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From Flashcardlet > Patho 7 - Blood > Flashcards

Patho 7 - Blood Flashcards

1
Q

What do the blood cells stem from embryonically?

A

Mesoderm

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2
Q

What percentage of blood is cells?

A

45%

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3
Q

What percentage of blood is plasma?

A

55%

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4
Q

What organ produces and matures blood cells?

A

Bone marrow

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5
Q

What percentage of plasma is water?

A

90%

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6
Q

What is the remaining 10% of plasma comprised of?

A

Proteins, mainly albumin

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7
Q

What is serum?

A

The fluid remaining after blood clots

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8
Q

Which part of the bone marrow actively produces blood cells?

A

Red marrow

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9
Q

What does yellow marrow do?

A

Serves as a storehouse for fat, can become red marrow if necessary

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10
Q

Where is red marrow located within the bone?

A

Central cavity of bones

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11
Q

What bones contain red marrow?

A 
Spine
Pelvis
Ribs, sternum
Femur, tibia
Cranium
Proximal ends of long bones
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12
Q

Wy does only 25% of red marrow produce red cells if they are the most abundant cellular component?

A

75% of red marrow produces white blood cells because they have a shorter life span

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13
Q

What binds to albumin?

A

Transport hormones
Fatty acids
Bilirubin

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14
Q

What is hematopoiesis?

A

Generation of blood cells

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15
Q

What is the common ancestor of all blood cells?

A

Pluripotent hematopoietic stem cell

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16
Q

What are the specialized multi potent stem cells of the blood cells?

A

Progenitor cells - lymphoid and myeloid

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17
Q

Which blood cells are derived from the lymphoid line?

A

B and T lymphocytes

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18
Q

Which blood cells are derived from the myeloid line?

A

All cells other than lymphocytes

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19
Q

Where are the cellular elements of the blood produced in the fetus?

A

Liver and spleen, long bones

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20
Q

What is extra medullary hematopoiesis?

A

Blood cell production by the liver and spleen in an adult

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21
Q

What is hemoglobin?

A

Compound in RBCs to which oxygen attaches for transport from lungs to tissues

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22
Q

What substances does the synthesis of hemoglobin require?

A

Iron
B12
B6
Folic acid

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23
Q

Which blood cells do not have a nucleus?

A

RBC do not have nucleus

WBC have nucleus

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24
Q

What organ stimulates the production of RBCs, and with what hormone?

A

Kidney stimulates production with EPO

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25
Q

What organ removes old RBCs?

A

Spleen

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26
Q

How long does it take for a pluripotent stem cell to mature to a reticulocyte?

A

One week

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27
Q

How long does it take for a reticulocyte to mature to a RBC?

A

1-2 days

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28
Q

What does the percentage of reticulocytes in the blood reflect?

A

How active the marrow is in producing new RBCs

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29
Q

What is the lifespan of lymphocytes and monocytes?

A

Days

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30
Q

What is the lifespan of granulocytes?

A

Days

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31
Q

What is the lifespan of platelets?

A

7-10 days

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32
Q

Why do you need to stop aspirin use a week before surgery?

A

Because the lifespan of a platelet is about a week, and aspirin acts on the platelet for the lifespan of the platelet

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33
Q

What stimulates the kidney to produce EPO?

A

Amount of oxygen delivered to the kidney by RBCs

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34
Q

What WBCs show up first in viral infections?

A

Lymphocytes

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35
Q

What WBCs show up first in bacterial infections?

A

Neutrophils

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36
Q

What tests are included in the CBC?

A
  • WBC count
  • WBC differential
  • RBC count
  • Hemoglobin
  • Hematocrit
  • Platelet count
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37
Q

What is hematocrit?

A

The percentage of RBCs in the blood volume

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38
Q

What three values are used to calculate the RBC indices?

A

MCV - mean cell volume
MCHC - mean cell Hgb concentration
MCH - mean cell Hgb

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39
Q

What are red cell indices?

A

Measurement of the size and hemoglobin content of the average RBC

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40
Q

What is the MCV?

A

Average size of a RBC

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41
Q

What is the MCH?

A

Average amount of hemoglobin in an average RBC

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42
Q

What is the MCHC?

A

Average concentration of hemoglobin per unit of volume in the average RBC

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43
Q

What type of hemoglobin is the normal hemoglobin?

A

Hemoglobin A

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44
Q

How do you determine the hematocrit from the hemoglobin value?

A

Hgb x 3 = Hct%

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45
Q

What is the problem in RBC production if the reticulocyte is low?

A

Problem in the bone marrow

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46
Q

What is the problem in RBC production if the reticulocyte is high?

