Chico Recommended Flashcards
(82 cards)
necrosis vs apoptosis
Apoptosis is programmed cell death. It is a regulated and controlled part of a cell’s life cycle and is advantageous. Apoptosis can be used by the body to limit tissue expansion and to eliminate some precancerous cells. The nature of apoptosis is that cells die, but do not trigger inflammation, as cellular debris is cleaned out by other mechanisms. Insufficient apoptosis can lead to uncontrolled cell growth, which can lead to cancer. The average adult experiences 50-70 million programmed cell deaths per day.
Necrosis is defined as traumatic cell death. This is usually caused by factors external to the cell or tissue such as infection, trauma or toxins. In contrast to apoptosis, necrosis is almost always detrimental. It causes uncontrolled release of products into the extracellular space causing inflammation and local cell destruction.
Cardinal signs of inflammation
pain, heat, swelling, redness, loss of function
4 components of the tissue repair process.
- ) Hemostasis in which the bleeding stops.
- ) Inflammation occurs to clean up the dead/damaged tissue.
- ) Proliferation of local healing cells ( as you explained in the notes) bringing in the healing crew.
- ) Scar formation ( exception: regenerative tissue)……With regeneration, cells grow to replace the injured with virtually little to no scarring.
- ) Maturation: tightening up the tissue for long term.
Differentiate between an embolus and a thrombus
A thrombus is a blood clot (solid mass of platelets and/or fibrin) that forms inside a vessel when clotting mechanism is activated with injury, and adheres at that location. It can happens at a site where artherosclerotic plaque has ruptured, further occluding blood flow.
An embolus is anything that travels through the blood vessels until it reaches a vessel that is too small to let it pass. When this happens, blood flow is stopped or severely limited by clot. Emboli are usually blood clots, such as pieces of thrombus that have broken free or blood that has become stagnant such as in atrial fibrillation, and start traveling through body
ischemia vs. infarct
Ischemia is cell injury or distress due to hypoxia, generally to lack of blood flow. Cells are distressed but still viable, and as blood flow is restored, they recover. The classic example of ischemia is Angina Pectoris.
Infarct is cell death due to lack of oxygen/blood flow. Cells are no longer viable and necrose. The classic example of infarction is a Myocardial Infarction.
All cells pass through a period of ischemia before infarction occurs. For some cells, this is shorter, 1-3 hours (brain), while for others it can be as long as 6 hours (extremities).
humoral and cellular immunity
The humoral response (or antibody‐mediated response) involves B cells that recognize antigens or pathogens that are circulating in the lymph or blood (“humor” is a medieval term for body fluid).
The cell‐mediated response involves mostly T cells and responds to any cell that displays aberrant MHC markers, including cells invaded by pathogens, tumor cells, or transplanted cells.
Innate vs Adaptive
Innate immunity refers to nonspecific defense mechanisms that come into play immediately or within hours of an antigen’s appearance in the body. These mechanisms include physical barriers such as skin, chemicals in the blood, and immune system cells that attack foreign cells in the body. The innate immune response is activated by chemical properties of the antigen.Natural Killer T Cells and Neutrophils are the principle cells involved.
Adaptive immunity refers to antigen-specific immune response. The adaptive immune response is more complex than the innate. The antigen first must be processed and recognized. Once an antigen has been recognized, the adaptive immune system creates an army of immune cells specifically designed to attack that antigen. Adaptive immunity also includes a “memory” that makes future responses against a specific antigen more efficient. T Helper Cells, B cells that produce antibodies, Cytotoxic T Cells, and macrophages are the principle cells involved, along with antigen presenting cells such as macrophages and dendritic cells.
Role of the HLA proteins in antigen presentation
The HLA system encodes for proteins on the surface of cells that are responsible for regulation of the immune system in humans. Among other functions HLAs present peptides from both inside the cell and outside the cell for T-cells to destroy.
The HLA system is used to identify ‘self’ from ‘non-self’, which can be seen in cases such as organ transplants and their rejection.
4 types of immune hypersensitivity reactions
- Immediate (type I) hypersensitivity: is a rapid IgE (turns on histamine) and mast cell-mediated vascular and smooth muscle response that occurs in genetically susceptible people. We know these responses as allergies. Histamine reaction: is very immediate: hay fever, allergies. If it is anaphylaxis, then it is immediate and gone within an hour or so. Asymptomatic reaction: bronchial restriction. Associated with hives. Short lived unless ingested.
