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Pathophys. Exam II
Flash Cards for our second pathophysiology exam
| Question | Answer |
|---|---|
| What is a mature red blood cell called? | Erythrocyte |
| What is the Erythrocyte's function? | To carry oxygen |
| Why does a red blood cell (RBC) have a concave structure? | Allows for more surface area, which allows a greater potential for exchanging oxygen. |
| What is the structure of Hemoglobin? | It is 2 pairs of polypeptide chains (2 alpha & 2 beta). It is a Quaternary protein. Each subunit has 1 iron-containing heme unit. |
| The production of each chain is controlled by individual genes with five different loci... Implication? | More risk for mutation leading to different levels of severity. Beta genes would have more severe mutations because there are less genes coding for the beta chain. |
| How many heme units are in hemoglobin? and what is the heme units purpose? | There is one heme unit per subunit, so in hemoglobin there are 4 hemeunits. Their purpose is to bind oxygen. |
| Why does the membrane of the RBC need to be extremely strong and extremely flexible? | It has to be strong enough to be shot out of the heart and flexible enough to squeeze through capillaries |
| What is the rate of hemoglobin synthesis by RBC's depend on? | The availability of Iron for heme synthesis. |
| What happens if a patient is iron-deficient? | If you don't have a unit of iron, you can not make an effective functional hemoglobin. So you don't make heme, so hemoglobin doesn't have heme, so your RBC's cant carry oxygen |
| How can a person become iron-deficient? | Iron comes from your diet, so if you don't get enough iron in your diet (red meat, leafy green vegetables), you will be iron-deficient. Are anemic (tired,weak). |
| Who is at risk for being iron-deficient? | Women, vegetarians, peptic ulcers (slow chronic blood loss), blood loss |
| What happens to iron once it is in the blood stream? | It doesn't dissolve in plasma. It encounters transferrin and becomes bound to it. Then it can be transported to the liver or bone marrow. |
| What happens to iron if it is transported to the liver? | Ferritin binds to the iron and stores it in the liver. If there is not enough iron in the blood it can be transported back to the blood stream. |
| What happens if it is transported to the bone marrow? | Used to make red blood cells. |
| What is the spleen and it's purpose? | It is a lymph organ that filters blood. It is made up of small convoluted blood vessels. It is a pruning ground of RBCs, because if the RBC is not strong enough to make it through the vessels, it will lyse. |
| What is erythropoiesis? | It is the process by which new RBC's are made. |
| Where does erythropoiesis occur? | It occurs in the bone marrow. |
| What is erythropoietin and where is it produced? | It is produced by the kidney. It is the growth factor for RBC. The kidney monitors blood pressure, flow, sodium concentration, and it is an oxygen sensor. It can detect low tissue oxygen and release erythropoietin, which stimulates the bone marrow. |
| How does the erythropoietin stimulate the bone marrow? | It causes the stem cells to commit to being red blood cells. The stem cells then go through replication and maturation eventually spitting out nucleus. |
| What is reticulocytes? | They are red blood cells that are not fully matured. It fully matures once released in the blood flow for a couple of days. |
| Why are reticulocytes counted? | Red blood cells tend to last around ~120 days. So you can look at the reticulocytes and tell if red blood cells are still being made and whether there is a problem with bone marrow or not. |
| What is the driving force for erythropoietin? | Hypoxia (high altitude, smokers, low blood pressure, heart attach victims, shock) |
| What happens while a red blood cell ages? | Metabolic activity decreases and membrane thins & weakens. |
| What is heme changed to in the blood and why? | Heme is not very soluble so it is changed to bilirubin which is soluble. |
| Where is bilirubin sent to? | Once it is changed from heme. It is sent to the liver. The liver sends it out with its bile to the gall bladder. Then the bile is sent to the intestines, then out of the body. |
| What is Jaundice? | It is a build up billirubin in the blood that turns a person skin yellow. Means the liver is not working well. |
| Why do babies have jaundice? | Their liver is not fully functional and their blood steams are full of the mother's RBC, the mother's RBC begin to lyse, so there is an excess amount of conjugated bilirubin which the liver can not keep up with. |
