Test your understanding with these related questions
A 36-year-old man presents to his primary care physician because of shortness of breath. He is an office worker who has a mostly sedentary lifestyle; however, he has noticed that recently he feels tired and short of breath when going on long walks with his wife. He also has had a hacking cough that seems to linger, though he attributes this to an upper respiratory tract infection he had 2 months ago. He has diabetes that is well-controlled on metformin and has smoked 1 pack per day for 20 years. Physical exam reveals a large chested man with wheezing bilaterally and mild swelling in his legs and abdomen. The cause of this patient's abdominal and lower extremity swelling is most likely due to which of the following processes?
Practice US Medical PG questions for Pulmonary hypertension. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Pulmonary hypertension Explanation: ***Right ventricular dysfunction secondary to pulmonary hypertension*** - This patient's long history of smoking, chronic cough, and wheezing suggest significant **chronic obstructive pulmonary disease (COPD)**, which leads to **hypoxemia** and **pulmonary hypertension**. - **Pulmonary hypertension** increases the workload on the **right ventricle**, eventually leading to **right heart failure** (cor pulmonale), characterized by peripheral edema (leg swelling) and ascites (abdominal swelling). *Excessive protease activity* - While excessive protease activity (e.g., elastase) is implicated in the pathogenesis of **emphysema** by destroying alveolar walls, it does not directly cause peripheral edema and ascites. - This process primarily leads to **airflow obstruction** and **gas exchange abnormalities**, which can indirectly contribute to pulmonary hypertension but is not the direct cause of the peripheral edema. *Damage to kidney tubules* - **Acute tubular necrosis** or chronic kidney disease can cause edema due to impaired fluid and electrolyte balance, but the patient's symptoms (dyspnea, wheezing, smoking history) point strongly to a primary pulmonary and cardiac etiology. - While diabetes can cause nephropathy, there is no information to suggest acute kidney injury or chronic kidney disease leading to such severe edema. *Hyperplasia of mucous glands* - **Hyperplasia of mucous glands** in the bronchi is characteristic of **chronic bronchitis**, contributing to the chronic cough and airway obstruction. - This pathology primarily affects airway clearance and airflow, rather than directly causing systemic edema or ascites. *Defective protein folding* - **Defective protein folding**, such as in **alpha-1 antitrypsin deficiency**, can lead to early-onset emphysema and liver disease. - While this could fit with a pulmonary presentation, it is less common than smoking-induced COPD and does not directly explain the edema and ascites caused by right heart failure.
Pulmonary hypertension Explanation: ***Elevated pulmonary artery pressure*** * The patient's long history of **heavy smoking** and progressive exertional dyspnea, wheezing, plethoric face, distended jugular veins, and lower extremity edema are highly suggestive of **cor pulmonale** due to chronic obstructive pulmonary disease (COPD). * **COPD** leads to chronic hypoxia and vasoconstriction of pulmonary arteries, increasing **pulmonary artery pressure**, which eventually causes right ventricular failure (cor pulmonale) manifested by the systemic venous congestion symptoms. *Coronary plaque deposits* * While **coronary plaque deposits** can lead to chest discomfort, the prominent signs of **right-sided heart failure** (jugular venous distension, lower extremity edema) and chronic respiratory symptoms point away from isolated coronary artery disease as the primary cause. * The patient's wheezing and long smoking history are more indicative of a **respiratory rather than purely cardiac origin** for his dyspnea. *Chronic respiratory acidosis* * **Chronic respiratory acidosis** can occur in severe COPD, but it is a **consequence** of impaired gas exchange, not the primary cause of the patient's presenting symptoms of shortness of breath and chest discomfort with signs of overt heart failure. * While important, acidosis alone does not explain the **physical findings of right heart failure** such as jugular venous distention and peripheral edema. *Increased left atrial pressure* * **Increased left atrial pressure** is characteristic of **left-sided heart failure**, which typically presents with pulmonary edema (rales, pink frothy sputum) and symptoms like orthopnea and paroxysmal nocturnal dyspnea. * This patient's symptoms, particularly the **plethoric face, distended jugular veins, and lower extremity edema**, are classic signs of **right-sided heart failure**, not left-sided heart failure. *Decreased intrathoracic gas volume* * **Decreased intrathoracic gas volume** is usually seen in restrictive lung diseases (e.g., pulmonary fibrosis), not obstructive diseases like COPD, where gas trapping leads to **increased intrathoracic gas volume**. * The patient's wheezing and long smoking history are classic for **obstructive lung disease**, which is associated with air trapping and hyperinflation, rather than decreased lung volumes.
