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Clinical Lab > CBC > Flashcards

CBC Flashcards

1
Q

Hemogram/CBC components

A

RBC
Hemoglobin - number
Hematocrit - percentage of blood containing Hb
Indicies (MCV**, MCH, MCHC)
WBC count -differentials
- Neutrophils
- Lymphocytes
- Monocytes
- Eosinophils
- Basophils
Platelets count

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2
Q

anemia: main DX parameter + signs and sx

A

Main parameter to dx anemia: LOW HEMOGLOBIN **

Signs and symptoms of anemia:
- fatigue
- pale (nails and conjunctiva)
- tachycardia + tachypnea: physical compensation
- hypotension
- chest pain (rarely)

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3
Q

Physical compensation of RBC anemia

A

Tachycardia + increase RR
… Long Term–> Hypertrophy –> Heart needs more O2–> Body doesnt have–> Heart Failure

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4
Q

Production compensation of RBC anemia

A

Kidneys and liver increase EPO release which then increases reticulocytes and RDW

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5
Q

RBC definition

A

-mature RBC in blood

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6
Q

hmg

A

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

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7
Q

Hematocrit (Hct) definition and what causes low/high Hct levels

A

Definition: measures the proportion of RBCs in the blood
- expressed as a percentage or ratio of volume of RBCs relative to total blood volume
- ex: 40% HCT = 40 mL of red blood cells in 100 mL of blood
-Hct is approx 3x hmg
-direct relationship with hmg

Low HCT:
- anemia

High HCT with normal HMG:
- dehydration

High HCT with high HMG:
- high altitude
- pulmonary disease
- polycythemia vera

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8
Q

Effect of IV Fluids on Hematocrit and Hemoglobin

A

Administering intravenous (IV) fluids can lead to a dilution of blood component
- HCT: DECREASES because of increased plasma volume
- Hemoglobin: unchanged

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9
Q

Mean Corpuscular hemoglobin concentration(MCHC):

A
  • Assesses the CONCENTRATION of hemoglobin + size (? - idk her slides says it does)
  • indicates how dense the hemoglobin is within RBCs: COLOR
  • Hb/Hct
  • Hypochromic: pale color bc not dense
  • normochromic
  • hyperchromic: very dense

Think using watercolor paint: more concentrated = higher pigment/color

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10
Q

Mean Corpuscular Hemoglobin(MCH):

A
  • WEIGHT of hemoglobin in the RBC
    -Hgb/RBC count
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11
Q

Mean Corpuscular Volume (MCV)

A

aka the QUALITY of RBCs, dense or not dense enough?
- Hct/RBC
- checks the SIZE or VOLUME of RBC
- helps to classify TYPES of anemia

Low MCV: microcytic
Normal MCV: normocytic
High MCV: macrocytic

“the only one that doesnt have Hb in the name -> numerator is HCT”

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12
Q

types of anemia + which parameter

A

-normocytic
-microcytic
-macrocytic
-defined by MCV

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13
Q

red cell distribution weight (RDW)

A

Measurement of the RANGE in the volume and size of your RBC
- aka: 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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14
Q

reticulocyte count + reticulocyte index

A

reticulocyte count = # of immatures RBC
-normally only 0.5-1.5%
-90-120 days life span of RBC
-high reticulocyte count: indicates effective bone marrow response to anemia
- low reticulocyte count: indicates inadequate production of RBCs

Reticulocyte index: corrected count that takes into account degree of anemia + reticulocyte lifespan
Less than 2%: decreased production problem
Greater than 2%: increased destruction or blood loss
- bleeding
-hemolysis

