Bsi Test 1

Front 1

What is the functions of blood?

Back 1

1)Transports Oxygen, waste products, nutrients, hormones, enzymes

2)Regulates blood clotting, body temperature, Ph balance (contains compounds and ions), and fluid levels

3)Protects against pathogens through lymphocytes

Front 2

What are Erythrocytes?

Back 2

RBC's that lack nuclei, have a bi-concave shape, and contains hemoglobin that carries up to 4 oxygens to tissue and CO2 back to the lungs

Front 3

What are the functions of blood plasma?

Back 3

To carry nutrients, hormones, waste products, antibodies, and proteins

Front 4

What are Albumins and their function?

Back 4

Albumins are the smallest and the most abundant of the plasma proteins

They regulate water movement between blood and intersitial fluid. And they act as transport proteins to carry ions, hormones, and lipids

Front 5

What are Globulins and their function?

Back 5

Globulins are the second largest group of plasma proteins

Also known as Ig, they are secreted by B-cells to protect the body

Alpha-globulins and larger beta-globulins bind, support, and protect water-insoluble molecules

Front 6

What is Fibrinogen and its function?

Back 6

Fibrinogen is a plasma protein responsible for blood clot formation

Front 7

Name the different types of Leukocytes.

Back 7

Granulocytes
1)Neutrophils: are phagocytic
2)Eosinophils
3)Basophils: allergic reactions b/c they release histamine

Monocytes: become macrophages

Lymphocytes: become B/T cells which secret antibodies and mount immune responces

Front 8

What is Erythropoesis?

Back 8

The production of RBC's

Front 9

Where are RBC's produced?

Back 9

Up until about 20 years old RBC's are prduced in the marrow of the femur and tibia

After 20, they are produced in the marrow of the vertebra, sternum, and ribs. But there production decreases with age

Front 10

What is Hemopoiesis?

Back 10

It is the production of blood cells from pluripotential (undifferentiated) hemopoietic stem cells

Front 11

What types of cells can be produced from pluripotent stem cells?

Back 11

The cells either become myeoloid: erythrocyte, platelets, macrophages, neutrophils, eosinophils, or basophils

Or they become Lymphoid: B/T cells

Growth and differentiation of these cells is dependent on enviornemntal factors

Front 12

What are Megakaryocytes?

Back 12

They are cells that remain in the bone marrow near blood sinuses. They extend processes into the blood vessel and release platelets

Front 13

What are the stages of RBC differentiation?

Back 13

1) Pronormoblast (proerythrocyte): youngest RBC, once formed it divides several more times

2) Early Normoblast (basophilic normoblast): small nucleus, chromatin is dense, very little hemoglobin

3) Intermediate Normoblast (polychromatophilic normoblast): Nucleus is dense and cytoplasm shows signs of hemoglobin production

4) Late Normoblast (orthochromatic normoblast): Nucleus is very dense and cytoplasm is almost full of hemoglobin

5) Reticulocyte: the RBC extrudes the nucleus and is finished

Diapedesis: the RBC passes from the marrow into the blood where it will fully mature in 1-2 days

Front 14

What is Erythropoietin and its function?

Back 14

It is a hormone mainly produced by the kidney (renal tubular epithelial cells) that stimulates RBC production by increasing the production of pronormoblasts from stem cells

Front 15

What is Hemostasis and the steps involved?

Back 15

It is the prevention of blood loss by:

1) Vascular compression caused by thromboxane A released by platelets, nervous reflexes, and local humoral factors from traumatized factors

2) Formation of platelet (thrombocyte) plug. Platelets adhere to damaged cells by means of glycoproteins (exposed collagen and laminin), after adherence they swell and secret ADP and thromboxane which will cause more platelet adherence, this is activated by thrombin

3) Formation of blood clot: Prothrombin activator forms as a result of blood vessel damage. In the presence of sufficient Ca, prothrombin activator converts prothrombin (a plasma protein made continually by the liver) is converted into thrombin. Thrombin enzymatically converts fibrinogen into fibrinogen monomers which will polymerize into fibrin fibers. These cross-link to form the clot.