A

Demand for RBCs in the body is high - maybe the spleen is prematurely destroying the RBCs

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47
Q

What hormones stimulate the production of WBC?

A

Interleukin

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48
Q

Why do blood diseases feature too many or too few cells?

A

Because of an imbalance in the production or loss of cells

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49
Q

How many protein strands and iron molecules make up hemoglobin?

A

4 protein strands

4 iron

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50
Q

What conditions can cause the improper assembly of hemoglobin?

A
  • Genetic conditions interrupt synthesis of protein strands

- Loss/dietary deficiency of iron

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51
Q

What do malignancies of WBCs produce?

A
  • Large numbers of abnormal WBCs

- Crowd out normal cells in marrow and blood

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52
Q

What is anemia?

A

Abnormally low hemoglobin in the blood

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53
Q

What is anemia caused by?

A
  • Blood loss (hemorrhage)
  • Premature RBC destruction (hemolytic)
  • Insufficient RBC production
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54
Q

What is anemia a clinical sign of, in general?

A

Always a sign of some underlying condiiton

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55
Q

What are some symptoms of anemia?

A
  • Low RBC count
  • Fatigue
  • SOB
  • Weakness
  • Palor
  • Tachycardia
  • Palpitations
  • Tachypnea
  • Angina
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56
Q

Why does tachycardia present with anemia?

A

The body demands more oxygen so the heart needs to pump more frequently

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57
Q

What are some specific symptoms of hemolytic anemia?

A
  • Increased bilirubin
  • Jaundice
  • Skin can be ashy/pale too
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58
Q

What is the body trying to establish when experiencing anemia?

A

Trying to reestablish perfusion - increase cardiac output

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59
Q

What does chronic hemorrhage cause, in terms of type of anemia?

A

First causes anemia of hemorrhage, but can cause failed red blood cell production due to iron deficiency (because body cannot recycle iron from lost blood)

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60
Q

What are the two problems that blood loss causes?

A

Loss of oxygen carrying capacity, and loss of iron

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61
Q

What is dilutional anemia?

A

Volume of lost red cells is initially replaced by water and albumin synthesis by liver - experienced until marrow can replace the lost RBCs

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62
Q

What conditions result in chronic blood loss?

A
  • Menstruation

- Intestinal bleeding (undetected colon cancer)

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63
Q

What happens to bone marrow with hemolytic anemia?

A

Active, hyper cellular bone marrow - works overtime to replace dying cells

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64
Q

What happens to the kidney with hemolytic anemia?

A

Increased EPO to stimulate RBC production

Splenomegaly

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65
Q

What happens to reticulocyte counts in hemolytic anemia?

A

High reticulocyte count

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66
Q

Why does hemolytic anemia present with increased bilirubin levels?

A

Bilirubin is a metabolic product of hemoglobin breakdown

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67
Q

What type of anemia (cytic/chromic) presents with acute hemorrhage?

A

Normocytic normochromic

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68
Q

What type of anemia (cytic/chromic) presents with chronic hemorrhage?

A

Microcytic hypochromic

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69
Q

Why does chronic hemorrhage produce microcytic hypo chromic anemia?

A

Body is not recycling iron

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70
Q

What is iron deficiency anemia commonly caused by?

A

GI bleeds

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71
Q

What are four diseases causing hemolytic anemia?

A

Hereditary spherocytosis
Glucose 6 Phosphate Dehydrogenase deficiency
Sickle cell disease
Thalassemia

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72
Q

What is hereditary spherocytosis?

A

Genetic disorder of structural protein (spectrin) in the red cell membrane that renders cells stiff and spherical rather than flexible and biconcave

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73
Q

Why are RBCs destroyed more readily in hereditary spherocytosis?

A

Cells are less able to deform themselves to successfully pass through the spleen

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74
Q

What is the structural protein that is defective in hereditary spherocytosis?

A

Spectrin

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75
Q

What is G6PD deficiency?

A

X linked recessive genetic disorder that causes deficiency of G6PD in red cells

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76
Q

What is G6PD?

A

Important in the supply of energy to stabilize the red cell membrane

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77
Q

What does deficiency of G6PD cause?

A

Destabilization of membrane, rendering RBCs fragile and susceptible to destruction

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78
Q

What hemoglobin is associated with sickle cell anemia?

A

Molecularly defective Hemoglobin S

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79
Q

What mutation occurs in sickle cell anemia?

A

Valine is substituted for glutamic acid in the beta globin chain - chromosome 11

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80
Q

Why does Hgb S cause sickling?

A

Hgb S is less soluble than Hgb A (normal hemoglobin), so sites with low oxygen levels cause the Hgb to form a gel that causes RBCs to deform in a sickle shape

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81
Q

What is a sickle crisis?

