Hematology/Neoplasms Flashcards

(177 cards)

1
Q

a test to measure Hgb S

A

hemoglobin electrophoresis

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2
Q

low hemoglobin and hematocrit, small red blood cells, and an increased total iron binding capacity are all signs of…

A

iron deficiency anemia

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3
Q

lab test used to to evaluate red blood cell size

A

mean corpuscular volume

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4
Q

best laboratory test for detecting a clotting factor defect

A

aPTT

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5
Q

beta thalassemia minor, the genetic defect is in the ________

A

Hemoglobin

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6
Q

Cancers arise in cells that have alterations in the ______

A

genes

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7
Q

these are high at birth & cont to rise in some healthy infants during the 1st yr of life; steady decline occurs throughout childhood and adolescence until adult values reached

A

lymphocytes (neutrophils, eosinophils, monocytes)

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8
Q

For full-term neonates: these are comparable to counts in adults and remain so throughout infancy and childhood

A

platelets

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9
Q

normal erythrocyte life span in full-term infants

A

60-80 days

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10
Q

normal erythrocyte life span in pre-term infants

A

20-30 days

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11
Q

erythrocytes have many ______ in full-term infants

A

reticulytes

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12
Q

normal erythrocyte life span in children/adolescents/adults

A

120 days

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13
Q

aging causes erythrocytes to ________ while maintaining normal lifespan

A

replenish more slowly

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14
Q
Causes of \_\_\_\_\_\_\_ in Aging
Fe++ depletion
Decreased total serum Fe++
Decreased Fe++ binding capacity
Decreased intestinal Fe++ absorption
A

erythrocyte replacement slowing

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15
Q
Signs of \_\_\_\_\_\_\_ in the hematological system:
Platelet adhesiveness increases
Lymphocyte function decreases
T-cell function declines
Humoral system less responsive
A

Aging

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16
Q

large cells with normal Hgb

A

macrocytic normochromic anemias

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17
Q
Risk Factors for \_\_\_\_\_\_\_\_:
Dietary deficiency
alcoholism
cirrhosis
malabsorption
increased requirement state (pregnancy)
A

folate anemia

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18
Q

low maternal folate leads to ______

A

neural tube defects

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19
Q

Lab Findings in ________:

  • Low RBC
  • Low Reticulocytes
  • Low WBC
  • Low Plt
  • Low serum Folate
  • High MCV
  • High Homocysteine
  • Normal MCHC / MCH
  • Normal methylmalonic acid
A

folate anemia

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20
Q

Folate deficiency leads to abnormal _______ in RBC (as in B12 deficiency)

A

DNA synthesis

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21
Q

Both ________ have defective DNA synthesis in the bone marrow

A

folate and B12 anemia

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22
Q
Clinical Manifestation of \_\_\_\_\_\_\_:
Mild: 
fatigue
weakness
lethargy
pale skin
irritability
SOB (nonspecific and vague)
Severe: 
cheilosis (scales and fissures of the lips and corners of the mouth)
stomatitis (inflammation of mouth)
painful ulcerations of buccal mucosa & tongue (burning mouth syndrome)
dysphagia
flatulence
watery diarrhea
***Generally don’t see neurologic or psychiatric manifestations**
A

Folate Anemia

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23
Q

condition with high MCV: the RBC’s are large w/ normal Hgb, MCHC, MCH

A

macrocytic anemia

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24
Q

a measure of the concentration of haemoglobin in a given volume of packed red blood cel

A

mean corpuscular hemoglobin concentration (MCHC)

