821435
| Question | Answer |
| What type of imbalance leads to Diabetes insipidus, what is the general cause of the balance and the symptoms? | -ADH deficiency due to posterior pituitary damage. -Number one cause is head trauma that damages the hypothalamus. -Causes a huge output of urine and intense thirst. -Must keep well hydrated. |
| What imbalance causes Syndrome of Inappropriate ADH Secretion (SIADH) and what are the symptoms? | ADH hypersecretion (after neurosurgery, trauma, or secreted by cancer cells). -Results in retention of fluid, headache, disorientation. -Must restrict fluids and monitor blood sodium levels. |
| Hypersecretion of Growth Hormone (GH) results in? | Gigantism |
| Hypersecretion of Growth Hormone (GH) in adults results in? | Acromegaly. -Enlarged hands and feet, soft tissue growth, jaw brow, heart |
| Hyposecretion ofGrowth Hormone (GH) in children leads to? | Pituitary dwarfism. |
| Myxedemia | Severe hyperthyroidism caused by hyposecretion of Thyroid Hormone (TH) |
| Hashimoto's Thyroiditis | Hyposecretion of Thyroid Hormone(TH). -Most common cause of hypothyroidism. -Autoimmune disease. -Something causes T cells to attack thyroid. -Test for antibodies. |
| Endemic Goiter | Enlargement of the thyroid do to lack of iodine. -Hyposecretion of Thyroid Hormone (TH). |
| Cretinism | Hyposecretion of Thyroid Hormone (TH) in infants. -Results in dwarfed stature and mental retardation. |
| Graves' Disease | Caused by hypersecretion of Thyroid Hormone (TH). -Most common cause of hyperthyroidism. -Characterized by goiter and exopthalmos (enlargement of one or both eyes) |
| Hyperparathyroidism due to tumor | Parathyroid hormone imbalance. -Bones soften and deform. -Elevated Ca2+ depresses nervous system and contributes to formation of kidney stones. |
| Hypoparathyroidism | Following gland trauma or removal or dietary magnesium deficiency. -Results in tetany, respiratory paralysis and death. |
| Aldosteronism | Hypersecretion of Aldosterone due to adrenal tumors. -Hypertension due to extansive Na+. -Excretion of K+ leading to abnormal function of neurons and muscle. |
| Addison's Disease | Hyposecretion of glucocorticoids (cortisol). -Also involves deficit of mineralcorticoids (aldosterone). -Decrease in glucose and Na+ levels. -Weightloss, severe dehydration, and hypotension |
| Cushing's Syndrome | Hypersecretion of Glucocorticoids (Cortisol). -Depresses cartilage and bone formation. Inhibits inflammation (slowing tissue repair). Depresses the immune system. -Promotes changes in cardiovascular, neural and gastrointestinal function. |
| Diabetes mellitus (DM) | Due to hyposectretion of insulin (type 1, autoimmune) or hypoactivity (type 2) of insulin. (Dependent v. Insulin resistance - inability to bind the receptor). -Blood glucose levels remain high-->nausea-->higher blood glucose levels (fight or flight response). -Glycosuria: glucose spilled into urine. -Fats used for cellular fuel-->lipidemia; ifsevere-->ketones(ketone bodies) from fatty acid metabolism-->ketonuria and ketoacidosis. -Untreated ketoacidosis-->hypernea (disrupted heart activity and O2 transport and depression of nervous system)-->coma and death possible. |
| Diabetes mellitus signs | 1. Polyuria: huge urine output (Glucose acts as osmotic diuretic). 2. Polydipsia: excessive thirst (from water loss due to polyuria). 3. Polyphagia: excessive hunger and food consumption (Cells cannot take up glucose and are starving) |
| Hypoglycemia | Excessive insulin secretion. -Low blood glucose levels. -Anxiety, nervousness disorientation, unconsciousness, even death. -Treated by sugar ingestion. |
| Oxytocin | Strong stimulant of uterine contraction. -Triggers milk ejection. -Plays a role in sexual arousal. -Acts as a neurotransmitter in the brain. |
| Antidiuretic hormone | Prevents the formation of urine. -Helps avoid dehydration or water overload. -Alcohol inhibits ADH release and causes copious urine output. |
| Growth Hormone aka Somatotropin | Produced by somatotropic cells. -Increases blood levels of fatty acids; encourages use of fatty acids for fuel; increase protein synthesis. -Decreases rate of glucose uptake and metabolism. -Glycogen breakdown and glucose release into blood (anti-Insulin effect) |
| Gherlin | Hunger hormone. -Increases storage of energy. -Increases appetite. -Often occurs with lack of sleep. |
| Thyroid stimulating hormone | Produced by thyrotropic cells of anterior pituitary. -Stimulates normal development and secretory activity of thyroid. -Inhibited by rising blood levels of thyroid hormone that act on both the pituitary and hypothalamus (negative feedback system) |
| Adrencorticotrpic Hormone (ACTH) | Secreted by corticotropic cells of anterior pituitary. Stimulates adrenal cortex to release corticosteroids. -Regulated by corticotrpin releasing hormone in daily rhythm. -Internal and external factors can effect release of CRH (fever, hypoglycemia, stress..) -Negative feedback system shuts off both CRH and ACTH |
| Gonadotropins in females | Leutinizing hormone (LH) works with FOllicle Stimulating hormone (FSH) to cause maturation of the ovarian follicle. -LH works alone to trigger ovulation. -LH promotes synthesis and release of estrogen and progesterone. |
| Gonadotropins in males | LH stimulates interstitial cells of the testes to produce testosterone. FSH important in sperm production. |
| Prolactin (PRL) | -Stimulates milk production. -Role in males not well understood. -Blood levels rise toward end of pregnancy. -Suckling stimulates PRL release and promotes continued milk production. -Hypersecreation causes inappropriate lactation, lack of menses, infertility in females, and impotence in males. Possibly caused by pituitary tumor. |
| Thyroid hormone | -Affects virtually every cell in the body. -Increases metabolic rate and heat production. -Regulation of tissue growth and development. -Maintenance of blood pressure. |
| Calcitonin | Puts calcium in the bone. |
| Parathyroid hormone | Goal is to increase blood calcium. -Promotes activation of vitamin D. |
| Aldosterone | Most important mineralocorticoid. -Increase sodium back into the blood. -Maintains sodium balance. |
| Cortisol | Help the body resist stress by keeping blood sugar levels relatively constant. -Maintaining blood volume and preventing water shift into tissue. |
| Epinephrine | Stimulates metabolic activities, bronchial dilation, and blood flow to skeletal muscles and heart |
| Norepinephrine | Influences peripheral vasoconstriction and blood pressure |
