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TEST 3 - Advanced Pathophysiology Summer 2024 UTA 5315, Exams of Nursing

TEST 3 - Advanced Pathophysiology Summer 2024 UTA 5315 Mitral Valve Stenosis Answer - - Characterized by NARROWING of mitral valve - Normal is 4-6 cm -Narrowed is less than 2.5 cm - Caused by RHEUMATIC FEVER -More common in WOMEN -Oxygenated blood comes back into heart into the left atrium and down through the mitral valve to the left ventricle - Complex: Stenosis leads to volume/pressure in left atrium, which results in atrial hypertrophy/dilation, which increases pressure/volume in the pulmonary circulation & causes PULMONARY EDEMA - Simplified: Skinny mitral valve doesn't let blood pass through easily, so blood backs up into the left atrium and causes it to swell, then backs up into the lung and causes resp. symptoms -S/sx: dyspnea, hemoptysis, a-fib, dysphagia, pulmonary hypertension

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TEST 3 - Advanced
Pathophysiology Summer
2024 UTA 5315
Mitral Valve Stenosis Answer - - Characterized by NARROWING of mitral
valve
- Normal is 4-6 cm
-Narrowed is less than 2.5 cm
- Caused by RHEUMATIC FEVER
-More common in WOMEN
-Oxygenated blood comes back into heart into the left atrium and down
through the mitral valve to the left ventricle
- Complex: Stenosis leads to volume/pressure in left atrium, which results
in atrial hypertrophy/dilation, which increases pressure/volume in the
pulmonary circulation & causes PULMONARY EDEMA
- Simplified: Skinny mitral valve doesn't let blood pass through easily, so
blood backs up into the left atrium and causes it to swell, then backs up
into the lung and causes resp. symptoms
-S/sx: dyspnea, hemoptysis, a-fib, dysphagia, pulmonary hypertension
Mitral Valve Regurgitation Answer - -Characterized by INCOMPLETE
CLOSURE of mitral valve
-Caused by MITRAL VALVE PROLAPSE (flaps don't close together properly,
leaving valve ajar); more common in WOMEN; STICKING CHEST PAIN
-Blood in left ventricle backs up to left ventricle during systole (mitral valve
should be closed during systole/contraction of heart)
-Leads to atrial dilation/hypertrophy, increased pulmonary vascular
pressure/volume, PULMONARY EDEMA
-S/sx: Dyspnea, rales, pansystolic murmur, S3 & S4 heart sounds
Aortic Valve Stenosis Answer - -Most common valvular disease
-Most common causes are aortic valve CALCIFICATION (stiffening) in
people over 60; congenital aortic valve stenosis in people less than 30
-Normal valve 3 cm; symptoms seen when valve less than 1 cm; severe
when valve is less than 0.5 cm
-Narrowed valve prevents outflow from left ventricle to aorta. This backs
up blood to the left atrium and ultimately floods the lung causing
PULMONARY EDEMA
S/Sx: Pulmonary hypertension/edema, poor outflow of aorta to body (aorta
sends out oxygenated blood to body), causing fainting or chest pain
Simplified: Aorta is stiff and can't send out oxygenated blood properly
to the body, depriving tissues of oxygen. Blood gets backed up into
lungs, causing pulmonary edema.
Aortic Valve Regurgitation Answer - -Valve is TOO WIDE or TOO NARROW,
blood doesn't pass through effectively, causing back flow of blood into the
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Download TEST 3 - Advanced Pathophysiology Summer 2024 UTA 5315 and more Exams Nursing in PDF only on Docsity!