A

Periods of acute severe abdominal or bone pain caused by vascular occlusion

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82
Q

What causes sickle crises?

A

Infection, dehydration, acidosis, or physiologic stress

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83
Q

What is Thalassemia?

A

Inherited microcytic hemolytic anemia that impairs the synthesis of the alpha or beta polypeptide chains of globin protein in hemoglobin

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84
Q

What does the genetic defect in thalassemia affect?

A

Amount of hemoglobin synethsized

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85
Q

What does the defective globin protein in thalassemia cause?

A

Renders RBC membrane fragile and susceptible to hemolysis

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86
Q

Which thalassemia is more severe, minor or major?

A

Major

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87
Q

Which thalassemia is more common, minor or major?

A

Minor

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88
Q

What kind of anemia is sickle cell (cytic/chromic)?

A

Normocytic normochromic

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89
Q

What kind of anemia is thalassemia (cytic/chromic)?

A

Microcytic hypochromic

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90
Q

What kind of hemoglobin has a higher affinity for oxygen?

A

Hemoglobin F - fetal

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91
Q

What causes the RBCs to change their shape?

A

Oxygen cannot bind correcly

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92
Q

Are sickle cell anemia RBCs always sickled?

A

No, only after hypoxic damage occurs

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93
Q

What are two common infections that trigger sickling of RBCs?

A

Salmonella and Strep pneumonia

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94
Q

Is sickle cell anemia dominant or recessive gene?

A

Recessive

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95
Q

What are some symptoms of sickle cell anemia?

A
  • Infarct in fingers and toes, retina, pulmonary, renal
  • Necrosis of bones
  • Osteomyelitis
  • Splenomegaly
  • Splenic atrophy (infarct)
  • Gall stones
  • Bone marrow hyperplasia
  • Skin ulcers
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96
Q

How do we treat sickle cell anemia?

A

Pain control, hydration, and proper vaccination (to prevent infections that trigger episodes)
Increase in fetal hemoglobin synthesis

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97
Q

What kinds of anemia are due to insufficient RBC production?

A

Iron deficiency
Macrocytic/megaloblastic
Anemia of chronic disease
Aplastic anemia

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98
Q

What are the causes of iron deficiency anemia?

A

Usually blood loss
Poor intestinal absorption
Low dietary intake
Increased demand for iron caused by normal growth and development

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99
Q

What is the cause of iron deficiency anemia in adults over 50, until proven otherwise?

A

Colon cancer - occult bleeding from the GI tract

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100
Q

Where is 80% of the body’s iron?

A

RBCs

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101
Q

Where is 20% of the body’s iron?

A

Ferritin

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102
Q

What is ferritin?

A

Iron protein complex found in bone marrow, liver, spleen, and skeleta lmuscle

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103
Q

What is transferrin?

A

Iron transported from one place to another bound to blood protein transferrin

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104
Q

What is total tarnsferrin measured by?

A

TIBC

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105
Q

What is TIBC?

A

Total iron binding capacity - ability of transferrin to bind to iron

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106
Q

Is TIBC high or low in iron deficiency anemia?

A

High TIBC

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107
Q

What is pre anemic iron deficiency?

A

Stage before anemia when stores are being depleted - anemia does not occur until stores are completely exhausted

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108
Q

What do RBCs look like in iron deficiency anemia?

A

Small and pale

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109
Q

What are the lab values for iron deficiency anemia?

A
  • Low hemoglobin
  • Low hematocrit
  • Low iron
  • Low ferritin
  • High TIBC
  • High transferrin
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110
Q

What is the reticulocyte count in iron deficiency anemia?

A

Low reticulocytes

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111
Q

What is macrocytic anemia due to?

A

Deficiency of B12 or folic acid

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112
Q

What is B12 and folate essential for?

A

DNA synthesis

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113
Q

What happens to cell production if there is a decrease in B12 and folate?

A

Cell cannot be made because DNA cannot be produced

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114
Q

Why are the cells in macrocytic anemia large if DNA cannot be produced?

A

RNA synthesis still continues, so cells that are made have a large nucleus and abundant cytoplasm

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115
Q

What deficiency are alcoholics prone to?

A

Folate deficiency

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116
Q

What deficiency are vegetarians prone to?

A

B12 deficiency - B12 abundant in meat

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117
Q

What does B12 absorption require?

A

Requires intrinsic factor

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118
Q

Where is B12 absorbed?

A

B12 is bound to intrinsic factor and is absorbed in the ileum

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119
Q

What is pernicious anemia?