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25
average mass of hemoglobin per red blood cell in a sample of blood
mean corpuscular hemoglobin (MCH)
26
Autoimmune disorder that causes destruction of the parietal cells in the stomach with complete loss of intrinsic factor
Pernicious (B12 Deficiency) Anemia
27
enzyme that is necessary for the absorption of B12
intrinsic factor
28
``` Risk Factors for ______: Alcoholism cirrhosis bariatric surgery H. pylori medications (H2 blockers, proton pump inhibitors) ```
Pernicious (B12 Deficiency) Anemia
29
ineffective DNA synthesis in RBC production in bone marrow that produces megaloblasts that do not mature properly and die off early (happens slowly)
B12 deficiency patho
30
_____ mostly affects older women (median age = 60)
Pernicious (B12 Deficiency) Anemia
31
``` Lab Findings of _______ Low RBC Low Reticulocytes Low WBC Low Plt - High MCV - High homocysteine - High methylmalonic acid -Normal MCHC / MCH -Norm-low serum cobalamine (B12) ```
Pernicious (B12 Deficiency) Anemia
32
methylmalonic acid is high in pernicious anemia because...
B12 is needed to break it down
33
Clinical Manifestations of ________: vague, nonspecific sx (similar to folate deficiency) Severe cases: marked anemia & neurological deficits Marked anemia: -Weakness, fatigue -Paresthesias of feet & fingers -Difficulty walking -Loss of appetite -Abdominal pain Neurological deficits: -Peripheral nerve degeneration is r/t demyelinating lesions of spinal cord & cerebral cortex -myelin degeneration & loss of nerve fibers in the dorsal and lateral columns of the spinal column and cerebral cortex ***Megaloblastic Madness Delusions, hallucinations, outbursts, paranoid schizo ideation
Pernicious (B12 Deficiency) Anemia
34
small cell size with decreased Hgb | MCV, MCHC low
Microcytic Hypochromic Anemia
35
``` Causes of _______: Nutritional deficiency blood loss (slow-GI bleed, fast-hemorrhage) Less common: decreased GI absorption pregnancy renal failure ```
Iron Deficiency Anemia
36
______ results in pale, small RBCs with lower than normal Hgb concentration
Iron Deficiency Anemia
37
``` Lab Findings of ______: Low Hgb concentration Low reticulocytes Low RBCs Low MCV, MCH /MCHC Low serum Ferritin Low serum Fe++ Increased total Fe++ binding capacity ```
Iron Deficiency Anemia
38
``` Clinical Manifestations of _______: (s/sx depends on severity) Mild-moderate: no sx (explore hx of any bleeding or s/s of bleeding) Severe: fatigue headache palpitations decreased exercise tolerance weakness More advanced: sore tongue brittle or spoon-shaped nails (koilonychia) PICA ```
Iron Deficiency Anemia
39
Normal cell size and Hgb
Normochromic/Normocytic Anemias
40
anemia caused by accelerated destruction of RBCs in which Erythrocyte production is unable to keep up with destruction
Hemolytic Anemia
41
type of hemolytic anemia that occurs due to deficiency in CD55 and CD59, a complement mediated intravascular lysis of RBCs & release of Hgb
Paroxysmal nocturnal hemoglobinuria
42
type of hemolytic anemia in which autoantibodies against antigens normally on the surface of the erythrocyte are present: • Warm reactive antibody type • Cold agglutinin type • Cold hemolysin type (paroxysmal cold hemoglobinuria) **named according to the optimal temperature at which the antibody binds to the erythrocyte
Autoimmune hemolytic anemias
43
type of hemolytic anemia that is due to an allergic rxn against foreign antigens: the drug (penicillin, cephalosporins, hydrocortisone) "Hapten-Hypersensitivity"
Immune Hemolytic Anemia
44
Signs of _________: Jaundice - unconjugated bili (Icterus) Splenomegaly
Hemolytic Anemia
45
``` Signs of _______: anemia hemoglobinuria fatigue abd pain thrombosis ```
Paroxysmal nocturnal hemoglobinuria
46
Evaluation of _______: | Bone marrow aspirate showing abnormal increase in erythrocyte stem cells (erythroid hyperplasia)
Hemolytic Anemia
47
``` Lab Findings for _______: Low CBC High Hgb/Hct High reticulocytes Normal to High MCV ```
Hemolytic Anemia
48
Cause of ______: | Dehydration
Relative Polycythemia
49
``` Dehydration leads to decreased fluid in blood which means less floating space 2 groups of hemoconcentration -high Hgb/Hct/ RBC -Disturbed fluid balances -Stress-induced ```
Relative Polycythemia
50
Abnormal regulation of multipotent hematopoietic stem cells that is associated with a gene mutation and neoplastic transformation of bone marrow stem cells & absolute increased RBC mass
Primary Absolute Polycythemia | Polycythemia Vera
51
``` Key Points of ______: Rare in ages <40 Men>Women Cause unknown No cure Increased risk for stroke/ MI /HTN ```
Primary Absolute Polycythemia | Polycythemia Vera