| Melatonin | Timing of sexual maturation and puberty. -Day/night cycles (Circadium rhythm). -Physiological processes that show rhythmic variations (body temp, sleep, appetite). |
| Glucagon | Causes increased blood glucose levels |
| Insulin | Lowers blood glucose levels. -Enhances membrane transport of glucose into fat and muscle cells and, liver. -Inhibits glycogenolysis and gluconeogenesis. -Participates in neuronal development and learning and memory. -Increases protein synthesis. -Primary stimulus of release is elevated blood glucose levels. -Rising blood levels of amino acids and fatty acids also trigger release. |
| Estrogen | Maturation of reproductive organs. -Appearance of secondary sexual characteristics. -With progesterone causes breast development and cyclic changes in uterine mucosa. |
| Testosterone | Initates maturation of male reproductive organs. -Causes appearance of males secondary sex characteristics and sex drive. -Necessary for normal sperm production. -Maintains reproductive organs in funcitonal state. |
| Leptin | Appetite control. -Stimulates increased energy expenditure. -Drops with sleep deprivation. |
| Resistin | Insulin antagonist |
| Adiponectin | Enhances sensitivity to insulin. |
| Gastrin | Stimulates release of HCl |
| Secretin | Stimulates liver and pancreas |
| Cholecystokinin | Stimulates pancreas, gallbladder, and hepatopancreatic sphincter. |
| Seratonin | Acts as a paracrine (gastric motility) |
| – Atrial natriuretic peptide (ANP) | Decreases blood Na+ concentration, therefore lowers blood pressure and volume |
| Erythropoietin | Signals production of red blood cells |
| Renin | Initiates the renin-angiotensin-aldosterone mechanism |
| Anemia | Blood has abnormally low oxygen carrying capacity. It is a symptom rather than a disease itself. Blood oxygen levels cannot support normal metabolism. |
| Hemorrhagic anemia | Rapid blood loss (ex. stab wound). Treated by blood replacement. |
| • Chronic hemorrhagic anemia | Slight but persistent blood loss. Hemorrhoids, bleeding ulcer. Primary problem treated. |
| Iron deficiency anemia | Caused by hemmorrhagic anemia, low iron intake, impaired absorption. -Most common nutrient deficiency anemia. -Iron supplements to treat. |
| Pernicious anemia | Autoimmune disease. Destroys stomach mucosa. -Lack of intrinisic factor (protein needed to absorb 99% of B12). Leads to deficiency of B12. -RBCs cannot divide leading to macrocytic (larger cell) anemia. -Treated with B12 injections, sublingual or nasal gel. -Also caused by low dietary B12. -1% of B12 is absorbed passively. |
| Renal anemia | Lack of EPO (erythropoeitin). Often accompanies renal disease. -Treated with synthetic EPO. |
| Aplastic anemia | Destruction or inhibition of red marrow by drugs, chemicals, radiation, viruses. -Usually cause unknown. -Treateed short-term with transfusions; longterm with transplanted stem cells. |
| Hemolytic anemia | Premature RBC lysis. -Caused by Hb abnormalities (ex. Sickle cell), incompatible transfusions, infections. |
| • Thalassemias | Typically mediteranean ancestry. -One globin chain absent or faulty. -RBCs thin, delicate, absent or faulty. -Most common genetic order worldwide. -Many subtypes from mild to severe. |
| Hemoglobin S | One amino acid wrong in globin beta chain. -RBCs crescent shaped when unload O2 or blood O2 low. -RBCs rupture easily and block small vessels. -Poor O2 delivery, pain. |
| – Sickle-cell anemia | Defective gene codes for abnormal Hb. -Have two defective genes for sickle cell. -Causes RBCs to become sickle shaped in low oxygen situations. - The sickle cells rupture easily. -If only one defective gene then considered sickle cell trait. Usually do not have symptoms, but can pass it on to their children. -This trait gives increased immunity to malaria. -Disease occurs in 1/500 African American births. |
| • Polycythemia vera | Bone marrow cancers lead to excess RBCs. -Severely increased blood viscosity. |
| • Secondary polycythemia | Less O2 available (High altitude) or EPO production increases leading to higher RBC count. -Blood doping. |
| Leukopenia | Decrease in WBCs |
| Leukocytosis | WBC count over 11,000/mm^3. -Normal response to bacterial or viral invasion, strenuous exercise, anesthesia, surgery |
| Neutrophils | • Most numerous WBCs • Also called Polymorphonuclear leukocytes (PMNs or polys) • Contain hydrolytic enzymes or defensins • 3-6 lobes in nucleus; ~twice size of RBCs • Very phagocytic—"bacteria slayers" |
| Eosinophils | •Bilobed nucleus •Granules lysosome like •Role in allergies and asthma •Role in modulating immune respones |
| Basophils | •Rarest WBCs •Granules contain histamine; inflammatory chemical that acts as a vasodilator to attract WBCs to inflamed sites. •Are functionally similar to mast cells. |
| Lymphocytes | •Second most numerous WBC •Mostly in lymphoid tissue, few circulate in the blood. •Crucial to immunity •T lymphocytes act against virus-infected cells and tumors •B lymphocytes give rise to plasma cells which produce antibodies** |
| Monocytes | •Largest leukocytes •Leave circulation, enter tissues, and differentiate into macrophages. •Actively phagocytic cells; crucial against viruses, intracellular bacterial parasites, and chronic infections. •Activates lymphocytes to mount an immune response. |
| Leukemia | Cancer that leads to the overproduction of abnormal WBCs •Names according to the abnormal WBC clone involved •Myelod leukemia involves myeloblast descendents •Lymphocytic leukemia involves lymphocytes |
| Acute leukemia | Derives from stem cells •Primarily effects children |
| Leukemia | •Cancerous leukocytes fill red bone marrow •Immature non-funtional WBCs in blood stream •Death from internal hemmorhage; overwhelming infections. •Treated with irradiation, antileukemic drugs, stem cell transplants. |
| Infectious mononeucleosis | •Highly contagious viral disease •Epstein-Barr virus •High numbers of atypical agranulocytes •Symptoms: tired, achy, chronic sore throat, low fever •Runs course with rest |
| Thrombocytopenia | Deficient number of circulating platelets. •Petichiae appear due to spontaneous, widespread hemorrhage •Due to suppression or destruction of red bone marrow (malignancy, radiation, drugs) •Platelet count less than 50,000 •Treated with transfusion of concentrated platelets. |
| Hemophilia A | Most common type •Factor VIII deficiency •77% of all cases |
| Hemophilia B | Factor IX deficiency |
| Hemophilia C | Mild type. •Factor XI deficiency. |