TEST 3 - Advanced

Pathophysiology Summer

2024 UTA 5315

Mitral Valve Stenosis Answer - - Characterized by NARROWING of mitral valve

  • Normal is 4-6 cm -Narrowed is less than 2.5 cm
  • Caused by RHEUMATIC FEVER -More common in WOMEN -Oxygenated blood comes back into heart into the left atrium and down through the mitral valve to the left ventricle
  • Complex: Stenosis leads to volume/pressure in left atrium, which results in atrial hypertrophy/dilation, which increases pressure/volume in the pulmonary circulation & causes PULMONARY EDEMA
  • Simplified: Skinny mitral valve doesn't let blood pass through easily, so blood backs up into the left atrium and causes it to swell, then backs up into the lung and causes resp. symptoms -S/sx: dyspnea, hemoptysis, a-fib, dysphagia, pulmonary hypertension Mitral Valve Regurgitation Answer - -Characterized by INCOMPLETE CLOSURE of mitral valve -Caused by MITRAL VALVE PROLAPSE (flaps don't close together properly, leaving valve ajar); more common in WOMEN; STICKING CHEST PAIN -Blood in left ventricle backs up to left ventricle during systole (mitral valve should be closed during systole/contraction of heart) -Leads to atrial dilation/hypertrophy, increased pulmonary vascular pressure/volume, PULMONARY EDEMA -S/sx: Dyspnea, rales, pansystolic murmur, S3 & S4 heart sounds Aortic Valve Stenosis Answer - -Most common valvular disease -Most common causes are aortic valve CALCIFICATION (stiffening) in people over 60; congenital aortic valve stenosis in people less than 30 -Normal valve 3 cm; symptoms seen when valve less than 1 cm; severe when valve is less than 0.5 cm -Narrowed valve prevents outflow from left ventricle to aorta. This backs up blood to the left atrium and ultimately floods the lung causing PULMONARY EDEMA S/Sx: Pulmonary hypertension/edema, poor outflow of aorta to body (aorta sends out oxygenated blood to body), causing fainting or chest pain Simplified: Aorta is stiff and can't send out oxygenated blood properly to the body, depriving tissues of oxygen. Blood gets backed up into lungs, causing pulmonary edema. Aortic Valve Regurgitation Answer - -Valve is TOO WIDE or TOO NARROW, blood doesn't pass through effectively, causing back flow of blood into the

left ventricle

Hyperlipidemia Answer - Leading cause of coronary artery disease

Most commonly affects promximal portions of coronary arteries, larger branches of carotid arteries, circle of Willis (base of brain), large vessels of lower extremities, renal arteries, mesenteric (intestinal) arteries Consequences of Atherosclerosis Answer - Reduced blood flow Coronary artery disease, myocardial infarction, carotid artery disease, cerebral vascular disease, stroke, mesenteric ischemia, peripheral vascular disease, renal artery stenosis Congenital Heart Disease Answer - -Most common heart disease affecting children -Etiology is unknown in 90% of cases Causes: Genetic/environmental factors (multifactorial factors) Primary genetic factors (single gene disorders, chromosome disorders) Sole environmental factors (Accutane/isotretinoin for acne, alcohol, maternal rubella infection) Maternal Risk Factors: Age over 45, prior child with heart defect, poorly controlled diabetes during pregnancy, alcohol, congenital infection during pregnancy (rubella), aspirin, lupus, Dilantin/phenytoin/diphenylhydantoin for seizures LEFT to RIGHT shunt (Congenital heart defect) Answer - -Oxygenated blood from the left side of the heart mixes with unoxygenated blood in the right side of the heart. -Oxygen saturation on left side is usually 95%, whereas right side is 75%

  • As blood mixes, right side's oxygen saturation increases to 80% or more -VOLUME OVERLOAD occurs on RIGHT side of heart occurs, leading to PULMONARY HYPERTENSION, which causes RIGHT VENTRICULAR HYPERTROPHY, (secondary to pulm. hptn.), and LEFT VENTRICULAR HYPERTROPHY(secondary to blood being returned to left ventricle) Eisenmenger Syndrome: Reversal of left to right shunt to a right to left shunt. Eisenmenger Syndrome Answer - 1. Increased blood flow returns to lungs rather than to the rest of the body.
  1. Blood vessels become stiff and narrow - permanent damage.
  2. Increased pressure of the blood flow in the lung becomes so great that the direction of blood flow through the shunt reverses.
  3. Oxygen-poor (blue) blood from the right side of the heart flows into the left ventricle and is pumped to the body and tissues do not receive enough oxygen.
  4. Results in late-onset cyanosis (as in, later in life) and clubbing of fingernails. Ventricular Septal Defect (most common congenital heart defect) Answer - -Hole allowing blood to move from left ventricle to the right ventricle -Sign: Harsh holosytolic murmur at the lower left sternal border (high-

