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717 Cards in this Set
- Front
- Back
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What is pathology?
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The study of disease as a basic science and a branch of medicine
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What is the role of a clinical pathologist?
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A person who determines the specifics of the disease: the type, prognosis and treatment
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What are the top three causes of death in Canada?
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Cardio-vascular 37%
Cancer 28% Respiratory diseases 9% |
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What is the major cause of death globally and what is this due to?
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The major cause of death globally is infectious disease and this is in part due to malnutrition
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What was the increase in life expectancy due to?
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A decrease in infant and youth mortality due to our ability to control infectious diseases though SANITATION, IMMUNIZATION, and the DEVELOPMENT of ANTIBIOTICS and BETTER NUTRITION
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How do environmental factors compare to genetic factors?
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Environmental factors are as important if not more than genetic factors
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If a father died from a heart attack, will the son also?
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No, alot of the risk factors are reversible by changes in life-style. For instance, exercise increases
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What is a symptom?
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Something that the sick individual has to tell another person, it is NOT DIRECTLY VISIBLE
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What is a sign?
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Something that another person can detect, see or verify
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What is a lesion?
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A physical change in the tissue
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What is a sequel?
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A secondary event resulting from a primary event (direct consequence)
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What is a complication?
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Is something that MAY or MAY not occur as a result a primary event
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What is a biopsy?
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The study of a tissue taken from a patient for determining the course of action in treating their disease
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How can a biopsy be performed?
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A surgeon can take a sample of tissue directly or it can be removed by endoscopy
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What is histopathology?
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Studies tissue sections through various staining and immunohistochemical methods to determine what causes the disease
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What is cytology?
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The specialty that studies individual cells which can be removed from a living organism
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What is important to do when studying disease?
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Look at alterations in individual cells
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What are some functions of epithelial tissue?
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It can be protective and secretory, as well as absorptive
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What are four types of epithelium?
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Simple or stratified squamous
Simple or stratified cuboidal Simple or pseudostratified columnar Different combinations of the above |
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What are some functions of connective tissue?
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They are structural and contractile
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What are some examples of where connective tissue is found?
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In muscle, neurons, fibroblasts secreting collagen
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What can happen to a normal cell under stressful conditions?
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A normal cell is adaptable and will undergo reversible adaption by altering its steady state.
-If the stress is maintained for a long period or if it has a high magnitude then the adaption cannot cope and the cell is reversibly injured. If the injury is severe, the cell can die by necrosis or have permanent subcellular alterations |
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What is atrophy?
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The individual cells shrink in size, resulting in a decreased organ size
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What are some causes of atrophy?
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1- Decreased workload
2- Loss of innervation 3-Diseases (ex: polio) 4-Inadequate blood supply 5-Inadequate hormonal stimulation 6-Malnutrition |
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What is similar about the reaction of cells to the causes of atrophy?
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The cells try to match the resources to the activity thats is required so it undergoes autophagy to make itself smaller.
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What is autophagy?
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When a cell digests part of itself
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What is hypertrophy?
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The cells get bigger
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What are the two types of hypertrophy?
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Physiological and pathological
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What is an example of physiological hypertrophy?
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Athletes have greater size in cardiac muscle cells
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What are two examples of causes of pathological hypertrophy?
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Cardiac infarct
Enzyme induction |
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How does a cardiact infarct result in pathological hypertrophy?
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A part of the tissue is no longer able to contract, so the rest of the heart has to work extra hard to be able to meet the requirements of the body to properly pump blood
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How does enzyme induction cause pathological hypertrophy?
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This is hypertrophy in the ER caused by high exposure to drugs, smoking, alcohol and certain chemicals
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What is hyperplasia?
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An increase in the number of cells
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What is an example of physiological hyperplasia?
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Changes are reversible. Smooth muscle cells in the uterus during pregnancy
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What is an example of pathological hypertrophy?
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The prostate gland with increasing age
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What is an example of combined hypertrophy and hyperplasia?
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The uterus during pregnancy
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What is metaplasia?
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The substitution of one cell type for another
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What is an example of pathological metaplasia?
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In smokers, stratified squamous epithelial cells replace the normal columnar epithelial cells.
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Why is the replacement of the normal columnar epithelial cells with squamous cells a problem?
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Squamous cells lack cilia and the mucociliary transport system is disrupted
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What type of consequences result from metaplasia?
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A normal adaption mechanism and sometimes loss of function
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What is the key difference between metaplasia and dysplasia?
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In metaplasia, we have substitution with DIFFERENT cells but that are still NORMAL
In dysplasia, the cells are DIFFERENT AND ABNORMAL |
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What is characteristic of dysplasia?
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Increased rate of mitosis, Uneven distribution of shape and size of cells
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How is dysplasia a significant type of lesion?
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It can be a precancerous lesion that can lead to cancer
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What is anaplasia?
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Cancerous cells
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What is metastasis?
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The anaplastic cells require the ability to migrate and invade other tissues
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What are the four vulnerable target areas of the cells that are more rapidly affected by stressful circumstances than some of the other functions of the cell?
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Mitochondria
Plasma membrane ER Nucleus |
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What does the extent of the injury depend on?
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The type, the duration and the severity of the CAUSE
The type, health and adaptability of the CELL |
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What is hypoxia?
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Lack of oxygen
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What is the most common reason for hypoxia?
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Ischemia
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What is ischemia?
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Inadequate blood supply reducing the amount of nutrients and oxygen delivered
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What are the two most important tissues affected by ischemia?
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The heart and the brain
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What does a reduced blood supply to a section of the heart result in?
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Death of cardiac muscle cells of that section if there is no accessory blood supply
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What are some accessory blood supplies to the heart?
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Anastomoses or directly from the endocardium
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What is anastomosis?
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A network of streams that branch out and reconnect
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In ischemic injury to the heart, what determines if the person will survive?
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The size of the group of cells that die
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What is a possible result of ischemic injury to the brain?
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Impairment (due to part of brain not functioning) or death
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What is the most common cause of ischemia?
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Atherosclerosis
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What is atherosclerosis?
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Forming a plaque on the wall of a blood vessel which can grow or trigger a lot to form on top of it, resulting in impaired blood flow to the point where cells die!
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What are other causes of ischemia?
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Thrombus formation
Embolism Compression Structural changes Vessel spasm |
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What is a thrombus?
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Formation of a CLOT on the wall of the blood vessel
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What is an embolism?
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A moving clot in the vessel which causes reduced blood flow
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What is compression?
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Anything outside the vessel compressing it
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How can structural changes result in ischemia?
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Alteration of normal endothelial function or atherosclerosis
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How does a vessel spasm result in ischemia?
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Since there is smooth muscle in vessel walls, the contraction of these results in the narrowing and therefore decreased flow
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What is another cause of hypoxia besides ischemia?
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Impaired erythrocytes
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How does the impairment of erythrocytes cause decreased oxygen?
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The ability of the erythrocytes to transport O2 is impaired
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What would be a cause of the impaired ability of erythrocytes to transport O2?
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Anemia or CO poisoning
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How does anemia result in impaired erythrocyte ability?
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Inadequate number of RBCs and hemoglobin (lower capacity to carry oxygen)
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How does CO poisoning impair erythrocytes?
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CO occupies the sites on Hb that O2 binds to, preventing the transport of oxygen to the rest of the body
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What are some different factors in cellular physical injury?
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Mechanical
Thermal Altered pressure Radiation exposure Electrical shocks |
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What is behind the most prevalent injury mortality rate?
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Road-traffic injuries
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What is the most important factor that comes into play in CHEMICAL injury?
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Dosage (too much of anything is toxic)
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What are some biological agents that cause disease?
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Bacteria and virus cause infectious diseases
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How can bacteria interact with the cell?
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Directly contact, or through secreting toxins
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Which virus is considered to be the major cause of the common cold?
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Rhinovirus
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How is the cell affected by the life cycle of a virus?
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The cell can be DAMAGED when viruses replicate and often DIES when the virus lyses the cell in order to release newly formed viral particles (results in membrane rupture or altered cytoskeleton)
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What are the two pathologies viruses can cause?
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Cell death or cancer (by altering genetic material)
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How does the immune system come into play in viral infections?
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The virally infected cell often dies as a result of the immune system trying to kill the cell
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What does the immune response require?
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Sacrificing the infected cells so that the virus doesn't spread
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Which cells trigger virally infected cell death?
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Fc receptors on NK cells recognize bound antibody and the NK cell kills the virally infected cell
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What are three immune reactions that can lead to cell death?
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-NK cells
-Cytotoxic T cells -Complement system |
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What is a congenital genetic abnormality?
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A person is born with a genetic abnormality that will make the person more vulnerable to cell injury and death
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What is an aquired genetic abnormality?
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Through exposure to radiation, chemicals, etc
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How is albinism an example of a congenital genetic abnormality?
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They have been born with a genetic defect and they are unable to produce melanin and therefore do not have protection from UV light
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What are two types of injury causes that are due to food intake?
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Obesity
Malnutrition |
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What are some consequences of the lack of supply to cells in hypoxic injury?
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A decreased production of ATP in the mitochondria
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What does a decreased production of ATP in the mitochondria lead to?
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Decreased activity in the Na/K ATPase pump
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Which cells will be affected by this decreased activity of the Na/K ATPase pump and how?
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Cells that depend on a well-regulated ionic content/voltage gradient such as neurons or muscle cells, and they will stop functioning
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What is a way that cells try to compensate for this lack of oxygen?
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Increased glycogen breakdown for supplying other sources
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What does the breakdown of glycogen result in?
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A decrease in pH in the cytosol due to lactic acid production
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What is a consequence of the change in pH?
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Changes in the chromatin structure in the nucleus
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What are the first signs of hypoxic cell injury?
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Swelling of the cell due to an accumulation of ions inside of it
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What forms on the cell surface in hypoxic injured cells?
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Microvilli and blebs
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What happens to the mitochondria and ER?
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Swelling of mitochondria, and dilation of ER (resulting in ribosome detachment)
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What does this change in ER result in?