| Disemminated Intravascular Coagulation (DIC) | •Widespread clotting blocks occur in intact vessels. Severe bleeding occurs because residual blood unable to clot. •Occurs as pregnancy complication; septicemia or incompatible blood transfusions. |
| Hemolytic Disease of the newborn aka Erythroblastosis fetalis | Only occurs in Rh- mom with Rh+ baby. •Rh- mom exposed to Rh+ blood of fetus during delivery of first baby - baby healthy. Mother now synthesizes Rh+ antibodies. •Second pregnancy mom's ani Rh+ antibodies cross placenta and destroy RBCs of Rh+ baby. •Baby treated with prebirth transfusions and exchange transfusions after birth. •Rhogam serum prevents mom from becoming sensitized. |
| Transfusion reactions | Occur if mismatched blood infused. •Donor's cells attacked by recipient's plasma agglutinins --> Agglutinate and cause clogged vessels-->rupture and release Hb into the bloodstream •Result in diminished O carrying capacity, diminished blood flow beyond blocked vessels, Hb in kidney tubules leads to kidney failure. |
| Pericarditis | Inflammation of pericardium. •Roughens membrane surfaces leading to pericardial friction rub •Cardiac tamponade: excess fluid sometimes compresses the heart leading to limited pumping ability. |
| **Pathway of blood through the heart | Right atrium-->tricuspid valve-->right ventricle-->pulmonary semilunar valve-->pulmonary trunk--> pulmonary arteries-->lungs-->pulmonary veins-->left atrium-->bicuspid valve-->left ventricle-->aortic semilunar valve-->aorta-->systemic circulation |
| Incompetent valve | Blood backflows so heart repumps same blood over and over |
| Valvular stenosis | Stiff flaps constrict opening causing the heart to exert more force to pump blood |
| Angina pectoris | Thoracic pain caused by fleeting deficiency in blood delivery to myocardium. •Cells weakened. •Not permanent |
| Myocardial infarction | Aka Heart Attack. •Prolonged coronary blockage •Areas of cell death repaired with noncontractile scar tissue •Permanent damage |
| Sinoatrial (SA) Node | Pacemaker of the heart in the right atrial wall •Generates impulses about 75x/minute (sinus rhythm) |
| Atriventricular (AV) node | Delays impulses about 0.1sec allowing atria to respond and complete contraction before the ventricle contact. |
| Arrhythmias | Irregular heart rhythms |
| Fibrillations | Rapid, irregular contractions that are useless for pumping blood causing circulation to cease and leading to brain death. •Defibrillation to treat. |
| Ectopic focus | Defective SA node. •Sets high rate •AV node may take over setting junctional rhythm of 40-60beats/min |
| Heart block | Defective AV node •Few (partial) or no (total) impulses reach ventricles. •Ventricles beat at an intrinsic rate too low for life. •Artificial pacemaker to treat |
| Main Factors Effecting Stroke Volume | 1. Preload 2. Contractility 3. Afterload |
| Stroke Volume: Preload | Degree of stretch of cardiac muscle cells. •Frank-starling law of the heart: The more the heart fills with blood during diastole, the greater the force of contraction during systole (most significant factor) |
| Stroke Volume: Contractility | Contractile strength at a given muscle length, independent of muscle stretch and EDV |
| Stroke Volume: Afterload | Pressure that must be overcome for ventricles to eject blood out of the heart and into the artery. *Hypertension and atheroscerosis increase afterload, resulting in reduced SV |
| Extrinsic factors effecting Stroke Volume | 1. Acidosis 2.Anoxia (extreme hypoxia) 3.Increased extracellular K+ 4. Calcium channel blockers |
| Hypocalcemia | Depresses heart caused by to little calcium int he blood |
| Hypercalcemia | Increased heart rate and contractility due to too much calcium in the blood |
| Hypokalemia | Feelble heartbeat, arrhythmias due to too little potassium |
| Hyperkalemia | Alters electrical activity leading to heart block and cardiac arrest due to too much potassium. |
| Tachycardia | Abnormally fast heart rate(>100beats/min), If persistent may lead to fibrillation. |
| Bradycardia | Heart rate slower than 60 beats/min. May result in grossly inadequate blood circulation in athletes. May be desirable result in endurance training. |
| Congestive Heart Failure (CHF) | Progressive condition. CO is so low that blood circulation inadequate to meet tissue needs. •Reflects weakened myocardium caused by clogged arteries, persistent high blood pressure, mult myocardial infarcts, dilated cardiomyopathy. |
| Purpose of valves | Heart valves ensure unidirectional blood flow through the heart |
| Arteries | Carry blood away from the heart. •Oxygenated except for pulmonary circulation and umbilical vessels of fetus. •Smaller lumen than veins and no valves. |
| Veins | Carry blood toward heart chambers. •Have larger lumens than arteries •Have valves to prevent backflow |
| Factors aiding venous return | 1. Muscular pump: contraction of skeletal muscles "milks" blood toward heart; valves prevent backflow. 2. Respiratory pump:pressure changes during breathing move blood toward heart by squeezing abdominal veins as thoracic veins expand 3. Venoconstriction: under sympathetic control pushed blood toward heart. |
| Hypertension | High blood pressure •Sustained, elevated arterial pressure of 140/90 or higher. |
| Othostatic hypotension | Tempory low blood pressure and dizziness when suddenly rising from sitting or reclining position. |
| Chronic hypotension | Hint of poor nutrition and warning sign for Addison's disease or hypothyroidism |
| Acute hypotension | Important sign of circulatory shock; threat for surgical patients and those in ICU |
| Hypovolemic shock | Results from large-scale blood loss. Too little volume so pressure down. |
| Vascular shock | Results from extreme vasodilation and decreased peripheral resistance. •Vascular: blood vessels dialte so pressure drops. •Ex: Anaphylactic shock |
| Cardiogenic shock | Results when an inefficient heart cannot sustain adequate circulation. •Ex: myocardial infarcts |
| Three important sources of peripheral resistance | 1. Blood viscosity:the stickiness of blood due to formed elements and plasma proteins. Increased viscosity = increased resistance 2.Total blood vessel length: the longer the vessel the greater the resistance encountered 3.blood vessel diameter: Greatest influence on resistance. |
| As resistance increases, blood flow ____________ | decreases |
| As resistance decreases, blood flow ______________ | Increases |