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15
Q

peripheral blood smear

A

-number, shape, and appearance
- sickle cell: look at peripheral blood smear

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16
Q

serum iron + components of RBC

A

-essential component of hemoglobin
-lack of iron -> cant build hemoglobin

components of RBC:
-folic acid
-b12
-iron

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17
Q

shilling test

A

B12 deficiency testing*
-Radio labeled B12 given orally
-Urine collected 24 hrs, checked for B12 level
-normal: 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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18
Q

coomb’s test

A

-used to detect ANTIBODIES that act AGAINST the surface of your RBC
-autoimmune destruction of RBCs -> hemolytic anemia
-presence of these ANTIBODIES = immune
hemolytic anemia

immune hemolytic anemia:
- blood does not contain enough RBC because they are destroyed prematurely
- presence of antibodies
-possible jaundice

“Honey COOMBs = yellow = jaundice”

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19
Q

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

A

1) Anemia of CHRONIC disease: chronic inflammation ds
- Rheumatoid Arthritis
- lupus
- chronic infections
- malignancy
-bone marrow not as active to produce RBC or EPO deficient

2) Renal disease- Deficient EPO

3) Aplastic anemia: insuffient bone marrow
- Fanconi anemia: Inherited aplastic anemia
- Blackfan-Diamond syndrome: Inherited bone marrow failure
- Parvovirus infection causing aplastic anemia (bone marrow can be suppressed) -> temporary

4) Drug or toxins

“PRO-LIFE” - “CLIMB FDR Paranoia”
- Prolife: proliferation
- Chronic diseases
- Lupus/ rheumatoid arthritis (autoimmune)
- Infections (chronic)
- malignancy
- Blackfan-Diamond syndrome
- Fanconi anemia
- Drugs/Toxins
- Renal disease
- Parvovirus infection

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20
Q

anemia diff dx: maturation (trouble assembling)

A

Vitamin deficiencies:
- Vitamin B12 deficiency: Pernicious anemia
- Folate deficiency- normo or macro
- Iron deficiency- normo or micro

Sideroblastic:
- Iron in the mitochondria has abnormal sequestration
-ringed sideroblasts

Lead poisoning
- Inhibited heme synthesis
- decreased survival of RBC

“if you Mature = LIFe SaVe -> as you mature you get older and your life is save+ have a better diet - vitamins, iron, folate”
-Maturation anemia ddx
-Lead poisoining
-Iron deficiency
-Folate deficiency
-Sideroblastic
-Vitamin B12 deficiency

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21
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

“3 Ms 2Is DW H” -> Don’t Worry be Happy -> think dont break down (hemolysis) -> be happy! (reach lol)
- Metabolic abnormalities
- Membrane abnormalities
- Mechanical hemolysis: valves
- Immune hemolytic anemia
- Infectious causes
-Drugs
- Wilson
- Hemoglobinopathies

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22
Q

anemia diff dx: hemorrhage (disappearing act!)

A

-hypersplenism: overactive spleen -> excess destruction of RBCs
-acute/chronic hemorrhages: bleeding

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23
Q

microcytic dx

A

Microcytic: MCV < 80 fL
-MC: iron deficiency ***

Normal reticulocyte:
- iron deficiency ***
-Sideroblastic
-Anemia of Chronic Disease
-Thalassemia

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

“In Small Anemias, Cells Tire + High HIME”
- Iron deficiency
- Sideroblastic
- microcystic anemias: normal reticulocytes
- Chronic diseases
- Thalassemia

High HIME: high reticulocyte
- Hereditary spherocytosis
- immune hemolytic
- membrane defect
- enzyme defect

Think of the cells tiring because of their high hime (princess) -> cells at work vibes

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24
Q

iron deficiency causes

A

-blood loss- MC
-menorrhagia: heavy menstrual bleeding
-diet low in iron

25
Q

thalassemia

A

inherited blood disorder: mutations in gene for GLOBULIN CHAINS
- typically microcytic presentation
- cause abnormal RBC morphology which causes destruction of RBCS -> anemia
- category: hemolytic anemia - intrinsic hemoglobinopathies

Alpha thalassemia:
- decreased production of alpha globin chains
-Present at birth
-typically microcytic
-Range from no symptoms to fatal - depends on if both parents passed it

