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Pathophysiology > Hematology > Flashcards

Hematology Flashcards

1
Q

Platelets are also called

A

thrombocytes

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2
Q

RBC are also called

A

erythrocytes

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3
Q

cytotoxic T cells function

A
  • kill virus infected and damaged cells
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4
Q

helper T cell functions

A
  • help cytotoxic T cells and B cells in their immune functions
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5
Q

B cells functions

A
  • produce antibodies
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6
Q

-lysis

A

cell membrane rupture

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7
Q

-plasty

A

make

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8
Q

cyt-

A

cell

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9
Q

-osis

A

unusual condition

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10
Q

Hematocrit

A

% of blood volume that is RBC

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11
Q

Hemoglobin

A

of hemoglobin in the blood

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12
Q

ESR

A

rate at which RBCs settle out of suspension

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13
Q

reticulocyte count

A

of immature RBC

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14
Q

Anemia can be caused by

A
  • losing too much blood (hemorrhagic)
  • destroying too much; rupturing of red blood cells (hemolytic)
  • not making enough, lack of iron, protein, vit.B12 (nutritional deficiency)
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15
Q

symtoms of general anemia

A
  • fatigue
  • weakness
  • dyspnea
  • pallor
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16
Q

how does the body compensate for decreased hemoglobin associated with anemia

A
  • tachycardia
  • dizziness
  • impaired hemoglobin
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17
Q

low oxygen supply to the spinal column can result in

A
  • paresthesia, weakness, impaired reflexes
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18
Q

low oxygen associated with anemia can result in

A

nausea, vomiting, and anorexia

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19
Q

ischemic tissue can be associated with

A

fever

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20
Q

All symptoms of anemia

A
  • shortness of breath, rapid and pounding heartbeat, dizziness, fatigue
  • pallor or yellow (jaundice)
  • impaired healing
  • paresthesia, balance disturbances, weakness, spasticity, reflex abnormailities
  • abdominal pain, neausea, vimiting, anorexia
  • low grade fever (ischemic tissue)
  • PICA
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21
Q

what is PICA

A

eating items that are not typically though of as food

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22
Q

why do some patients with anemia experience PICA

A

body is trying to replenish needed nutrients

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23
Q

examples of loss or destruction anemia

A

Normocytic - normochromic anemia
aplastic anemia
post hemorrhagic anemia
hemolytic anemia

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24
Q

aplastic anemia

A
  • stops producing enough new RBC
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25
Q

Normocytic-Normochromic Anemias

A
  • normal in size and hemoglobin content
  • insufficient numbers of RBC
  • there is no change in the cells itself; not enough cells
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26
Q

Post hemorrhagic anemia cause

A
  • sudden blood loss
  • normal iron stores
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27
Q

post hemmorhagic anemia treatment

A
  • stop bleeding
  • restore blood volume (isotonic IV fluids)
  • transfusion
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28
Q

signs and symptoms of acute hemorrhage anemia

A
  • orthostatic hypotension, altered mental status, cool/clammy skin, tachycardia, hyperventilation, decreased pulse pressure
  • Late sings: decreased urine output, decrease in BP
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29
Q

how does the body try to compensate for hemorrhage anemia

A
  • body will initially try to compensate for blood loss through peripheral vasoconstriction
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30
Q

hemolytic anemias are caused by

A

premature destruction
- hemolytic disease of newborns
- infections (E.Coli, salmonella, snake bites, malaria)

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31
Q

hemolytic disease of newborns

A
  • Rh incompatibility
  • 1st baby has separate blood circulation, 2nd baby that is Rh positive mother antibodies will destroys RBCs
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32
Q

hemolytic uremic syndrome is caused by

A

Infections
- E. Coli (several days of diarrhea can lead to low RBC count)
- Snake Bites (venom induced consumption coagulopathy)
- malaria (cause RBCs to rupture) –> sickel cell anemia

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33
Q

consumption coagulopathy

A

platelet disorder which can lead to prolonged or excessive bleeding

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34
Q

hemolytic anemias symptoms

A
  • abnormal paleness
  • yellowish skin, eyes and mouth (jaundice)
  • dark colored urine
  • fever
  • weakness
  • dizziness
  • confucion
  • cant handle physical activity
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35
Q

hemolytic anemias treatments

A
  • blood transfusions, medications, plasmapheresis surgery, bone marrow and stem cell transplants, lifestyle changes
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36
Q

plasmapheresis

A

plasma is separated from the blood cells
- plasma is replaces with another solutions such as saline or albumin, or plasma is treated and then returned to the body

