General Study Tips and Recommendations

NR507 Midterm Exam Study Guide General Study Tips and Recommendations  Topics and content on guides are intended to focus student attention when reading/studying and some topics may be repeated in multiple chapters.  Multiple test items are derived from the same topic areas to encourage deeper comprehension.  Students must have a broad understanding of content and not simply memorize passages in textbooks or articles.  Information contained in the chapters as well as boxes and table within the chapters may include test items.  Exam questions represent various levels of cognitive learning. You are expected to analyze, synthesis, and evaluate patient scenarios in order to answer the questions.  Read all of the answers BEFORE reading the stem of the question. This will help you focus on the key content and not get distracted by extraneous information. Once you have selected your answer, read the question one more time to ensure that the best answer has been chosen.  Utilize your time well by not rushing. You will have plenty of time to read each question for understanding before you select your final answer. Major Content Topics: Alterations in Immunity & Inflammation    Hypersensitivity Immunodeficiency Autoimmunity Alterations in Hematologic Function         Anemia Role of erythropoietin in RBC production Primary site of RBC production Anemia Microcytic anemias Macrocytic anemias Normocytic anemias Hemoglobinopathies Alterations of Cardiovascular Function  Coronary artery disease Definition: imbalance between myocardial oxygen demand and supply from coronary arteries Prolonged O2 demand on the heart leads to Myocardial Infraction Cause: Atherosclerosis of coronary arteries with myocardial ischemia Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 PATHO: LDL in blood overtime starts to stick to artery wall. It grows over time which limits the blood flow to heart. As people do activity, sob and chest pain with activities. Goes away with rest.-stable angina Unstable: plaque rupture: artery wall messed up, body sends clotÝng factors to artery to repair it and forms a thrombus. ACS: Thrombus keeps growing and growing which stops blood flow : unstable angina (chest pain unrelieved by rest and nitroglycerin doesn’t relieve chest pain. Once thrombus completes blocks blood flow= MI(heart muscle dies) Non-modifiable: age(men > 45 y/o ; women > 55 y/o), family history modifiable:: Elevated LDL(BAD) & Decreased HLD(Good), Hypertension, Diabetes, smoking Present as Stable Angina, Prinzmetal Angia, Acute Coronary Syndrome(unstable angina, Non ST elevation, MI, NSTEMI, STEMI Chronic Ischemia heart disease, sudden cardiac death) Less common cause: Coronary Embolus: A-Fib, Infective endocarditis, left atrial or ventricular thrombus, cardiac cath Vasculitis(CAD in Children): * Kawasaki disease (medium vessel vasculitis cause coronary artery aneurysm) Vasospasm: reduce blood flow Aortic Valve Stenosis: not enough blood to coronaries leading to myocardial ischemia Causes of concentric ventricular hypertrophy: HTN, hypertrophic cardiomyopathy d/t more heart muscle to supply Stable(Plaque) Angina(hasn’t ruptured) (Near -total occlusion w/ no infraction of b/c atherosclerotic plaque grows slowly gives heart to develop **collateral circulationRerouting**)- that supplies the hyperperfused area Secondary to Myocardial Ischemia(Reversible Cell Injury) Atherosclerotic plaque occluding > 75% of coronary artery lumen S/S chest pain with activity, sob, fatigue-goes away with rest Infraction: Irreversible cell injury or death Described as : Deep poorly localized squeezing, crushing, suffocating, retrosternal pain(jaw, neck, arm) Other symptoms: sob, nausea, vomiting, diaphoresis, fatigue, dizziness *** Reproducible during: Physical exertion or Emotional Stress*** Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Relieved w/in 5 min with : Rest and Sublingual nitroglycerin** Risk Factors: smoking, obese, overweight, High Cholesterol, Sedentary life style, family history TEST ECG: Normal at Rest Stress Test: Abnormal Cardiac Markers : Always Normal like TROPONIN why because of ischemia but no infarction Prinzmetal Angina (variant Angina) No atherosclerotic plaque instead the coronary artery undergoes vasospasm(narrowing the lumen) Angina at Rest Cause: smoking, cocaine, alcohol, triptans(Given with patients with migraines ) 24 hour ECG(Holter Monitor)---Transmural Ischemia ***Results: Transient Elevation of ST-Segment ; Troponin Levels Normal**(no infraction) Diagnosis: Low dose of VASOCONSTRICTIVE meds: ERGONVINE (provoke vasospasm and transient elevation of ST Segment Treatment: Calcium channel blockers and nitroglycerin(relax vascular smooth muscle and cessation of trigger) Unstable Angina or Acute Coronary Syndrome: Medical Emergency Not relieved with rest or nitro 1. Unstable Angina** Near-to (incomplete ) occlusion ECG: ST Segment Depression, T Waves Inversion, Troponin Levels are Normal(no myocyte necrosis) 2. NSTEMI **infarction beneath endocardium called** subendocardial infarct** Troponin Levels : Elevated ECG: ST-Segment Depression and T wave Inversion (Ischemia-reversible) 3. STEMI: Thrombus occludes 100% of the lumen ECG: ST- Segment Elevation (Acute Transmural Infarction involves the whole wall) (Injury-irreversible) CM: Sudden new onset angina or increase in severity of existing stable angina Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 ATYPICAL Presentation: older people, females, diabetics-SOB, Fatigue, dizziness Cause: Thin fibrous cap and rich lipid core = increased risk of rupture Key Cardiac Biomarkers 1. Troponin **Increased 2-4 hours AFTER INFARCTION, peak = 48 hours, stay increased 7-10 days 2. CK-MB ** increased 2-4 hours AFTER INFARCTION, peak 24 hours, normal after 48 hours **Diagnosis reinfarction Locate Infarct & Vessels involved based on ECG(locate leads with ST Elevation) Now for your exam, you might be asked to locate the infarct and the vessel involved based on the on the ECG. This can be done by locating which leads had the ST elevation: V1 and V2 involvement is an anteroseptal MI, which means the left anterior descending artery, or LAD is involved. V3, V4 involvement is an anteroapical MI, which means the distal part of the LAD is involved. V5, V6 involvement is an anterolateral MI, which involves the LAD or left circumflex artery. Lateral MI involves leads I and aVL, and the left circumflex is occluded. Inferior MI involves leads II, III and aVF with the right coronary artery being the culprit. Inferior wall myocardial infarctions are very high yield because they can also present as epigastric abdominal pain instead of chest pain. RCA occlusion can also cause right ventricular infarction, but right sided leads would have to be obtained to see that. Finally, whenever there is ST depression with tall R-waves in V1 to V3, then a posterior MI involving the posterior descending artery is a possibility. Therefore, posterior leads V7-V9 must be obtained in such a scenario Timeline: In the first 24 hours, the heart looks grossly normal. On light microscopy, after 4 hours, coagulative necrosis begins, and the necrotic myocardial cells hypercontract, giving them a