| As resistance increases, blood pressure __________ | increases |
| As resistance decreases, blood pressure ___________ | decreases |
| Baroreceptor Reflexes | Short-term mechanism of blood pressure regulation. •Increased blood pressure stimulates baroreceptors to increase input to vasomotor center. •Causes arterial dialtion and venodilation •Stimulates cardioinhibitory center leading to decreased blood pressure •Ie increased heart rate leads to lower stroke volume which leads to decreased blood pressure |
| Chemoreceptor reflexes | Chemoreceptors detect increase in CO2 or decrease in O2 and pH •When chemoreceptors stimulated, they increase cardiac output (increase stroke volume and heart rate) which leads to an increase in blood pressure. •Stimulates vasoconstriction leading to increase in BP |
| Norepinephrineand epinephrine effects on blood pressure | Cause an increase in blood pressure via vasoconstriction and increase cardiac output. |
| Antidiuretic hormone effects on blood pressure | Causes intense vasoconstriction in cases of extremely low blood pressure |
| Angiotensin II effects on blood pressure | Causes vasoconstriction to increase blood pressure |
| ANP effects blood pressure | caused blood pressure and volume to decline |
| Nitric oxide effects blood pressure | It is a brief and potent vasodilator causing BP to decrease |
| Alcohol effects blood pressure | Causes blood pressure to drop by inhibiting ADH |
| Direct Renal Regulation effects on blood pressure | Alters blood volume independently of hormones. •Increased blood pressure or blood volume causes elimination of more urine thus lowering blood pressure. •Decreased blood pressure or volume causes kidneys to conserve water and BP rises. |
| Renal Regulation: Indirect mechanism | Renin-angiotensin-aldosterone mechanism. •Decrease in blood pressure stimulates the release of renin which converts angitensinogen from liver to angiotensin I. Angiotensin converting enzyme converts angiotensin I to angiotensis II. •Angiotensin II increases blood volume which stimulates aldosterone secretion, ADH release, and triggers hypothalamic thirst center. Causes vasoconstriction. |
| Lymph Nodes | Filter lymph:macrophages destroy microorganisms and debris. •Immune system activation:lymphocytes activated and mount attach against antigens. |
| Spleen | Largest lymphoid organ •Site of lymphocyte proliferation and immune surveillance and response (identify foreign pathogens in blood). •Cleases blood of aged cells and platelets •Stores breakdown products of RBCs (iron) for later use. •Stores blood platelets and monocytes •May be site of fetal erythrocyte production |
| Thymus | Important functions in early life. •Stops growing during adolescence then gradually atrophies (functional tissue replaced with fatty tissue) but still produces immunocompetent cells slowly. •Does not directly fight antigens. Functions strictly in T cell maturation. |
| Mucosa-associated Lymphod Tissue (MALT) | Lymphoid tissue in mucus membranes throughout the body •Protects from pathogens trying to enter the body •Largest collections of MALT found in tonsils, peyers patches, appendix •Also in mucosa of respiratory and genitourinary organs; rest of digestive tract |
| Tonsils | Simplest lymphoid organs •Palantine tonsils (most commonly removed), Lingual tonsil, Pharyngeal tonsil, Tubal tonsils •Gather and remove pathogens in food or air •Trap and destroy bacteria and particulate matter •Allow immune cells to build memory for pathogens |
| Peyers patches | Clusters of lymphoid follicles •Destroy bacteria preventing them from breaching intestinal wall •Generate memory lymphocytes |
| Appendix | Destroy bacteria preventing them from breaching intestinal wall •Generate memory lymphocytes |
| T Cell Maturation (Becoming immunocompetent) | T cells mature in the thymus under negative and positive selection tests. •Positive selection: Selects T cells capable of recognizing self MHC proteins; failures are destroyed by apoptosis. •Negative selection:Prompts apoptosis of T cells that bind to self antigens. Ensure self-tolerance. •Only 2% of T cells survive this selection process |
| B cell maturation | B cells mature in the red bone marrow. •Positively selected if they make antigen receptors. •Self reactive B cells are eliminated by apoptosis (clonal deletion), Undergo receptor editing, Are inactivated (anergy) if they escape from the bone marrow |
| Activation of B and T cells | Immunocompetent B and T cells not yet exposed to the antigen are called naive •They are sent from primary lymphoid organs (bone marrow, thymus) to secondary lymphoid organs (lymph nodes, spleen, etc.) to increase chance of encounter with antigen. •Activated when find matching antigen |
| IgM | First antibody released •Potent aggluinating agent •Readily fixes and activates complement •Has highest ability to bind •Monomer found on the surface of B cells as receptors |
| IgA | Antibody found in mucus and other secretions including saliva, tears, colostrum, breast milk •Helps prevent entry of pathogens |
| IgD | Functions as a B cell receptor |
| IgG | 75-85% of antibodies found in plasma. •From secondary and late primary responses •Crosses placental barrier |
| IgE | Active in some allergies and parasitic infections •Mediates Type I sensitivity by causing mast cells and basophils to release histomine. •Defends agains parasitic worms by causing eosinophils to produce worm destroying enzymes |
| Antibody Mechanisms | •P.L.A.N.• Precipitation, Lysis (by complement fixation), Agglutination and Neutralization |
| Cytotoxic T cells | Directly attack and kill other cells •Activated cytotoxic T cells circulate in search of body cells displaying antigen they recognize. •They target virus infected cells, cells with intracellular bacteria or parasites, cancer cells, foreign cells. •Perforins drill holes in the cell, granzymes enter and causes apoptosis •Cytotoxic T cell binds specific membrane receptor on target cell and stimulates apoptosis |
| Natural Killer Cells | Use the same mechanisms as cytotoxic T cells, but are non-specific in their targets |
| Helper T cells | Play central role in adaptive immune response •Activate both humoral and cellular arms •Help activate B and T cells •Induce T and B cell proliferation •Their cytokines recruit other immune cells •Without Helper T cells, there is no immune response |
| Innate Immune System Defenses | First Line:Skin and mucus membranes •Second line: Phagocytosis, natural killer cells, Inflammation, Antimicrobial proteins, Fever |
