The Audio PANCE and PANRE Physician Assistant Board Review Podcast

Welcome to episode 99 of the Audio PANCE and PANRE Physician Assistant/Associate Board Review Podcast.

Join me as I cover ten PANCE, PANRE, and EOR™ review questions from the Smarty PANCE Instagram/Facebook page and the smartypance.com board review website.

Special from today’s episode:

Below you will find an interactive exam to complement today’s podcast.

The Audio PANCE/PANRE and EOR PA Board Review Podcast

I hope you enjoy this free audio component to the examination portion of this site. The full board review course includes over 2,000 interactive board review questions and is available to all members of Smarty PANCE.

Listen Carefully Then Take the Practice Exam

If you can’t see the audio player, click here to listen to the full episode.

Podcast Episode 99: Ten PANCE/PANRE and EOR Topic Blueprint Questions

1. A 42-year-old male on lithium presents with polyuria, nocturia, and polydipsia. Laboratory findings are remarkable for slightly elevated sodium. Which of the following is the most likely diagnosis?

A. Neurogenic diabetes insipidus

The answer is B. Nephrogenic diabetes insipidus

Nephrogenic diabetes insipidus (DI) is a condition where the kidneys are resistant to the effects of ADH. Nephrogenic DI can occur secondary to lithium toxicity or chronic lithium use, pregnancy, inherited disorders, and electrolyte issues. Clinical features include polyuria, nocturia, and polydipsia. Serum sodium is either normal or high.

In this patient, lithium has entered the collecting duct, accumulated, and interfered with ADH’s capacity to increase water permeability. Treatment options for this patient include amiloride or thiazide diuretics. In general, whether or not lithium is discontinued depends on many factors.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Endocrinology ⇒ Pituitary Disorders ⇒ Diabetes insipidus

Also covered as part of the Internal Medicine EOR and Emergency Medicine PAEA EOR topic list

2. A 50-year-old female presents with poor appetite, low energy, poor concentration, and feelings of hopelessness on most days for the past 3 years. She denies suicidal ideation. She has never had a past manic or hypomanic episode. Which of the following is the best treatment option?

A. Haloperidol

The answer is B. Fluoxetine

This patient has dysthymia, or persistent depressive disorder. The DSM V criteria follow:

Like other psychiatric disorders, symptoms can’t be attributable to drugs, and the symptoms must cause distress/impairment. 1st line treatment is selective serotonin reuptake inhibitors and psychotherapy.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Psychiatry ⇒ Depressive disorders ⇒ Persistent depressive disorder (dysthymia)

Also covered as part of the Psychiatry EOR, Emergency Medicine EOR, and Pediatric PAEA EOR topic list

3. An 85-year-old male with a history of chronic kidney disease presents to the ER with muscle cramps. Laboratory studies reveal potassium of 7.8 mEq/L. EKG reveals peaked T waves. Which of the following is the best initial med to give?

A. Insulin

The answer is E. Calcium gluconate

Hyperkalemia is caused by many things: iatrogenic (ACEI/ARBs), cellular destruction (hemolysis, tumor lysis syndrome, burns), renal failure, adrenal insufficiency, etc. Symptoms are nonspecific and include muscle weakness, N/V, decreased DTRs, etc. Classically on EKG, you may see peaked T waves (there are many other findings though…such as QRS widening, PR interval prolongation, sine-wave, etc). Management for severe hyperkalemia includes calcium gluconate (stabilizes the resting membrane potential of the myocardial membrane), shifting potassium intracellularly (via beta-agonists, sodium bicarbonate, insulin), and removing potassium (via diuretics, kayexalate, or hemodialysis).

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Renal System ⇒ Fluid and Electrolyte Disorders ⇒ Hyperkalemia/hypokalemia

Also covered as part of the Emergency Medicine EOR and General Surgery PAEA EOR topic list

4. A 28-year-old male with sickle cell disease presents to the ER with chest pain, dyspnea, and a cough for the past day. Vitals are remarkable for SpO2 91% and T 102.2F. A CXR reveals bilateral pulmonary infiltrates. On physical exam the patient is alert, speaking in full sentences, and breathing without accessory muscle use. Which of the following is the most appropriate management option for this patient?

A. Surgical consultation, antibiotics, plasmapheresis, IVIG

The answer is B. Pain control, hydration, blood transfusions, oxygen, antibiotics, VTE prophylaxis

The patient has acute chest syndrome (ACS), which is defined as a new radiodensity on CXR with fever and/or pulmonary symptoms. It occurs due to vaso-occlusion in the pulmonary microvasculature, subsequently leading to deoxygenation of hemoglobin and sickling of RBCs. ACS is the main cause of death in patients with sickle cell disease (SCD). About 1 in 2 patients with SCD get ACS.