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Prevention of de novo protein synthesis
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What can eventual cell death result from?
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Degradation of the lysosomal membrane which will cause its contained enzymes to digest the cellular content (autolysis)
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What are some changes in the cell that are reversible?
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Organelle dilation, ribosome disaggregation, blebbing
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What are some characteristics of the "point of no return"?
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Mitochondrial high amplitude swelling, changes in the mitochondrial matrix, violent blebbing
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What are some irreversible changes of the cell?
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Membrane rupture, organelle dispersal, lysosomal breakdown, inflammatory response activation, free Ca2+ rise
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What is problematic about the rise in calcium levels in the cell due to hypoxic injury?
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The increased Ca2+ levels can activate various enzymes which will cause serious alterations in cellular membrane and cytoskeleton
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What can enzyme activation by calcium lead to?
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Activation of endonucleases, proteases, and phospholipases
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How can calcium induced enzyme activation lead to blebbing?
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Activation leads to disruption of the cytoskeleton which causes blebbing
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What is a free radical?
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An atom with an unpaired electron that makes it very reactive and chain reactions
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What is superoxide?
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O2 with an extra electron
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What is superoxide dismutase?
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Can scavenge free radicals that are in the form of superoxides or are O2 derived
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Where are some instances that free radicals can be produced?
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Metabolic reactions
Inflammatory reactions Radiation Reperfusion Chemicals |
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What is reperfusion injury and why does it form free radicals?
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It is when an oxygen deprived tissue starts to receive oxygen again but too quickly, producing hydrogen peroxide, superoxide, hydroxyl radical, chemicals
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What can free radicals do to the cell?
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-Cause lipid peroxidation in PM and organelle membranes
-Remodelling of phospholipid's FA chains -Cross links w/ disulfide bonds -FA oxidation -Lipid cross linking -Protein strand breaks -phospholipid modification |
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How do antioxidants protect against free radicals?
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THey contribute an electron
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What are some intracellular enzymes that can protect against free radicals?
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Catalases and Glutathione peroxidase
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How do the enzymes catalase and glutathione peroxidase act to protect against free radicals?
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They scavenge superoxide
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How do certain vitamins/antioxidants help protect us?
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Fix free radicals BEFORE they have an opportunity to enter the cell and harm us
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What is necrosis?
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The death of some cells within a living organism, and these cells that die can be replaced
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What is necrosis stimulated by?
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An external agent
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What is coagulative necrosis?
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The skeletal framework of the cell is kept in place after it dies, the region is removed and replaced with scar tissue by inflammatory cells
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What is an example of coagulative necrosis?
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A myocardial infarct
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What is liquefactive necrosis?
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The damaged tissue is filled with fluid containing inflammatory cells
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Where is liquefactive necrosis seen?
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In an abcess (permanent hole)
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When can liquefactive necrosis occur in the lung?
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In bacterial infection
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When can liquefactive occur in the brain?
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After ischemic necrosis to the brain
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What is caseous necrosis?
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The material replacing the dead cells is a semi-solid
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What is gangrene?
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Happens when there is coagulative necrosis followed by bacterial infection
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Where are the two most common places that gangrene can occur?
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At the surface of the body and in the intestine (due to the increased presence of bacteria)
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Why is the most common place on the body surface for gangrene occurance the toes?
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Inadequate blood flow (due to diabetes)
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What is apoptosis?
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Programmed cell death that is more rapid than necrosis and does NOT cause inflammation!
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What happens in apoptosis?
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The cell is triggered to destroy itself: it disintegrates into membrane bound sacs (blebs) that are phagocytosed by nearby cells
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When can apoptosis be triggered?
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In some infections against an immune response (against virally infected cells), or in disease states, embryogenesis, menstrual cycle, GI tract, after spinal cord injury, etc...
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What are the sequence of events in apoptosis?
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1-Loss of surface contact with other cells
2-Shrinkage 3-Organelles are intact 4-Nuclear changes (breaks up into fragments) 5-Phagocytosis |
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What are two ways that apoptosis can be initiated?
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Through membrane receptors or from internal mechanisms
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What are some of these internal mechanisms that trigger apoptosis?
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Radiation, viral infections, immune mechanisms, and mitochondrial agents
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What is an extracellular ligand that can classically trigger apoptosis?
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FasL
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How does FasL act to trigger apoptosis?
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It enforces trimerization of the FasR, which recruits the FADD (Fas associated death domain) which leads to the activation of a series of enzymes called caspases which activate/trigger apoptosis)
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What is another ligand that can activate the caspase system?
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The extracellular protein TNF, binds to its receptor, allows forces trimerization but instead recruits TRADD (which is similar to FADD)
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What is one way to block apoptosis through TRADD?
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The transcription factor NFkB blocks genetic mechanisms necessary for apoptosis
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What is an example of a mitochondrial protein that triggeres caspase activity and therefore apoptosis?
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Cytochrome C
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How do caspases execute their apoptosis promoting function?
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They disrupt cytoskeletal elements and DNA
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What are Heat Shock Proteins (HSP) and why are they important?
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They are protein chaperones which are involved in protein folding- the 3D structure of a protein is vital to their function
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What type of proteins are HSP responsible for folding?
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Damaged proteins and HSP are upregulated in various types of injury
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What happens to misfolded proteins that cannot be folded properly?
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They are ubiquinated and destroyed
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How does apoptosis compare to necrosis?
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-Usually much faster
-Requires active synthesis in a dying cell -Does not trigger inflammation -Occurs routinely, in some tissues |
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What is lipofuscin?
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A product of normal metabolism, a harmless lipid protein conjugate that the cell is not able to break down and accumulates with time.
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When can melanin accumulate?
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With excessive exposure to UV light
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What can form when calcium accumulates in the cell?
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CaPO4 crystals. Ca may accumulate in atherosclerotic deposits causing blood flow problems
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What is the microcirculation?
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Occurs in tissues, blood comes in the arteriole side, goes into a capillary bed, and then small venules in the venous system
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What are the four signs of inflammation?
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Redness, hotness, swelling (edema) and pain
Sometimes, loss of function can occur |
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What are true capillaries surrounded by?
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A single layer of endothelial cells
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What controls the amount of blood flow flowing through the capillary bed?
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The smooth muscle contracting in the arterioles
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What occurs during normal circumstances (concerning the capillary bed)?
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The blood flow is reduced because of a phenomenon known as shunting
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How does the circumstances in the capillary bed change in an inflammatory reaction?
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There is increased blood flow
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What causes the increased blood flow in the capilalry bed during inflammation?
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The blood vessels dilate
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What is hyperemia?
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Increased blood flow
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What is a consequnce of the hyperemia in infection?
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The site turns red and has an increased temperature
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What happens to the permeability of the microcirculation in infection?
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It is increased
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How is fluid forced out of the microcirculation?
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By the hydrostatic pressure
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What is osmotic pressure?
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Forces fluid to be retained within the microcirculation by a pressure exerted by plasma proteins
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How does the hydrostatic force compare to the osmotic on the arteriole side?
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Hydrostatic force is greater than the osmotic, and therfore fluid flows out
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How does the hydrostatic force compare to the osmotic pressure on the venule side?
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Hdyrostatic foce is less than osmotic, therefore there is a net reabsorption
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What is transudate?
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Fluid that bathes tissues
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What does transcudate contain?
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Water, small molecules (such as ions, nutrients etc...)
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Normally, what is NOT found in the transudate?
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Large protein molecules such as albumins and globulins
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What happens to hydrostatic pressure in acute inflammation?
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It is increased
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What is a result of this increased pressure?
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There is a leakage of some of the proteins into the surrounding tissue
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What results from this protein leakage?
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The proteins exert an osmotic pressure, retaining fluid in the tissue. This results in the venule side becoming leaky
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What other alteration in the endothelial cells allows proteins to leak out that would not normally?
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Contraction of the endothelial cells create spaces between them
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What is edema?
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Excess interstitial fluid
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Why do endothelial cells contract?
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They are activated by release of specific mediators (the majority of which are released from mast cells)
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What is a major mediator released from mast cells and what are some consequences of its release?
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Histamine is a major mediator causing vasodilation and contraction of the endothelial cells
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What happens to the microvasculature permeability in an immediate transient reaction?
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The permeability change peaks in 5 minutes and is gone within 30
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What happens to the microvasculature permeability in a mild reaction?
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Swelling is due to level of venules only
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What happens to the microvasculature permeability in a sustained reaction?
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There is an effect on ALL the microcirculation
-A much greater amount of protein and fluid flowing through the region |
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What happens to the microvasculature permeability in a prolonged delayed reaction?
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There is a delayed reaction because the cell needs to synthesize new mediators
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What are some examples when a prolongued delayed reaction takes place?
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Exposure to UV light
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What is margination?
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In an inflammatory reaction, fluid and proteins are lost, resulting in an increased concentration of RBCs which clump and decrease flow rate. They become compressed against the endothelial wall
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What does the "rolling" and "sticking" of leukocytes to endothelial cells depend on?
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Selectin and Integrin activity
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What is the first event in this rolling and adhesion process?
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P-selectin redistributes on the surface of the endothelial cell
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What is the redistribution of P-selectin triggered by?
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Inflammatory mediators such as histamine and thrombin
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What is the role of selectins?
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To provide a binding site for leukocytes
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What is the role of integrins?
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Allows the leukocytes to bind to cell adhesion molecules and adhere
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Which step converts the rolling leukocyte to one that is stuck?
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The activation of integrin
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What is the stage after margination?
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Transmigration
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What is transmigration?
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The leukocyte is able to get out of the blood vessel between two endothelial cells
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What allows a leukocyte to pull itself through the junction between endothelial cells?
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Its pseudopod- which experiences mutal recognition and binding and it knows where to go
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What are collagenases?
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THey are secreted by the tip of the pseudopod and create a hole in the basement membrane that surrounds endothelial cells, allowing the leukocyte to pass through.
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What are the 5 types of white blood cells?
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B lymphocytes, T lymphocytes, Monocytes, Eosinophils, Neutrophils
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What are neutrophils?