| How much of the hematocrit should be RBCs? | ~ 40% |
| What is polycythemia? | It is an excess of RBC's in the hematocrit compared to normal. It can be due to high altitude, cancer, etc. |
| What are things you notice about red blood cells to tell if they are healthy? | Color, Size, Shape |
| What is anemia? | Anemia it a lack of healthy red blood cells. It is not a disease, but a condition, because it is a deficiency and it is an indication of a disease process or alteration in the body. |
| What are types of anemia? | * Blood Loss (trauma) * Hemolytic * Defective RBC Production |
| What are two types of Blood Loss Anemia? | Acute Blood Loss and Chronic Blood Loss |
| Why does chronic blood loss cause iron-deficiency? | The gradual continuous loss of red blood cells is leeching iron from the system |
| What are two types of inherited hemolytic anemia? | Sickle Cell Anemia and Thalassemia. They both effect the production of hemoglobin |
| What is sickle cell anemia caused from? | It results from a point mutation in the beta chain of hemoglobin. A Valine replaces every glutamic acid in the chain. |
| What happens when a person with sickle cell anemia has a cell deoxygenated? | The abnormal HgB molecule aggregates and polymerizes to form a gel. This distorts or sickles the RBC |
| Why does replacing glutamic acid with valine causes sickling? | Valine has much more hydrophobic interactions with other hydrophobic groups on hemoglobin causing them to aggregate. |
| What is a crenated cell? | Crenated is an intermediate shape between sickle and normal shape. |
| What are the two forms of sickle cell disease and where is there a high incidence of it? | The two forms are: homozygous and heterozygous. There is a high incidence of it in places where malaria is prevelent. |
| What is the homozygous form of sickle cell disease? | 2 effect HgB genes, the 2 beta genes, so 80 to 95% of HgB is altered. |
| What is the heterozygous form of sickle cell disease? | One abnormal HgB gene. It is a milder form because only 40% of HgB is altered. |
| Why is there chronic hemolytic anemia with people who have sickle cell disease? | There is premature destruction of RBC's due to the cells being rigid causing them to lyse easily. |
| Why is there blood vessel occlusion with people who have sickle cell anemia? | The sickle cells block blood vessels and they adhere to the vascular endothelium triggering platelet activation. |
| What are some factors that exacerbate sickling? | Cold, stress, physical exertion, sleep (all of these increase oxygen demand or decrease oxygen levels). Also dehydration, diarrhea, and acidosis. |
| What are some long term effects of sickle cell disease? | Anemia, severe pain, organ failure, acute chest syndrome, stroke, growth retardation, splenic injury, hyperbilirubemia, life threatening infections. |
| What are some treatment options for sickle cell disease? | Avoid stress, prophylactic antibiotics, full immunizations, hydroxyurea, bone marrow transplant, Arginine (vasodilator, prevent plateleet aggregation |
| what is thalassemia? | a genetic defect that results in defective synthesis of alpha or beta chains of hemoglobin |
| What populations does alpha and beta thalassemia occur in? | Alpha occurs in asian populations and beta in italian and greek populations |
| What are some manifestations of thalassemia? | Depends on severity of gene mutation. The cells tend to be pale and small. Hemolysis and anemia occurs due to the accumulation of unaffected chain. |
| What are the 4 alpha thalassemias? | 1)Alpha trait: 1 defective gene, asymptomatic. 2)Alpha Thal. minor: 2 defective genes, mild 3)Hemoglobin H Disease: 3 defective genes, common in asians,chronic moderate anemia, most important clinically. 4)Alpha Thal. major: 4 defective genes, fatal. |
| What are the 2 beta thalassemias? | 1)Thalassemia minor: 1 defective gene, mild-mod anemia, asymptomatic unless stressed. 2)Thalassemia major: severe anemia, increased erythropoiesis, iron overload |
| What patients are at greatest risk for iron deficiency? | Menstruating women, chronic blood loss, vegetarians, pregnant women, adolescents |
| What are manifestations of iron deficiency? | Lack of hemoglobin synthesis, small & pale cells, hypoxemia, fatigue, sores, poikilocytosis, and anisocytosis |
| What is poikilocytosis? | Irregular shape red blood cells |
| What is anisocytosis? | irregular size red blood cells. brittle hair, nails, mouth |
| What is pica? | Bizarre syndrome of eating odd substances, ice, dirt, clay, paint with severe iron defiency |