Patients may present with chest pain, extremity pain, and shortness of breath. Causes of ACS include fat emboli, infection, asthma, oversedation, and post-op issues. Treatment typically includes fluids, oxygen, pain control, blood transfusions, antibiotics, and VTE prophylaxis.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Hematology ⇒ Hemoglobinopathies ⇒ Sickle cell anemia

Also covered as part of the Internal Medicine EOR and Emergency Medicine PAEA EOR topic list

5. Which of the following is the most common cause of bacterial sialadenitis?

A. Bacteroides

The answer is B. Staphylococcus aureus

Bacterial sialadenitis is defined by inflammation of a salivary gland due to a bacterial infection. It is most commonly caused by Staphylococcus aureus. Usually, bacterial sialadenitis happens in the setting of a salivary gland stone (reduced salivary flow leads to bacteria building up in the mouth). Other risk factors include bad oral hygiene and old age. The most common gland affected is the parotid gland.

Clinical features include acute onset of fever, chills, and swelling/tenderness of the affected gland (possible to see purulent drainage). The treatment is broad-spectrum antibiotics: IV ampicillin-sulbactam. Surgical drainage is needed if an abscess develo

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint EENT ⇒ Salivary disorders ⇒ Sialadenitis

Also covered as part of the Family Medicine PAEA EOR topic list

6. A 52-year-old female presents to the clinic complaining of chronic bone pain, constipation, and fatigue. Her last lab results reveal a decline in the glomerular filtration rate. Which of the following is the most likely diagnosis?

A. Acute myelogenous leukemia

The answer is C. Multiple myeloma

The patient has multiple myeloma, which is a clonal proliferation of abnormal plasma cells. It can present with “BREAK” symptoms: Bone pain, Recurrent infections, Elevated calcium, Anemia, and Kidney failure. A serum and urine protein electrophoresis will reveal a monoclonal spike. Other diagnostic studies include a CT or MRI (reveals lytic bone lesions), peripheral blood smear (normocytic anemia in rouleaux formation), and urinalysis (Bence Jones proteins aka free light chains).

The definitive diagnosis is a bone marrow biopsy. Treatment is high-dose chemotherapy with autologous hematopoietic cell transplantation.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Hematology ⇒ Neoplasms, premalignancies, and malignancies ⇒ Multiple myeloma

Also covered as part of the Internal Medicine PAEA EOR topic list

7. A 56-year-old post-menopausal G0P0 female presents to the clinic complaining of abnormal uterine bleeding and weight loss for the past 5 months. Physical exam is unremarkable. Which of the following is not a risk factor for this patient’s likely diagnosis?

A. Nulliparity

The answer is E. Late menarche

The patient has endometrial cancer, the most commonly encountered gynecologic cancer. The cardinal symptom is abnormal uterine bleeding. Other clinical features include pelvic pain, pelvic masses, and weight loss.

Risk factors include conditions or medications that lead to chronically increased estrogen levels, such as nulliparity, tamoxifen, anovulation, and obesity. Early menarche and late menopause would be risk factors, not late menarche.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Reproductive System ⇒ Neoplasms of the breast and reproductive tract ⇒ Endometrial cancer

Also covered as part of the Women’s Health PAEA EOR topic list

8. Which of the following are the two most common etiologies of peptic ulcer disease?

A. H. pylori and NSAIDs

The answer is A. H. pylori and NSAIDs

Peptic ulcer disease (PUD) is a common GI disease defined by a defect in the mucosal lining of the stomach or duodenum. The two most common causes are H. pylori and NSAIDs. Other more rare culprits include Zollinger-Ellison Syndrome, cancer, stress, and radiation. Surprisingly, patients are asymptomatic about 70% of the time. Common symptoms are epigastric abdominal pain, dyspepsia, and bloating. Overall, an upper endoscopy is the best diagnostic test. A biopsy should be done for ulcers with malignant features on all gastric ulcers.

The preferred treatment is PPIs. If H. pylori is the cause, an antibiotic regimen is warranted (e.g., amoxicillin, clarithromycin, and a PPI).

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint GI and Nutrition ⇒ Gastric Disorders ⇒ Peptic ulcer disease

Also covered as part of the Internal Medicine EOR, Emergency Medicine EOR, Family Medicine EOR, and General Surgery EOR topic list

9. A 72-year-old male smoker with a history of cancer presents to the clinic for an annual physical. Vitals are unremarkable. On physical exam, you notice erythema along the course of a superficial vein on his left leg. The area is mildly tender to palpation. The left leg is also larger than the other leg. Which of the following is the next best step?

A. Treat with NSAIDs and warm compresses

The answer is B. Order a duplex ultrasound

The patient has superficial thrombophlebitis, which is inflammation involving a superficial vein along with the presence of a superficial clot. Risk factors include varicose veins, estrogen, prior DVT, cancer, and hypercoagulable states. Clinical features include tenderness, induration, pain, and erythematous skin over a superficial vein.

In many cases, duplex ultrasound is needed to rule out a concurrent DVT (studies show that up to 25-50% of patients with superficial thrombophlebitis have a concurrent DVT). Treatment includes NSAIDs, warm/cold compresses, extremity elevation, and compression therapy. The decision to initiate anticoagulation for superficial thrombophlebitis depends on many factors.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Cardiology ⇒ Vascular Disease ⇒ Phlebitis/thrombophlebitis

10. A 63-year-old male with a history of hepatitis C presents with a pruritic rash located on the flexor surfaces of his wrist. On physical exam, you observe purplish papules with flat-tops. Which of the following is the most likely diagnosis?

