Mid Term Study Guide NR 507

Mid Term Study Guide NR 507

Pulmonary

1. Concepts of Anticholinergic Drugs and Asthma: Anticholinergic drugs block acetylcholine binding, primarily in the lungs, promoting bronchiole dilation by decreasing the parasympathetic response. Examples like tiotropium and ipratropium are fast-acting.
2. Bronchitis & Associated Pathogenesis: Bronchitis begins with exposure to an irritant, such as tobacco smoke, which triggers bronchiole smooth muscle constriction, mucus secretion, and the release of inflammatory mediators like histamine, prostaglandins, and leukotrienes. Chronic bronchitis develops over long periods (3 months for over 2 consecutive years) leading to smooth muscle hypertrophy, increased bronchoconstriction, hypertrophy and hyperplasia of goblet cells, mucus hypersecretion, and epithelial cell metaplasia, resulting in non-ciliated squamous cells and fibrosis in the bronchial wall. This condition also causes thickening and rigidity of the bronchial basement membrane, narrowing bronchial passageways, and leading to symptoms like weight loss, loss of appetite, and muscle weakness due to increased protease activity and destruction of lung tissue.
3. Chronic Bronchitis and Related Acid/Base Disturbance: In chronic bronchitis, hypercapnia (CO2 retention) leads to respiratory acidosis due to compromised ventilation, especially during exhalation, resulting in alveolar hyperinflation.
4. Perfusion: Perfusion refers to the actual exchange of O2 and CO2 in the bloodstream via the alveoli and pulmonary capillaries. It typically describes the delivery of blood to an organ or tissue.
5. Blood Flow Between the Heart and Lungs in Chronic Bronchitis: Poor ventilation in chronic bronchitis causes right-to-left shunting, where deoxygenated blood passes from the right ventricle to the lungs to the left ventricle without adequate perfusion. The kidneys respond by secreting erythropoietin, increasing RBC production and O2-carrying capacity. This increases blood volume, the workload on the pulmonary and cardiovascular systems, leading to pulmonary hypertension, increased workload on the right ventricle, cardiac hypertrophy, and eventually right-sided heart failure or Cor Pulmonale.
6. Asthma Signs and Symptoms: Asthma is characterized by coughing (especially at night), chest tightness, shortness of breath, wheezing during exhalation, and rapid breathing. These symptoms are due to airway inflammation, bronchial hyperactivity, smooth muscle spasms, excessive mucus production, and obstruction leading to decreased alveolar ventilation.
7. Bronchioles in Asthma: The bronchioles, which consist of three layers surrounding the lumen or airway passageway, play a significant role in asthma. The innermost layer is composed of columnar epithelial cells and goblet cells, the middle layer is the lamina propria embedded with connective tissue and immune cells, and the outermost layer is smooth muscle cells responsible for the airway’s ability to constrict and dilate. In asthma, these protective features become overactive, leading to inflammation, damage to host tissue, smooth muscle hypertrophy, excessive mucus production, and bronchioles spasm.
8. Alveolar Hyperinflation with Asthma: Increased mucus production by goblet cells during the inflammatory process forms mucus plugs that block alveolar passageways, leading to air trapping and hyperinflation, which can erode airway tissue.
9. Polycythemia Vera: Polycythemia vera is a rare blood disease where the body produces too many RBCs, thickening the blood and increasing the risk of blood clots. It often results from chronic low oxygen levels, prompting the kidneys to increase erythropoietin secretion, stimulating RBC production. Patients with chronic bronchitis often exhibit elevated hematocrit levels and may develop secondary polycythemia vera.
10. Mechanism of Action of Anticholinergic Drugs to Treat Asthma: Anticholinergic drugs bind to muscarinic receptors, blocking acetylcholine action. They reduce bronchomotor tone, leading to bronchodilation and decreased parasympathetic response.

