Lecture 1 Flashcards

1
Q

Leukocytes

A

white blood cells

Consists mainly of neutrophils (60%) that fight infection and play a role in immune system

Normal Level: 5,000-10,000

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2
Q

Erythrocytes

A

red blood cells

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3
Q

Eosinophils

granulocyte

A

1-4% of leukocytes

role in ending allergic reactions and in fighting parasitic infections

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4
Q

Granulocytes

A

contains granules

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5
Q

Neutrophils

granulocyte

A

primary pathogen-fighting cells (60-65%)

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6
Q

Basophils

granulocyte

A

Blood cells; release heparin, histamine, and other inflammatory mediators (.3-.5%)

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7
Q

Mast Cells

A

tissue cells; release heparin, histamine, and other inflammatory mediators; involved in allergic reactions

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8
Q

Pathogen

A

foreign substance; viral, bacterial, chemical etc

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9
Q

Agranulocytes

A

No granules

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10
Q

Lymphocytes (30%)

A

B cells, T cells, Natural killer cells

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11
Q

B cells

A

Produce antibodies, fight from a distance

ex: coaches

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12
Q

T cells

A

cell to cell combat, fight hand in hand

ex: players

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13
Q

Natural Killer Cells

A

Kill antibody generating cells

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14
Q

T-helper cells

A

activate immune response

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15
Q

Cytotoxic T cells

A

cell-mediated immunity

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16
Q

monocytes–>Macrophages

A

antigen-presenting cells; produce inflammatory mediators (3-8%)

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17
Q

lymph node

A

filter your blood; spleen helps do this

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18
Q

Leukopenia

A

decrease in absolute number of leukocytes in blood

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19
Q

Neutropenia (agranulocytosis)

A

virtual absence of neutrophils (congenital and acquired)

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20
Q

Aplastic anemia

A

all myeloid cells affected (anemia, thrombocytopenia, and agranulocytosis)

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21
Q

Infectious Mononucleosis

A

Epstein-Barr Virus (EBV)

self limiting lymphoproliferative disorder

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22
Q

HIV

A

white blood cells deficiencies

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23
Q

Leukemia

A

Malignant neoplasms of hematopoietic stem cells

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24
Q

Acute Leukemia

A

Progenitor cells
Sudden and stormy onset
S/S: fatigue, night sweats, weight loss, bruising, bone pain, low grade fever

Depressed bone marrow function

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25
Q

Chronic Leukemia

A

Fully differentiated myeloid and lymphoid cells

onset is usually slow with non specific symptoms such as weakness and weight loss

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26
Q

Leukemia Lymphocytic

A

immature lymphocytes
progenitors
Originate in bone marrow but filter to spleen, lymph nodes, CNS, and other tissues

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27
Q

Leukemia Myelogenous

A

Pluripotent myeloid stem cell in bone marrow

Interfere with maturation of all blood cells including granulocytes, erythrocytes, and thrombocytes

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28
Q

Acute Lymphocytic Leukemia (ALL)

A

Most common in children 66-75% of all childhood cancers
Pre-B or Pre-T cells
Lymphoblasts

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29
Q

Acute Myelogenous Leukemia

A

Mainly in older adults can be seen in children and young adults (65-70ish)

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30
Q

Chronic Lymphocytic Leukemia (CLL)

A

Clonal malignancy of B-lymphs
Average age of diagnosis is 72 years old
Rare younger than 40
Diagnostic hallmark of CLL is isolated increased lymphocytes
Increased WBC with >75% lymphocytes
Hypogammaglobulinemia common (increased risk for infection)

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31
Q

Chronic Myelogenous Leukemia (CML)

A

Progenitor cell disorder
33% of all leukemia and is common in older adults

3 phases:

  1. Chronic Phase
  2. Accelerated Phase
  3. Terminal Phases

PHILADELPHIA CHROMOSOME

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32
Q

Leukemia Diagnosis

A

Blood and bone marrow studies
Assessment findings: splenomegaly (spleen enlargement), generalized lymphadenapathy (soreness of the lymph nodes), and hepatomegaly (enlarged liver)

Bone marrow aspiration, lumbar puncture

33
Q

Leukemia Treatment

A

Chemotherapy- kills every cell, good or bad

Bone marrow or stem cell transplant (ALL, AML if other treatments have failed)

34
Q

Malignant Lymphomas

A

solid tumors involving lymphoid tissue

35
Q

Non-Hodgkin Lymphoma

A

malignant transformation of either T or B cell differentiation
Most commonly originate in lymph nodes then spread throughout the body to multiple organs

36
Q

Hodgkin Lymphoma (aka Hodgkin’s Disease)

A

Reed-Sternberg Cell
typically originate in a single lymph node and then spreads to contiguous nodes
Malignant B cells invade lymphoid organs
Usually just one lymph node

37
Q

Non Hodgkin Lymphoma

S/S

A

painless lymphadenopathy isolated or widespread

diagnosis: lymph node biopsy, CT, MRI, bone scans

Treatment: depends on histologic type, stage, and clinical status of person
Localized Radiation
Chemo/Radiation Combined(most common)

