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human bio > blood n immunology > Flashcards

blood n immunology Flashcards

1
Q

Functions of the blood

A

Blood has three general functions:
Transportation.
Transports gasses (O2, CO2), Nutrients, Heat and waste products, Hormones from endocrine glands to other body cells.
2.Regulation.
pH of body fluids.
Body temperature; Water allows transportation of heat to be lost through skin.
Blood osmotic pressure affects water content of cells.
3.Protection.
Blood clotting to prevent fluid loss.
WBCs to protect againstdisease through killing bacteria & producing antibodies.
Influence immunity through proteins such as interferons & complement

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2
Q

Blood Plasma

A

When cells removed from blood, straw coloured liquid called plasmaremains.
Plasma is 91.5% water, 7% proteins, 1.5% solutes
Proteins in blood, (plasma proteins) synthesized mainly by liver.

Albumins, (54% of all plasma proteins).
- help maintain proper blood osmotic pressure
Globulins(38% of plasma proteins), includeantibodies.
Fibrinogen(7% of plasma proteins); a key protein in forming blood clots.

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3
Q

Formation of Blood Cells

A

Process by which cells of blood develop is called hemopoiesis.

Red bone marrow is main site of hemopoiesis

Red bone marrow is highly vascularized connective tissue within microscopic spaces in spongy bone tissue.

0.1% of red bone marrow cells are cells called pluripotent stem cells.

Pluripotent stem cells have the capacity to develop into many different types of cells.

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4
Q

Formation of Blood Cells pt2

A

Pluripotent stem cells generate two other types of stem cells, that have a reduced number of cellular options: myeloid stem cells and lymphoid stem cells.

Myeloid stem cells present in red bone marrow.
Differentiate into red blood cells, platelets, and white blood cells except lymphocytes.

Lymphoid stem cells begin their development in red bone marrow but complete it in lymphatic tissues.
Differentiate into T and B lymphocytes and natural killer (NK) cells.

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5
Q

Formation of Red Blood Cells (RBCs/ erythrocytes)

A

Contain oxygen‐carrying protein haemoglobin; gives blood its red colour.
Haemoglobin also transports a quarter of CO2 in blood.
RBCs biconcave discs. Lack nucleus and other organelles.
Being biconcave increases surface area to enhance diffusion of gas molecules in and out of RBC.
They cannot reproduce.
All internal space used for O2 & CO2 transport (and to convert CO2 to HCO3- and H+)

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6
Q

Recycling of old RBC products

A

Globin and heme portions of haemoglobin are split apart.
Globin is broken down into amino acids, to be reused.
Iron removed from heme, transferred to muscle and liver to be stored as ferritin or transferred back to bone marrow.
Non-iron portion of heme is converted tobilirubinand transported to liver.
Bilirubin secreted into bile, into intestine.

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7
Q

Haemoglobin

A

Comprises 4 globin chains and 4 Iron containing Haem Units.

Haemoglobin binds reversibly with O2 to form oxyhaemoglobin

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8
Q

Oxyhaemoglobin dissociation curve

A

Normal arterial saturation is 95-100%.

If curve moves to right, Hb will give up O2 easier

Active tissues have higher temperature, higher CO2, lower pH so preferentially receive the O2 within Hb.

Carbon monoxide preferentially binds Hb stopping transport of O2 from lungs into blood

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9
Q

Control of RBC production

A

Tissue hypoxia can be due to anaemia, poor blood flow, reduced oxygen content of blood.

Erythropoietin (EPO) is a hormone

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10
Q

Blood groups

A

Surfaces of red blood cells contain genetically determined assortment ofantigenscomposed of glycolipids and glycoproteins.

These antigens, calledagglutinogens, occur in characteristic combinations. Based on presence or absence of various antigens, blood is categorized into differentblood groups.

We will focus on two major blood groups: ABO and Rh.

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11
Q

ABO Blood Group

A

ABO blood group based on two antigens calledAandB.
People whose RBCs have only antigen A have type A blood.
Those who have only antigen B are type B.
People with both A and B antigens are type AB
People with neither A or B are type O.

Plasma contains antibodies against ABO groups that are not normally present in the person.
Plasma does not contain antibodies that could react with the antigens on the persons own red blood cells.