Cardiovascular

1. Review Concepts of Cardiac Output: Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV). CO is the volume of blood ejected by each ventricle per minute (e.g., 75 bpm x 70 ml = 5.25 L/min). CO decreases with age at a rate of 1% per year after the age of 30. CO is crucial for understanding heart failure and the relationship between HR and SV.
2. Concepts of Cardiac Contractility: Contractility, or the ionotropic state, is determined by calcium availability and its interaction with actin and myosin. Sympathetic stimulation increases contractility, while low levels of ATP (due to ischemia, hypoxia, or acidosis) decrease it.
3. Preload and Afterload Concepts:
   • Preload: The degree of myocardial fiber stretch before contraction, influenced by the end-diastolic ventricular volume (EDV). It can be increased by conditions like CHF and hypervolemia and decreased by cardiac tamponade or hypovolemia.
   • Afterload: The tension the ventricle must develop during systole to open the semilunar valves and eject blood. It is influenced by ventricular wall thickness, arterial pressure, and ventricle chamber size. Afterload increases with systemic hypertension, valve disease, and COPD and decreases with hypotension or vasodilation.
4. Systole and Diastole: Systole is the phase when the heart contracts to pump blood out, while diastole occurs when the heart relaxes after contraction. Systole causes blood ejection into the aorta and pulmonary trunk, while diastole allows the heart chambers to fill with blood.
5. Heart Valves: When They Open and Close: The heart has four valves: two atrioventricular valves (tricuspid and bicuspid) and two semilunar valves (pulmonary and aortic). These valves ensure unidirectional blood flow and open/close in response to myocardial contractions and pressure changes. For example, during RV contraction, the tricuspid valve closes, and the pulmonary valve opens, allowing blood flow into the lungs.
6. The Production of Heart Sounds S1 and S2:
   • S1: The first heart sound, caused by the closure of the bicuspid (mitral) and tricuspid valves at the start of systole.
   • S2: The second heart sound, caused by the closure of the semilunar valves (pulmonic and aortic) marking the end of systole.
7. Stenosis of the Heart Valves and Effects: Aortic valve stenosis occurs when the heart’s aortic valve narrows, preventing blood flow from the heart into the aorta and the body during systole. Symptoms include a systolic murmur, abnormal heart sounds, angina, and chest pain. Bicuspid (mitral) valve stenosis impairs blood flow from the left atrium to the left ventricle, often due to rheumatic heart disease, leading to symptoms like shortness of breath, edema, palpitations, and fatigue.
8. Stroke Volume: Stroke volume is determined by preload, contractility, and afterload, with a normal stroke volume being about 70 ml.
9. Cor Pulmonale: Cor Pulmonale is the abnormal enlargement of the right side of the heart due to lung or pulmonary vessel issues. It is defined as the right ventricle’s inability to provide adequate blood flow into pulmonary circulation, commonly caused by pulmonary hypertension or worsening left-sided heart failure.
10. Heart Failure: Heart failure is a cardiac dysfunction where the heart cannot provide adequate cardiac output, resulting in insufficient tissue perfusion. Left-sided heart failure (CHF) involves the left ventricle’s inability to pump blood into systemic circulation, often due to hypertension, cardiac hypertrophy, or MI, leading to pulmonary edema and dyspnea. Right-sided heart failure causes blood to back up into the vena cava and systemic veins, leading to jugular distention, hepatosplenomegaly, and peripheral edema. High-output heart failure, caused by conditions like hyperthyroidism or nutritional deficiencies, initially allows the heart to meet demands but eventually leads to failure.
11. Hypertension: Pathophysiology: Hypertension (HTN) is a consistent elevation of systemic arterial blood pressure caused by increased cardiac output and/or total peripheral resistance. Primary HTN is often genetic or idiopathic, while secondary HTN results from another disease. HTN can lead to target organ damage, including retinal changes, renal disease, CHF, CAD, stroke, or dementia.
12. Calcium Binding and Troponin: Calcium ions released from the sarcoplasmic reticulum bind to troponin, causing a shift in tropomyosin and exposing myosin binding sites, leading to muscle fiber contraction. ATP is required to facilitate this interaction.

Hematology

1. Hematopoiesis: Hematopoiesis is the formation of blood cells, occurring in different sites throughout life. In fetuses, it begins in the yolk sac, then the fetal liver and spleen, and eventually in the bone marrow. In adults, it primarily occurs in the red marrow of large bones. Hematopoiesis is stimulated by factors such as infiltration of yellow marrow with red marrow cells and faster proliferation and differentiation of stem cells.
2. Risk Factors for Developing Anemia: Risk factors for anemia include poverty, age, a diet lacking iron, vitamin B12, and folic acid, menstruation, intestinal disorders (e.g., Crohn’s or celiac disease), pregnancy, chronic conditions (e.g., cancer, kidney disease, ulcers), family history, autoimmune disorders, alcoholism, exposure to toxic chemicals, and certain medications.
3. Iron Deficiency Anemia: Iron deficiency anemia (IDA) is a microcytic hypochromic disorder characterized by small cells with low hemoglobin levels. The most common cause is insufficient iron intake or chronic/occult bleeding. Pathologically, decreased iron levels lead to reduced hemoglobin synthesis, resulting in smaller and paler red blood cells.
4. Erythrocyte Function and Lifespan: The primary function of erythrocytes is gas exchange, transporting oxygen bound to hemoglobin and a small amount of CO2. The typical lifespan of an erythrocyte is 100-120 days.
5. Sickle Cell Anemia: Sickle cell anemia is an inherited disorder of the erythrocytes, characterized by a single amino acid change on the beta chain of hemoglobin, leading to elongated and less effective hemoglobin molecules. This results in oxidative stress, sickling of red blood cells, and various complications, including an increased risk of stroke, splenic damage, and kidney damage.
6. Thalassemia: Thalassemia is an inherited autosomal recessive disorder caused by mutations in the alpha or beta chains of hemoglobin, leading to varying degrees of red blood cell distortion and dysfunction. The severity of the disorder can range from minor, asymptomatic cases to severe, life-threatening conditions like Cooley’s Thalassemia.
7. Pernicious Anemia: Pernicious anemia is a macrocytic normochromic anemia characterized by unusually large cells with normal hemoglobin levels. It is often related to an autoimmune reaction, particularly against GI tissue, leading to decreased intrinsic factor production and subsequent vitamin B12 malabsorption. This results in impaired DNA synthesis and nerve cell myelination, causing neuropathies associated with pernicious anemia.
8. Hemolytic Anemia: Hemolytic anemia is characterized by the lysis of red blood cells. Causes include infections, transfusion reactions, hemolytic disease of the newborn, autoimmune reactions, and certain drugs. Pathologically, premature destruction of red blood cells occurs due to enzymes, toxins, immune responses, or chemical effects.
9. Erythropoietin: Erythropoietin is a growth factor produced in the kidneys (and to a lesser extent the liver) in response to tissue hypoxia. It binds to hemocytoblasts, triggering a series of genetic and enzymatic changes that lead to the development of mature erythrocytes.
10. Function of Hemoglobin: Hemoglobin has a unique chemical structure that allows it to bind four oxygen molecules. It plays a critical role in tissue oxygenation, efficiently carrying oxygen from the lungs to body tissues and aiding in CO2 and hydrogen transport back to the lungs.
11. Development of Anemia Due to Gastrectomy: Gastrectomy procedures result in the loss of GI cells that produce intrinsic factor, necessary for vitamin B12 absorption. Inadequate B12 levels lead to decreased DNA synthesis and reduced RBC production, resulting in pernicious anemia.
12. Effect of Being Transfused with the Incorrect Blood Type: Transfusion with the incorrect blood type can cause a hemolytic transfusion reaction, leading to hemolytic anemia. The immune system attacks the transfused RBCs, which can be life-threatening.

