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Adv Patho > Hematology > Flashcards

Hematology Flashcards

1
Q

What do erythrocytes do and what is another name for them?

A
  • RBC
  • transport hemoglobin which carries O2 from the lungs to the tissues
  • most abundant cells of blood
  • lack nucleus and ctoplasmic organelles
  • live 100-120 days
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2
Q

Where are RBC produced?

A
  • early gestation in yolk sac, then liver, and last month in bone marrow
  • marrow of all bones amkes RBS until 5 years old
  • 5 and older most RBC produce in verebrae, sternum, ribs, an dilia
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3
Q

What do pluripotential hematopoetic cells become and where do they origiante

A
  • Originate in bone marrow
  • stem cell for erythroyctes
  • pluripotent stem cell–erythroyce–erythroblast–reticulocyte–erythrocyte
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4
Q

What stimulates RBC production

A

-erythropoietin is hormone released in kidneys that stimulate hematopoietic stems tobecome proerythroblasts that become RBCs

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5
Q

What are factors that can decrease oxygenation?

A
  • low blood volue
  • anemia
  • poor blood flow
  • pulmonary disease
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6
Q

What makes up hemoglobin

A
  • 4 polypeptide chanes (globins-2 apha and 2 beta)
  • and 4 Fe (heme)
  • 1 oxygen molecules can bind to 1 Fe so 1 hemoglobin cell can carry 4 molecules of oxygen (or 8 atmos of oxygen)
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7
Q

What is polycthemia and what can cause it

A
  • excessive RBCs
  • causes: dehydration, incrased erythropoietin secretion in response to chronic hypoxia, high altitudes, smokers, COPD, CHF
  • increased risk for blood clots, increase size of spleen and liver
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8
Q

What happens with RBC die?

A
  • undergo hemolysis by marcophages
  • macrophages release the Fe of RBC and they are trasnported as transferrin which can be used new new RBCs or stored as ferritin
  • porphyrin from RBC in converted to bilirubin, relased into the blood, transported to liver and secreted as bile
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9
Q

what is porphyrin

A

-protein in RBC that helps bind Fe to hemoglobin

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10
Q

How does anemia develop?

A
  • decreased RBC production
    • deficiency Fe, B12, folate
    • co-morbid conditions
    • inflammation and inflammatory state
    • erythropoietin
  • loss of RBCs (blood loss)
  • RBC production is abnormal (sickle cell, thalassemia)
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11
Q

What is MCV (mean corpuscular volume)

A
  • how big or small RBC is (aka average size)
  • small associated with: iron deficiency anemia, thalassemia
  • large associated with: b12 deficiency, folic acid deficiency, vit b deficiency, liver disease, hypothyroidism
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12
Q

What is MCHC (mean corpuscular hemoglobin concentration)?

A
  • how red or how much hgb is in RBC
  • low means RBCs do not have enough hgb
  • low associated with anemia
  • high means concentrated amount of hgb in RBC
  • high associated with sickle cell, autoimmune autolyic disease, severe burns, smokers
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13
Q

What is RDW (red cell distribution width)?

A
  • measures range and volume size of RBC
  • normal high RDW could mean nutrition deficiency or anemia, DM, heart disease, liver disease, kidney disease, cancer
  • low RDW means most of RBCs are the same size
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14
Q

Ferritin test

A
  • indicates amount of stored iron
  • blood protein that contains iron
  • measures amount of ferritin in blood
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15
Q

What is transferrin?

What does TIBC test?

A
  • transferrin is ability of the body to transport iron
  • main protein that binds to Fe and transports it throughout the body
  • produced in liver
  • low: inflammation and malignancy
  • high: iron deficiency anemia
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16
Q

Where is iron produced

A

liver

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17
Q

What is hemolytic anemia

A

RBC and destroyed faster then they are made

-inherited blood disorders: sickle cell, thalasseia, bone marrow disorder

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18
Q

MCV <80

Hypochromic <27

A

iron deficiency
anemia of chronic illness
thalassemia
sideroblastic anemia

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19
Q

Normocytic (MCV 80-100)

Normochromic (MCHC>=27)

A 
anemia of chronic illness
sickle cell
aplastic anemia
hymolyic anemia
CKD
HIV
acute blood loss
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20
Q

Macrocytic (MCV>100)

