Nu 735Anemia Flashcards

1
Q

Hematopoisis

A

On going formation blood cells

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2
Q

Erythropoises (EPO)

A

lHormone regulate RBC
Linked to O2
Produced in Kidney
Apoptosis> Abcess of EPO leading to cel death

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3
Q

Iron, B12, Folate (B9)

A

Iron > “fuel hormone”
Erythroblast require productio of : B12 and Folate B9
Erythropoiesis.> Deficiensy in B12 and Folate

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4
Q

RBC

A

Hgb: blood’s O2 carrying capacity
Hct: volume of RBC to whole blood
MCV: Size RBC
MCH: amount of Hgb in RBC
MPV: average of plt
Reticulocyte Count: **immature **RBC > measure production and rease RBV

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5
Q

Mean Corpuscular Volume (MCV) =
Determine Size RBC

A

MCV< 80 : micro
a. Iron Deficiensy Anemia ( Not enough Iron to make Hgb leading fewer RBC formed

MCV: 80 to 100 = Normocytic

MCV>100 macrocytic
a. Folate / B9 deficiecy
B12 deficiency

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6
Q

Reticulocyte Count

A
  • “Immature RBC”
    Measures Production of RBC by bone marrow and
  • Elevated RC = Hemolysis (Hemolytic Anemia, Acute Blood loss; Vitamin B12 B9 defifiensy)
    *** Low RC **> Erythropoiesis > 2/2 bone marrow due to reduction erythroblast .
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7
Q

Lactate Dehydrogenase (LDH)

A

Ensyme Found in all body tissues
Catalyzes to pyruvate (production of glycolysis )
Elevated Hemolitic Anemia b/c it’s floating around

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8
Q

Haptoglobin

A

Plasma protenin produce in Liver
Clear free RBC
Low : Hemoliti Anemia

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9
Q

Hemolitic Anemia Labs

A

LDH = High
Haptoglobin = low
Reticolyte count = Hight

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10
Q

Ferritin and Fe +

A

Ferrtin is protein that contains iron
**Primary stored iron **
Fe require for cell groth
Low Iron leading to Toxicity and Death

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11
Q

Transferrin, TIBC % Saturation

A

Measure capacity to transfer Iron

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12
Q

Reticular Counnt deficiensy
Hypo- Proliferative Anemia

A

**Key Points: **
* 75 % of all cases has
* Low Reticulocytes with **normal **RBC Morphology
* Reticulocyte production index <2

*** Causes: **
* Mild to mod Fe deficiency
* Marrow damage
* Inadeuate EPO production
* Impaired O2 d/t metabolic Diseases

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13
Q

Maturation Anemia
Reticular Count Formation

A

Low Reticular Count +
Both Macrocytic /Microcytic Anemia

RC normal index <2

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14
Q

Types of Anemia

A
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15
Q

Iron Def Anemia
TX Plan

A
  • Fe Sul 300 to 325 mg po TID
    Duration : 3month
    Improve around 2 month
    Increased storage in around 6 month
    Considratiion: **
    Take on empty stomach
    Avoid antacids or milk
    Add Vit C (increase absorption)

Venofer
Indication: GI intolernce or malabsortion
Duratio 5 days

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16
Q

Iron Deficiensy **

**Iron Deficiency Anemia :
Most common cause of Anemia

  • Bleedding
  • Nutrition Defficit **
    *
A
  • Diagnosis:
    MCV <80 > micrositic
    MCH low > Hyochromic
  • **Pathophysiology: ***
    Fe + loss > storage
  • Etiology:
    Chronic blood loss
    Indadequate Fe intake
    Impair absorption

*** S/s : **
Smooth tonque
Brittle or spoon nails aka koilonychia
PICA aka ice chewing, unusual cravings for food (consider malabsorption )

Lab
Low Hgb, Hct, RBC
Low MCV, MCHC
Low Ferritin/Iron
**High TIBC **
% transfering saturation

****Common patient charateristics : **
Infant, Pregnant, Female, or Elderly

Next Step”
Search for underlying cause (source of
bleeding,
nutrition deficiency

  • **Population **
    Infant
    Pregnant
    Female
    Elderly
17
Q

Vitamin B12 Deficiency

A
  • Dx
    High MCV > Macrocytic
  • Pathophysiology
    a. B12+Intrinsic factor (glycoprotein) made from stomach lining
    Asorpotion: absorption occur ilium (last part of small intestine just last part of large intestine )
    b. B12 require for RBC division > RBC enlarged > macrocytic
    c. RBC not able to leave marrow > Anemia
18
Q

B12 Etiology

A
  • Vegan Diet : lack of B12
  • **Pernicious Anemia : Auto-immune destroy Intrinsic Factor **
  • Post-Gastrectomy: Mechanical loos of stomach lining
  • **Ileal Resection: Celiac Diseas (insrisit factor ) (deodenum and jejunum) **
  • Sevre chronic Pancreitis
  • Alcoholism
  • Crohn’s Disease
19
Q

B12 S/s

A

a. ** Neurologic**
B12 require for myelination CNC
> Paresthesia: tingling
> Memory Loss:

**b. Increase Homocystine **
Increase riskCVD
c. Glossitis : Inflemation of tonque
**d. GI :

20
Q

Supplemental ?