38
Q

Hodgkin Lymphoma

S/S

A

painless lymph node enlargement
Sometimes c/o dyspea and prolonged cough
Mediastinal mass may be discovered on CXR

Diagnosis: Lymph node biopsy with presence of Reed- Sternberg cells
CT, CXR, MRI, Bone scan

Treatment: Radiation and chemotherapy; no option must do both

39
Q

Multiple Myeloma

A

B Cell malignancy of terminally differentiated plasma cells.
Monoclonal paraprotein
Proliferation of malignant plasma cells in the marrow and osteolytic bone lesions throughout the system

manifestations: blood and bone marrow
plasma cell dyscrasias
osteoclasts
paraproteins secreted by plasma cells cause hyperviscosity of body fluids and may break down into amyloid that can cause heart failure and neuropathy

40
Q

Hemostasis

A

process that maintains the integrity of a closed high pressure circulatory system after vessel injury

41
Q

Blood Cells Platelets

A

Normal level: 150,000- 400,000 per microliter

42
Q

Platelets (Thrombocytes)

A

live 8 to 9 days in circulation
many stored in the spleen
released when needed
large fragments of megakaryocytes in bone marrow

43
Q

Thrombopoietin

A

platelet production
made in liver, kidney, smooth muscle, bone marrow

production controlled by thrombopoietin

44
Q

Plasma Proteins

coagulation factor

A

circulate as inactive procoagulation factors
most are synthesized by the liver
von Willebrand factor made by megakaryocytes and endothelium

45
Q

Coagulation Factors

A
Constrict blood vessels
von Willebrand factor 
-->platelet Adhesion
Degranulation of platelets--> ADP, TXA--> platelet aggregation
Calcium-->coagulation cascade
46
Q

Coagulation

A

Clotting is not expected to be the permanent solution to vessel injury.
blood clotting is accompanied by processes designed to control the coagulation cascade and dissolve the clot once bleeding has been controlled.

47
Q

Clot formation and Dissolution

A

5 stages

  1. Vessel Spasm
  2. Formation of platelet plug
  3. Blood coagulation or development of fibrin clot
  4. Clot retraction
  5. Clot dissolution
48
Q

vonWillebrand factor

A

helps platelets change shape and adhere to vessel wall

49
Q

Hypercoagulability

A

increased platelet function (thrombocytosis):
platelet adhesion, formation of platelet clots, disruption of blood flow
smoking, high cholesterol, diabetes mellitus, and hemodynamic stress

Increased clotting activity (genetic & acquired):
Genetic- factor V (Leiden mutation)
polycythemia- sickle cell disease, hyperestrogenic state of pregnancy, oral contraceptions, smoking obesity

50
Q

Thrombocytopenia

A

decrease in circulating platelets (<100,000/microliter)
increased risk for bleeding
splenic sequestration, decreased platelet production, dilution

51
Q

Immune thrombocytopenic Purpura (ITP)

A

Autoimmune disorder that results in platelet antibody formation and destruction of platelets.

52
Q

Drug-Induced Thrombocytopenia

A

Some sulfa, quinine, quinidine

heparin

53
Q

Thrombotic Microangiopathies

A

Platelets are consumed by increased levels of fibrin

Thrombotic Thrombocytic purpura (TTP), hemolytic- uremia syndrome (HUS)

54
Q

Inherited

coagulation disorder

A

hemophilia A (factor VIII defiency)- x linked recessive

Von willebrand Disease (factor IX deficiency)
Autosomal Dominant

55
Q

Acquired

coagulation disorders

A

Liver disease
gallbladder disease
Vitamin K deficiency (Fat soluble vitamin)

56
Q

Problems of Hemostasis

hemophilia

A

“loves to bleed” are genetic disorders

Types:
Hemophilia A(VIII)- most common
Hemophilia B (IX)
vo Willebrand’s disease

57
Q

Problems of Hemostasis
(hemophilia)

Manifestations

A
Slow, persistent bleeding from minor traumas and cuts
Delayed bleeding after minor trauma
Epistaxis
GI bleeding (ulcers, gastritis)
Hematuria
Ecchymoses and SQ hematomas
Hemarthrosis
Pain, neurological symptoms from hematoma putting pressure on nerves
58
Q

hemophilia

A

the ability to form blood clots is reduced

59
Q

Problems of Hemostasis

Thrombocytopenia

A
Reduction in platelets below 150,000
Causes:
Chemotherapy
Aspirin/NSAID therapy
Types:
Immune Thrombocytopenic Purpura
Thrombotic Thrombocytopenia Purpura
Heparin-Induced Thrombocytopenia and Thrombosis Syndrome
60
Q