A 
b12 deficiency
folate def.
myelodysplastic syndrome
adverse drug reaction
alcohol abuse
hypothyroidism
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21
Q

Iron deficiency anemia

A
  • HYPOCYTIC
  • most common anemia
  • diet deficiency
  • malabsorption issue (chrons/gastric bypass)
  • pregnancy
  • increase in children during periods of growth
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22
Q

Thalassemia

A
  • Autosomal recessive disorder
  • can be Alpha or Beta types (Alpha less severe)
  • mutation of Hgb A: change in ratio changes structure of Hgbb making RBCs less stable and more likely to breakdown
  • treat with Fe infusions, but risk o iron overload
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23
Q

Anemia of Chronic Illness

A
  • 2nd most common anemia

- result of chronic infection or disease, inflammation

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24
Q

What do proinflammatory cytokines do?

A

generally regulate growth, cell activation, differentiation, and homing of the immune cells to the sites of infection with the aim to control and eradicate the intracellular pathogens, including viruses

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25
Q

What is hepcidin?

A
  • HYPOCYTIC OR NORMOCYTIC
  • controls Fe absorption in blood and secretion of Fe in GI tract
  • blocks the release of Fe from reticuloendothelial system
  • decreases oral iron absorption–leading to Fe deficiency.
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26
Q

What is hemolytic anemia

A
  • destruction of RBCs

- can be due to genetics, autoimmune disorders, adverse drug reactions

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27
Q

What labs would you see increased and decreased in hemolytic anemia?

A

Increased labs: bilirubin, phosphorous, uric acid, hemoglobinuria
Decrease labs: haptoglobin

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28
Q

What is aplastic anemia?

A

Disorder of stem cells: may be congenital, r/t chemo, viral infections (hepatitis), autoimmune d/o. Dx with bone marrow biopsy

body stops producing enough new blood cells

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29
Q

Pancytopenia

A

RBC, WBC, platelets are decreased

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30
Q

Sickle Cell Anemia

A

NORMOCYTIC (small sz RBC)
-genetic (autosomal recessive) hemolytic anemia
-Africans
RBC with Hgb S have low oxygen capacity
-sickle cell crisis
-risk of CVA, MI, pulmonary injury
-triggered by infections, dehydration, and hypoxia

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31
Q

Pernicious Anemia

A
  • aka B12 deficiency
  • normal cell death
  • cause by inability to absorb B12, dietary deficiency, autoimmune
  • s/s: symptoms of anemia, paresthesia, decreased balance, sore tongue, increased homosysteine an amino acid that b12 breaks down to create other chemicals your body needs (high levels associated with dementia, stroke)
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32
Q

What happens if you have a folate deficiency?

A
  • impaired RNA and DNA snythesis
  • cause by: dietary deficiency, poor absorption (elderly and ETOH), drug effects (aspirin competes with FA for binding sites)
  • can cause fetal neural tube defects (effect brain and spinal developement)
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33
Q

What are leukocytes for?

A
  • mobile units of the body’s immune response

- formed in bone marrow and lymph tissue

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34
Q

What types of leukocytes are there?

A
  1. Granulocytes (made in bone marrow)

2. monocytes and Lymphocytes which become B or T cells

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35
Q

Types of WBCs

A
  1. Agranular (“cytes”) : lymphocytes and monocytes
  2. Granular (“phils”) : neutrophils, eosinophils, basophils

-formed and stored until needed

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36
Q

Agranulocytes

A
  • live longer than granulocytes
  • Lymphocytes live weeks to months while monocytes 10-20 hr in blood and deposit in tissue where they can survive for months
  • respond to inflammation
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37
Q

Granulocytes

A
  • short lived

- survive in tissue 4-5 days

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38
Q

What do lymphocytes do?

A

-identify and neutralize foreign objects
-make T and B cells
seen in infections with inflammation
-low count in chemotherapy and steroid use

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39
Q

What do monocytes do?