A. Atopic dermatitis

The answer is C. Lichen planus

Lichen planus is a skin disorder characterized by a rash associated with the 5 Ps: polygonal, pruritic, papules, plaques, and purple. It commonly affects the wrists and ankles. Lichen planus can also cause the classic Wickham’s striae, which are white-lacelike lines (usually in the oral mucosa). A risk factor is hepatitis C.

A skin biopsy can help confirm the diagnosis. Treatment includes high potency topical corticosteroids. If a patient has an extensive form of lichen planus, then phototherapy, acitretin, or systemic steroids may help.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Dermatology ⇒ Papulosquamous Disorders ⇒ Lichen planus

Also covered as part of the Family Medicine EOR and Pediatric EOR topic list

Looking for all the podcast episodes?

This FREE podcast series is limited to every other episode, you can download and enjoy the complete audio series by becoming a Smarty PANCE member.

I will be releasing new episodes every few weeks. Smarty PANCE is now discounted, so sign up now before it’s too late!

Additional resources and links from the show

This Podcast is available on iOS and Android

Download the Interactive Content Blueprint Checklist

Follow this link to download your FREE copy of the PANCE/PANRE/EOR™ Content Blueprint Checklists

Print it up and start crossing out the topics you understand, marking the ones you don’t, and making notes of key terms you should remember. The PDF version is interactive and linked directly to the individual lessons on Smarty PANCE.

Smarty PANCE is not sponsored or endorsed by, or affiliated with, the NCCPA or the Physician Assistant Education Association (PAEA). All trademarks are the property of their respective owners.

Welcome to episode 98 of the Audio PANCE and PANRE Physician Assistant/Associate Board Review Podcast.

Join me as I cover ten PANCE, PANRE, and EOR™ review questions from the Smarty PANCE Instagram/Facebook page and the smartypance.com board review website.

Special from today’s episode:

Below you will find an interactive exam to complement today’s podcast.

The Audio PANCE/PANRE and EOR PA Board Review Podcast

I hope you enjoy this free audio component to the examination portion of this site. The full board review course includes over 2,000 interactive board review questions and is available to all members of Smarty PANCE.

Listen Carefully Then Take the Practice Exam

If you can’t see the audio player, click here to listen to the full episode.

Podcast Episode 98: Ten PANCE/PANRE and EOR Topic Blueprint Questions

1. An 81-year-old female presents to the ER with acute onset of low back pain. She complains of bowel dysfunction and loss of sensation over her inner thighs. Physical exam reveals decreased lower extremity reflexes. Which of the following is the best diagnostic test for the likely diagnosis?

A. Lumbar radiographs
B. MRI of the lumbosacral spine
C. CSF fluid analysis
D. Scoliosis studies
E. None of the above

The answer is B. MRI of the lumbosacral spine

Cauda equina syndrome is a surgical emergency caused by severe stenosis in the lumbar spine (often due to acute disc herniation).

Clinical manifestations include bowel/bladder dysfunction, decreased lower extremity reflexes, sciatica, saddle anesthesia (loss of sensation over the perineum, buttock, medial aspect of thighs), and decreased anal sphincter tone. Symptoms can develop acutely or chronically.

An emergent MRI of the lumbosacral spine is the preferred diagnostic test. Surgery is the preferred treatment.

Click here to view the Smarty PANCE lesson

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Musculoskeletal ⇒ Spinal Disorders ⇒ Cauda equina syndrome

Also covered as part of the Emergency Medicine PAEA EOR topic list

2. Which of the following is the most common cause of Cushing syndrome?

A. Iatrogenic
B. Bronchogenic carcinoma
C. Pituitary adenoma
D. Adrenal adenoma
E. Obesity

The answer is A. Iatrogenic

Cushing syndrome is a condition defined by too much cortisol. The most common cause of Cushing syndrome is exogenous steroid therapy (i.e., medical providers prescribing steroids). Other causes include a pituitary ACTH-secreting adenoma, adrenal tumors, and ectopic ACTH production from neoplasms. Classic clinical features include buffalo hump, moon-facies, purple striae, easy bruising, weight gain, depression, and weakness.

Laboratory tests will be remarkable for elevated cortisol. Late night-salivary cortisol or 24-hour urinary free cortisol is typically the initial screening test. A low-dose dexamethasone test can be done. Referral to an endocrinologist is usually done at this point (or even prior).

Click here to view the Smarty PANCE lesson

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Endocrinology ⇒ Adrenal Disorders ⇒ Cushing’s syndrome

Also covered as part of the Internal Medicine EOR, Family Medicine EOR, and Emergency Medicine PAEA EOR topic list

3. A 73-year-old female presents with facial flushing, wheezing, and watery diarrhea for a few months. Her symptoms are worsened by certain foods. Which of the following is the best initial diagnostic study to order for the suspected diagnosis?

A. 5-HIAA in urine
B. Serum ACE levels
C. Chest radiograph
D. Upper endoscopy
E. Bronchoscopy

The answer is A. 5-HIAA in urine

Carcinoid tumors are uncommon tumors that originate from neuroendocrine cells and secrete serotonin. The most common site is the appendix, but they can also be found in the lungs, kidney, etc.