Problems of Hemostasis
(Thrombocytopenia)

clinical manifestations

A

Bleeding (post-procedure)
Petechiae, purpura, ecchymosis
Hemorrhage

61
Q

Problems of Hemostasis

Disseminated Intravascular Coagulation, DIC

A

Serious bleeding and thrombotic disorder
MEDICAL EMERGENCY
Is an abnormal response of the normal clotting cascade stimulated by a disease process or disorder.
in pregnant women, someone with multiple trauma

62
Q

Disseminated Intravascular Coagulation (DIC)

A
Obstetric Conditions:
Abruption placentae, Dead fetus syndrome, Amniotic fluid embolism
Cancers:
APML, metastatic cancer
Infection:
Sepsis, bacterial meningitis, parasitic infections
Trauma:
Burns, snake bite, heatstroke
Blood Transfusion reactions
63
Q

Problems of Hemostasis
(Disseminated Intravascular Coagulation)

clinical manifestations

A
No well-defined sequence
Weakness, malaise, fever
Bleeding
Thrombosis
Pallor, petechiae, purpura, hematomas, hemoptysis, hematuria, etc.
EKG changes
64
Q

Complete Blood Count (CBC)

A
Blood test that measures the levels of:
RBCs
WBCs
Platelets
Hemoglobin (Hgb)
Hematocrit (Hct)
Other “Differentials” in the RBCs and WBCs
65
Q

Erythrocytes

A

red blood cells
contain hemoglobin that carries oxygen

Normal Level
RBCs 
Men – 4.2-5.4
Women – 3.6-5.0
Hemoglobin (11-15)
Men – 14-16.5
Women – 12-15
Hematocrit (35-45)
Men – 40%-50%
Women – 37%-47%
66
Q

Erythropoiesis

A

production of red blood cells
after birth RBC’s ar3e normally produced in bone marrow

RBC’s live approx 120 days

67
Q

Anemia

A

abnormally low number of circulating RBC’s, level of Hgb or both

decreased o2 carrying capacity

causes:
decreased RBC production
Blood loss: acute and chronic
increased RBC destruction

68
Q

Blood loss Anemia

A

Trauma

chronic blood loss (iron deficiency anemia)

69
Q

Hemolytic Anemia

A

transfusion reaction
sickle cell anemia
Destruction of RBC’s at a rate that exceeds production.

Clinical manifestations
Jaundice
Spleen and/or liver enlargement
Renal failure secondary to hemoglobin accumulation in the renal tubules
All other S/S of anemia

Complications
Infection secondary to spleen failure
Aplastic and hemolytic crisis
Organ infarction

70
Q

Acute Blood Loss

A

anemia caused by blood loss
Result of a sudden hemorrhage.
Clinical Manifestations
10 % - None
20% - No detectable S/S at rest, tachycardia and postural hypotension w/activity
30% - Normal supine BP at rest, postural hypotension and tachycardia with exercise
40% - BP, CVP, and CO below normal at rest; rapid, weak pulse and cold clammy skin
50% - Shock and potential death

71
Q

Chronic blood loss

A

Examples:
PUD
Hemorrhoids
Menstrual and postmenstrual blood loss

72
Q

Thalassemia

A

A group of diseases that have an autosomal recessive genetic basis involving inadequate production of normal hemoglobin.

Clinical manifestations
Pallor
All other symptoms of anemia
Develops by two years of age and causes developmental delays
Splenomegaly and hepatomegaly – jaundice
73
Q

Megoblastic Anemias

A

A group of anemias caused by impaired DNA synthesis and characterized by the presence of LARGE RBC’s

Types: 
Iron deficiency anemia 
Cobalamin (Vitamin B12) deficiency 
Gastritis
Gastrectomy
Folic acid deficiency
Poor nutrition, malabsorption in small intestine
Alcohol abuse
Hemodialysis
74
Q

Aplastic Anemia

A

A disease in which the patient has a general pancytopenia (decrease in all blood cell types) and hypocellular bone marrow
May be caused by chemotherapy

Clinical manifestations
Anemia symptoms
Thrombocytopenia
Neutropenia 
Diagnostic studies
CBC
Total serum iron and TIBC
75
Q

Polycythemia

A
Production and presence of TOO MANY RBC’s
Clinical manifestations
Hypertension secondary to hypervolemia
Headache, pain, dizziness, visual disturbances
Pruritis from histamine release 
Angina, heart failure, thrombophlebitis
Blood vessel distention
Stroke, PE and other “clot” disorders
76
Q

Gerontologic Considerations

A

Number of stem cells and bone marrow deplete with age, thus causing problems with the following:
number of RBC’s (anemia)
clotting ability
ability to fight infection
oxygen transportation
compensation for an acute or chronic disorder

77
Q

Pediatric Considerations

A

Hyperbilirubinemia in the neonate:
Increased serum bilirubin
Most common cause of jaundice in neonate
Can place the neonate in danger of brain damage
Treated with phototherapy or exchange transfusion

78
Q

Hemolytic Disease of the newborn:

A
Erythroblastosis fetalis (rh + mother and rh- infant)
Rh positive infant and Rh negative mother