Patho Exam 6 Mod 11&12

• BIO280/BIO280V Exam 6 prep scheduled in week 12.
• Exam covers Modules 11 and 12.
• The exam is available for online access in Week 13.
• The exam opens Monday at 12am and closes Wednesday at 11:59pm.
• The format is a 50-question unit exam (multiple choice, select all that apply, etc.).
• All unit exams use Respondus Lockdown Browser and require scanning the work area and room.
• Exams are not open book, and do not allow internet access, notes, paper, or pencils.
• Whiteboards are permitted if the blank board is shown at the start and end of the exam.
• For technical issues, contact [email protected] immediately and include the instructor.
• Key Terms Lists from weekly pre-lecture videos/slides guide learning.
• Exam Prep Sessions are available and recordings are posted; listening to recordings twice is recommended.
• Unit exams make up 50% of the overall grade.
• Tutoring is available via the LSC site (myjoyce.edu) with course-specific dates/times.
• Student Outlines (Appendix B) offer practice questions, quizlets, and worksheets.

Acute Kidney Injury

• Focus on the causes of pre/renal/post types.
• Focus on signs/symptoms of each phase: oliguric, diuretic, and recovery.
• Pre-renal AKI involves decreased renal blood flow.
• Renal AKI involves damage to the renal architecture, specifically acute tubular necrosis, often secondary to ischemia or toxins.
• Post-renal AKI results from obstruction of the urinary outflow system.

Kidney Conditions

• Acute tubular necrosis: pathophysiology
• Bladder cancer: signs and symptoms
• Chronic kidney disease: anemia development, causes, pathophysiology, labs
• End-stage chronic kidney disease: signs/symptoms, electrolyte imbalances
• Hydronephrosis: outcome of this condition
• Incontinence (types): pathophysiology and signs/symptoms of each
• Kidney failure lab work: impacts on creatinine and GFR levels
• Kidney stones: causes of the different types
• Nephritic syndrome: pathophysiology, signs/symptoms
• Nephrotic syndrome: signs/symptoms
• Polycystic kidney disease: pathophysiology

Ear and Eye Conditions

• Ear infections: pathophysiology
• Open vs. Closed angle glaucoma: pathophysiology, signs/symptoms
• Otitis media involves infection of the inner ear.
• Otitis media can result in the blockage of the eustachian tube due to inflammation.
• Glaucoma is characterized by sudden accumulation of pressure, where the iris blocks the drainage canal.
• Open-angle glaucoma develops slowly, with the iris in the correct position.
• Closed-angle glaucoma's iris is suddenly pushed against the cornea.