Carcinoid syndromes develop 10% of the time; clinical features include flushing, sweating, wheezing, and watery diarrhea. These symptoms are due to the release of serotonin and can be precipitated by foods high in tyramine or ethanol.

The best initial diagnostic study is a 24-hour measurement of urinary excretion of 5-HIAA (Note: 5-HIAA is a degradation product from 5HT). Surgical resection is the definitive treatment of choice.

Click here to view the Smarty PANCE lesson

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Pulmonary ⇒ Pulmonary Neoplasms ⇒ Carcinoid tumors

Also covered as part of the Internal Medicine PAEA EOR topic list

4. Which of the following is the most common cause of Mallory-Weiss Syndrome?

A. Iatrogenic
B. Vomiting
C. Abdominal trauma
D. Hiatal hernia
E. Corrosive ingestion

The answer is B. Vomiting

Mallory-Weiss Syndrome (MWS) is defined by a mucosal tear at or below the gastroesophageal junction. MWS is one of the most common causes of an upper GI bleed. It is most commonly due to forceful vomiting. It is classically associated with alcoholism (binge drinking), but really anything that can cause vomiting can lead to a tear. Other causes include iatrogenic, trauma, hiatal hernia, and corrosive ingestion. Diagnosis is made via upper endoscopy. Intervention is rarely necessary, but if needed, the patient can undergo surgery or embolization. Do not confuse this with Boerhaave syndrome, which is an actual perforation of the esophagus!

Click here to view the Smarty PANCE lesson

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint GI and Nutrition ⇒ Esophageal Disorders ⇒ Mallory Weiss tear

Also covered as part of the Internal Medicine EOR and Emergency Medicine PAEA EOR topic list

5. A 51-year-old male presents to the clinic complaining of “band-like pressure” around his head. He has been more stressed lately. Which of the following is the most likely diagnosis?

A. Cluster headache
B. Migraine with aura
C. Sinus headache
D. Tension headache
E. Medication overuse headache

The answer is D. Tension headache

A tension-type headache (TTH) is the most common headache. It usually presents with steady, aching, “band-like” pain that circles the entire head. There may also be tightness in the posterior neck muscles. Precipitants include anxiety, depression, and stress.

You should treat any underlying depression and/or anxiety. NSAIDs and acetaminophen are the first-line abortive treatment options for mild-moderate TTHs. For long-term prophylactic treatment, amitriptyline is preferred.

Click here to view the Smarty PANCE lesson

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Neurology ⇒ Headaches ⇒ Tension headache

Also covered as part of the Internal Medicine PAEA EOR topic list

6. Which of the following physical exam findings would you expect in a patient with mitral regurgitation?

A. Holosystolic blowing murmur best heard at the apex with radiation to the axilla
B. Diastolic blowing murmur at the left upper sternal border
C. Systolic ejection crescendo-decrescendo murmur at upper right sternal border
D. Mid-systolic harsh murmur best heard at the left upper sternal border
E. None of the above

The answer is A. Holosystolic blowing murmur best heard at the apex with radiation to the axilla

Mitral regurgitation (MR) is characterized by a blowing, holosystolic murmur at the apex with radiation to the axilla. It can be acute or chronic. Acute causes include endocarditis and papillary muscle rupture; chronic causes include mitral valve prolapse (MVP), rheumatic fever, cardiomyopathy. The most common cause of MR is MVP.

Remember, regurgitation murmurs will often have blowing sounds, while stenotic murmurs are harsh and rumbling. Diagnosis should be made with an echocardiogram. Treatment (repair vs. replace vs. medical therapy) depends on many factors.

Click here to view the Smarty PANCE lesson

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Cardiology ⇒ Valvular Disorders ⇒ Mitral regurgitation

Also covered as part of the Emergency Medicine EOR topic list

7. Which of the following is not an expected clinical manifestation of polyarteritis nodosa?

A. Kidney failure
B. Livedo reticularis
C. pANCA positive
D. Pulmonary fibrosis
E. Hypertension

The answer is D. Pulmonary fibrosis

Polyarteritis nodosa is a systemic vasculitis of medium-sized vessels (specifically involving the nervous system and GI tract) that leads to thrombi and microaneurysms. It is associated with hepatitis B, HIV, and drug reactions. Clinical features include fever, hypertension, livedo reticularis, abdominal pain, and arthralgias. Remember patients may be positive for pANCA, but are ANCA negative.

A definitive diagnosis is made via biopsy of involved tissue (or mesenteric angiography). What sets polyarteritis nodosa apart from other vasculitides is that it spares the lungs. Treatment includes high-dose steroids. The prognosis is not really good.

Click here to view the Smarty PANCE lesson

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Musculoskeletal ⇒ Rheumatologic Disorders ⇒ Polymyalgia rheumatica

Also covered as part of the Internal Medicine PAEA EOR topic list

8. An 8-year-old female presents to the clinic with her dad. She is complaining of left ear pain and pruritus for the past few days. The physical exam is remarkable for drainage and pain on tragal pressure. The tympanic membrane can’t be visualized. Which of the following is the best treatment option?