-Multiple VSDs are associated with Tetralogy of Fallot, Cri du Chat Syndrome, and Fetal Alcohol Syndrome. -Associated with development of atrial septal defects, patent ductus arteriosus, coarction (congenital narrowing) of aorta, aortic valve stenosis, INCREASED RISK FOR DEVELOPING ENDOCARDITIS at some point in life ( infection of the heart's inner lining, usually involving the heart valves) Atrial Septal Defect (most common congenital heart defect in adults) Answer - -Most common cause is a patent foramen ovale (hole) that does not close -Associated with FETAL ALCOHOL SYNDROME and DOWN SYNDROME -Sign: Midsystolic murmur at upper sternal border -Increases risk for EMBOLUS Patent Ductus Arteriosus Answer - Patent ductus arteriosus (PDA) is a persistent opening between the two major blood vessels leading from the heart. The opening, called the ductus arteriosus, is a normal part of a baby's circulatory system before birth that usually closes shortly after birth. If it remains open, however, it's called a patent ductus arteriosus. Sign: Machine-like murmur heard continuously throughout systole and diastole Reversal may occur if pulmonary hptn occurs from increased blood flow through the pulmonary artery. If this happens, unoxygenated blood will enter the aorta below the level of the subclavian artery and the child will be cyanotic in the lower body, but not in the upper body. Associated with congenital rubella, Tetralogy of Fallot, respiratory distress syndrome, and transposition of great vessels (unoxygenated blood does not pick up oxygen in lungs and is pumped back to body) Right to left shunt Answer - Tetralogy of Fallot is most common cyanotic congenital heart defect. Impaired gas exchanged r/t decreased pulmonary blood flow Right side of heart = Deoxygenated Left side = Oxygenated

  1. Deoxygenated blood is mixed with oxygenated blood.
  2. Blood on left side has oxygen saturation decrease from 95% to 80% or lower.
  3. Cyanosis may or may not develop depending on how low the oxygen saturation on the left side drops. -Left side oxygen saturation 85% or high, cyanosis is not likely to occur. -Left side oxygen saturation below 80% is indicative of a large amount of blood being shunted and will result in cyanosis. Tetralogy of Fallot Answer - Most common cyanotic congenital heart defect Tetralogy of Fallot involves four heart defects: 1.A large ventricular septal defect
  4. Pulmonary stenosis
  1. Right ventricular hypertrophy 4.An overriding aorta Heart Failure Risk Factors Answer - -Age (most common over 65 y/o) -Ischemic heart disease -Obesity -Diabetes -Hypertension -Excessive ETOH use -Congenital heart disease -Valvular heart disease -Myocarditis -Cardiomyopathy (stiffening of heart muscle) -Renal failure Heart Failure Clinical Manifestations Answer - -Volume overload -Poor perfusion secondary to pump failure Heart Failure with REDUCED Ejection Fraction, SYSTOLIC Heart Failure, LEFT- SIDED heart failure Answer - -LEFT-SIDED HEART FAILURE, SYSTOLIC HEART FAILURE, but right ventricular systolic dysfunction can happen too -IMPAIRMENT in LEFT VENTRICULAR CONTRACTION (SYSTOLE) -Most common CAUSE is MYOCARDIAL INFARCTION. Other causes are myocarditis and cardiomyopathies.
  2. Decrease in contractility in left ventricle will decrease stroke volume (volume of blood pumped from left ventricle with each beat).
  3. Cardiac output (amount of blood pumped from heart per minute) decreases.
  4. Left ventricular end diastolic (relaxation of heart) volume (preload) increases - not enough blood got pumped out of left ventricle during systole (contraction), so more is hanging around during diastole (relaxation).
  5. Ventricular remodeling occurs.
  6. Preload (amount of blood in ventricle during relaxation) further increases over time, causing causing a dilation of the ventricle and further compromises contraction and cardiac output.
  7. Myocytes deteroriate. The systolic dysfunction (low cardiac output) results in 2 processes being triggered: -Baroreceptor activation: Baroreceptors notify the medulla to turn on sympathetic nervous system because heart is not pumping out enough blood. The catecholamines epinephrine and norepinephrine cause vasoconstriction, increased afterload, increased blood pressure, increased heart rate. This increases work loard of heart, causes hypertrophy & dilation of left ventricle, and further impairs contractility. -Renin Angiotensin Aldosterone System (RAAS): Activated by decreased renal blood flow. Causes vasoconstriction, which increases afterload and blood pressure, but contributes to worsening of left ventricular hypertrophy/dilation and worsens contractility.

