Krafts- Anemia Flashcards

1
Q

What are the most important causes of IDA?

A

GI Bleed

Menorrhagia in premenopausal women

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2
Q

What are the signs of IDA?

A

Pale, spoon nails, smooth tongue, PICA

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3
Q

What is the morphology of IDA?

A

Hypochromic and microcytic cells

Anisocytosis and Poikilocytosis

Decreased Reticulocytes

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4
Q

What are the labs for IDA?

A

Decreased serum Fe

Increased TIBC

Decreased Ferritin

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5
Q

What are the three types of anemia related to size and what happens in a nut shell?

A

IDA:

Decraesed iron–> decreased Hb–> Decrased RBC prod–> Anemia

Thalessemia:

Genetic defect in Hb–> make less Hb (protein that binds O2 in RBCs)–> fewer RBCS–> Anemia

Megaloblastic Anemia:

Inhibition of DNA–> decreased production of RBC–> Anemia

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6
Q

What is thalessemia?

A

When you have a defect in Hb and you can’t make enough alpha or beta chains

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7
Q

What are the characteristics of Apha Thalassemia?

A

Deletion of alpha genes–> not enough alpha chain and excess/unpaired beta

More common in asians and blacks

Carrier and thal trait: asymptomatic

HbH disease: mod to severe

Hydrops fetalis: fatal in utero

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8
Q

What are the characteristics of beta thalassemia?

A

Defective beta chains–> leads to a decrease in the amt of beta chains in Hb–> excess/unapired alpha chains

Mediterraneans, blacks, asians

Thal minor: asymptomatic

Thal major: variable severity, usually presents in infancy

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9
Q

What is the morphology of Thalessemia?

A

Target cells

Hypochromicc and microcytic

ansiocytosis and poikilocytosis depending on severity

Increased RBC count

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10
Q

What are the characteristics of Megaloblastic Anemia?

A

Defective DNA synthesis

Nuclear/cytoplasmic asynchrony–> HUGE cytoplasms w/ immature nuclei

Deficiency in B12/Folate

Macrocytic anemia w/ oval macrocytes and hypersegmented neutrophils

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11
Q

What are the anemias of abnormal shape?

A
  1. Hereditary Spherocytosis
  2. AIHA
  3. Sickle Cell
  4. G6PD Def
  5. MAHA
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12
Q

What are the characteristics of hereditary spherocytosis including the triad of clinical sxs?

A

Genetic defect in spectrin–> loss of SA–> Spherocyte

Normochromic, normocytic, w/ TONS OF SPHEROCYTES

Splenectomy

Triad: Jaundic, Anemia, Splenomegaly

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13
Q

What is Warm Autoimmune Hemolytic Anemia (WAHA)?

A

For unknown reasons/infection/autoimmune disorder >

Your IgG starts to coat RBCs when it’s WARM >

Macrophages DIGEST or BITE RBC >

Spherocytes or Bite cells (b/c the membrane is compromised) >

Spherocytes get stuck in spleen and are destroyed >

Warm Autoimmune Hemolytic Anemia

warm is GOOD–> IgG

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14
Q

What is cold autoimmune hemolytic anemia?

A

infection or lympoproliferative disease >

IgM and complement coating RBC >

IgM falls off in warm body parts, but in cold forms bridges across RBCs leading to clumbing

Complement- lyses RBCs

>

Hemolysis aggravated by the cold

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15
Q

How do you diagnose both warm and Cold AHA?

A

DAT

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16
Q

What is sicle cell anemia (hemoglobinopathy)?

A

Genetic Defect (more common in blacks)>

Pt mut in beta chain of Hb (V–> G)>

RBC assumes sickle shape>

vaso-occlusion and hemolysis>

Splenectomy>

Nucleated RBC, Target cells, Howell-Jolly Bodies, Pappenheimer bodies

17
Q

What is G6PD Deficiency?

A

*You need G6PD to generate NADPH so that glutathione can remove ROS from cells.

Exposure to oxidants (fava beans, drugs) overwhelms your system>

Can’t reduce ROS >

ROS attacks Hb>

Hb breaks down, globin denatures and sticks to RBC membranes >

HEINZ body>

Spleen bites out Heinz body>

Bite cell

18
Q

What is microangiopathic hemolytic anemia (MAHA)?

A

Micro-angiopathic (Small blood vessels)

Increased coagulation factors in small blood vessels>

RBC getting cut by fribrin>

Physical trauma>

Sphistocytes/Traingulocytes>

Spleen destroys

ANEMIA

19
Q

What are the anemias of normal size and shape?

A

Anemia of blood loss

Anemia of chronic disease

Anemia of renal disease

Anemia of liver disease

Aplastic anemia

20
Q

How does anemia from normal blood loss appear?

A

Trauma–> blood loss at first does not present as anemia because blood still looks normal. After 2-3 days reticulocytes appear indication that new blood is being made.

21
Q

What is anemia of chronic disease?

A

Infection or inflammation (IL-7) causes the overproduction of hepcidin which leads to the increase in Fe storage. An increase in iron storage presents as anemia.

22
Q

How can anemia occur with liver disease?

A

W/ end-stage kidney failure, there is a lack of EPO, leading to malformed RBCs call echinocytes–spiny RBCS.

23
Q

What percentage of pts w/ liver disease have anemia and what do cells look like?

A

3/4 of pts w/ liver disease are anemic

there are multiple causes

Cells are acanthocytes. Pointy spikes off a round cell.

24
Q

What is aplastic anemia?

A

Aplastic = empty

Bone marrow/cells are damaged>

Pancytopenia (reduced number of RBC/WBC produced)>

Blood smear/bone marrow look empty>

Anemia

*idiopathic, drugs, viruses, pregnancy

25
Q

What are the clinical findings related to aplastic anemia?

A

Anemia- pallor dizziness, fatigue

Leukopenia- recurrent infection

Throbocytopenia- bleeding, bruising