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Pathophysiology > Hematologic > Flashcards

Hematologic Flashcards

1
Q

The hematological system

4 main components

A

Plasma
Red blood cells
White blood cells
Platelets

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2
Q

Anemia

A

A condition in which the blood doesn’t have enough healthy red blood cells

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3
Q

Describe the composition of blood

A

Plasma is 55% of blood
(7% proteins; 92% water, 1% other solutes)

Formed elements are 45% of blood
(platelets; leukocytes; erythrocytes)

Leukocytes:

  • neutrophils (40-60%)
  • lymphocytes (20-40%)
  • monocytes (2-8%)
  • eosinophils (2-4%)
  • basophils (0.5-1%)
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4
Q

Discuss the function of plasma and plasma proteins

A

Plasma is 55% of blood
(7% proteins; 92% water, 1% other solutes)

Function: Maintains BP and regulates body temperature, supplies proteins for blood clotting, immunity and maintains proper PH.

  • Albumins function as carriers and control the plasma oncotic pressure
  • Globulins are carrier proteins and immunoglobulins (antibodies)
  • Clotting factors (mainly fibrinogen)
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5
Q

Discuss the structure and function of the cellular components of blood

A

Platelets:

  • disk-shaped cytoplasmic fragments of megakaryocytes
  • essential for blood coagulation and control of bleeding
  • about a 10 day lifetime in blood (not true cells)
  • Thrombopoietin is the main regulator (stimulating factor) for platelet formation; regulates platelets b/c bound by platelets

Cellular Components:

  • Erythrocytes (RBCs) are the most abundant cell in the body; responsible for tissue oxygenation; bioconcavity and reversible deformity
  • 120 day life cycle
  • Leukocytes (WBCs):
    Lymphocytes (B & T cells);
    Monocytes;
    Granulocytes (Basophils, Eosinophils, Neutrophils)
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6
Q

Identify the role of the mononuclear phagocyte system

A

Consists of monocytes that differentiate w/out dividing and reside in the tissue for months or years.

MPS cells ingest and destroy (phagocytosis) unwanted materials and foreign protein particles, circulating immune complexes, microorganisms, debris, defective/ injured erythrocytes, and dead neutrophils. Osteoclasts are multinucleate MPS that originate from monocyte cell lineage and specialize to allow function of lacunar bone resorption and are also known to be phagocytic.
Body’s main line of defense against bacteria in the blood.

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7
Q

Identify the process of hematopoiesis and the role of hematopoietic stem cells

A

Blood cell production.

Formed from stem cells in bone marrow(myeloid tissue).

Regulation by growth factors - controls for correct proportions of each cell type

Mesenchymal Stem Cells (MSCs):
- Stromal cells, that can differentiate into a variety of cells → incl. osteoblasts, adipocytes, and chondrocytes (produce cartilage), but from there cannot differentiate into other cell types any longer.

Hematopoietic stem cells (HSCs):
- Progenitors of all hematologic cells

Both populations of stem cells undergo self-renewal in the bone marrow to replace the ones that undergo differentiation.

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8
Q

Explain erythropoiesis, focusing on the role of erythropoietin in this process

A

Erythropoiesis is the process which produces RBCs (erythrocytes). It is stimulated by decreased O2 in circulation (hypoxia), which is detected by the kidneys causing the secretion of the hormone erythropoietin. This hormone stimulates proliferation and differentiation of red cell precursors, which activates increased erythropoiesis in the hemopoietic tissues, ultimately producing erythrocytes.

Erythropoietin → hormone that stimulates erythrocyte production; made in the kidney and its main stimulus is hypoxia, but also decreased RBCs, decreased Hb synthesis, decreased blood flow, hemorrhage and increased O2 consumption by tissues.

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9
Q

Explain the function of hemoglobin in the human body

A

o Oxygen carrier.
o Carbon dioxide carrier.
o Gives the red color to blood by Fe2+ ions
o Maintains the shape of the red blood cells.
o Acts as a buffer.
o Interacts with other ligands.
o Degradation accumulates physiologically active catabolites.