wavy appearance. During this period, arrhythmias can occur because the infarction disrupts the electrical flow through the myocardium. **Premature ventricular arrhythmias or PVCs are the most common arrhythmia**, but these are benign. Ventricular arrhythmias like ventricular tachycardia or fibrillation are the most common cause of sudden cardiac death, which is death within 1 hour of symptom onset. Ex: However, ventricular arrhythmias due to coronary artery disease are a more common cause of death in athletes over 35 years old, whereas hypertrophic cardiomyopathy is more common in those under 35 years old. Other complications include heart failure and cardiogenic shock, which are the most common cause of death from MI in the hospital. Right coronary artery occlusion, the infarcted right ventricle dilates, pushing the interventricular septum onto the left ventricular cavity, causing decreased left ventricular filling, which results in a decreased stroke volume and hypotension. You can differentiate between right and left ventricular failure clinically, Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 because in a right ventricular failure, the lungs are clear on auscultation, and there is elevation of jugular venous pressure. It’s important to look for a right ventricular MI because veno-dilating medications like nitroglycerin are contraindicated in these cases, as they further decrease the preload, worsening the hypotension. 1 to 3 days after the infarction, the affected area appears grossly red. On light microscopy, there’s extensive coagulative necrosis, and a large amount of neutrophils have infiltrated causing acute inflammation. That inflammation can spread towards pericardium, causing postinfarction fibrinous pericarditis. This presents with a low-grade fever, and sharp, pleuritic chest pain, meaning it increases with inspiration. 3 to 14 days after the infarction, macrophages come over to clean up the necrotic mess, and soft, yellow granulation tissue begins to develop to repair the infarcted tissue. This soft granulation tissue is quite weak, so there’s a risk of interventricular septum or ventricular free wall rupture. Interventricular septum rupture typically presents at around 3 to 5 days as a left-to-right ventricular septal defect, which presents as a new holosystolic murmur at the left sternal border, and increased oxygen saturation in the right ventricle. Ventricular free wall rupture classically occurs in anterior wall STEMIs, and presents at around 5 to 14 days. As a result, large amounts of blood leak into the pericardial cavity, causing a pericardial tamponade. Sometimes, the rupture is contained by the adherent pericardium, producing a balloon-like sack of blood called a ventricular pseudoaneurysm. This pocket of blood is static, and stasis promotes clotÝng, producing what’s called a mural thrombus. Bits of this thrombus can embolize to the systemic circulation, resulting in peripheral complications like a stroke. Rupture of the papillary muscles, small muscles that anchor to the atrioventricular valves by the chordae tendineae. This usually occurs 2 to 7 days post-infarction. Normally, the anterolateral papillary muscle receives a dual blood supply from both the LAD and the left circumflex artery. The posteromedial papillary muscle, however, is solely supplied by the posterior descending artery, so it’s more at risk of rupture, and this can cause acute-onset mitral regurgitation and pulmonary edema. 2 weeks to a couple of months post-MI, macrophages invade the tissue, and the healing process begins with the formation of granulation tissue, which is a type of scar tissue that’s yellow and soft, along with some new blood vessels, in a process called neovascularization. This scar tissue may cause the ventricular wall to bulge out, forming a true ventricular aneurysm. Therefore, there is a risk of developing heart failure, as well as a mural thrombus due to stasis of blood flow in that area Another complication during this period is Dressler syndrome, a fibrinous pericarditis that occurs secondary to formation of autoantibodies that target serosal surfaces like the pericardium. Treatment Unstable Angina & NSTEMI Antiplatelet Therapies, anticoagulant therapy, coronary angiography & revascularization aka reperfusion therapy STEMI Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Reperfusion Therapy PCI(percutaneous coronary Intervention) Angiography-image xrays to visualize clot or angioblastyballoon or stent placement Fibrinolytic Therapy (meds to break downs fibin in blood clots) Anticoagulants  Heart failure Left side = Lungs Right side =venous circulation Heart failure is a clinical syndrome used to describe the inability of the heart to pump enough blood or a point at which the heart can’t supply enough blood to meet the body’s demands. This can happen in two ways, either the heart’s ventricles can’t pump blood hard enough during systole, called systolic heart failure, or not enough blood fills into the ventricles during diastole, called diastolic heart failure. In both cases, blood backs up into the lungs, causing congestion or fluid buildup, which is why it’s also often known as congestive heart failure, or just CHF. Systolic heart failure. OXYGENATED BLOOD backs up into the lungs Systolic heart failure(Left sided HF, PULMONARY EDEMA) Heart failure with REDUCED ejection fraction Left ventricular systolic dysfunction Systolic is the SQUEEZING phase of heart Left ventricle can’t properly eject blood properly An EF of 40% or less is a diagnosis for heart failure: Echo, heart carth, Nuclear stress test One way to think about this is that the heart needs to squeeze out a certain volume of blood each minute, called cardiac output, which can be calculated as the heart rate multiplied by the stroke volume. The heart rate is pretty intuitive, but the stroke volume is a little tricky. Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 For example, an adult heart might beat 70 times per minute and the left ventricle might squeeze out 70ml per beat, so 70 x 70 equals a cardiac output of 4900 ml per minute, which is almost 5 liters per minute. Now, the stroke volume is only a fraction of the total volume. The total volume might be closer to 110 ml, and 70ml is the fraction that got ejected out with each beat, the other 40ml kind of lingers in the left ventricle until the next beat. In this example, the ejection fraction would be 70ml divided by 110 ml or about 64%, a normal ejection fraction is around 50-70%. Ejection fraction depends on contractility, preload, and afterload Now, in systolic heart failure, there’s decreased contractility of the left ventricle, which causes a decreased cardiac output because the stroke volume is low. This means there’s also a decreased ejection fraction. During diastole blood returns to the ventricles and combines with the leftover blood that didn’t get pumped out during systole, and this is called the EDV or end diastolic pressure volume. With systolic heart failure, don’t forget that EDV is high, because there’s more blood leftover after each heartbeat. ** Regarding the end diastolic pressure or EDP, which is the pressure that’s found in the ventricle at the