contracting!*

-Catecholamines - epinephrine & norepinephrine make heart pump harder -Increases in intracellular calcium -Decreased sodium in blood (decreases activity of the sodium/calcium exchanger) -DIGITALIS: increases intracellular calcium What decreases contraction and promotes r? (improves diastolic heart failure) Answer - Diastolic heart failure needs help relaxing! -Beta Blockers: Block effects of catecholamines. Metoprolol, Bystolic -Acidosis -Hypoxia/hypercapnia -Calcium channel blockers Systole Answer - Contraction of heart as it shoots blood Diastole Answer - Relaxing of heart so it can fill with blood Systolic heart failure Answer - Heart can't contract Diastolic heart failure Answer - Heart can't relax Coronary artery dominance Answer - 85% of people are right dominant Right dominant - posterior descending artery arises from right coronary artery Left dominant - posterior descending artery arises from left circumflex artery (about 8% of population) Codominant - posterior descending artery arises from both the left & right coronary arteries Most common site of coronary artery occlusion Answer - Left circumflex artery So if a left dominant person has an occlusion in the left circumflex artery, they have a higher chance for poor outcomes. Dysphagia in coronary artery disease Answer - When left atria enlarges (as in from occlusion r/t coronary artery disease), it enlarges and compresses the esophagus. It can also compress the left recurrent laryngeal nerve and cause hoarseness. Coronary Artery Disease: Risk Factors Answer - Advanced age, male, post- menopausal, family history, dyslipidemia, hypertension, smoking, diabetes, obesity, sedentary lifestyle, diet high in fat. Why does hypertension put a person at increased risk for developing coronary artery disease? Answer - Causes endothelial damage, making it easier for cholesterol to accumulate in damaged area, also triggers inflammatory response and allows buildup of more cholesterol, macrophages, foam cells, platelets

  1. Oxygen reserves are used up.
  2. Glycogen (storage unit for glucose) decreases.
  3. Glycolysis (breakdown of glucose by enzymes, releasing energy) is not able to supply all the needed energy to the heart, leading to less ATP production.
  4. Hydrogen ions & lactic acid accumulate from the anaerobic metabolism (anaerobic metabolism is the creation of energy through the combustion of carbohydrates in the absence of oxygen).
  5. Myocardial cells deprived of nutrients lose contractility and result in a diminished contraction.
  6. Ischemic cells release catecholamines (fight/flight hormones), further stressing the heart & increasing risk for arrythmias & heart failure. 8. Norepinehrine (a catecholamine) decreases insulin secretion and hyperglycemia occurs (body tries to get more sugar in blood to fuel heart). This can be seen by 72 hours post MI and is associated with increased mortality.
  7. Angiotensin II is released causing vasoconstriction, thereby increasing afterload (contraction) and myocardial work load. How long can cardiac cells remain viable in a severely hypoxic (heart attack) state? Answer - 20 minutes. After 20 minutes, coagulative necrosis occurs. Reperfusion Injury Answer - -Caused when blood flow is restored -Triggers release of TOXIC OXYGEN RADICALS from when myocytes were deprived of oxygen, CALCIUM INFLUX, and PH CHANGES (this causes persistently open mitochondrial permeability and contributes to cell death) Troponins Answer - -Detected in 2-4 hours of onset of pain -Peak in 24 hours -Disappear in 7-10 days Complications of MI Answer - -Cardiac dysrhythmias: PVCS are most common. Most common cause of death is V-Fib and is associated with cardiogenic shock.
  • Left ventricular failure and pulmonary edema: Usually occurs within first 24 hours. -Cardiogenic Shock: Results from a large infarct. High mortality. Associated with V- Fib.
  • Ventricular free wall rupture: Occurs in 4-7 days. Associated with thrombosis of the LAD (left anterior descending) coronary artery. Results in cardiac tamponade from hemorrhage into the pericardial space. Cardiac tamponade is compression of the heart due to fluid collecting in the sac surrounding the heart. -Papillary muscle rupture: Acute onset of mitral valve regurgitation and left side heart failure. Associated with inferior MIs due to thrombosis of RCA (right coronary artery)

-Ventricular septum rupture: Produces a left to right shunt (ventricular septal defect), causing right heart failure. Associated with thrombosis in the LEFT ANTERIOR DESCENDING ARTERY - WIDOW MAKER!

