Lecture 2-Exam 2 Flashcards
1
Q
What are the blood functions (4)
A
- Transport-> solutes, gases, hormones
- Homeostasis-> for BP
- Hemostasis
- Immunity-> WBCs that travel in blood
2
Q
What is the blood composition? (with percentages)
A
3
Q
What are anticoagulants? What is prevented?
A
- EDTA, citrate, or heparin (from basophils)
- Prevents Ca2+ binding (Ca2+ critical blood clotting)
4
Q
What is therapeutic plasma exchange?
A
Plasmapheresis
5
Q
What are the main osmotically active plasma solutes?
A
Na+ Cl− and HCO3− main osmotically active plasma solutes. Osmotic pressure changeable.
6
Q
What do the proteins in the blood form? Is it unstable or stable?
A
Proteins in the blood form the oncotic pressure, also known as colloidal osmotic pressure. Relatively stable
Proteins pull water over
7
Q
Is plasma charged? If so what is the charge?
A
Plasma is electroneurtral
8
Q
What are the different plasma proteins and their function?
A
9
Q
What are the different plasma lipids?
A
- Cholesterol: free cholesterol and cholesterolester
- Triglyceride
- Phospholipids
10
Q
What are the different plasma lipoproteins?
A
- Apoprotein (apo)
- Lipoprotein (apoptein+lipids): below is from low density to high density
* Chylomicron (CM)
* VLDL
* LDL
* IDL
* HDL
11
Q
A
Na+: extracellular
12
Q
A
Chloride: extracellular
13
Q
What are the main extracelluar cation and anion?
A
NaCl
14
Q
What are carbohydrates in the blood
A
Glucose
15
Q
- What are the break down by-products of lipids in the blood?
- What are the lipid and water soluble Vitamins?
A
- By-products: ketones
- Lipid: Vit A,D,K,E
- Water: Vit B12, and C
16
Q
- Elevated LDL increased risk of what
- What does reduced HDL levels indicate?
- Who has high triglyceride levels?
- What are other risk predictors of CVD?
A
- Elevated LDL (the form that takes cholesterol to tissues), increases risk of cholesterol plaque buildup in arterial walls (atherosclerosis)
- Reduced HDL levels indicate decreased ability to remove excess cholesterol.
- Many people with obesity, heart disease, and/or diabetes also have high triglyceride levels.
- Several ratios, such as the LDL/HDL ratio and the total cholesterol/HDL ratio, are also used as risk predictors.
17
Q
- What is elevated in hepatitis?
- What is increased with bile duct obstruction?
- What is used to monitor general liver damage?
A
- ALP is elevated in hepatitis
- ALT is commonly increased with bile duct obstruction
- AST levels are used to monitor general liver damage
18
Q
- What is bilirubin? What is it produced by?
- Depending on its form, bilirubin levels can be used to identify what?
A
- Bilirubin is a waste product of the liver, produced from RBC breakdown and recycling.
- Depending on its form (conjugated or unconjugated), bilirubin levels can be used to identify a problem that occurs before the liver (e.g., hemolytic anemia), a problem within the liver (e.g., cirrhosis), or a problem after the liver (e.g., bile duct blockage).
19
Q
- Abnormalities in an electrolyte panel (i.e., electrolytes and HCO3−) commonly what?
- What components are used to assess liver health and function?
A
- Abnormalities in an electrolyte panel (i.e., electrolytes and HCO3−) commonly predict problems with fluid balance, such as edema or hypertension.
- The * components are used to assess liver health and function.
20
Q
What are all the cells in formed elements of blood?
A
21
Q
Hematopoietic stem cells reside predominately where? How is the stem cells pushed down a lineage?
A
Hematopoietic stem cells reside predominately in the red bone marrow (axial, humerus, hip, epipitis bone) and can be further differentiated into various lineages by a group of cytokines that are collectively called colony- stimulating factors.
22
Q
- Platelets come from what?
- Monocytes turn into what?
A
- Platelets are fragments of megakaryocytes
- Turns into a macrophage when in tissue
23
Q
What are eosinophils, basophils, monocytes, and lymphocytes?
A
- Eosinophils are inflammatory cells that defend against parasitic infections.
