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Infections 1. Discuss the differences between bacterial and viral infections (recall from micro). A: bacterial infections can be acute or chronic. They can be in various environments, they reproduce by binary fission, they respond to antibiotics. Usually localized Viral needs a host cells to mult...

Infections 1. Discuss the differences between bacterial and viral infections (recall from micro). A: bacterial infections can be acute or chronic. They can be in various environments, they reproduce by binary fission, they respond to antibiotics. Usually localized Viral needs a host cells to multiply, does not respond to antibiotics, chronic, produce fever 2. Discuss the locations, advantages, and disadvantages of resident (normal) flora (A&P and current content) Normal Flora Bacteria that normally inhabit the body are referred to as normal flora. They live cooperatively with the body and usually do not cause disease. In fact, these bacteria contribute to a healthy balance of bacteria in the body, keeping out abnormal and potentially more dangerous bacteria and other organisms skin; mucous membranes of the eye, nose, and mouth; upper and lower GI tracts; upper respiratory tract; urethra; and vagina. Benefits: 1. Produces enzymes which facilitate digestion of fatty acids and large polysaccharides 2. Synthesizes essential metabolites (e.g., vitamins K and B) 3. Releases antibacterial substances that are toxic to pathogenic microorganisms 4. Competes with pathogens for nutrients and blocks attachment of the pathogens to the epithelium, an obligatory first step in the infectious process 5. Fosters adaptive immunity by inducing the growth of gut-associated lymphoid tissue, an important site in the development of both local and adaptive immunity 6. Contributes to bidirectional communication between the brain and the GI tract (brain–gut axis) which has implications for cognitive function, behavior, pain modulation, stress responses, and disease Cons: Prolonged treatment with broad-spectrum antibiotics can alter the normal microbiome, decreasing its protective activity, and leads to an overgrowth/mutation of pathogenic microorganisms. opportunistic pathogens —that is, they are harmless under normal conditions but can cause disease in immunocompromised individuals who lack the usual defense mechanisms 3. Describe the modes of transmission of microbes (micro and current content). A: Contact, Vehicle, and vector. Contact: Direct Contact Direct contact transmission involves direct physical contact of the infectious agent between hosts, such as by person-to-person contact. Common forms of direct contact transmission include: Touching Kissing Sexual intercourse Fecal-oral route (poor hygiene) Examples of pathogens transmitted in this matter include: Agents causing respiratory tract infections Staphylococcal infections Measles Scarlet fever Sexually transmitted diseases indirect contact transmission involves a pathogen being transmitted from the reservoir to the susceptible host by an inanimate object called a fomite. Examples of fomites include: Tissues and handkerchiefs Towels and linens Wrestling mats Toys Clothes Diapers Money Eating utensils and drinkware Medical equipment and devices Contaminated needles—a common fomite for the transmission of human immunodeficiency virus (HIV) and hepatitis B and C Droplet transmission occurs when infectious agents are transmitted through respiratory droplets released into the air traveling less than 1 meter. Examples include: Normal exhaling Laughing Coughing Sneezing (the most effective form of droplet transmission) Common droplet transmitted infections include: Common cold Influenza Pneumonia Pertussis Vehicle: Airborne transmission involves the spread of pathogens by droplet nuclei (droplets of mucus), aerosols, and dust that travel more than 1 meter from the reservoir to the host. Aerosols can originate from coughing or sneezing, as well as from air conditioning and other cooling systems. Pathogens can attach themselves to dust particles and are transmitted by air via sweeping, mopping, changing of bed linens, changing of clothes, or simple dusting. Waterborne transmission occurs due to untreated or poorly treated sewage. Examples of specific infections include: E. Coli: transmit via uncooked meat, food contaminated by fecal material; swimming in contaminated water Hepatitis A: transmit via contaminated food, water contaminated with human feces Salmonellosis: transmit via contaminated poultry, eggs, and meat; fecal-oral route Bodily fluid transmission occurs when contaminated bodily fluids are handled, predominantly in the health care setting. Special precautions should be taken when handling these types of fluids:  Blood Urine Saliva Other bodily fluids: can be reservoirs for different pathogen Foodborne transmission involves pathogens in or on foods that are improperly prepared (incompletely cooked, poorly processed under unsanitary conditions, not refrigerated, or poorly refrigerated). This type of contamination can occur due to normal microbial flora and zoonotic pathogens; it can also occur due to parasitic worms that alternate between human and animal hosts. Cholera: transmits via ingestion of contaminated water, raw or partially cooked fish, or shellfish Gastroenteritis (Norwalk virus): transmits via ingestion of contaminated seafood and handling of contaminated food Salmonella: transmits via