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Physiology > PHS 203 Blood Physiology 3 WBC and Hemostasis > Flashcards

PHS 203 Blood Physiology 3 WBC and Hemostasis Flashcards

1
Q

Difference between rbc and wbc

A

WBCs differ from RBCs in many aspects.
1. Larger in size.
2. Irregular in shape.
3. Nucleated.
4. Many types.
5. Granules are present in some type of WBCs.
6. Lifespan is shorter

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2
Q

Types of granulocytes

A

i. Neutrophils with granules taking both acidic and
basic stains.
ii. Eosinophils with granules taking acidic stain.
iii. Basophils with granules taking basic stain

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3
Q

Types of agranulocytes

A

i. Monocytes.
ii. Lymphocytes.

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4
Q

Function of Monocytes

A

Monocytes: Defend against infection by cleaning up damaged cells
- precursor pf tissue macrophages

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5
Q

Function of basophils (and nucleus shape)

A

Basophils:
- Produces an allergic response like coughing, sneezing or a runny nose
- secrete histamine which results in inflammation associated with asthma
- role in signalling when infectious agents invade the body

Shape of nucleus: irregular

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6
Q

Function of eosinophils (and nucleus shape)

A

Eosinophils:
- Identify and destroy parasites, cancer cells and assists basophils with your allergic response

Shape of nucleus: bilobular connected by thin chromatin strand

Shape of nucleus: bilobed

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7
Q

Function of lymphocytes

A

Lymphocytes:
T cells, involved in inntae immunity, they are natural killer cells which kill tumore cells

B cells to protect against viral infections and produce proteins to help you fight infection (antibodies).
They produce plasma cells and are involved in cell-mediated immunity

Shape of nucleus: round with an indentation

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8
Q

Function of neutrophils (and nucleus shape)

A

Neutrophils
- Help protect your body from infections by killing bacteria, fungi and foreign debris
- the most numerous of all leukocytes in the body
- 1st line of defence for the body’s immune system
- main component of pus

Shape of nucleus: multilobular connected by chromatin strands

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9
Q

What is hemostasis?

A

Hemostasis is defined as arrest or stoppage of bleeding

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10
Q

What are the stages of hemostasis?

A
  1. Vasoconstriction
  2. Platelet plug formation
  3. Coagulation of blood
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11
Q

Describe vasoconstriction

A

Immediately after injury, the blood vessels (usually arterioles and small arteries) constrict and decrease the loss of blood from damaged portion.
When the blood vessels are cut, the endothelium is damaged and the collagen is exposed.
Platelets adhere to this collagen and get activated. The activated platelets secrete serotonin and other vasoconstrictor substances which cause constriction of the blood vessels. Adherence of platelets to the collagen is accelerated by von Willebrand factor. This factor acts as a bridge between a specific glycoprotein present on the surface of platelet and collagen fibrils.

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12
Q

Describe the platelet plug formation

A

Platelets get adhered to the collagen of ruptured blood vessels and secret adenosine diphosphate (ADP) and thromboxane A2. These two substances attract more and more platelets and activate them. All these platelets aggregate together and form a loose temporary platelet plug or temporary hemostatic plug, which closes the ruptured vessel and prevents further blood loss. Platelet aggregation is accelerated by platelet­ activating factor (PAF).

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13
Q

Describe the coagulation of blood

A

During this process, the fibrinogen is converted into fibrin. Fibrin threads get attached to the loose platelet plug, which blocks the ruptured part of blood vessels and prevents further blood loss completely.

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14
Q

State Landsteiner law

A

Landsteiner law states that: 1. If a particular agglutinogen (antigen) is present in the RBCs, corresponding agglutinin (antibody) must be absent in the serum.
2. If a particular agglutinogen is absent in the RBCs, the corresponding agglutinin must be present in the serum.
Though the second part of Landsteiner law is a fact, it is not applicable to Rh factor

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15
Q

What are the 2 categories of abnormal hemoglobin

A
  1. Hemoglobinopathies
  2. Hemoglobin in thalassemia and related disorders.
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16
Q

What are hemoglobinopathies?

A

Hemoglobinopathy is a genetic disorder caused by abnormal polypeptide chains of hemoglobin.

i. Hemoglobin S: It is found in sickle cell anemia. The α-chains are normal and β-chains are abnormal.
ii. Hemoglobin C: The β-chains are abnormal. It is found in people with hemoglobin C disease, which is characterized by mild hemolytic anemia and splenomegaly.
iii. Hemoglobin E: Here also the β-chains are abnormal. It is present in people with haemoglobin E disease which is also characterized by mild hemolytic
anemia and splenomegaly.
iv. Hemoglobin M: It is the abnormal haemoglobin present in the form of methemoglobin. It occurs
due to mutation of genes of both in α and β chains, resulting in abnormal replacement of amino acids. It is present in babies affected by hemoglobin M disease or blue baby syndrome. It is an inherited disease, characterized by methemoglobinemia.