A

Autoimmune disease featuring autoantibodies against gastric mucosal cells that produce intrinsic factor - cannot absorb B12

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120
Q

What conditions result in the inability to absorb B12 in the ileum?

A
  • Crone’s disease
  • Gastric bypass
  • Bowel resection
  • Pernicious anemia
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121
Q

Why does Crone’s disease affect the ability to absorb B12?

A

Disease of ileum - cannot absorb B12

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122
Q

Why does gastric bypass affect the ability to absorb B12?

A

Lack ability to secrete intrinsic factor

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123
Q

What is aplastic anemia?

A

Primary bone failure

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124
Q

What elements are affected in aplastic anemia?

A

Failure to produce RBC, WBC, and platelets (pancytopenia)

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125
Q

What is the common cause of death from aplastic anemia?

A

Hemorrhage due to low platelet count

Infection due to low WBC count

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126
Q

What causes aplastic anemia?

A
  • Idiopathic
  • Autoimmune
  • Drugs
  • Large fat content in marrow
  • Genetic defects
127
Q

What kind of anemia is aplastic (cytic/chromic)?

A

Normocytic normochromic

128
Q

What is anemia of chronic disease?

A

Any depression of bone marrow production

129
Q

What are the three mechanisms of anemia of chronic disease?

A
  • RBC survival is shortened
  • Erythropoiesis impairment
  • Iron utilization impairment
130
Q

What chronic diseases usually cause anemia of chronic disease?

A

Malignant neoplasms
Chronic infections
Chronic autoimmune diorders
Kidney and liver failure

131
Q

How do inflammatory mediators affected anemia of chronic disease?

A

Infere with mechanism that transports iron from storage into red cell production
Interfere with EPO production in kidney

132
Q

What kind of anemia is anemia of chronic disease (cytic/chromic)?

A

Normocytic normochromic

133
Q

What is polycythemia?

A

Excess number of RBCs in blood

134
Q

Where are blood specimens collected, and why?

A

Collected from peripheral pool, which is more concentrated than central pool

135
Q

What is relative polycythemia?

A

Increase in peripheral red blood cell counts due to low plasma volume - Apparent polycythemia because total RBC count is normal

136
Q

What conditions cause relative polycythemia?

A
  • GI loss
  • Fluid loss (dehydration)
  • Diarrhea
  • Stress - overweight, anxious, hypertensive patients
137
Q

What is absolute polycythemia?

A

Increase in total RBC mass - actual increase in total number of RBCs in the body

138
Q

What is primary absolute polycythemia?

A

Stems from overproduction of RBCs in the bone marrow

139
Q

What is secondary absolute polycythemia?

A

Increased RBC counts due to a condition outside bone marrow that stimulates it to produce more RBCs

140
Q

What are some examples of causes of secondary absolute polycythemia?

A 
Lung disease (smoking)
Life at high altitude
Renal tumors (secrete more EPO)
141
Q

Why does lung disease cause secondary absolute polycythemia?

A

Hypoxia stimulates kidney to produce more EPO

142
Q

What condition is primary polycythemia?

A

Polycythemia vera

143
Q

What is polycythemia vera?

A

Bone marrow malignancy causing a proliferation of primitive bone marrow red cell precursors

144
Q

What are the three elements of normal hemostasis?

A
  • Coagulation
  • Blood vessel factors
  • Platelets
145
Q

What are the steps of normal hemostasis?

A

A, Injury occurs.
B, Temporary vasoconstriction
C, Blood contacts tissue, platelets accumulate, and coagulation begins.
D, Further platelet aggregation occurs, and coagulation produces a web of fibrin in the wound.
E, Hemorrhage stops as fibrin traps red cells and blocks further bleeding.

146
Q

What does prolongation of PTT indicate?

A

Intrinsic pathway defect

147
Q

What does prolongation of PT indicate?

A

Extrinsic pathway defect

148
Q

What does prolongation of both PTT and PT indicate?

A

Common pathway defect

149
Q

What does a prolonged bleeding time indicate?

A

Platelet deficiency or abnormality

150
Q

What does bleeding from fragile vessels result from?

A

Vascular or platelet deficiency

Vitamin C deficiency

151
Q

What kind of diseases often affect blood vessels?

A

Autoimmune

152
Q

What might cause bleeding from low platelet counts or platelet malfunction, causing fragile vessels?

A
  • Toxins or drugs
  • Marrow failure
  • Hypersplenism
  • Immune thrombocytopenia
153
Q

How does hypersplenism cause platelet malfunction?

A

Too many platelets are removed from circulation

154
Q

What does capillary bleeding appear as?

A

Petechiae

155
Q

What does von Willebrand factor do?