contaminated poultry, eggs, and meat Vector Biological vectors transmit pathogens but also serve as a host for a part of the pathogen’s life cycle (vector-borne diseases). Biting insects are typical biological vectors that affect humans. Mosquitoes: Malaria, yellow fever, elephantiasis, dengue, viral encephalitis, West Nile virus Ticks: Lyme disease, Rocky Mountain spotted fever Fleas: Bubonic plague, endemic typhus Lice: Epidemic typhus Blood-sucking flies: African sleeping sickness, river blindness Blood-sucking bugs: Chagas’ disease Mites: Scrub typhus Mechanical vectors passively carry pathogens on their body (typically feet/legs) from one host to another. Houseflies, face-flies, blow-flies: cause foodborne illness, dysentery, intestinal worms Cockroaches: cause foodborne illness, typhoid fever, viral diseases, human enteric protozoa (i.e., giardiasis) Dung Beetles: cause Toxoplasma gondii (toxoplasmosis)  Hospital-acquired infections (HAIs), also referred to as nosocomial infections, are those that occur in health care facilities, including hospitals, nursing homes, doctors’ offices, and dental offices. Most infections in health care facilities are spread by direct contact between persons or contaminated objects. Common nosocomial infections include: Urinary tract infections (most common) Pneumonia Diarrhea Surgical wound infection C. difficile interrupts the distribution of normal flora allowing the bacteria to multiply causing severe diarrhea and ultimately death in some cases. MRSA infections are common nosocomial infections that are difficult to treat due to growing resistance to multiple antibiotic medications, not just methicillin. 4. Describe the factors determining host resistance (current content). A: Age Underlying health Immune status Genetics Malnutrition Examples of Host Resistance Increased Microbial Virulence, Intact skin and mucous membrane, Body secretions—stomach acid, tears, Nonspecific phagocytosis, Effective inflammatory response, Absence of disease, Interferon production (virus) 5. Explain the factors contributing to pathogenicity and virulence of microbes (current content). Adhesion: presence of bacterial capsule and pili Colonization: spore formation, reproduction/replication of microbes Invasion: entry of large number of organisms into body Evasion of host defenses: viral mutation and replication Toxogenesis: production of exotoxins, endotoxins, and destructive enzymes A: Pathogenicity: capability of microbe to cause disease -Virulence: severity (ability to cause host an infection) Adhesion Specific: lock and key, permanent/irreversible, Nonspecific: Hydrophobic interactions (water repelling): This increases propensity of adhesion; the more hydrophobic cells, the stronger the surface is to adhesion. Electrostatic attraction: This is the attractive or repulsive interaction between organisms with an electric charge; adhesion increases through attraction. Atomic and molecular vibrations: This creates a force of attraction for pathogens. Brownian movement: Random movement of microscopic particles suspended in a liquid or gas aids adhesion. Recruitment and trapping by biofilms: Microbial biofilms are complex bacterial communities often seen on implanted medical devices; they attract or recruit organisms for proliferation by altering the texture of the surface to meet the needs of the pathogen. colonize: establish themselves without immediate infection impacted by: motility, Adherence, invasion, competition Invasin: Extracellular proteins or enzymes that have the ability to damage or destroy host cells are known as invasins and are critical in the invasion factor of virulence. Invasins disrupt the host cell membrane and break down the primary and secondary defense barriers facilitating growth and proliferation of the pathogen. Evade: Avoid contact, Inhibiting engulfment, Surviving inside phagocyte, Producing toxins  Produce toxins: An aggressive strategy used to produce substances that kill or damage phagocytes either before ingestion or after ingestion Most act as enzymes that lyse cell membranes and destroy leukocytes and red blood cells Endotoxins: released once bacteria is destroyed Exotoxins: secrets by living bacteria 6. Discuss methods of preventing and controlling infection (current content).. In class: Cleaning surfaces, Cover mouth, wear mask, Wear gloves,, gowns, Hand Washing, water treatment A:-No major chain of events=no infection (prevention) -How?= good diet, exercise, immunizations, sleep, decrease stress, good hygiene, proper hand washing -cleaning of clothing/surroundings -Sterilize tools (heat or chemicals) -Disinfect inanimate objects -Antiseptics (used on living tissue)(hand-sanitizer 7. Describe the stages in the development and course of an infection (current content).. 