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DMD 5247 > Bikman - Anemia > Flashcards

Bikman - Anemia Flashcards

1
Q

What are the two main components of complete blood count (CBC)? Why?

A
  1. Hemoglobin
    - More red when oxygenated means more hemoglobin
  2. Hematocrit
    - How much of what’s in the tube is made of RBCs
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2
Q

What is the most common anemia worldwide?

A

Iron-deficiency

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3
Q

Anisocytosis

A

Size variation

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4
Q

Poikilocytosis

A

Shape variation

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5
Q

What is anemia?

A

A reduction below normal in Hb or RBC #.

Symptoms:

  • Pale skin
  • Mucus membranes
  • Jaundice (if hemolytic)
  • Breathlessness
  • Tachycardia
  • Dizziness
  • Fatigue

Not enough of RBCs or Hb or not enough vitamin B12 (aids in cell formation) or if it’s not moving around as it should

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6
Q

What are the three causes of anemia?

A
  1. Blood loss
  2. Excessive RBC destruction
    - Extracorpuscular reasons
    - Intracorpuscular reasons
  3. Insufficient RBC production
    - Too little material
    - Too little RBCs
    - Not enough room
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7
Q

Anemia induced by blood loss

A

Cause: trauma resulting in acute blood loss
- After 2-3 days, reticulocytes spike (normal is 1%)

Kidneys release erythropoietin and goes to bone marrow and activates erythropoiesis, releasing reticulocytes (RBC precursors) which mature in the blood to erythrocytes

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8
Q

Anemia induced by excessive RBC destruction - what are some signs of destruction and some signs of production?

A

Destruction

  • Increased bilirubin (breakdown of RBCs)
  • Increased LDH (where RBCs get their energy b/c no mt)
  • Reduced haptoglobin

Production

  • Increased reticulocytes
  • Nucleated red cells in blood
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9
Q

Erythrocyte destruction

A
  • Lifespan of RBC is ~120 days
  • RBC destroyed by macrophages in spleen and liver
  • RBC recycling
  • – Globin (into AA)
  • – Heme (Fe-containing part) used in liver, spleen, bone marrow
  • – Remainder converted to bilirubin
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10
Q

Unconjugated bilirubin is toxic

A
  • Bilirubin + Albumin complex
  • Lipid soluble
  • Damage cell membranes
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11
Q

Bilirubin elimination

A
  • Unconjugated bilirubin is taken up by the liver and other cells
  • Conjugated via glucuronyl transferase (makes bilirubin water soluble)
  • Conjugated bilirubin is excreted with bile to the small intestine
  • – Can be eliminated from body in feces
  • Some bilirubin in the intestine is converted into urobilinogen by intestinal bacteria
  • – Most excreted via feces
  • – Some reabsorbed into the blood and liver can further metabolize urobilinogen and excrete it as bile
  • Small amounts of urobilinogen are excreted from the body in the urine
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12
Q

What is jaundice? How can we treat it?

A

Excess bilirubin accumulation in the body
- Skin, nails, whites of eyes

Toxic to brain cells.

Tx:

  • Tx cause of condition
  • Blood transfusion
  • Sun/UV rays make bilirubin water soluble
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13
Q

What is jaundice caused by?

A

Excess bilirubin production due to RBC destruction
- Surpasses liver’s ability to conjugate

OR

  • Decreased bilirubin excretion
    1. Reduced hepatic uptake (hepatitis, cirrhosis)
    2. Decreased conjugation (hepatitis, cirrhosis, enzyme deficiency)
    3. Bile duct obstruction (tumor, stone)
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14
Q

Dx and Tx of Jaundice

A

Location determined by

  • Color of feces and urine
    1. Light or clay-colored feces and dark urine
    • Extrahepatic obstructive jaundice = obstruction of bile duct
  1. Normal to light colored feces and light urine
    - Intrahepatic obstructive jaundice = damaged hepatocytes; cirrhosis, hepatitis, liver failure
  2. Dark feces and urine
    - Hemolyic anemia
  • X-ray, CT scan, liver biopsy can provide evidence of presence of stone, tumor, hepatitis, cirrhosis
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15
Q

Extrahepatic obstructive jaundice

A

Light or clay colored feces, dark urine

Obstruction of the bile duct

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16
Q

Intrahepatic obstructive jaundice

A

Normal to light-colored feces, light urine

Damaged hepatocytes from cirrhosis, hepatitis, liver failure

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17
Q

Hemolytic anemia

A

Dark feces and urine

Overloading the process, destroying too much

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18
Q

What are the extracorpuscular hemolytic anemias?

A
  • Microangiopathic hemolytic anemia

- Autoimmune hemolytic anemia

19
Q

Microangiopathic hemolytic anemia

A

Extracorpuscular hemolytic anemia

  • Physical trauma to RBCs
  • Schistocytes (RBC fragments)

Causes:

  • Artificial heart valve
  • Malignancy
  • Obstetric complications
  • Sepsis
  • Trauma
20
Q

Autoimmune hemolytic anemia

A

Extracorpuscular

Warm

  • IgG - more active at higher temp
  • Spleen
  • Spherocytes

Cold

  • IgM, complement - more active at lower temp
  • Intravascular hemolysis
  • Agglutination

Type II

21
Q

What are the intracorpuscular hemolytic anemias?