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37
Q

Iron deficency anemia classification

A

Microcytic-Hypochromic anemia

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38
Q

Pernicious Anemia (vit.B) classification

A

macrocytic-mormochromic anemia

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39
Q

Floate deficency anemia classifications

A

macrocytic normochromic anemia

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40
Q

Aplastic anemia classificication

A

normocytic- normochromic anemia

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41
Q

sickle cells anemia classification

A

Normocytic-normochromic anemia

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42
Q

Microcytic hypochromic anemia cell size

A
  • cells small in size, light in color
  • small and low hemoglobin
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43
Q

Microcytic hypochromic anemia causes

A
  • inadequate intake of dietary iron or a chronic loss of blood
  • insufficient iron delivery to bone marrow or impaired iron use within bone marrow
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44
Q

Microcytic hypochromic anemia incidence

A

Men- higher in childhood
women - during reproductive years until menopause

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45
Q

women suffer iron deficient anemia as a result of

A

excessive mentraul bleeding

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46
Q

men suffer iron deficent anemia as a result of

A

ulcer, histal hernias, esophageal varices, cirrhosis, hemorrhoids, ulcerative colitis, cancer

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47
Q

How does IDA progress

A
  • depleting iron stores
  • creating iron deficient RBC
  • hemoglobin deficient blood cells enter circulation to replace old RBC
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48
Q

IDA symptoms

A
  • fatigure, weakness, dyspnea, pallor,
    LATE: fingernails become brittle and spoon shaped, tongue papillae atrophy (soreness and burning), Angular stomatitis (sores in the corner of the mouth
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49
Q

Pernicous Anemia cell size

A
  • large cell, normal color (without vit.B12 and folic acid cells do not decrease in size)
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50
Q

Causes of pernicious Anemia

A

lack of intrinsic factor (vit.B cannot be absorbed)
- inflammation of the gastric muscosa (body attacks healthy cells)
- H. pylori bacterium (reduces stomach acid = reduced absorption)
- alcohol intake, smoking

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51
Q

Pernicious anemia classification

A

Macrocytic-normochromic

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52
Q

how long can pernicous anemia take to develop

A

20-30 years

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53
Q

pernicous anemia signs and symptoms

A
  • mood swings, other GI issues, cardiac and kidney alterations
  • LATE: anemia weakness, fatigue, pallor/jaundice, paresthesia (tingeling) of feet and fingers, difficulty walking, loss of appetite, weight loss, sore tongue (smooth and beefy red)
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54
Q

Folate Deficiency Anemia calssification

A

Macrocytic-normochromic

55
Q

Folate Deficiency Anemia cell

A

large cell, normal color

56
Q

Folate Deficiency Anemia cause

A

lack of folic acid (essential for RNA and DNA synthesis within maturing erythrocytes)
- chronic malnurishment
- alcoholics

57
Q

Folic Acid Deficent Anemia

A
  • painful ulcerations (scales and fissures) in the mouth
  • burning mouth syndrome (scalding or tingleing feeling in the mouth)
  • dysphagia, watery diarrhea
58
Q

Folic Acid Deficient Anemia

A
  • oral folate
  • adjustment of dietary intake
  • prophylactic treatment in pregnancy
59
Q

reason for prophylactic treatment in pregnancy

A

prevent neural tube defects such as spina bifida

60
Q

aplastic anemia cells

A

too many cells are being made
without growth

61
Q

aplastic anemia occurs more frequecy in

A

teens and early 20s

62
Q

aplastic anemia causes

A

Autoimmune disease - attack your own stem cells
radiation and chemotherapy treatment
radiation and chemotherapy treatments
- idiopathic - greater than 50%
- exposure to radiation or certain toxic chemical, viral infections (hepatitis)
- congenital from chromosomal abnormalities
- damage to bone marrow erythropoiesis

63
Q

aplastic anemia symptoms

A
  • manifests as typical anemia - but it is pancytopenia
  • leukopenia and infections, thrombocytopenia
  • easy bruising
64
Q

how is aplastic anemia diagnoised

A

bone marrow biospy

65
Q

aplastic anemia treatment

A

antirejection
- transfusions, or a blood and bone marrow transplant

66
Q

Sickle-Cell Anemia causes

A

an inherited RBC disorder in which there arent enough healthy RBC
- recessive genetic link
- linked to aferican, carbbean, or indian ancestory