1.Infections agent (bacteria, fungi, viruses, protozoa, Based on Transmissibility, virulence,pathogenicity) ) 2.. Reservoirs (Animal (carrier), Human (carrier) , Non-living (bacteria mainly can survive)) 3.. Port of exit  (Gastrointestinal, Genitourinary, Respiratory, Skin (bleed,cut) ,Mucous membranes) 4.. Transmission (Contact: direct,indirect,droplet:sneeze,cough,laugh) Vehicle: Airborne, Waterborne, Bodily fluid, Foodborne Vector: Biological: Carry and serves as a living space, Mechanical: carry only on body Hospital acquired: NOSOCOMIAL Common infections: UTI, Pneumonia,DIarrhea, Wound infection Common Bacteria: C.difficile: encapsulated , MRSA: Methicillin-resistant Staphylococcus aureus Bacteria) 5.. Port of entry (Mucous membrane, skin, Conjunctiva, parenteral(VEIN)) 6. Susceptible host (Age, Underlying health, Immune status, Genetics, Malnutrition) 8. Describe typical, local, and systemic signs of infection (current content). -local infections: location in the body (redness, swelling, pain, lymphadenopathy, Exudate/purulent) -systemic infection: Signs=(fever, leukocytosis, Elevated ESR, Fatigue, weakness, anorexia, headache,) (septicemia: pathogens in blood)(bacteremia: bacteria in blood)(toxemia: toxins in the blood)(viremia: presence of virus in the blood) 10. Describe the respiratory infection influenza, including the cause, transmission, immunization, incidence, manifestations, and possible complications (current content). Patho: flue Reservoir: respiratory tract, Human Portal of exit: mouth and nose Mode of transmission: droplet/airborne, direct Portal of entry- mouth,eyes,nose Susceptible Host: Age, immune status Pathogensis: Entry and replication: Hemagglutinin(HA) allows adherence to cells (respiratory) Neuraminidase(NA) helps virus release particles. surface proteins, makes it virulent and patho. Destroys the lining of the respiratory tract. Immune response: fever,chills,body ache. Adaptive immune response: antibodies Virulence and pathogen: Ability to change, reproduce, Antigenic shift- new strains changes HA and NA. Types A B C(less common) Immunization: Annual vaccination needed Incidence: 5 - 20 % of the population in North America. complications- severe respiratory distress, pneumonia NOTES: Infererons: group of signaling proteins, Used for cancer treatment, Influence activity of nearby host cells Respiratory Disorder 1. Describe the causes, signs, and symptoms of and effects of common respiratory infections, including influenza, pneumonia, and tuberculosis (current content).. Influenza: Cause flu signs and symptoms: Fever and chills, muscle ache and fatigue cough and sore throat Effects: Pneumonia and Sepsis- Influenza can lead to severe complications such as secondary bacterial pneumonia or sepsis, especially in high-risk populations. Worsening of Chronic Conditions The flu can exacerbate pre- existing conditions like asthma, heart disease, and diabetes, increasing the need for hospitalization. Neurological Complications Rare but severe complications like encephalopathy and seizures can occur, especially in children under 5 years. Pneumonia: caused by bacteria, viruses, fungi, protozoa, or parasites. Signs and symptoms:Cough with sputum( yellow or green-Bacterial), Fever and chills SOB Effects: Acute Respiratory Failure- Severe pneumonia can cause respiratory failure, requiring ventilatory support to maintain oxygen levels. Sepsis and Septic Shock- Bacterial pneumonia can lead to sepsis if it spreads to the bloodstream, which is often life- threatening and requires intensive care. Pleural Effusion and Empyema: Pneumonia may cause fluid buildup around the lungs, known as pleural effusion. If the fluid becomes infected, empyema can occur, necessitating surgical drain Tuberculosis: Caused by mycobacterium TB affecting the lungs Signs and symptoms: Persistent cough( more than 3 weeks, sputum or blood) , night sweats/fever chest pain and fatigue Effects:Pulmonary Damage- Tuberculosis primarily affects the lungs, causing scarring and reducing lung function, leading to chronic respiratory issues. Extrapulmonary Spread- TB can spread beyond the lungs to infect organs like the brain, spine, and kidneys, causing meningitis or renal impairment. Multidrug-Resistant TB (MDR-TB) Inadequate treatment can lead to MDR-TB, which is difficult and costly to treat, with only 40% of patients accessing proper ca 2. Describe the possible outcomes of aspiration (current content, Sherpath).. Aspiration pneumonia occurs as a result of abnormal entry of material from the mouth or stomach into the respiratory tract. This aspirated material triggers an inflammatory response and subsequent pneumonia. The most common form of aspiration pneumonia is a primary bacterial infection, and usually more than one organism is identified on sputum culture. If the aspiration is of acidic gastric contents, this can cause chemical pneumonitis. This is non-infectious and may not require antibiotic therapy. However, a secondary bacterial infection can occur about 48 to 72 hours later. Pneumonia, Bronchial inflammation, collapse of airways 3. Discuss the causes, signs and symptoms and effects of obstructive pulmonary diseases, including asthma and chronic obstructive pulmonary disease (current content).. Asthma: Cause : allergens and exercise Signs and symptoms(acute): Wheezing SOB, mucus build up, airway obstruction, chest tightness, persistent cough Effects: Status Asthmaticus A severe, prolonged asthma attack that does not respond to standard treatment, requiring emergency care. Frequent Hospitalizations: Recurrent asthma exacerbations can lead to repeated hospital admissions, impacting patient quality of life. Airway Remodeling: Chronic inflammation can lead to permanent structural changes in the airways, reducing lung function overtime. COPD: Cause: Smoking, pollutants, Genetic factor(AA1) Signs and Symptoms Chronic cough, Dyspnea on exertion, wheezing and chest tightness Effects: Chronic inflammation, Alveolar damage, Irreversible airway obstruction, Respiratory Infections, cor pulmonale, Acute exacerbations 4. Explain the purpose of pulmonary function testing