| Autoimmune diseases | Body attacking itself •5% of adults in North America (2/3 women) have an autoimmune disease •There are no cures for autoimmune diseases •Vitamin D deficiency linked to autoimmune diseases such as MS |
| Mechanisms of Autoimmune Disease | Weakly self reactive lymphocytes may be activated by foreign antigens that resemble self; New self-antigens may appear generated by gene mutations, changes in self antigen by hapten attachment or infectious damage, release of novel self-antigens by trauma |
| Hypersensitivities | Differentiation based on how long it takes and whether it involves antibodies or T cells. •I,II,II are all antibody mediated and IV is Tcell mediated. •Immediate, subacute and delayed hypersensitivities. |
| Immediate (accute) Hypersensitivity | Begin seconds after contact •Does not occur on first contact but sensitizes person •May be local or systemic •Histamines released making blood vessels dilated and leaky causing runny nose, hives, watery eyes •Systemic response is anaphylactic shock |
| Subacute Hypersensitivites: Cytotoxic (Type II) Reactions | Slow onset (1-3 hours) and long duration (10-15hours) •Antibodies bind to antigens on specific body cells, stimulate phagocytosis and complement mediated lysis of cellular antigens •Ex: mismatch blood transfusions |
| Subacute hypersensitivities: Immune complex (Type III)hypersensitivity | Occurs withing 1-3 hours •Antigens widely distributed in blood or body •Insoluble antigen-antibody complexes form •Complexes cannot be cleared from particular area of the body •Intense inflammation, local lysis and killing by neutrophils •Ex: systemic lupus, farmer's lung |
| Delayed hypersensitivities: Type IV | T cell mediated •Slow onset (1-3 days) •Cytokine activated macrophages and cytotoxic T cells cause damage •Ex: allergic contact dermititis •Agents act as haptens •TB skin test depends on this reaction |
| AIDS | Cripples immune system by interfering with activity of Helper T cells •Opportunistic infections occur including pneumocystis pneumonia and Kaposi's sarcoma •Is now the 6th leading killer of Americans ages 25-44 •Caused by retrovirus HIV •Transmitted via body fluids •HIV multiples in lymph nodes throughout asymptomatic period ~10yrs if untreated •97%of persons will develop antibodies in first 3 months following infection, in rare cases it can take up to 6 months. •HIV enters cell and uses reverse transcriptase • High mutation rate •Treated with antiviral drugs: Fusion inhibitors, Integrase inhibitors, Reverse transcriptase and protease inhibitors. •Antiretroviral vaginal gel reduces risk by 50% |
| Hodgkin's Disease | Acquired immunodeficiency •Cancer of B cells •Leads to immunodeficiency by depressing lymph node cells |
| Severe Combined Immunodeficiency Syndrome | Genetic defect. •Marked deficit in B and T cells •Defective adenosine deaminase enzyme •Metabolites lethal to T cells accumulate •Fatal if untreated; treated with bone marrow transplants |
| Rhinitis | Inflammation of nasal mucosa •Spreads from nose to throat to chest •Spreads to tear ducts and paranasal sinuses causing blocked sinus passageways leading to air absorbed causing a vacuum and then a sinus headache. |
| Atelectasis | Lung collapse due to plugged bronchioles that cause the collapse of aveoli. •Most common cause of Atelectasis is pneumothorax which is air in the pleural cavity. •Treated by removing air with chest tubes |
| Inspiration | Diaphragm and external intercostals contract, thoracic volume increases leading to a drop in intrapulmonary pressure, Air flows into the lungs down the pressure gradient |
| Expiration | Quiet expiration is normally a passive process •Inspiratory muscles relax, thoracic cavity volume decreases leading to an increase in pressure and air flows out of the lungs down the pressure gradient •Forced expiration is an active process and uses abdominal and internal intercostal muscles |
| Asthma/Allergies | As airway resistance rises, breathing movements become more strenuous. •Severe constriction or obstruction of bronchioles •Can prevent life-sustaining ventilation •Can occur during acute asthma attacks; stops ventilation •Epinephrine dilates bronchioles, reduces air resistance |
| Hypoxia | Inadequate O2 delivery to tissues leading to cyanosis (turn blue) |
| Anemic hypoxia | Too few RBCs; abnormal or too little Hb |
| Ischemix hypoxia | Impaired/blocked circulation |
| Histotoxic hypoxia | Cells unable to use O2 as in metabolic poisons (block the binding of O2) |
| Hypoxemic hypoxia | Abnormal ventilation; pulmonary disease |
| Carbon monoxide poisoning | Especially from fire; 200x greater affinity for Hb than oxygen. •Form of histotoxic hypoxia |
| COPD | Exemplified by chronic bronchitis and emphysema. •Irreversible decrease in ability to force air out of the lungs •Treated with bronchdilators, corticosteroids,oxygen, surgery •History of smoking in 80% of patients •Coughing and frequent pulmonary infections •Most develop respiratory failure accompanied by respiratory acidosis, hypoxemia |
| Chronic bronchitis | Inhaled irritants lead to excessive mucus and inflamed & fibrosed lower respiratory passageways which cause obstructed airways causing impaired lung ventilation and gas exchange causing frequent pulmonary infections. |
| Emphysema | Destruction of aveoli causes them to lose their elasticity so they can't expand and receive O2. Leads to use of accessory muscles for breathing which causes exhaustion from energy use. |
| Asthma | Active inflammation of airways precedes bronchospasms. •1/12 in N. America suffer |
| Tuberculosis | Infectious disease caused by Mycobacterium tuberculosis •Symptoms include fever, night sweats, weight loss, racking cough, coughing up blood •Treatment is a 12 month course of antibiotics •There are resistant strains |
| Lung Cancer | Leading cause of cancer deaths in North America •90% of all cases result from smoking •Metastasizes rapidly and widely, most victims die within 1 yr. |
| Lung Cancer: Adenocarcinoma | 40% of cases •Originates in peripheral lungs, bronchial glands, alveolar cells |
| Squamous cell Carcinoma | 20-40% of cases •In bronchial epithelium |
| Small cell carcinoma | 20% of cases •Contains lymphocyte like cells that originate in primary bronchii and subsequently metastasize |
| Cystic Fibrosis | Most common lethal genetic disease in North America •Abnormal, viscous mucus clogs passageways leading to increased bacterial infections. •Affects lungs, pancreatic ducts, reproductive ducts •Treatments include mucus dissolving drugs, manipulation to loosen mucus, antibiotics |