4) Plasminogen is trapped in clots as they form. Damaged tissue releases tissue plasminogen activator (t-PA) which cverts plasminogen into plasmin (a proteolytic enzyme) which removes the clot. Plasmin can digest Factors V,VIII,XII, and prothrombin. Free circulating plasmin is inhibited by antiplasmin

Front 16

Describe the Extrinsic Pathway of Hemostasis?

Back 16

1) Tissue trama releases Factor III (tissue factor)

2) Factor III along with Factor VII in the presence of Ca activates Factor X

3) Factor Xa along with Factor III and Factor V, in the presence of Ca, forms prothrombin activator

Front 17

Describe the Intrinsic Pathway of Hemostasis?

Back 17

1) Blood trauma activates Factor XII and releases platelet phospholipids

2) Factor XIIa activates Factor XI

3) Factor XIa activates Factor IX

4) Factor IXa in conjunction with Factor VIIIa (antihemophilla factor), platelet phospholipids, and Factor III activates Factor X

5) Factor Xa along with Factor III and Factor V, in the presence of Ca, forms prothrombin activator

Front 18

Explain the importance of Vitamin K.

Back 18

Vitamin K, which is continually made in the GI tract by bacteria, is necessary for the formation of Prothrombin, Factors VII, IX, and X, and Protein C

Vitamin K is fat-soluble and a GI disease or liver disease (failure to secrete bile which aids in digestion) can cause a decrease in Vitamin K absorption

Front 19

Explain Hemophilia.

Back 19

1) Hemophilia A (Classic Hemophilia): is the most common form (85%). It arises from a variety of mutations in the Factor VIII gene which is important for activating Factor X

Patients suffer joint and muscle hemorrage, easy bruising and prolonged bleeding.

Treatment is acomplished by the infusion of Factor VIII concentrates

2) Hemophilia B: is caused by a deficieny (due to mutations) in Factor IX. Clotting will occur it just takes longer

Front 20

Describe the three inherited disorders in fibrinogen

Back 20

1) Afibrinogenemia: (a complete lack of fibrinogen) this is an autosomal recessive disease that is very rare

2) Hypofibrinogenemia: (reduced levels of fibrinogen) characterized by levels being below 100mg/dl (normal is 250-300) and it can be acquired or inherited

3) Dysfibrinogenemia: (presence of dysfunctional fibrinogen) this condition is extremely heterogenous (different) affecting any of the functional properties of fibrinogen

There can also be deficiencies in fibrin stabilizing factor (Factor XIII)

Front 21

Describe von Willebrand Disease (vWD)

Back 21

This disease is due to an inherited deficiency in von Willebrand factor (vWF) and is the most common inherited bleeding disorders (occuring 2x more frequently then hemophilia A).

The result of this disease is defective platelet adhesion and it causes a secondary deficiency in Factor VII (b/c vWF helps stabilize Factor VIII)

Front 22

Describe Antithrombin Deficiency

Back 22

Antithrombin inhibits thrombin, Factor IX and X by forming a stable complex with them.

Deficiencies (autosomal dominant) results from mutations that affect its synthesis or affect its heparin binding site. Heparin increases the activity of antithrombin by 1000x.

Symptoms could include deep vein thrombosis and pulmonary embolism

Front 23

Explain Thromboembolic conditions

Back 23

1) Left side emboli, originating in left side of the heart can travel to the brain or kidneys.

2) Right side emboli, originating in the venous system can plug vessels in the lung causing pulmonary embolism.

These conditions are almost always caused by the slowing of the blood which allows for accuminlation of procoagulants

Front 24

How would one treat or prevent intravascular clots?

Back 24

1) An injection of Tissue Plasminogen Activator (t-PA) would help disolve the clot.

2) Streptokinase can be given to activate plasminogen to plasmin

3) Drugs like Plavix inhibits ADP from binding to its receptor. ADP and thromboxane A activates other platelets causing them to adhere to the origional platelets (by means of changing their shape)

Front 25

Describe Hemoglobinopathy

Back 25

1) Qualitative abormalities: (sickle cell anemia) has a mutation in the beta-globin that converts a glutamic acid codon (GAG) into a valine codon (GTG), resulting in heoglobin tetramers that cluster upon deoxygenation in the tissue.