- Antibody-mediated (type II) hypersensitivity: Antibody-mediated (type II) reactions result when antibodies are directed against antigens on the surface of cells or other tissue components. The deposition of the antibody can have a variety of detrimental effects, including inflammation, opsonization and phagocytosis, or functional derangements Antibodies that attack the cells.
- Immune complex-mediated (type III) hypersensitivity: Immune complex-mediated (type III) hypersensitivity results when complexes of antibodies and antigens deposit in vascular walls or other tissues and cause an inflammatory response. This type of pathology is commonly implicated in vasculitis and arthritis. Could be virus or drug induced.
- Cell-mediated (type IV) hypersensitivity: Cell-mediated (type IV) hypersensitivity results from an inappropriate or excessive immune reaction that is mediated by a specific subset of CD4+ helper T cells (Th-1 and Th-17 cells) or by CD8+ Cytotoxic T cells. These reactions are the basis for disease such as Crohn’s disease and multiple sclerosis. Delayed hypersensitivity reaction. No antibody involvement.
Benign vs Malignant
Benign neoplasms grow locally and their growth is limited. They do not spread to other tissues.
Three characteristics of Malignant neoplasms are that they i) grow uncontrollably, ii) invade into adjacent tissue, and iii) metastasize, to other, distant, tissues.
genetic mutations in etiology of cancer
Cancer cells are genetically mutated cells that have altered control of their cellular division, differentiation, and apoptosis. Once this occurs a clone of cells derived from the original mutated cell grows uncontrollably and becomes cancerous. Genetic mutations can vary depending on where they occur/originate, ie organs. Cancer generally involves several mutations before a cell becomes cancerous. Early mutations can affect policing mechanisms that repair defective DNA as it is transcribed, and this increases the rate of future mutations in this cell line.
transmission of HIV
- -Penetrative sexual intercourse
- -Direct injection with HIV-contaminated drugs, needles, syringes, blood or blood products
- -From HIV-infected mother to fetus in utero, through intrapartum inoculation from mother to infant or during breast-feeding
- -Rare cases have been reported to the CDC of HIV transmission via acupuncture, artificial insemination , tattoo, and human bite. Most of the incidents have occurred due to the use of a used needle and the transfusion of body fluids such as blood.
Presentation of HIV
After exposure to the HIV virus an incubation period lasting 2-4 weeks, but sometimes up to ten months occurs. After this time, HIV related factors are detectable in the blood and an individual will usually display primary infection symptoms such as fever, myalgias, headache, lymphadenopathy and nausea lasting up to 28 days. After the initial infection early stages of the AIDS disease will usually present around 6 months.
Hep A
- Type:
- Incubation:
- Transmission:
- Acute Infection:
- Groups at Risk:
- Serious consequences:
- Leads to chronic Infection?
RNA, and theres a vaccine
- 2 to 6 wks
- Fecal-oral Route (contaminated water, on food)
- Acute Infection = Initial: Fever, nausea, Rt upper quadrant pain, diarrhea, fatigue. Within days: jaundice, dark urine, light stools, rash. Symptoms last 1-3 months, up to 6 months
- Groups at Risk = Low Socioeconomic areas of poor sanitation or travellers to these areas
- Serious consequences = Acute death is rare, more common w/ compromised LVR function and age
- Leads to chronic Infection? = Rarely leads to chronic illness
Hep B
- Type:
- Incubation:
- Transmission:
- Acute Infection:
- Groups at Risk:
- Serious consequences:
- Leads to chronic Infection?
DNA, and theres a vaccine
- 4/ 6 wks to 6 months
- Blood/Body Fluids (needle sharing, blood transfusion, sexual contact, perinatal infection, rarely open sores)
-Acute infection (jaundice, anorexia, nausea, abdominal pain up to 3 months). Less severe than Hep A, but lasts longer. 30% don’t have chronic infection, 70% mild or asymptomatic
30% infected w/ acute hep B following resolution show low levels of virus even yrs later, but rare to progress to chronic Hep B (possible long lasting immune response)
- Groups at Risk = Individuals w/ high risk behaviors: IV Drug use, high risk sexual factors: multiple partners
- Serious consequences = ● Chronic active hepatitis ● Chronic LVR disease and cirrhosis ● Liver cancer ● Kidney failure ● Inflammatory arthritis
-Leads to chronic Infection = Most persons with acute disease recover with no lasting liver damage; acute illness is rarely fatal
Hep C
- Type:
- Incubation:
- Transmission:
- Acute Infection:
- Groups at Risk:
- Serious consequences:
- Leads to chronic Infection?