end of diastole, this will also be high**, because the volume at the end of diastole is high as well. Systolic heart failure is mainly caused by low contractility which can happen with** ischemia caused by myocardial infarction**, where a part of the cardiac tissue is damaged, so it won’t contract properly anymore. MI is the primary cause of decreased contractility Myocardial Ischemia =inflammatory, immune, neurohumoral changes (activation of SNS and RAAS) that mediate a process called ventricular remodeling Ventricular remodeling-disruption of the normal myocardial extracellular structure =myocyte contractile dysfunction Contractility decreased, stroke volume decreased, left ventricular end-diastolic volume increased(Preload) Preload increases with decreased contractility (IV fluids, renal failure, mitral valvular dz) Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Frank Sterling Law: cardiac output can improve up to a certain point, preload continue to rise, dilation of myocardium leads to dysfunction of the sarcomeres and decreased contractility Another cause is **dilated cardiomyopathy, where the ventricle is dilated and weakened** Left-sided heart failure develops from damage to the myocardial heart muscle making the heart weak causing a weaker pump usually from MI where the heart muscle dies and now can't contract at all so we commonly get heart failure after a big Mi heart attack or an ischemia disease before a heart attack like in CAD or ACS where plaque Narrows the oxygen tubes or the coronary arteries resulting in the left ventricle sort of suffocating from that lack of oxygen which again results in a weaker pump but in this case causing systolic heart failure meaning a squeeze failure basically the heart fails to squeeze blood forward so fluid fills the lungs causing pressure and this is called pulmonary hypertension Symptoms in left heart failure the blood starts to back up into the lungs, specifically in the pulmonary veins and capillary beds which can increase the pressure in these vessels. This leads to fluid moving from the blood vessels to the interstitial space causing ** edema, or congestion.** **Crackles (rales) on Auscultation-** In the alveoli of the lungs, all the extra fluid makes oxygen and carbon dioxide exchange a lot harder, and therefore patients have **dyspnea or trouble breathing**. Another symptom is **orthopnea,** which is difÏculty breathing when lying down flat. This is because there’s more venous return from the legs and the gut to the heart, which increases the amount of blood backing up into the pulmonary circulation. paroxysmal nocturnal dyspnea, which is when the sensation of not being able to breathe wakes a person at night. Such individuals often sleep using more pillows in order to keep their upper body a bit elevated. This will lower the venous return and ease lung congestion. **The extra fluid in the lungs causes crackles or rales on auscultation**. If enough fluid fills the capillaries in the lungs, they can rupture, causing blood to leak into the alveoli. Alveolar macrophages then eat up these red blood cells, which causes them to take on this brownish color from iron build-up. And then they’re called** “hemosiderin-laden macrophages”, also known as “heart failure cells”.** **Decreased cardiac output**, not enough blood is reaching vital organs. As a result, an individual with heart failure may also present with fatigue. Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Decreased blood flow to the **kidneys activates the renin-angiotensin-aldosterone system, which will increase sodium and water reabsorption in the kidneys, ultimately causing fluid retention**. You’d think this is good, because** it increases blood volume** which **increases end diastolic volume** and based on the frank starling mechanism, it will **increase contractility** Unfortunately, in the long term large portions of this extra fluid will end up leaking into the tissues, which worsens the **pulmonary edema **and it will also lead to** peripheral edema**. “pitÝng edema” because the tissue is visibly swollen and when you apply pressure to it - it leaves a “pit.” Apart from this, the low cardiac output will also activate the sympathetic nervous system, which **increases left ventricle contractility**, but also activates the **renin-angiotensin-aldosterone system**. left heart failure, on auscultation, you can hear an extra sound, **either S3, or, less commonly, S4**. S3 is a low-pitched sound that comes right after S2. S3-systolic Ventricle overly compliant (increased blood into chamber **Ventricle Gallop** S4-diastolic Ventricles Stiff(atria contract harder) **Atrial Gallop** D: DifÏcult breathing R: Rales/crackles O: Orthopnea W: Weakness N: Nocturnal Paroxysmal Dyspnea I: Increased Heart Rate (Sinus Tach) N: Nagging Cough( Pink frothy sputum) G: Gain weight (pitÝng edema) Treatment for Left Sided Heart Failure always end in “IDE” Think the body is dride Furosemide Bumetanide H: HOB 45 Simi-High Fowlers Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 O: Oxygen P: Push Furosemide + Morphine E: End all sodium and fluids Diastolic Heart failure-Right sided heart failure -Heart failure with preserved (Normal) ejection fraction -Left ventricular diastolic dysfunction Diastole is the filling or RESTING phase of heart Ventricles is too stiff to allow for filling of blood Diastolic heart failure: Which is where the cardiac contractility is sufÏcient but not enough blood is returning to the ventricles. In this case, again, the **stroke volume is low, but the ejection fraction is normal*** So for example, the total volume might be lower than normal, say about 69 mL, and we pump out 44 mL, so if we divided 44 by 69, we get 64%, which is in the normal range. With diastolic heart failure, we need to look at the end diastolic pressure, or the EDP, as well. The problem is that the left ventricle isn’t compliant enough, so when the ventricle is filling during diastole, the pressure within will rise, so keep in mind that ** EDP is elevated during diastolic heart failure.** Also remember that with **diastolic heart failure, EDV is normal, at least in the beginning**, because the atria are capable of squeezing more blood into the ventricle. cause of diastolic heart -***ventricular hypertrophy***, where the ventricular myocardium gets thicker, and this decreases the ability of the chamber to stretch when filling. Heart failure can be systolic or diastolic and can affect the right ventricle, or the left ventricle, or both ventricles, which is called Biventricular Heart Failure For your exams, it’s important to remember that the **main cause of right heart failure is left heart failure** When **right heart failure isn’t caused by left heart failure, but by a pulmonary cause, we refer to this as cor pulmonale ** , pulmonary hypertension, fibrotic lungs “ Stiff lungs”,COPD, **Right Side HF Obstructive sleep apnea** Symptoms of right heart failure: Most common cause: Left sided HF Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Since left heart failure increases the pressure in the pulmonary artery, this will make it harder for the right ventricle to pump blood into it. Other causes of right-sided heart