52
``` Lab Findings for _______: Absolute increase in RBC mass leukocytosis (increased WBC) thrombocytosis (increased plt) increased uric acid (due to excess proliferation) normal O2 sat ```
Primary Absolute Polycythemia | Polycythemia Vera
53
``` Clinical Manifestations of ________: s/sx are all d/t increased blood viscosity • SOB • Dizziness • Red-colored face • Bluish extremities ```
Primary Absolute Polycythemia | Polycythemia Vera
54
Acute, self-limiting viral infection of B lymphocytes usually caused by Epstein Barr Virus (EBV) (~85% of cases)
Infectious Mononucleosis
55
``` Viral Causes of ______: Epstein Barr cytomegaly adenovirus HIV Hep A Influenza A & B Rubella ```
Infectious Mononucleosis
56
Bacterial Causes of _______: | Toxoplasmosis and Diphtheria
Infectious Mononucleosis
57
Bacterial Causes of _______: | Toxoplasmosis and Diphtheria
Infectious Mononucleosis
58
- Virus enters oropharynx, nasopharynx, or salivary epithelial cells & spreads to lymphoid tissue & B cells - Virus causes widespread infxn of B lymphocytes that have receptors for the EBV Meanwhile, the unaffected B lymphocytes produce IgG, IgM, & IgA against the virus Cell-mediated response is in the form of cytotoxic T cells & cytokines that directly attack the EBV infected cells This immune response produces cellular proliferation in the lymphoid tissue--specifically nodes, tonsils, spleen, & liver.
Patho of Infectious Mononucleosis
59
Labs for ______: CBC (Differential with at least 50% lymphocytes and 10% atypical lymphocytes- classic triad, high leukocytes) Monospot (qualitative test for heterophilic antibodies which increase as the illness progresses) EBV specific antibodies positive IgM antibodies (may not appear for 7-10 days)
Infectious Mononucleosis
60
``` Clinical Manifestations of ________: Sore throat Sore, Inflamed tonsils Exudate on tonsils (grey, thick) Fatigue (can last up to 2 months) Malaise Arthralgia ***Classic triad of symptoms: Fever, pharyngitis, and lymphadenopathy of the cervical lymph nodes (lasts 7-20 days) ```
Infectious Mononucleosis
61
incubation of Infectious Mononucleosis
30-50 days
62
prodomal phase of Infectious Mononucleosis with sx of fever, arthralgia, malaise
3-5 days
63
Adults 40 and older with mononucleosis are more likely to have infection from _______ or _________
cytomegaly virus or bacterial
64
Mononucleosis is more common in ages ______with ______/1000 cases per year
15-35 | 6-8
65
State of hypercoagulability which increases risk of thrombosis
thrombophilia
66
type of thrombophilia that results from defects in proteins that are involved in hemostasis  Inherited conditions (mostly autosomal dominnt) that increase risk for thrombosis  Ex: Factor V Leiden
Primary (hereditary)
67
type of thrombophilia that is caused by condition/disease that promotes venous stasis or changes in coagulation factors  Ex: Pregnancy
Secondary (acquired)
68
Genetic disease that is the most common hereditary thrombophilia
Factor V Lieden
69
Key Points of ________: - Increases the risk of blood clots - Alters clotting factor V - Protein C cannot be degraded - Hormonal birth control increases risk even without this factor – so women are screened
Factor V Lieden
70
Labs for _____: Protein C Genetic Testing
Factor V Lieden
71
_______ increases risk for ischemic stroke, DVT, & MI
Factor V Lieden
72
30% of patients w/ DVT or PE have ______
Factor V Lieden
73
Lab Findings for ______ & ______: Prolonged PTT Normal Platelets and INR
Hemophilia and Von Willebrand Disease
74
Lab Findings for ______: Platelet Count <150,000 Normal PT/PTT/INR
Immune Thrombocytopenia Purpura (ITP)
75
most common blood disorder in children with the highest Incidence between 6mo – 2yrs old that is caused by ingesting too much cow’s milk which has a heat labile protein that casues inflammation and chronic intestinal blood loss
Iron Deficiency Anemia
76
Clinical Manifestations of _______: | Fatigue, weakness, dizziness, SOB, Tachycardia, HA, Leg cramps, Pale skin
Hemolytic Disease of the NB
77
``` Labs for _______: -Microcytic RBCs -Low MCV, MCH and MCHC -Hemoglobin electrophoresis (may be used to determine type of abnormal hemoglobin) Unconjugated bilirubin ```
Hemolytic Disease of the NB
78
Lab that tests for antibodies that stick to RBCs and cause hemolysis
Coombs
79
lab test used to detect antibodies that are stuck to the surface of RBC and cause hemolysis and anemia -Positive test indicates that these antibodies are present
Direct Coombs
80
lab test that detects free-flowing antibodies against certain RBC - Most often done to see if there is a potential transfusion reaction - Positive: there are antibodies present and blood crossmatch is incompatible