67
Q

Sickle Cell anemia signs and symptoms

A

Vaso-occlusive crisis
- blood vessel occulsion
- causes vasospasms (extremely painful)
Sequestration Crisis
- blood pooled in spleen
Chronic hemolytic anemia
- diminished erythropoiesis

68
Q

Sickle Cell Anemia treatment

A
  • adequate hydration and pain medications
  • stem cells transplant or bone marrow transplant
  • oxygen
69
Q

what is the leading cause of dealth in children with sickle cell anemia

A

pneumonia
- affected spleen increases the risk of infection

70
Q

Anemia due to chronic disease

A

Rheumatoid - inflammation in joints decreases production
Lupus - have antibodies against erythropoietin
Infection - decreases life span, impaired iron metabolism, impaired erythropoiesis
Chronic blood loss - impaired iron stores

71
Q

adaptive immunity cells

A
  • B and T cells
  • denititic cells
72
Q

Innate immunity cells

A
  • neurophils, eosinophil, basophil, macrophage, dendritic cells
73
Q

dendritic cells

A

form the bridge between the innate and adaptive immune response (via antigen presentation to lymphocytes)

74
Q

leukocytes function (B and T cells)

A
  • ingests foreign material and cellular debris
  • destroys infectious agents and cancer cells
  • inflammation medication
  • produces antibodies
75
Q

Leukocytosis

A

a condition in which the white cells (leukocyte count) is above the normal ranfe in the blood

76
Q

Leukocytosis is a protective mechanism for

A
  • inflammation, infection, anesthesia, surgury, pregnancy
  • malignancies: leukemia or hematologic disease (HIV, anemia)
77
Q

leukocytosis sings and symtoms

A
  • fever
  • feeling weak, tired or sick
  • feeling dizzy, faint, or sweaty
  • pain or tinglinf in arms, legs or abdomen
  • trouble breathing, thinking or seeing
  • loosing weight without trying or poor appetite
78
Q

Leukopenia

A

decreased leukocytes in the blood

79
Q

leukopenia causes

A

Cancer or disease of the bone marrow
- antibiotics can destroy WBC

80
Q

decreased WBC =

A

increased risk of infection

81
Q

Leukopenia signs and symptoms

A

fever and chills, frequent infections that will not go away

82
Q

neutrophils increase due to

A

infection

83
Q

neutrophils decrease due to

A

chemotherapy

84
Q

Increased eosinophils is due to

A

allergies, parasitic infections

85
Q

decreased eosinophils is due to

A

stress, medications

86
Q

increased basophils is due to

A

inflammation, infection, allergies

87
Q

decreased basophils is due to

A

acute infection, hyperthyroidism

88
Q

increased monocytes is due to

A

late stage of infection

89
Q

decreased monocytes is due to

A

prednisone use

90
Q

increased lymphocytes is due to

A

viral infections, endocrine dysfunction

91
Q

decreased lymphocytes are due to

A

immunodeficency, cancer, treatment

92
Q

What is infectious mononucleosis

A

over production of T cells

93
Q

what is the most common cause of infectious mononucleosis

A

Epstein-Barr virus (EBV) herpes

94
Q

main transportation of infectious mononucleosis

A

saliva
- kissing disease

95
Q

infectious mononucleosis symptoms

A

headache, malaise, joint pain, fatigue
- sore throat, fever, lymph node enlargement and fatigue
- may experience fatigue for 1-2 months
- may experience splenomegaly

96
Q

Leukemia

A

overproduction of malignant leukocytes
- overcrowding of bone marrow and decreased production and function of normal leukocytes: causing pancytopenia

97
Q

what are the 2 types of

A
  • acute lymphocytic leukemia
  • acute myeloid leukemia
98
Q

ALL, CLL

A

too many lymphoblasts (immature lymphocytes)

99
Q

AML, CML

A

too many myeloblasts (immature granulocytes)

100
Q

Acute

A
  • rapid increase in immature blood cells
  • rapid progression and accumulation of the malignant cells over weeks or months
  • immediate treatment is required in acute leukemia
  • most common forms of leukemia in children
101
Q

