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
Q

Hemolysis Anemia:
Hemolitic Anemia

A

TyPes:
**A. Intravascular **
* Mechanical
* Toxic Damage
**B. Extraslalar **
Autoimmune
RBC Detreoy issuce with Spleen and Liver

26
Q

Sicle Cell Disease:
Mutatio of B globulin

A
  • 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
Q

Sickle Cells Trait vs Disease

A

**a. Trait: **
Carry out one copy of HbS
Asymptomatic
b. Disease
HbSS (two copies HbS)
Symptomatic

28
Q

Sickle Cell Crisis Causes

A

Infection
Fever
Dehydration
Excessive Exercies
Changes in temperature
Hypoxia
Anxiety
____________________________

Teach not to excerte themself
Ovoid change tempareture
Avoid Dehydration

29
Q

Sickle Cell S/s

A

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
Q

Sickle Cell TX

A

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
Q

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
*****

A

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

  1. **
32
Q

Sideroblastic Anemia
Management and Contrainticatio

A

**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
Q

Aplastic Anemia
Findings on Bone Marrow associate wtih Aplastic Anemia

A

Fatty Bone Marrow

34
Q

Treatment Options for Aplastic Anemia
Mild
Severe

A

**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
Q

Reason for Thalassemia Fatality

A

High Iron due to Mlt blood transfusion