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12
Q

Rh Blood Group

A

Similar to ABO system but people either express RH antigen (85% of population) or not.
If Rh+ve you don’t have Rh antibodies
If Rh-ve you don’t have antibodies unless transfused with Rh+ blood or pregnancy with Rh+ baby (father must be Rh+)
Pregnant women who are Rh- may be offered injection of antibodies against Rh+ to mop up any Rh+ RBCs that are released by baby into mothers circulation

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13
Q

White blood cells

A

Divided into 2 groups
Granulocytes-these have granules in cytoplasm. When they are stained, granules either turn red (eosinophils, blue, basophils or don’t stain (neutrophils)

The most common are neutrophils

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14
Q

Neutrophils

A

Constantly circulate in blood & lymph.

Attracted to dead cells or bacteria in tissue.

Squeeze through gaps in capillary walls to engulf the bacteria inside cell (phagocytosis) and expose it to toxic chemicals within their lysosomes.

Pus is dead tissue, bacteria, live and dead neutrophils

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15
Q

Other granulocytes

A

Eosinophils
Red staining of granules
Specialist cell to deal with parasites to big to be phagocytosed by releasing toxic chemicals around parasite.
Especially worms

Also involved in allergic inflammation such as asthma.

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16
Q

Other granulocytes pt2

A

Basophils
Granules stain blue
Basophils circulate in blood
Mast cells similar but fixed in tissue
Associated with autoimmune inflammatory processes as they contain histamine

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17
Q

Agranulocytes

A

Lymphocytes circulate in blood and present in lymph nodes
Subdivided into B-lymphocytes that make antibodies
T-lymphocytes involved in immune response but don’t make antibodies

Monocytes are long lasting phagocytic cells (unlike neutrophils)
Some are mobile, others are fixed to do specific monitoring roles and called macrophages (big eaters) where they influence immunity by releasing chemicals called cytokines

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18
Q

Platelets

A

Small, no nucleus.
Bud off from megakaryocytes in red bone marrow
Circulate in blood
Form platelet plug to control bleeding (haemostasis)
Release chemicals that promote vascular spasm and blood clotting.

Aspirin reduces the stickiness of platelets

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19
Q

Haemostasis

A

A sequence of responses that stops bleeding.

When blood vessels damaged, the haemostatic response must be quick, localized to region of damage, and carefully controlled.

Three mechanisms are involved:
vascular spasm,
platelet plug formation,
blood clotting (coagulation).

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20
Q

Haemostasis pt 2

A

Vasoconstriction reduces blood flow to region
Platelets sense defect and become activated (sticky) and release further vasoconstrictors.
Platelets from a plug where platelets bind together and to vessel wall.
Activate clotting factors circulating in blood to convert to active forms and make fibrin clot

21
Q

Clotting cascade

A

Multiple clotting factors involved
Final stages are activating prothrombin to thrombin and fibrinogen to fibrin
Deposits as threads and traps blood cells and other proteins (plasminogen) in blood clot.

22
Q

Blood clot

A

Plasminogen trapped in clot will eventually be activated to plasmin and dissolve clot

23
Q

When things go wrong

A

Anaemia
Low haemoglobin levels/red blood cells
Multiple causes:
-Production inefficient
-Blood loss more than normal
Patient may be tired/breathless/pale looking

24
Q

Terms used to describe RBCs

A

Normochromic-normal colour
Normocytic-normal size
Microcytic-small
Macrocytic-larger than normal
Hypochromic-paler than normal
Haemolytic-destruction faster than normal
Megaloblastic-cells large & immature

25
Q

Iron deficiency anaemia

A

May be inadequate intake (major source red meat)
Inability to absorb the Fe from gut (Malabsorption)
-coeliac disease reduces surface area of small intestine)
Higher than normal requirements
-Pregnancy
-heavy periods

Increase blood loss- cancer colon

26
Q

Iron deficiency anaemia

A

RBCs smaller and paler

27
Q

Pernicious anaemia

A

RBCs are large and may keep nuclei
Due to folate deficiency or B12 deficiency

Folate deficiency due to dietary intake
Vitamin B12 deficiency often due to failure to absorb vitamin.
Stomach produces a protein (intrinsic factor) that binds B12 to allow it to be absorbed in small intestine.
Autoimmunity against these cells causes B12 deficiency

28
Q

Haemolytic anaemia

A

RBCs are destroyed faster than normal
Bone marrow can’t keep up

Sickle cell anaemia
Genetic sequence for Hb different causing amino acid changes.
When deoxygenated, shape of RBCs changes to sickle shape.
Body senses these and rapidly destroys them.
Sickling also blocks small capillaries.
Causes obstruction blood flow

29
Q

White cell disorders

A

Neutropenia
Granulocytes low
Indicates damage in bone marrow-chemicals, bone marrow disorders, chemotherapy
Risk of infections increased

Leucocytosis
Raised WBCs
Normal response to infections-returns to normal
Long term-leukaemia

30
Q

Leukaemia

A

Causes
Genetic factors-changes in DNA occur in everyone over time
Increased with ionising radiation or chemicals

Acute leukaemia’s
Bone marrow taken over by the cancer cells so RBCs and platelets may reduce

Chronic leukaemia less aggressive but may progress to more acute type eventually.