Secondary Pneumothorax Answer - -Caused by injury -Tension pneumothorax occurs when air is trapped in the thoracic cavity and cannot escape. Site of the injury on the pleural membrane acts as a one-way valve and only allows air into the thoracic cavity. -Person may experience complete lung collapse. Sings: Deviated trachea, shortness of breath, hypotension. Pulmonary Edema Answer - Accumulation of water in alveolar sacs. Prevents proper exchange of gases. Symptoms: Dyspnea, chest pain, hypoxia, ORTHOPNEA, PAROXYSMAL NOCTURNAL DYSPNEA *Most common CAUSE is LEFT-SIDE HEART FAILURE. Backup up blood increases capillary hydrostatic pressure which pushes fluid into the alveolar sac. Acute Respiratory Distress Syndrome Answer - Type of respiratory failure which results from massive lung inflammation and widespread alveolar capillary damage Damage significantly impairs gas exchange and the patient will have significant issues with oxygenation Causes: Pneumonia, sepsis, massive trauma, burns, aspiration, DIC, pancreatitis Three Phases of ARDS Answer - 1. inflammatory Phase. Occurs in first 72 hours following initial insult or injury. Inflammatory cascade increases capillary permeability, allowing fluid, proteins, blood cells to leak out of circulation into pulmonary interstitium (extracellular area). Gas exchange is impaired.

  1. Proliferative Phase. Pulmonary edema resolves. Lasts 1-2 weeks. Intra- alveolar exudate turns into granulation tissue and worsens the hypoxemia.
  2. Fibrotic Phase. Occurs between 14-24 days. Alveoli undergo fibrosis (hardening), causing a decrease in respiratory function that may be permanent. Direct ARDS/Pulmonary ARDS Answer - Results from direct lung injury (pneumonia, aspiration, near drowning, inhaling toxins) Indirect ARDS/Extrapulmonary ARDS Answer - Results from injury other than in lungs (head trauma, burns, multiple transfusions, pancreatitis) Asthma Answer - -Reactive airway disease triggered by an allergic reaction -IgE mediated reaction -Airway narrows, causing dyspnea and wheezing -Results in smooth muscle hypertrophy, goblet cell hyperplasia, thickening and hyalinization of the basement membranes, proliferation of eosinophils, bronchial mucous plugs. -Exacerbations often trigged by viral infection. -RSV is most common asthma trigger for infants and toddlers Asthma in Children Answer - -Affects boys more often -Severity is largely based on socioeconomic status -Vit D deficiency may play a role in asthma. Vit D is anti-inflammatory

and mediates t-cell immune responses

-Klebsiella Pneumoniae: Common in hospitalized, debilitated patients, diabetics, and alcoholics. Elderly infected with this bacteria have a high mortality! -Haemophilus Influenza: Commonly seen in infants and children. Occurs in adults with COPD. Healthcare-Associated Pneumonia Answer - -Occurs in any individual who has had contact with healthcare system -Patients who have received infusion therapy or dialysis or have resided in a nursing home within 90 days of the diagnosis are said to have a healthcare-associated pneumonia -Common causes: Gram-negative (harder to treat) Klebsiella, Pseudomonas aeruginosa, E-Coli Hospital-Acquired Pneumonia Answer - -Diagnosed 48 hours after admission to hospital -Common causes: Gram-negative (harder to treat) Klebsiella, Pseudomonas aeruginosa, E-Coli Tuberculosis Answer - -Most commonly occurs in disadvantaged populations -Caused by mycobacterium tuberculosis -Spread via droplets containing the organism Tuberculosis Stages Answer - 1. Primary infection: Macrophages engulf the mycobacterium and form a granuloma (mass) called a Ghon. Inflammatory cascade is triggered. Center of lesion necroses and eventually calcifies. This infection is usually asymptomatic and does not cause active disease.

  1. Secondary infection: Ghon has activated and the infection has spread to additional sites within the lung. SIGNS OF INFECTION OCCUR: fever, hemoptysis, pleural effusion, wasting, weight loss. Lesions often occur in the apices (highest point of lung). These individuals are infectious and can spread disease! Mycobacterium can spread to other parts of the body via blood or lymphatic systems. During what stage of TB infection is the patient infectious and has signs/symptoms? Answer - Secondary infection Lung cancers Answer - -Usually malignant -Most cancer lesions are metastatic lesions from from a different primary cancer -Lung cancer = leading cause of death from cancer in men and women -Smokers develop 90% of primary lung cancer tumors -Most common primary lung cancer tumors are small cell and squamous cell carcinomas
  • There are no good screening tests to diagnose lung cancer in early stages, so most get diagnosed in late stages -Complications: Superior vena cava syndrome, hoarseness, pleural effusion, malnutrition, weight loss Pulmonary Atrial Hypertension Answer - -Hypertension in pulmonary artery

-Mean pulmonary arterial pressure greater than 25 at rest (normal is 15-18)