Beta thalassemia:
- Decreased beta hemoglobin chains
-Produced after fetal hemoglobin is replaced with adult hb (contains beta chains), 3-6 months
-Range from no symptoms to transfusion dependent
-blood cell appearance: target cells and basophilic stippling (small blue dots due to ribosomal clusters)

26
Q

Increased reticulocytes:

A
  • suggests bone marrow is responding to anemia and releasing more immature RBCs (reticulocytes)
  • hemolysis usually always in INCREASED RETICULOCYTE counts
27
Q

MC normocytic anemia

A

-blood loss
-normal MCV

28
Q

normocytic anemia ddx: reticulocyte normal

A
  • acute bleeding/blood loss
    -chronic anemia disease
    -Early Iron deficiency
    -Early folate or B12 deficiency
    -Medication effect

If others excluded, consider:
-Red blood Cell aplasia: bone marrow fails to make enough RBCs
-Myelodysplasia: bone marrow ds
-Paroxysmal Nocturnal Hemoglobinuria: rare

“Normal + normal reticulocytes: do the ABC-MED” -> if its not normal we need to “RAMP” it up

ABC-MED:
- acute bleeding
- B12
- Chronic ds
- Medication effects
- Early folate, B12, iron deficiency
- Diet: think vitamins - b12, iron, folate

RAMP:
-Red blood cell Aplasia
- myelodysplasia
- paroxymal nocturnal hemoglobinuria

29
Q

normocytic anemia dx: multiple cytopenias

A

Condition where there is reduction in the number of 2+ types of blood cells: RBCs, WBCs, platelets and cause lead to anemia

Types of multiple cytopenias:
- myelodysplasia: bone marrow disorders
- bone marrow inflitration: cancer cells invade bone marrow and disrupt function
- aplastic anemia: bone marrow fails to produce enough of all 3 types of blood cells

Multiple cytopenias: tournament with more than one type of blood cell affected -> think sports -> “MBA”
-Myelodysplasia
- bone marrow inflitrates
- Aplastic anemias

30
Q

normocytic anemia diagnosis: reticulocyte increased

A

PROBABLE hemolysis
- means no blood loss

31
Q

macrocytic diagnosis: reticulocyte low

A

-B12 deficiency **
- Folate deficiency **
-Liver disease
-Hypothyroidism
-Down Syndrome
-Medication effect
- after r/o all other things: probable myelodysplasia

Low B12 + folate -> confirms deficiency

“My FaT BoLD MarshmalLOW” -> fat think macrocytic size
- Medication effects
- Folate deficiency
- a
- Thyroid (hypothyroidism)
- B12 deficiency
- o
- Liver ds
- Down syndrome
- Myelodysplasia
- LOW reticulocytes

32
Q

macrocytic diagnosis: reticulocyte high

A

-hemolysis
-blood loss
- partially treated hypo-regenerative macrocystic anemia

“High HP can have Blood Loss and still be ok”
-High reticulocyte count
- hemolysis
- partially treated hypo-regenerative anemia (PTHRA)
- blood loss

33
Q

hemolytic anemia: intrinsic

A

Intrinsic - body is breaking it down due to the construction of RBCs

Intrinsic = “MEH”
Membranopathies:
- hereditary spherocytosis
- hereditary elliptocytosis

Enzymopathy:
- G6PD deficiency: RBCs cannot absorb oxidative stress and form “Heinz Bodies”
- Heinz bodies = denatured Hb from oxidative damage

Hemoglobinopathies
- sickle cell
- thalassemia
- Hemoglobinopathies = structural defect in Hb

34
Q

hemolytic anemia: extrinsic

A

Extrinsic - something outside of the RBC acting on it

Microangiopathic Hemolytic:
- create environment to mechanically shear RBCs
- peripheral blood film: schistocyte appearance
Blood Transfusion Reaction
Immune Hemolytic
Malaria

Fetal Rh Compatibility

“My Ex BIt Fetal Malaria” -> biting something -> causes bleeding/oozing -> extrinsic hemolytic anemia causes