| What is Vit. B12 used for? | It is an essential co-factor for red blood cell dna synthesis and maturation |
| What is vit b12 deficiency anemia? | A rare condition that causes megaloblastic anemia (enlarged RBCs). there is an excess rna and protein production |
| What is pernicious anemia? | Inability to absorb B12 through the gut. There is impaired production of the intrinsic factor by the gut. |
| What is Folic Acid used for? | Necessary for RBC DNA synthesis and RBC maturation. |
| What is folic acid deficiency? | Due to malnutrition, alcoholism, or intestinal malabsorption syndromes. It can cause neural tube defects in a fetus. |
| What is aplastic anemia? | Damage to the stem cells in the bone marrow. Several different things can cause it: radiation, toxins, anti-cancer drugs, chemicals, etc |
| Why do we have an inflammatory response? | It is a protective response, eliminates the initial cause of the injury as well as any necrotic cells that result from the injury. It also dilutes, destroys, or neutralizes and sets the stage for healing. |
| What are the signs of inflammation? | Rubor (redness), Tumor (swelling), Calor (heat), Dolor (pain), and functio laesa (loss of function) |
| What are the 2 components of acute inflammation? | 1)Vascular stage: response of blood vessels to injury 2)cellular stage: response of immune cells to injury |
| What is Vascular Response? | Brief vasoconstriction of small vessels and followed by rapid dilation of local arterioless and venules (redness and warmth). Also increased capillary permeability. |
| What is the point of edema in inflammation? | to flood and dilute out injurious toxins. |
| What purpose does the increased capillary permeability serve? | Stagnation of blood flow limits spread of bacteria and toxins. It facilitates the movement of WBC's out of blood vessels |
| What is cellular response? | It is the movement of white blood cells into the area of injury. It is set up by vascular response. |
| What are neutrophils? | They are phagocytic granulocytes that are first responders. They generate toxic free radicals the begin to digest and destroy organisms. They only last 10 hours |
| What are basophils? | They are pro-inflammatory granulocytes. they release histamine and other inflammatory mediators (keeps inflammatory reaction going) |
| What are eosinophils? | They regulate inflammation and are toxic to parasites. |
| What are monocytes? | Long lived white blood cells. They migrate into tissues and become macrophages. |
| What is the WBC response? | 1) Margination 2) Transmigration 3)Chemotaxis 4)Phagocytosis |
| What is Margination? | The WBCs move to the edges of the blood vessels. They are able to do this because the blood flow has slowed down around wound. |
| What are adhesion molecules? | molecules in the walls of the blood vessel that allows the wbc to latch on for a bit. This allows it to migrate into the tissue. |
| What is transmigration? | It is when WBC move from the blood vessels into the tissue. |
| What is Chemotaxis? | It is the process of the WBC's following chemicals released from the bacteria and injured cells. |
| What is phagocytosis. | The WBC begin to engulf debris and bacteria and break it down. |
| What role does cytokines play in inflammation? | They help to stimulate immune response and they help attract white blood cells to the area. |
| Where are Mast cells distributed? | throughout the body in the connective tissues. They tend to run adjacent to blood vessels |
| What do mast cells contain? | granules with numerous inflammatory mediators (histamine, leukotrienes, prostaglandins) that are released when tissues are injured. |
| What is SRS-A? | Slow reacting substance for anaphylaxis |
| What is arachidonic acid? | 20 carbon fatty acid found in cell membranes. It is released by cell injury or inflammation. Used to synthesize prostaglandins and leukotrienes. |
| What do leukotrienes do? | Induce smooth muscle contraction. Constricts pulmonary airways. Increases microvascular permeability. |
| What do prostaglandins do? | Induces vasodilation and bronchoconstriction. Inhibits inflammatory cell function |
| What do thromboxane do? | Vasoconstriction and bronchoconstriction. It also promotes platelet function. |
| Corticosteroids inhibit the formation of: | Leukotrienes, prostaglandins, thromboxanes, and arachidonic acid |
| What is the regeneration stage of tissue repair? | Occurs in parenchymal (functional) cells that are capable of cell proliferation, THe lost functional tissue is repaired with new functional tissue. No loss of function and little or no evidence of injury. |