Indirect Coombs
81
an unstable and insoluble form of Hgb resulting from defective Hgb synthesis in Sickle Cell Disease
HBs
82
genetic defect in which valine replaces glutaminic acid in Hgb
Sickle Cell Disease
83
RBC with high levels of HBs are very sensitive to ________ so they fold or "sickle"
low O2 states
84
Sickling is reversible except when _____ are present in very high percentage
HBs
85
In ________, anemia is caused by rapid death of defective RBCs that have only 16-20 day lifespan
Sickle Cell Disease
86
Sickle Cell Disease is _______ ________ Disorder (must have a defective gene from both parents to show phenotype)
Autosomal Recessive
87
This occurs when a child inherits Hb S from one parent and normal hemoglobin (Hb A) from the other and this heterozygous carrier rarely has symptoms
Sickle Cell Trait
88
Symptoms of Hgb S do not appear until age ______ when fetal Hgb is replaced by Hgb produced by the infant
6 months
89
Clinical Manifestations of ______: • Recurrent pain • Disability • Organ damage • Increased infections (most common cause of death) • Early death (people are now living into 40-50s)
Sickle Cell Disease
90
Group of inherited disorders caused by variant or missing genes that affect how the body makes Hgb (microcytic hemolytic anemia)
Thalassemias
91
The type of _______ (alpha or beta) depends on the type of Hgb that is low or missing
Thalassemias
92
``` Inhereited Severity of _________: Carrier Intermedia Trait/Minor: heterozygous inheritance may not have sx Major: homozygous inheritance- may require blood transfusions ```
Thalassemias
93
Thalassemias is a ________ ________ disorder
autosomal recessive
94
Hemolysis of reticulocytes leads to elevated iron and indirect bilirubin
patho of Thalassemias
95
Type of hemophilia: Factor VIII deficiency • Most common inherited coagulation disorder that leads to excessive bleeding • X-linked (boys only) • Often discovered during circumcision
Type A (classic)
96
Type of hemophilia: Factor IX deficiency | • X-linked
Type B (Christmas disease)
97
type of hemophilia: Factor XI deficiency • Autosomal recessive • Occurs in boys and girls • Less severe
Type C
98
Autosomal dominant (most) disorder affecting Factor VIII deficiency (key clotting protein) and platelet dysfunction • Most common bleeding disorder for both men and women • Carried on chromosome 12
Von Willebrand Disease
99
protein that binds factor VIII and platelets and BV walls to create platelet plugs.
Von Willebrand protein
100
Clinical Manifestations of ______: Hematoma formation Persistent bleeding from minor laceration
Von Willebrand Disease
101
Lab Findings of ________: Prolonged aPTT Normal platelets and INR
Von Willebrand Disease
102
Antiplatelet antibodies bind to platelet plasma membranes causing platelet sequestration & destruction resulting in low platelet count & increased risk of hemorrhage usually occuring after a viral infection→ large amount of antigen in blood → formation of immune complexes → bind to platelets → platelet destruction
Immune Thrombocytopenia Purpura in Children
103
``` Key Points of _______: • Type II hypersensitivity • Resolves when antigen is removed • Persistent cases can last 3-12 months • Autoimmune or primary thrombocytopenic purpura ```
Immune Thrombocytopenia Purpura in Children
104
``` Clinical Manifestations of _________: Bruising generalized petechial rash asymmetrical bleeding spontaneous bleeding (Platelet count <15,000) resulting in • Petechiae • Ecchymosis • Purpura ```
Immune Thrombocytopenia Purpura in Children
105
Lab Findings for _______: Platelet count <150,000 Normal PT/ INR/PTT
Immune Thrombocytopenia Purpura in Children
106
caused by changes in expressions of the genes involved in cell division
Cancer
107
ONE CELL can generate widespread metastatic disease
monoclonal origin of cancer
108
NOT inherited from one human generation to another • UNLESS mutation is present in a gene that regulates cell division in a germline cell, then it CAN be inherited and this mutation in germline cells can significantly increase the risk
Cancer
109
_______ develops as a results of 3 interacting factors: • Environmental exposure to carcinogens • Health of immune function • Genetic predisposition
Cancer
110
This germline mutation is present in one BRCA 1 allele throughout all of the person’s cells. The cells have essentially already gone through half of initiation at conception and require only one additional allele mutation followed by promotion for the malignancy to occur. While the person carries genetic changes which could lead to development of cancer, they have not inherited the cancer itself – it requires further mutation/changes to develop into cancer.