failure include chronic lung disease. Lung diseases, such as emphysema or pulmonary embolism, make oxygen exchange harder. In response to low oxygen levels, or hypoxia, the pulmonary arterioles constrict, and the pulmonary blood pressure rises. This makes it harder for the right side of the heart to pump against and can lead to right-sided hypertrophy and heart failure. In right-sided heart failure, blood gets backed up to the body, and so individuals will have congestion in the veins of the systemic circulation. One common manifestation of this is jugular venous distention, where the jugular vein that’s relatively close to the heart becomes enlarged and distended. Also in the body, when blood backs up to the liver, it causes venous congestion there and eventually, fluid can move into its interstitial spaces, causing the liver to become enlarged, which is called hepatomegaly. There’s a special name for this particular type of hepatopathy, called congestive hepatopathy. On pathology, there’s a so called** “nutmeg liver”**, because you can see the congested hepatic venules and veins as dark spots and it actually looks like a grated nutmeg! If the liver is congested for long periods of time, patients can eventually develop cirrhosis and liver failure, which is called cardiac cirrhosis. Finally, fluid that backs up into the interstitial space in the soft tissues of the legs causes **pitÝng edema** S: swelling in legs, feet ,abdomen (Ascites) W: weight gain E: edema(peripheral pitÝng) L: Large neck vein (JVD) L: Lethargic I: Irregular Heart Beat(A Fib) N: Nausea (congestin of liver, pressure on stomach) G: girth of abdomen Labs/Test Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 HBNP: > 100 Echocardiogram: Measures the ejection fraction less than 40% confirms Heart failure Hemodynamic monitoring (Increased central venous pressure and pulmonary artery wedge pressure) (ANYTHING OVER 8 IS NOT GREAT)  Heart valve disorders Patho-when blood flow direction is compromised through the valves and cardiac output is compromised Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Rheumatic fever can develop after streptococcal infection like strep throat, which is caused by Streptococcus pyogenes. This particular group of streptococcus has an antigen that lumps it into a group called “group A”, and they also produce an enzyme called streptolysin, which causes hemolysis. Some of these strep bacteria have a protein on their cell wall called “M protein”, and this particular protein is highly antigenic, meaning that the immune system sees it and recognizes it as a foreign molecule and produces antibodies against it. Now, this becomes a problem when these antigens cause a phenomenon called molecular mimicry. M proteins can be structurally similar to human proteins, which means the antibodies that target them will also target our own tissue. In this case, they are similar to proteins found in the myocardium and heart valves. Once bound to cardiac tissue, the antibodies activate nearby immune cells, which causes a cytokine-mediated inflammatory response and tissue destruction. This is also an example of what’s called a type 2 hypersensitivity reaction. Carditis. The inflammation can affect the endo, myo, and pericardium. Since the endocardium includes the valves, they too are affected. A high yield fact to remember is that the mitral valve is most commonly affected, although the aortic and tricuspid valve can also be affected. In the acute phase of the illness, mitral regurgitation is most Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 common. Later on, fibrosis around the valve causes its leaflets to fuse together, giving it a fish-mouth-like appearance. This fusion narrows the valve opening, and so we get mitral stenosis. Stenosis, where there’s narrowing of the valvular orifice that prevents adequate outflow of blood, and insufÏciency or regurgitation, where the valvular leaflets fail to close correctly and are unable to prevent backflow of blood. In order to make things easier to remember, we’ll classify valvular disease based on what type of murmurs you hear on auscultation. Remember there are two normal heart sounds; S1, caused by the mitral and tricuspid valves closing at the beginning of systole, and S2, caused by the aortic and pulmonary valves closing at the beginning of diastole. aortic stenosis. The aortic valve is typically made up of three leaflets: the right, left, and posterior leaflet and it opens during systole to allow blood to be ejected to the body. During diastole, it closes to allow the heart to fill with blood and get ready for the next systole. Aortic stenosis is when the aortic valve doesn’t open all the way and it gets harder to pump blood into the aorta. Aortic stenosis is usually caused by chronic mechanical stress that damages endothelial cells around the valves, causing **fibrosis and calcification*, which hardens the valve and makes it more difÏcult to open completely. This type usually shows up in late adulthood, so for your exams, remember that this is more common in individuals over 60 years old. Now, if there’s aortic stenosis in a younger individual, the cause could be due to a bicuspid valve. These abnormal valves are more at risk of fibrosis and calcification since the mechanical stress is now being split by just two leaflets. Okay, let’s go over auscultation now. With aortic stenosis, since blood has to flow through a narrow aortic valve, there’s turbulence which creates noise, or a murmur. This initially gets louder as more blood flows past the opening and then quieter as the amount of blood flowing subsides. This is called a crescendo-decrescendo murmur and you can hear this right after S1. This sound is best heard in the aortic area and typically radiates in the carotids. The intensity of the murmur increases as the pressure gradient between the left ventricle and the aorta increases. So, the narrower the stenosis, the louder the murmur. Now, normally, S2 has two components: the aortic component and the pulmonary component since the valves don’t close at the same time. Typically, the aortic valve closes first and then the pulmonary valve. But with aortic stenosis, the aortic valve closes later than expected and so it may close at the same time with the pulmonary valve, in which case you’ll hear a soft S2. Another important clue that will likely show up on your exam is the ejection click, since the valve fuses together or hardens, it doesn’t open as easily. And so as the left ventricle contracts, it creates this high pressure that eventually pushes on the valve until it finally snaps open, causing a clicking sound. In aortic stenosis, the pulse is described as being “parvus and tardus”. That’s because the valve doesn’t fully open so there’s less blood flow and the pulse is weak, or “parvus”, and there’s a delay in the opening of the valve that occurs a bit later than expected, so, the pulse is also late, or “tardus”. Even though the ventricle tries to pump out more blood, the heart still might struggle to get enough blood through the narrowed opening and then to the rest of the body. Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 For example, if there’s a reduction in blood flow to the brain, it could lead to syncope, and a reduction in blood flow through the coronary arteries to the heart’s own myocardium could cause chest pain and angina. Individuals might not initially experience symptoms at rest, and problems only occur during exercise or exertion because there’s an increase in the demand for oxygen. So, during exercise, they can also experience dyspnea. With aortic regurgitation, blood flows back from the aorta into the left ventricle during diastole. About half of the cases are caused by aortic root dilation where the leaflets are also pulled apart, making it harder for the valves to fit together and close all the way so some blood ends up flowing backwards. Besides aortic root dilation, regurgitation can also happen due to valvular damage from something like rheumatic fever, infective endocarditis, or from a bicuspid aortic valve which doesn’t close properly. The typical auscultation in aortic regurgitation is a high-pitched early decrescendo diastolic murmur, which you can hear right after S2. It’s caused by the blood flowing back through the valve. Now, since blood is leaking back from the aorta into the left ventricle, the left ventricular end diastolic volume increases. Because there is a volume overload, the left ventricle responds by undergoing eccentric hypertrophy, which increases the stroke volume, or the amount of blood that the left ventricle pumps out during systole. More blood pumped out of the heart per squeeze requires more pressure, so systolic blood pressure increases. However, during diastole, there’s less blood volume in the aorta since some has leaked back into the ventricle, which means that diastolic blood pressure decreases. A higher systolic pressure and lower diastolic pressure means an increase in pulse pressure, which is just systolic pressure minus diastolic pressure. A large pulse pressure is referred to as a hyperdynamic circulation. People with hyperdynamic circulation have bounding pulses, or water-hammer pulses because the blood slams like a hammer against the walls of the arteries with each heartbeat. In chronic and severe cases, these bounding pulses can be dramatic enough that they cause head bobbing that’s in tune with the heartbeat. Over time, aortic regurgitation can progress to left heart failure. Normal murmur: function (increased blood flow in normal valve) Abnormal murmur: abnormal pathologic(dysfunctional valve) Mitral regurgitation(insufÏcient) Mitral valve can not close completely, blood back flows into LA Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Mitral Stenosis Mitral valve can not fully open or is narrow, blood can’t get into LV Aortic regurgitation(insufÏcient) Aortic valve can’t close completely, blood back flows into LV Aortic stenosis Aortic valve can not open or is narrowed, blood can’t get out of the LV Subjective data: asymptomatic, with a heart murmur If co is compromised: chest pain, sob, weakness fatigue Systolic murmur: aortic stenosis or mitral reg Diastolic murmur: aortic reg or mitral stenosis If co is compromised decreased bp, increased HR, weak pulses, slow capillary refills , cool, diaphoretic or dusky skin Function and Alterations of the Pulmonary System  Mechanics of breathing Physiology: Conducting zone: nose, pharynx, larynx, trachea, and bronchi; Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Respiratiory zone : respiratory bronchioles, alveolar ducts, and alveoli. Lining the lumen of the airways you’ve got the** epithelium, mostly composed of one layer of ciliated pseudostratified columnar epithelial cells ** up until the beginning of terminal bronchioles, where it is replaced by cuboidal cells. Cilia-are responsible for eliminating larger particles like dust that reach the terminal bronchioles by moving them towards the pharynx, where they are coughed out. The epithelium also contains the goblet cell which makes the mucus within the airway. basement membrane and loose connective tissue, called the lamina propria, which together with the epithelium makes up the mucosa Lamina propria + epithelium= mucosa Smooth muscle + connective tissue make up= submucosa Submucosa-which is where the bronchial mucinous glands that secrete the majority of the mucus into the lumen of the bronchi live. Finally, in the bronchi, there is a layer of cartilage below the submucosa which stiffens the bronchus and helps to keep it open. Gas exchange: The role of lungs; remove carbon dioxide from body and to replenish the body with fresh oxygen Heart and lungs work together to make this happen Alveoli sacs: where gas exchange occurs Alveolus: sac that fill with air when one breathes in and allows that air to pass across a membrane into a blood vessel(alveolar capillary) Alveolus contracts back down(deflating Normal breathing brings fresh oxygen down your trachea and into your lungs with an inhale. As you exhale, carbon dioxide exits your lungs. As you inhale and exhale, your chest and ribs expand and contract to allow for the air going in and out. Diaphragm  Inhaling The diaphragm contracts and flattens, moving down and creating a vacuum in the chest cavity. This allows the lungs to expand and fill with air.  Exhaling Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 The diaphragm relaxes and returns to its dome shape, moving up in the chest cavity. This reduces the space in the chest cavity, causing the lungs to deflate and forcing air out. The diaphragm is a dome-shaped muscle at the base of the lungs that plays a key role in breathing. Diaphragmatic breathing, also known as belly breathing, involves breathing in a way that fully engages the diaphragm. This type of breathing can help you exchange oxygen and carbon dioxide more efÏciently, and can also lower your blood pressure and slow your heartbeat.  Obstructive and Restrictive Lung Diseases Obstructive-allows limitation due to airway obstruction a group of conditions, characterized by obstruction of airflow, which traps air inside the lungs Example: COPD, ASTHMA Rationale: because the airway is narrowed down or severely obstructed, exhaled air comes out more slowly than normal, and at the end of a full exhalation, an abnormally large amount of air still remain in the lungs. This an obstructive respiratory deficit, and it’s marked by several changes which can be seen on pulmonary function tests or PFTs, like spirometry and plethysmography. Spirometry when you breathe into a tube attached to a machine called a spirometer, which measures the amount of air you breathe in and out, and how quick you do it. Plethysmography is when you are placed inside a sealed chamber and asked to breathe through a mouthpiece, which measures the pressure generated by your breathing to calculate the amount of air inside your lungs. Obstructive lung diseases, first, there’s an 1. is the amount of air left in the lungs after exhaling as much as you can= increase in residual volume or RV, -which is the amount of air remaining in the lungs at the end of a normal exhalation = increased functional residual capacity or FRC,. 