| What cells are capable of regeneration? | Labile cells, stable cells |
| What are labile cells? | the cells that continue to divide throughout life. constantly going through mitosis. |
| What are stable cells? | The cells that have stopped growing because it has reached its full potential, but can regenerate if needed. The stroma (connective tissue and blood vessels) must be intact to be able to regenerate. |
| What is connective tissue replacement? | When cells that can not divide are destroyed, they are replaced with scar tissue that is not functional. |
| What are the three stages of tissue repair? | 1) Inflammatory phase. 2)Proliferative phase 3)Maturational phase |
| What is the inflammatory phase? | Hemostasis (blood clotting), vascular and cellular inflammatory responses, 24-48 hours |
| What is the proliferative phase? | Begins in 2-3 days may last 3 weeks. Production of collagen, release of growth factors, proliferation of vascular endothelium, and proliferation of epithelial cells at edges (to seal top of wound) |
| What is granulation tissue? | A tissue in the process of repair. It is a spongy yellowish tissue. |
| What is the maturational phase? | Also known as remodeling, 3 weeks to 6 months post injury. Remodeling of repaired tissue to give maximal strength. Continued activity of fibroblasts and collagen |
| What is primary intention? | Small wound that repair quickly and completely |
| What is secondary intention? | Larger wounds that require longer to heal and often leave significant scar tissue. |
| What is keloids? | abnormal formation of scar tissue during wound repair. Most common in african americans |
| What are factors effecting wound healing? | Malnutrition, blood flow and oxygen delivery, age, impaired immune or inflammatory response, infection, wound separation, or foreign bodies |
| How does malnutrition effect wound healing? | Lack of proteins and amino acids, vitamins, carbohydrates, etc. |
| What is Kwashiokor? | Protein malnutirtion, GI disease where it is not absorbing effectively |
| How does blood flow and oxygen delivery affect wound healing? | blood flow and oxygen delivery supply nutrients for repair, remove debris, require oxygen to generate free radicals |
| How does infection, wound separation, and foreign bodies affect wound healing? | It prolongs inflammation, inhibits activity of fibroblasts, prevents contact of wound edges. |
| How do sutures enhance wound healing? | It brings the edges of the wound together |
| When was HIV discovered? | 1986 |
| How is HIV transmitted? | Contact with blood and body fluids, sexual contact, IV drug use, infected blood products, maternal-fetal transmission (can cross placenta, and breastfeeding) |
| How does HIV replicate? | Can not replicate independently. Must use host cell replication machinery (obligate parasite). |
| What is unique about the RNA HIV virus? | Double strand of identical RNA. It is a retrovirus, so it must have its RNA genome copied into DNA in order to be replicated. |
| How many coatings does the RNA have and what are they? | 3, protein capsule, protein shell, and a lipid bi-layer |
| What is on HIVs lipid bi-layer? | peplomers (spikes) that are organ of attachment made up of gp120 and gp41. they use cD4 as sites of attachment. |
| Where is CD4 found? | Helper T cells |
| This glycoprotein is used by HIV to attach to human CD4 | gp120 |
| What is reverse transciptase? | Copies RNA into DNA. it is needed because our body does not produce this enzyme. |
| What is HIV integrase? | Integrates the virus genome into the host cell genetic material. |
| What is HIV protease? | A protein modifying/cleaving enzyme. After the viral proteins are produced and before they are functional, they have to be modified/cleaved to be functional. |
| What are the 8 steps of the HIV life cycle? | 1. Binding 2. Fusion 3. Reverse Transcription 4. Integration 5. Transcription 6. Translation 7. New Virus Assembly and Budding 8. Maturation |
| What is reverse transcription? | translating the RNA into DNA |
| What is intergration? | Integrating the virus DNA into the host genetic material |
| What is transcription? | translating the virus dna to mRNA |
| What is translation? | The coding of the mRNA into proteins,etc |
| What is maturation? | The modifying and cleaving of the proteins to make it functional. |
| The drug AZT (Zidovudine) acts by? | Inhibiting HIV replication |
| What are the three phases of HIV infection? | 1. Primary infection 2. Chronic Asymptomatic (latency) 3. Overt AIDS |