-My: Microangiopathic hemolytic
- Extrinsic hemolytic anemia
- Blood transfusion reaction
- Immune
- Transfusion reaction
- Fetal Rh compatibility
- Malaria

35
Q

erthrocytosis

A

Definition: Hemoglobin elevated, TOO MANY RBCs

Causes:
-Myeloproliferative neoplasm: Polycythemia vera - chronic overproduction of RBCs
-Reactive erythrocytosis
-Spurious erythrocytosis: just dehydration
- Secondary polycythemia: factors external to bone marrow stimulate RBC production
-Smoking
-High altitude
-Lung disease / fibrosis
-Renal Cell Carcinoma (elevated EPO)
-Cerebellar hemangioblastoma (elevated EPO)

“My RESPECTS High”
-Myeloproliferative neoplasm: Polycythemia vera
- Reactive erythrocytosis
- EPO: renal cell carcinoma and cerebellar hemangioblast
- Spurious erythrocytosis
- Pulmonary diseases/fibrosis
- Elevation: high altitude
- Cigarette smoking
- Thirst
- Secondary Polycythemia
- High: erthrocytosis = High Hemoglobin

36
Q

myeloid vs lymphoid

A

Myeloid stem cell:
- RBC
- Platelets
- granulocytes (eosinophils, basophils, neutrophils)

Lymphoid stem cells: lymphoblasts
-B lymphocyte
- T lymphocyte
- natural killer cells

37
Q

differential count: neutrophil

A

Normal WBC count: 40-70%

Low Neutrophils:
-bone marrow depression: chemo or radiation
-Typhoid
- measles & rubella
- systemic lupus erythematosus
-If VERY low: consider patient on isolation (chemotherapy)- immature neutrophils stop being produced -> low immunity

High Neutrophils: ACUTE INFECTIONS -
- neutrophils will have immature bands
-> 70%: left shift -> bacterial infection + rise in banded neutrophils during bacterial infection)

“CRIB MeLT -> NEUTROPHILS”
- Chemo
- Radiation
- Isolation
- Bone marrow depression
- Measles
- Lupus: systemic lupus erythematosus
-Typhoid

38
Q

differential count: lymphocytes

A

Normal: 20-25%

Low:
- heart failure
- renal failure
- corticosteroid therapy

High: “PAST - U”
- Pertussis
- Autoimmune disease
- Syphilis
- Tuberculosis
- Ulcerative colitis

lymphocytes: think high adaptive/memory immunity vs compromised immunity situations

“PAST U” -> Memory (the past) + Lymphocytes

39
Q

differential count: monocytes

A

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

40
Q

differential count: eosinophils

A

Normal: 1-6%

Low values seen in:
- high stress
- trauma
- surgery
- Cushing’s syndrome (cortisol)

High:
- allergies
- parasitic infections
- skin diseases

“HTCS - eosinophils got their Head in The Clouds when they’re low”

41
Q

differential count: basophils

A

Normal: 0-2%

Low:
- hyperthyroidism
- pregnancy
- ovulation

High: Hypersensitive conditions
- ulcerative colitis
- histamines (allergic REACTIONS)

“Think fat and oversensitive basophils”
fat:
- pregnant/ovulation
- hyperthyroidism (enlarged thyroid)

oversensitive:
- UC: super sensitive stomach
- too much histamines: hyperreactive allergic rxn

42
Q

neoplastic proliferation: lymphoid

A

B-cell neoplasms (memory):
-Bone marrow to lymph nodes to circulation
- B cells = antibody production

T & NK cell neoplasms:
-Stem to thymus to circulation
- T cells + NK = cellular immunity

Hodgkin lymphoma
- know diff between hodgkin and non-hodgkin
-Hodgkin lymphoma is distinguished from non-Hodgkin lymphoma by Reed–Sternberg cells