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-They are polymorphonuclear cells that are full of granules with pre-formed mediators/newly synthesized mediators
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What are some functions of the neutrophil?
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-Phagocytosing microbes
-Releasing inflammatory molecules |
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What are some effects of monocytes/macrophages?
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-Phagocytose bacteria
-Produce inflammatory mediators -Synthesize molecules -Initate the immune response -Scavenge (cleanup) -Induction of general effects |
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What are some molecules that monocytes/macrophages synthesize?
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Molecules affecting:
-Antibacterial defences -Antiviral defences -Blood clotting -Cell growth -Vascular growth -Tumor growth -Collagen production |
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What are some general effects that monocytes/macrophages can induce?
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Fever, Acute phase reaction, cachexia
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What is cachexia?
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Lack of appetite
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What are eosinophils?
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Contain preformed granules with powerful mediators that can be key in allergic reactions
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What do platelets contain?
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Powerful mediators (not just for coaggulation)
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How do neutrophils and platelets interact?
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Compounds released by neutrophils can tell platelets what to do
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What are basophils?
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Contain powerful mediators and are partially vasoactive (changing permeability)
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What do monocytes become upon activation?
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Macrophages
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What are examples of macrophages in the brain?
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Microglial cells
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What are four catergories of cytokines that macrophages release?
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Interleukins, Chemokines, Growth factors, interferons
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What are interleukins?
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Chemical compounds that allow macrophages to communicate to one another
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What are chemokines?
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Compounds that have an ability to chemically attract
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What is the difference between lifespan of neutrophils/macrophages/
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Neutrophils come in right away but have a short lifespan
-After, monocytes replace them and become activated macrophages which stay in the tissue for the remainder of the inflammatory reaction |
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What is exudate?
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Fluid that flows out of microvasculature in situations of lesion/inflammation
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Compared to the transudate, what does the exudate have more of?
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Albumin
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How is the neutrophil able to be motile?
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It contains actin and myosin
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How does the neutrophil know which direction it should move?
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It extends its pseudopod, and on the surface of the neutrophil are many chemokine receptors. It will therefore move in the direction w/ the most chemokine
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|
|
What can some phagocytes digest?
|
Whole cells, fragments, dying cells, etc....
|
|
|
What are the three stages of phagocytosis?
|
Recognition
Engulfment Killing and Digestion |
|
|
What are some examples of receptors that macrophages have?
|
For bacterial constituents such as LPS and mannose
|
|
|
What does macrophage receptor binding trigger?
|
Release of cytokines that further the inflammatory process
|
|
|
What are opsonins?
|
They are something that label the bacteria to be destroyed
|
|
|
What are examples of opsonins?
|
Antibody or complement
|
|
|
What happens when the microorganism is engulphed?
|
It is surrounded, creating a phagosome.
|
|
|
What happens to the phagosome?
|
It fuses with the lysosome and creates a phagolysosome
|
|
|
What happens in the phagolysosome?
|
The microbes are destroyed with enzymes or other free radicals
|
|
|
What type of free radicals are releasedin the phagolysosome??
|
O or NO derived free radicals
|
|
|
How does the macrophage correct the problem of ingesting indigestible material?
|
When dividing, one daughter cell keeps the indigestible material, while the other formed is perfectly normal
|
|
|
How can surrounding tissue be damaged in phagocytosis?
|
If the phagocyte releases damaging materials before the organism is completely engulphed
|
|
|
What do endothelial cell selectins promote?
|
Weak attachment to leukocytes
|
|
|
What are spasmogens?
|
They cause the contraction of smooth muscle
|
|
|
When are vasoactive mediators involved?
|
In the initial aspect of the inflammatory response
|
|
|
What are vasoactive mediators responsible for and what are some consequences of their actions?
|
They are responsible for the vascular changes in inflammation (vasodilation and increased permeabiltiy), resulting in edema, swelling, and redness
|
|
|
What are some examples of vasoactive mediators?
|
Histamine, NO, serotonin, bradykinin, platelet activating factor (PAF), prostaglandins/leukotrienes, anaphylatoxins
|
|
|
What is responsible for releasing histamine?
|
Mast cell/basophil degranulation
|
|
|
Which cells release serotonin?
|
Platelets
|
|
|
What are plasma proteases?
|
Enzymes that act on protein precursors to produce activators of vascular permeability and complement
|
|
|
What is the first step of the classical pathway of complement?
|
C1 binds to 2 IgG molecules on their Fc portion
|
|
|
What does binding of C1 to the Fc portion of 2 IgGs trigger?
|
Formation of the C2/C3/C4 complex
|
|
|
Which fragments are released when the C2/C3/C4 complex forms?
|
C3a, C3b, C4a, C4b
|
|
|
What are C3a and C4a?
|
Anaphylatoxins
|
|
|
What are anaphylatoxins?
|
Vasoactive compounds that cause vasodilation of the microcirculation as well as an increase in vascular permeability
|
|
|
What is released when the membrane attack complex (MAC) forms?
|
C5a
|
|
|
What is the function of the released fragment C5a?
|
It increases vascular permeability and is chemotactic
|
|
|
What results after the formation of the MAC (C5/6/7/8)?
|
A hole is punched in the membrane of the microorganism
|
|
|
What creates the channel for the hole in the membrane of the microorganism?
|
Multiple C9 molecules
|
|
|
What are two other ways that complement can be activated?
|
The alternative pathway and the lectin binding pathway
|
|
|
How is the alternative pathway triggered?
|
Recognition of a foreign microorganism
|
|
|
How is the lectin binding pathway triggered?
|
Through recognition of mannose on the bacterial surface by a mannose binding protein
|
|
|
What are three consequences of complement?
|
Lysis
Chemotaxis Opsonization |
|
|
What is bradykinin?
|
It has vasoactive properties and is thought to be responsible for the lingering pain felt in inflammation
|
|
|
What are prostaglandins and leukotrienes formed from?
|
Arachidonic acid
|
|
|
How is arachidonic acid liberated from the membrane?
|
By Phospholipase-A2
|
|
|
How can phospholipase A2 action be reduced and how does this affect inflammation?
|
Corticosteroids can block PLA2 resulting in decreased amounts of prostaglandins and leukotrienes, resulting in a reduction in inflammation
|
|
|
What catalyzes the conversion of arachidonic acid to prostaglandin?
|
Cyclooxygenase enzymes
|
|
|
How can cycooxygenase enzymes be blocked?
|
By non steroidal anti-inflammatory drugs
|
|
|
What are some examples of NSAIDS that can block cyclooxygenases?
|
Aspirin/ibuprofen and indomethacin
|
|
|
How does the use of NSAIDS decrease pain?
|
Blocking prostaglandin synthesis lowers their ability to sensitive nocioceptive nerve endings to the action of other mediators
|
|
|
What are some of the physiological roles of prostaglandins?
|
Body temperature, bronchial tone, stomach mucosal lining, blood pressure, reproduction
|
|
|
In what cases do prostaglandins play a role in pathologies?
|
Fever, Ulcers, GI and reproductive problems, pain
|
|
|
What are cytokines?
|
Communication molecules
|
|
|
What do macrophages release?
|
Interleukins, tumor necrosis factor
|
|
|
What do the products released by macrophages do to endothelial cells?
|
Cause leukocyte adherence, prostaglandin synthesis, coagulation
|
|
|
What are acute phase reactions?
|
Fever, decreased appetite, reactions on the brain, liver, bone marrow, etc..
|
|
|
What are the effects of IL-1 and IL-6 on the liver?
|
They cause the liver to release more acute phase proteins (C-reactive protein, Mannose Binding protein)
|
|
|
What does the release of CRP and MBP from the liver result in?
|
Activation of compliment/opsonization
|
|
|
What type of effects do cytokines have on the bone marrow endothelium?
|
Neutrophil mobilization/phagocytosis
|
|
|
What results from cytokine IL-1/IL-6 action on the hypothalamus?
|
Increased body temperature
|
|
|
What resutls from cytokine IL-1/IL-6 action on fat/muscle?
|
Protein and energy mobilization to allow increased body temperature
|
|
|
What are the overall effects of IL-1/IL-6 action?
|
Decreased viral and bacterial replication, increased Ag processing, and specific immune response
|
|
|
What type of receptor are chemokine receptors?
|
G-protein coupled
|
|
|
Which cells release platelet activating factor?
|
Many cells, including endothelium and inflammatory cells
|
|
|
What does the release of PAF result in?
|
Increased permeability
Leukocyte aggregation/adhesion/chemotaxis Platelet activation |
|
|
What do activated platelets do?
|
Can secrete inflammatory mediators, vasoactive factors, growth factors, clotting/coagulation factors
|
|
|
What is nitric oxide and what is it released by?
|
It is a powerful vasodilator that is released by macrophages/endothelium
|
|
|
What happens to the excess fluid after an inflammatory response?
|
It is drained by the lymphatics
|
|
|
What do macrophages do after an inflammatory response?
|
They phagocytose dead neutrophils and necrotic cells
|
|
|
What are the important cells in acute inflammation?
|
Neutrophils, platelets, mast cells
|
|
|
What are the important cells in chronic inflammation?
|
Macrophages, lymphocytes, plasma cells
|
|
|
What are granulomas?
|
Fused macrophages with collagen and lymphocytes on the outside
|
|
|
How is the formation of a granuloma advantageous when there is a foreign body that is too big to be removed by any cell?
|
The formation of a granuloma surrounds and encases the foreign body
|
|
|
How is the formation of a granuloma advantageous when there is infection by an indestructible microbe?
|
The microbe is surrounded so it cannot infect other tissues
|
|
|
What is the formation of a granuloma induced by?
|
Il-1
|
|
|
Why would there be a granuloma with a caseous necrosis center?
|
The microbes can be destroyed in the center of the granuloma
|
|
|
What is serous inflammation?
|
The fluid exudate has a low protein/cell content, and the fluid can reabsorb after some time
|
|
|
What is fibrinous inflammation?