and significance of results (current content – limited to tidal volume and forced expiratory volume as related to COPD). What they are: PFTs are a group of non-invasive tests that assess lung volume, capacity, rates of flow, and gas exchange. The most common PFTs include spirometry, lung volume measurement, and diffusion capacity testing. Why they are used: ○ Diagnosis of lung diseases: PFTs are critical in diagnosing chronic lung conditions such as asthma, chronic obstructive pulmonary disease (COPD),  restrictive lung disease (like interstitial lung disease), and other pulmonary conditions. ○ Spirometry: Measures how much air a patient can inhale and exhale (FVC: forced vital capacity) and how quickly air can be exhaled (FEV1: forced expiratory volume in one second). Forced Expiratory Volume in 1 Second (FEV1) measures the volume of air a person can forcefully expel in the first second of the FVC maneuver A decreased FEV1/FVC ratio (< 70%) indicates obstructive lung diseases like COPD and asthma, while normal or elevated ratios with reduced lung volumes suggest restrictive lung diseases. ○ Tidal Volume (TV) ○ The amount of air inhaled or exhaled during a ○ normal, resting breath. ○ In COPD, airflow limitation and lung hyperinflation can impair the ability to fully exhale, leading to air trapping. To maintain adequate ventilation, patients often increase their tidal volume to compensate for the reduced efficiency of each breath. Cardiovascular Disorders 1. Explain how blood flow can be altered, including the formation of clots (thrombus), pieces of clots that move (emboli), and fatty deposits in the arteries (atherosclerotic plaques), as well as describe what varicose veins are (current content). 1. Thrombus Formation (Clot Formation): A thrombus is a blood clot that forms inside a blood vessel or the heart, often obstructing blood flow. Clot formation is part of the body's normal response to injury, but pathological thrombi can form under abnormal conditions. ○ Endothelial Injury: Endothelial cells line the inner walls of blood vessels and prevent clotting by releasing substances that inhibit platelet adhesion and coagulation. However, when these cells are damaged (due to trauma, high blood pressure, or atherosclerosis), the protective barrier is broken, exposing the underlying tissue (collagen) that promotes clot formation. ○ Platelet Activation: Once the endothelium is damaged, platelets adhere to the exposed collagen and become activated. Activated platelets release substances that recruit more platelets and initiate the formation of a platelet plug.  ○ Coagulation Cascade: The activation of platelets triggers a complex series of reactions called the coagulation cascade, where various clotting factors (proteins) are sequentially activated. This cascade ultimately leads to the conversion of fibrinogen (a soluble protein) into fibrin, which forms a mesh that stabilizes the platelet plug. ○ Thrombus Formation: The end result is the formation of a thrombus, consisting of a mesh of platelets and fibrin that seals the damaged vessel. If the thrombus grows too large or fails to dissolve, it can obstruct blood flow entirely. ○ Effects of a Thrombus: A thrombus can obstruct blood flow, depriving tissues downstream of oxygen and nutrients. In arteries, this can lead to ischemia (e.g., myocardial infarction or stroke), while in veins, it can cause venous insufficiency or deep vein thrombosis (DVT). 2. Embolus Formation (Embolism): An embolus is a piece of material (most commonly a piece of thrombus) that breaks off and travels through the bloodstream until it lodges in a smaller vessel, causing obstruction. Effects of an Embolus: Pulmonary embolism (PE): If a thrombus in a vein (often in the legs or pelvis) breaks off and travels to the lungs, it can lodge in the pulmonary arteries, causing life-threatening blockage. Symptoms include sudden shortness of breath, chest pain, and hypoxia. Cerebral embolism: An embolus traveling to the brain can cause a stroke by blocking blood flow to part of the brain. Systemic embolism: An embolus from the heart (e.g., in atrial fibrillation) may travel to the limbs, kidneys, or intestines, causing ischemia and damage to the affected organs. 3. Atherosclerotic Plaques (Fatty Deposits in Arteries): An atherosclerotic plaque is a build-up of lipids (cholesterol), inflammatory cells, and fibrous tissue within the arterial walls. Over time, plaques can narrow arteries and reduce blood flow, a condition known as atherosclerosis. Development of Atherosclerotic Plaques:  1. Endothelial Injury: The process begins with damage to the endothelial lining of arteries due to factors like hypertension, smoking, high LDL cholesterol, or diabetes. 2. Lipid Infiltration: LDL cholesterol penetrates the damaged endothelium and becomes oxidized, which triggers inflammation. 3. Foam Cell Formation: Macrophages (immune cells) engulf the oxidized LDL, transforming into foam cells and creating a fatty streak in the artery wall. 4. Plaque Growth: Smooth muscle cells migrate to the site, forming a fibrous cap over the lipid core, resulting in a more advanced plaque. 