A
  • phagocytosis
  • help other white blood cells remove dead or damaged tissues, destroy cancer cells, and regulate immunity against foreign substances
  • bigger than lymphocytes
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40
Q

Types of granulocytes

A

neutrophils
eosinophils
basolphils

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41
Q

Neutrophils

A
  • first responders in inflammation

- common in bacterial responses

42
Q

Eosinophils

A
  • engulf parasites

- look for parasitic infections and allergic responses

43
Q

Basophils

A

-help with allergic reactions and myeloproliferative disorders (ex: polycythemia vera, thrombocytosis)

44
Q

Leukemia

A
  • malignant d/o of leukocytes in bone marrow and blood
  • over production of leukocytes leads to overcrowding in bone marrow which leads to decreased production of normal hematopoietic cells that can overflow bone marrow and flow in blood and then infiltrate other organ-
  • uncontrolled proliferation of IMMATURE WBCs
45
Q

What are the 2 types of Leukemias

A
  1. Myeloid Leukemia: arise from monocytes (neutrophils, eosinophils, and basophils)
  2. Lymphoid Leukemia: T and B cells
46
Q

Difference between Acute and Chronic Leukemia

A

Acute: cells don’t mature; remain in “blast” form

Chronic: proliferation of immature leukocytes. They look like mature WBC but lack their functionality

47
Q

Types of Acute Leukemias

A
  1. Acute Myelogenous Leukemia (AML)- older adults; chromosomal translation issue
  2. Acute Lymphoblastic Leukemia (ALL)- seen mostly in kids; chromosomal translation issue with PHILADELPHIA chromosome (chromosome 22)
    - chromosomal translation is when one chromosome breaks of and switches with another chromosome
48
Q

Type of Chronic Leukemias

A
  1. Chronic Myelogenous Leukemia (CML)- caused by translocation of PHILADELPHIA chromosome
  2. Chronic Lymphoblastic Leukemia (CLL)
49
Q

Philadelphia Chromosome

A
  • chromosome 9 switches long arm with chromosome long 22
  • forms BCR gene which is like an on and off switch that stays on and forces immature myeloid cells to keep dividing leading to build up of premature Leukocytes in the bone marrow then in to blood causing hepatosplenomegaly
50
Q

CLL

chronic leukocyte leukopenia

A
  • B cells don’t mature fully
  • move into lymphatic tissues and can become lyphomas
  • B cell likely to produce auto-antibodies which can lead to immune thrombocytopenia and autoimmune hemolytic anemia
  • associated with Lymphadenopathy
51
Q

S/S of Acute leukemias

A
  • fatigue d/t anemia
  • easier bleeding d/t thrombocytopenia
  • infections d/t leukopenia
  • pain in bones d/t increase blast cell production
  • abd fullness d/t hepatosplenomegaly
  • lymphadenopathy d/t localized pain of lymph nodes
52
Q

T cell ALL

A

abnormal lymphoblasts migrateto thymus causing enlargement thus compressing the mediastinal structure

53
Q

CML

chronic myelogenous leukopenia

A
  • associated with hepatosplenomegaly
  • effects older adults
  • s/s easy bleeding, weight loss, pale skin, night sweats
  • associated Philadelphia chromosome
  • can progresse to AML (more serious)
  • treatment is BCR ABL tyrosine kinase inhibitors
54
Q

How is acute leukemias dx?

A
  • peripheral blood smear

- bone marrow biopsy

55
Q

How to differentiate between AML and ALL?

A
  • stain smear
  • myelobast: large cells, fine chromatin, prominent nucleolus, and auer rods
  • lymphoblast: smaller cells, coarse chromatin, scant nucleoli
56
Q

How is chronic leukemias dx?

A
  • lots of immature blood cells that look like mature cells, increase number of monocytes, granulocyres, and metamyelocytes, and myelocytes
  • abnormal B cell
57
Q

What are lymphomas

A
  • Malignant proliferation f lymphocytes in the lymphoid system
  • present with swollen lymph nodes, fatigue, weight loss, and abd swelling, puritis
58
Q

Hodgkin Lymphoma

A
  • dx with (lymphocytes) B cells called Reed-Sternberg
    cells
  • progress from one group of lymph nodes to another
  • linked to EBV and HIV infections
    -tumor derived from lymphocytes
    -cell divides uncontrollably and becomes a neoplastic cell
    -spreads to nearby lymph odes
    -made of large mononulcear cells or mutlinuccleated cells (aka Reed Sternberg cells)
    -dont produce antibodies like a normal b cell should
59
Q

Non Hodgkin lymphoma

A

-spreads non-conitugously

=extranodal sites (skin , GI tract, and brain)