Pulmonary hypertension Explanation: ***Metformin therapy*** - This patient has **newly diagnosed type 2 diabetes mellitus** with classic symptoms (polyuria, polydipsia, blurred vision) and laboratory confirmation (HbA1c 6.8%, glucose 180 mg/dL, glucosuria). - **Metformin is the first-line pharmacologic therapy** for type 2 diabetes according to current guidelines (ADA, AACE) due to its efficacy, safety profile, cardiovascular benefits, and low risk of hypoglycemia. - The patient's creatinine is normal (1.0 mg/dL), so metformin is not contraindicated. - Addressing the **symptomatic hyperglycemia** is the most appropriate next step in management. *ACE inhibitor therapy* - ACE inhibitors are indicated for diabetic patients with **hypertension and albuminuria** to provide renoprotection and slow progression of diabetic nephropathy. - While this patient has both hypertension (148/95 mm Hg) and proteinuria (1+), ACE inhibitor therapy should be initiated **after or concurrent with diabetes management**, not as the sole initial intervention. - The patient needs **glycemic control first** given symptomatic hyperglycemia, though ACE inhibitor would be an appropriate addition to the treatment regimen. *Low-carbohydrate diet* - **Lifestyle modifications** including medical nutrition therapy and exercise are foundational for managing type 2 diabetes and should be recommended. - However, given the patient's **symptomatic hyperglycemia** (HbA1c 6.8%, glucose 180 mg/dL with classic symptoms), lifestyle changes alone are **insufficient as the initial management**. - Pharmacologic therapy with metformin should be initiated immediately alongside lifestyle counseling. *Insulin therapy* - Insulin therapy is indicated for patients with **very high HbA1c** (typically >9-10%), **severe symptoms of hyperglycemia**, evidence of catabolism, or failure of oral agents. - This patient's HbA1c of 6.8% represents **relatively mild hyperglycemia** that is appropriately managed with metformin as first-line therapy. - Insulin is **not indicated** at this stage of disease. *Aspirin therapy* - **Aspirin for primary prevention** in diabetes is controversial; current guidelines suggest shared decision-making for patients at increased cardiovascular risk without high bleeding risk. - While this patient has cardiovascular risk factors (diabetes, hypertension, obesity, dyslipidemia), aspirin would be a **secondary priority** after addressing the acute metabolic derangements. - **Glycemic control takes precedence** over aspirin initiation in newly diagnosed diabetes.
Pulmonary hypertension Explanation: ***Tear in the tunica intima*** - The sudden onset of **severe anterior chest pain**, hypertension, and a **diastolic murmur** consistent with **aortic insufficiency** points strongly to an **aortic dissection**, which begins with a tear in the tunica intima. - Risk factors like **hypertension**, **smoking**, and **advanced age** increase the likelihood of aortic dissection. *Rupture of a bulla in the lung* - This would typically cause **pneumothorax**, leading to **sharp, pleuritic chest pain** and **dyspnea**, often with diminished breath sounds on the affected side. - A **cardiac murmur** and severe distress in the context of vascular risk factors are not characteristic of a ruptured bulla. *Perforation of the esophageal wall* - Esophageal perforation (Boerhaave syndrome) presents with **severe chest pain**, **vomiting**, and often **subcutaneous emphysema** or **pleural effusion**. - While it causes severe chest pain, the described **diastolic murmur** and absence of vomiting or other specific signs make this less likely. *Obstruction of the pulmonary arteries* - **Pulmonary embolism** (obstruction of pulmonary arteries) typically causes **sudden onset dyspnea**, **pleuritic chest pain**, **tachycardia**, and **hypoxia**, often without a significant cardiac murmur of this nature. - The oxygen saturation of 98% makes a large pulmonary embolism less probable. *Fibrofatty plaque in the aortic wall* - While common in patients with hypertension and smoking history, an **atherosclerotic plaque** in the aortic wall itself rarely causes acute, severe chest pain and a new diastolic murmur unless it leads to an **aortic dissection** or **rupture**. - This option describes a precursor to diseases like aortic dissection but not the acute event itself.