5. Plaque Rupture: Over time, the fibrous cap can weaken and rupture, exposing the underlying lipid core. This triggers clot formation at the site, which can further block blood flow and lead to events like a heart attack or stroke. Effects of Atherosclerosis: Coronary artery disease (CAD): Atherosclerosis in the coronary arteries reduces blood flow to the heart muscle, causing angina or, if the plaque ruptures, a myocardial infarction (heart attack). Peripheral arterial disease (PAD): Plaques in the arteries of the legs cause claudication (leg pain with walking) and, in severe cases, gangrene. Stroke: Plaque build-up in the carotid arteries or cerebral arteries increases the risk of an ischemic stroke. 4. Varicose Veins: Varicose veins are enlarged, twisted, and swollen veins that typically occur in the legs. They result from damaged or weakened venous valves that fail to prevent the backward flow of blood, causing blood to pool in the veins and leading to increased pressure and vein dilation. Causes of Varicose Veins: Valve dysfunction: Normally, veins have one-way valves that prevent blood from flowing backward as it returns to the heart. When these valves are weak or damaged, blood pools in the vein. Increased venous pressure: Prolonged standing, pregnancy, obesity, and age contribute to increased pressure in the leg veins. Complications of Varicose Veins: Chronic venous insufficiency (CVI): Long-standing varicose veins can lead to more severe venous disease, causing edema, skin changes, and venous ulcers. Deep vein thrombosis (DVT): Although less common, varicose veins can predispose a person to blood clot formation in deeper veins, increasing the risk of DVT. 2. Explain the differences between the types of high blood pressure: primary (essential), secondary, and complicated hypertension (current content). primary hypertension(overtime) has no identifiable, specific cause but is thought to arise from a complex interaction of genetic, environmental, and lifestyle factors. Secondary hypertension(suddenly) is caused by an identifiable underlying condition or disease renal artery stenosis and pheocromocytoma. Complicated hypertension(uncontrolled) refers to long-standing, poorly controlled high blood pressure that leads to target organ damage and increases the risk of serious complications. Heart, brain, kidney and eyes. 3. Explain how coronary artery disease progresses from the buildup of fatty deposits (atherosclerosis) to a heart attack (myocardial infarction) (current content). A:Fatty Deposits (Atherosclerosis): The process starts when cholesterol and other substances form a fatty plaque in the walls of the coronary arteries, which supply blood to the heart muscle. Narrowing of Arteries: Over time, these plaques can harden or rupture, narrowing the arteries and restricting blood flow to the heart. This can cause chest pain (angina) during physical activity, as the heart muscle gets less oxygen. Plaque Rupture and Clotting: Sometimes, the plaque breaks open or ruptures. When this happens, blood platelets rush to the site, and a blood clot forms. Heart Attack: If the clot is large enough, it can completely block the artery, cutting off the blood supply to part of the heart muscle. This causes the death of heart tissue, known as a myocardial infarction, or heart attack. 4. Describe peripheral arterial disease and chronic venous insufficiency, focusing on their causes, how they develop, and their symptoms (current content). A: PAD refers to a condition where the arteries that supply blood to the limbs (usually the legs) become narrowed or blocked, typically due to atherosclerosis. The narrowed arteries cannot supply enough oxygen-rich blood to meet the muscle demands, particularly during activity. Stage 1 Asymptomatic, Stage 2 claudication,  Stage 3&4 rest pain and tissue necrosis. As the disease progresses, ischemia (lack of oxygen) may occur even at rest. Symptoms include intermittent claudication- Rest pain, Skin changes, reduced hair growth, pale skin, weak pulse and ulcers. Gangrene Chronic Venous Insufficiency (CVI) Causes: Valve Dysfunction: Weak or damaged valves that allow blood to flow backward. Blood Clots: Previous deep vein thrombosis (DVT) can harm veins. Varicose Veins: Enlarged veins that lead to valve issues. Age: Veins become weaker over time. Obesity: Extra weight increases pressure on leg veins. Pregnancy: Increased blood volume and pressure can cause CVI. Development: Venous hypertension: Blood pools in veins due to valve failure. Vein Stretching: Chronic pressure causes veins to widen and malfunction. Tissue Changes: Poor blood flow leads to skin and tissue problems. Symptoms Appear: As the condition worsens, symptoms become more noticeable. Symptoms: Swelling: In legs and ankles. Pain/Discomfort: Aching or heaviness, especially after standing. Skin Changes: Color changes, dryness, or thickening near ankles. Varicose Veins: Visible, swollen veins. Ulcers: Open sores near the ankles. Restless Legs: Urge to move the legs. 7. Explain the differences between left-sided and right-sided heart failure, focusing on their causes, how they develop, and their symptoms (current content). Hematology Disorders 1. Compare the pathophysiology and manifestations of select red blood cell disorders (current content). Iron deficiency anemia: Pathophysiology: Nutritional or blood loss-related: Iron is essential for hemoglobin synthesis, and iron deficiency leads to decreased hemoglobin production and smaller, paler RBCs (microcytic, hypochromic anemia).  Causes include inadequate dietary intake, poor absorption or chronic blood loss (e.g., gastrointestinal bleeding, heavy menstruation). Severe liver disease, infection and cancer Manifestations: 1. Fatigue, weakness, and pallor due to decreased oxygen delivery to tissues. 