|
THe increased permeability allows fibrinogen to enter alveoli and lay down fibrin
|
|
|
What is Legionaire's disease?
|
A respiratory disease where the deposition of fibrin is permanent, resulting in impaired function
|
|
|
What is an ulcer?
|
An area of necrosis on an epithelial surface
|
|
|
Where are common sites of ulcer formation?
|
On the skin surface or the GI tract
|
|
|
What occurs at the base of the ulcer?
|
Cell death and chronic inflammation
|
|
|
What occurs at the surface of the ulcer?
|
Reduced blood flow
|
|
|
How is fever triggered?
|
IL1/6 and TNF act on the hypothalamus to release prostaglandins, which triggers shivering and thus an increase in body temperature
|
|
|
How is fever advantageous?
|
Which a minimal increase in temperature, the motility of leukocytes is increased
|
|
|
What is leukocytosis?
|
A systemic affect of inflammation where cytokines stimulate the bone marrow resulting in a greater proliferation of stem cells into all cells into the circulation
|
|
|
What are labile cells?
|
Cells that are continually cycling
|
|
|
How can labile cells be regenerated/replaced?
|
They can quickly replace themselves because of their fast division rate
|
|
|
What are stable cells and how are they replace?
|
Stable cells have the ability to divide, but only when it is necessary for them to be replaced
|
|
|
What are permanent cells replaced by when damaged and why?
|
They are replaced by scar tissue (fibrosis) because there is no stem cell that can replace them
|
|
|
What are some examples of permanent cells?
|
Neurons, cardiac myocyte
|
|
|
What are some examples of stable cells?
|
Hepatocyte
|
|
|
What are some examples of labile cells?
|
Squamous cells of the epithelium
|
|
|
What happens in partial damage to a neuron?
|
The Schwann cells can help guide growth of the axon
|
|
|
What happens in the case of motor neuorn loss?
|
A nearby motor neuron can sprout to re-ineervate some of the muscle
|
|
|
What is neuron sprouting an example of?
|
Hypertrophy
|
|
|
What is angiogenesis?
|
Old blood vessels sprout- example of hyperPLASIA
|
|
|
What are the roles of fibroblasts?
|
-Make the extracellular matrix
-Proliferate during repair/healing -Deposit collagen -Become myofibroblasts |
|
|
When are myofibroblasts important?
|
In wound contraction
|
|
|
What is the order of cell activity in tissue injury?
|
Platelets, Neutrophils, Macrophages, Fibroblasts, Lymphocytes
|
|
|
What is a primary union/first intentioN?
|
A neat injury, heals quickly
|
|
|
What is a secondary union?
|
There is missing a piece of tissue, therefore there is a bigger scar and wound contraction might be necessary
|
|
|
How do myofiboblasts help decrease the size of the scar?
|
They pull together the edges of the wound
|
|
|
What is a keloid?
|
Overactive myoblasts- results in a huge scar
|
|
|
What type of cells are adipocytes?
|
Stable cells
|
|
|
What is the global rate of death due to infectious diseases?
|
1/4 of deaths
|
|
|
In poorer countries, what fraction of the deaths can be attributed to infectous disease?
|
1/2
|
|
|
Who is most vulnerable to infectious disease?
|
Children under 5
|
|
|
In order of decreasing incidence, list the most common diseases caused by infectious agents
|
Pneumonia, AIDS, diarrheal diseases, TB, malaria, measles
|
|
|
Which bacteria was recently discovered to be a source of ulcers?
|
H. pylori
|
|
|
How is malaria transmitted?
|
Via a mosquito (vector in this case)
|
|
|
What are the three factors influencing infectious disease?
|
Genetic, Environment, Lifestyle
|
|
|
What host factors are essential in fighing off parasite infection?
|
The general state of the indivudal:
-their nutrition, age, body integrity, underlying conditions -Their specific/nonspecific resistance |
|
|
What abilities of the parasite allow it to infect easily?
|
The dosage, ability to colonize and spread, their virulence, protection from host, toxigenicity
|
|
|
What are two primitive techniques that were discovered to control infectious disease?
|
Sanitation, quarantine
|
|
|
When did antibacterial drugs become available?
|
In the 1950's (60 yrs ago)
|
|
|
What was one of the first antibacterial drugs?
|
Penicillin became available during WWII
|
|
|
What are four reasons why there has been a decrease in death due to tuberculosis?
|
Improved sanitation, better nutrition, effective drugs, immunization
|
|
|
What are pathogenic microbes?
|
Harmful
|
|
|
What are commensal microbes?
|
They have no impact
|
|
|
What are symbiotic microbes?
|
They are beneficial
|
|
|
What are some areas in the body that harbor beneficial microbes?
|
The respiratory tract, digestive tract, genitourinary tract
|
|
|
What are some driving forces for the co-evolution of bacterial-host relationship?
|
-Bacterial genetic diversity
-Capacity for rapid growth -High population density |
|
|
What is an opportunistic infection?
|
Microbes that cause infection given the opportunity to do so will.
If the defense system is poor, some microbes can cause problems even if they are normally harmless |
|
|
What was the Black Death spread by?
|
A rat flea
|
|
|
How did rat fleas start transmitting this to humans?
|
After the rats died, the rat flea turned to humans
|
|
|
How is Lyme disease transmitted?
|
By the deer tick
|
|
|
How is West Nile Virus transmitted?
|
Via mosquitoes
|
|
|
What are some examples of route of transmission of infectious diseases?
|
Airborne
Droplet Hand contact Human-human Food borne Water borne Insect borne |
|
|
What is an example of an infectious disease transmitted by the airborne route?
|
Tuberculosis is transmitted by small droplet nuclei
|
|
|
WHat is an example of an infectious disease that is transmitted by the droplet route?
|
Influenza is transmitted in larger droplet nuclei
|
|
|
What is an example of an infectious organiam that is transmitted via hand contact?
|
Rhinovirus
|
|
|
What is an example of an infectious disease transmitted by the airborne route?
|
Tuberculosis is transmitted by small droplet nuclei
|
|
|
What are some ways that humans can transfer infectious microorganisms to another human?
|
Across the placenta
Sexual transmission Air-borne Blood-borne |
|
|
WHat is an example of an infectious disease that is transmitted by the droplet route?
|
Influenza is transmitted in larger droplet nuclei
|
|
|
What is an example of an infectious organiam that is transmitted via hand contact?
|
Rhinovirus
|
|
|
Why don't microorganisms indiscriminately infect every tissue in the body?
|
They have receptors for specifc cell surface markers
|
|
|
What are some ways that humans can transfer infectious microorganisms to another human?
|
Across the placenta
Sexual transmission Air-borne Blood-borne |
|
|
Why don't microorganisms indiscriminately infect every tissue in the body?
|
They have receptors for specifc cell surface markers
|
|
|
Which cells do polioviruses recognize?
|
CNS
|
|
|
Which cells do chickenpox viruses recognize?
|
The skin
|
|
|
Which cells do measles recognize?
|
Lungs
|
|
|
Which cells do mumps recognize?
|
The salivary gland
|
|
|
Which cells does hepatitis B virus recognize?
|
The liver
|
|
|
How does the muco-ciliary tract work to rid of infectious microorganisms?
|
The macrophages climb up the tract and are swallowed. THe pH of the HCL in the stomach kills the bacteria or virus ingested
|
|
|
How does the GI tract protect against infection?
|
Normal flora block pathogenic bacteria attachment
|
|
|
How do Mycobacteria resist host defense?
|
Mycobacteria prevent lysosomal fusion to endosome
|
|
|
What is antigenic variation?
|
A stategy by the pathogen to block the hosts recognition system. It varies either the antigen or the coat polysaccarides so any previously aquired immunity is nonfunctional
|
|
|
When are babies most vulnerable?
|
At 6 months of age
|
|
|
Why are babies most vulnerable at 6 months of age?
|
-In utero, the mothers IgGs are transfered to the fetus
-After birth, these Ab start to deplete and are lowest at 6 months (baby hasnt aquired the ability yet to synthesize enough of its own antibodies) |
|
|
What is bacteremaia?
|
If microbial contamination persists at a low level in the blood
|
|
|
What is sepsis?
|
If microbial contaminations persists at high levels in the blood
|
|
|
What is antibiotic resistance a result from?
|
Using it for viral infections or as a method of prophylaxis (prevention)
|
|
|
What are the host defenses against VIRAL infection?
|
Macrophages/Lymphocytes
|
|
|
What is the host cell response to viral infection?
|
Reduced host protein synthesis
Cell lysis or fusion Neoplastic transformation |
|
|
What is a latent infection?
|
Virus is inactive but still present
|
|
|
What is an example of a latent infection?
|
Infection with Varicella, which later in life gives rise to Shingles
|
|
|
How do antibodys block infection?
|
They bind to the virus receptor, and therefore the virus cannot attach
|
|
|
How many cases of measles are there per year?
|
30-40 million, 600 000 deaths
|
|
|
What is the only virus that has been completely eradicated?
|
Small pox
|
|
|
What are different sites for antiviral drug action?
|
Entry
Uncoating Nucleic acid synthesis Viral particle production Exit |
|
|
Where does influenza infect?
|
The respiratory tract
|
|
|
What type of cells do influenza viruses have a selective affinity for?
|
Tracheobronchial epithelial cells
|
|
|
What distinguishes influenza from the common cold?
|
Systemic symptoms
|
|
|
What are the respiratory symptoms of influenza?
|
Nose and throat
|
|
|
What are the systemic symptoms of influenza?
|
Headache, myalgia, muscle pain, fever, pain
|
|
|
What is a major complication of influenza?
|
Pneumonia
|
|
|
How is influenza transmitted?
|
Can be through hand but it is mostly through aerosol droplets
|
|
|
What does epidemic mean?
|
A significant number of people in a localized region get sick
|
|
|
What does pandemic mean?
|
The illness/disease is spread worldwide
|
|
|
Which pandemic occurred in 1918 and how many people died?
|
Spanish Influenza, 40-50 million deaths
|
|
|
Which pandemic occured in 1957 and how many people died?
