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Clin Lab > Blood Cells > Flashcards

Blood Cells Flashcards

1
Q

Hemogram/CBC

A

-RBC count
-hmg
-hct
-indicies: MCV**, MCH, MCHC
-platelet count

-WBC- differential:
-neutrophils
-lymphocytes
-monocytes
-eosinophils
-basophils

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2
Q

anemia

A

-low hmg***
-signs and symp of anemia- fatigue, tachypnea, pale (nails and conjunctiva), tachycardia, hypotension, chest pain (rarely)
-physical compensation- EPO
-production compensation- reticulocytes will increase

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3
Q

RBC

A

-mature RBC in blood

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4
Q

hmg

A

-iron containing protein found in RBC
-carriers of oxygen and CO2

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5
Q

Hct

A

-proportion of RBC %
-low- anemia
-high hct with normal hmg- dehydration
-high hct with high hmg- high altitude, pulmonary disease, polycythemia vera
-indicates dehydration
-direct relationship with hmg
-if you give IV fluids -> lower Hct (%) -> hmg unchanged?
-Hct is approx 3x hmg

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6
Q

indices

A

-MCV*: size or volume of RBC (Hct/RBC count) -> helps to classify types of anemia
-MCV- aka the quality, dense or not dense enough?
-MCH: weight of hemoglobin in the RBC (Hgb/RBC count)

-MCHC: Assesses both the size of the RBC as well as the concentration of hemoglobin (Hgb/Hct)
-MCHC assesses hypochromic (smaller and not dense), normochromic, hyperchromic

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7
Q

types of anemia

A

-normocytic
-microcytic
-macrocytic
-defined by MCV

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8
Q

red cell distribution weight (RDW)

A

-measurement of the range in the volume and size of your RBC
-the precision of the RBC
-when all the RBCs are similar -> RDW is normal
-when some RBCs are small or some large -> RDW is elevated
-“the poor mans reticulocyte count”- if reticulocytes are high RDW is high (new cells measure bigger) -> compensating for anemia
-if someone is anemic and RDW is low -> why arnt they compensating?

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9
Q

reticulocyte count

A

-immature RBC
-normally only 0.5-1.5%
-90-120 days life span of RBC
-the new amount of RBC being made

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10
Q

peripheral blood smear

A

-number, shape, and appearance

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11
Q

serum iron

A

-essential component of hmg
-lack of iron -> cant build hmg
-deficiency- diet, chronic GI bleed

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12
Q

components of RBC

A

-folic acid
-b12
-iron

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13
Q

shilling test

A

-B12 testing
-Radio labeled B12 given orally
-Urine collected 24 hrs, checked for B12 level
-8-40% should be excreted
-If less with dose of intrinsic factor then indicative of pernicious anemia
-B12 deficiency- macrocytic anemia

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14
Q

coomb’s test

A

-used to detect antibodies that act against the surface of yourRBC
-autoimmune destruction of RBCs -> hemolytic anemia
-presence of these antibodies indicates condition -> hemolytic anemia
-hemolytic anemia- blooddoes not contain enoughRBCbecause they are destroyed prematurely
-possible jaundice

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15
Q

anemia diff dx: Proliferation (Can’t produce!)

A

-Anemia of CHRONIC disease
-bone marrow not as active to produce RBC or EPO deficient
-Anemia of Chronic disease- inflammation (Rheumatoid Arthritis, lupus, chronic infections, malignancy) -> low EPO
-Renal disease- Deficient EPO
-Fanconi anemia- Inherited aplastic anemia (bone marrow issue)
-Blackfan-Diamond syndrome -> Inherited bone marrow failure
-Parvovirus- Infection causing aplastic anemia (bone marrow can be suppressed) -> temporary
-Drug or toxins

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16
Q

anemia diff dx: maturation (trouble assembling)

A

-Vitamin B12 deficiency- Perncicous anemia -> poor quality membranes
-Folate deficiency- normo or macro
-Iron deficiency- normo or micro
-Sideroblastic- Iron in the mitochondria has abnormal sequestration (Ringed)
-Lead poisoning- Inhibits heme synthesis & decreased survival of RBC

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17
Q

anemia diff dx: hemolysis (broken down!)