2. Second, there’s a small reduction in forced vital capacity or FVC, which measures the amount of air a person can breathe out forcefully after taking as deep a breath as possible -a significant reduction in forced expiratory volume in one second or FEV1, which measures the total amount of air that can be forcibly exhaled in the first second of the FVC test. This is because these individuals have a narrow airway, which hinders how fast air can leave the lungs. Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 3.Third,(decrease FEV1/FVC) there’s a decrease in the ratio of FEV1 to FVC secondary to the disproportionate decrease in FVC and FEV1. The ratio measures the amount of air a person can forcefully exhale in one second relative to the total amount of air they can exhale. ***Decrease in the ratio of FEV1 to FVC is considered the hallmark of obstructive lung disease and can also be used to figure out the severity of the obstruction*** 4. Fourth, the total lung capacity is either normal or increased, unlike restrictive lung diseases, where it almost always is decreased. The reason why TLC may increase is that in some obstructive lung diseases, like emphysema, there’s air trapping and lungs hyperinflate. TLC is calculated by adding the volume of air left in the lungs after exhalation or the residual volume with the FVC. 5.Fifth, there might also be a V/Q mismatch, where the V stands for ventilation, which is the air you breathe in, and the Q stands for perfusion, which is blood flow. A V/Q mismatch happens because the blood flow is normal but the lungs don’t receive enough oxygen due to airway obstruction, and this is measured by a test called a pulmonary ventilation/perfusion scan. Over time, this can lead to hypoxemia, because there’s not enough oxygen in the blood. In order to keep the V/Q ratio constant, as the ventilation decreases, the pulmonary vessels start to constrict in order to reduce perfusion to the areas that do not participate in gas exchange. This is called hypoxic vasoconstriction, and it leads to pulmonary hypertension. Over time, pulmonary hypertension puts a strain on the right heart, and can lead to right heart failure, or cor pulmonale; which manifests as jugular venous distention, peripheral edema, and hepatomegaly due to congestion. finally, it’s important to assess the gas exchange, which varies, depending on the particular disease. This is done by measuring the diffusing capacity of the lungs for carbon monoxide, also known as DLCO. This test involves asking the individual to inhale a small amount of carbon monoxide and seeing how well it diffuses. Another high yield concept is how obstructive lung disease can change the flow-volume loop which is used to show airflow on the y axis as it relates to lung volume on the x axis. So imagine taking the deepest breath you can and then exhaling it out as forcefully as possible. The volume you’re gonna exhale is the forced vital capacity, and what will be left after maximal expiration will be the residual volume. And these two combined give us the total lung capacity. Now since in most cases of obstructive lung disease, the residual volume is increased while the total vital capacity is normal or increased, the loop will typically show a shift to the left.  Chronic Obstructive Pulmonary Disease The condition is characterized by obstruction of airflow due to either chronic bronchitis or emphysema. Sometimes patients can have one or the other; however, most patients have elements of both chronic bronchitis and emphysema at the same time. In addition, the triggers of the inflammation of the airway are often the same, and include environmental triggers, like inhalation of toxic substances such as tobacco smoke, or occupational pollutants like dust and silica. Chronic Bronchitis Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Chronic bronchitis is an inflammation of the tracheobronchial tree that leads to increased mucus production by hyperplasia of goblet cells Cause: a trigger, usually smoking, irritates the mucosa of the airways, leading to hypertrophy and hyperplasia of mucinous glands in the main bronchi and goblet cells in the bronchioles. One test that’s used post-mortem is** the Reid index**, which measures the ratio of the thickness of the bronchial mucinous glands layer relative to the total thickness of the wall between the epithelium and the glands. Findings :Normally, the ratio should be less than 0.3, but for people with chronic bronchitis it can be over 0.4. Hyperplasia and hypertrophy of the mucinous glands increases mucus production in both the main bronchi and the bronchioles, which causes airway obstruction. V/Q mismatch signs and symptoms of chronic bronchitis include :CHWP productive cough due to excess mucus secretion wheezing from the narrowing of the airways. Crackles or rales can be heard on auscultation of the lungs, which are caused by the popping open of small airways. hypoxemia and hypercapnia, both secondary to the mucus plugs blocking air exchange. obstruction of the airflow can get so bad that deoxygenated blood from the right side of the heart reaches the left side without any participation in gas exchange in the pulmonary capillaries. This is called a shunt What causes some people to develop cyanosis(bluish discolartion of the skin)? A Shunt high yield fact is that these individuals are sometimes referred to as “blue bloaters”. a mucus plug obstructing the airways, there’s a high risk for pneumonia behind the obstruction. Classic symptoms of pneumonia include high fever, chills, confusion or irritability, worsening dyspnea and changes in sputum color, thickness or amount. Emphysema permanent enlargement and loss of elasticity of the alveolar wall secondary to alveolar injury(alveolar sacs). Matched V/Q Defect Caused by irritants like tobacco smoke that triggers inflammation in the alveoli. Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Patho: The way this happens is that neutrophils gather and release destructive proteases like elastase which breaks down the elastin in alveolar walls, making them weaker, so the alveoli collapse during exhalation. Alveoli also lose their ability to stretch and recoil so they can’t return to their normal shape. The result is alveoli trap a tiny bit of air distal to the point of collapse. Alveoli are organized in clusters, called acini. And depending on which part of the acini are affected, we can have one of three types of emphysema.   