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Pathology 2 > Exam 3 Hematologic Slide Set 1 > Flashcards

Exam 3 Hematologic Slide Set 1 Flashcards

1
Q

Hematopoesis from the start of life

A
  • Stem cells in the yolk sac at 3rd week of development
  • Cells migrate to the developing liver at 3 months
  • Blood islands migrate from yolk sac to bone marrow at 4 months
  • ALL the bone marrow is active in producing blood cells at birth
  • Production is isolated to specific marrow sites by puberty
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2
Q

Red Marrow sites in adulthood

A

Where blood cells are being produced…

  • vertebrae
  • ribs
  • skull
  • pelvis
  • proximal epiphyseal portions of the humerus & femur
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3
Q

Process of hematopoesis

A

-Pluripotent stem cells give rise to the full line of blood cells, which includes: RBCs, WBCs (neutrophils, lymphocytes, eosinophils, monocytes, & macrophages), platelets, plasma cells, mast cells, NK cells, B cells & T cells.

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4
Q

RBC facts

A
  • They transport O2 with hemoglobin! :D
  • They consist of 90% hemoglobin! (That’s why they’re red!)
  • Their normal life span is 90-120 days!
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5
Q

Anemia defined

A

Decreased amounts of RBCs (size, numbers, or both), decreased hematocrit, decreased hemoglobin.

Characterized by low O2 transport capacity of the blood.

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6
Q

Polycythemia defined

A

INCREASED amounts of RBCs!

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7
Q

Anemia is due to what??

A
  • Blood loss
  • Impaired RBC production
  • Increased RBC destruction
  • A combination of the above
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8
Q

Examples of Anemias

A
  • Blood loss
  • G6PD
  • Iron-deficiency anemia
  • Hereditary spherocytosis
  • Pernicious anemia
  • Thalassemia
  • Sickle-cell anemia
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9
Q

Sx of Anemia

A
  • Pallor
  • Increased rate/weak pulse
  • dyspnea
  • palpitations
  • dizziness
  • fatigue
  • headaches
  • faintness/syncope
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10
Q

The simplest breakdown of anemia classifications

A

Loss or Decreased Production

I.e.:
Excessive blood turnover (Hemorrhage or Hemolysis)
or
Failure of blood production

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11
Q

Blood Loss

A
  • Can be massive & acute or slow & chronic (GI, Gyn, or GU)
  • Sx vary with degree of anemia & rate of development
  • A rapid drop is not tolerated as well, and thus is more symptomatic than a similar loss that is slow over time
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12
Q

Normal Response to Acute Blood Loss

A
  • Lose too much = death
  • Otherwise, volume rapidly restored as water is shifted from interstitial fluid compartment into the blood
  • Hemo-dilution lowers hematocrit
  • Decreased oxygenation (of renal JGA cells) triggers EPO production
  • Reticulocytes (young RBCs, just lost nucleus) start to appear in the peripheral blood, can climb from 1.5% to 15% within a week of the event
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13
Q

Polychromasia

A

A disorder, high # of immature red blood cells found in the bloodstream. Cells stain grayish blue/purplish instead of normal red/pink. Usually an indication of bone marrow stress.

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14
Q

Normal lab value for reticulocytes

A

0.5%-1.5% in circulating blood

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15
Q

When does chronic blood loss cause anemia?

A

1- if the rate of loss exceeds bone marrow’s capacity to restore it
2- if the iron sotres are inadequate

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16
Q

These organ systems are usually involved with chronic hemorrhage…

A

“Gee, why am I anemic??”

GI - ulcer, colitis, cancer
Gynecologic - excessive menstrual flow, cancer
Genitourinary - cancer or stone

17
Q

Hemolytic Anemias - Characterization

A

Characterized by: shortened RBC life span, Hgb breakdown products accumulating, marked increase in erythropoiesis in BM.