A

-Hemoglobinopathies- spleen kills RBCs due to poor quality RBCs
-Immune hemolytic anemia- autoimmune
-Infectious causes of hemolysis
-Membrane abnormalities
-Metabolic abnormalities
-Mechanical hemolysis- valve replacements
-Drug or toxins
-Wilson disease- Copper in RBC, cell damage -> Kayser-Fleischer rings on eyes

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18
Q

other anemia diff dx

A

-hypersplenism
-hemorrhage (disappearing act!)

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19
Q

microcytic dx

A

-MC_ iron deficiency
-normal reticulocyte:
-Sideroblastic
-Anemia of Chronic Disease
-Thalassemia- common for Mediterranean descent

-high reticulocyte: (body is trying to compensate)
-immune hemolytic
-hereditary spherocytosis- inherited RBC disorder -> loss of biconcave shape, lack central pallor
-membrane or enzyme defects

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20
Q

iron deficiency causes

A

-blood loss- MC
-menorrhagia
-diet low in iron

21
Q

thalassemia

A

-Mutations in gene for globulin chains
-1. Decreased alpha hemoglobin chains = alpha thalassemia
-Present at birth
-typically microcytic
-Range from no symptoms to fatal - depends on if both parents passed it
-2. Decreased beta hemoglobin chains = beta thalassemia
-Produced after fetal hemoglobin is replaced with beta, 3-6 months.
-Range from no symptoms to transfusion dependent

-Target cells and basophilic stippling (small blue dots due to ribosomal clusters)

22
Q

MC normocytic anemia

A

-blood loss
-normal MCV

23
Q

normocytic anemia diagnosis: reticulocyte normal

A

-isolated anemia:
-chronic anemia disease
-Early Iron deficiency
-Early folate or B12 deficiency
-Medication effect

-If others excluded, consider:
-Red blood Cell aplasia
-Myelodysplasia
-Paroxysmal Nocturnal Hemoglobinuria

24
Q

normocytic anemia diagnosis: reticulocyte increased

A

-means no blood loss -> probable hemolysis

-multiple cytopenia:
-myelodysplasia
-bone marrow infiltration
-aplastic anemia

25
Q

macrocytic diagnosis: reticulocyte low

A

-B12
-Folate
-Liver disease
-Hypothyroidism
-Down Syndrome
-Medication effect
-Myelodysplasia
-low B12 + folate -> confirms deficiency

26
Q

macrocytic diagnosis: reticulocyte high

A

-hemolysis
-blood loss
-hypo-regenerative

27
Q

hemolytic anemia: intrinsic

A

-1. hemoglobinopathies- sickle cell or thalassemia
-2. membranopathies- hereditary spherocytosis or hereditary elliptocytosis
-3. enzymopathy: G6PD -> oxidative stress or “Heinz Bodies”

28
Q

hemolytic anemia: extrinsic

A

-Immune Hemolytic
-Microangiopathic Hemolytic- Small blood vessels shearing RBC or Schistocytes
-Malaria
-Blood Transfusion Reaction
-Fetal Rh Compatibility

29
Q

erthrocytosis

A

-Hemoglobin elevated
-Myeloproliferative neoplasm - Polycythemia vera
-Reactive erythrocytosis
-Spurious erythrocytosis- just dehydration

-Secondary polycythemia:
-Smoking
-High altitude
-Lung disease / fibrosis
-Renal Cell Carcinoma (elevated EPO)
-Cerebellar hemangioblastoma (elevated EPO)