2. Activity intolerance 3. Glossitis (inflamed tongue) and angular cheilitis (cracks at the mouth corners). 4. Brittle nails and hair loss. 5. Restless legs syndrome B12 deficiency: Macrocytic anemia: Vitamin B12 is necessary for DNA synthesis, especially in RBC precursors. A deficiency impairs DNA replication, leading to the production of large, immature RBCs (megaloblastic anemia). Causes include pernicious anemia (autoimmune destruction of intrinsic factor needed for B12 absorption), dietary deficiency (vegetarians/vegans), or malabsorption (e.g., Crohn’s disease, gastric surgery). Chronic gastritis, gastrectomy, aging Manifestations: Anemia symptoms: Fatigue, pallor, and shortness of breath. Neurological symptoms: Numbness, tingling in hands and feet, difficulty walking (due to nerve demyelination). Cognitive changes: Memory loss, confusion, and mood changes in severe cases. Impaired coordination and balance Folate deficiency: Pathophysiology: Macrocytic anemia similar to vitamin B12 deficiency because folate is also essential for DNA synthesis in RBC precursors. Causes include poor dietary intake (common in alcoholics), malabsorption (e.g., celiac disease), or increased requirements (e.g., pregnancy). medication Manifestations: Similar to B12 deficiency anemia, with fatigue, pallor, and shortness of breath. diarrhea may occur. Pregnant women may have an increased risk of giving birth to babies with neural tube defects (e.g., spina bifida).  Hemolytic Anemia Pathophysiology: Characterized by premature destruction of RBCs, which may be due to intrinsic factors (sickle cell disease) or extrinsic factors (e.g., autoimmune disorders, infections,). The increased rate of RBC destruction leads to increased erythropoiesis and the release of immature RBCs (reticulocytosis). Hemolysis results in an elevated level of free hemoglobin and bilirubin. Manifestations: Anemia symptoms: Fatigue, pallor, and shortness of breath. Sickle cell disease(normocytic) Autosomal recessive mutation Rigid sickle-shaped cells Causes microvascular occlusion RBC’s are more prone to hemolysis Pathophysiology- -Genetic mutation causes “sickling” Deoxygenated conditions, Acidosis, Dehydration -Causes chronic hemolysis and vas occlusion -Episodic exacerbations known as “sickle cell crisis Manifestations- Pain Fatigue Pallor Jaundice Organ damage Delayed growth and puberty Sickle cell crisis: Acute exacerbation caused by: Infection Hypoxia  Dehydration Stress Temperature extremes Types: Vasoocclusive Most common, blockage of small blood vessels Acute chest syndrome Life-threatening, vaso-occlusion in the lungs Splenic sequestration Splenic enlargement leading to acute anemia Aplastic crisis Triggered by infections Hemolytic crisis Accelerated destruction of RBC’s Manifestations: Sudden severe pain Shortness of breath Fever Severe fatigue or weakness Enlarged spleen Anemia Aplastic anemia Pathophysiology: Rare condition Bone marrow fails to produce new blood cells Key features  Anemia Leukopenia Thrombocytopenia Causes: ○ Idiopathic (unknown cause) in many cases. ○ Autoimmune destruction of bone marrow stem cells. ○ Exposure to toxins, such as benzene or certain medications (chemotherapy, antibiotics like chloramphenicol). ○ Viral infections (e.g., Epstein-Barr virus, hepatitis). ○ Radiation or chemotherapy. ○ Genetics Manifestations: ○ Fatigue And weakness ○ Dyspnea on exertion ○ Pallor ○ Frequent infections ○ Bruising, bleeding ○ Abnormalheartbeat Primary Polycythemia (Polycythemia Vera): Pathophysiology: ○ Abnormal overproduction of RBCs in bone ○ marrow ○ Myeloproliferative disease ○ Considered a malignancy Secondary Polycythemia: Pathophysiology: ○ Low oxygen triggers the body to produce more RBCs (Compensatory) ○ Common in people with chronic lung disease ○ Erythropoietin stimulates RBC production ○ Causes include: Chronic lung diseases (e.g., COPD, sleep apnea). Living at high altitudes, where oxygen levels are lower. Chronic heart disease. Kidney tumors that secrete excess EPO. Smoking, which reduces oxygen levels in the blood Manifestations: Hypertension Heart failure Skin changes “ruddy” look Splenomegaly Headache and dizziness Dyspnea Visual disturbances 2. Explain the pathophysiology and manifestations of various leukocyte disorders (current content). Leukemias-Overview Uncontrolled production of abnormal WBCs Undifferentiated Immature Nonfunctional Abnormal WBCs crowd out other blood components Infiltrate other organs disrupting normal Function Acute: Rapidly progressing Immature WBC’s Caused by genetic disorders, radiation, chemotherapy Acute symptoms: fatigue, fever, bruising, infections Life-threatening if untreated Chronic Slow progressing Abnormal mature WBC’s Affects older age individuals  Initially asymptomatic, symptoms develop over time Increased risk of infections, anemia, bleeding Can transform into acute Thrombocytopenia: Decreased production, increased destruction or sequestration Caused by autoimmune disorders, viral infections, chemotherapy, medications Signs and symptoms: bruising, nosebleeds, prolonged bleeding, petechiae, heavy menstruation Complications: hemorrhaging, internal Bleeding Thrombocytosis- high platelet count Overproduction of platelets Caused by chronic inflammation, cancer, iron deficiency, bone marrow disorders Signs and symptoms: typical asymptomatic, headaches, dizziness, weakness, chest pain Complications: thrombosis, stroke, MI, DVT Differentiate anemia, coagulopathies, leukemias, and polycythemias. Anemia: Low RBC count, hemoglobin/hematocrit; presents with fatigue and pallor. Coagulopathies: Normal RBCs but abnormal clotting; presents with bleeding or clotting disorders. Leukemias: Abnormal WBC production; presents with symptoms of infection, anemia, bleeding. Polycythemias: Elevated RBC count; presents with thickened blood, risk of clotting. Exemplar diseases: 3. Atelectasis (Sherpath only): Atelectasis is the collapse of lung tissue. There are three types of atelectasis: 1. Compression atelectasis is caused by external pressure exerted by tumor, fluid, or air in the pleural space or by abdominal distention pressing on a portion of lung, causing alveoli to collapse. 