- Basophils release histamine, causing the inflammation of allergic and antigen reactions.
- Monocytes migrate from the blood stream and become macrophages.
- Lymphocytes contain three cell types that participate in the immune system.
24
Q
What are rough values of RBC, Hbg and Hct?
A
25
* In evaluating patients for hematologic diseases, it is important to determine what? Why?
* The Hct can only be used to determine what?
* determine the total number of circulating RBCs and the Hgb concentration in the blood
* This information is used to determine whether the patient is anemic.
* The Hct can only be used to determine anemia when fluid status is taken into account.
* With a given RBC count, Hgb, and Hct, several other important blood indices can be derived.
26
What is normal, low and high hematocrit including the disease?
27
RBC:
What binds reversibly and irreversibly?
* O2 binds reversibly to iron atoms in heme (**oxyhemoglobin**).
* CO2 binds reversibly to globin (**carbaminohemoglobin**).
* CO binds almost irreversibly
28
Where do each one bind to:
* Co2:
* O2:
* Co2: globin part
* O2: heme part
29
Where can mutations be in RBCs? What does it lead to?
Mutations can occur anywhere in the five gene loci resulting in the production of abnormal Hgb molecules leading to hemoglobinopathies:
* sickle cell anemia
* thalassemias
30
What is the pathway if a person is hypoxemia?
31
What is the lineage of forming RBC?
32
What are the precursors of RBCs?
* Amino acids
* Iron
* Folic acid
* Vit B12: absorbed by intrinsic factor and if low->pernicious anemia
33
How is red blood cells broken down?
34
What are the two different areas of the spleen?
* Red pulp: RBC degrade
* White pulp: Immune fxn
35
What are the three RBC diseases d/t change in size?
36
What are the three RBC diseases d/t change in shape?
37
What are the three RBC diseases d/t change in color?
38
What are the three RBC diseases d/t being immuture cells?
39
What are the four RBC diseases d/t other issues?
40
What is the normal shape, diameter of a RBC? What does RBC contain?
Erythrocytes have the shape of biconcave disks, with a diameter of about 7 μm and a maximum thickness of 2.5 μm. They contain several hundreds of hemoglobin molecules, each consisting of four polypeptide chains (two α and two β), with each chain containing iron bound to its heme group.
41
* Unconjugated and conjugated bilirubin is measured clinically to detect and monitor what?
* Blood samples with high bilirubin are said to be what?
* Where is jaundice seen?
* The increase in bilirubin to a level that can be visually detected is what?
* measured clinically to detect and monitor liver or gallbladder dysfunction
* Blood samples with high bilirubin are said to be **icteric**, which is evident as a yellow-green tint and increased stickiness.
* Those with icteric blood develop jaundice. The yellow coloration that is characteristic of jaundice can be seen in the skin, particularly under the fingernails.
* The increase in bilirubin to a level that can be visually detected is a serious situation because a high level of bilirubin that is not bound to plasma proteins is neurotoxic.
42
What are the 3 different causes of anemia?
43
44
What is erythroblastosis fetalis? Mothers are given what?
45
46
* Steps in phagocytosis and intracellular killing by what?
* What WBC is the first defensive cells to be recruited to a site of inflammation?
* Steps in phagocytosis and intracellular killing by neutrophils.
* Neutrophils are the first defensive cells to be recruited to a site of inflammation.
47
Platelets:
* How are they formed?
* What is the lifespan?
* What granules are in platelets?
*
* Platelets have an average lifespan of 15 to 45 days, but many of them are immediately consumed as they participate in day-to-day hemostasis
* Granules: Serotonin, Ca, Enzymes, ADP, PDGF
48
* Several factors stimulate megakaryocytes to release what?
* What are those factors?
* Release platelets within the bone marrow sinusoids.
* This includes the hormone thrombopoietin, which is mainly generated by the liver and the kidneys and released in response to low numbers of circulating platelets.
49
What is the structure of platelets? What do they possess?
Platelets have no nucleus but possess important proteins, nucleotide, and other factors, which are stored in intracellular granules and secreted when platelets are activated during platelet aggregation in response to vascular injury.
50
What are the steps after blood vessel trauma?
51
What are the factors in the coagulation cascade?