| Increased altitude leads to _____ atmospheric pressure | Decreased |
| Acute Mountain Sickness | Atmospheric pressure and O2 levels lower. •Headaches, shortness of breath, nausea, dissiness •In severe cases lethal cebreal and pulmonary edema •Common in travelers to ski resorts |
| Unloading of O2 | •PO2: as the concentration of O2 decreases, the rate of unloading increases •Temperature: as the temperature increases, the rate of unloading increases •Blood pH: as pH decreases (becomes more acidic) the rate of unloading increases •PCO2: As concentration of CO2 increases the rate of unloading increases |
| Carbohydrates are mechanically digested in ____________ | •Mouth •Stomach |
| Lipids are mechanically digested in __________ | •Mouth •Stomach |
| Proteins are mechanically digested in ________________ | •Mouth •Stomach |
| Carbohydrates are chemically digested in ____________ | •Mouth by amylase •Small intestine by pancreatic enzymes |
| Lipids are chemically digested in ____________ | •Stomach •Small intestine |
| Proteins are chemically digested in ___________ | •Stomach •Small intestine |
| Chemical digestion of proteins in the stomach | HCl is produced in the stomach which converts pepsinogen to pepsin. •Pepsin breaks the bonds between amino acids |
| Secretin | Released when fatty or acidic chyme enters the duodenum •Causes secretion of biocarbonate rich pancreatic juice. •Pancreatic juice stimulates the liver to make bile • |
| Cholecystokinan | Stimulates release of enzyme rich pancreatic juice •Causes the gallbladder to contract releasing bile into the small intestine •Causes the hepatopancreatic sphincter (Sphincter of Oddi) to relax |
| Gastrin | Increases gastric secretions •Plays essential role in stomach secretion and motility •Relax the ileocecal sphincter •Allow chyme to pass into large intestine |
| Liver | Accessory digestive organ •Largest gland in the body Has four lobes (right, left, caudate, quadrate) • |
| Gallbladder | Accessory digestive organ •Stores and concentrates bile by absorbing water and ions •Releases bile via the cystic duct |
| Pancreas | Accessory digestive organ •Exocrine function: Acini cells secrete pancreatic juice which breaks down all categories of food stuff •Endocrine function:Pancreatic islets release insulin (Beta cells) and glucagon (alpha cells) • |
| Carbohydrate Absorption | Absorbed via facilitated diffusion. Enter the capillary bed in the villi then transported to the liver via the hepatic portal vein |
| Dental Caries (Cavities) | Gradual demineralization of enamel and dentin by bacterial action •Dental plaque adheres to teeth •Acid dissolves calcium salts •Without salts organic matter digested by proteolytic enzymes •Daily brushing and flossing help prevent |
| Gingivitis | Plaque calcifies to form tartar •Tartar disrupts the seal between gingivae and the gums •Anaerobic bacteria infect gums •Infection reversible if tartar removed |
| Periodontitis | Autoimmune •Destroy periodontal ligament •Activate osteoclasts dissolving bone •Risk factors: smoking, diabetes, piercing |
| Gastritis | Inflammation by anything that breaches the mucosal barrier |
| Peptic Ulcer | Erosion of the wall of the stomach (gastric ulcer), esophogus (esophageal ulcer), duodenum (duodenal ulcer) •Most caused by H. pylori •10-15% caused by H. pylori though estimated 50% of population has H.pylori •Chronic NSAIDS users account for 15-30% of gastric ulcers |
| GERD | Burning, radiating substernal pain that occurs when acidic gastric juice regurgitates into esophagus. •Common in persons with hiatal hernia |
| Hepatitis | Inflammation of the liver most often due to viral infection •More common in men •Hep B: 40% of cases, transmitted by bodily fluids •Hep A: 32% of cases, Transmitted fecal-oral, contaminated food, water. •Hep C: Characterized by persistent or chronic liver infections, more than 4 mil Americans, 10,000 die/yr |
| Cirrhosis | Progressive, chronic inflammation of the liver that typically results from severe chronic hepatitis or chronic alcoholism. •Liver becomes fatty and fibrous |
| Gallstones | Crystallization of cholesterol int eh gallbladder due to insufficient bile salts or lecithin or excessive cholesterol. •More common in females due to estrogen imbalances. |
| Diverticulitis | Inflammation of the diverticula that can cause rupture and leakage of feces into the peritoneal cavity. |
| Celiac disease | Gluten damages the intestinal villi and reduces the length of the microvilli •Autoimmune disease •Treated by eliminating gluten from diet |
| Colon Cancer | Second largest cancer death in males and females. Number 2 in both populations put together. |
| Effects of Angiotensin II | •Contricts arteriolor smooth muscle causing increase in BP •Stimulates reabsorption of Na+ •Stimulates the hyppothalamus to release ADH and ativates the thirst center •Prompts aldosterone release from adrenal cortex • |
| Renin-Angiotensin Mechanism | Main trigger for aldosterone release •Renin catalyzes production of Angiotensin from angiotensinogen released by the liver •ACE converts angiotension I to angiotensin II which causes vasoconstriction, secretion of aldosterone, increases ADH, increases thirst |
| Pyelitis | Infection of renal pelvis and calyces |
| Pyelonephritis | Infection/inflammation of entire kidney |
| Renal failure | Causes uremia syndrome - ionic and hormonal imbalances, metabolic abnormalities, toxic molecule accumulation •Treated with hemodialysis or transplant |
| Kidney Stone | Crystalized calcium oxalate (75%), magnesium ammonium phosphate (15%), uric acid (10%). •Larger stones block ureter, cause pressure and pain in kidneys •Risk factors: chronic bacterial infection, dehydration, urine retention, increase in blood Ca, increase in pH of urine •#1 way to decrease risk is proper hydration |
| Urinary tract infection | 40% of all women get UTI •Symptoms: dysuria, urgency and frequency, fever, back pain and headache if kidneys involved. |
| incontinence | usually from weakened pelvis muscles •Stress incontinence: (laughing, coughing), increased intra-abdominal pressure forces urine through external sphincter. •Overflow incontinence: Urine dribble when bladder overfills |
| Polycystic Kidney Disease | Many fluid-filled cysts interfere with function. •Autosomal dominant form is less severe but more common •Autosomal recessive is more severe. •Cause unknown but involves defect in signaling proteins |