Pulmonary hypertension Explanation: ***Positive bubble study*** - The patient's symptoms, including **cyanosis** (**bluish tinge to the lips**), **clubbing**, and **right ventricular heave**, suggest **Eisenmenger syndrome**, a late complication of a **left-to-right shunt** that has reversed due to pulmonary hypertension. - A positive bubble study on echocardiography would confirm the presence of a **right-to-left shunt**, characteristic of Eisenmenger syndrome, by showing microbubbles crossing from the right to the left side of the heart. *Mitral insufficiency* - While mitral insufficiency can cause a murmur and heart failure symptoms, it does not typically lead to the **cyanosis** and **clubbing** described. - The absence of a murmur, despite a history of one, points away from a significant current insufficiency. *Aortic stenosis* - Aortic stenosis is characterized by an **ejection systolic murmur** that would likely be heard on examination, contradicting the scenario where no murmur is audible. - It usually presents with a different constellation of symptoms, such as angina, syncope, and heart failure, without the prominent cyanosis or clubbing seen here. *Dynamic left ventricular outflow tract obstruction* - This is characteristic of **hypertrophic obstructive cardiomyopathy (HOCM)**, which can cause exertional syncope. - However, HOCM does not typically lead to **cyanosis**, a **right ventricular heave**, or **clubbing**, which are strong indicators of a right-to-left shunt. *Ventricular aneurysm* - A ventricular aneurysm is a bulging of the ventricular wall, often a complication of a **myocardial infarction**, which is unlikely in a 27-year-old with a history of a "heart murmur since childhood." - It typically presents with symptoms related to heart failure, arrhythmias, or embolism, and would not explain the prominent **cyanosis** and **clubbing**.
Pulmonary hypertension Explanation: ***Liver cirrhosis*** * This patient has **metabolic syndrome**, characterized by **central obesity** (waist >88 cm in women), **hypertension** (≥130/85 mm Hg), **low HDL cholesterol** (<50 mg/dL in women), **elevated triglycerides** (≥150 mg/dL), and **type 2 diabetes mellitus**. * Metabolic syndrome is strongly associated with **non-alcoholic fatty liver disease (NAFLD)**, which affects **70-90% of patients** with this condition. * NAFLD can progress to **non-alcoholic steatohepatitis (NASH)**, then to **hepatic fibrosis**, and ultimately **cirrhosis**—making this patient's greatest long-term risk without intervention. * NAFLD is now the **leading cause of chronic liver disease** in developed countries, and the combination of obesity, insulin resistance, and dyslipidemia directly promotes hepatic lipid accumulation and inflammation. *Incorrect: Osteoporosis* * While common in post-menopausal women, **obesity is generally protective against osteoporosis** due to increased weight-bearing stress on bones and higher estrogen levels from adipose tissue aromatization. * No specific risk factors for osteoporosis (e.g., corticosteroid use, smoking, low calcium intake) are present. *Incorrect: Rheumatoid arthritis* * This is an **autoimmune condition** not associated with metabolic syndrome. * The patient has no symptoms of joint pain, morning stiffness, or synovitis that would suggest rheumatoid arthritis. * Metabolic factors do not increase the risk of developing rheumatoid arthritis. *Incorrect: Subarachnoid hemorrhage* * While **hypertension** is a risk factor for hemorrhagic stroke, subarachnoid hemorrhage is more specifically associated with **ruptured aneurysms** or **arteriovenous malformations**. * The patient's moderately elevated blood pressure poses some cardiovascular risk, but this is not the greatest risk compared to the progressive liver disease associated with metabolic syndrome. *Incorrect: Central sleep apnea* * **Central sleep apnea** (cessation of respiratory effort) is primarily associated with **heart failure**, **stroke**, or **opioid use**—not metabolic syndrome. * **Obstructive sleep apnea** (OSA) is what's associated with obesity and metabolic syndrome, but that is not an option here. * While this patient may be at risk for OSA, central sleep apnea is not the primary concern in metabolic syndrome.