Respiratory Conditions

• Acute respiratory distress syndrome: pathophysiology
• Acute vs. Chronic bronchitis: causes
• Asthma: pathophysiology, signs/symptoms
• Atelectasis: pathophysiology, signs/symptoms
• Chronic obstructive pulmonary disease: signs/symptoms, complications
• COVID: pathophysiology
• Cystic fibrosis: complications
• Deep vein thrombosis: complications
• Emphysema: pathophysiology, impacts on surfactant
• Flail chest: pathophysiology
• Hemothorax: pathophysiology
• Hypoxia: signs/symptoms
• Influenza: pathophysiology
• Obstructive sleep apnea: pathophysiology
• Pneumoconiosis: pathophysiology
• Pneumonia: pathophysiology
• Pulmonary embolism: risk factors, signs/symptoms, pathophysiology behind the VQ mismatch
• Pulmonary hypertension: why this causes right-sided heart failure
• Tension pneumothorax: signs/symptoms
• Ventilation/Diffusion/Perfusion: examples of these issues
• Ventilation involves inhalation and exhalation.
• Perfusion is blood flow to pulmonary vessels.
• Diffusion (oxygenation) is gas exchange at the alveolar level.
• Ventilation: Issues include asthma, COPD, obstructive sleep apnea, phrenic nerve damage.
• Diffusion: Alveoli fill with fluid as with pulmonary edema, pneumonia, ARDS, and emphysema.
• Perfusion: Pulmonary embolism and primary pulmonary hypertension are issues.
• Upper respiratory tract infections are usually viral and resolve with symptom management or supportive care like for influenza.
• Lower respiratory tract infections are viral or bacterial acute bronchitis.
• In lower respiratory tract infections, more aspirations occur in the right lung.
• Infections impair gas exchange.
• Hypoxia is impaired oxygen to the tissues.
• In hypoxia, low O2 is detected by the carotid body within the carotid artery.
• The respiratory system will respond by breathing faster in hypoxia.
• Signs and symptoms of hypoxia include headache/confusion, dyspnea/coughing, tachycardia, and cyanosis.
• Atelectasis is the collapse of a section of alveoli, impairing gas exchange; it is a partial collapse.
• Atelectasis usually results from a blockage of a bronchiole by disease or post-operation.
• Influenza is a respiratory condition that infects the epithelial cells in the respiratory tract, leading to pulmonary inflammation.
• Influenza's signs and symptoms include high fever, runny nose/sore throat/cough, myalgia, and N/V/D.
• COVID is a viral infection of the pulmonary alveolar epithelial cells, leading to alveolar wall damage.
• COVID's signs and symptoms include fever, cough/dyspnea, fatigue, sore throat, taste/smell loss, and GI distress.
• Acute, bacterial pneumonia affects the lower respiratory tract.
• Pneumonia requires antibiotics.
• In pneumonia, there is isolation in one lung area, with fluid or pus collecting in the alveoli.
• Pneumonia has a high risk for hypoxemia, especially in older patients, who may need supplemental O2.
• Symptoms of pneumonia include shortness of breath, fever, productive cough, weakness, confusion, crackles, and crepitations.
• Asthma involves bronchoconstriction and inflammation, leading to increased mucous production/recurrent airway obstruction.
• Asthma signs and symptoms include dyspnea, expiratory wheezing, cough (especially at night), and tachypnea.
• Asthma is primarily a ventilation issue.
• Common asthma triggers include exercise and allergens.
• COPD is a chronic inflammatory condition combining emphysema and chronic bronchitis.
• COPD carries a high risk of developing pulmonary hypertension and right-sided heart failure.
• Emphysema involves gradual damage and scarring to the alveoli.
• In emphysema, air sacs rupture, creating one big air pocket instead of many small ones; air trapping occurs.
• A loss of surfactant in emphysema creates incomplete exhalation.
• Emphysema reduces surface area and prevents O2 from moving through the bloodstream.
• There is also a lack of O2 and CO2 exchange across the alveolar-capillary membrane.
• Chronic bronchitis involves inflammation of the bronchi and bronchioles, causing bronchial injury.
• There is dysfunctional mucociliary movement and excess mucus secretions with chronic bronchitis.
• Chronic bronchitis is commonly caused by toxins or irritants.
• Signs and symptoms include dyspnea, chronic cough, barrel chest, hypoxia, hypercapnia/hypercarbia, polycythemia, respiratory.
• There is acidosis, pursed-lip breathing, and cyanosis.
• With CO2 narcosis, there is a tolerance for high CO2, so the drive to breathe is hypoxemia.
• High-flow O2 to increase O2 sat turns off the hypoxic drive from the brain stem, causing higher CO2 levels.
• Pneumoconiosis (black lung) leads to scarring, pulmonary fibrosis, airway obstructions, and poor expansion with inflammation.
• Pneumoconiosis causes include inhalation of coal dust, silica, and asbestos.
• Prevention for pneumoconiosis involves using masks and other personal protective equipment.
• Obstructive Sleep Apnea (OSA): Pharyngeal/Laryngeal muscles relax, leading to reduced respiration & hypoxia
• Body wakes itself up when it senses that it is not getting enough oxygen, leading to daytime fatigue/sleepiness, & memory defects
• OSA Risk factors: obesity, male, alcohol, smoking, congestion/infection
• Over time OSA can also lead to pulmonary hypertension and eventually right sided heart failure; this is called cor pulmonale.
• Pulmonary hypertension is characterized by increased resistance to blood flowing from the heart to the lungs
• Damage in the lungs increases artery pressure causing the heart to work harder
• Pulmonary artery hypertension causes increased right ventricular strain and ultimately right sided heart failure
• Increased arterial HTN
• Harder for heart to pump to lungs
• If right sided heart failure – systemic s/sx
• Primary – unknown cause/ Secondary: causes include COPD, PE, OSA, Pulmonary fibrosis
• Acute Respiratory Distress Syndrome (ARDS): Results in massive inflammation/ Causes vasodilation and ultimately alveolar edema usually following a life-threatening injury, This is widespread pulmonary inflammation. It leads to impaired gas exchange and pulmonary infiltrates/ Diffusion issue/ S/S: dyspnea, rapid breathing, fever, productive cough
• Cystic Fibrosis: Autosomal, Recessive Disorder/ Abnormal secretions that cause airway obstructions, Recurrent lung infections, Hypoxia
• Pancreas = Mucus production blocks pancreatic enzymes from entering GI tract, Nutrient malabsorption, Weight loss, Pancreatic failure, Replacement of pancreatic enzymes
• Pulmonary Embolism (PE): Obstruction of a pulmonary artery by a dislodged thrombus
• Usually from a DVT with Symptoms of DVT: Unilateral leg swelling, leg tenderness, and redness & VQ mismatch with Adequate ventilation but no perfusion
• Pulmonary Embolism Risk factors: Femur fracture, deep vein thrombosis, immobility, cancer, birth control pills, pregnancy, smoking, obesity
• Symptoms of PE: SOB, hemoptysis, pleuritic chest pain, syncope, hypoxemia