43
Q

neoplastic proliferation: myeloid neoplasms

A

-acute myeloid leukemia
-myeloproliferative neoplasms

44
Q

platelets

A

-Small fragments from megakaryocyte
-Forms the plug of the clot
-cannot be immature

what inhibits platelets:
- aspirin
- hypothermia

45
Q

Coagulation Cascade: Intrinsic Pathway

A

involves factors: XII, XI, IX, VIII -> 12, 11, 9, 8

1) factor XII is exposed to collagen, kallikrein, and high molecular weight kininogen (HMWK) and become activated to XIIa
2) XIIa activates XI
3) XIa activates IX
4) IXa binds with VIIIa (activated by thrombin) and activates X
5) Xa joins common pathway

46
Q

Coagulation Cascade: Extrinsic Pathway

A

1) injury to skin tissue/endothelial tissue exposing tissue factor (factor III) to the blood
2) Tissue factor (III) then becomes bound with calcium and factor VIIa to activate factor X
- Factor VII is present in the blood
- factor Xa is part of common pathway

involves: III, VII -> 3, 7

47
Q

Coagulation Cascade: Common Pathway

A

factors: X, V, II, I, XIII -> 1, 2, 5, 8, 10

1) Xa, Va, and calcium bind together and activate II
2) IIa activates factor I to Ia
3) thrombin cleaves factor XIII into XIIIa
4) Factor XIIIa binds Ia with calcium to make stable fibrin clot

48
Q

Coagulation cascade: what factors in each pathway

A

Intrinsic: 12, 11, 9, 8
- factor 9: christmas tree factor/hemophilia B
- factor 8: hemophilia A

Extrinsic: 3, 7
- factor III: tissue factor

Common: 10, 5, 2, 1, 13
- factor I: fibrinogen
- factor II: prothrombin
-factor XIII: fibrin stabilizing factor

49
Q

bleeding disorders: hemophilia A

A

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

50
Q

bleeding disorders: hemophilia B

A

-Christmas Disease
-Deficiency of factor IX
-Increased PTT

51
Q

bleeding disorders: Von Willebrands disease

A

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

von willebrand’s factor: plasma protein involved with platelet adhesion

52
Q

bleeding disorders: thrombcytopenia

A

-Low platelet count
-sx: petechiae - small red dots on skin

Causes:
- Post viral infections
- Immune
- Transfusion reaction
- Anticoagulants: Heparin
- Sepsis

Thrombocytopenias = PITAS -> pita bread kinda rhymes

53
Q

Anticoagulants and what factor they impact

A

Warfarin: VII, XI, X (intrinsic + extrinsic)
Apixaban, rivaroxaban: Xa
Dabigatran: IIa
Heparin: Xa, IIa

54
Q

bleeding time

A

-How long to stop bleeding
-tests platelet function
-Finger prick, blotted till bleeding stopped and timed
-normal: 1-3 min

55
Q

clotting time

A

-Time for blood outside body to clot
-Test tube clot formation timed
-normal: 8-15 min

56
Q

prothrombin time (PT) + INR

A

PT: checks efficacy of EXTRINSIC pathway and common pathway
-Factors II, V, VII and X
-Significant inter-laboratory variability
- PT can vary based on lab -> INR is the normalized calculation for the variability
-PTT never varies

International normalized ratio (INR):
- created to offset lab variability
- normal: 1-1.3
- order with pt

57
Q

What causes PT to increase?

A

-warfarin use
-Vit K deficiency
- liver disease
- disseminated intravascular coagulation
- massive blood transfusion
- hypothermia

58
Q

platelet count + when is it decreased/increased

A

-Number in the blood

Decreased in:
- viral infections
- drug reactions

Increased in:
- high altitude
- strenuous exercise

59
Q

partial thromboplastin time (PTT)

A

-Efficacy of intrinsic and common pathway!
-Factors I, II, V, VlII, IX, X, XI and XII -> you need to know this
- common: 1, 2, 5, 10, 13
-intrinsic: 12, 11, 9, 8

Clinical Lab (17 decks)

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