Pulmonary hypertension Explanation: ***Weight Loss*** - The patient's **BMI of 39 kg/m²** indicates **class III obesity**, which is the strongest modifiable risk factor for **obstructive sleep apnea (OSA)**. The clinical presentation—**daytime fatigue**, morning headaches, unrefreshing sleep despite adequate sleep duration, and hypertension—strongly suggests OSA. - While **polysomnography** is the gold standard for confirming OSA, the clinical diagnosis is evident in this case. **Weight loss** is the most important initial therapeutic intervention, as even modest weight reduction (10% of body weight) can significantly improve or resolve OSA in obese patients. - Weight loss reduces upper airway collapse by decreasing fatty tissue deposition around the pharynx and improving lung volumes. This addresses the underlying pathophysiology rather than just treating symptoms. - This intervention also addresses his **hypertension** (180/110 mm Hg), which is commonly associated with and exacerbated by OSA. *Caffeine avoidance* - While excessive caffeine can disrupt sleep architecture, the patient's symptoms—particularly **morning headaches** and **unrefreshing sleep despite sleeping in**—are not characteristic of caffeine-induced insomnia, which typically presents with difficulty initiating sleep. - These symptoms, combined with obesity and hypertension, point strongly to a sleep-related breathing disorder rather than a stimulant effect. *Screening for depression* - Fatigue is indeed a cardinal symptom of major depressive disorder, but the specific pattern here—**morning headaches** (from nocturnal hypercapnia/hypoxemia), **unrefreshing sleep**, and **obesity with hypertension**—is far more consistent with OSA. - Depression screening could be considered if symptoms persist after addressing the sleep disorder, as untreated OSA can contribute to or worsen mood disorders. *Alcohol avoidance in the evening* - **Alcohol consumption** (2-3 beers daily) does worsen OSA by relaxing upper airway dilator muscles and suppressing arousal responses to hypoxemia. Evening alcohol avoidance would be a beneficial **adjunctive measure**. - However, while helpful, this intervention is less impactful than weight loss. The patient's **severe obesity** (BMI 39 kg/m²) is the predominant and most modifiable risk factor, making weight loss the priority intervention that will have the greatest effect on reducing OSA severity. *CT head* - CT head would be indicated if there were focal neurological deficits, papilledema, or features suggesting increased intracranial pressure or structural brain pathology. - This patient's **neurological exam is unremarkable**, and his headaches are characteristic of OSA (worse in the morning due to nocturnal CO₂ retention, improving throughout the day). Imaging is not warranted.
Pulmonary hypertension Explanation: ***Obstructive sleep apnea*** - This patient's symptoms of **dyspnea, lower extremity swelling, frequent nocturnal awakenings, and excessive daytime sleepiness**, in conjunction with **obesity (BMI 37)**, **hypertension**, and specific **oropharyngeal abnormalities** (small orifice, enlarged tongue and uvula, low-lying soft palate), are highly suggestive of **obstructive sleep apnea (OSA)**. - The echocardiographic findings of a **mildly dilated right ventricle** and **elevated systolic pulmonary artery pressure** (cor pulmonale) without left heart abnormalities are a common consequence of chronic hypoxia and hypercapnia associated with severe OSA. *Chronic obstructive pulmonary disease* - While the patient is a 35-pack-year smoker, the absence of a **cough** and **clear lungs to auscultation** make COPD less likely. - A Ventilation-Perfusion scan showing **no abnormalities** further decreases the likelihood of significant parenchymal lung disease often seen in COPD. *Pulmonary thromboembolism* - Although dyspnea is a symptom of pulmonary thromboembolism, the **insidious onset over a year** and the absence of acute symptoms like pleuritic chest pain or hemoptysis make it unlikely. - A **normal ventilation-perfusion scan** effectively rules out significant pulmonary thromboembolism. *Idiopathic pulmonary artery hypertension* - This diagnosis typically presents with **progressive dyspnea** and signs of **right heart failure**, similar to the patient's presentation. - However, the patient's severe **risk factors for OSA (obesity, oropharyngeal features)** provide a more specific and likely underlying cause for the observed pulmonary hypertension, rather than idiopathic. *Heart failure with a preserved ejection fraction* - This condition is characterized by dyspnea and edema with normal or near-normal left ventricular ejection fraction. - However, the echocardiogram specifically states **no abnormalities of the left heart**, which would typically show some signs of diastolic dysfunction in HFpEF. The primary findings point to right heart strain.