2.Obstructive (absorption) atelectasis results from obstructed or hypoventilated alveoli as the air is gradually absorbed out of the alveoli and into the blood. 3. Surfactant impairment (adhesive) atelectasis results from decreased production or inactivation of surfactant, which is necessary to reduce surface tension in the alveoli and thus prevent lung collapse during expiration. Surfactant impairment can occur because of premature birth and from any serious lung injury, such as occurs with aspiration, acute respiratory distress syndrome, anesthesia induction, or mechanical ventilation. 4. Aspiration (Sherpath only) bronchial inflammation and collapse of airways distal to the obstruction Aspiration of oral or pharyngeal secretions can lead to aspiration pneumonia. Aspiration of acidic gastric fluid may cause severe pneumonitis 8. Hypertension Triggering of compensatory mechanisms to regulate blood pressure Baroreceptors Atrial natriuretic peptide Modifiable: Obesity, Poor diet, Smoking, Alcohol use Non-modifiable- Age, Genetics, Family history (Consider lifestyle and environmental factors) Often asymptomatic (silent killer) Headaches Dizziness Blurred vision Chest pain Complications: CAKE Cardio-Ischemic or hemorrhage stroke Neurological (brain)- Dementia,stroke Kidney- Chronic disease Eye-visual changes 9. Aterio and atherosclerosis Endothelial Injury- Arteriosclerosis begins with damage to the endothelial lining of arteries due to factors like hypertension, smoking, or high cholesterol levels. Inflammatory Response- Injury to the endothelium leads to an inflammatory response. Macrophages and other immune cells are attracted to the site to aid in repair. Formation of Atheroma- Lipoproteins, especially LDL, accumulate in the arterial wall, leading to the formation of fatty streaks, which evolve into atheromas. Plaque Maturation- Smooth muscle cells migrate to form a fibrous cap over the atheroma. The plaque may calcify, reducing arterial elasticity and contributing to vessel narrowing. Nonmodifiable Risk Factors These include age, gender, and genetics. Genetic predispositions influence serum lipid levels and receptor function. Modifiable Risk Factors - Lifestyle Obesity, smoking, poor diet, and sedentary lifestyle Modifiable Risk Factors -Conditions like hypertension, diabetes mellitus, and hyperlipidemia exacerbate atherosclerosis. Manifestations: Cardiovascular System- Atherosclerosis in coronary arteries can lead to angina, myocardial infarction, and congestive heart failure. Cerebral Circulation- In the brain, atherosclerosis can cause transient ischemic attacks(TIA) and cerebrovascular accidents (stroke), leading to neurological deficits. Peripheral Arterial Disease- (PAD)In peripheral arteries, it can cause intermittent claudication and gangrene, especially in the lower extremities. Complications: Myocardial Infarction, Stroke, Aneurysm, Peripheral Arterial Disease (PAD) 10. Acute coronary syndrome Mechanism of Coronary Artery Blockage Plaque Rupture: ACS often starts with the rupture of an atherosclerotic plaque in a coronary artery, exposing the underlying tissue and triggering thrombus formation. Thrombus Formation: The formation of a blood clot (thrombus) at the site of plaque rupture can partially or completely obstruct coronary blood flow. Ischemia and Infarction: Blockage of a coronary artery leads to ischemia (restricted blood flow) and, if prolonged, myocardial infarction (heart attack) with tissue necrosis. Vasospasm Contribution: Coronary artery vasospasm can also contribute to ACS by reducing blood supply, often triggered by factors like stress or drug use Risk factors: Nonmodifiable Risk Factors- Age, gender, and family history Modifiable Risk Factors - Lifestyle Smoking, obesity, physical inactivity, and unhealthy diet are significant modifiable risk factors for ACS. Modifiable Risk Factors - Medical Conditions like hypertension, diabetes mellitus, and dyslipidemia Signs and symptoms: SOB, Angina chest pain, Diaphoresis and nausea, Fatigue and dizziness Different Types of Angina Stable, Unstable, and Variant Angina Stable Angina: Occurs predictably with physical exertion or stress. It is often relieved by rest or nitroglycerin. Unstable Angina: A more severe form that occurs unpredictably, often at rest, and signals an increased risk of myocardial infarction. Variant (Prinzmetal) Angina: Caused by a spasm in the coronary arteries, often occurring at rest and typically not related to physical exertion. Complications: Heart Failure, Arrhythmias, Cardiogenic Shock, Sudden Cardiac Arrest 11. Heart failure: “Pump” problem Systolic dysfunction (contraction) Diastolic dysfunction (relaxation) Both lead to reduced cardiac