|
Asian Flu, 1-2 million deaths
|
|
|
Which pandemic occured in 1968 and how many people died?
|
The Hong Kong Flu, 700 000 people died
|
|
|
Which pandemic occured in 1977 and how many deaths occured?
|
Russian Flu, no excess deaths
|
|
|
What type of genome does influenza have?
|
RNA genome
|
|
|
How many types of influenza are there?
|
A, B and C
|
|
|
What is the outer capsule of influenza derived from?
|
Host plasma membrane
|
|
|
What does the outer capsule of influenza contain?
|
Hemagglutinin
Neuraminidase M1 protein M2 protein |
|
|
What is characteristic of Influenza C viruses?
|
They only have SEVEN distinct segments of RNA
-They only have HA variants on their surface |
|
|
What is characteristic of Influenza A and B viruses?
|
They have 8 segments of RNA
They have variations of both HA and NA on their surfaces |
|
|
What type of variation can influenza type A viruses undergo?
|
Antigenic drift and shift
|
|
|
What type of variation can influenza type B viruses undergo?
|
Antigenic drift
|
|
|
What type of variation can influenza type C viruses undergo?
|
None- they are stable
|
|
|
What is the role of the HA protein in influenza?
|
It allows the virus to recognize the host cell
|
|
|
How many HAs exist?
|
16
|
|
|
How many NAs exist?
|
9
|
|
|
How many HAs regularily infect humans?
|
3
|
|
|
How many NAs regularily infect humans?
|
2
|
|
|
What is antigenic drift?
|
There is a slow genetic change that is occuring all the time
|
|
|
What do the mutations in the HA epitopes lead to?
|
The neutralizing antibodies no longer bind
|
|
|
What is antigenic shift?
|
Occurs when RNA segments are exhanged between viral strains in a secondary host
|
|
|
Which species is capable of carrying a huge number of viruses?
|
Wild water birds
|
|
|
What is genetic reassortment?
|
Occurs in species that can be infected by multiple species specific strains, and different strands of RNA can be exchanged, resulting in a new variant of the virus
|
|
|
What is the genetic type of the Avian Influenza?
|
H5N1
|
|
|
How is H5N1 generally transmitted?
|
Can be transmitted directly from birds to people, however this is a typical occurance
|
|
|
What are some key differences between H5N1 and H1N1?
|
-H1N1 spreads easily in the respiratory tract and is rarely fatal
-H5N1 spreads slowly through the respiratory tract but is fatal |
|
|
Why is H5N1 often fatal?
|
The receptors for the virus are deeper in the lungs
|
|
|
How did the current H1N1 arise?
|
First, the classic swine H1N1, Human H3N2 and Avian recombined to form the North American swine.
-The North American swine virus reassorted with the Eurasian swine, resulting in the current H1N1 |
|
|
What does the viral HA recognize?
|
Sialic acid
|
|
|
How does influenza enter the cell?
|
Through an endosome
|
|
|
What is NA responsible for?
|
Allowing the virus to escape
|
|
|
How can the virus eject its genetic material into the cytoplasm?
|
Once in the endosome, the acidification changes the properties of HA, allowing the virus to fuse its membrane to that of the endosome, releasing its genetic content
|
|
|
How can the genetic material be seperated from the M1 proteins?
|
An ion channel M2 allows protons to enter the viral particle
|
|
|
What is amantadine for?
|
Blocks the M2 ion channel, which in turn blocks viral replication
|
|
|
What happens during influenza release?
|
HA binds to host cell receptors, and NA cleaves the virus free
|
|
|
What are the defense mechanisms against influenza?
|
Cytokines
NK cells Antibodies |
|
|
What does the nomenclature of an influenza strain depend on?
|
Virus type
Geographic origin Isolate number Year HA:NA |
|
|
How can the genetic material be seperated from the M1 proteins?
|
An ion channel M2 allows protons to enter the viral particle
|
|
|
What is amantadine for?
|
Blocks the M2 ion channel, which in turn blocks viral replication
|
|
|
What happens during influenza release?
|
HA binds to host cell receptors, and NA cleaves the virus free
|
|
|
What are the defense mechanisms against influenza?
|
Cytokines
NK cells Antibodies |
|
|
What does the nomenclature of an influenza strain depend on?
|
Virus type
Geographic origin Isolate number Year HA:NA |
|
|
What is an example of this use of nomenclature in naming influenza viruses?
|
AH1N1/NewCaledonia/20/99
|
|
|
Which type of influenza is amantadine effective against?
|
Type A
|
|
|
What can be used to treat both influenza A and B?
|
Neuraminidase inhibitors
|
|
|
What is Reye's syndrome?
|
A rare event that has neurological consequences when aspirin is given to children with influenza
|
|
|
What type of genome do Herpes viruses have?
|
DNA genome
|
|
|
How many types of herpes are there? How many cause disease?
|
There are 9 known types of herpes, 8 of which cause disease
|
|
|
What are the three subfamilies of herpes?
|
Alpha, beta, gamma
|
|
|
What are the alpha herpes viruses?
|
-Herpes simplex type 1 (Human herpes virus 1)
-Herpes simplex type 2 (Human herpes virus 2) -Varcicella-zoster (Human herpes virus 3) |
|
|
What are the beta herpes viruses?
|
-Cytomegalovirus (Human Herpes Virus 5)
-Exanthum subitum (Human Herpes Virus 6) -Roseola infantum (Human Herpes Virus 7) |
|
|
What are the gamma herpes viruses?
|
-Epstein barr (Human Herpes Virus 4)
-Kaposi's Sarcoma associated (Human Herpes Virus 8) |
|
|
What happens once herpes enters?
|
It is carried along microtubules to the nucleus
|
|
|
When does a latent herpes virus reactivate?
|
In states when an individual is immunocompromised
|
|
|
What is the tropism of herpes viruses?
|
They hide in neurons or leukocytes
|
|
|
Which herpes viruses are neurotropic?
|
HSV-1, HSV-2, and VZV
|
|
|
Which herpes viruses are blood-borne?
|
CMV, EBV, HHV-6,7,8
|
|
|
Which type of receptor do herpes viruses bind?
|
TNF/NGF protrein receptor via the herpes glycoprotein (gD)
|
|
|
What does HSV-1 cause?
|
The classic cold sore
|
|
|
Where does HSV-1 travel?
|
It gets into the sensory nerve endings and travels to the trigeminal ganglion
|
|
|
How is latent infection established?
|
Through retrograde transport
|
|
|
What is anterograde transport?
|
How reactivation occurs
|
|
|
What happens during anterograde transport?
|
THe virus exits the nerve endings and attacks the skin region
|
|
|
At what rate does reactivation occur?
|
At a rapid rate (9 mm/hr)
|
|
|
What is the main defense against herpes virus?
|
Cell mediated immunity
|
|
|
What is whitlow?
|
When dentists get herpes infection in their hands
|
|
|
What is HSV-1 encephalitis?
|
It is when an immunocompromised individual has the virus, and it can go throughout the brain and cause necrosis of the temporal lobe
|
|
|
Which herpes virus causes genital herpes?
|
HSV-2
|
|
|
Infection with which herpes virus gives cross-resistance to HSV-2?
|
HSV-1, but these individuals are still carriers of HSV-2
|
|
|
What is the prevalence of Herpes?
|
1/5
|
|
|
What is Acyclovir?
|
Inhibits HSV DNA polymerase
|
|
|
What does Varicella Zoster Virus cause?
|
Chicken pox
|
|
|
Where does VZV usually enter?
|
The lungs
|
|
|
How does primary viremia in VZV infection occur?
|
The virus enters, replicates in the lymph nodes, so it can enter the circulation where it travels to the liver and spleen and can replicate there
|
|
|
How does secondary viremia in VZV infection occur and how does this result in transmitting the virus to otheres?
|
The virus is transported by mononuclear cells to the skin and mucous membranes, where it is released into respiratory secretions
|
|
|
Where does VZV establsh its latent infection?
|
In the dorsal root gangion
|
|
|
What results upon reactivation of VZV?
|
Shingles
|
|
|
What are some characteristics of shingles?
|
When it comes out of the nerve endings, it causes intense lesions (cell lysis in the epidermis)
|
|
|
What is post herpetic neuralgia?
|
A risk in Shingles, that the nerves are damaged in reactivation
|
|
|
What can EBV cause?
|
Mononucleosis
|
|
|
What cell type does EBV target?
|
B cells
|
|
|
Where does the virus remain for the duration of the host's life?
|
Immortalized lymphocytes
|
|
|
What can cytomegalovirus cause?
|
Ulcers in the GI tract, in the eye, congentical infection in offspring
|
|
|
What are PAMPs?
|
Pathogen associated molecular patterns
|
|
|
What are DAMPs?
|
Damaged associated molecular pattern
|
|
|
What is RIG-1?
|
RNA helicase that recognizes viral RNA in the cytoplasm
|
|
|
What are PRR?
|
Pattern Recognition Receptors
|
|
|
What is the role of IL-22?
|
Promotes repair
|
|
|
What is the role of IL-17?
|
Recruits neutrophils
|
|
|
What is TepC?
|
A protein produce by E.coli in the gut, that inactivates the response system
|
|
|
Which antibodies are mainly produced in the lungs?
|
IgA
|
|
|
Which immunoglobulins do B cells produce first?
|
IgM and IgD, then IgE and IgG
|
|
|
Where are B cells found in the lymph node?
|
In the cortex
|
|
|
Where are T cells found in the lymph node?
|
The paracortex
|
|
|
Where do B cells undergo affinity maturation?
|
In the germinal centre
|
|
|
What happens when B cells mature?
|
THey switch their isotypes
|
|
|
What happens when a B cell matures?
|
It becomes a plasma cell committed to making one type of antibody
|
|
|
How do B cells turn into plasma cells?
|
They can either be activated by TH2 helper cells, or they can activate into a plasma cell without the assistance of a T cell
|
|
|
Where does gene rearrangement of T cells occur?
|
In the bone marrow
|
|
|
Where does positive and negative selection of T cells occur?