A. Oral amoxicillin
B. Neomycin/polymyxin B/hydrocortisone drops
C. Oral cefepime
D. Oral steroids
E. Ciprofloxacin/dexamethasone drops

The answer is E. Ciprofloxacin/dexamethasone drops

The patient has otitis externa (aka swimmer’s ear), which is inflammation of the external auditory canal. The most common bacterial cause is Pseudomonas aeruginosa (~40%). Risk factors include water exposure, trauma, ear devices, and dermatologic conditions. Clinical features include ear pain, pruritus, auricular discharge, pain/tenderness when pressure is applied to the tragus, and hearing loss.

Treatment is topical ear antibiotic/steroid drops. Medication options include neomycin/polymyxin B /hydrocortisone and ciprofloxacin/dexamethasone. **Remember that aminoglycosides are ototoxic and should be avoided when the tympanic membrane can’t be visualized!**

Click here to view the Smarty PANCE lesson

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint EENT ⇒ Ear Disorders ⇒ External ear ⇒ Otitis externa

Also covered as part of the Pediatric EOR, Family Medicine EOR, and Emergency Medicine PAEA EOR topic list

9. Which of the following correctly depicts the typical clinical features of Parkinson’s disease?

A. Pill-rolling tremor, bradykinesia, rigidity, masked facies
B. Loss of declarative episodic memory, apraxia, olfactory dysfunction
C. Visual hallucinations, REM sleep behavior disorder, gait issues
D. Hyperorality, apathy, socially inappropriate behavior
E. None of the above

The answer is A. Pill-rolling tremor, bradykinesia, rigidity, masked facies

Parkinson’s disease is a neurodegenerative disease. Its 3 cardinal features are tremor (“pill-rolling” at rest), bradykinesia, and rigidity. Tremor is the presenting feature in most patients. Other clinical features include hypomimia (masked facies), speech impairment, mood disorders (depression or anxiety), dysphagia, shuffling gait, stooped posture, sleep issues, cognitive dysfunction, and autonomic dysfunction.

It is mainly a clinical diagnosis. When patients respond to dopaminergic drugs, this supports the diagnosis. The mainstay of treatment is levodopa or dopamine agonists (pramipexole, ropinirole). For mild disease, monoamine oxidase type B inhibitors or amantadine can be given.

Click here to view the Smarty PANCE lesson

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Neurology ⇒ Movement Disorders ⇒ Parkinson’s disease

Also covered as part of the Internal Medicine EOR and Family Medicine PAEA EOR topic list

10. A 72-year-old male presents with an abnormal change in bowel habits and fatigue. The physical exam is remarkable for pale conjunctiva and a palpable abdominal mass. His hemoglobin is 10 mg/dL. Which of the following is likely to be elevated?

A. Alpha-fetoprotein
B. CEA
C. CA-125
D. CA 19-9
E. AAT1

The answer is B. CEA

The patient has colorectal cancer (CRC), which is the third most common cause of cancer death in the U.S. The USPSTF suggests screening at age 45 for individuals with an average risk. Patients may present with alarming “red flag” symptoms, a bowel obstruction, or CRC may just be found via routine screening. The most common symptom is a change in bowel habits (~70%). Other symptoms include rectal bleeding, iron deficiency anemia, and pain.

Initial diagnostic tests include colonoscopy, CBC, fecal occult blood testing, and tumor markers like carcinoembryonic antigen (CEA). CEA is more often used for surveillance and not screening though (since its sensitivity for CRC is only 46%).

Click here to view the Smarty PANCE lesson

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint GI and Nutrition ⇒ Gastrointestinal System Neoplasms ⇒ Colon cancer

Also covered as part of the Internal Medicine EOR, Family Medicine EOR, General Surgery PAEA EOR topic list

Looking for all the podcast episodes?

This FREE podcast series is limited to every other episode, you can download and enjoy the complete audio series by becoming a Smarty PANCE member.

I will be releasing new episodes every few weeks. Smarty PANCE is now discounted, so sign up now before it’s too late!

Additional resources and links from the show

This Podcast is available on iOS and Android

Download the Interactive Content Blueprint Checklist

Follow this link to download your FREE copy of the PANCE/PANRE/EOR™ Content Blueprint Checklists

Print it up and start crossing out the topics you understand, marking the ones you don’t, and making notes of key terms you should remember. The PDF version is interactive and linked directly to the individual lessons on Smarty PANCE.

Smarty PANCE is not sponsored or endorsed by, or affiliated with, the NCCPA or the Physician Assistant Education Association (PAEA). All trademarks are the property of their respective owners.

Welcome to episode 97 of the Audio PANCE and PANRE PA board review podcast.

Today is a bonus episode rounding out this fabulous five-part podcast series with Joe Gilboy PA-C, all about cardiac murmurs. In this week’s episode, we continue our discussion of cardiac murmurs with ten PANCE and PANRE murmur questions.

We’ll cover the ins and outs of all the NCCPA content blueprint valvular disorders and learn how to identify and differentiate them from one another.

If you haven’t already, make sure to listen to our previous podcast episodes where we covered tricuspid stenosis, aortic valve murmurs, mitral valve murmurs, pulmonic valve murmurs, and HOCM and MVP.

Below is a transcription of this podcast episode edited for clarity.

