:
Large-large cells-LARGE NUCLEOLI

Gene rearrangements:
BCL-Gene rearrangements of BCL2 and BCL6

34
Q 
Burkitt Lymphoma
how to remember:
-Who does it affect
-What causes it
-What gene causes it?
A

who does it affect?:
-Burkitt-kitt-kid:most common childhood malignancy in central africa

what causes it?
-Ebstein Barr Virus
(burkitt has two t’s, Barr has two r’s

What gene causes it?

  • Burkitt-kit-tik which rhymes with mic
  • caused by the MYC oncogene
35
Q

Hodgkin Lymphoma

  • What is it?
  • Who does it affect?
A

What is it?
-Clonal neoplasms of B lymphocytes

Affects who?
-Burkitt was for kids, Large BCL for adults, Hodgkin is the intermediate (10-30 year olds)

36
Q

Hodgkin Lymphoma

  • Cause
  • Dx
  • how to remember these
A

Cause
-arises from a single node or chain of nodes: staging is important as a result

Dx:
-Reed-Sternberg cells: large atypical mononuclear/multinuclear tumor cells

“Sternberg…Staging”

37
Q

Multiple Myeloma

-What (use definition to remember pathophysiology_

A

malignant disorders of terminally Differentiated B lymphocytes
-uncurable (untreated: 6 mo survival, chemo: 3 yr survival)

terminally Differentiated b lymphocytes

  • Destructive lesions*
  • Diffuse Demineralization*
  • Dysregulation of D cyclin
  • what happens to bone marrow cuz of dysregulated d cyclin

terminally differentiated B lymphocytes
-secrete abnormal ab called Bence-jones protein which Block up or destroy lining of kidneys

Path4 My Cards (6 decks)

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