Genitourinary/Renal

1. Anatomy and Physiology of the Kidney: The kidney consists of three distinct areas: the renal cortex (outer), renal medulla (middle), and renal pelvis (inner). The nephron, the functional unit of the kidney, performs ultrafiltration. It consists of Bowman’s capsule and a tubular system, surrounded by two capillary beds. The nephron’s function includes maintaining homeostasis, filtering blood, producing urine, maintaining pH and BP, and eliminating waste.
2. Nephron Damage: Kidney diseases often attack the nephrons, causing them to lose their filtering ability. Nephron damage, often irreversible, leads to increased creatinine levels, changes in renal vasculature, and the potential shunting between efferent and afferent arterioles.
3. Tubular Reabsorption and Tubular Secretion:
   • Tubular Reabsorption: This process involves the selective return of water and solutes from the nephron tubule system back into the bloodstream.
   • Tubular Secretion: This process involves moving waste materials and excess ions from the bloodstream into the nephron tubule system for excretion.
4. Conditions Associated with Renal Failure: Conditions leading to renal failure include unresolved acute kidney injury, hypertension, diabetes mellitus, and systemic lupus.
5. Calculi Blockage of the Ureter: Kidney stones, which often form due to elevated levels of substances like calcium and uric acid, can block the ureter. Smaller stones may pass on their own, while larger stones may require intervention.
6. Benign Prostatic Hypertrophy (BPH): BPH is the enlargement of the prostate gland, which can compress the urethra and lead to partial or complete urinary tract obstruction. BPH can cause acute kidney injury post-renal failure.
7. Prerenal, Intrarenal, and Postrenal Disease:
   • Prerenal: Caused by renal hypoperfusion due to severe hypotension or decreased cardiac output.
   • Intrarenal: Often results from acute tubular necrosis or acute glomerulonephritis.
   • Postrenal: Caused by urinary tract obstruction, such as BPH, calculi, inflammation, or tumors.
8. Glomerulonephritis: Glomerulonephritis is inflammation of the glomeruli due to immunologic responses, infections, or other factors. It leads to glomerular injury, resulting in proteinuria, hematuria, edema, and renal failure.
9. Treatment for Renal Failure: Treatment of acute kidney injury requires individualized therapy focusing on correcting fluid and electrolyte imbalances, managing blood pressure, preventing infections, and maintaining nutrition. In advanced renal failure, dialysis or transplantation may be necessary.
10. Blood Hydrostatic Pressure: Blood hydrostatic pressure is the force exerted by water in the blood against the inside wall of Bowman’s capsule, essential for blood pressure in the glomerulus and facilitating filtration.
11. Kidney Filtration: Nephrons perform ultrafiltration, where blood enters the glomerulus, and blood pressure forces water and dissolved substances into Bowman’s capsule, starting the process of urine formation.
12. Role of Angiotensin Converting Enzyme (ACE): ACE converts angiotensin I to angiotensin II, which stimulates aldosterone secretion, acts as a potent vasoconstrictor, and regulates blood pressure and fluid balance.
13. Role of the Macrophage: Macrophages play a crucial role in immunity by performing phagocytosis, regulating lymphocyte activation, and aiding in the activation of T and B lymphocytes.