The sickling of the cells makes them inflexable and causes them to clog the fine blood capillaries

2) Quantitative abnormalities: are mutations in hemoglobin synthesis.

Front 26

What are the two types of resistance?

Back 26

1) Innate (nonspecific) defenses: are present at birth and provide immediate but general protection against pathogens. Mechanical and chemical barriers like the skin and mucus membranes are the first line of defence.

2) Immune defenses: developes more slowly and involves activation of specific lymphocytes (T/B Cells) to fight pathogens.

Front 27

Explain the Lymphatic System

Back 27

The begining of the lymphatic system is the lymphatic capillaries. The end of endothelial cells overlap and form the capillaries, allowing for leakiness. As fluid pressure increases, anchoring filaments connecting the capillaries to surrounding tissue pulls the capillaries open, allowing for intersitial fluid to enter

Lymph is intersitial fluid that has passed into lymphatic vessels, these vessels are a passive return system that allows fats, proteins, and microorganisms (macrophages) to easily enter.

The functions of lymphatic vessels are to allow defense cells to migrate, allow pathogens to be transported to lymph nodes, and help maintain fluid balance.

Lymphatic vessels flow through lymph nodes (which are encapsulated by masses of B/T Cells). After exiting the nodes, lymph passes from trunks into two main channels:

1) Thoracic (left lymphatic) duct: is the main duct for return of lymph to blood that drains into the left subclavian vein.

2) Right lymphatic duct: drians into the right subclavian vein.

Front 28

Map the flow of lymph

Back 28

1) Blood Capillaries
2) Intersitial spaces
3) Lymphatic Capillaries
4) Lymphatic Vessels
5) Lymphatic Ducts
6) Subclavian Veins

Front 29

List and describe Primary Lymphoid Organs

Back 29

1) Red Bone Marrow: is found in flat bones and in the epiphyses of long bones. Hemopoietic stem cells give rise to lymphoid cells which form B/T Cells. (T Cells must travel to the thymus to become immunocompetent)

2) Thymus: is a bi-lobed organ located behind the sternum. It contains lobules that are seperated by trabecula. The outer cortex of the lobule contains a large number of T Cells, dendritic cells (assist T Cells in maturation by presenting antigens), epithelial cells (thought to aid in the maturation of T Cells), and macrophages.

Only about 2% of T Cells survive maturation and enter the inner medulla of the lobule.

The Inner Medulla contains mature T Cells, epithelial cells, dendritic cells, macrophages, and thymic corpuscles (which are epithelial cells arranged into concentric layers that degenerate and become filled with karatin)(May also be the site of T Cell death)

Front 30

List and describe Secondary Lymphoid Organs

Back 30

1) Spleen: is the largest single mass of lymphatic tissue that contains a hilus were the splenic artery and vein form.

White Pulp: is lymphatic tissue arranged around branches of the splenic artery. This tissue contains lymphocytes (B/T Cells) and macrophages.

Red Pulp: contains blood filled venous sinuses and splenic cords which contains erythocytes, macrophages, lymphocytes, plasma cells (Mature B Cells), granulocytes (neutrophil, eosinophil, basophil). It is also responsible for about 1/3 of the bodies platelet supply.

2) Lymph Nodes: The outer cortex contains primary lymphatic nodules which primarily contains B Cells, and sceondary lymphatic nodules which form in responce to antigens and form plasma cells and memory B cells.

The inner cortex of the lymph node, which does not contain nodules, houses T-Cells and Dendritic cells (which present antigens to the T-Cells and activate them).

The Medulla of the lymph node contains B-Cells, Plasma Cells, and Macrophages that have migrated from the cortex.

Foreign substances are trapped by reticular fibers within the sinuses of the node. Macrophages and Lymphocytes destroy them.

Front 31

Describe the first line of defense for the innate immune system

Back 31

1) Skin: contains tight junctions that prevent easy entry. Shedding removes microbes, and the low pH of secretions inhibit bacterial growth.