A

Allows platelets to aggregate and form an initial plug

156
Q

Does aspirin affect for the life of the platelet or life of the drug?

A

Life of the platelet

157
Q

Do anti-inflammatory drugs affect for the life of the platelet or life of the drug?

A

Life of drug

158
Q

How does aspirin affect platelets?

A

Blocks cyclooxygenase, so that thromboxane A2 is not formed, so platelet aggregation doesn’t occur

159
Q

What is excessive bleeding always associated with?

A
  • Fragile blood vessels
  • Low platelet count
  • Defective platelet function
  • Decreased coagulation factor activity
160
Q

Where does bleeding related to platelet disorders usually occur?

A

Capillary sized blood vessels

161
Q

Where does bleeding related to coagulation factors usually occur?

A

Larger vessels

162
Q

Where are coagulation factors made?

A

Liver

163
Q

Why does excessive bleeding result with liver failure?

A

Liver is supposed to produce coagulation proteins

164
Q

When is intarvascular clotting abnormal?

A

ALWAYS and secondary to another disease

165
Q

What proteins are a good measure of liver function?

A

Coagulation factors

166
Q

What three deficiencies can interfere with platelet aggregation?

A
  • Platelets
  • Von Willebrand factor
  • Factor VIII
167
Q

What kind of receptors are present on cell membranes for binding von Willebrand factor?

A

Glycoprotein receptors

168
Q

How are drugs with an affinity for the glycoprotein receptors on cell membranes used?

A

Used for patients experiencing heart attack - platelets cannot accumulate because vWF can’t adhere to the receptor

169
Q

What is classic hemophilia?

A

Hemophilia A - x linked genetic deficiency of factor VIII - can cause spontaneous bleeding in joints

170
Q

What is von Willebrand disease?

A

Causes reduced platelet adherence

171
Q

Why does DIC cause a tendency towards hemorrhage?

A

DIC consumes clotting proteins, leaving insufficient clotting proteins to support normal clotting

172
Q

What conditions initiate DIC?

A
  • Abruptio placenta
  • Amniotic fluid embolus
  • Preeclampsia
  • Gram negative sepsis
  • Malignancy
  • Severe tissue trauma
  • Sepsis
173
Q

What are three results of DIC?

A
  • Hemolysis
  • Thromboses
  • Hemorrhage
174
Q

What is the most common hereditary bleeding disorder?

A

Von Willebrand disease

175
Q

What coagulation factors are produced by the liver?

A

II, V, VII, IX

176
Q

What are local factors that can cause thrombosis?

A
  • Turbulent flow
  • Stasis
  • Endothelial cell damage
177
Q

What are the two cases where abnormal coagulation factors promote thromboses?

A

Lupus anticoagulant

Factor V Leiden

178
Q

What is another name for lupus anticoagulant?

A

Antiphospholipid antibody

179
Q

What patients have lupus anticoagulant?

A

Occurs in 10% of patients with SLE, most patients do not have SLE

180
Q

What is factor V Leiden?

A

An abnormal form of coagulation factor V that causes increased risk of thrombi

181
Q

What two factors increase your risk of developing clots with factor V Leiden?

A

OCP and smoking

182
Q

What is the WBC count of leukopenia?

A

Below 4,000

183
Q

What is agranulocytosis?

A

Critically low numbers of neutrophils (less than 200 cells/mL)

184
Q

What are some causes of neutropenia?

A
  • Accelerated removal
  • Drug induced, usually by damage to marrow
  • Crowding of marrow
  • Autoimmune
185
Q

What are patients at increased risk with neutropenia?

A

Bacterial and fungal inspections

186
Q

How does the normal flora affect patients with neutropenia?

A

Even colonizations of normal flora can be overwhelming

187
Q

What is the most common site for serious infection in neutropenia?

A

Respiratory tract

188
Q

What is lymphopenia caused by?

A

Steroid therapy

AIDS

189
Q

What kind of infection causes lymphocytosis?

A

Viral infection

190
Q

What kind of infection causes neutrophilia?

A

Bacterial infection

191
Q

What is a left shift?

A

Increased number of band neutrophils

192
Q

What kind of leukocytosis is benign?

A

Reactive - secondary leukocytosis due to bacterial infection or inflammation

193
Q

What kind of leukocytosis is malignant?

A

Leukemia

194
Q

When would a left shift in band neutrophils occur?

A
  • Acute infection or inflammation - increased need

- Malignancy - marrow is bursting full of cells

195
Q

Where is the malignancy of lymphoma located?

A

Malignancy in tissues - no malignant cells in blood

196
Q

Where is the malignancy of leukemia found?