centriacinar or centrilobular emphysema Most common Only damages the central or proximal alveoli of the acinus. This is the pattern seen with cigarette smoking and it typically affects the upper lobes of the lungs. Panacinar emphysema, where the entire acinus, usually in the lower lobes, is uniformly affected Often associated with alpha-1 antitrypsin deficiency. Since the alveolar neutrophils are always releasing proteases to help clear the debris, the body protects itself by releasing alpha-1 antitrypsin, which is a protease inhibitor that prevents excessive collateral damage. Now, those with alpha-1 antitrypsin deficiency have no way to stop the proteases, so they end up with damaged air sacs earlier in life, especially if they smoke, since it will attract more neutrophils to the area. Paraseptal emphysema Distal alveoli of the acinus are most affected Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Affects the lung tissue on the periphery of the lobules, near the interlobular septa that separate each lobule. S/s of emphysema SOB, Hyperventilation, weight loss Barrel Chest      COPD Diagnosis To start with, pulmonary function tests can help detect any changes in lung volumes associated with obstructive lung disease. if COPD seems likely, an inhaled bronchodilator, like albuterol is given to the person, and pulmonary function tests are measured again to see if the obstruction is reversible. Reversibility is defined as more than 12% increase in FEV1 after administering the bronchodilator. Ok so note that unlike asthma, COPD is an irreversible disease so giving a bronchodilator should not change the values too much. This means that if the FEV1 doesn’t increase by more than 12% after the bronchodilator, then COPD is the likely diagnosis. Next, it’s important to find out if the individual has predominantly chronic bronchitis, emphysema or both. Diagnosis of chronic bronchitis is clinical and based on a productive cough that lasts for at least 3 months, and over a period of 2 or more years. Another clue for you is a complete blood count showing polycythemia, which is an increase in the red blood cell number. Individuals with chronic bronchitis develop secondary polycythemia as a response to chronic hypoxemia, which triggers increased production of erythropoietin by the kidneys. Diagnosis of Emphysema can’t be diagnosed clinically as it is defined by structural changes in the lungs. Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698      This means an x-ray or CT scan is needed, which might show enlargement of the air spaces, increased anterior-posterior diameter, a flattened diaphragm, and increased lung field lucency. Additionally, a DLCO might also show a decrease in the lung’s diffusing capacity secondary to alveolar wall destruction, unlike those with chronic bronchitis. Alpha-1 antitrypsin deficiency screening is done in those who develop COPD without having any risk factors. Treatment of COPD **Reducing risk factors, like stopping smoking Managing associated illnesses. Because infections often trigger COPD exacerbations, people should be given the influenza vaccine annually**. If an infectious exacerbation does happen, these individuals may need a course of antibiotics, corticosteroids, inhaled short-acting bronchodilators, including beta-agonists like albuterol and muscarinic agents like ipratropium as well as supplemental oxygen.  Be careful, though, as giving too much oxygen could potentially be harmful in patients with COPD.  In healthy individuals, the stimulus of respiratory drive is normally the partial pressure of carbon dioxide or PaCO2, which stimulates the central chemoreceptors in the medulla.  In those with longstanding hypoxemia, this role is attributed assumed by the partial pressure of oxygen or pO2, which stimulates the peripheral chemoreceptors in the carotid and aortic bodies.  ***So if you give too much oxygen to someone with COPD, their only respiratory stimulus disappears, which leads to respiratory failure***  Long-term treatment of COPD include long-acting agents if short-acting agents can not relieve symptoms.  Other options include long-acting beta-agonists like formoterol and long-acting muscarinic agents like tiotropium or umeclidinium.  Now, in some individuals with severe hypoxia, or there’s cor pulmonale, home supplemental oxygen might be also needed.  Asthma(respiratory acidosis) Episodic disorder caused by inflammation and hyperresponsiveness of the bronchial smooth muscle, leading to reversible bronchoconstriction 3 key players: Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 1. Smooth muscle: constricts and dilates to breathe (during an asthma attack, the smooth muscle is only constricting= chest tightness and trouble breathing) 2. Mucosal Lining – during an asthma attack, becomes inflamed=narrow airway leads to decreased airflow (coughing, wheezing, air trapping) 3. Goblet cells(w/in the mucasal lining) produce mucus to keep bacteria out(increase mucus production=worsening coughing, wheezing, air trapping) specific causes of asthma ultimately unknown, it’s thought to be due to a combination of genetic and environmental factors, like air pollution, cigarette smoke, and car exhaust, as well as allergens** Some worth remembering include dust, animal dander, cockroaches, and mold. For your exam, don’t forget that aspirin has also been known to trigger symptoms in some individuals with asthma. Aspirin-induced asthma has to do with leukotriene B4 overproduction, which is a compound that results in bronchospasm and increased mucus production. What’s especially high-yield is that aspirin-induced asthma is often combined with nasal polyps and chronic sinusitis. causes a Type I hypersensitivity reaction. It starts when the trigger causes an excessive activation from type 2 helper T cells, or Th2 cells, and causes them to produce cytokines like IL-4. These cytokines cause B lymphocytes to produce IgE antibodies against the foreign antigens. These then coat mast cells and cause them to release granules containing histamines, leukotrienes, and prostaglandins. These inflammatory mediators cause bronchoconstriction and edema which leads to airway obstruction. Another cytokine released by Th2 cells is IL-5, which activates eosinophils and these cells release more inflammatory mediators which contribute to the symptoms. Initially these inflammatory changes are reversible, but over time irreversible changes take place, like scarring and fibrosis in the basement membrane of the airways, causing permanent reduction of airway diameter. Furthermore, there’s smooth muscle hypertrophy and hyperplasia that worsens the obstruction. The signs and symptoms of asthma come and go, and tend to be more frequent in winter or when exposed to an irritant such as cigarette smoke. An asthma episode can include coughing and a feeling of chest tightness due to airway irritation, but also tachypnea, dyspnea, and wheezing, due to airway edema. Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Okay, the first step of diagnosis is asking for a personal or a family history of asthma, atopic eczema, and allergy Next, it’s important to conduct pulmonary function tests. Now, because asthma is an episodic obstructive lung disease, these tests show the typical signs of obstructive pulmonary disease only when the individual is having symptoms. If asthma seems likely, an inhaled bronchodilator is given to the person, just as in COPD. Note that unlike COPD, giving a bronchodilator should reverse the pulmonary function tests measurements back towards normal, confirming the diagnosis. Diagnosis is asking for a personal or a family history of asthma, atopic eczema, and allergy Next, it’s important to conduct pulmonary function tests. Now, because asthma is an episodic obstructive lung disease, these tests show the typical signs of obstructive pulmonary disease only when the individual is having symptoms. If asthma seems likely, an inhaled bronchodilator is given to the person, just as in COPD. Note that unlike COPD, giving a bronchodilator should reverse the pulmonary function tests measurements back towards