[00:00:00] Welcome back, everybody. This is Joe Gilboy. I work with Stephen Pasquini over there at Smarty PANCE. And today is the most dreaded podcast of all because you know what I’m going to do. That’s right. I’m going to ask cardiac murmur questions.

And I know it’s the most dreaded thing in the world. Let’s do this together because what I want to try to do here is make sense of it all. So, let’s just kind of recap some basic rules before we start going down this thing. You know, the previous lectures, what have I been barking about? What’s Joe been saying? First – inspiration, right? Expiration left.

[00:00:40] Inspiration, right? Expiration left. So, with inspiration, the right-sided murmurs sound louder. So that’s the tricuspid and the pulmonic valve regardless of if it’s stenosis or regurgitation. Expiration – left. What am I saying? Everything on the left side sounds louder with expiration, whether it’s aortic or mitral – your call.

[00:01:01] It can be stenotic or regurgitation, it doesn’t matter, but it’ll sound louder. What is squatting? Squatting is a party. So, what are you doing? You’re bringing it all the blood flow back home. And so, if I bring all the blood flow back home, just from a laminar flow physics point of view, I bring more blood flow back home to the heart, more blood flow over a valve specifically with a diseased disease valve, it sounds louder.

[00:01:29] So, right off the bat, squatting will do what? It’s going to make all my murmurs sound louder. That’s the whole point to decrease venous return. In other words, take blood flow away from the heart. What do I do? Well, those are going to be Valsalva and standing. So, what am I doing when I do Valsalva and standing?

[00:01:56] Taking blood flow away from the heart. So, what’s going to happen to all my murmurs when I stand and perform Valsalva? It takes blood flow away from the heart. Exactly. And then hand grip. What did handgrip do? So, in school, what’d you learn about hand grip? Well, it increases afterload, right? So, what they’re really saying to you is this, and this is how I want you to visualize it.

[00:02:18] When I do hand grip, what I’m really doing is this. You’re right. I’m increasing the afterload. But you must stop and think this one out for a second, folks. What’s really in the heart? Which valve must fight afterload?

[00:02:39] Say you increase the peripheral vascular resistance for whatever reason. So, you increase the afterload, who fights it? And your answer will be… oh, wait for a second, Joe, that’s the aortic valve in the left ventricle. Exactly. So, when I perform handgrip, who am I really challenging? Oh, I’m challenging the aortic valve and everything behind it.

[00:03:00] Exactly. So that’s the point I need inside your head? Then remember our last podcast was about our low-volume lovers. Who were our low-volume lovers? Who were the special needs murmurs that really like low volume? They’re like, hey, I like low volume, not high volume. I like low volume. Who was that?

[00:03:19] That was HOCM and mitral valve prolapse. What did they both like? They both like low volume. So, they’re the opposite of all my regular murmurs. They go in the opposite direction. All right, everybody got that? I am not going to give you a list of answers. So, what I’m going to do is I want you to listen to what I’m going to say. I’m going to say the test question twice.

[00:03:47] And then I want you to pause the podcast. Just put it on pause and think about your answer before I explain it. All right. Is everybody with me? Because that’s the best thing to do. All right, here we go.

Murmur Question #1:

[00:04:11] You have a 76-year-old gentleman that presents to your emergency room and comes in complaining of shortness of breath and chest pain on physical exam. You notice an upper sternal murmur that sounds louder with squatting and goes away with hand grip—one more time. Upper sternal border, sounds louder with squatting, and goes away with hand grip. Who am I?

[00:04:45] So upper sternal border. This will be my aortic and pulmonic area. Well, it goes away with handgrip. So, who’s that going to be? So, what happens with hand grip? I increase my afterload. Which valve fights the afterload? The aortic valve. It’s not pulmonic because the pulmonic valve is not fighting the afterload; it is fighting the lung. So, this has to be aortic stenosis, which makes sense for the syncope and the shortness of breath. So aortic stenosis is going to do what? Well, squatting, that’s a party. Of course, it will sound louder. We could actually throw expiration in here as well, couldn’t we? We sure could, but it’s the handgrip. That differentiates it, doesn’t it? Because the handgrip made the murmur go away. And what did the handgrip do? I keep telling you I want you to view handgrip like sitting on your aortic valve, and you can barely open up squeak, squeak, squeak, squeak.

[00:05:47] You can barely open up. Now imagine sitting on that valve. Can it open up now? And you’re like, no, it goes away. Exactly. And that’s the point I’m trying to make. The answer is aortic stenosis.

Murmur Question # 2

[00:06:21] I have a 45-year-old gentleman who comes in with shortness of breath and chest pain. The murmur sounds louder with inspiration. It’s located at the upper sternal border. And I am also noticing that the patient has right ventricular hypertrophy and right bundle branch block on EKG. Who am I?

[00:06:44] Upper sternal border. Well, who are we talking about? The aortic valve or the pulmonic valve. Inspiration → right and expiration → left. So, this murmur sounds louder with inspiration, so I know that this is on the right side. Then it’s got to be the pulmonic valve. And now they’re telling me I’ve got right ventricular hypertrophy and right bundle branch block. Then blood must be backing up into the right ventricle.