A
  • Sickle cell anemia
  • Thalassemia
  • Hereditary spherocytosis
  • Howell-Jolly bodies
  • G6PDH deficiency
22
Q

Sickle Cell Anemia

A

Intracorpuscular

  • Hemoglobinopathy
  • Single aa substitution in beta chain (Val for Glut Acid)
  • Heter vs homozygous
  • African ethnicity

Aggregates and polymerizes, clogging the vessels -> ischemic necrosis or spleen infarction

23
Q

Thalassemia

A

Intracorpuscular

Hypochromic, microcytic anemia

  • Can’t make enough alpha or beta chain
  • Increased RBC synthesis (EPO)
  • Medullary expansion due to increased erythropoiesis

alpha: SE asian
beta: Mediterranean

24
Q

Hereditary Spherocytosis

A

Intracorpuscular

  • Many spherocytes
  • Caused by a spectrin defect
  • Splenectomy is curative
  • RBCs form polymers and get trapped in the spleen = SPLENOMEGALY
25
Q

Howell-Jolly bodies

A

Intracorpuscular

Evidence of markedly decreased splenic function

Small remnant of the nucleus intracorpuscular anemia

26
Q

G6PDH deficiency

A

Intracorpuscular

  • Low G6PDH > Higher peroxides > Cell lysis
  • ROS exposure kills RBCs
  • Development (and removal) of Heinz bodies
  • – Form bite cells

Not producing enough glutathione (removes ROS) = increase in ROS and hydroxide radicals, killing the cell

27
Q

What are Heinz bodies?

A

Globin denatures, sticks to RBC membranes

28
Q

Bite cell symptoms and triggers

A

Some are asymptomatic
Others have ‘episodes’

Triggers: fava beans, drugs

29
Q

Causes of anemia due to insufficient RBC production

A

Too material

  • Fe deficiency
  • Chronic disease
  • Megaloblastic

Too few erythroblasts
- Aplastic anemia

Not enough room
- Myelophthistic anemia

30
Q

Iron deficiency anemia effects

A

Insufficient RBC production b/c of too little material

Microcytic, hypochromic anemia

  • Atrophic glossitis
  • Koilonychia
31
Q

What are some causes of iron deficiency anemia?

A

Causes

  1. Decreased iron intake
    - Poor diet
    - Poor absorption
  2. Increased iron loss
    - GI bleeding
    - Menses
    - Hemorrhage
  3. Increased iron requirement
    - Pregnancy
32
Q

Causes of anemia due to chronic disease

A

Normochromic, normocytic anemia

Disrupted Fe metabolism
- Increased hepcidin in the liver

33
Q

Causes of megaloblastic anemia

A

Normochromic, macrocytic anemia

Reduced B12/folate in the body
- Generally due to inadequate absorption through INTRINSIC FACTOR

You need folate for cell division.
You can’t absorb B12 if you don’t have enough IF.

34
Q

What is a subtype of megaloblastic anemia?

A

Pernicious anemia

35
Q

What is pernicious anemia?

A

Normochromic, macrocytic anemia

  • Decreased RBC synthesis due to low vitamin B12 in the body (due to low IF)
  • Nutritional B12 deficiency is rare
  • IF deficiency
  • – Autoimmune disease of stomach
  • – GI surgery (i.e. gastric bypass surgery, losing the part of the stomach)
  • – Chronic gastritis
36
Q

How does pernicious anemia manifest and how do you treat it?

A

Low levels of B12 in blood and low uptake of B12 from intestine (measured with radioactive B12).
Disease develops slowly due to large sores of B12 in the liver (may take over 1 year)

Tx: B12 injections

37
Q

What do the RBCs and neutrophils look like in megaloblastic anemia?

A

Normochromic, macrocytic anemia

Hypersegmented neutrophils

38
Q

What is the Schilling test?

A

A clinical test to determine whether a patient has pernicious anemia (B12 absorption)

39
Q

How do you perform Stage 1 of the Schilling test?

A

Stage 1

  • Feed patient radiolabeled B12
  • Inject B12 one hour later

Normal: At least 10% of B12 in urine over 24 hr
Abnormal: <10% B12 in urine

40
Q

How do you perform Stage 2 of the Schilling test and when would you do it?

A

If B12 levels are abnormal after Stage 1 test. (<10%)

Stage 2
- Feed patient radiolabeled B12 AND give them IF

Normal B12 levels = patient has PA
Still low B12 = patient has GI pathology (i.e. Crohns, etc)

41
Q

What are some causes of aplastic anemia?

A

Normochromic, normocytic anemia
(Too few RBCs)

  1. Idiopathic
  2. Drugs/chemicals
  3. Viruses
  4. Pregnancy
  5. Fanconi anemia
42
Q

What are some histological features of aplastic anemia?

A

Pancytopenia
- Bleeding and compromised immune function

Hypoplastic (empty) bone marrow

43
Q

Myelophthisic anemia causes and histological features?

A

Normochromic, normocytic anemia

Infiltration of bone marrow by tumors or fibrosis

Possible pancytopenia
Dacryocytes

DMD 5247 (7 decks)

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