52
What is lymph, lymphatic vessels, lymphatic tissues, lymphatic organs?
* Lymph: The recovered fluid
* Lymphatic vessels: Transport the lymph
* Lymphatic tissues: Composed of aggregates of lymphocytes and macrophages that populate many organs in the body
* Lymphatic organs: Defense cells are especially concentrated in these organs. Separated from surrounding organs by connective tissue capsules
| UNDER LOW PRESSURE
53
Why do we have the lymph system?
Fluid is lost in the intitisal space and the lymph system picks it up to maintain fluid levels
54
What is primary and secondary lymphoid organs?
* Primary: thymus and bone marrow-> B+T cells mature here to become immunocompent
* Secondary: Tonsils and adenoids, lymph nodes, BALT (bronchi), spleen, MALT (mucosa), GALT (gastro)
55
Where can lymph be dumped back into the venous system?
* Right lymphatic duct: jxn at IJV and RSV
* Thoracic duct: jxn at IJV and LSV
56
* Pathogens contain what? What are different ones?
* What are immunogens?
* What are haptens?
* **Pathogens** contain antigens - some are surface antigens and some within the pathogen.
* **Immunogens** are antigens that activate the immune system
* **Haptens** are antigens that do not activate the immune system, but become immunogenic when
linked to a carrier molecule.-> Pollen
| * Infection activates the immune system.
* Self-tolerance
57
What is the break down of the innate and adaptive defenses?
58
What is immunity?
Resistance to disease
59
Dr. H notes: overview of immune system
As part of the innate immunity, the human body has natural measures to prevent entry of microbes. When these barriers are overcome, a foreign invader first encounters phagocytes. Complement may bind to the invader and facilitate its phagocytosis or lysis. Inflammation may develop. If the innate immune system cannot destroy the invader, the adaptive immune system is activated with T and B lymphocytes as its effectors. Although the innate and adaptive immune systems are characterized by contrasting functions and timing, they work closely together and rely on each other to succeed in removing invading pathogens.
60
What is the first, second and third line of defense?
61
What are t cells and b cells used for?
* t cells: pathogens that are intracellular (viral or cancer)
* B cells: pathogens that are extracellular
62
Skin and mucosa first line of defense: What are the functions of skin and mucous membranes?
* Skin: Mechanical barrier; dry, nutrient poor, acid mantle, antimicrobial (acidic) proteins, mucus with lysozyme (enzyme to breakdown microbe)
* Mucous membranes: mucus traps, lysozyme
63
fill in
64
Innate Internal Defenses
* When is protection given?
Protection if microorganisms invade deeper in tissues
65
Innate Internal Defenses:
* What are the immune cells
* What are antibacterial proteins?
* What this system cause?
A.- Immune Cells: Phagocytes, Natural Killer (NK) cells, Mast cells, WBCs
B.- Antibacterial proteins: Interferons, Complement proteins
C.- Inflammation
D.- Fever
66
Fill in for the immune cells of innate immunity
67
what are the steps in phagocytosis and intracellular killing by neutrophils?
68
What is evident in chronic granulomatous disease? What does it cause?
The important role of the **NADPH oxidase (NOX)** for efficient host protection against invading pathogens becomes evident in chronic granulomatous disease, which is caused by the lack of phagocytic NADPH oxidase and is characterized by recurrent life-threatening bacterial and fungal infections.
69
What are the steps for macrophages function?
70
How does the NK cells work?
71
* NK cells have same mechanism of action as what?
* NK cells are less what? What is this compared to?
* What do NK cells continually do?
* Same mechanism of action as a cytotoxic T-lymphocyte uses in the adaptive cellular immunity.
* NK cells are less specific in which pathogens they destroy compared to cytotoxic T-cells.
* NK cells continually patrol body looking for pathogens and diseased host cells, whereas T-cells must be activated.
72
* Cellular secretions of antimicrobial proteins do what?
* What are two types of antimicrobial proteins?
* Attack microbes or hinder their ability to reproduce
* Two types: Interferons and Complement proteins
73
What are interferons and what are their functions?
Viral infected cells secrete interferons
* An SOS to neighboring cells
Functions:
* Induce other cells to secrete Anti-viral proteins
* Activate macrophages and mobilize NK cells
74
Explain the whole process of interferons
75
What are complement proteins and what are the functions?