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17
Q

What is Methemoglobinemia

A

Methemoglobinemia (MetHb) is a blood disorder in which an abnormal amount of methemoglobin (oxidized hemoglobin) is produced.

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18
Q

What is Cyanocobalamin?

A

Vitamin B12 (Cyanocobalamin)
Vitamin B12 is the maturation factor necessary for erythropoiesis.
Source
Vitamin B12 is called an extrinsic factor since it is obtained mostly from the diet. Its absorption from the intestine requires the presence of the intrinsic factor of Castle.
When necessary, it is transported to the bone marrow to promote the maturation of RBCs. It is also produced in the large intestine by the intestinal flora.

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19
Q

Where is Vitamin B12 stored

A

In the liver and small quantities in the muscle

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20
Q

Action of vitamin B12

A

Vitamin B12 is essential for the synthesis of DNA in RBCs.
Its deficiency leads to failure in the maturation of the cell
and reduction in cell division. Also, the cells are
larger with fragile and weak cell membranes resulting in
macrocytic anemia.

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21
Q

Why is vitamin B12 called anti pernicious factor?

A

A deficiency of vitamin B12 causes pernicious anemia.
So, vitamin B12 is called anti pernicious factor.

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22
Q

What is a normal Mean Corpuscular Volume (MCV)?

A

90 cu µ (78 to 90 cu µ).

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23
Q

How does MCV change the name of a rbc

A

When MCV is normal, the RBC is called normocyte.
When MCV increases, the cell is known as a macrocyte
and when it decreases, the cell is called a microcyte

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24
Q

What is MCV

A

MeanCorpuscular volume
MCV is the average volume of a single RBC and it is expressed in cubic microns (cu µ)

25
Q

What is MCH?

A

MCH is the quantity or amount of hemoglobin present in one RBC
C. It is expressed in micro­microgram or picogram
(pg)

26
Q

What is the normal value for Mean Corpuscular Hemoglobin (MCH)

A

Normal value of MCH is 30 pg (27 to 32 pg).

27
Q

What is MCHC?

A

Mean Corpuscular Hemoglobin Concentration (MCHC) is the concentration of hemoglobin in one RBC

28
Q

Normal value of MCHC?

A

Normal value of MCHC is 30% (30% to 38%).

29
Q

Which is the most important absolute value in the diagnosis of anemia?

A

MCHC

30
Q

How does MCHC affect change the name of rbc?

A

When the MCHC(Mean corpuscular hemoglobin concentration) decreases, the RBC is known hypochromic.

31
Q

What is CI?

A

Color index is the ratio between the percentage of
hemoglobin and the percentage of RBCs in the blood.
Actually, it is the average hemoglobin content in one cell of a patient compared to the average hemoglobin content in one cell of a normal person

32
Q

Normal value for CI

A

Normal color index is 1.0
(0.8 to 1.2). However, it is useful in determining the type of anemia. It increases
in macrocytic (pernicious) anemia and megaloblastic anemia. It is reduced in iron deficiency anemia. And, it is normal in normocytic normochromic anemia

33
Q

5 Characteristics of adaptive immunity

A
  1. Timing of response: this develops over a long period of time (time of response is slow)
  2. Immune response is highly specific: This refers to the ability of the immune system to recognize non-self-antigens and respond in a specific manner to them, rather than responding in a random manner.
  3. Memory response: the initial contact with a molecule eliciting an immune response(antigen) leaves an imprint of information.
  4. Recognition of pathogens: it recognizes pathogens using memory cells (T and B cells) and activated B cells. B cells are lymphoid cells concerned with humeral immunity (short lived), T cells are the type of white blood cells, can also be called T lymphocyte and thymocyte.
  5. Self-limitation: The adaptive immune response wanes with time after antigenic stimulation, returning the immune system to its resting basal state, a process called homeostasis.
34
Q

What is Adaptive immunity?

A

Adaptive immunity involves specialized immune cells and anti-bodies that attack and destroy foreign invaders and are able to prevent diseases in the future by remembering what those substances look like and mounting a new immune response. It may last for a few weeks or months or even a lifetime.

35
Q

Secondary causes of polycythemia vera

A

1) Dehydration
2) Pulmonary Fibrosis
3) Living at a high altitude
4) Carbon monoxide exposure
5) Kidney cancer

36
Q

Vasoconstriction is purely a local phenomenon T/F

A

TRUE

37
Q

Adherence of platelets to the collagen is accelerated by what?

A

von Willebrand factor

38
Q

What is Hypercoagulability/Thrombophilia and what does it cause?

A

This is when the blood clots too much or too easily. This is dangerous because those clots can develop or get stuck in different places in the body and cause severe, life-threatening problems. Examples of these problems include:
* Stroke.
* Deep vein thrombosis (DVT) which can then cause a pulmonary embolism.
* Heart attack.