2) Mucus Membranes: mucus is primarily made of mucin and its viscosity allows it to trap microbes. Mucus also contains Defensins which is an antimicrobial peptide that can kill +/- bacteria and enveloped viruses like HIV.

Front 32

Describe the Complement System

Back 32

The main functions of the complement system is to recruit inflammatory cells, opsonization of pathogens (coating them with opsin, like C3b or IgG, in order for the pathogen to be destroyed), or direct killing of the pathogen by late complements.

The complement system is activated by three pathways, all of which activate C3:

1) Classical pathway: the binding of IgG or IgM antibodies.

2) Lectin pathway: the binding of MBL to bacterial surfaces which activates C4 and C2.

3) Alternative Pathway: C3 is spontaneously activated and C3b attaches to host cells or pathogens. (Activation of Classical and Lectin Pathways activates this pathway)

After C3 is activated, C3b binds to the membrane of the pathogen, confining complement activation to the pathogen only. Smaller C3a and fragments of C4 and C5 promote inflammation by recruiting phagocytes and lymphocytes.

C3b can also activate C5b, which forms a membrane attack complex (the binding of C5b,C6,C7,C8,C9) (C7 causes the complex to bind to the membrane) (C9 punches a hole in the membrane causing it to lyse)

Many activated components of the complement system are inherently unstable and rapidly become inactive unless they bind to another complement.

Front 33

What can activate Helper T Cells?

Back 33

1) Dendritic Cells (antigen-presenting cells)

2) Memory B-Cells

Front 34

How are Helper T Cells activated?

Back 34

Two signals are needed to activate Helper T Cells.

1) Class II MHC complex containing a peptide fragement binds to the Helper T Cell. (Co-stimulatory proteins CD4 or CD8(killer T-Cells) is released that activates Lck within T-Cell, Lck phos. CD3, ZAP-70 docks to phos-CD3, LCK activates ZAP-70)

2) B7 proteins expressed by the antigen-presenting cell binds to the CD28 receptor on the Helper T-Cell

After the Helper T-Cell is activated it secretes IL-2 and presents IL-2 receptors on its surface. This allows for proliferation and differentiation.

Once activated T-Cells express CTLA-4 which binds to B7 proteins on antigen-presenting cells thus keeping activation in check.

Front 35

What is a Type 1 Hypersensitivity Reaction?

Back 35

A Type 1 Hypersensitivity Reaction (immediate or anaphylactic) may involve reaction on the skin, eyes, nose, throa, or gut.

Reaction time is usually 15-30 minutes from time of exposure. It is IgE mediated and primarly contains mast cells and basophils.

Front 36

What is a Type 2 Hypersensitivity Reaction?

Back 36

A Type 2 Hypersensitivity Reaction (cytotoxic) normally contains antigens that are endogenous.

Reaction time is minutes to hours. It is mediated by IgM or IgG and complement to heighten response, also contains neutrophils.

Front 37

What is a Type 3 Hypersensitivity Reaction?

Back 37

A Type 3 Hypersensitivity Reaction (immune complex) may be general or involve individual organs.

Reaction time is 3-10 hours. It is mediated by soluble immune complexes (Mainly IgG or IgM bound to antigen) and complements (C3a, C4a, C5a). The damage is done by platelets and neutrophils.

Front 38

What is a Type 4 Hypersensitivity Reaction?

Back 38

A Type 4 Hypersensitivity Reaction (cell mediated) can be caused by autoimmune, infectious diseases (tuberculosis, leprosy), or contact dermatitis (poision ivy).

Reaction peaks at about 48 hours. It is mediated by T-Cells, there are no antibodies involved.

Front 39

Explain what is meant to be atopy

Back 39

When someone is atopy they tend to produce high levels of IgE antibodies, which will allicate an allergic reaction.

The activation of Helper 2 T-Cells is responsible for the evelated IgE levels. This is due to the fact that the body has not gone through "immune deviation" and antigen-presenting cells are releasing IL-4 and IL-13 instead of IL-12, which is causing more TH2 cells to activate more B-Cells that produce IgE (with the help of NF-kb and STAT-6)

This condition can be genetic or related to the type of enviornment the patient lived in. Possible treatments include IFN-y(activates macrophages not B-Cells), IL-12/18(stimulates TH1).