Pulmonary hypertension Explanation: ***Abnormal elastic properties of the aorta*** - Chronic **hypertension** (11 years) is the #1 risk factor for aortic dissection, causing **cystic medial degeneration** (breakdown of elastic fibers and smooth muscle in the tunica media). - This degenerative process results in **abnormal elastic properties** and weakening of the aortic wall, predisposing to dissection. - The tearing pain, blood pressure differential between arms, and CT findings of intimal flap are classic for **Type B aortic dissection**. - While often associated with connective tissue disorders in younger patients, cystic medial degeneration is also the pathophysiologic result of chronic hypertension in older patients. *Aortic atherosclerosis* - Atherosclerosis primarily affects the **intima** layer, while aortic dissection occurs in the **media** layer. - Though hypertension and smoking contribute to atherosclerosis, this is not the primary predisposing mechanism for dissection. - The underlying pathology is medial degeneration with abnormal elastic properties, not atherosclerotic plaque. *Coronary atherosclerosis* - This affects the coronary arteries supplying the heart, not the aortic wall structure. - Does not explain the anatomical location of dissection or the tearing interscapular pain. - Not a predisposing factor for aortic dissection. *Hypertensive urgency* - This refers to elevated blood pressure without acute end-organ damage. - The patient has **aortic dissection**, which represents acute end-organ damage (hypertensive emergency, not urgency). - While hypertension can precipitate dissection, the underlying **predisposing factor** is the chronic medial wall changes (abnormal elastic properties), not the acute blood pressure elevation itself. *Aortic coarctation* - This is a **congenital** narrowing of the aorta, typically diagnosed in childhood or young adulthood. - Classic finding is upper extremity hypertension with **lower extremity hypotension** (opposite pattern from arm-to-arm differential seen in dissection). - The patient's age, presentation, and 11-year history of essential hypertension make this unlikely.
Pulmonary hypertension Explanation: ***Lipohyalinosis*** - This patient's history of **hypertension** and **diabetes** are major risk factors for **lipohyalinosis**, which leads to **lacunar infarcts** and presents with sudden onset **pure motor hemiparesis**, as seen with the left arm weakness. - The elevated blood pressure of 177/118 mmHg further supports a diagnosis involving **cerebral small vessel disease** secondary to chronic hypertension. *Bridging vein tear* - A bridging vein tear would typically lead to a **subdural hematoma**, characterized by a **gradual onset of symptoms** like headache, confusion, and neurological deficits, often following trauma, which is inconsistent with the sudden onset in this case. - While the patient recently fell off a horse, his symptoms are acute and focal, not typical of the delayed presentation often seen with subdural hematomas. *Cerebellar bleeding* - **Cerebellar bleeding** usually presents with symptoms such as **ataxia**, **nystagmus**, vertigo, and vomiting, along with potential truncal instability, which are not the primary symptoms observed here. - While the patient has some mild abnormality on the finger-nose test, the predominant symptom is **pure motor weakness** of the left arm, making a cerebellar bleed less likely. *Berry aneurysm rupture* - A **berry aneurysm rupture** typically causes a **sudden, severe headache** (thunderclap headache), neck stiffness, photophobia, and altered mental status due to subarachnoid hemorrhage, which are not reported by the patient. - The patient's primary complaint is **focal motor weakness** and mild confusion, not the classic diffuse hemorrhagic symptoms of aneurysm rupture. *Hypertensive encephalopathy* - **Hypertensive encephalopathy** presents with a more generalized and rapidly progressive decline in neurological function, including severe headache, altered mental status, seizures, and visual disturbances, usually with **diastolic blood pressure >120 mmHg**. - While the patient's blood pressure is high, the presentation of **focal motor deficit without severe headache** or global neurological decline makes this less likely than a lacunar stroke due to lipohyalinosis.