BRCA 1 suppressor gene mutation
111
``` Characteristics of _______ Tumor: • Grow slowly • Well-defined capsule • Not invasive • Well-differentiated • Low mitotic index • DO NOT metastasize ```
Benign
112
``` Characteristics of ______ Tumor: • Grow Rapidly • Not encapsulated • Invasive • Poorly differentiated • High Miotic Index • Can spread distally (Metastasis) ```
Malignant
113
Stage of Metastatic Disease • A carcinogen causes genetic mutation that activates proto oncogenes which inactivates tumor suppressor genes. • The mutation is not evident until PROLIFERATION • Proliferation is required for cancer development! • Initiation is irreversible • It only takes ONE transformed cell to start the cancer process
Initiation
114
Stage of Metastatic Disease: • Occurs when mutant cells begin to proliferate through the enhancement of the growth of the initiated cell. • Promoters: infection, hormones, nutritional factors, cigarette smoke, etc. • Cancer synthesize telomerase when they become malignant. This process of synthetization allows the cell to have immortality as it continually regenerates the telomeres. • Cells are not immortal and can divide only a certain number of times. • Telomeres are protective caps on each chromosome and are held in place by telomerase • Telomeres become smaller and smaller with each cell division • Cancer cell telomeres do not become smaller with cell division and telomeres can be restored, leading to continued division and immortality. • Cancer cells are P-53 deficient which allows the cell to escape apoptosis, though DNA is grossly abnormal.
Promotion
115
Stage of Metastatic Disease: • Continued genetic changes that occur over time- gives survival changes to cancer cells (the cell begins to display malignant behaviors) • Some cells will have growth advantage and proliferate more readily. • Some cells are able to develop a separate blood supply through tumor angiogenesis factor (TAF)
Progression
116
Stage of Metastatic Disease: • Loss of differentiated function, cell becomes more efficient in cell division → METASTASIS • Metastasis occurs when cancer cells escape the tissue of origin and initiate colonies of cancer at distant sites via blood and lymph circulation.
Metastasis
117
Genes associated w/ initiation of cancerous behavior in a cell that are promitotic and induce cells to divide and proliferate ***Mutations occurs less frequently,
Oncogenes
118
the loss of oncogene sensitivity to suppressor gene regulation leads to....
oncogene overexpression
119
normal cellular gene that is growth promoting. | ***When this is erroneously activated, it becomes an oncogene and promotes cancer
Proto-oncogenes
120
these genes regulate a group of growth-promoting genes and suppress tumor formation • They inhibit mitosis and trigger apoptosis • Mutation and under-expression of this gene is associated with cancer development
Tumor Suppressing Gene
121
Examples of _______: P-53- suppresses tumor formation RB Tumor suppressor - this is inactivated in occurrences of Retinoblastoma BRCA 1 - Inactivated in occurrences of Breast and Ovarian Cancer BRCA 2- Inactivated in occurrences of ovarian, breast, and prostate carcinomas
Tumor Suppressing Genes
122
Mutations in _________ (even if only in one allele), reduces the ability of the suppressor gene products to inhibit the activity of the promitotic oncogenes
Tumor Suppressing Genes
123
Mutations in suppressor genes alleles or DNA repair genes cause most _________
cancer
124
* Occurs usually as a result of environmental exposure or unknown factors * No observable pattern of inheritance * Mutations of carcinogenesis disrupt regulation of cell division (usually somatic cells) * Not present in higher-than-expected levels within three family generations
Sporadic Cancer
125
* Occurs at a higher-than-expected frequency within a family * Does not demonstrate observable pattern of inheritance * Family may have higher-than-expected incidence of several cancer types * Those who develop cancer are older (usually over 60)
Familial Cancer
126
• Cancer that occurs with an observable autosomal dominant pattern within a family • Diagnosis at much younger-than-expected ages • Caused by germline mutations in suppressor genes • RISK is inherited - NOT the actual cancer *****Risk is greatly increased, but NOT absolute. (AGING, IMMUNOCOMPROMISED ALSO INCREASES PERSONAL RISK)
Inherited Cancer
127
immature form of RBC
reticulyte
128
disruption of dna synthesis of blast cells in bone marrow produces megaloblasts (large abnormally shaped RBC with normal Hgb)