A

Malignant cells are present throughout the bone marrow and in peripheral blood

197
Q

Which is more easily described, leukemia or lymphoma?

A

Leukemia

198
Q

What leukocyte response would be elicited in response to bacterial infection?

A

Granulocytosis

199
Q

What leukocyte response would be elicited in response to viral infection?

A

Lymphocytosis

200
Q

What leukocyte response would be elicited in response to parasitic infection?

A

Eosinophilia

201
Q

What is infectious mononucleosis caused by?

A

Epstein Barr virus

202
Q

What leukocyte response would be elicited in mononucleosis?

A

Atypical lymphocytosis

203
Q

What is lymphadenopathy?

A

Enlarged lymph nodes

204
Q

When are enlarged lymph nodes worrisome?

A

Absence of apparent infection or injury, because they may contain malignant cells

205
Q

What is lymphadenitis?

A

Benign inflammatory change in lymph nodes - infection of lymph nodes

206
Q

What causes the enlargement of lymph nodes?

A

Increased number of cells being filtered through the node due to malignancy, autoimmune, or infection

207
Q

What is reactive hyperplasia of lymph nodes?

A

Enlargement of the lymph node

208
Q

What is reactive lymphadenitis?

A

Due to inflammation

209
Q

What is cat scratch disease?

A

Acute lymphadenitis caused by rickettsial type organisms

210
Q

How does cat scratch disease present?

A

Axillary or neck lymph node will enlarge a few weeks after

211
Q

What does the biopsy of a lymph node in cat scratch disease show?

A

Typical chronic inflammatory reaction

212
Q

What organism causes cat scratch disease?

A

Bartonella henselae

213
Q

What malignancy presents as lymphadenopathy?

A

Lymphoma

214
Q

What is acute lymphocytic leukemia?

A

Malignant proliferation of immature lymphocyte precursors, usually B cells

215
Q

What type of patients typically get ALL?

A

Children

216
Q

What percentage of childhood leukemias are ALL?

A

80%

217
Q

What condition do children have that increases the risk of ALL by 15-20 times?

A

Down syndrome

218
Q

How many chromosomes present with ALL in 1/3 of all cases?

A

47 or more

219
Q

Which is more common in ALL, B cell subtype, or T cell?

A

80% of cases are B cell subtype

220
Q

What is the characteristic of the bone marrow in ALL?

A

Hypercellular - blasts accumulate in marrow and crowd out other cell types

221
Q

Where do malignant cells infiltrate in ALL?

A 
Lymph nodes
Spleen 
Liver
Bones
Meninges
222
Q

What symptoms present with ALL?

A 
Bone pain
Lymphadenopathy
Hepatospleomegaly
Headache
nerve paralysis
Pain
223
Q

What percentage of ALL patients are in remission after chemotherapy, and what percentage are cured?

A

95% in remission

75% cured

224
Q

What is a different expression of the same disease as CLL?

A

Small cell lymphocytic lymphoma (SLL)

225
Q

What is the difference between CLL and SLL?

A

SLL - few lymphocytes in blood (or normal levels)

CLL - many lymphocytes in blood

226
Q

What is the most common leukemia?

A

CLL

227
Q

What is the onset of CLL?

A

Onset is slow, most patients are asymptomatic

228
Q

What are the symptoms of CLL?

A 
Malaise
Mild fever
Minimal lymphadenopathy
Weight loss
Loss of appetite
229
Q

What happens to normal B cells in CLL?

A

Normal B cells are in short supply as malignant B cell proliferate, and B cells an’t produce antibodies to fight infections

230
Q

What patients get CLL?

A

Median age is 60, males are 2 times more likely than females

231
Q

Which cell lineage is more common in CLL, B or T cell?

A

B cell lineage is 95%

232
Q

What values diagnose CLL?

A

Lymphocyte count greater than 4000

WBC count greater than 20000

233
Q

What do plasma cell proliferations produce?

A

Benign or malignant proliferations that produce antibody or light/heavy chains

234
Q

What are the two types of lymphoma?

A

Hodgkin

Non hodgkin

235
Q

What are plasma cell proliferations?

A

Overgrowths of a single clone of plasma cells

236
Q

Why is it detrimental for plasma cell proliferations to make antibodies?

A

These antibodies are functionally useless and are produced at the expense of normal antibodies

237
Q

What are Bence Jones proteins?

A

Free light chains that are small enough to pass out of the renal glomerulus and into the urine

238
Q

What are the effect of Bence Jones proteins on the kidney?

A

Toxin to the kidney

239
Q

What happens to the appearance of the lymph node in leukemia and lymphoma?