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10
Q

Explain how iron (as Fe2+, Fe3+, and bound to transferrin) is used, focusing on how hemoglobin can carry oxygen, including the cycle of oxy-, deoxy-, and met- hemoglobin

A
  • Each globin subunit of the hemoglobin molecule can bind with one Fe 2+ ion.
  • Affinity of hemoglobin towards oxygen is gained by the Fe2+ion. Each Fe2+ can bind with one oxygen molecule
  • The binding of oxygen oxidizes Fe2+ into Fe3+. Oxyhemoglobin → oxygen-bound hemoglobin When blood reaches an oxygen deficient tissue, oxygen is dissociated from hemoglobin and diffused into the tissue. The O2 is the terminal electron acceptor in the process called oxidative phosphorylation in the production of ATP.
  • The removal of O2 turns the iron into its reduced form. Deoxyhemoglobin → oxygen-unbound hemoglobin. Oxidation of Fe2+ into Fe3+ creates methemoglobin which cannot bind with O2.
  • Methemoglobin Fe3+ loses O2 but can still oxidize → tissues
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11
Q

List several situations that lead to increased leukocyte production

A

An increased production of white blood cells to fight an infection

A reaction to a drug that increases white blood cell production

A disease of bone marrow, causing abnormally high production of white blood cells

Acute lymphocytic leukemia à an immune system disorder

Acute myelogenous leukemia (AML)

Allergy, especially severe allergic reactions

Chronic lymphocytic leukemia

Chronic myelogenous leukemia

Drugs, such as corticosteroids and epinephrine

Infections, bacterial or viral

Myelofibrosis (a bone marrow disorder)

Polycythemia vera

Rheumatoid arthritis (inflammatory joint disease)

Smoking

Stress, such as severe emotional or physical stress

Tuberculosis

Whooping cough

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12
Q

Describe the role of platelets in hemostasis

A

Platelet accumulation at the site of injury is considered the first wave of hemostasis and the second wave of hemostasis is mediated by the blood coagulation pathway. Platelets play a central role in a series of sequential events during the platelet accumulation (i.e. platelet adhesion, activation, and aggregation) and are also actively involved in cell-based thrombin generation, which markedly amplifies the blood coagulation cascade. Thus, platelets contribute to both the first and the second waves of hemostasis

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13
Q

Lab values for complete blood count (CBC)

WBC

A

WBC: 5,000 -10,000 /mm3

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14
Q

Lab values for complete blood count (CBC)

Hgl

A

Hgl: Male: 13.2-17.3 Female: 11.7-15.5 g/dL

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15
Q

Lab values for complete blood count (CBC)

Plt

A

150,000-400,000 /uL

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16
Q

Define anemia

A

Blood condition classified by their causes or by the changes that affect the size, shape, or substance of the erythrocyte.

Condition marked by a deficiency of red blood cells or of hemoglobin in the blood, resulting in pallor and weariness. Not enough RBCs to carry adequate oxygen to the body’s tissues.

Lab values to look for anemia
HGB (14-18 g/dl) and HCT (35%-45%)

17
Q

List the various methods of classifying the anemias

A

Classifying anemias cytic refers to the size

Classifying anemias chromic refers to the color. No iron not able to take the stain

Anisocytosis refers to the size of blood

Poikilocytosis refers to shape of blood.

Microcytic
Normocytic
Macrocytic

18
Q

Describe the manifestations of anemia and discuss the pathophysiology that generates them

A

The fundamental alteration of anemia is a reduced-oxygen carrying capacity of blood. Consistency and blood volume reduced, movement of interstitial fluid into blood causing plasma volume, causing viscosity to decrease (blood thins) causing hyperdynamic circulatory state and eventually increasing stroke volume and heart rate.

19
Q

Compare and contrast the pathophysiology underlying iron deficiency, pernicious, and folate
deficiency anemias

A

Pernicious anemia (PA)- due to absence of intrinsic factor (IF) enzyme required for gastric absorption of vitamin B12.

Folate deficiency- folate is essential in RNA and DNA synthesis with erythrocyte. Folate is absorbed in upper small intestine and stored in liver.

Iron deficiency (IDA)- most common throughout the world, blood loss of 2-4 ml/day causes IDA- from use of medication, surgical procedures, insufficient dietary intake, eating disorders.

20
Q

Describe the normocytic-normochromic anemias

A

Characterized by erythrocytes that are relatively normal in size and hemoglobin content but insufficient in number

Do not share any common etiology, pathologic mechanism, or morphologic characteristics

Less common than the macrocytic-normochromatic and the microcytic-hypochromatic anemias

Five distinct anemias are:
Aplastic - damage to bone marrow erythropoiesis

Posthermorrhagic - acute blood loss

Acquired hemolytic - immune destruction of erythrocytes

Hereditary hemolytic - e.g. sickle cell - destruction by eryptosis

Anemia of chronic inflammation - multiple causes

21
Q

Describe the multiple system manifestations of polycythemia vera related to the increased
viscosity and volume of blood

A

Secondary is the most common of the two, it is a physiological response from erythropoietin secretion caused by hypoxia. (physiological or pathological)

Primary- polycythemia vera is a stem cell disorder with hyperplastic and neoplastic bone marrow alterations.