31
Q

Haemorrhagic disease

A

Thrombocytopenia
Lowered platelets
Reduced production
-e.g., in leukaemia
Ionising radiation
Chemotherapy
Increased destruction

32
Q

Abnormalities of clotting factors

A

Dietary
-Vitamin K (fat soluble vitamin stored in liver)
-Liver disease
-coeliac disease

Congenital disorders
Haemophilia
-Genes present on X chromosome

33
Q

Haemophilia A & B

A

Congenital disorders
Genes present on X chromosome
Mainly affects males as only have 1 X chromosome.
Main type Factor VIII (8) deficiency Haemophilia A
Factor IX (9) deficiency called Haemophilia B

Treatment with fresh frozen plasma or recombinant factor 8 (or 9)

34
Q

Inflammatory response

A

Red, hot, swollen, painful

= Increased blood flow, fluid accumulation, inflammatory mediators released

Fluid accumulation-capillary leakage
Increased body temperature interleukin-1 from WBCs

Pain –compression nerves and release of chemicals that increase nerve sensitivity

35
Q

Antibody-mediated immunity

A

When B-cells meet antigen they have receptor for, they proliferate and differentiate into plasma cells, making antibodies against antigen.

They also interact with t-cells increasing cell mediated killing of microbe.

Plasma cells that make antibody are short lived.

Memory B-cells long lived & respond to second exposure

36
Q

5 types of antibodies

A

After antigen exposure, first Ab is IgM, then changes to IgG.

37
Q

Immunoglobulin A
(gA)

A

Found in body secretions like breast milk
and saliva, coats epithelial membranes and
prevents antigens crossing them and invading
deeper tissues

38
Q

IgD

A

made by B cells and displayed on their surfaces. Antigens bind here to activate B cells

39
Q

IgE

A

Found on cell membranes of, for example,
basophils and mast cells; if it binds its antigen,
it activates the inflammatory response. This
antibody is often found in excess in allergy

40
Q

IgG

A

Is the largest, longest-lived and most common
antibody type. It attacks many different
pathogens and crosses the placenta to
protect the fetus

41
Q

IgM

A

Produced in large quantities in the pi nery
response and is a potent activator of
complement

42
Q

Cell-mediated immunity

A

Macrophages phagocytose microbe & put bits of microbe onto its surface to signal to T-cells. (Macrophages are antigen presenting cells)
Cytotoxic T-cells kill antigen/microbe
Helper T-cells stimulate T-cell response and antibody (B-cell responses)
-release cytokines to signal extra response
-these cells infected by HIV
Regulatory T-cells turn off response-sometimes faulty in autoimmune responses
Memory T-cells-long lived rapid response if re-exposure

43
Q

Interdependence of T- and B- cells

A

T helper cells release cytokines that stimulate T-cell and B-cell responses

44
Q

Types of acquired immunity

A

Active naturally acquired-e.g., catch chickenpox (clinical and subclinical infection as with covid.)

Active artificially acquired- e.g., vaccination

Passive naturally acquired- maternal foetal transfer through placenta or breast milk

Passive artificially acquired-injection with antibodies-e.g., Rh antibodies

45
Q

When things go wrong

A

Immunodeficiency

Primary-genetic defect

Secondary-severe malnutrition, leukaemia, chemotherapy, splenectomy, HIV infection

46
Q

Hypersensitivity(allergy)

A

When immune response out of proportion to something that is generally harmless

47
Q

Autoimmune disease

A

Immune response against self. Examples:

Rheumatoid arthritis-synovial membrane of joints
Graves disease-Ab bind to TSH receptors in thyroid and cause XS thyroxine release
Glomerulonephritis-glomerular membranes
Type 1 diabetes-pancreatic islet beta-cells

48
Q
A

human bio (10 decks)

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