30
Q

myeloid vs lymphoid

A

-myeloid stem cell -> RBC or Platelets or grandulocytes
-lymphoid stem cells -> lymphoblast -> B lymphocyte (memory) or T lymphocyte or NKC

31
Q

immature neutrophils

A

-left shift- surge of banded neutrophils (immature neutrophils) -> major infection
-platelets cant be immature

32
Q

differential count: neutrophil

A

-40-70%
-> 70% left shift -> bacterial infection
-Low in bone marrow depression like chemo or radiation
-Low with typhoid, measles & rubella, systemic lupus erythematosus
-High in ACUTE INFECTIONS! Immature bands.
-Left shift (rise in bands during bacterial infection)
-If very low, consider patient on isolation (chemotherapy)- immature neutrophils stop being produced -> low immunity

33
Q

differential count: lymphocytes

A

-20-25%
-Low in heart failure, renal failure and corticosteroid therapy
-High in tuberculosis, syphilis, pertussis, autoimmune disease and ulcerative colitis

34
Q

differential count: monocytes

A

-2-10%
-high in bacterial infections
-can also be high in viral

35
Q

differential count: eosinophils

A

-1-6%
-allergies
-Low values seen in: high stress, trauma, surgery and Cushing’s syndrome (cortisol)
-High in parasitic infections, skin diseases and allergies

36
Q

differential count: basophils

A

-0-2%
-allergic reactions
-Low in hyperthyroidism, pregnancy and ovulation
-Hypersensitive conditions like ulcerative colitis, histamines

37
Q

neoplastic proliferation: lymphoid

A

-B-cell neoplasms (memory):
-Bone marrow to lymph nodes to circulation
-Antibody production

-T & NK cell neoplasms:
-Stem to thymus to circulation
-Cellular immunity

-Hodgkin lymphoma - know diff between hodgkin and non-hodgkin

38
Q

neoplastic proliferation: myeloid neoplasms

A

-acute myeloid leukemia
-myeloproliferative neoplasms

39
Q

platelets

A

-Small fragments from megakaryocyte
-Forms the plug of the clot
-Aspirin can inhibit & hypothermia
-cant be immature

40
Q

bleeding disorders: hemophilia A

A

-Deficiency of factor VIII
-Profuse hemorrhage
-Classic hemophilia
-Increased PTT

41
Q

bleeding disorders: hemophilia B

A

-Christmas Disease
-Deficiency of factor IX
-Increased PTT

42
Q

bleeding disorders: Von Willebrands disease

A

-Decreased von willebrand’s factor
-MC clotting disorder
-Increased bleeding time

43
Q

bleeding disorders: thrombcytopenia

A

-Low platelet count
-Petechiae
-Causes:
-Immune, Drugs (Heparin), post viral, transfusion reaction, sepsis

44
Q

bleeding time

A

-How long to stop bleeding
-Platelet function
-Finger prick, blotted till bleeding stopped and timed
-1-3 minutes

45
Q

clotting time

A

-Time for blood outside body to clot
-Test tube clot formation timed
-8-15 minutes

46
Q

prothrombin time (PT)

A

-PT can vary based on lab -> INR is the normalized calculation for the variability
-PTT never varies
-PT - extrinsic
-efficacy of the extrinsic pathway and the common pathway
-Factors II, V, VII and X
-Significant inter-laboratory variability
-9.5- 13.5 seconds
-Increased in warfarin use, liver disease, Vit K deficiency, disseminated intravascular coagulation, massive blood transfusion, hypothermia
-international normalized ratio (INR): created to offset lab variability -> 1-1.3

47
Q

platelet count

A

-Number in the blood
-150,000- 350,000
-Decreased in some viral infections, drug reactions
-Increased in high altitude, strenuous exercise

48
Q

partial thromboplastin time (PTT)

A

-Efficacy of intrinisc and common pathway!
-Factors I, II, V, VlII, IX, X, XI and XII -> you need to know this
-Normal 60-70 seconds

Clin Lab (14 decks)

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