60
Q

s/s hodgkin lymphoma

A
  • painless cervical adenopathy
  • nodular scelrosis
  • fever, night sweats, weight loss
61
Q

How to dx hodgkin lymphoma

A

CT scan and lymph node biopsy

62
Q

Treatment of hodgkin lymphoma

A
  • chemo

- radiation

63
Q

Non Hodgkin Lymphoma

A
  • absence of Reed Sternberg cell
  • derived B and T cells
  • genetic mutation b and t cells that should die, but continue to divide and multiply
64
Q

Burkitt Lymphoma

A
  • non hodgkins
  • B cell lymphoma
  • assoc with EBV
  • presents ats tumors of jaw and facial bones or abd
65
Q

Risk factors for Non Hodgkins

A
  • family hx
  • chemical exposure
  • infection with cancer r/t virus (EBV, HIV, Hep c)
  • immune suppression from transplant
66
Q

Non Hodgkin t cell lymphoma

A
  1. adult t cell lymphoma: caused by human t lyphmotrophic virus that causes a viral dna mutation
  2. mycosis fungoides: t cell lymphoma of skin; red rash
67
Q

S/S of Non Hodgkins

A 
-painless lyphadenopathy
fever
night sweats
weight loss
- exrtranodal involvement: bowel obstruction, fatigue, easy bruising, recurrent infections, weakness and loss of sensation in legs
68
Q

Dx Lymphoma and treatment

A

CT and lymph node biopy

-chemo or radiation or rituximab (antibody infusion to help aptopsis)

69
Q

Multiple Myeloma

A

-malignancy of plasma cells

70
Q

Multiple Myeloma-slow proliferation of tumor cells in bone marrow

A
  • increased production of IgG

- Bence Jones protein found in urine

71
Q

Multiple Myeloma-lytic bone lesions

A
  • myeloma cells-lead to hepatic growth factor and paraythyroid hormone which lead to cytokine production that leads to osteoclast activation that increases bony reabsorption
  • bones lesions lead to incrased serum calcium levels which increases chance of fractures and renal failure
72
Q

What does vascular constriction do?

A

Causes smooth muscle to contract which activates the humoral response» platelys begin to arrive and secrete thromboxane A2 (TXA2) which increases platelet expression and splatelet aggregation
-low dose aspirin inhibits TXA2

73
Q

Steps of platelet plug formation

A
  1. Adhesion
  2. Activation
  3. Aggregation
74
Q

What is clot formation

A
  • starts when when bleeding is not stopped by a platelet plug alone
  • may be triggered by immune/inflammatory response
  • platelet aggregate and fibrin thread form a true clot in 3-6 minutes
  • after 20-60 minutes clot retrace to further occlude
75
Q

What 2 pathways make up the coagulation cascade?

A
  1. Extrinsic: primary pathway; measured by PT; shorter way; once the damage to vessel is done, the endothelial cells release (transmembrane receptor tissue factor)_ TF which goes on to activate factor 7 and 7a. factor 7a activates factor 10 into factor 10a.
  2. Intrinsic: supports and amplifies extrinsic pathway; measured by PTT; takes longer than extrinsic-more factors have been activated and converted
76
Q

What does thrombin do?

A
  • clotting promoter

- Converts fibrinogen to fibrin. Fibrin fibers join with aggregated platelets to form a clot

77
Q

How is thrombin from the blood removed?

A
  • absorbed by fibrin fibers
  • antithrombin III (AT3) blocks the effects of thrombin on fibrinogen, inactivating thrombin
  • heparin works with AT3 to increaseremoal of thrombin 100 fold
  • heparin is produced by mast cells and basophils
78
Q

What is plasmins role in clot dissolution?

A

When a clot is formed, plasminogen is entrapped. Over time, endothelium releases tissue plasminogen activator (t-Pa) which coverts it to plasmin to remove the clot after the vessel has healed.

79
Q

What do proteolyric enzymes do?

