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Hematological Flashcards

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1
Q

Thrombocytopenia

A

platelet count of <100,000

<50,000 hemorrhage from minor trauma

<15,000 spontaneous bleeding

<,10,000 severe bleeding

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2
Q

Causes of thrombocytopenia

A

hypersplenism, autoimmune disease, hypothermia, viral and bacterial infections that cause DIC

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3
Q

Clinical Manifestations of Thrombocytopenia

A

petechiae and purpura

frank bleeding from mucous membranes (epistaxis, m=hematuria, menorrhagia, bleeding gums)

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4
Q

Types:

Anemia

Normochromic macrocytic anemia

hypochromic-microcytic anemias

iron defeciency anemias

A
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5
Q

reduction of the total number of erythrocytes in the circulating blood or in the quality or quantity of the hemoglobin

A

*impaired erythrocyte production

*acute or chronic blood loss

* increased erythrocyte destrution

or a combination of the above

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6
Q

*Classifications

*etiology

*morphology (based on MCV, MCH, MCHC values)

*size: identified by terms that end in “-cytic”

*macrocytic (large), microcytic (small), normocytic (normal)

*

A

*hemoglobin content

-identified by terms that end in -“chromic”

Normochromic (normal amount), hypochromic (decreased amount)

*other descriptors of erythrocytes associated with some anemias: Anisocyotis (RBC’s are present in various sizes)

Poiklicytosis: RBC’s are present in various shapes

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7
Q

Anemia

Physiologic manifestation

A

reduced oxygen carrying capacity

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8
Q

Classic anemia symptoms

A

fatigue, weakness, dyspnea, pallor

-variable symptoms based on severity and the ability of the body to compensate

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9
Q

Hpoxia

physiologic anifestation of anemia

A

reduced oxygen carrying capacity

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10
Q

Cardiovascular FX and anemia

A

increased preload, heart rate and stroke volume;

reduced afterload

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11
Q

Respiratory Fx and anemia

A

Dyspnea

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12
Q

Nervous system fx and anemia

A

myelin degeneration and parasthesias

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13
Q

Gastrointestinal fx and anemia

A

pain, nausea, vomiting and anorexia

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14
Q

Other fx related to anemia

A

due to hypoxemia and tissue hypoxia

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15
Q

Megaloblastic anemias

A

RBC are unusually large

  • Defective DNA synthesis die to deficiencies in vitamin B12 or folate and coenzymes for nucear maturation and the DNA synthesis pathway
  • RNA processes occur at a normal rate (results in unequal growth of the nucleus and cytoplasm)
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16
Q

Most common type of MACROCYTIC anemia

A

*Caused by lack of intrinsic fact or from th gastric parietal cells which is required for vitamin B12 absorption

-may be a congenital or autoimmune disorder (auto antibodies against intrinsic factor)

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17
Q

Increasing risk factors for pernicious anemia include:

A

past infection with H-Pylori

  • gastrectomy
  • proton-pump inhibitors
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18
Q

Macrocytic anemia: Pernicious

SXS’s

A

Weakness, fatugue

paresthesias of feet and fingers/difficulty walking

loss of appetite, abdominal pains, weight loss

sore tongue thta is smooth and beefy red secondary to atrophic glossitis

*lemon-yellow sallow skin and a result of a combination of pallor and icterus

*neurological symptoms from nerve demyelination

*Not reversible-even with treatment

Often unrecognized in older adults die to subtle, slow onset and presentation

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19
Q

Treatment

A

Parenteral or high oral doses of Vitamin B 12

*if untreated, death will occur

-Life long treatment is required

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20
Q

Folate (Folic acid) Deficiency

A

folate is an essential vitamin for RNA ans DNA synthesis

*absorption of folate offurs in the upper small intestine; it os not dependent on any other facilitating factors

*common in alcoholics and individuals with chronic malnourishment

*associated with neural tube defects in the fetus

*

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21
Q

Clinical findings of folate defeciency anemai:

