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308 Test 3 > Hematological > Flashcards

Hematological Flashcards

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
Q

Hypochromic-microcytic

CAUSES:

A
  • 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)
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26
Q

Hypochromic-Microcytic

manifestations

A

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

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27
Q

what do you evaluate in iron-deficiency anemia?

A

serum ferritin

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28
Q

Treatment of Iron-Defiency anemia

A

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

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29
Q

Iron Deficiency Anemia

A
  • 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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30
Q

50-55% of blood volume

Organic and inorganic elements

A
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31
Q

Leukemia is:

Uncontrolled proliferation of malignant leukocytes and results in

A
  • overcrowding of bone marrow
  • decreased production and function of normal hematopoietic cells:
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32
Q

Clssification of Leukemia

A

Predominant cell of origin: Myeloid or Lymphoid

rate of progression: acute or chronic

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33
Q

Acute Leukemia

A

Presence of undifferentiated or immature cells (usually blast cells)

-rapid onset with narrow window in which to treat

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34
Q

Chronic Leukemia

A

Predominant cell is mature but does not function normally

-slow progression

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35
Q

Acute lymphocytic Leukemia

A
  • 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
Q

Cause of ALL

Acute Lymphocytic Leukemia

A

Unclear cause

genetic susceptibility

environmental factors

viral infections

37
Q

Clinical Manifestations of ALL

A

Pallor

fatigue

petechiae

purpura

bleeding

fever (hypermetabolism and infections)

bone pain

38
Q

Test for ALL

A

Bone marrow aspirtion for BLAST cells

39
Q

Treatment of ALL

A

Combinatoin chemotherapy

-radiation

4 phases (induction of remision; preventative therapy for the central nervous system; intensification (consolidation) and maintenance

40
Q

Acute Myelogenous leukemia (AML)

A

Most common adult leukemia (mean is 67)

-down syndrom increases the risk

-

41
Q

Acute Myelogenous Leukemia

A

abnormal proliferation of myeloid precursor cells-

  • decreased rate pf apoptosis
  • arrest in cellular differentatin
  • Mutation in receptor tyrosine kinase FLT3
42
Q

Risk factors for AML

A

Exposure to radiation, benzene and chemotherapy

-hereditary conditions

43
Q

Chronic Myelonegous Leukemia

A

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
Q

CLL

A

common is adults older than 50 (70% are asymptomatic at dg)

  • affects monoclonal B lymphocytes
  • has a familial tendency
45
Q

Manifestations of CLL

Chronic Lymphocytic Leukemia

A

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
Q

Testing:

A

bone marrow

peripheral blood smear

47
Q

RAPID

CHILDREN

SURVIVAL RATE:91%

PRIMARY CELL: GREATER THAN 3% LYMPHOBLAST AND B CELLS

A

rAPID ONSET

MOST COMMON IN CHILDREN

SURVICAL RATE 91%

LYMHOCYTES AND b CELLS

48
Q

progression is slow

adults

survival rate 85%

monoclonal B is primary cell

A

slow

mostly adults

85% survival

monoclonal B cell

49
Q

AML

RAPID

Most common ADULT FORM

survival rate 24%

precursor myeloid cells

A

Progression/onset rapid

most common adult form

24% survical

precursor meyloid cells

50
Q

CML

Slow onset

Mostly is adults

NO CURE

neutrophilic or eosinophilic or clonal

arise from hematopoietic stem cell

A

chronic old people

slow

adults

no cure

neutrophilic, eosinophilic, clonal

arise from hematopoitic stem cell

51
Q

Vaso occlusive crisis (thrombotic crisis)

A

Sickling s in Microcirculation, extremely painful and symmetric

-hands and feet exhibit painful swelling (hand-foor syndrome)

52
Q

Neutropenia: reduction in circulating neutrophils

A

Primary or secondary

53
Q

Primary Neutropenia

A

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
Q

Causes of Neutropenia

A

Prolonged Infection

  • decreased production
  • reduced neutrophil survival
  • abnormal neutrophil distribution and sequestration
55
Q

Severe Neutropenia

A

less than 500/microliter

56
Q

Granulocytopenia

AKA: Agranulocytosis

Causes

A

Interference with hematopoiesis

immune mechanisms

chemotherapy destruction

ionizing radiation

SEPSIS caused by agranulocytosis usually results in death within 3-6 days

57
Q

Eosinophila

A

-elevated eosinophil count

hypersensitivity reactions trigger the release of eosinophilic chemotactic factor of anaphylaxix from mast cells

58
Q

Causes of eosinophilia

A

allergic disorders

parasitic invasions

59
Q

Eosinopenia

A

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
Q

Iron cycle:

Ferrtitn

transferrin

A

Ferritin: major intracellular iron storage protein-

-precursor to ferritin is apoferritin (ferritin without iron)

TRANSFERRIN:

-transfers iron in circulation

precursor is apototransferrin

61
Q

Hematocrit or PCV: %%

A

percentange of RBC’s in total blood volume: approximately 3XHgb

62
Q

Normal range for Hct

A

40-52% men

35-47% women

63
Q

HgB

A

total amount of HgBin the blood

more accurately reflects the changes in plasma volume

64
Q

Range for HgB

A
  1. 5-6.0 (men)
  2. 8-5.2 (women)
65
Q

MCV

A

Volume or SIZE of single RBC

Normal Range:

80-100 fl

66
Q

MCH

A

Total amount of HgB in a RBC

Range: 26-34 pg

67
Q

MCHC

A

Average concentration or %percentage of HgB in a single RBC

Normal Range: 32-36%

68
Q

RDW

A

estimate of RBC size

normal Range: 12-13.5%

69
Q

Retic

A

Immature RBC, reflects bone marrow Fx

Normal Range 0.5-2.0%

70
Q

Retic Index

A

RI=retic count x (hct/45) c (1/1.85)

Normal range:

<2% hypoproliferative anemia

>3 increase RBC production

71
Q

Nutritional Requirements for Erythropoiess (with IF)

A

Proteins

Vitamins

Minerals

72
Q

Proteins (amino Acids)

for erythropoieses

A

Proteins (amino acids)

-structural supports

synthesis of hemoglobin

73
Q

vitamins

in erythropoiesis

A

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
Q

Minerals in erythropoiesis

A

Iron: hemoglobin synthesis

Copper: required for moblization of iron from tissues to plasma

75
Q

Idiopathic thrombocytopenic purpura

A

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
Q

Manifestations

A

petechiae and purpura, progressing to a major hemorrhage

77
Q

Acute, self-limiting infection of B lumphocytes transmitted by saliva through personal contact

A

Commonly called EBV (epstein-barr virus): 85%

78
Q

Other viral agents resembling IM

A

CMV

hapatitis

influenza

HIV

79
Q

Hodgkins Lymphoma

A

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
Q

Sideroblastic anemia

A

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
Q

Sideroblastic anemia

clinicical manifestations

Hypochromic microcytic anemias

A

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
Q

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

A
83
Q

Aplastic anemia

A

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
Q

Posthemorrhagic anemia:

Acute blood loss from the vascular space

A

clinical manifestations depends on severity of blood loss

tx: IV of saline, dextran, albumin or plasma large volume:fresh whole blood

85
Q

hemolytic

A

accelerated destruction on RBC’s

congenital vs acquired

intravascular vs extravascular hemolysis

86
Q

paraoxysmal nocturnal hemoglobunuria

A

defiency in complement regulatory genes: cause complement mediated Intravascular lysis and releae of Hgb

-anemia, hemoglobinuria, sever fatigue, abdominal paon and thrombosis

87
Q
A

308 Test 3 (4 decks)

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