Characterized as Extravascular/Intravascular and/or Extrinsic/Intrinsic

18
Q

Hemolytic Anemias - Extravascular v. Intravascular

A
  • Extravascular hemolysis: Spleen (mononuclear phagocytic cells) normally destroy RBCs, can contribute to hemolytic anemias! Also sickle cell anemia & hereditary spherocytisis
  • Intravascular hemolysis: destruction of RBCs in the vascular compartment - mechanical trauma (heart valves, marathons & bongo drums), antibody fixation (mismatched blood transfusion), toxic injury to RBCs (malaria, septic shock). Peripheral smear would show multiple fragmented RBCs - helmet cells & schistocytes
19
Q

Hemolytic Anemias - Intrinsic v. Extrinsic

A
  • Intrinsic: genetic & hereditary RBC diseases (sickle cell, hereditary spherocytosis). May see schistocytes or spherocytes. Can include disorders of rBC membrane, RBC enzyme deficiencies, disorders of hemoglobin synthesis. Often have a + family hx. Can be FURTHER divided into: Abnormal hemoglobin, abnormal RBC metabolism, or abnormal hemoglobin SYNthesis.
  • Extrinsic: cause is extrinsic TO THE RBC - heart valve prosthesis/AV shunts, malarial infection, lead poisoning or snake venom, hypersplenism (abnormal sequestration of RBCs in spleen), acquired hemolytic anemias (autoimmune - IgG against RBCs)
20
Q

Autoimmune causes of Extrinsic Hemolytic Anemias

A

Can be Primary/Idiopathic or Secondary to…

-lymphoma, carcinoma, sarcoidosis, collagen vascular dz (lupus or RA)

21
Q

Immune hemolysis is caused by…

A

Bad blood transfusions

Fetal/Maternal incompatibility… ?? What the hell even is this card? Ugh.

22
Q

What’s Hemoglobin?

A
  • metallo-proteins made of 2 identical pairs of chains
  • Hb F during fetal/neonatal period is made of 2 alpha & 2 gamma chains
  • After 1 year, the adult profile is present: over 95% adult hemoglobin (Hb A, 2 alpha chains, 2beta chains) & 2-3.5% of hemoglobin A2
23
Q

Sickle Cells

A
  • *A single point mutation in the beta-globulin creates hemoglobin S.
  • Autosomal recessive inheritance of the dz
  • RBCs sickle at low pH & low O2, sickling is initially reversible. Low pH reduces oxygen’s affinity for hemoglobin!
  • Shorter life span! 20 days**
24
Q

Sickle Cell Disease prevalence in US & Africa

A
  • ~8% of American blacks are heterozygous for Hb S = carriers or “sickle cell trait” = 40% Hb S, 60% HbA?
  • Homozygous = almost 100% Hb S
  • 2 million Americans have trait
  • 1 in 500 African-Americans develops sickle cell anemia
  • In Africa 1/100 develop dz
  • Newborns have several months of protection from fetal hemoglobin
25
Q

HbSC disease

A

Hemoglobin C has higher affinity to deoxygenated HbS & HbA

  • HbSC dz is milder than full sickle cell
  • Sx: hematuria, retinal hemorrhages & aseptic necrosis of femoral head
  • 2-3% American blacks are asymptomatic HbC/HbA heterozygotes
  • 1 in 1250 has HbSC dz
26
Q

Sickle Cell Anemia

A
  • MCHC influences pathogenesis
  • Increased MCHC (from intracellular dehydration?!) facilitate sickling & thus vascular occlusion
  • Conditions decreasing MCHC (alpha-thalassemia) will have milder sx’s/dz b/c it reduces globin synthesis
  • Clinical manifestations: chronic hemolysis & ischemic tissue damage from occlusion of small blood vessels
  • Pathogenesis of microvascular occlusions: I can’t add to this card because I MUST pee now & it’s written in tiny stupid print.

Pathology 2 (9 decks)

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