A

Diges fibrin fibers and fibrinogen , prothrombin, and FActos V, VIII, and XII

80
Q

Hypercoagulable Disorders

A

VIRCHOW TRIAD- factors that contribute to venous thomosis

  1. venous stasis
  2. vessel damage
  3. hypercoagulable states
81
Q

Acquired Thrombosis

A
  • can be arterial or venous
  • risk factors: immobility, MI, malignancy, obesity, estrogen therapy, pregnancy, sickle cell
  • treatment: ASA, heparin and mobilize to reduce stasis
82
Q

Factor V Liden

A
  • inherited
  • autosomal dominant
  • mutation of of the bloods factor V protein which increases the chance of blood clots
83
Q

Antiphospholipid Syndrome

A
  • acquired
  • autoimmune syndrome with antibodies to plasma proteins and clotting factors
  • more common in women and results in pregnancy complications
84
Q

Thrombotic Thrombocyropenia Purpura (TTP)

A
  • genetic or autoimmune
  • high amounts of von Willebrand Factor (sticky platelets)
  • platelets don’t stick to the blood vessel wall, but to each other causing anemia, thrombocytopenia and microvascular thrombi
85
Q

What is thrombocytopenia?

A

Low blood platelet count which help stop bleeding by cluming and forming plus in blood vessels during injury. Low blood platelet increases chance of bleeding.

86
Q

Primary Immune (idiopathic) Thrombocytopenia Purpura

A
  • viral
  • platelets are phagocytized by macraophges and presented to CD4 cells that cause IgG antibodies to bind to platelets
  • HIT
  • s/s: easy bruising, bleeding, and pinpoint sized reddish purple spots on the legs
87
Q

Hemophilia A

A
  • inherited
  • most common
  • x lined recessive
  • deficiency in factor 8
  • normal platelets and prolonged aPTT
  • intrinsic pathway issue
88
Q

Hemophilia B

A
  • inherited
  • x linked recessive
  • deficiency factor 9
  • normal platelets and prolonged aPTT
  • intrinsic pathway issue
89
Q

von Willebrand Disease

A
  • inherited-autosomal dominant; most common inheritited bleeding disorder
  • decrease in vWF leads to decreased platelet adhesion and increased bleeding
90
Q

Disseminated Intravascular Coagulation (DIC)

A

-clotting and bleeding d/o
abnormal clumps of thickened blood (clots) form inside blood vessels. These abnormal clots use up the blood’s clotting factors, which can lead to massive bleeding in other places. Causes include inflammation, infection, and cancer.
-releases procoagulants d/t widespread endothelia injury which leads to microvascular clots
-proteins that control blood clotting become overactive

91
Q

Lab finding of DIC

A
  • decreased platelets and clotting factors

- increased PT, apTT, and d dimer

92
Q

Why are microvascular clots in DIC bad?

A

b/c clots cause obstruction to distal tissue which lead sto cell death; tend to have multi organ failure and near tissues dying

93
Q

What are the key components of a hemoglobin molecule?

A
  • globin
  • oxygen
  • heme protein
94
Q

What are the 2 by products of RBC destruction and how are they removed?

A
  1. bilirubin: sent to liver then large intestines where it broken down and expelled in feces
  2. globin that is not phagocytized are removed from the circulation through the kidneys
95
Q

What does a right shift in the oxygen hemoglobin dissociation curve mean?

A

hemoglobin has a decreased affinity for oxygen which makes it more difficult to bind to oxygen

96
Q

What does a left shift in the oxygen hemoglobin dissociation curve mean?

A

hemoglobin has an increased affinity for oxygen which makes it easier to bind to oxygen

97
Q

What are examples of normal variations in hemoglobin and why would you expect these variations?

A
  1. Hb A: adults; 2 alpha and 2 beta
  2. Hb A2: adults, made of 2 alpha and 2 delta chains
  3. Hb F-found in fetus; 2 alpha and 2 gamma chains
98
Q

What RBC tests can help in assessing anemia?

A
  1. TIBC
  2. ferritin blood test
  3. transferrin test
  4. serum iron test
99
Q

What do iron studies assess and what do abnormal results indicate?

A

Iron studies measure the amount of iron in the blood that is stored in tissues. An abnormal iron study when indicate anemia

100
Q

What is Virchow’s triad?

A

3 critical elements important in development of thrombosis

  1. venous stasis
  2. activation on blood coagulation
  3. vein damage
101
Q

How does again impact coagulation?

A

blood coagulation capacity increase with aging put older adults at a higher risk for a thrombosis

Adv Patho (23 decks)

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