A

Pernicious Anemia
Auto-immune destroys intrinsic factor
* **Check Homocysteine: **
Hight level can lead to CVP
Intrinsic Factor (IF):
Type I : blocks combining IF and B12
Type II: Prevent attachment fo IF to Ilium
**Absorption of B12: **
in illium : last part of small intestine befor large int

21
Q

B12 TX

A

**Permicious Anemia :
Life long B12

**Anemia due to poor absorption:
**vit B12 1000mg SQ IMQD
For 7 days; then
weekly for 4 wks
Montly maintance **

22
Q

**Anemia or Chronic Disease: **

Second most common after Iron Deficiensy

Dx: **
Mild to Moderate microcytic or Normacytic
Pathyphysiology:
Decrease Erthrocytes lifespan

A

**Dx: **
Mild to Moderate microcytic or Normacytic
Pathyphysiology:
Decrease Erthrocytes lifespan

Etiology
Inlflamation, Organ Failure, Advanced age, Malignancy, Cirrhosis
**Lab and Dianositic
**Microcytic/Normacitic
** Ferritin : normal to high
* Iron: High
*TIBC : Low
% Tranfering : HigH
* RBW: Normal
* Iflammatory Markers: ESR and CRP

**Treatmen: **
Manage underlying Pathology
**Erythropoietin (procrit): ** Indication Hgb <10 + anemia
Transfusion
Consult HemOnc + GI
*
**Common Patient : **
Treat underlying contidtion;
Consider Erythropoesis

23
Q

Blood Loss/Hemolysis Anemia

A

**Pathophysiology: **
Increased RBC destructio

**Labs: **
Reticulocyte >2.5

**Hemolysis:
**Destruction RBC Increased
Elevation reticular Count >300%

Hemorrhagic
Less retic production 2/2 limited Fe +

24
Q

Blood Loss/Hemolysis Anemia: Causes

A

a. Hemorrhage

**b. Hemoglobinopathy: **

  • Sickle Cell (Intravascular +Extravascular)
  • Thalassemia
  • **c. Hemolytic **
    Intravascular (Mechanical and toxic damage
    Extavascular (RBC are destroyed: Spleen , liver)
25
Hemolysis Anemia: Hemolitic Anemia
TyPes: **A. Intravascular ** * Mechanical * Toxic Damage **B. Extraslalar ** Autoimmune RBC Detreoy issuce with Spleen and Liver
26
Sicle Cell Disease: Mutatio of B globulin
* Pathophysiology: a. **Mutation of beta globin (changes the 6th amino acid ) Hemoglobin S b. HbS Polymerizes reversibly leading to i. ** Stiffen** RBC membrane ii Increases** viscosity** 1) Potassium leakage 2) Calcium leakage III Dehydration
27
Sickle Cells Trait vs Disease
**a. Trait: ** Carry out one copy of HbS Asymptomatic **b. Disease** HbSS (two copies HbS) Symptomatic
28
Sickle Cell Crisis Causes
Infection Fever Dehydration Excessive Exercies Changes in temperature Hypoxia Anxiety ____________________________ Teach not to excerte themself Ovoid change tempareture Avoid Dehydration
29
Sickle Cell S/s
A. **Hallmark sigh** * Acute pain * Low Hgb * Elevated Retic * b. Agrenulocytosis: ( type of production of WBC drops leading to infection * Tissue Ischemia * End organ Damage * **Slenic Sequenstration: ** ii. Spleen accumulates (splenogemgaly) +destroyes RBCs rapidly leading to relatively Anemia Leading to **Hemolytic Crisis **Acute Chest Syndrome**: 2/2 concomitant PNA+ PE (high mortaliity) i. Chest pain, Tachypnea, fever, cough II. Pulmonary Crises > Pulmonary HTN > Co Pulmonary III Increased mortality
30
Sickle Cell TX
**Hydroxyurea** 10 to 30mg/kg/day (mainstay) Titrate to wBC of 5 to 8,000 Antihistamin(Zyrtec) NOT Benadryl NSAIDs **Supportive: ** Hydration Pain Supplemental oxygen
31
**Thalassemia's** Micrositic Anemia 1**.Background: ** a. Typically dianosed is childhood *****Test: ******************** b. Lve expectancy arount 30 yrs secondary to Due to Toxic Iron due to excessive Blood Transfusion*******************
1**.Background: ** a. Typically dianosed is childhood b. Lve expectancy arount 30 yrs secondary to excessive Iron 2**.Pathology** a. Genetic b. Alpha and beta globolin biosynthesis > diminished Hgb teramer production 3. Epidemiology: mediterranean, Asia (alpha), Africa (beta), Medle east **3.Labs** Microcytic Hypochromic Hgb Elecrophoresis (electrocutes Hgb) > elevated globin wiht exception to alpha thalassemia train S/s : Hematosphlenogegly Chipmunk face Long bone vertebral fx 4. **
32
Sideroblastic Anemia Management and Contrainticatio
**Managment: ** * Removal of toxic agents * * Pyridoxine (Vit B 6) * Thiamin (B1) and or Folic Acid (B9) * Transfusion i. Monitor Fe leve ****Contraintication** Splenectomy Thromolica Contraindication congenital Blastic Anemia those for anexplained Anemia
33
Aplastic Anemia Findings on Bone Marrow associate wtih Aplastic Anemia
Fatty Bone Marrow
34
Treatment Options for Aplastic Anemia Mild Severe
**Mild Aplastic ** i. Trasfusions ii. Removing offendign expore *** Severe Aplastic Anemia ** i. Hematopoietic stem cell trasplant (cure) 1) Lab: human leukocyte antigen (HLA Typing) 2) Best Option: fully histocompatiblity sibling donor II. Remove offendig exposure III Consult: HemOnc IV Immunosupression therapy Antithymocyte globulin (ATG ) + cyclosporine
35
Reason for Thalassemia Fatality
High Iron due to Mlt blood transfusion