| What is HIVs primary infection? | 2-4 weeks, acute flu-like syndrome, very high viral loads |
| What is latency? | Median time 10 years, few overt signs or symptoms, persistent lymphadenopathy (swollen lymph nodes) possible, viral load low |
| What is overt AIDS? | CD4 cell counts are <200 cells/mcL, can lead to death in 2-3 years without treatment, viral load rises, opportunistic infections, cancers, virus may enter CNS |
| What are the 4 types of HIV progressors? | Typical, rapid, slow, long-term non progressors |
| What is HARRT? | Highly active anti retroviral therapy |
| What is induction chemotherapy? | Induce remission, radiation, and wipe the bone marrow, then you prep for a new bone marrow transplant |
| What is the other receptor besides gp120 that HIV attaches to? | CCR-5 receptor |
| What are opportunistic infections? | Infections that take advantage when your immune system is down. They normally do not occur in a person with a healthy immune system. |
| What are 2 opportunistic cancers? | Kaposi Sarcoma, Burkitt's Lymphoma |
| What are some opportunistic infections? | CMV (Cytomegalovirus), R jiroveci pneumonia, TB (HIV is due to a major resurgence of this), and candidiasis |
| This opportunistic fungus can cause oral thrush in HIV patients: | Candida |
| AIDS Dementia Complex is: | Late stage manifestation, direct HIV effects on the brain, motor and mental impairment, amnesia, personality disorders |
| What are the current targets of HIV drugs? | Fusion inhibitors, chemokine receptor inhibitors, Reverse transcriptase inhibitor, protease inhibitor, integrase inhibitor |
| Why has it been so difficult to produce an effective HIV vaccine? | There are a large number of strains and a high amount of mutation |
| What is hypersensitivity? | Excessive or inappropriate activation of the immune system |
| What are four types of hypersensitivity? | Type I - Immediate, Type II - Antibody mediated, Type III - Immune-Complex Mediated, Type IV - T-cell mediated |
| Type I Hypersensitivity: | Begins rapidly after antigen exposure, allergic reaction, involves 2 main cells (Helper T-cells, mast cells) |
| What are the steps of Type I first exposure? | 1. exposure to the antigen (swelling, redness) 2. production of AB (IgE) against antigen (should not happen) 3. IgE coats the surface of Mast cells (should not happen). Minimal systemic effects with first exposure |
| What happens when you are exposed again to Type I antigen? | The IgE-coated mast cells degranulate and cause widespread release of Histamine, Prostoglandins, and Leukottrienes |
| What is anaphylaxis? | Systemic, life-threatening hypersensitivity reaction. systemic release of histamine, prostaglandins, and leukotrienes causing hypotension, bronchospasm, marked edema, angioedema, itching, GI cramps |
| What are treatment options for patients with anaphylactic shock? | drug to dilate the airways, antihistamines, IV fluids, corticosteroids |
| What is type II hypersensitivity? | Mediated by IgG or IgM. Results in cell destruction. Antibodies are made inappropriately against stuff that should not be an antigen. Grave's disease, blood mis-match |
| What is type III hypersensitivity? | Accumulation and deposition of insoluble antigen-antibody complexes. May occur following widespread infection. Neutrophils try to destroy complexes but only worsen inflammation. |
| In type III, antigen-antibody complexes may deposit in blood vessel walls causing: | Vasculitis, Glomerunephritis |
| What is serum sickness? | Is a type III reaction with widespread deposition of AG-AB complexes in tissues and blood vessels. Causing: Vasculitis, joint pain, renal damage, rash, etc. Ex: Penicillin, food reaction, etc |
| What is Type IV T-cell mediated hypersensitivity? | Principle mechanism of response against certain bacteria, viruses, fungi, and protozoa. It involves direct cell mediated cytotoxicity and delayed hypersensitivity mediated by excess cytokine release from T-cells |
| What are examples of Type IV? | TB, HBV, Poison Ivy, Contact dermatitis, Latex allergy |
| What is the thinking behind type IV? | the immune system is trying to attack the antigens, which damages the skin. Delayed reaction can take hours to days after exposure because it is a cell mediated response. |
| What is a peanut allergy? | Type I |
| What is a blood transfusion mis match? | Type II |
| What is a delayed hypersensitivity due to cytokines? | Type IV |
| What is poison ivy? | Type IV |
| What is a deposition of AG-AB complexes? | Type III |
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