|
In the bone marrow
|
|
|
What happens if a self-reactive T cell exists?
|
A T regulatory cell will suppress it
|
|
|
How are self-reactive T cells typically removed?q
|
The thymus screens fo rthem and removes them by inducing apoptosis
|
|
|
How do NK cells know when to act?
|
If there is no inhibitory receptor, such as in tumor cells, the NK cell will induce cell death (by apoptosis)
|
|
|
What is a type I hypersensitivity reaction?
|
IgE-mediated
|
|
|
What does IgE protect against?
|
Parasitic diseases
|
|
|
WHat happens after the plasma cell produces IgE?
|
The IgE binds to a mast cell via its Fc portion
|
|
|
What happnes when the same antigen is encountered again?
|
2 IgE molecules are cross-linked, generating a signal
|
|
|
What does the signal of 2 IgE cross-linking cause?
|
Release of Ca2+
|
|
|
What is a result of the release of Ca2+?
|
The release of pre-formed mediators from the mast cell
|
|
|
What are some of these mediators released by mast cells?
|
Histamine, proteases, and chemotactic actors and well as cytokines
|
|
|
What type of effect does the release of cytokines have in a type I hypersensitivty reaction?
|
Vasodilation, Vascular leakage, Smooth muscle spasm, intense itching
|
|
|
What is an adjuvant?
|
A substance that modifies the effect of other agents without having much of an effect on their own
|
|
|
What is sarafotoxin?
|
A potent vasoconstrictor from snake bites that stimulates mast cell degranulation to inactivate the toxin
|
|
|
What does release of IL-10 by mast cells result in?
|
Blocking T cells and therefore the decrease in the inflammatory response
|
|
|
What do immediate/late phase type 1 reactions result from?
|
Different mediators are released: histamine/leukotrienes
|
|
|
Where does the immediate phase have an effect?
|
Smooth muscle in gut, airways, and blood vessels
|
|
|
What are hay fever and bronchial asthma examples of?
|
Anaphylactic disease
|
|
|
What happens to the first exposure of pollen with those with Hay fever?
|
IL4 drives B cells to produce IgE in response to pollen antigens, which binds to mast cells
|
|
|
What happens in the second exposure to pollen?
|
The mast cell releases its contents
|
|
|
What is dyspnea?
|
Difficulty breathing
|
|
|
Where does Dander come from?
|
Skin of animals
|
|
|
What does cholera toxin activate?
|
Dendritic cells
|
|
|
What component of mites allow them to act on TLR?
|
LPS component
|
|
|
What is type 2 hypersensitivity?
|
Antibody Dependent
|
|
|
What happens in hemolytic anemia?
|
An antibody binds to the RBC and complement results in phagocytosis or lysis
|
|
|
What happens in drug induced hemolysis?
|
An immune complex of the drug/Ab occurs, which can join onto RBCs
|
|
|
What happens in Rh incompatibility?
|
The first time an Rh- mother has an Rh+ fetus, she will develop anti-Rh antibodies after birth
The second time the mother has a baby that is Rh+ the child will be born with hemolytic anemia |
|
|
What is a danger in the child being targeted with the anti-Rh antibodies?
|
The high levels of bilirubin that develop can cross the blood brain barrier and result in a depressed mentality
|
|
|
How is Rh incompatibility treated?
|
The mother is given anti-Rh antibodies (that CANNOT cross the placenta) and these destroy any incoming Rh+ RBCs before they have a chance to sensitize the mother, and she will therefore not produce any anti-Rh Abs that CAN cross the placenta, and therefore the dangerous reaction will not occur
|
|
|
What is Myasthenia Gravis?
|
A disease in which the ability to use muscles is degenerated, movement is slow and breathing is troublesome
|
|
|
What causes Myasthenia Gravis?
|
An Ab against the Ach receptor is produced, and therefore Ach cannot access its receptor and therefore the signal to the muscle is incomplete
|
|
|
What is a treatment of Myasthenia Gravis?
|
The use of acetylcholinesterase inhibitors to block breakdown of Ach
|
|
|
What is Type 3 Hypersensitivity?
|
The formation of immune complexes that deposit on epithelial or endothelial surfaces which attracts neutrophils and destroys the tissue
|
|
|
What are some examples of Type 3 hypersensitivity reactions?
|
Vasculitis, Glomerulonephritis
|
|
|
What is vasculitis?
|
The destruction of vessels in the process of a Type 3 reaction
|
|
|
What is type 4 hypersensitivity?
|
Cell mediated
|
|
|
What are the four Type 4 Hypersensitivity reactions?
|
Delayed Hypersentitivity
Contact Hypersensitvity Gluten sensitivity Eye Trauma |
|
|
What is a hapten?
|
A small molecule that can elicit an immune response only when it is attached to a large carrier such as a protein
|
|
|
What does gluten sensitvity cause?
|
Celiac disease
|
|
|
What happens in Celiac disease?
|
The villi of the small bowel atrophy
|
|
|
What happens during eye trauma?
|
Introcular protein antigens that were previously sequestered are now released. These antigens are NOT recognized as self and they go to the lymph nodes where T cells are activated, return to the eyes, and induce an immune response
|
|
|
What does UV light cause?
|
Expression of RANKL, which causes Langerhans cells to increase T Regs
|
|
|
What is a result of the increase in T Regs due to UV light exposure?
|
A suppressed immune response
|
|
|
What is dermatomyosiitis?
|
It is an autoimmune disorder that results in destruction of muscle fiberes due to inflamation
|
|
|
What is rheumatoid arthritis?
|
It is an autoimmune disorder, in which the inflammation results in destroyed joints.
|
|
|
What is the difference between rheumatoid arthritis and osteoarthritis?
|
Osteoarthritis is not an autoimmune disorder but is due to trauma. There is symmetry in the involved areas in rheumatoid arthritis but not in osteoarthritis
|
|
|
What is synovial fluid?
|
It is produced by mesothelial cells, and lubricates the joint (surrounds the cartilage and bone)
|
|
|
What happens in rheumatoid arthritis?
|
The cartilage is destroyed, and the synovial membrane is inflamed.
|
|
|
What is a pannus?
|
A membrane of tissue that forms that has bone marrow derived cells, that releases factors that eventually result in cartilage destruction
|
|
|
What is an antibody mediated autoimmune disorder of the thyroid?
|
Hyperthyroidism
|
|
|
What is a cell mediated autoimmune disorder of the thyroid?
|
Hypothyroidism
|
|
|
What happens in hyperthyroidism?
|
An antibody is formed that acts as an agonist to cells that produce thyroid hormone
|
|
|
What is characteristic of hyperthyroidism?
|
Low TSH but high T3/T4
|
|
|
What is characteristic of hypothyroidism?
|
High TSH and low T3/T4
|
|
|
What are some consequences of SLE (Systemic Lupus Erthematosus)?
|
-Lesions in small blood vessels, thrombi in glomerular capillaries, fibrinous pericarditis, etc..
|
|
|
How many people are living with HIV/AIDS and where are the majority of these cases?
|
33.4 million w/ HIV/AIDS and 22 million of these are in Sub-saharan Africa
|
|
|
What are the three main ways of HIV transmission?
|
Sexual contact, IV, infected mother to newborn
|
|
|
What happens when the HIV virus penetrates the skin?
|
It is taken into dendritic cells that infect CD4+ T cells
|
|
|
What is HIV taken up into in dendritic cells?
|
Birbeck granules
|
|
|
What happens in these Birbeck granules?
|
The virus is partially degraded and some portions escape and infect lymphocytes
|
|
|
Where is most of the HIV in the blood?
|
In memory cells (and therefore in a latent, dormant state) and therefore treatment is often ineffective
|
|
|
Why are anti-HIV antibodies ineffective?
|
The virus is constantly evolving and changing its antigenic composition
|
|
|
How does the composition of the viral coat make it difficult for antibodies to bind?
|
Some of the proteins are highly glycosylated and do not bind well to antibodies
|
|
|
How many structural genes does HIV have?
|
3: Gag, Pol and Env
|
|
|
How many genes does HIV encode for and how many proteins does it make?
|
9 genes for 15 proteins
|
|
|
What does HIV protein Vif do?
|
Inactivates the host restriction factor APOBEC
|
|
|
Which molecule that if present, makes some primates HIV resistant?
|
ITRIM5alpha
|
|
|
What is aspergillosis?
|
Common fungal infection which can penetrate the blood vessels and destroy them
|
|
|
What is toxoplasmosis?
|
Resulting from infection with Toxoplasma gondii, that resides in muscle and brain tissue. The suppressed immune system in HIV patients cannot deal with the spores and tissue destruction results
|
|
|
What is progressive multifocal leukoencephalopathy?
|
Caused by the virus: HIV replciates in white matter of the brain and destroys the myelin
|
|
|
What are the main opportunistic infections that result in HIV infection?
|
-Pneumonocystis carin
-Toxoplasma gondii -Mycoses -Mycobacterium -Cytomegalic -Papovirus |
|
|
What results from Pneumocystis carin infection?
|
lung disease
|
|
|
Where does mycoses occur?
|
Mouth and esophagus
|
|
|
Where does mycobacterium infect?
|
Mostly in the lung
|
|
|
Where does cytomegalic infection occur?
|
Mostly in the eyes
|
|
|
What is a result of papovirus infection?
|
Brain destruction
|
|
|
What is the current therapy in treating HIV?
|
Valproic acid and HAART
|
|
|
What does LEDGF do?
|
Helps integrase action
|
|
|
How does chromatin remodelling of drugs help with HIV infection?
|
It activates synthesis of HIV proteins in latent cells making them visible to the immune system
|
|
|
What is the role of Vpu?
|
Vpu frees newly made viruses
|
|
|
What is Immune Reconstiution Inflammatory Syndrome?
|
A consequence of HAART and recovery of the immune system
-The immune system now acts against antigens in tissues (but is too strong? need to suppress!) |
|
|
What is the difference in viral load and CD4 count in patients w/ AIDS that were untreated and those exposed to HAART?
|
With HAART, the viral load dropped within months an dthe CD4+ count was stabilized, only slightly lower than normal.