Complement proteins
* ~20 plasma proteins that circulate in an inactive form
* Major mechanism for destroying foreign substances
Functions of Activated Complement:
* Enhances inflammation
* Promotes phagocytosis
* Causes cell lysis
76
* What is inflammation?
* What are the key signs of acute inflammation?
A local defensive response to tissue injury, including trauma and infection
Key signs of acute inflammation:
1. Redness
2. Heat
3. Swelling
4. Pain
77
78
Fever:
* Results from what?
* What is the systemic response to?
* What is exposed to foreign substances? What do they secrete?
* What does pyrogens do?
* Results from trauma, infections, drug reactions, brain tumors, and other causes
* Systemic response to invading microorganisms
* Neutophils and macrophages exposed to foreign
substances secrete pyrogens
* Pyrogens reset the body’s thermostat upward
| Important to hide necessary things (zinc, etc) that pathogens need
79
Fill in for adaptive immunity
i. Specificity
ii. Diversity
iii. Memory
80
What is the process of immunocompetence of lymphocytes?
81
What is humoral immunity?
Humoral immunity is mediated by secreting antibodies
82
What is the process after b cells were activated?
Only the clone of the lymphocyte that has the unique ability to recognize the antigen of interest proliferates and generates progenitor cells. These cells are specific to the inducing antigen but may have different functions. In the case of B cells, plasma cell clones produce antibodies, and memory cell clones enhance subsequent immune responses to the specific antigen. In the case of T cells, the clones become either effector cells or memory cells. Clonal selection occurs in secondary lymph organs such as the local lymph nodes.
83
What does plasma cells need a lot of?
Lots of ATP+proteins for antibodies-> why we get tired
84
What type of cells prevent the over amount of Immune system cells
Reg or suppressor cells
85
What are the different antibodies + their structures and where does a pathogen bind?
* Antibodies are immunoglobulins (Ig) with five isotypes (IgA, IgD, IgE, IgG, IgM).
* The basic unit of each isotype is a monomer that consists of two heavy chains and two light chains held together in a Y-configuration by disulfide bonds. The heavy chains are different for the various isotypes.
* Each end portion of the “Y” is called Fab because it is the fragment that contains the antigen-binding site.
* When secreted from plasma cells, IgG, IgD, and IgE consist of one monomer, IgA of two (dimer), and IgM of five (pentamer).
86
* B cells receptors resembles what?
* What do t-cell receptors contain?
* The B-cell receptor resembles a membrane-associated Ig monomer
* The T-cell receptor contains a Fab-like structure.
87
88
When the antigen-antibody complex is formed in adaptive immunity, what are the different pathways that can be taken?
89
* What is the complement system? What does it contain and do?
* What is the difference of classical and alternative pathway?
* The complement system attacks the surface of foreign cells.
* Over 20 different complement (C) proteins supplement antibody activity in a cascade of events to eliminate pathogens.
* The goal is to produce opsonin C3b, anaphylatoxins, chemoattractants C4a, C3a and C5a, and the membrane attack complex (MAC).
* The MAC inserts into membranes of cells and causes their lysis.
* Antigen–antibody (Ag–Ab) complexes and other (e.g., C-reactive protein and lectin pathway components) activate the classical pathway.
* Spontaneously hydrolyzed C3 and pathogen surface molecules (e.g., lipopolysaccharides) activate the alternative pathway and other (e.g., lectin pathway components).
* The lectin pathway is initiated in response to microbial surfaces (mannose).
* The classical and alternative pathways use structurally different but functionally identical enzymes C3 convertase and C5 convertase.
90
What is the difference between a primary and secondary response to a pathogen (adaptive)?
91
For humoral immunity:
* What is naturally acquired and artifically acquired for both active and passive ways?
92
Cell-mediated response involves activation of what? What is released?
* Cell-mediated response involves activation of T cells and release of cytokines.
93
What are the different pathways that a t cell can take? What are the carriers and final products?
94
What is the pathway of t cells after antigen recognition?
95
What is teh mechanism of target cell killing by cytotoxic t cells?
96
What are the different pathways that the Helper t cell do?
97
