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KCSU17 Patho/Pharm Submodule 1 > Hematologic Pathology > Flashcards

Hematologic Pathology Flashcards

1
Q

platelets

A

cytoplasmic fragments of megakaryocytes

fxn: stop bleeding

lifespan = 8-9 days, 30% of numbers are on reserve in spleen

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2
Q

eyrthrocytes

A

RBCs

most numbers

life span: 3-4 months in circulation

large surface area (surface:volume) so they can quickly pick up and dump oxygen

flexible: can get into small capillaries

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3
Q

where are WBCs produced?

A

Bone marrow, lymph nodes and spleen

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4
Q

types of WBCs

A
  1. neutrophils
  2. lymphocytes
    3, eosinophils
  3. basophils
  4. monocytes
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5
Q

neutrophils

A

45-70%

actively phagocytic cells (fights foreign invaders)

dominate in acute inflammation and bacterial infections

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6
Q

lymphocytes

A

35-40%

long living, predominate in WBC of children

rotation between circulation and lymph nodes

predominate in a viral infection

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7
Q

eosinophils

A

5-10% (MINOR)

when they are high: NAACP

N= neoplasm 
A= allergies
A= airway disease
C=connective tissue disease 
P= parasites
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8
Q

basophils

A

3-7% (LEAST common)

allergic reactions

histamine and heparin release

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9
Q

monocytes

A

3-5%

actively phagocytic cells

become macrophages when they move from the blood to the tissues

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10
Q

hematopoietic stem cells

A

progenitor cells that are found in bone marrow

common “ancestor” for all blood cells, growth factors/hormones differentiate

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11
Q

thrombopeotin

A

stimulates platelet production

produced by liver, kidney, skeletal muscle, bone marrow

low platelet count stimulates thrombotic production

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12
Q

hormones that stimulate WBC production

A

G-CSF
GM-CSF
IL3

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13
Q

what hormone stimulates RBC production?

A

erythropoeitn

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14
Q

Erythropoetin

A

RBC production hormone

stimulated for release by kidney

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15
Q

what stimulates eruthropoetin release from kidney?

A

low peripheral blood O2

problematic bc may promote blood viscosity (decreasing blood flow rate)

hypoxia can have other causes (such as smoking) that could be harmed by increased viscosity

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16
Q

most important white cells disorders

A

malignancies

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17
Q

spleen functions

A

identification and removal of tagged cells (cells with Igs)

storage of platelets

removal of red blood cells (damaged or old)

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18
Q

what causes damage to the spleen

A

mononucleosis
liver disease
cancer

if damaged, it won’t weed out potential invaders or rupture during trauma

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19
Q

sequelae if spleen is removed

A

immunocompromised

especially sensitive to encapsulated organisms (spleen is best at grabbing these) (meningitis nicesiaria, etc.)

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20
Q

cancer that starts in progenitors cells of WBCs

A

leukemia

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21
Q

When a progenitor cell becomes a leukemic cell:

A

maturation process is arrested (stops)

cell division is then accelerated and apoptosis is limited

resulting in many copies of immature cells

builds up in the bone marrow and crowd out the normal cells (eventually spread to other cells)

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22
Q

two categories of leukemia

A
  1. lymphotic or myeloid leukemia

2. acute or chronic leukemia

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23
Q

leukemias developing from lymphoid cell line

A

lymphocytic

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24
Q

leukemias developing from WBCs, RBCs, and platelet precursors

A

myeloid

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25
Q

acute leukemia

A

leukemias that progress rapidly and are fatal if not treated quickly

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26
Q

chronic leukemia

A

leukemias that progress slowly, come from more mature progenitors

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27
Q

what typically causes the signs and symptoms of leukemia?

A

deficiencies of the other cell likes

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28
Q

Main symptoms of leukemia

A 
fatigue 
dyspnea on exertion 
stollens nd bleeding gums
fevers
recurrent infections 
petechiae
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29
Q

B symptoms of leukemia

A

occur bc of the malignancy

weight loss, fevers, right sweats, muscle wasting

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30
Q

signs of leukemia

A

splenomegaly
hepatomegaly
petechiae
pallor

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31
Q

acute lymphocytic leukemia

A

ALL

most common in children 2-5 yrs (another peak in elderly)

common cause is genetic mutation (haven’t ID what)

Very likely to survive if a child, minimal numbers of adults survive

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32
Q

chronic lymphocytic leukemia

A

CLL

most common type in US adults

sometimes rapid progression, most cases is indolent

often patient is asymptomatic at time of discovery (accidental finding on routine CBC)

often monitored without specific treatment until it progresses

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33
Q

Acute Myelogenous Leukemia

A

AML

cancer of any WBC besides lymphocytes

occurs in bone marrow when cells arrest in earliest stage of differentiation and begin proliferating

other cell lines in bone marrow are crowded out (resulting in neutropenia (low other WBCs) anemia, and thrombocytopenia)

more common in developed nations, caucasians

median age is 70 (effects all ages)