A

Severe cheilosis: scales and fissures of the lips and corners of the mouth

stomatitis: mouth inflammation
- painful ulderations of the buccal mucosa and tongue; characteristic of burning mouth syndrome
- dysphagia, flatulence and watery diarrhea

Neuro sxs’s are usually not seen

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22
Q

Treatment of folate deficency anemia

A

oral dose of folate is administered daily until normal blood levels are obtained

-life long treatment is NOT necessary

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23
Q

Characterized by red blood cells that are abnormally small and contain reduced amounts of hemoglobin

They are related to:

A

Disorders of iron metabolism

  • disorders of porphyrin and heme synthesis
  • disorders of globin synthesis
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24
Q

Iron deficiency anemia

hypochromic-microcytic anemia

A
  • Most common type of anemia worldwide
  • Highest risk: older adults, women, infanct and those living in poverty
  • associated with cognitive impairment in children
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25
Hypochromic-microcytic CAUSES:
- inadequate dietary intake - excessive blood loss - chronic parasite infections - metabolic or functional iron deficiency - menorrhagia (excessive bleeding during menstration) - iron deficiency anemia dn folate deficiency anemia are two leading causes of anemia in pregnancy - use of medications that cause GI bleeding (ASA, NSAIDS) - surgical procedures that decrease stomach actidity - intestinal transit time and absorption (Gastric bypass) - eating disroders (pica)
26
Hypochromic-Microcytic manifestations
fatigue, weakness, shortness of breath pale earlobes, palms and conjunctiva brittle, thin coarsly ridged and spoon-shaped nails (koilonychia) red, sore painful tongue angular stomatitis: dryness and soreness in the cornders of the mouth --become symptomatic when hgb is 7-8
27
what do you evaluate in iron-deficiency anemia?
serum ferritin
28
Treatment of Iron-Defiency anemia
identify and eliminate sources of blood loss - iron replacement therapy: iron dextran - Sodium ferric gluconate comples in sucrose (Ferrlecit) and iron sucrose injection (Venofer) Duration of therapy: 6-12 months after the bleeding has stopped, but may continue for 24 months
29
Iron Deficiency Anemia
- Most common blood disorder of infancy and childhood - stored iron: greatest stores are 4-8 weeks after birth Dietary Iron: is needed after 16-20 weeks of age - lack of iron intake or blood loss - manifestations: irritability, decreased activity intolerance, tachycardia, weakness, lack of interest in play and Pica
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50-55% of blood volume Organic and inorganic elements
31
Leukemia is: Uncontrolled proliferation of malignant leukocytes and results in
- overcrowding of bone marrow - decreased production and function of normal hematopoietic cells:
32
Clssification of Leukemia
Predominant cell of origin: Myeloid or Lymphoid rate of progression: acute or chronic
33
Acute Leukemia
Presence of undifferentiated or immature cells (usually blast cells) -rapid onset with narrow window in which to treat
34
Chronic Leukemia
Predominant cell is mature but does not function normally -slow progression
35
Acute lymphocytic Leukemia
- Most common malignancy of childhood - greater than 30% lymphoblasts in bone marrow or blood - Genetic Anomoly: Philadelphia Chromosome (reciprocal translocation results in abnormal chromosome and occurs between chromosomes 9 abd 22)
36
Cause of ALL Acute Lymphocytic Leukemia
Unclear cause genetic susceptibility environmental factors viral infections
37
Clinical Manifestations of ALL
Pallor fatigue petechiae purpura bleeding fever (hypermetabolism and infections) bone pain
38
Test for ALL
Bone marrow aspirtion for BLAST cells
39
Treatment of ALL
Combinatoin chemotherapy -radiation 4 phases (induction of remision; preventative therapy for the central nervous system; intensification (consolidation) and maintenance