-In untreated patients, the viral load stabilized but the CD4+ count decreased for years |
|
|
Where are glial cell precursors found?
|
In the ventricular system of the brain
|
|
|
What are the three types that glial cell precursor can differentiate into?
|
1-Oligodendroglial
2-Astrocytes 3-Microglial/Macrophages |
|
|
What are oligodendroglial cells responsible for?
|
Making myelin for the CNS (Schwann cells make it for the PNS)
|
|
|
What is myelin?
|
Lipid substance covering axons of the neurons to ensure maximal electric conduction along the axon
|
|
|
What are astrocytes?
|
Maintain the blood brain barrier and provide nutrition and general guidance to neurons
|
|
|
What do astrocytes produce to repair the CNS?
|
FIlaments that are similar to collagen (but not negatively charged- which would disrupt the function of neurons)
|
|
|
What are microglial-macrophages?
|
Bone marrow derived and are responsible for immune function and repairing damaged brain cells
|
|
|
What are the three possible structures of microglial-macrophages?
|
-Rounded w/ stored fat
-Small cell-body with processes -Rod-like |
|
|
What is neurophagia?
|
Macrophages eating damaged or infected neurons
|
|
|
What are the four causes of Cerebral infection?
|
-Bacteria
-Viral -Parasitic and Fungal -Prions (unique to CNS) |
|
|
What is meningitis?
|
Inflammation of the meninges (coverings) that surround the brain
|
|
|
Where is meningitis infection primarily established BEFORE proceeding to the brain?
|
The nose and pharynx
|
|
|
What is pia mater?
|
The thin membrane found closest to the brain
|
|
|
What is the subarachnoid space?
|
Found betwen the pia mater and the arachnoid membrane
|
|
|
What is the dura mater?
|
The meninge that is furthest way from the brain
|
|
|
What does the subarachnoid space contain?
|
CSF (Cerebral Spinal Fluid) and blood vessels (subarachnoid space)
|
|
|
Where is bacteria generally localized?
|
In the subarachnoid space
|
|
|
What is the glial limitans?
|
Thin layer of glial tissue between the pia and the cortex
|
|
|
Who is most likely to get meningitis?
|
Neonatals
|
|
|
What are some symptoms of meningitis?
|
Severe headache, fever, vomiting, neck stiffness, drowsiness/confusion, photophobia
|
|
|
What are some causes of CNS disease?
|
-Epidural abscess
-Purulent leptomeningitis -Brain abscess -Tuberculosis meningitis (at the base of the brain) -Neuropsyphilis -Lyme disease |
|
|
What is the most common cause of meningitis in neonates (newborns)?
|
E.coli, Group B streptococci, L. monocytogenes, S.pneumoniae
|
|
|
What are the most common causes of meningitis in children?
|
Neisseria meningitides S.pneumoniae, H. influenza
|
|
|
What are the most common causes of meningitis in adults?
|
S. pneumoniae and N meningitides
-Also, gram negative bacilli and Listeria species |
|
|
What level of pus is fatal in purulent meningitis?
|
A small amount of pus that collects around the brain is fatal
|
|
|
Which bacterial species can cause meningitis in immune-compromised individuals?
|
Cryptococcus bacteria
|
|
|
What are the lesions caused by Neisseria meningitides?
|
-Large hemorrhagic blotches on the skin due to small thrombi
-Hemorrhages in the eye -Infarct (necrosis) in the finger tips -Fatal bleeding in adrenal gland |
|
|
Where does Nesseria meningitides colonize?
|
The naso-pharynx, travels to the blood stream and then the CSF (where there is no real immunity)
|
|
|
What does N. meningitides induce?
|
Coagulation
|
|
|
What component of N.meningitides sets off the innate system?
|
The capsule (that has an LPS component)
|
|
|
What is the infection of the CNS by Tuberculosis meningitis secondary to?
|
Pulmonary infection
|
|
|
What does Tuberculosis meningitides infection involve?
|
The base of the brain (where the cranial nerves are located There is also local tissue and blood vessel destruction, as well as penetration into the brain
|
|
|
What was one of the 1st drugs against TB introduced?
|
Streptomycin
|
|
|
What does bacterial induced release of mediators result in meningitis?
|
Inreased intercranial pressure, because of the formation of thrombocytes that cause leakage of blood vessels and an increase in the cranial volume. Decrease blood flow leads to necrosis and death
|
|
|
What is dangerous about the formation of abscesses in the brain?
|
The collagen in the fibrous tissue that is laid down during the healing process is NEGATIVELY charged and this irritates the electricalyl charged cortex, resulting in seizures
|
|
|
What is encephalitis?
|
Inflammation of the brain
|
|
|
What are the most common VIRAL CAUSES Of encephalitis?
|
Echovirus, Coxsackie A and B, Herpes simplex virus, mumps, measles, and adenovirus
|
|
|
What can occur upon reactivation of the latent HSV?
|
Fatal necrotizing encephalitis
|
|
|
What is a key difference between viral meningitis and encephalitis?
|
Viral encephalitis destroys the tissue, lymphocytes, and macrophages
|
|
|
What is used to classify viruses?
|
Their homing instinct (target organ)
|
|
|
What are the viruses whose target organ is the meninges?
|
Mumps, Enteroviruses, Coxsackieviruses, HIV
|
|
|
What are the viruses whose target is the motor neurons?
|
Polio and enteroviruses
|
|
|
What are the viruses whose target is the oligodendritic cells?
|
Papoviruses (in immunocompromised individuals)
|
|
|
What are the viruses whose target are the neurons and glia?
|
HSV, rabies, measles)
|
|
|
What are the viruses whose target is the microgliaA?
|
HIV
|
|
|
What are the viruses whose target is the dorsal root ganglia?
|
Varcicella zoster
|
|
|
What are the viruses whose target is the fetal nervous system?
|
Rubella, Cytomegalovirus
|
|
|
What is the most common CNS infection?
|
HIV
|
|
|
What is the most common parasitic infection of the CNS?
|
Malaria
|
|
|
What is the only strain of malaria that can have an effect on the CNS?
|
P. falciparum
|
|
|
What does P. falciparum do to the brain?
|
It infects RBCS causing them to adhere to the endothelium of blood vessels and creating small infarcts in the brain
|
|
|
What is the mosquito that is the vector that carries parasites and infects humans?
|
Anopheles
|
|
|
In what form does the parasite enter the human and travel to the liver to replicate?
|
Sporozoite
|
|
|
In what form does the parasite leave the liver to infect blood cells and spread to the brain?
|
Merozoite
|
|
|
What is another term for Prion diseases and what do they cause?
|
Spongiform encephalopathies- makes holes in the brain
|
|
|
What are some Spongiform Encephalopathies?
|
-Creutzfeld-jakob disease
-Gerstmann-Straussler-Scheinker -Kuru -Scrapie (Mad Cow!) |
|
|
What part of the brain does prion disease affect?
|
-Cerebral cortex
-Cerebellum -Brain stem -Thalamus |
|
|
What is a prion?
|
A protein that undergoes a configurational change from normal (PrPc) to beta-pleated abnormal (PrPsc), which cannot be degraded
|
|
|
How is diagnosis of prion formation conducted?
|
Synaptic type staining and plaque staining
|
|
|
What happens in patients with MS (Multiple Sclerosis)?
|
Patients lose their myelin sheath in the CNS and the spinal cord, resulting in a loss of function of neurons
|
|
|
How is the myelin destroyed in patients with MS?
|
It is thought that cell-mediated autoimmune reactions take place and destroy the oligodendrocytes that make myelin for 3-4 axons
|
|
|
What are some common symptoms of patients with MS?
|
Loss of:
-function, vision, autonomic control, coordination, sensation, movement |
|
|
What results from the damaged caused from the demyelination in MS?
|
Periventricular plaques where the white matter (myelin) is destroyed
|
|
|
What are two important components of myelin?
|
Proteolipid Protein and Myelin Basic Protein
|
|
|
How do the components of myelin tie into the autoimmune component of MS?
|
It is thought that the proteolipid protein is presented by an APC as foreign
|
|
|
How is the myelin destroyed in patients with MS?
|
It is thought that cell-mediated autoimmune reactions take place and destroy the oligodendrocytes that make myelin for 3-4 axons
|
|
|
What are some common symptoms of patients with MS?
|
Loss of:
-function, vision, autonomic control, coordination, sensation, movement |
|
|
What results from the damaged caused from the demyelination in MS?
|
Periventricular plaques where the white matter is destroyed
|
|
|
What are two important components of myelin?
|
Proteolipid Protein and Myelin Basic Protein
|
|
|
How do the components of myelin tie into the autoimmune component of MS?
|
It is thought that the proteolipid protein is presented by an APC as foreign
|
|
|
How is it thought that T cell/APC interaction causes damage in MS?
|
=Excess glutamate, excess CA into oligodendrocytes and neurons, resulting in the relase of proteases and enzymes
|
|
|
What is acute demylination?
|
Exposure of sodium channels on the axon at the nodes
|
|
|
What is chronic demylination?
|
Sodium channels grow bigger or appear between the node (partial function is restored)
|
|
|
What are some immediate effects of cerebral trauma?
|
Scalp laceration
Skull fracture Cerebral contusions Cerebral lacerations Intracranial hemorrhage Diffuse axonal injury |
|
|
What are some delayed effects of cerebral trauma?
|
Ischemia, hypoxia, Cerebral swelling, Infection
|
|
|
What are common sites of brain trauma?
|
-Coup and contre-coup (frontal and occipital lobes)
|
|
|
What is the genetic control of aging?
|
There is a certain amount of times a cell can divide in its lifespan
|
|
|
What is Werner's disease?
|
The doubling time of cells is markedly reduced and someone with this disease will age prematurely, dying at 15 with the same diseases as someone that is 80 or 90
|
|
|
What is presbyopia?
|
A disorder associated with aging that begins at age 55-70, is the inability of the lense to change shape and focus light clearly on the retina. This is possibly due to a disorder of the CILIARY MUSCLE
|
|
|
Why do elderly people "shrink"?
|
Loss of the inter-vertebral disks resulting in the compression of the vertebral column
|
|
|
What happens to telomeres as we age?
|
They become shorter and shorter as cells replicate due to the mechanism of DNA Pol. If they are not replaced by telomerase, then eventually there will be none left and this will lead to cell dysfunction which is part of aging.
|
|
|
Why are germ cells and stem cells immortal?
|
They have telomerase
|
|
|
What are some genes that are involved in the age-mechanism apoptosis?
|
Bcl-2, Myc, p53, and APO-1/Fas
|
|
|
How is thought that caloric restriction increases our life span?
|
Minimizes free radical destruction, triggers our "survival reflex" which involves insulin production and growth hormone levels
|
|
|
How are the mitochondria thought to be important in the aging process?