A

Loss of follicular pattern

240
Q

Do malignant cells circulate in plasma cell proliferations? Where are they located?

A

Malignant cells do not circulate - they proliferate in the bone marrow

241
Q

What patients are affected by multiple myeloma?

A

Elderly

242
Q

Where is the malignancy in multiple myeloma?

A

Osseous tissue - bone

243
Q

What happens when fibroblasts and macrophages secrete IL 6 in the bone marrow in multiple myeloma?

A

IL 6 serves as a growth factor for myeloma cells

244
Q

What antibodies are produced in excess in plasma cell proliferations?

A

IgG (most common) or IgA

245
Q

How do the Bence Jones proteins affect the kidney?

A

Excreted in the urine, can damage the renal tubule cells and eventually lead to renal failure

246
Q

What gene is expressed in myeloma cells?

A

DKK1

247
Q

What does DKK1 do in multiple myeloma?

A

Interferes with the differentiation of osetoblast precursor cells, favoring activity of osteoclasts

248
Q

What is Waldenstrom macroglobulinemia?

A

IgM is produced in excess, causing thick, viscous blood

249
Q

What is multiple myeloma a malignancy of?

A

B cells

250
Q

What is a monoclonal spike?

A

Monoclonal “M” protein - Increase in antibodies seen in plasma cell proliferations

251
Q

What protein found in urine is indicative of multiple myeloma?

A

Bence Jones

252
Q

What happens when DKK1 genes increase osteoclastic activity?

A

Break down bone
Release of calcium
Punch out lesions in bone in the spine and skull

253
Q

What blood count disorder is seen with multiple myeloma?

A

Pancytopenia - proliferation of plasma cells crowds out ability to produce other cells

254
Q

What symptoms present with Waldenstrom macroglobulinemia?

A 
Headaches
Dizziness
HTN
Fatigue
Stroke
Blurred vision
(All due to hyper viscous blood inability to reach head)
255
Q

Where are malignant plasma cells found in multiple myeloma?

A

Do not circulate in blood, appear as nodular masses in bone marrow

256
Q

What happens to immunoglobulin levels in multiple myeloma?

A

Malignant plasma cells crowd out normal plasma cells causing a decline in production of normal antibodies

257
Q

Which cell types are more aggressive in lymphoid leukemia, B or T cell?

A

T cell is more aggressive (B cell is more common)

258
Q

What does a child present with in the office that makes us suspicious of ALL?

A

Idiopathic, persistant fevers

259
Q

What does the gene defect in CLL cause?

A

Stops the lymphocytes from apoptosis - immortal lymphocytes

260
Q

What kind of immunity is lost with CLL?

A

B cell immunity - no antibodies are made

261
Q

What symptoms are seen in all leukemias?

A

Abnormal WBC count
Enlargement of lymph nodes
Splenomegaly

262
Q

Does lymphoma have an abnormal WBC count?

A

No - malignancy of lymphoid tissue

263
Q

What is the characteristic of lymphoma tumors?

A

Sold tumors

264
Q

What are the most common ages for Hodgkins lymphoma?

A

10-20, after 50

265
Q

What infection can cause Hodgkin lymphoma?

A

Epstein Barr virus

266
Q

What type of Hodgkin lymphoma is the most common type (70%)?

A

Nodular sclerosis

267
Q

Where does a tumor of Hodgkin lymphoma start and progress to?

A

Starts in single node and spreads continuously to neighboring nodes of the group

268
Q

What are the common lymph node sites for the start of Hodgkin lymphoma?

A

Cervical and mediastinal

269
Q

Does Hodgkin lymphoma involve other structures besides lymph nodes?

A

NO

270
Q

What kind of immunity is lost with Hodgkin lymphoma?

A

Defective cell mediated (T cell) immunity

271
Q

What is the malignant cell type of Hodgkin lymphoma?

A

Reed Sternberg cell

272
Q

Is clinical staging more important in Hodgkin lymphoma or non Hodgkin lymphoma, and why?

A

Hodgkin lymphoma because of its tendency to spread in stepwise fashion

273
Q

What is the origin of non Hodgkin lymphoma?

A

Multiple sites involved - multi centric origin

274
Q

What sites does non Hodgkin lymphoma involve?

A 
Lymph nodes
GI tract
Liver
Lung 
Bone marrow
275
Q

Which is more aggressive, Hodgkin lymphoma or non Hodgkin lymphoma?

A

Non Hodgkin lymphoma

276
Q

What fraction of non Hodgkin lymphoma arise in organs other than the lymph nodes?

A

1/3

277
Q

What are the two main types of non Hodgkin lymphoma?

A

Diffuse and follicular

278
Q

What is follicular lymphoma?