macrocytic normochromic anemias | folate + B12 deficiency anemias
129
gastrectomy makes you think...
pernicious anemia
130
What is it that causes parasthesis of the fingers and hands in B12 deficiency?
demyelination in the spinal cord
131
What does B12 + folate deficiency do in the bone marrow that lead to macrocytic anemia?
DNA synthesis of the RBC disrupted
132
What symptom is seen in all anemias?
fatigue
133
spoon-shaped nails
koilynichia
134
type of Hgb that is present in newborns but slowly fades away with age
Hgb F
135
normal type of Hgb
Hgb A
136
type of Hgb present in sickle cell disease
Hgb S
137
myeloproliferative disorder, increase in RBCs resulting in an increase in blood viscosity leading to clinical symptoms such as HTN
polycythemia
138
most common type of polycythemia that is due to chronic hypoxemia increased erythopoitein production increase in RBC w/o increase in WBC or platelets *seen in individuals w/ lower O2 serum concentration (high altitude or smokers)
secondary polycythemia
139
condition that usually occurs after a viral infection that leads to a large amount of antigen in the blood that forms immune complexes with circulating antibodies that bind to receptors on platelets and cause platelet destruction
Autoimmune or Primary Thrombocytopenic Purpura
140
Primary Thrombocytopenic Purpura is a Type ___ Hypersensitivity
2
141
Clinical Manifestations of ________: | Bruising, generalized petechial rash, asymmetrical bleeding
Autoimmune or Primary Thrombocytopenic Purpura
142
Lab Findings for ______: o Low platelet count o Increased bleeding time o Normal PT, PTT, & INR
Autoimmune or Primary Thrombocytopenic Purpura
143
type of polycythemia that is due to dehydration because decreased fluid within bloodstream it looks like there are more RBCs but really you just have less floating space
Relative Polycythemia
144
First test to order when patient presents with fatigue
CBC
145
increase in reticulocyte count tells us what?
bone marrow is responding to a decrease | increase related to treatment with iron
146
MCV tells us what about RBC?
size
147
MCH tells us what?
weight/mass of Hgb per RBC
148
MCHC tells us what?
Hgb concentration of average RBC?
149
bleeding time tells us what?
how long it takes to clots?
150
bleeding time is testing which RBC?
platelets
151
Hgb electrophoresis
differentiates between Hgb A, S or F
152
Which test is most sensitive for detecting clotting factor defects?
aPTT
153
aPTT and PTT tests screen for what?
clotting factor defects
154
D-dimer is a screening test for what?
blood clots
155
Mutations of Rb (tumor suppressing gene) are inherited via ____?
autosomal dominant or sporadic
156
How does chronic inflammation cause cancer?
cell mutation due to inflammatory process of releasing O2
157
tumor markers are found where?
blood, spinal fluid, urine
158
ca125 screening is for?
ovarian cancer
159
chromosome instability may result in the over expression of _______
oncogenes
160
pernicious anemia caused by autoimmune destruction of parietal cells that make intrinsic factor
megaloblastic anemia
161
macrocytic anemias
pernicious anemia B12 deficiency anemia folate deficiency anemia
162
microcytic anemias
iron deficiency anemia | thalassemia (inherited)
163
normocytic anemias
hemolytic anemia | post-hemorrhagic anemia
164
lymphocyte function ______ with age (in particular cellular immunity)
decreases
165
BRCA1 gene is associated which cancers?
breast, ovarian, prostrate
166
type of Hgb seen with beta-thalassemia
HgbA2
167
folate is stored in the _____
liver
168
folate absorption occurs in the ______
small intestine
169
most common form of autoimmune hemolytic anemia
warm antibody
170
``` Causes of _______: hypoxemia **most common increased plasma osmolality/volume low temperature decreased pH dehydration ```
Sickling
171
these negatively regulate proliferation
tumor suppressing genes
172
Hep B, Hep C, Epstein Barr & HPV have all been linked to...
cancer development
173
genes that encode proteins to repair DNA whose loss of function results in increased mutation rates and cancer rates
caretaker genes
174
test used to detect antibodies that are stuck to the surface of RBCs, These antibodies sometimes destroy RBCs and cause anemia.
Direct Coombs
175
______ direct coombs test means there are antibodies that act against the RBCs
positive
176
test that looks for free flowing antibodies against certain RBCs -most often used to see if there is a blood transfusion reaction
Indirect Coombs
177
______ indirect coombs test means there are free flowing antibodies that will act against RBCs that the body views as foreign= incompatible blood match
positive