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THey produce reactive oxygen species during metabolism.
-They also undego genetic changes and their activity decreases |
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What is a genetic factor to why it is thought women live longer than men?
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If the long arm is present on the Y chromosome they will die before women
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What is osteoporosis?
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Degeneration of the skeletal bone structure
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What are the two types of cells involved in bone growth?
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Osteoblasts and osteoclasts
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What is the role of osteoblasts?
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Make new bone
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What is the role of osteoclasts?
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Dissolve bone by use of a proton pump which produces HCl
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Why is it thought that women tend to develop osteoporosis quickly after menopause?
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Due to the decrease in estrogen levels
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How does estrogen help preserve bone integrity?
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-Osteoblasts produce a chemical agent called a RANK receptor that induces osteoclast maturation when their macrophage precursor binds to it. Estrogen blocks the RANK receptor and therefor osteoclast maturation
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What is the reagent that estrogen stimulates the release of that blocks the RANK receptor?
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Osteoprotegerin
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At what bone minearal density do hip fractures begin?
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0.79
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What drug should be taken for treating osteoporosis and how does it work?
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Reveromycin A- induces apoptosis of osteoclasts
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What should our diet be supplemented with to prevent/treat osteoporosis?
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Calcium and Vitamin D to increase deposition
Statins- stimulate bone formation Bisphosphonates- inhibit bone resorption |
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When would bone formation induction using parathyroid hormone supplements be necessary?
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In cases of severe osteoporosis
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What is osteoarthritis caused by?
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Wear and tear on the bones
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What leads to osteoarthritis?
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The cartilage will wear down on the bone until the heads are rubbing against each other
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What are Herberdon's Nodes?
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Swelling of joins resulting from the growth of new bone around the edges of the joint
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What is characteristic about cartilage in osteoarthritis?
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Loss of proteoglycans in the cartilage resulting in brittle cartilage, opposed to its normal flexibility
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What is Parkinson's disease?
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People with this disorder have an inability to move with any great fluidity because the control mechanism in the vasoganglia, thalamus and brain stem is abnormal
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Where are alot of neurons lost in Parkinson's?
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The substantia nigra (Dopamine producing area of brain)
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At what point in the loss of neurons does Parkinson's set in?
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At about 80% neuron loss
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What are Lewy bodies?
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Characteristic of Parkinson's they are a filamentous mass in the remaining neurons in the substantia nigra
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What happens in Alzheimer's?
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A marked atrophy of the brain: the hippocampus, entorhinal cortex (important memory cortex that preprocesse input signals for the hippocampus) and cerebral cortex shrink
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What happens to the ventricles and other spaces in the brain?
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They get bigger
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How are "senile plaques" formed in Alzheimer's?
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THe accumulation of beta-pleated, insoluble amyloid proteins that resist proteases
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What is one of the best indicators of Alzheimer's?
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The formation of neurofibrilary tangles in the brain
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What are the precursors of amyloid proteins normally?
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Transmembrane proteins
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What happens if alpha secretases act on the transmembrane amyloid precursor?
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The fragments are soluble
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What happens if beta-secretases act on the amyloid transmembrane precursor?
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The fragment is insoluble and will aggregate in tangles, inducing TAU
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What is TAU?
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A microfilament associated protein
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How do presenilin proteins affect amyloid production?
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A genetic mutation in these proteins results in the amyloid production
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What is dementia defined as?
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An acquired and persistent impairment of intellectual facilities and impairment of the person's capacity for personal and social responsibilities
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What does pre-clinical Alzheimer's present?
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The involvement of the TEMPORAL cortex (ability to speak and remember things decreases)
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What does mild-moderate Alzheimer's present?
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The frontal lobe (social skills and manners go downhill)
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What does advanced Alzheimer's present?
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It involves much of the brain and all social skills are lost, memory is gone, and other functions are markedly impaired
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What are some other types of dementias?
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Alzheier's
Parkinson's Pick's Disease Vascular Dementia Familial Congophilic Angiopathy |
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What is Frontal Lobe Dementia?
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The abnormal protein is in the nucleus instead of the cytoplasm
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What is Congohilic Angiopathy?
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The amyloid plaques are in the blood vessels, resulting in the easy rupture of the vessels
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What is a polyQ expansion?
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When plaques form in the nucleus (like in Frontal Lobe Dementia)
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What is the number 1 cause of death in children?
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Primary undernutrition
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What are some powerful adaptive changes in starvation?
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-Na/K pump decreases its activity, resulting in K loss
-Temperature homeostasis is reduced -Menstrual cycle arrests -Sperm production is affected -Infertility -Decreased immune response |
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What can happen during re-feeding?
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A surge of electrolytes
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What can happen in Bulimia as a result of vomiting?
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-Loss of HCl from the stomach resulting in alkalosis
-Loss of electrolytes K+, Na+, Cl |
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What can result from the loss of electrolytes in bulimia nervosa?
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Cardiac arthymias
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What can happen as a result of voluntary vomiting in Bulimia?
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Gastric rupturing as well as aspiration pneumonia (food in lungs)
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Are adipocytes homogenous?
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No. The characteristics of fat cells are different in different locations
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How is BMI calculated?
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Weight/height =kg/m^2
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What is a normal BMI?
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20-24
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What is an obese BMI?
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Over 30
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What is the BMI of someone that is morbidly obese?
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Greater than 40
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What happens when one goes from normal to overweight?
|
Hypertrophy of adipocytes occurs
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What happens in category 2 and 3 of obesity?
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Hyperplasia begins (there is max hypertrophy of adipocytes)
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What happens when someone loses the weight?
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The cells shrink back to their normal size, but hyperplasia remains
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What is lipoprotein lipase?
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Takes in free FA into the adipocytes
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What are adipokines?
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Secreted from adipocytes which travel to the hypothalmus, affecting appetite and feeding
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What is leptin?
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Released when adipocytes take in food
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What happens when leptin reaches the brain?
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Triggers a decrease in food intake/increases energy expenditure
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Where are the majority of the alpha adrenergic receptors on adipocytes for MALES?
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In the abdomen
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Where are the majority of alpha adrenergic receptors on adipocytes for FEMALES?
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The periphery
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Where is fat deposited initially?
|
Subcutaneously (under the dermis0
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Where is fat deposited after subcutaenous deposition initially?
|
Intraperitoneal (abdominal cavity) adipose tissue develops
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How does the turnover of triglycerides compare in the periphery and in the abdomen?
|
The abdomen turns over its triglycerides more quickly than those in the periphery
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What does free FA from adipocytes do in the liver?
|
Hyperlipidemia
Hyperinsulinemia Hyperglycemia |
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What poses a greater risk: abdominal obesity or peripheral obesity?
|
Abdominal
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What is RMR?
|
Resting Metabolic Rate- biggest use of energy (3/4)
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What happens to RMR in starvation?
|
It DECREASES
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What is RMR proportional to?
|
Lean body mass: more energy will be burnt sittin gif you are made of more protein than fat
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What is thermogenesis?
|
If someone exercises, they can still lose weight even if they eat alot
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What is the causative problem of type 2 diabetes?
|
Obesity
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What is metabolic syndrome?
|
Hyperinsuliemia, Hyperglyemedia, Low HDL cholesterol, abnominal obesity
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What happens if there is a drastic reduction in calories?
|
Cut down utilization of energy, decreased activity of the Na/K pump, decrease in muscle mass, changes in thyroid hormone, decreased RMR, out put of noradereniline
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What happens in weight cycling?
|
When you lost weight you lose more muscle mass than fat. Weight is regained in fat, and your body composition continually shifts to more fat and less muscle
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How is hunger affected by the increased level of fats?
|
Adipocytes signal to the brain, increasing hunger
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What do cigarettes kill the largest number of people from?
|
Cardiovascular disease
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|
What are ciliotoxins?
|
Impair the ability to clean the lungs
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|
What is the main carcinogen in cigarretes?
|
Benzo-a-pyrene (BAP)
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What are some things that smoking causes that cripple us?
|
Coronary heart disease
Peripheral vascular disease Stroke Lung disease |
|
|
What does coronary heart disease caused by smoking involve?
|
Increase in hypertension, CO in lung, atherosclerosis (clogged arteries), platelet aggregation,
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|
Why does smoking cause peripheral vascular problems?
|
It causes inadequate blood flow
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|
What type of effect does nicotonine/autonomic nervous system have?
|
Causes vasoconstriction
|
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|
What is HIGHER in second hand smoke?
|
The side stream smoke (coming out of the lit end) has a higher chemical content
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|
What is the first stage of alcoholic liver disease?
|
Fatty liver - turns yellow
|
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|
What happens in the second stage of alcoholic liver disease?
|
Scarring and fibrosis
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|
What type of effects does alcohol have on the brain?
|
Acts on: ion channels, membrane lipids, G protein coupled receptors
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|
What else can alcohol cause?
|
Myopathy, pancreatic damage, GI tract cancer, colon cancer, esophagus cancer, intestinal damage, testicular atrophy
|
|
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How does acute alcohol consumption affect the CNS?
|
It is a CNS depressant
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Which organs does chronic alcohol consumption affect?
|
Heart, GI tract, Reproductive system,
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