Chest Trauma

• Pneumothorax: Collapse of lung due to separation of visceral and parietal pleura with Hemothorax- blood in pleural space & Pleural effusion- fluid in pleural space
• Tension Pneumothorax: Collapse of the lung causing hemodynamic instability due to pressure on the right side of the heart → MEDICAL EMERGENCY w/ Right heart compression makes it so that blood cannot return to the heart/ This will lead to hypotension, tachycardia, tracheal deviation toward unaffected side, jugular vein distention, and absent breath sounds on one side

Flail Chest:

• Flail Chest. Broken ribs at multiple locations causes part of the chest wall to move inward with inspiration/ Results in decreased ventilation

Client with flank/groin pain, vomiting, hematuria, and hyperparathyroidism

• Suspected conditions include polycystic kidney disease, bladder cancer, acute kidney injury

Labs Indicating Kidney Injury

• High creatinine
• Low glomerular filtration rate
• High BUN

Pathophysiology of Chronic Kidney Disease

• Kidney damage leads to reduced glomerular filtration, resulting in excess fluid and waste accumulation.
• Inherited disorder causes multiple cysts develop in kidneys, causing them to enlarge.
• Antigen-antibody complex causes inflammation of the glomerulus

Potential Causes of Pre-Renal Acute Kidney Injury

• Dehydration
• Hemorrhage
• NSAIDs
• Hypovolemic shock

Client with acute kidney injury and IV drug use

• Kidney injury is from obstruction of urine outflow from the kidney

Client with BPH experiencing urge to pee even after urinating

• The nurse suspects overactive bladder

Potential Final Outcome for Client with Hydroureter

• Peripheral edema
• Incontinence
• Inability to concentrate urine

Dietary Changes for Client with Chronic Kidney Disease

• The client should decrease sodium intake
• The client should increase potassium intake
• The client should begin taking vitamin D supplement

Signs and Symptoms of Nephritic Syndrome

• Foamy urine
• Cola-colored urine
• RBCs in the urine
• Hyperlipidemia
• Hypertension

Client with diabetes mellitus, edema, hyperlipidemia, proteinuria, and foamy urine

• There is damage to the blood vessels in the glomerulus, causing increased permeability in the glomerulus
• As well as an antigen-antibody complex causing inflammation of the glomerulus, causing a leaky basement membrane

Diffusion Disorders

• Pneumonia
• Asthma
• Acute Respiratory Distress Syndrome
• Pulmonary Embolism
• Emphysema

Client with perfusion to lung area but no ventilation causing respiratory distress

• This is a Shunting V/Q mismatch

Client recovering from surgery experiencing collapsed alveoli

• This is Atelectasis

Asthma

• Bronchoconstriction is a component of asthma
• Inflammation is a component of asthma
• Signs and symptoms include dyspnea, wheezing, and cough

Pathophysiology of Emphysema

• Gradual damage/scarring to the alveoli results in a loss of surfactant

Client with sepsis exhibiting dyspnea, rapid breathing, fever, and productive cough

• Widespread inflammation causes vasodilation and alveolar edema
• Scarring and fibrosis of the lungs
• Separation of visceral and parietal pleura results in partial lung collapse

Client with cystic fibrosis asking about disease impact on daily life

• May experience hypoxia due to buildup of secretions
• At increased risk for pulmonary infections
• Replacement pancreatic enzymes may be started

Client with viral infection affecting alveolar wall epithelial cells

• Nurse to expect dyspnea

Client with difficulty breathing, absent breath sounds on right, and blood in space of right lung

• Diagnosis to suspect is Hemothorax
• As well as Tension Pneumothorax
• As well as Pneumothorax
• As well as Pleural effusion

Risk Factors for Pulmonary Embolism

• Femur Fracture
• DVT
• Immobility
• Smoking
• Recent viral infection

Glomerulonephritis (Nephritic Syndrome) Details

• Glomerulonephritis involves inflammation of the glomerulus.
• Antibodies attack the glomerulus, or an antigen/antibody complex circulates in the bloodstream, clogging the glomerulus.
• Risk factors include being immunocompromised, hepatitis viral infections, bacterial infections (e.g., strep), SLE, IgA nephropathy, and Goodpasture’s syndrome.
• Signs and symptoms include hypertension and oliguria (less than 400 mL/24-hour period).