Front 40

List and explain the 8 steps of HIV replication

Back 40

1) Attachment: The virus binds to the CD4 receptor on the Helper T-Cell via gp120, then it binds to the cytokine receptor (CCR5 or CXCR4) to activate internalization.

2) Virus Internaliation: the virus evelope peptides fuse with the Helper T-Cell membrane. The HIV fusion protein inserts and interacts with the cell membrane, rearrangement of the fusion protein provides the energy needed for the virus to fuse into the cell (fusing w/h the cell uncoates the virus).

3) DNA Synthesis: copies of the RNA are made then mirror copies are reverse transcribed to make double stranded DNA (takes place in cytosol)

4) Integration: the dsDNA enters the nucleus. Integrase inserts the dsDNA into the chromosomal DNA.

5) Transcription: the virus now utilizes the T-Cell's transcription factors and RNA polymerase in order to convert it's viral DNA into mRNA.

6) Translation: T-Cell's own rRNA are used to make viral polyproteins.

7) Cleavage: the protease cuts the viral polyproteins into individual proteins to make new copies of the virus (what is found in the origional HIV virus)

8) Assembly: proteins and viral RNA are assembled into new virus envelope and exocytosed from the cell.

Front 41

Explain the 4 phases of deep wound healing

Back 41

1) Inflamation: a blood clot forms on the surface and blood vessel which loosely unites wound edges. Vasodilation occurs and and infiltration of neutrophils, macrophages, and mesenchymal cells (produce fibroblasts).

2) Migratory phase: clot becomes scab, epithelial cells migrate beneath scab to bridge wound. Fibro blasts begin making collagen fibers and glycoproteins (scar tissue) and damaged blood vessels begin to re-grow.

3) Proliferation phase: continued epithelial, fibroblast, and vessel growth.

4) Maturation phase: Scab sloughs off, collagen fibers become more organized, and vessels are resotred.

Front 42

List and describe the 5 layers of the epidermis

Back 42

1) Stratum Basale (deepest/bottom layer): is a single row of cuboidal or columnar kerantioncytes that is attached to the dermis. It contains stem cells that can develope into keratinocytes and migrate up.

Consists of Melanocytes, Langerhans cells, and Merkel cells.

2) Stratum Spinosum (thornlike): is made up of 8-10 layers of keratinocytes (some of which are able to divide) containing Langerhans cells and Melanocytes.

3) Stratum Granulosum (Important transition layer): contains 3-5 layers of cells undergoing apoptosis. It contains keratohalin which converts tonofilaments into keratin and contains lamellar granules retard water loss and penetration of microbes.

4) Stratum Lucidum (present only on hairless areas): contains 3-5 layers of flattened dead keratinocytes, which is needed for areas of high friction.

5) Stratum Corneum (horn): contains 25-30 layers of dead keratinocytes for protection. This layer is continuously shed and replaced and between teh cells are lipids from lamellar granules.

Front 43

Describe the two regions of the dermis

Back 43

1) Papillary region: is about 1/5 of the total dermis and it consists of areolar connective tissue and fine elastin fibers.

The dermal papillae contains capillary loops, Meissner corpuscles (touch receptor), and free nerve endings (pain and temperature).

2) Reticular region: is located in the deeper dermis and consists of dense irregular connective tissue (which consists of bundles of collagen and course elastin fibers).

Located in this region are adipose cells, hair follicles, nerves, sebaceous glands (oil), and sudiferous glands (sweat).

Front 44

Describe the Subcutaneous layer

Back 44

It is a layer that lies below the dermis but is not part of the skin. It consists of areolar and adipose tissue.

Fibers that extend from the dermis anchor the skin to the subQ (subQ then anchors to underlying tissue and organs)

The subQ layer stores fat, blood vessels that nourish the skin, and contains Pacinian corpuscles (pressure receptors)

Front 45

List and describe the different types of glands found in the skin

Back 45

1) Sebaceous glands (oil): are simple branched acinar glands that lies in the dermis and opens into the neck of a hair follicle.