Clinical manifestations: increased coagulability, blood viscosity and blood pressure. Thick blood, headache, drowsiness, angina.

22
Q

Describe the different types of alterations in leukocyte function

A

Leukocytosis- Increase in leukocytes. A normal protective physiologic response to physiologic stressors (like infection)

Leukopenia- decrease in leukocytes. Not normal and not beneficial. Low WBC count predisposes a patient to infections.

23
Q

Define granulocytosis and agranulocytosis, explaining what “shift to the left” and “shift to the
right” mean in this context

A

Granulocytosis- is an increase in granulocytes (neutrophils, eosinophils or basophils) begins when stored blood cells are released. Premature release of immature cells is responsible for the phenomenon known as shift-to-the-left or leukemoid reaction. This refers to the microscopic detection of disproportionate numbers of immature leukocytes in peripheral blood smears. Visualize cellular differentiation, maturation, and release as progressing from left to right instead of vertically. The early release of immature white cells prevents the completion of the sequence and shifts the distribution of leukocytes in the blood toward those on the left side of the diagram. This phenomenon is seen on the blood smear of individuals’ w/ leukemia. As infection of inflammation diminishes, and granulopoiesis replenishes circulating granulocytes, a shift-to-the-right or return to normal occurs.

Agranulocytosis-is when granulocyte count is extremely low. Usually when it occurs, hematopoiesis is arrested in the bone marrow or cell destruction increases in circulation. This leads to infection, general malaise, septicemia, fever, tachycardia, & ulcers in the mouth and colon. If untreated sepsis results in death within to 3 to 6 days.

24
Q

Classify leukemia as it relates to the maturity of the cells and appearance of the total leukocyte count and differential

A

Leukemia involves uncontrolled proliferation of malignant (cancerous) leukocytes, (WBCs) which cause an overcrowding of bone marrow and decreased production and function of normal hematopoietic cells (responsible for the formation of blood cells). The proliferating leukocytes overcrowd the bone marrow and other cells are inhibited.
- The classification of leukemia is based on: the cell of origin (either myeloid or lymphoid—from the bone/spinal cord or lymph node) AND the degree of differentiation (rate of growth) before the cell became malignant (cancerous).

25
Q

List the various causes of impaired hemostasis

A

Commonly associated with liver dysfunction, often caused by Vitamin K deficiency or liver disease

Vitamin K deficiency: vitamin K is required for the synthesis and regulation of prothrombin, as well as both coagulant and anticoagulant factors.

Liver disease: certain liver diseases can lead to defects in the clotting system, fibrinolytic systems, and platelet function

26
Q

Discuss the conditions that predispose an individual to the development of thrombi, defining
the “Virchow triad”

A

Thrombus: clot attached to a vessel wall.
Embolus: A piece of thrombus that detached and is circulating.
There are several factors for developing thrombi called the Virchow Triad.
1: Atherosclerosis- initiates platelet adhesion/aggregation= further damage/occlusion.
2: abnormalities of blood flow
A: Turbulent- platelets and endothelial cells are activated.
B: Stasis- platelets remain in contact w/ endothelium for extended periods. When clotting factors are not diluted by fresh blood, thrombi is activated.
C: Hypercoagulation of blood. This is a rare cause of thrombus. It can by primary (hereditary) or secondary (acquired).

27
Q

Identify the main pathophysiology that accounts for 90-95% of hemophilias

A
  • May be inherited or caused by spontaneous mutation of factor gene
  • Body loses the ability to clot blood, results in life-threatening bleeding
28
Q

What happens if there is not enough water in the blood?

A

-Water contains 92% in plasma

  • Blood volume decrease
  • Leading to a drop in blood pressure
  • When blood pressure drops too low, your organs won’t receive the oxygen and nutrients they need
29
Q

The wall of blood vessel?

A

Single-layer of endothelial cells

30
Q

Thrombopoietin is a)__________ produced by the b)________ and c)________ which regulates the production of d)________.

TPO also known as e)________ growth and development factor

A

a) Protein
b) liver
c) Kidney
d) Platelets

e)Megakaryocyte

31
Q

Blood clotting 4 steps

A 
1) Platelets activate
   Become sticky to plug hole/ not strong enough
2) Clotting factor
     reinforce platelets
3) Fibrin acts as glue
4) Other cells support the clot
32
Q

a) Erythropoiesis?
b) What cause?
c) What hormone involve?

A

a) A process that produces red blood cells
b) Hypoxemia
c) Erythropoietin(produce by kidney)

33
Q

Normal white blood cell (WBC, leukocyte) count?

A

5,000–10,000 WBCs/mm

34
Q

Normal Red blood cell (RBC) count?

A

Pathophysiology (11 decks)

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