Nephrotic Syndrome Details

• Nephrotic syndrome involves losing large amounts of protein (more than 3.5g/dL/24 hrs).
• It is caused by glomerular damage, not an inflammatory condition.
• Symptoms and clinical findings include proteinuria leading to edema, hypoalbuminemia, and hallmark symptoms of peripheral edema and hyperlipidemia.
• The release of aldosterone occurs to compensate, leading to water and salt retention, increasing edema and weight gain and hypertension.
• Hyperlipidemia (high cholesterol) and potential for pleural effusion are involved.
• Foamy urine is a common presentation due to albuminuria.

Causes of Pre-Renal Issues

• Hypovolemia
• Dehydration
• Hemorrhage
• Hypovolemic shock
• Trauma
• Cardiovascular disorders
• Atherosclerotic disease
• Vasodilation

Compensation for Pre-Renal Issues

• The body compensates with the RAAS system and ADH release

Renal/Intrarenal Issues

• Renal/Intrarenal issues cause damage to the renal architecture.
• Acute tubular necrosis results from destruction of tubular epithelial cells, leading to necrosis, sloughing of cells, cast formation, edema, and tubular obstructions, resulting in oliguria.
• Other causes include glomerulonephritis, kidney transplant rejection, nephrolithiasis, certain medications, recreational drugs, and IV contrast.

Post-Renal Issues

• Post-renal damage includes obstruction of the urinary outflow system.
• Causes include BPH, nephrolithiasis, and blockage of the ureters, bladder, or urethra.

Hydroureter Details

• Hydroureter results from an accumulation of urine in the ureter.
• The steps include occlusion or ureter leading to urine accumulation.
• Increased hydrostatic pressure follows, leading to dilation of the ureter and renal pelvis (hydronephrosis).
• Increased glomerular pressure then occurs, decreasing glomerular blood flow and the glomerular filtration rate while increasing pressure.
• This can lead to tubular atrophy, loss of nephrons, and inability to concentrate urine.

More on Chronic Kidney Disease

• It is caused by constant injury to the kidney and loss of nephrons resulting from diabetes mellitus and hypertension.
• Progressive and irreversible damage to the glomerulus leads to a buildup of fluid and waste products.
• As creatinine and BUN increase, GFR decreases.
• Other signs and symptoms include hyperkalemia, hypocalcemia, anemia (low hemoglobin related to decreased erythropoietin), high hydrogen ions (metabolic acidosis), decreased GFR, increased BUN/creatinine, increased intravascular volume, and confusion (uremia).
• Medication adjustments may be necessary, and dialysis or transplant may be needed.

Polycystic Kidney Disease Details

• It is an autosomal dominant inherited disorder causing fluid-filled sacs on the kidney, leading them to enlarge and stop functioning.
• Leads to hypertension, renal failure, and fluid-filled cysts can develop in other places.

Bladder Cancer Details

• The most common type is urothelial carcinoma caused by chronic irritation, resulting in dysplasia.
• The signs and symptoms include painless, intermittent gross hematuria.
• Other symptoms include a sensation of incomplete bladder emptying and UTI-like symptoms.

Nephrolithiasis (Kidney Stones) Details

• General signs and symptoms include abrupt flank pain/radiating pain to the groin, nausea/vomiting, and hematuria.
• Oxalate stones (most common) result from too much oxalate or calcium (Ca) and not enough fluid (i.e., dehydration).
• Urate stones (uric acid) result from loss of too much fluid (i.e., chronic diarrhea, malabsorption) or underlying conditions such as a diabetic client, metabolic syndrome, and high protein diets.
• Phophate stones result from renal tubular acidosis.
• Cystine stones result from too much cystine in the urine.
• Xanthine Stones: tiny crystals come together, may see some abdominal pain & hematuria
• Struvite stones are due to bacteria and are commonly seen in UTIs.