| Metabolic Acidosis | All acid-based abnormalities other than those caused by PCO2 levels in blood; indicated by abnormal HCO3- levels. •Second most common cause of acid-base imbalance •Causes: too much alcohol, excessive loss of HCO3- (diarrhea), Accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation and kidney failure |
| Metabolic alkalosis | Much less common than acidosis •Indicated by rising blood pH and HCO3- •Causes: Vomiting of the acid contents of the stomach, Intake of excess base, Constipation in which excessive bicarbonate is reabsorbed •pH above 7.8 can lead to excitation of the nervous system causing muscle tetany, exterme nervousness, convulsions, death often from respiratory arrest |
| Respiratory acidoses | The most common cause of acid-base imbalance •Hypoventilation (shallow breathing) results in respiratory acidosis •Occurs when a person breathes shallowly or gas exchange is hampered by diseases such as pneumonia, cystic fibrosis or emphysema |
| Respiratory alkalosis | Hyperventilation results in respiratory alkalosis •Can occur from stress, anxiety attack, bleeding, bleeding, heart or lung disorder, infection, oxygen deficiency from high altitude |
| Benign Prostatic Hyperplasia (BPH) | Hypertrophy of the prostate •Causes difficulty urinating. •Increases risk of bladder infection •Natural treatment: Saw palmetto |
| Prostatitis | Inflammation of the prostate |
| Prostate cancer | Second most common cause of cancer death in men (after lung cancer) •(Second most common cause of cancer death in both sexes combined is colorectal) |
| Breast Cancer | usually arises from the epithelial cells of small ducts. •Risk factors:early onset of mentruation and late menopause, no pregnancies or first pregnancy late in life, family history •10% are due to hereditary defects •70% of women with breast cancer have no known risk factors |
| Ectopic Pregnancy | Development of an embryo or fetus outside of the uterine cavity •Most common site is the uterine tube •Women who smoke are 2x more likely due to niccotine paralyzing the cilia in the uterine tube •Risk factors:smoking, scarring from PID, uterine tube surgery, previous ectopic pregnancies |
| Gonorrhea | bacterial infection of the mucosae of reproductive or urinary tracts. •Transmission: spread by contact with genital, anal, and pharyngeal mucosae •More than 700K new cases/yr •Prevention: condemns •Males: urethritis, painful urination, discharge of pus •Females:20% no S & S, Abdominal discomfort, vag discharge, abnormal uterine bleeding. Can lead to PID. •Treatment: Antibiotics |
| Syphilis | Bacterial infection transmitted sexually by direct contact with sore. •Can be contracted congenitally. Infected fetus still born or death shortly after birth. •Infection asymptomatic 2-3 weeks •A painless chancre appears at the site of infection and disappears in a few weeks. •If remains untreated secondary signs appear several weeks later lasting 3-12 weeks. Include pink skin rash, fever, joint pain. •Latent period may or may not progress to tertiary syphilis. Characterized by lesions of the CNS, blood vessels, bones, skin. •Condems must cover sore •Treatment: Penicillin |
| Chlamydia | Most common bacterial STD •Responsible for 25-50% of PID diagnosed. •Transmitted via sex or mom to baby during vaginal birth. •Symptoms: Urethritis, penile and vaginal discharges, abdominal, rectal, testicular pain, painful intercourse, irregular menses. Can cause arthritis and UTIs in men and sterility in women. Treatment: Tetracycline class drugs |
| Genital Warts | Caused by HPV. •Second most common STD in US. •100 types HPV •40HPV that can infect genitals •Increase risk of cancer in infected area •The types of HPV that cause warts are not the same ones that cause cancer. •90% of cases the body's immune system clears HPV naturally in 2 years. •30% of genital warts go away without treatment •50% of sexually active men and women get it at some point in their lives. •3/4 of Americans between 15-49 have been infected with HPV •Gardisil works against 6,11,16,18. 6,11 responsible for 90% of genital warts. 16,18 responsible for 70% of cervical cancer. |
| Genital Herpes | Caused by human herpes virus type II. •Characterized by latent periods and flareups. •1/6 of people aged 15-49 •Virus released from sores, but also released when no sores via viral shedding. •Treatment: Anti-viral drugs, no cure |
| Oogenesis | Begins in the fetal period where oogonia multiply by mitosis and store nutrients. Primary oocytes develop in primordial follicles. •Have about 200K to 2mil at birth. 40K remain at puberty. •Primary oocytes begin meiosis but stall in prophase 1. •Each month after puberty a few primary oocytes are activated. •One is selected each month to resume meiosis •Result is two haploid cells:Secondary oocyte and a first polar body •The secondary oocyte arrests in metaphase II and is ovulated. •If penetrated by sperm it completes meiosis II yielding an ovum (gamete) and a secondary polar body. |
| Spermatogenesis | Sequence of events that produces sperm in the seminiferous tubules of the testes •Takes 65-75 days •Each day 300mil complete spermatogenesis •Begin with mitosis •Meiosis I and II result in 4 daughter cells. •Meiosis I primary spermatocyte become two secondary (haploid) spermatocytes •Meiosis II each secondary spermatocyte turn into 2 spermatids •Spermatids lose excess cytoplasm and form a tail becoming sperm. |
| Ovarian Cycle | Monthly sequence of events associated with the maturation of an egg. •Two consecutive phases in a 28 day cycle. •Follicular phase, Ovulation, Luteal Phase |
| Follicular Phase of Ovarian Cycle | 1. Primordial follicle is activated 2. Follicle enlarges to become primary follicle 3. Primary follicle becomes a secondary follicle 4. Secondary follicle becomes a late secondary follicle. 5. Late secondary follicle becomes a vesicular follicle - the primary oocyte completes meiosis I |
| Ovarian Cycle: Ovulation | Ovary wall ruptures and expels the secondary oocyte. •Mittleschmerz is twinge of pain sometimes felt at ovulation •1-2% of ovulations release more than one secondary oocyte |
| Luteal Phase of Ovarian Cycle | Ruptured follicle collapses •Granulosa cells and internal thecal cells form corpus luteum •Corpus luteum secretes estrogen and progesterone •If no pregnancy the corpus luteum degenerates into a scar in 10 days •If pregnancy occurs, corpus luteum produces hormones until the placenta takes over at about 3 months. HCG produced |