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34
Q

blast cell

A

a primitive, undifferentiated blood cell, often found in the blood of those with acute leukemia

(AML)

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35
Q

Chronic myelogenous leukemia

A

gradual progression

most often found in older adults

accounts for a small amount of leukemias

philadelphia chromosome

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36
Q

philadelphia chromosome

A

reciprocal translocation between long arms of chromosomes 22 and 9

CML

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37
Q

patient has this type of leukemia:

  • 62 yr old black male
  • high serum levels of lymphocytes found on routine labs
  • asymptomatic
A

Chronic lymphocytic anemia

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38
Q

patient has this type of leukemia:

  • 73 yr old white female
  • blasts present in blood
  • low neutrophil, platelet, and RBC counts
A

acute myelogenous leukemia

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39
Q

patient has this type of leukemia:

  • 4 yr old hispanic boy
  • quick progression
  • high lymphocyte progenitor counts
A

acute lymphocytic leukemia

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40
Q

patient has this type of leukemia:

  • gradual progression
  • Philadelphia chromosome
A

chronic myelogenous leukemia

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41
Q

to diagnose any type of leukemia this procedure myst be done

A

bone marrow biopsy

genetic analysis of WBCs

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42
Q

bone marrow biopsy tells us

A

definitive diagnostic test

tells us if one cell line is at higher numbers than the others

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43
Q

genetic analysis of WBCs tells us

A

possible mutations of the cancer cells that may be important for determining treatment

can be targeted by a cancer drug and limits collateral damage

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44
Q

lymphoma

A

cancer of MATURE lymphocytes

OUTSIDE bone marrow

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45
Q

broad division of lymphomas

A

Hodgkin’s

Non-Hodgkin’s

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46
Q

how do we diagnose lymphoma?

A

lymph node biopsy with genetic analysis of specimen

excision of node from: cervical, axilla, inguinal

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47
Q

s/s of lymphoma

A

lymphadenopathy

hepatomegaly, splenomegaly, or abdominal mass

pruritus

b symptoms

cytopenia symptoms

mediastinal mass

48
Q

B symptoms of lymphomas

A

unexplained weight loss

unexplained fever

drenching night sweats

49
Q

cytopenia symptoms

A

decreased WBCs, RBC, platelet #s

50
Q

staging of lymphoma (4)

A

histology
extent of disease
symptoms and performances
status of patient

once we know the stage, we recommend treatment

51
Q

treatment for lymphoma

A

low grade: watchful waiting

higher stage: XT, CXT, bone marrow transplant

52
Q

multiple myeloma

A

malignancy of plasma cells in bone marrow and bloodstream

plasma cells overproduce an Ig protein (toxicity) - may cause *acute kidney injury *

produces lytic lesions in the bone, causing pathologic fractures

53
Q

CBC results of multiple myeloma

A

plasma cells crowd out the other cell lines in bone marrow

causes anemia, neutropenia, thrombocytopenia

54
Q

multiple myeloma diagnosis

A

monoclonal spike on serum and urine protein electrophoresis (SPEP and UPEP)

normal: high albumen spike, low Igs
MM: high albumen and one high Ig (two peaks)

55
Q

multiple myeloma Ig production

A

may cause acute kidney injury (blocks up the tubules so no filtration or waste removal)

hypervicosity

amyloidosis (abnormal` protein folding)

56
Q

erythropoesis

A

development of RBCs

only occurs in bone marrow

57
Q

what does an RBC synthesize as it grows?

A

Hemoglobin

released from bone marrow into blood when 80% done

58
Q

reticulocyte

A

RBC released into blood prior to maturation

has about 80% of its Hg, matures in 24 hours

59
Q

hemoglobin

A

4 iron and 4 protein chains that form a stable porphyrin ring

60
Q

components of adult HgB

A

2 alpha and 2 beta chains

61
Q

components of fetal HgB

A

2 alpha and 2 gamma chains

these gamma chains have a higher O2 affinity so they suck up more oxygen

at birth: 50% adult, 50% fetal but by 6 months, they are all adult

62
Q

raw materials required for erythropoiesis

A
  1. iron
  2. b-12, folate, and proteins
  3. adequate bone marrow
63
Q

how do RBCs get iron?

A

via absorption from dietary intake in duodenum

recycled from breakdown of RBCs (most)

64
Q

how do RBCs get B-12, folate and other proteins?

A

absorption from the gut

via diet

65
Q

what is the site of RBC construction?

A

bone marrow

66
Q

decrease in RBC mass?