A

Follicular microscopic appearance

279
Q

What is diffuse lymphoma?

A

Uniform microscopic appearance, Lack follicles

280
Q

Which non Hodgkin lymphoma type is more aggressive?

A

Diffuse

281
Q

Which non Hodgkin lymphoma has a better prognosis?

A

Follicular - less aggressive

282
Q

What lymph node symptom is present in Hodgkin lymphoma?

A

Painless lymphadenopathy

283
Q

What characterizes acute myeloid leukemia?

A

Abrupt onset

Immature forms of malignant cells - blasts

284
Q

What are the symptoms of acute myeloid leukemia?

A 
Decreased blood cells
Bone pain and tenderness due to expanding marrow
Enlarged lymph nodes, liver, and spleen
Headache, confusion
Vomiting
Dyspnea
285
Q

What causes headache in acute myeloid leukemia?

A

Hyperviscosity from leukostasis

286
Q

What is leukostasis?

A

Large amount of blood cells causes sluggish blood flow and in the brain, inefficient oxygen and glucose delivery

287
Q

What causes dyspnea in acute myeloid leukemia?

A

Results from plugging of small pulmonary vessels, increased, pressure, rupture, and infiltration of airspace which interferes with oxygen exchange

288
Q

What is chronic myeloid leukemia characterized by?

A

Mature forms of malignant cells

289
Q

What are the symptoms of chronic myeloid leukemia?

A

Generalized fatigue
Pallor
Low grade fever
Night sweats

290
Q

What does the abrupt onset of AML also present with?

A

Hemorrhage or infection

291
Q

What is the Philadelphia chromosome?

A

Shortened chromosome 22 with a translocation from chromosome 9 presenting with CML

292
Q

What are the phases of CML?

A

Indolent
Accelerated
Blast crisis

293
Q

What is the indolent period of CML?

A

May last about three years, asymptomatic

294
Q

What is the accelerate phase of CML?

A

Becomes resistant to treatment, anemia and thrombocytopenia become worse

295
Q

What is the blast crisis phase?

A

Terminal phase of quick evolution into AML

296
Q

What can AML evolve from?

A

Primary disease

Evolve from chronic myeloproliferative disorder

297
Q

What can CML evolve into?

A

Primary disease
Evolve into myeloproliferative disorder
Evolve into AML

298
Q

What is a chronic myeloproliferative disorder?

A

Group of related diseases that arise from myeloid stem cells

299
Q

What are the four disorders of chronic myeloproliferative disorder?

A
  • Polycythemia vera
  • CML
  • Malignant (essential) thrombocythemia
  • Myeloid metaplasia with myelofibrosis
300
Q

What are two important features of chronic myeloprolierative disorders?

A

Myelofibrosis

Extramedullary hematopoiesis

301
Q

What malignant cells predominate in polycythemia vera?

A

Malignant RBCs

302
Q

What malignant cells predominate in CML?

A

Malignant granulocytes

303
Q

What malignant cells predominate in malignant or essential thrombocythemia?

A

Malignant megakaryocytes

304
Q

What happens to malignant cells in myeloid metaplasia with myelofibrosis?

A

Malignant cells undergo metaplasia to fibrous tissue - bone marrow changes into fibrous tissue with fat

305
Q

What stage is myeloid metaplasia with myelofibrosis in other syndromes?

A

End stage of other disorders - fatal

306
Q

What is the function of the spleen?

A

Filters filtrate
Removes old blood cells
Removes blood cells labeled with antibody
Site of many immune reactions (APC)

307
Q

What is splenomegaly?

A

Enlarged spleen

308
Q

What causes splenomegaly?

A 
Acute viral infections
Chronic autoimmune disease
Liver disease
Heart failure
Mononucleosis
Malaria
Lymphoma 
Leukemia
Cirrhosis
309
Q

What is hypersplenism?

A

Enlarged spleen may become overactive and remove more than the normal number of red cells, white cells, and platelets

310
Q

What can result from hypersplenism?

A

Hemolytic anemia
Leukopenia
Thrombocytopenia

311
Q

What happens in DiGeorge syndrome?

A

Hereditary immune deficiency of the thymus where T cells do not mature and B cells then don’t get T helper cell stimulation

312
Q

What is myasthenia gravis?

A

Acquired autoimmune disease in which antibodies block ACh receptors and transmission of nerve signals across neuromuscular synapse

313
Q

What are the tumors of the thymus gland that are associated with myasthenia gravis?

A

Thymoma

314
Q

Are thymomas benign or malignant?

A

Usually benign, but can still cause problems due to growth

From Flashcardlet (133 decks)

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