39
Q

What is Hypocoagulability and what does it cause?

A

When the blood doesn’t clot well, any injury becomes a much more dangerous event. It also means a greater risk for injuries to organs and blood vessels inside the body, which can then cause internal bleeding. Certain types of cancer like leukemia can cause you to bleed too easily. Conditions that keep your blood from clotting are often genetic, also. Some examples of genetic conditions include:
* Hemophilia
* Von Willebrand disease
* Inherited thrombocytopenia (low platelet count).

40
Q

Explain Albumin’s buffer action

A

The imidazole group of histidine is an effective contributor. Albumin is the greatest protein buffer as it has 16 histidine residues. It is slightly acidic and because of its negative charge, it balances many positively charged molecules such as Hydrogen calcium potassium etc hence performing its function as a buffer

41
Q

How does plasma/ plasma proteins regulate blood acidity?

A

Plasma( proteins )functions as a ph regulator under the protein buffer system and offer 15 percent of the buffering capacity of blood.

It is dependent on the pk of ionizable group of amino acids. Amino acids contain positively charged amino groups and negatively charged carboxyl groups, these charged regions bind with hydrogen and hydroxyl ions thus functioning as buffers.

Because of the amphoteric nature of plasma proteins, they can combine with both acids and bases. In acidic pH, the amino group of proteins act as a base and is converted to ammonia when it accepts a proton.

42
Q

Applicability of Landsteiner’s Law

A

i. The first law holds true for all types of blood grouping
ii. The second law is a fact for ABO blood groups
iii. The Rh, M, N and other blood groups do not follow the second part of Landsteiner’s law.

43
Q

Describe the sickle cell disease

A

Hemoglobin consist of 4 polypeptide chains; 2 alpha chains and 2 beta chains. The Hbb gene provides instructions for making the beta globin, mutations of the Hbb gene affects the beta globin.

It occurs when a person inherits two abnormal copies of the beta-globin that makes the hemoglobin, one from each parent. It is INHERITED AUTOSOMAL RECESSIVE PATTERN, causing erythrocytes to be sickled crescent shape and affect multiple organ systems.

It is diagnosed with a blood test and usually manifest by 5-6 months of age
Symptoms include: swelling in hands and feet, bacterial infections, attacks of pain. The complications that can occur as a result of this disorder include chronic pain, aseptic bone necrosis, kidney problems, and pulmonary hypertension.

44
Q

Role of cyanocobalamin in erythropoiesis

A

Cyanocobalamin is under the maturation factor for erythropoiesis. It is an extrinsic factor because it can only be gotten from diet. Most of it is stored in the liver, while some are stored in the muscles. When it is necessary, it is transported to the bone marrow to promote maturation of Red Blood Cells. It is essential for the synthesis of DNA in Red Blood Cells.

45
Q

Why is the spleen is called “graveyard of RBC?

A

The destruction occurs mainly in the red pulp of the spleen because the diameter of the spleen capillaries is very small.

46
Q

Describe the process of the destruction of RBC (fate of RBC’s)

A

Destroyed RBCs are fragmented and hemoglobin is released from the fragmented part. Hemoglobin is immediately phagocytized by macrophages of the body, particularly the macrophages of the liver (Kupffer cells), spleen and bone marrow.
Hemoglobin degraded into iron, globin, porphyrin. Iron combines with the protein called apoferritin to form ferratin, which is stored in the body and reused later in erythropoiesis. Globin enters the protein depot for later use. Porphyrin is degraded into bilirubin, which is excreted by the liver through bile.

47
Q

What is a bleeding disorder?

A

Bleeding disorders are a group of health conditions in which there is a problem with the body’s blood clotting process. These disorders can lead to heavy prolonged bleed after an injury. Bleeding can also begin on it’s own, bleeding disorders can cause abnormal bleeding, both outside and inside the body. Some bleeding disorders can drastically increase the amount of blood leaving the body.

48
Q

Factor I

A

Fibrinogen

49
Q

Factor II

A

Prothrombin

50
Q

Factor III

A

Thromboplastin (Tissue factor)

51
Q

Factor IV

A

Calcium

52
Q

Factor V

A

Labile factor (Proaccelerin or accelerator
globulin)

53
Q

Factor VII

A

Stable factor

54
Q

Factor VIII

A

Antihemophilic factor (Antihemophilic
globulin)

55
Q

Factor IX

A

Christmas factor

56
Q

Factor X

A

Stuart-Prower factor

57
Q

Factor XI

A

Plasma thromboplastin antecedent

58
Q

Factor XII

A

Hageman factor (Contact factor)

59
Q

Factor XIII

A

Fibrin-stabilizing factor (Fibrinase).

Physiology (5 decks)

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