It secretes sebum which is a triglyceride, cholesterol, and protein mixture meant to prevent drying and moisture lose.

2) Sudoriferous gland (sweat): the Eccrine sweat gland secrets less viscous (active) sweat and is used for temperature regulation and waste removal.

The Apocrine sweat gland mostly found in the subQ secrets more viscous sweat used scent.

3) Ceruminus gland: is a modified sweat gland found in the subQ layer and opens directly into the ear that secrets a waxy substance used to trap microbes

Front 46

What can Plasmin digest?

Back 46

1) Digests fibrin fibers
2) Fibrinogen
3) Factor V
4) Factor VIII
5) Prothrombin
6) Factor XII

Front 47

List and describe the different classes of Helper T-Cells

Back 47

1) TH1: when an antigen presenting cell activates a Helper T-Cell, that dendritic cell can release different cytokines to cause the Helper T-Cell to differentiate. If the dendritic cell relases IL-12 then the TH will differentiate into a TH1 and that TH1 can activate macrophages by presenting them with a MHC II complex, CD40 ligand, and release IFN-y. They can also activate cytotoxic T-Cells b/c IFN-y increases the efficiency of antigen presentation by dendritic cells to T-Cells.

2) TH2: if the dendritic cell releases IL-4, then the TH will differentiate into a TH2. That TH2 can activate B-Cells by presenting it with a MHC II complex and a CD40 ligand. These TH2 cells also release IL-4, IL-13, IL-5, IL-10.

Front 48

Describe IgA

Back 48

IgA is a secretory Ig found in tears, saliva, milk, respiratory and intestional secretions.

IgA is an eight chain dimer that can bind to 4 different antigens. It can neutralize various toxins and metabolites.

Front 49

Describe IgD

Back 49

IgD is mainly found inserted into the membranes of B-Cells and plays a role in B-Cell maturation.

Front 50

Describe IgM

Back 50

IgM is the first class of antibody made by the developing B-Cell. It is also the major antibody secreted in responce to an initial exposure to an antigen.

It is a pentameric molecule that can bind to 10 different antigens. It is used to opsonize antigens and its presence in the blood stream indicates a recent infection.

Front 51

Describe IgE

Back 51

IgE antibodies bind to the Fc receptors of mast cells and basophils. They act as a receptor for these cells and plays a big role in allergic reactions, due to mast/basophils releasing histamin and cytokines that can cause inflammation.

It is a four chain dimer (Y-shaped) that can bind to 2 different antigens.

Front 52

Describe IgG

Back 52

IgG is the major antibody found in the blood. It is produced in large quanties during the secondary immune responce.

It is used for opsinaziation and it's tail (Fc) region triggers phagocytosis by macrophages.

It is Y-shaped and is the only antibody passed from mother to fetus via placenta.

Front 53

How can T-Cells kill target cells?

Back 53

1) T-Cells can bind to target cells and focus their centrosome and Golgi on the target cell and release Perforin, which punches a hole in the target cell. Then the T-Cell releases Granzyme B which enters the cell via the perforin channel and activates the caspase cascade.

2) The T-Cell can also express the Fas ligand which binds to the Fas receptor on the target cell causing the "death domain" of the Fas receptor to recruit procaspase-8 which cross-cleave each other and activate the caspase cascade.

Front 54

Explain how the TLR-4 is activated

Back 54

1) LPS binds to LBP in blood
2) LBP binds to CD14
3) CD14 complex activates TLR4
4) Adapter protein MyD88 is recruited
5) MyD88 recruits IRAK
6) IRAK autophosphorilates and activates TRAF6
7) TRAF6 activates TAK1
8) TAK1 leads to the activation of NF-kb and the activation of Jun/Fos which leads to the transcription of target genes

Front 55

What are Keratinocytes?

Back 55

They are found in about 90% of epidermal cells and are release Lamellar granules that helps prevent against mositure lose

Front 56

What are Melanocytes?

Back 56

They are found in about 8% of eipdermal cells and are used to protect keratinocytes against UV damage