| Aldosterone effects on Sodium Balance | Regardless of presence of aldosterone, 65% of Na+ reabsorbed in proximal tubules and 25% in loops of henle. Na+ never secreted into filtrate •Aldosteron increased reabsorption of remaining Na+ in distal convoluted tubule and collecting duct |
| ANP Effects on Sodium Balance | Increases excretion of Na+ and water •Released in response to stretch •Decreases ADH, renin and aldosterone production |
| Aldosterone Effect on Potassium | Stimulates K+ secretion (and Na+ reabsorption) •Increased K+ in adrenal cortex stimulates secretion of aldosterone |
| Estrogen Effect on Sodium | Increases reabsorption |
| Progesterone Effect on Sodium | Decreased Na+ reabsorption (blocks aldosterone) •Promotes N+ and H2O loss |
| Glococorticoids (cortisol) Effect on Sodium | Increased Na+ reabsorption •promotes edema |
| Hormones that increase sodium reabsorption | AGE Aldosterone, Glucocorticoids, Estrogen |
| Hormones that cause excretion or inhibits reabsorption of sodium | ANP, Progesterone |
| Considerations regarding the ability to kill microbes | 1. The number of microbes, the more there are, the harder to kill 2. Duration of exposure 3. Types of microbes involved 4.Temperature - the lower the temp, the harder to kill 5. Concentration of the chemical agent 6.pH - alkaline is better for killing microbes 7.Environment - is there blood, mucus, feces vomit? All will decrease accessibility to microbes 8.Endospore formation. |
| Action of Antimicrobial Agents: Alteration of membrane permeability | Going to kill microbes by bursting/shriveling microbe, letting contents leak out, letting unwanted items come in |
| Action of Antimicrobial Agents: Denature proteins | Ie, Unfold proteins. If proteins do not have the proper 3d shape, they can't function. Enzymes are a big target of this. |
| Action of Antimicrobial Agents: Damage nucleic acids | Mess with DNA/RNA duplication, transcription, translation |
| Physical Methods of Microbial Control: Heat | Denatures proteins. Inexpensive. Widely applicable (can work on almost any microbe if hot enough) Fast. Reliable. Sources of heat: Dry heat (oven), Moist heat (boiling), Moist heat + pressure (autoclave), Pasteurization (holding, flash, ultra high temp) |
| Physical Methods of Microbial Control: Cold | Decreases metabolism, growth and reproduction. Fridge: halts the growth of most pathogens |
| Physical Methods of Microbial Control: Drying | Removes water. Works because water is required for metabolism. Lyosphilization: removal of water under a vacuum |
| Physical Methods of Microbial Control: Filtration | Pores in the filter will trap the microbes. THe key is making sure you use small enough pores. Ex: Surgical mask |
| Physical Methods of Microbial Control: Osmotic pressure | Will cause microbe to either burst or shrivel. Jams, jellies, honey maple syrup |
| Physical Methods of Microbial Control: Radiation | Damages the DNA/RNA of the microbe. Ionizing radiation: irradiating just half our meat would prevent 900K cases of e. coli. Non-ionizing radiation: ultraviolet light. |
| Chemical Methods of Microbial Control: Phenol/Phenolics | Effective against gram+ bacteria and some fungi. Works by altering membrane permeability and denaturing proteins. Phenolic is more effective and less expensive than phenol. |
| Chemical Methods of Microbial Control: Soap and detergents | Effective against a broad range of microbes. Works by mechanical removal of microbes. Surfactant - decreases surface tension in water. |
| Chemical Methods of Microbial Control: Alcohol | Effective against vegetative bacteria, enveloped viruses, fungi and protozoa. Works by denaturing/dissolving lipid membranes and denaturing proteins. Need to be 70% alcohol to be effective. |
| Chemical Methods of Microbial Control: heavy metals | Effective against a broad range of microbes. Work by denaturing proteins. Silver, mercury, zinc. |
| Chemical Methods of Microbial Control: Chlorine | Effective against a broad range of microbes. Works by denaturing proteins. |
| Chemical Methods of Microbial Control: Iodine and Iodaphors | Effective against a broad range of microbes. Works by denaturing proteins. |
| Chemical Methods of Microbial Control: Aldehydes | Effective against all microbes. Can be a sterilent. Works by denaturing proteins |
| Chemical Methods of Microbial Control: Gaseous sterilizers | Effective against all microbes. Sterilent. Works by denaturing proteins. |
| Chemical Methods of Microbial Control: Hydrogen peroxide | Effective against anaerobes. Works as an oxidizing agent (steals electrons from nucleic acids, proteins, lipids). Can also denature proteins. |
| Compound 606 | Paul Ehrlich. Compound 606 called Salvarson. Worked on bacteria that caused syphilis. Was toxic to humans so only used for a few years. |
| Prontosil | Gerarg Domagk. Effective against gram + bacteria including staph and strep. Daughter with arm infection from sewing needle. |
| Alexander Flemming | Contaminated streak plate where mold grew, bacteria did not. Mold was penicillium. Unable to isolate substance which he named penicillin. |
| - Howard Florey & Ernst Chain | Isolated penicillin. |
| - Selman Wacksman | Streptomycin and over 20 additional antibiotics. First to use term antibiotic. |
| Antibiotic | A product of or derived from the metabolism of a microorganism. |
| Antimicrobial Drug | Synthesized in the lab. |
| Ideal qualities of an antibiotic/antimicrobial drug | 1.Inhibit or kill the pathogen without harming the host. 2. Cause no allergic reaction in the host 3.Stable as a liquid or solid 4.Remain in specific tissue long enough to be effective 5.Inexpensive 6.Inhibit or kill pathogen before resistance develops 7.Not kill normal flora |
| Targets of antibiotics/antimicrobial drugs | 1. Bacterial cell wall 2.Disrupt membranes 3.Nucleic acid synthesis 4.Block protein synthesis 5.Interfere with metabolic pathways ***Viruses have none of these targets |
| Narrow spectrum antibiotic/antimicrobial drug | Only effective against a limited number of microbes. Less damage to normal flora. Use when you know the pathogen. |
| Broad spectrum antibiotic/antimicrobial drug. | Effective against multiple microbes. Use if pathogen is unknown. kills normal flora - increases risk of secondary infection. Might need probiotics. |
| How to determine which antibiotic/antimicrobial drug to use. | Gram stain. Kirby-bauer. |
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