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NURS 5315 Advanced Pathophysiology Exam 3 2026/2027 – 150+ Questions & Answers | Cardiovascular, Respiratory, Shock, TBI, ICP, Stroke & Seizures | UTA

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This NURS 5315 Advanced Pathophysiology Exam 3 2026/2027 resource is an extensive 70-page exam study guide with 150+ questions and detailed answers designed around major cardiovascular, pulmonary and neurological pathophysiology concepts. The document provides explanation-based answers rather than simple answer keys, helping students review disease mechanisms, risk factors, clinical manifestations, physiologic compensation, complications and important diagnostic concepts. Major areas include valvular heart disease, atherosclerosis, congenital heart defects, heart failure, coronary artery disease, myocardial infarction, respiratory disorders, shock, traumatic brain injury, intracranial pressure, stroke and seizure disorders. The cardiovascular pathophysiology section begins with valvular disorders, including mitral stenosis, mitral regurgitation, aortic stenosis and aortic regurgitation. It connects structural valve abnormalities with changes in pressure, ventricular or atrial remodeling, pulmonary vascular congestion and characteristic manifestations. Atherosclerosis is explored through endothelial injury, inflammation, LDL accumulation, macrophage activity, foam-cell formation, fatty streaks, smooth-muscle proliferation, fibrous plaque formation and eventual ischemia or infarction. Congenital cardiovascular disease is addressed through left-to-right and right-to-left shunts, Eisenmenger syndrome, ventricular septal defect, atrial septal defect, patent ductus arteriosus and Tetralogy of Fallot. The questions emphasize changes in oxygen saturation, pulmonary hypertension, ventricular hypertrophy, cyanosis and characteristic murmurs, while also reviewing maternal and environmental risk factors associated with congenital heart abnormalities. The heart-failure material differentiates heart failure with reduced ejection fraction (HFrEF), heart failure with preserved ejection fraction (HFpEF), systolic dysfunction, diastolic dysfunction and right-sided heart failure. Students review changes in contractility, preload, stroke volume and cardiac output as well as ventricular remodeling, sympathetic activation and the renin-angiotensin-aldosterone system (RAAS). The guide also connects left-sided failure with pulmonary congestion and right-sided failure with jugular venous distention, hepatosplenomegaly and peripheral edema. A particularly detailed section examines coronary artery disease and acute coronary syndromes. It reviews CAD risk factors, stable and Prinzmetal angina, unstable angina, NSTEMI and STEMI, followed by the cellular pathophysiology of myocardial infarction. Students encounter concepts involving myocardial ischemia, ATP depletion, anaerobic metabolism, lactic-acid accumulation, catecholamine responses, troponins and reperfusion injury. Complications covered include ventricular fibrillation, cardiogenic shock, pulmonary edema, ventricular free-wall rupture, papillary-muscle rupture, ventricular-septal rupture, mural thrombus, ventricular aneurysm and post-infarction pericarditis. The respiratory pathophysiology portion distinguishes restrictive and obstructive lung disease and reviews acute respiratory failure, croup, spontaneous and tension pneumothorax, pulmonary edema and acute respiratory distress syndrome (ARDS). ARDS is organized into inflammatory, proliferative and fibrotic phases and further differentiated into direct pulmonary versus indirect extrapulmonary injury. Students also receive substantial review of asthma, COPD, alpha-1 antitrypsin deficiency, emphysema, chronic bronchitis, pneumonia, tuberculosis, lung cancer, pulmonary arterial hypertension and cor pulmonale. The document connects airway remodeling and IgE-mediated responses with asthma, loss of elastic recoil and air trapping with emphysema, mucus hypersecretion with chronic bronchitis, and pulmonary hypertension with progressive right-ventricular workload and right-sided heart failure. Another major component covers circulatory shock, beginning with impaired tissue perfusion, hypoxia, anaerobic metabolism and lactic-acid production. The resource distinguishes the nonprogressive, progressive and irreversible stages of shock and reviews hypovolemic, cardiogenic, septic, neurogenic and anaphylactic shock, emphasizing the different mechanisms involving reduced circulating volume, pump failure, widespread vasodilation and immune-mediated responses. The neurological section provides extensive coverage of traumatic brain injury (TBI), including Glasgow Coma Scale assessment, primary versus secondary and tertiary brain injury, focal and diffuse injury, coup-contrecoup injuries, contusions, concussions, penetrating trauma and basilar skull fractures. It further differentiates intracerebral, epidural, subdural and subarachnoid hemorrhage, including the lucid interval associated in the document with epidural hematoma and the thunderclap headache associated with subarachnoid hemorrhage. Post-concussive syndrome and chronic traumatic encephalopathy (CTE) are also reviewed. The intracranial pressure and cerebral perfusion section explains the inverse relationship between ICP and cerebral perfusion pressure (CPP) and follows the progression from cerebral compensation to hypoxia, decreased consciousness and brain herniation. High-yield concepts include Cushing's triad, decorticate and decerebrate posturing, Cheyne-Stokes respirations, uncal herniation, central herniation, transcalvarial herniation and cerebellar tonsillar herniation. Stroke content covers thrombotic, embolic, lacunar and hemorrhagic strokes, along with transient ischemic attacks and the Circle of Willis. The guide associates cerebral vascular territories with characteristic neurological deficits, including the anterior cerebral, middle cerebral, posterior cerebral, basilar and cerebellar arteries, and reviews aphasia/dysphasia and other neurological manifestations following vascular occlusion. The document further reviews focal and generalized seizures, seizure aura, simple and complex partial seizures, Jacksonian march, automatisms, tonic and clonic seizures, tonic-clonic seizures, status epilepticus and non-convulsive status epilepticus. It also introduces acute confusional states and meningitis, giving students an integrated review of neurological dysfunction and associated pathophysiologic mechanisms. Relevant Students: This study resource is particularly relevant to University of Texas at Arlington (UTA) NURS 5315 students, advanced pathophysiology students, graduate nursing students, MSN students, nurse practitioner students, FNP and AGACNP learners, advanced practice nursing students and students preparing for Exam 3. Its systems-based explanations also make it useful for students who need concentrated review of cardiovascular, pulmonary, shock and neurological pathophysiology before advanced nursing examinations. Keywords: NURS 5315 Exam 3, NURS 5315 Advanced Pathophysiology, NURS 5315 Exam 3 questions and answers, NURS , UTA NURS 5315, UTA Advanced Pathophysiology Exam 3, advanced pathophysiology questions and answers, advanced pathophysiology exam, valvular heart disease pathophysiology, mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation, atherosclerosis pathophysiology, congenital heart defects, Eisenmenger syndrome, Tetralogy of Fallot, heart failure pathophysiology, HFrEF, HFpEF, coronary artery disease, acute coronary syndrome, NSTEMI pathophysiology, STEMI pathophysiology, myocardial infarction complications, ARDS pathophysiology, COPD pathophysiology, emphysema, chronic bronchitis, pneumonia pathophysiology, tuberculosis pathophysiology, pulmonary hypertension, cor pulmonale, shock pathophysiology, cardiogenic shock, hypovolemic shock, septic shock, neurogenic shock, anaphylactic shock, traumatic brain injury, increased intracranial pressure, cerebral perfusion pressure, Cushing triad, brain herniation, epidural hematoma, subdural hematoma, subarachnoid hemorrhage, stroke pathophysiology, TIA, embolic stroke, hemorrhagic stroke, seizure disorders, status epilepticus, meningitis, graduate nursing exam, nurse practitioner pathophysiology