Chronic

A
  • excessive build up of relatively mature, but still abnormal, WBCs
  • months or years to progress
  • chronic forms can be monitored for extended time before treatment to increase effectiveness
  • most common in the older population
102
Q

leukemia risk factors

A
  • exposure to rays before birth
  • previous chemotherapy
  • genetic conditions including Down Syndrome
  • family history
  • smoking, previous chemotherapy, exposure to ionizing radiation
103
Q

leukemia signs and symptoms

A

amenia and thrombocytopenia
- fatigue due to anemia
- fever due to infection
- anorexia
- wasting of the muscle
- difficulty swallowing

104
Q

CML

A
  • slow growing disease
  • immature myeloblasts
105
Q

CLL

A
  • slow growing
  • too many immature lymphocytes
  • most common in the western world (longer life expextency)
106
Q

3 stages of leukemia

A
  • chronic phase
  • acclerated phase
  • terminal blast phase
107
Q

chronic phase

A

2-5 years

108
Q

accelerated phase

A

6-18 months
- primary develop lymphadenopathy (swollen lymph nodes)
- can have a decrease in neutrophils (infections)

109
Q

terminal blast phase

A

3-6 months
- painful, liver enlargement

110
Q

normal platelets

A

150-400

111
Q

bleeding disorders are caused by

A
  • platelet disorders (primary)
  • coagulation defects (secondary)
  • or a combination of both
  • decreased platelet production, increased consumption or both
112
Q

Heparin Induced thrombocytopenia (HIT) occurs

A

5-10 days after administration

113
Q

Heparin Induced thrombocytopenia (HIT)

A
  • marked by decrease in platelet count
  • thrombocytopenia
  • prothrombotic state
114
Q

prothrombotic state

A

Venous - DVT and PE
Arterial - Ischemia

115
Q

Hemorrhagic Disorders

A
  • diminished levels of coagulation factors (hemophilia)
  • excessice clotting (thromboembolic)
  • pulmonary emobilism
116
Q

Hemorrhagic Disorders causes

A
  • vitamin K deficiency
  • liver disorder (Hemophilia)
117
Q

vitamin K deficency

A
  • required for the synthesis and regulation of prothrombin
  • pro-coagulation and anticoagulant factors
  • destroy normal flora of the GI tract
  • prenatal storage is low (not sufficent in breast milk)
118
Q

Sings of Hemorrhagic Disorders

A
  • excessive bleeding
  • brusiing easily
  • bleeds in the mucous membrane
  • stool that looks dark black (like tar) and contains some blood
119
Q

hemophilia

A

X linked inheritance

120
Q

primary structures of the lymphatic system

A

bone marrow and thymus gland
- development of WBC

121
Q

Secondary structures of the lymphatic system

A

spleen, lymph nodes, tonsils, Peyer’s patches (small intestine)
- maintains volume balance between blood and interstitial fluids
- initiates adaptive immune response

122
Q

Lymphadenopathy or adenopathy

A

disease of the lymph modes, abnormal in size or consistency

123
Q

what are the 4 causes of Lymphadenopathy or adenopathy

A

neoplastic disease, immunological or inflammatory conditions, endocrine disorders, or lipid storage disease

124
Q

lymphoma

A

cancer that begins in the lymph nodes
- result of genetic mutation or infection

125
Q

Hodgkins lymphoma

A

cancer moves from one lymph more to another

126
Q

Hodgkins lymphoma symptoms

A
  • fever, night sweats, and weight loss, nonpainful enlargement of the lymph nodes in the neck, arm or groin
  • sedemate rate increases
127
Q

what is consitered on e of the most treatable forms of cancer

A

Hodgkins disease

128
Q

lymphoma stage I

A

localized disease
- signle lymph node involvement

129
Q

lymphoma stage II

A

2 or more lymph nodes on the same side of the diaphragm

130
Q

stage 3 lymphoma

A

lymph nodes on both sides of the diaphragm

131
Q

stgae 4 lymphoma

A

involvement of extra lymphatic organs (spleen, thymus gland, tonsils, ileum, appendix)

132
Q

non-hodgkins lymphoma

A

tumors develop form lymphocytes
- more common

133
Q

non-hodgkins lymphoma risk factors

A
  • older, man, white
  • inherited immune disorders
  • autoimmune disease
  • HIV/AIDS
  • exposure to chemical/pesticides
134
Q

non-hodgkins lymphoma symptoms

A

may be mistakes for a severe cold or flue

Pathophysiology (19 decks)

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