normal, confirming the asthma diagnosis Do not have symptoms at the time we can try to induce asthma by performing the “methacholine challenge test”. Methacholine binds to muscarinic receptors on bronchial smooth muscle, causing mild bronchoconstriction. because an asthmatic’s bronchial smooth muscle is hyperresponsive, methacholine causes a 20% decrease in their FEV1 from the baseline. Now, it’s important to remember that the methacholine challenge test is highly sensitive, meaning that a negative test can rule out the diagnosis, but nonspecific, so a positive test doesn’t confirm the diagnosis.. DLCO is usually normal or slightly increased in asthma. Sputum analysis called Curschmann Spirals- These are shed, elongated epithelial cells that can form whorled mucous plugs. The plugs can be particularly dangerous because they not only block the exchange of air, but they also block inhaled medications from getÝng to the site of inflammation. Charcot-Leyden crystals, which look like hexagonal, double-pointed crystals formed by the breakdown of eosinophils secondary to IL-5 stimulation. decreased inspiration/expiration ratio. - In those with asthma, because the airway obstruction leads to prolonged expiration, the ratio can be 1 to 4 or sometimes even 1 to 5. Severe asthma might also develop something called pulsus paradoxus, which is a drop in systolic blood pressure of more than 10 milligrams Mercury during inspiration. Pulsus paradoxus results from a decrease in cardiac stroke volume with inspiration due to greatly increased left-ventricular afterload. This is caused by the dramatic increase in negative intrapleural and transmural pressure in someone struggling to breathe against significant airway obstruction Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 chest x-ray which might show signs of hyperinflation like a flattened diaphragm, blood eosinophil count and serum IgE level which might be increased. A skin reactivity test to various allergens can be also done. But the fact is that they are less sensitive, meaning that normal findings on these tests cannot exclude the diagnosis. TX .1. In acute exacerbations, a short acting bronchodilator like albuterol is often administered through an emergency inhaler. side effects, albuterol can cause tremor and arrhythmias 2 chronic asthma, corticosteroids like fluticasone or budesonide, which inhibit the synthesis of cytokines, are considered first-line therapy. 3. long-acting beta-agonist or a muscarinic antagonist bronchodilator can be added to control symptoms if corticosteroids are not enough. 4. If this fails, theophylline, a methylxanthine which likely causes bronchodilation by inhibiting phosphodiesterase, can be added to the treatment plan. However, this drug has limited use due to its cardiotoxicity and neurotoxicity. 5. Alternatively, antileukotrienes like montelukast and zafirlukast, which block leukotriene receptors, or zileuton, a 5-lipoxygenase pathway inhibitor that blocks the conversion of arachidonic acid to leukotrienes, can be given in addition to corticotherapy, especially in those with aspirin-induced and exercise-induced asthma. People with asthma should avoid or minimize contact with triggering substances Next, long-acting bronchodilators like salmeterol and formoterol can also be used for prophylaxis. Rarely, chromones like cromolyn, which work by preventing mast cell degranulation, can also be used to prevent acute asthma symptoms. Bronchiectasis is characterized by damaged and dilated bronchi and bronchioles secondary to chronic inflammation and mucus obstruction. There are many causes of chronic inflammation, like primary ciliary dyskinesia, where the cilia don’t move normally and that leaves mucus stuck in the airways. If primary ciliary dyskinesia is combined with situs inversus or reversal of the internal organs, chronic sinusitis, and bronchiectasis called Kartagener Syndrome Cystic fibrosis, when the mucus itself is extra-sticky, hard to sweep, and therefore it accumulates, causing obstruction and dilation of the bronchi and bronchioles and thus, bronchiectasis. Another cause you might find in a test is allergic bronchopulmonary aspergillosis, which is caused by a fungus called Aspergillus that triggers chronic inflammation and damage of the airways, which can progress to bronchiectasis. Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 And then there is airway obstruction, usually caused by tumors, foreign objects or anything else that can block the bronchus or bronchiole, which subsequently leads to pneumonia and chronic inflammation. inflammation, immune cells in the bronchi and bronchioles release cytokines that damage the ciliated epithelial cells and destroy the elastin fibers in the walls of the airway. As a result, the airways become dilated and becomes clogged with mucus chronic inflammation leads to scarring and fibrosis which narrows the airways, resulting in airflow obstruction. And as the ventilation decreases, it leads to hypoxic vasoconstriction, meaning that the pulmonary vessels start to constrict in order to reduce perfusion to the areas that do not participate in gas exchange and keep the V/Q ratio constant. If that’s widespread, it can lead to pulmonary hypertension and in time, cor pulmonale. Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698  Interstitial Lung Disease Interstitial lung disease encompasses a group of lung disorders characterized by inflammation and scarring of the lung tissue, specifically the interstitium.  Gas exchange: The primary function of the alveoli is to facilitate the exchan ge of oxygen and carbon dioxide between the lungs and the bloodstream. Ox ygen from inhaled air diffuses across the alveolar walls into the capillaries sur rounding the alveoli, where it binds to hemoglobin in red blood cells. At the sa me time, carbon dioxide produced by cellular metabolism in the body diffuses from the capillaries into the alveoli to be exhaled.  Surfactant production: Specialized cells in the alveoli called type II pneum ocytes produce surfactant, a substance that reduces surface tension in the al veoli. Surfactant helps prevent the alveoli from collapsing during exhalation, making it easier to breathe and facilitating gas exchange.  Lung defense: The alveoli are lined with immune cells, such as macrophage s, that help protect the lungs from infection and remove debris and pathogen s that may be inhaled.  Blood supply: The alveoli are surrounded by a dense network of capillaries, which allows for efÏcient exchange of gases between the alveoli and the bloo dstream. This network of capillaries ensures that oxygenated blood is delivere d to tissues throughout the body and that carbon dioxide is removed from the bloodstream. Downloaded by zena ahmad (zenaahmad772@gmail.com) lOMoARcPSD|35287698 Alterations of Renal and Urinary Tract Function: In addition to course readings and Edapt review, also review the recorded presentation on Acute and Chronic Renal Failure      Urinary Tract Infections Renal Calculi Urinary Incontinence Acute Kidney Injury Chronic Kidney Disease Alterations of the Male Reproductive Systems  Benign Prostatic Hypertrophy Downloaded by zena ahmad (zenaahmad772@gmail.com)