More Pulmonary hypertension US Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
Heart failure may present with dependent _____ edema due to increased hydrostatic pressure
Heart failure may present with dependent _____ edema due to increased hydrostatic pressure
pitting
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Question: Heart failure may present with dependent _____ edema due to increased hydrostatic pressure
Answer: pitting
Extra Information: Watch Congestive Heart Failure Clinical Manifestations [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-cardiac/videos/medical-pathophysiology-cardiac-heart-failure-congestive-heart-failure-clinical-manifestations?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/heart-failure?index=2] https://onlinemeded.org/spa/cardiology/heart-failure/acquire?ref=anki
Question: How does ejection fraction change in heart failure with systolic dysfunction? _____
Answer: Reduced EF
Extra Information: Watch Congestive Heart Failure Pathophysiology [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-cardiac/videos/medical-pathophysiology-cardiac-heart-failure-congestive-heart-failure-pathophysiology?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/heart-failure?index=3] https://onlinemeded.org/spa/cardiology/heart-failure/acquire?ref=anki
Question: What is the effect of cardiogenic shock on pulse pressure? _____
Answer: Decreased pulse pressure
Extra Information: Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/cardiac-parameters-of-physiologic-function?index=12] https://onlinemeded.org/spa/surgery-trauma/shock/acquire?ref=anki
Question: The skull, femur, and pelvic bones are most commonly affected in _____
Answer: Paget's disease
Extra Information: Watch Osteoporosis & Paget Disease of Bone [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-musculoskeletal-derm/videos/medical-pathophysiology-musculoskeletal-and-derm-bone-osteoporosis-and-paget-disease-of-bone?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] https://onlinemeded.org?ref=anki
Question: One consequence of renal failure is _____ and _____ retention with resulting hypertension, heart failure, and pulmonary edema
Answer: Na+
Extra Information: Watch Hypertension [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-vascular/videos/medical-pathophysiology-vascular-hypertension-hypertension?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] Watch Chronic Kidney Disease (CKD) [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-renal/videos/medical-pathophysiology-renal-congenital-and-chronic-kidney-disease-chronic-kidney-disease-ckd?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] https://onlinemeded.org/spa/cardiology/hypertension/acquire?ref=anki
Question: Consolidation (lobar pneumonia, pulmonary edema) may present with late inspiratory _____ [sound:30 SO - Bronchial Breath Sounds and Late-Inspiratory Crackles.mp3]
Answer: crackles
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Question: Transudative pleural effusion is characterized by _____ protein content
Answer: low
Extra Information: Watch associated Bootcamp video [https://app.bootcamp.com/med-school/pulmonology/videos/lung-pathology-special-topics?index=10] https://onlinemeded.org/spa/pulmonology/pleural-effusion/acquire?ref=anki
Question: Exudative pleural effusions must be drained due to risk of _____
Answer: infection
Extra Information: Watch associated Bootcamp video [https://app.bootcamp.com/med-school/pulmonology/videos/lung-pathology-special-topics?index=10] https://onlinemeded.org/spa/pulmonology/pleural-effusion/acquire?ref=anki
Question: Kidney stones can lead to severe complications including _____ and pyelonephritis
Answer: hydronephrosis
Extra Information: Watch Hydronephrosis & Urinary Tract Obstruction [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-renal/videos/medical-pathophysiology-renal-urinary-tract-obstruction-hydronephrosis-and-urinary-tract-obstruction?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/nephrology/videos/nephrolithiasis?index=2] https://onlinemeded.org/spa/nephrology/kidney-stones/acquire?ref=anki
Question: The _____ stage of ATN is characterized by tubular re-epithelialization
Answer: recovery
Extra Information: * Results in gradual increase in urine output with high-volume diuresis, decreased concentrations of K, Mg, PO4, and Ca due to slowly recovering tubular function Watch Acute Tubular Necrosis (ATN) [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-renal/videos/medical-pathophysiology-renal-acute-kidney-injury-acute-tubular-necrosis-atn?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/nephrology/videos/kidney-injury?index=8] https://onlinemeded.org/spa/nephrology/acute-kidney-injury/acquire?ref=anki
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