output and congestion Reduced oxygen supply to tissues (forward effect) Fluid buildup in lungs and tissues(backward effect) Risk factors: Modifiable Hypertension CAD Diabetes Non-Modifiable Age Genetics Family history Chronic conditions can contribute Fatigue Dyspnea on exertion Increased (HR, BP, RR) Hypoxia Muscle weakness Severe (decompensated) Dizziness, diaphoresis, cyanosis Altered mental status Bradycardia, hypotension, dysrhythmias Complications: Sudden cardiac death Cardiogenic shock Chronic kidney disease Fluid retention Pulmonary edema, pleural effusions Respiratory failure 12. Deep vein thrombosis Virchow’s triad(SHE) Hypercoagulability Stasis Endothelial injury Prolonged immobility Risk Factors of DVT Prolonged immobility, Cancer Heart failure, Inflammatory conditions,Genetic disorders, Obesity Smoking, Hormonal therapy Signs and Symptoms -Usually unilateral Swelling and pain -Skin changes- Red and warm -Can be asymptomatic Complications: Pulmonary embolism- Clot can travel to the lungs Post thrombotic Syndrome(STS) Chronic Venous Insufficiency- Recurrence damages veins 13. Peripheral arterial disease Results from atherosclerosis Reduced perfusion to the limbs Hypoxia and tissue damage Can progress to critical limb Ischemia Stage 1- Asymptomatic Stage 2 -Claudication Stage 3 and 4- Rest pain, Tissue necrosis Modifiable Smoking, Diabetes Non- modifiable: Age Family history, genetics Hypertension Hyperlipidemia a CKD Signs and symptoms : Intermittent claudication: Pain with activity, relieved with rest Rest pain Prominent at night Occurs with advanced disease Skin changes Reduced hair growth Pale skin Weak pulses Ulcers Complications: Impaired healing Ulcers and non-healing wounds Severe blockage Critical limb ischemia Gangrene Tissue death 14. Chronic venous insufficiency Valve Dysfunction- Problems with backflow Venous hypertension- Vascular congestion Chronic inflammation- Varicose veins and ulcers Risk Factors Modifiable:- Obesity, Sedentary lifestyle Non- Modifiable- Age, Women History of DVT Pregnancy Signs and symptoms: Due to prolonged increased pressure- Varicose veins After prolonged standing- Edema Thick, discolored- Skin changes Complications: Venous ulcers, infections Deep vein thrombosis 16. Aplastic anemia ( normochromic) Prevalence Rare but important disorder Typically occurring in conjunction with leukopenia and thrombocytopenia Categorized as pancytopenia, or generalized bone marrow failure Causes and Predisposing Factors Alteration of stem cells ○ Stem cells cannot multiply or differentiate ○ Causes inhibited RBC production Minimal symptoms until death Two forms: ○ Idiopathic: no known cause; most common form ○ Secondary: caused by bone marrow depression from cytotoxic medications, radiation therapy, and viral infections 17. Sickle Cell Anemia 18. Vit B-related anemias (folate deficiency, pernicious anemia) Pernicious Anemia Pathophysiology Vitamin B12 cannot be absorbed in the lower ileum without the presence of the intrinsic factor to bind with the vitamin. Mucosa atrophies occur because parietal cells cannot produce hydrochloric acid (achlorhydria). ○ This inhibits digestion of protein. ○ This inhibits absorption of iron, which may manifest as an iron deficiency anemia. B12 deficiency inhibits the maturing process of the RBCs. ○ This interferes with synthesis of DNA. ○ RBCs are extremely large (megaloblasts) with nuclei. ○ RBCs are destroyed prematurely, leading to anemia. Hemoglobin in these cells is normal, with ability to carry oxygen. Granulocytes are also affected, causing large hypersegmented neutrophils. The thrombocyte count is low. Clinical Manifestations Tongue is enlarged and red, swollen, painful, and shiny. Decreased gastric acid production causes nausea/vomiting. Absence of B12 causes demyelination of nerves and spinal cord: ○ This inhibits nerve conduction. ○ This may be irreversible. ○ This affects sensory fibers first and then motor fibers 19. Thrombocytopenia purpura and Thrombocytosis Thrombocytopenia- low platelet count Decreased production, increased destruction or sequestration Caused by autoimmune disorders, viral infections, chemotherapy, medications Signs and symptoms: bruising, nosebleeds, prolonged bleeding, petechiae, heavy menstruation Complications: hemorrhaging, internal Bleeding Thrombocytosis- high platelet count Overproduction of platelets  Caused by chronic inflammation, cancer, iron deficiency, bone marrow disorders Signs and symptoms: typical asymptomatic, headaches, dizziness, weakness, chest pain Complications: thrombosis, stroke, MI, DVT 21. Leukemia Uncontrolled production of abnormal WBCs Undifferentiated Immature Nonfunctional Abnormal WBCs crowd out other blood components Infiltrate other organs disrupting normal Function a. Acute vs chronic Acute: Rapidly progressing Immature WBC’s Caused by genetic disorders, radiation, chemotherapy Acute symptoms: fatigue, fever, bruising, infections Life-threatening if untreated Chronic Slow progressing Abnormal mature WBC’s Affects older age individuals Initially asymptomatic, symptoms develop over time Increased risk of infections, anemia, bleeding Can transform into acute b. Lymphocytic vs myelogenous Key Differences Cell Type Affected: ○ Lymphocytic: Affects lymphocytes. ○ Myelogenous: Affects myeloid cells (granulocytes, red blood cells, platelets). Progression: ○ Acute forms (ALL and AML) progress rapidly, while chronic forms (CLL and CML) progress more slowly.