40
Acute Myelogenous leukemia (AML)
Most common adult leukemia (mean is 67) -down syndrom increases the risk -
41
Acute Myelogenous Leukemia
abnormal proliferation of myeloid precursor cells- - decreased rate pf apoptosis - arrest in cellular differentatin - Mutation in receptor tyrosine kinase FLT3
42
Risk factors for AML
Exposure to radiation, benzene and chemotherapy -hereditary conditions
43
Chronic Myelonegous Leukemia
Usualy diagnosed in adults - Myeloproliferative disorder that also includes polycythemia vera, primary thrombosis and ideopathic myelofibrosis - Philadelphia chromosome is often present and BCR-ABL 1 causes initiation of CML
44
CLL
common is adults older than 50 (70% are asymptomatic at dg) - affects monoclonal B lymphocytes - has a familial tendency
45
Manifestations of CLL Chronic Lymphocytic Leukemia
Fatigue caused by anemia - bleeding resulting from thrombocytopenia - fever (infection) - anorexia, weight loss, diminished sensitivity to sour and sweet tastes - wasting away of muscle difficulty swallowing -CNS involvment
46
Testing:
bone marrow peripheral blood smear
47
RAPID CHILDREN SURVIVAL RATE:91% PRIMARY CELL: GREATER THAN 3% LYMPHOBLAST AND B CELLS
rAPID ONSET MOST COMMON IN CHILDREN SURVICAL RATE 91% LYMHOCYTES AND b CELLS
48
progression is slow adults survival rate 85% monoclonal B is primary cell
slow mostly adults 85% survival monoclonal B cell
49
AML RAPID Most common ADULT FORM survival rate 24% precursor myeloid cells
Progression/onset rapid most common adult form 24% survical precursor meyloid cells
50
CML Slow onset Mostly is adults NO CURE neutrophilic or eosinophilic or clonal arise from hematopoietic stem cell
chronic old people slow adults no cure neutrophilic, eosinophilic, clonal arise from hematopoitic stem cell
51
Vaso occlusive crisis (thrombotic crisis)
Sickling s in Microcirculation, extremely painful and symmetric -hands and feet exhibit painful swelling (hand-foor syndrome)
52
Neutropenia: reduction in circulating neutrophils
Primary or secondary
53
Primary Neutropenia
PRIMARY 1-congenital -cyclic neutropenia and neutropenia with congenital immunodeficiency disease 2-Acquired -multiple conditions (hyplastic anemia, aplastic anemia, leukemias, lymphoma (hodgkin, non-hodgkin), myelodysplastic syndrome SECONDARY NEUTROPENIA lower cound from other disorders (immune disorders/drugs)
54
Causes of Neutropenia
Prolonged Infection - decreased production - reduced neutrophil survival - abnormal neutrophil distribution and sequestration
55
Severe Neutropenia
less than 500/microliter
56
Granulocytopenia AKA: Agranulocytosis Causes
Interference with hematopoiesis immune mechanisms chemotherapy destruction ionizing radiation SEPSIS caused by agranulocytosis usually results in death within 3-6 days
57
Eosinophila
-elevated eosinophil count hypersensitivity reactions trigger the release of eosinophilic chemotactic factor of anaphylaxix from mast cells
58
Causes of eosinophilia
allergic disorders parasitic invasions
59
Eosinopenia
decrease in circulation numbers of eosinophils - usually caused by migration of cells to inflammatory sites - other causes: surgery, shock, trauma, burns or mental disress
60
Iron cycle: Ferrtitn transferrin
Ferritin: major intracellular iron storage protein- -precursor to ferritin is apoferritin (ferritin without iron) TRANSFERRIN: -transfers iron in circulation precursor is apototransferrin
61
Hematocrit or PCV: %%
percentange of RBC's in total blood volume: approximately 3XHgb
62
Normal range for Hct
40-52% men 35-47% women
63
HgB
total amount of HgBin the blood more accurately reflects the changes in plasma volume
64
Range for HgB
4. 5-6.0 (men) 3. 8-5.2 (women)
65
MCV
Volume or SIZE of single RBC Normal Range: 80-100 fl
66
MCH
Total amount of HgB in a RBC Range: 26-34 pg
67
MCHC
Average concentration or %percentage of HgB in a single RBC Normal Range: 32-36%
68
RDW
estimate of RBC size normal Range: 12-13.5%