[00:07:10] In other words, something must be backing up, which means the valve must be stenotic. Oh, I see your point. It’s stenotic, and the right ventricle is going to hypertrophy. Remember if you take right ventricular hypertrophy and let it go unopposed. You stretch, and you stretch, and you stretch, and you stretch, and you dilate, and you stretch, and you dilate and stretch that wall.

[00:07:28] What are you going to get? The wires are going to get busted. That’s right bundle branch block. For those of you thinking outside the box, and you’re telling me, Joe, if I dilate my left ventricle and just stretch it and stretch and a bust, the wires, I get left bundle branch? Exactly. No, that’s exactly what you’re going to get. So the answer to the question is pulmonic stenosis.

Murmur Question # 3

[00:07:45] You have a young 32-year-old female who recently immigrated to the United States from Indonesia and is currently working and has now been complaining of increasing shortness of breath at work. On exam, you hear a murmur at the left sternal border. It sounds louder with expiration and appears to be diastolic in nature. Who am I?

[00:08:38] So again, left sternal border. So that’s just about everybody but the pulmonic valve. The murmur sounds louder with expiration, so you know it will be on the left (louder with inspiration → right and louder with expiration → left). So, based on these parameters, I know I’m dealing with either the aortic valve or the mitral valve, and I am a diastolic murmur. So now you have to stop and think. So, this seems to be in the neighborhood of the mitral area, and it’s a diastolic murmur.

[00:09:00] So it can’t be mitral regurgitation. It has mitral stenosis, and that’s the correct answer. And then, of course, as I always say, you’ll see the test questions, do this all the time. They’ll talk about people who immigrated to the United States. And what they’re really saying to you is this. So, this lady most likely has some form of rheumatic fever.

[00:09:16] Maybe she had strep when she was a younger child and just wasn’t diagnosed. So, what they’re really sharing with you is this. As soon as I see the word immigrant, what they are really saying is this: Listen, this person is at high risk for TB. All right. That’s the one thing that we kind of worry about.

[00:09:29] The second thing is that their care is not as structured as ours. In other words, they slipped through the cracks. Could this patient have had a previous strep throat and had rheumatic fever, which led her to the mitral stenosis? Of course, she could.

[00:09:44] And that was the whole point to it. But again, it is expiration → left, left sternal border. Just about everybody is at the LSB, so that doesn’t really help. But it was on the left side. So, I know this is either going to be aortic or mitral. And then you told me it was diastolic, so this will fit mitral stenosis.

[00:10:06] So, just trying to get you to look at these murmurs differently. That’s all just more from a laminar flow physics point of view.

Murmur Question #4

[00:10:15] Next question. I have a 67-year-old female who comes in with an upper sternal border murmur. This murmur increases in intensity when she is squatting, and with handgrip, it decreases intensity with Valsalva and standing.

[00:10:41] One more time. This murmur increases in intensity with squatting and handgrip and decreases in intensity with Valsalva and standing. Who am I?

[00:10:54] So let’s think about this upper sternal border. So, what are we talking about? Pulmonic or aortic. They didn’t tell me what side right or left did they? However, they told me that this murmur increases in intensity with squatting – that’s everybody. So that’s not helping me, but they said it increases in intensity with hand grip. Stop. No stop right here.

[00:11:06] Handgrip, who’s that challenging? Pulmonic or aortic? Oh, that’s aortic, Joe. I see your point. That makes so much sense. It’s not pulmonic. So, this is going to be either aortic stenosis or aortic regurgitation.

[00:11:28] Well, let me think about this. You’re telling me that this murmur sounds louder with handgrip, and wait a second, it’s not shutting it off. It’s making it worse. This means that the valve is wide open. Oh, then this must be aortic regurgitation, and that’s the correct answer. And of course, you know, my low volume maneuvers – Valsalva and standing, of course, will make it go away. The answer is aortic regurgitation.

[00:11:51] So does everybody see this? I’m just trying to get you ready for the PANCE. But does every see how we’re looking at this now? This is what I keep hammering away at, approach this not from a memorization point of view but a laminar flow physics point. Stop memorizing!

[00:12:07] Start trying to make sense of this because once you make sense of this, it will flow so much easier for you. Ignore those things you memorized in PA school, those little four squares, the graphs, etc.. I’ve seen it all in my 30 years of teaching. You can’t teach me one more trick. And I laugh when I’m sitting here in my studio saying this to you because I know students better than students know students. And I get it, but I’m just trying to teach you what will help you the most on the boards.

Murmur Question #5

[00:12:36] Next question. I have a patient who is a 72-year-old gentleman with hypertension, diabetes, and coronary artery disease, who also smokes. He comes in complaining of increasing shortness of breath and bilateral leg swelling. He’s got a murmur noted on physical exam in the upper sternal border. The murmur sounds louder with inspiration. Squatting makes it sound louder. Standing and Valsalva make it go away. And this murmur appears to be diastolic in nature. Who am I?

[00:13:31] Upper sternal border (pulmonic and aortic area) and louder with inspiration. So, I’m on the right (inspiration → right and expiration → left). This has got to be pulmonic. So, it’s going to be pulmonic stenosis or pulmonic regurgitation. He’s a smoker. So, he’s got some pulmonary hypertension. I get it. And this is a diastolic murmur. So, what pulmonary valve disorder is diastolic?