A

anemia

67
Q

s/s of anemia

A 
fatigue 
palor/paleness
fainting/dizziness
altered menta status 
tachycardia/palpitations 
SOB
68
Q

what test uncovers anemia?

A

CBC

decreased HgB and Hct

69
Q

classifications of anemia

A

based on RBC size – via MCV

microcytic
normocytic
macrocytic

or by color (hypo chromic and normochromic) – not common bc subjective

70
Q

causes of normocytic anemia

A
  1. decreased production capability of marrow
  2. decreased stimulation to produce RBCs
  3. increased peripheral destruction of RBCs

anemia of chronic disease, chronic renal failure, hemolytic anemia, blood loss, aplastic anemia

71
Q

microcytic anemia

A

small size

due to abnormalities in hemoglobin production (inc hemoglobinopathies)

iron deficiency, thalassemia

72
Q

decreased RBC production capability of marrow

A

causes normocytic anemia

may be due to not enough space

aplastic anemia, anemia of chronic disease

73
Q

decreased stimulus to produce RBC

A

causes normocytic anemia

caused by chronic kidney disease

not enough stimulus to produce enough

74
Q

increased peripheral destruction of RBCs

A

causes normocytic anemia

hemolytic anemia, hereditary spherocytosis

bone marrow works fine, but RBC lasts less time before they die

75
Q

macrocytic anemia causes

A

due to vitamin deficiencies (B-12, folate)

may be due to drugs that inferred with DNA synthesis (aren’t able to mature properly)

clonal proliferation in bone marrow (myelodysplasia)

liver disease, alcoholism, hyperthyroidism, drugs (sulfa, AZT, CTX)

76
Q

ferritin

A

protein stored with iron in the liver

stays here until it is transported to marrow

77
Q

transferrin

A

protein responsible for transport of iron from liver to marrow

78
Q

acid environment encourages absorption

A

iron

b-12

79
Q

what causes iron deficiency to develop?

A
  1. inadequate iron intake in the diet (esp. vegetarians, breast fed infants)
  2. infants during periods of rapid growth
  3. inadequate re-utilization of iron present in red cells due to chronic blood loss (causes heavy menses, vascular disorder of colon)
80
Q

PICA

A

common in iron deficient patients

craving for/eating clay, dirt, ice

common in pregnant women, low SES

81
Q

iron deficient anemia may produce which conditions?

A

PICA
restless legs
esophageal webs

82
Q

Iron studies comprise which tests (+definition)

A
  1. iron level (FE concentration in serum)
  2. serum ferritin (est. iron stores)*
  3. transferrin (amount of iron transporting peptide)
  4. % saturation (%of transferrin bound to blood)

*serum ferritin is interpreted with caution bc can be influenced by infection and inflammation

83
Q

what pattern will show on iron studies in patient with iron deficiency

A
  1. iron level = LOW
  2. serum ferritin = LOW
  3. transferrin = HIGH (increases to catch more)
  4. % sat = LOW
84
Q

thalassemias

A

genetic mutation resulting in decrease in production of alpha and beta chains

will have over production of other chains that it doesn’t make (more beta cells if alpha def., etc.)

often found in patients of african, asian, or mediterranean ethnicities

can vary in severity

85
Q

extra medullary hematopoiesis

A

occurs in major thalassemias

inadequate hematopoiesis forces areas of the bone to try and produce RBCS – unfortunately this is not the problem, instead it is an inability to transport oxygen (genetic not space issue)

causes bossing of the skill, engaged maxilla, saddle nose

massive hepatosplenomegdaly (enlarged liver)

wasting of extremities

short stature

86
Q

thalassemia treatment

A

resource rich: hyper transfusion therapy (lifetime blood transfusions to minimized hematopoietic stimulation)

may cause iron overload

in poor countries: terminal

87
Q

mesoblastic anemia

A

form of macrocytic anemia

due to impaired DNA synthesis that therefore causes more cytoplasm to accumulate than normal

88
Q

labs for macrocytic anemia

A

B-12 and folate level check

may do TSH check in liver

89
Q

folate deficiency

A

comes from green leafy veggies

common in those with poor nutrition - alcoholics and those in low SES

causes macrocytic anemia

90
Q

b-12 deficiency

A

comes from animal protein

important for hematopoietic fxn and nervous fxn

absorbed from terminal ileum when complexed with INTRINSIC factor (via acid producing stomach lining)

91
Q

two types of b-12 deficiency

A

true b-12 def.

pernicious anemia

92
Q

who gets TRUE b-12 deficiency

A

vegetarians

Chron’s disease

93
Q

chron’s disease and B-12 def

A

inflammation of the ileum so can’t absorb B-12

94
Q

pernicious anemia

A

body produces B-12 but it has autoantibodies, lack of intrinsic factor, Abs bind to the B-12 instead

common in patients with atrophy of stomach lining (elderly), autoimmune dx, and removal of lining (ulcer, bypass)