69
Retic
Immature RBC, reflects bone marrow Fx Normal Range 0.5-2.0%
70
Retic Index
RI=retic count x (hct/45) c (1/1.85) Normal range: \<2% hypoproliferative anemia \>3 increase RBC production
71
Nutritional Requirements for Erythropoiess (with IF)
Proteins Vitamins Minerals
72
Proteins (amino Acids) for erythropoieses
Proteins (amino acids) -structural supports synthesis of hemoglobin
73
vitamins in erythropoiesis
Vitamins: B12- synthesis of DNA. maturation or erythrocytes, facilitator of folate metabolism -B6, E and panthothenic acid: heme synthesis --Folic Acid (Folate): synthesis of DNA and RN; matruration of erythrocytes C: Iron metabolism Riboflavin: Oxidative reactions Niacin: needed for respiration of mature erythrocytes
74
Minerals in erythropoiesis
Iron: hemoglobin synthesis Copper: required for moblization of iron from tissues to plasma
75
Idiopathic thrombocytopenic purpura
Pathyphysiology: - IgG antibody targets platelet glycoproteins - antibody-coated platelets are sequestered and removed fromt he circulation - Acute form develops after viral infections (one of the most common childhood bleeding disorders)
76
Manifestations
petechiae and purpura, progressing to a major hemorrhage
77
Acute, self-limiting infection of B lumphocytes transmitted by saliva through personal contact
Commonly called EBV (epstein-barr virus): 85%
78
Other viral agents resembling IM
CMV hapatitis influenza HIV
79
Hodgkins Lymphoma
Reed-Stemberg cells in the lymph nodes are necessary for diagnosis but not specific for hodgkin lymphoma, are derrived from malignant B cells that usually become bunucleate and release cytokines - B-Cell in the germinal center has unsuccessful immunoglobin gene rearrangement; it should undergo apoptosis, but survives - Virus may be involved in the pathogenesis - familial clustering suffest and unknown genetic mechanism
80
Sideroblastic anemia
makes up a group f disorders characterized by anemia Caused by a defect in mitochondrial heme synthesis - Ringed sideroblasts in the bone marrow are diagnostic - sideroblasts: erythroblasts cotain iron granules that have not been synthesized into hgb - aquired vs hereditary - reversible siderblastic anemia: associated with alcoholism myelodysplastic syndrome
81
Sideroblastic anemia clinicical manifestations Hypochromic microcytic anemias
Iron overload (hemachromaatosis) enlarged spleen (splenomegaly) and liver (hepatomegaly) Evaluation: bone marrow is diagnostic dimorphism: normucytic and normochromic cells concomitantly observed with microcytic-hypochromic cells
82
RBCs normal in size and Hgb concentration but insufficient in number No common cause, pathologic, mechanisms or morphologic characteristics exsit Occur less frequently than macro-cytic normochromic and microcytic-hypochromic anemias
83
Aplastic anemia
panctopenia reduction of absence of all 3 types of blood cells - most aplastic anemias are autoimmune; some are due to chemical exposure (benzene aresnic, chemo) - Pure RBC aplasia Fanconi anemia: rare genetic anemia from decects in DNA repair Pathyphysiology: characteristic lesion is a hypocellular bone marrow that has been replaced with fat -Clinical manifestations: hypoxemis, pallor (occasional brown pigmentation to the skin), weakness along with fever and dyspnea with rapidly signs of hemorrhaging if platelets are affected Evaluation: Bone Marrow Bx
84
Posthemorrhagic anemia: Acute blood loss from the vascular space
clinical manifestations depends on severity of blood loss tx: IV of saline, dextran, albumin or plasma large volume:fresh whole blood
85
hemolytic
accelerated destruction on RBC's congenital vs acquired intravascular vs extravascular hemolysis
86
paraoxysmal nocturnal hemoglobunuria
defiency in complement regulatory genes: cause complement mediated Intravascular lysis and releae of Hgb -anemia, hemoglobinuria, sever fatigue, abdominal paon and thrombosis
87

308 Test 3 (4 decks)

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