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NURS 5315 Advance
Pathophysiology - Exam 3 - UTA
EXAM Questions & Answers,
Well Elaborated | Already
Verified Test |100% Verified
solutions | 2026/2027 Latest!!

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




COPYRIGHT©PROFFKERRYMARTIN 2026/2027. YEAR PUBLISHED 2026. COMPANY REGISTRATION NUMBER: 619652435. TERMS OF USE.
PRIVACY STATEMENT. ALL RIGHTS RESERVED

, -Marked by EARLY DIASTOLIC MURMUR (on systole, heart contracts

and pushes blood up the aorta, but on diastole, heart relaxes and

ineffective aortic valve is not able to hold blood up in aorta, so blood falls

and makes a swish sound, which is the murmur)

-Most commonly caused by AORTIC ROOT DILATION(starting point of

aorta is too wide)

-Other causes: infective endocarditis, rheumatic fever, aortitis from

syphilis, coarctation (congenital narrowing of aorta), aortic dissection

(tear), ankylosing spondylitis (inflammatory arthritis)




-Acute: increases left ventricular end-diastolic pressure (LVEDP)

(increased blood back down in the left ventricle increases pressure),

decreased stroke volume (not much blood is being pushed from left

ventricle because blood's backed up and overwhelming left ventricle),

normal or decreased pulse pressure, decreased cardiac output (aorta is

not effectively pumping blood from heart)




Chronic: Body adjusts; LVEDP normalizes, systolic bp increases

(compensation: harder contraction to push blood out of aorta before it

falls back down to left ventricle), diastolic bp decreases (compensation:

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