RNA and NO VACCINE
- 1/2 wks to 6 months
- Blood Borne (IV Drug use, needle stick, perinatal, infected blood products or organs)
- Similar to B, but usually milder
- Groups at Risk = Individuals w/ high risk behaviors: IV Drug use, high risk sexual factors: multiple partners (same as B)
Americans born between 1945 -1965, or who received blood products prior to 1992
- Serious consequences = ● Chronic active hepatitis ● Renal failure ● Cirrhosis, liver failure ● Liver cancer ● Hematologic disease (lymphoma) ● Thyroiditis ● Diabetes type 2 *most common cause of LVR disease + LVR transplant in US although prevalence is 1.6%
- Leads to chronic Infection =
• 15%–25% of newly infected persons clear the virus
• 60%–70% of chronically infected persons develop chronic liver disease
Define hemorrhage
an escape of blood from a ruptured blood vessel, especially when profuse
Describe the process of hemostasis. What is the role of platelets? What is the role of the clotting factors?
Hemostasis allows blood to clot to stop bleeding. Platelets are stimulated by endothelial cell damage or other mediators, platelets adhere to the site of injury, causing a ‘plug’. Clotting factors activate prothrombin into thrombin, and this in turn activates fibrinogen into fibrin. Fibrin forms long molecular bands that stick to the site of injury, intermesh with platelets – both are needed!
Describe clinical presentation and course of Bacterial Endocarditis
- Infection of the inner lining of the heart, generally affecting heart valves
- Presents acutely in most cases…days
- If unchecked, leads to dysfunction of the heart valve, usually with new onset regurgitation
- Acute regurgitation more symptomatic than chronic
- Aortic and mitral acute regurgitation can be serious with high mortality
Common signs…
∠ Fever
∠ Positive blood cultures for the infecting bacterium
∠ May have evidence of embolic disease or rash
∠ May have acute onset congestive heart failure
∠ Usually, but not always, in the setting of an acute infection
∠ High risk in IV drug abusers
Describe clinical presentation and course of Meningitis
- Intense headache
- Stiff neck
- Fever
If the diagnosis is known, supportive measures are adequate and recovery usually complete
Describe clinical presentation and course of Tuberculosis
- Incubation period….variable usually less than 4-6 weeks, symptoms usually resolve by 10 weeks
- Mycobacterium TB circulates throughout the body, but most has particular affinity for the lungs.
- The immune system kicks in, and cleans up ALMOST all of the bacteria.
- Most people have NO symptoms with initial infection. Of those that do have symptoms…
⋅ Fever is most common, low-grade, noted in 70% of patients
⋅ Pleuritic chest pain in 25% of patients
⋅ Other rarer symptoms include arthralgias, cough, chest pain on swallowing
BP: Systolic & Dysolic
- Systolic – highest pressure level achieved in cardiac cycle, reflecting pressure immediately after left ventricle is done ejecting blood.
- Dysolic – lowest pressure measurable, usually, at the end of ventricular filling when left ventricle is about to contract.
140/90 - if any more then these numbers then high
pathogenesis of atherosclerosis and plaque formation
Start with microscopic damage to the wall from hypertension leading to fats deposit, it leaks over years, becomes calcified and slowly starts blocking the lumen
relationship between angina, myocardial infarction, and coronary artery disease
Angina – is defined as ischemic disease, caused by coronary artery occlusion, which is reversible and by itself does not cause death to myocardial cells, but causes some ischemic changes in affected cells. (Heart tissue is still ok, haven’t lost any cells)
Myocardial infraction – is defined as ischemic disease, caused by coronary artery occlusion, which without treatment would cause death to myocardial cells. (Heart cells are actually dying because of lack of blood flow. Irreversible damage. )
Coronary artery disease – can be asymptomatic, but ACS almost always represents a symptom such as unstable angina or myocardial infarction. Atherosclerotic plaques, the hallmark of atherosclerosis, progressively narrow the coronary artery lumen and impair antegrade myocardial blood flow.