95
Q

why may a healthy person experience normocytic anemia

A

following a trauma (including C-section)

surgical procedure

96
Q

anemia of chronic disease

A

decreased bone marrow ability to produce RBCs, Normocytic

caused by chronic inflammatory conditions (infection, autoimmune, malignancy), causes issue with ferritin, interferes with normal iron transport bc more iron is in storage

generally develops slowly and well tolerated

goal is to treat underlying disease causing the inflammation

97
Q

aplastic anemia

A

decreased BONE MARROW ability to produce RBCs

Normocytic anemia

severe damage to the bone marrow that destroyed stem cells, kills of progenitors

causes rapid anemia

may be caused by drugs, medications, toxic chemicals, CTX, XT, or autoimmune

98
Q

workup for anemia of chronic disease

A

iron: NORMAL
transferrin: NORMAL

serum ferritin: NORMAL/increased (bc of inflammation )

% sat: NORMAL, increased

99
Q

decreased stimulation of Red blood cells and anemia

A

caused by advanced chronic kidney disease

erythropoietin is not produced
also produces 2ndary HTN

100
Q

how is decreased stimulation of RBCs different than anemia of chronic disease?

A

anemia of chronic disease is an issue with iron transport, not enough in the blood more in storage, this is bc the kidney is not releasing erythropoietin so cells just aren’t being produced

101
Q

ABCDEs of peripheral RBC destruction in the blood

A 
A: Air (low O2) 
B: Box (shape)
C: Synthesis 
D: defective enzyme 
E: hostile environment
102
Q

hemolytic anemias caused by defective Hg

A

ex. disease sickle cell

due to genetics, produces Hgb S instead of Hgb A

abnormal HgB S deforms the RBC in crisis plugs capillaries if O2 is low

capillary plugging results in bone and organ damage, and rapid destruction of sickled cell causes anemia

103
Q

hemolytic anemias caused by shape problems

A

hereditary spherocytosis

congenital abnormalities in shape and flexibility (ALL RBCs)

RBCs become trapped in spleen and recycled prematurely

chronic low grade hemolytic anemia

104
Q

hemolytic anemias caused by defective Hg synthesis

A

alpha and beta thalassemia

person can’t produce (homo/major) or reduced production (minor) of alpha or beta HG chains

the chain that is produced accumulates in RBCs and shortens life span

105
Q

hemolytic anemias caused by defective RBC enzyme

A

G6PD Deficiency

G6PD metabolizes glucose and protects Hg from oxidation

total absence (male) or diminished presence (female) of enzyme means that susceptible during stressful situations

106
Q

hemolytic anemias caused by hostile environments

A

autoimmune Hemo. anemia

activation against RBC offing following drug injection or part of autoimmune disease, occurs without warning

sudden, onset hemolytic anemia

107
Q

RDW

A

red cell distribution

reads CBC and gives a bell curve of size distribution

narrow bell curve = MCV is truly value

wide bell curve = could mean that you have multiple anemias, must broaden scope and do other tests

108
Q

polycythemia

A

when the Hgb/Hct are above normal (too many RBCs)

two causes:

  1. polycythemia vera
  2. secondary polycythemia
109
Q

polycythemia vera

A

hyperplasia of RBC bone marrow precursor

abnormal turning on of genes

110
Q

secondary polycythemia

A

erthrocytosis bc of low oxygen levels

consequences: increased blood viscosity (could cause eventual CVA in CNS)

111
Q

hemochromatosis

A

genetic inability to excrete iron

iron overload causing O2 radical damage

iron disposition in organs to cause failure

treated with constant phlebotomy (blood is normal, can be donated)

112
Q

4 tests for evaluation of hemolytic anemia

A
  1. serum haptoglobin (decrease)
  2. LDH (increase)
  3. reticulocyte count (increase)
  4. peripheral blood smear

separate of CBC

113
Q

hemolytic anemia test definite + result:

Serum haptoglobin

A

haptoglobin = plasma protein that clears HgB

reduced if hemolysis

114
Q

hemolytic anemia test definite + result:

LDH

A

lactate dehydrogenase

intracellular enzyme, marker of lysis

elevated if hemolysis

115
Q

hemolytic anemia test definite + result:

reticulocyte count

A

normal is 1%

increases if there is hemolytic anemia bc bone marrow is trying to make more

116
Q

hemolytic anemia test definite + result:

blood smear

A

will show that there is more abnormal shape cell or fragments

if there are fragments = hemolysis

KCSU17 Patho/Pharm Submodule 1 (12 decks)

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