[00:13:51] You’re going to go, oh, this has got to be pulmonic regurgitation. Exactly and wait a second. Oh, that makes so much sense. All that pulmonary hypertension, with COPD and stuff like that. Oh, that makes so much sense. And then he’s going to have to fight it. And, of course, everything is going to back up into the right ventricle and then go to his legs. The answer is pulmonic regurgitation.

Murmur Question #6

[00:14:27] Next question. I have a 37-year-old female with a previous history of mitral valve prolapse.

[00:14:33] However, recently, she’s been coming in with increasing shortness of breath and was diagnosed with atrial fib. Physical exam shows a murmur that increases with squatting and sounds louder with handgrip. And this murmur increases in intensity in the left lateral decubitus position. This murmur also decreases in intensity with Valsalva and standing. Who am I?

[00:15:10] One more time. The murmur increases intensity with squatting. Also, hand grip, also left lateral decubitus position, and decreases in intensity with Valsalva and standing. Who am I?

[00:15:31] All right. So, let’s think about this, she had a previous history of mitral valve prolapse. I got it. But now she’s got increasing shortness of breath and a fib – oh something went wrong.

[00:15:41] Do people with mitral valve prolapse get a fib? No, not at all. And so now this murmur is going to increase in intensity with squatting so that’s not helping me, but the hand grip, it increases with hand grip. So, wait a second. Let me think about this. So, there I am handgrip sitting on the aortic valve, which means the left ventricle has got to fill up with more blood and the left ventricle is going to contract with more blood.

[00:16:07] And then that mitral valve that should stay closed is actually blowing right on through. And if I put them in that left lateral decubitus position, that’s bringing the mitral valve to the surface. So let me think about this for a second, Joe. Hold on here. So, you’re telling me that the left lateral decubitus position brings the mitral valve to the right?

[00:16:31] So whether it be mitral stenosis or mitral regurgitation, that’s the maneuver, it’ll bring it closest to the chest. So, you hear it better. And we could argue expiration in this question, but this clue wasn’t given to me here. And does everybody see the most common cause for mitral regurgitation is actually mitral valve prolapse that goes untreated?

[00:16:48] And that’s how we get it. And then, of course, they start irritating the left atria, which is how they get the AFib. But now, does everybody understand how the handgrip made it worse? Again let’s think about it. Your hand gripping. What are you doing? Increasing the pressure behind the aortic valve.

[00:17:05] What’s the left ventricle going to do? Remember the Frank-Starling thing? What did Frank say? When you increase afterload, you’re going to increase preload. What’s the left ventricle going to do? Fill up with more blood. And there’s that mitral regurgitation valve – come and go as you please. Now that left ventricle goes to contract, what’s it going to do?

[00:17:20] Oh, it will push more blood flow against my regurgitant mitral valve. Exactly. And that’s the correct answer – mitral regurgitation.

Murmur Question #7

[00:17:31] Next question. I have this 67-year-old gentleman who comes in complaining of right-sided heart failure. He’s also got some right atrial enlargement, and he also has bilateral lower extremity edema. During the exam you note a mid-diastolic murmur at the left lower sternal border that increases in intensity with inspiration, sounds louder with squatting, and goes away with standing and Valsalva. Who am I?

[00:18:09] Again, mid-diastolic murmur, left lower sternal border, increasing with intensity with squatting and inspiration, goes away with Valsalva and standing. Who am I?

[00:18:30] Let’s think about it. So, what did we get in the question? Well, we got the word inspiration. So, what do we know? Oh, that’s on the right. And then we said left sternal border.

[00:18:39] So who’s that? Everybody. But it’s not the pulmonic valve or the aortic valve. So, who are we talking about if it’s on the right and not the pulmonic valve? The tricuspid valve. And then you told me that it was mid-diastolic. So, wait a second. The tricuspid valve, what’s the diastolic murmur associated with the tricuspid valve? Is this regurgitation or stenosis? Oh, this is stenosis. The answer is tricuspid stenosis.

[00:18:59] What are your low volume maneuvers? Standing and Valsalva. Usually, with these maneuvers, all of the murmurs will go away. The low volume lovers are murmurs that sound louder with low volume. That’s HOCM and mitral valve prolapse.

Murmur Question #8

[00:19:13] Next question. I have a murmur that is holosystolic in nature that is located on the left midsternal border and sounds louder with squatting and inspiration. This murmur also goes away with Valsalva and standing. Who am I?

[00:19:40] One more time. I am a holosystolic blowing murmur. I’m located at the left midsternal border. I sound louder with inspiration and squatting, and I go away with standing and Valsalva. Who am I? So holosystolic means, it’s probably most likely some type of regurgitation and now you’re telling me that it’s on the left midsternal border that’s everybody. But the key piece of information you gave me is inspiration, which means this is right. Which means it’s going to be the tricuspid valve. Now you’re telling me it’s holosystolic, so that can’t be tricuspid stenosis because that is diastolic. So, this is going to be tricuspid regurgitation. The answer is tricuspid regurgitation.  

[00:20:29] Then there’s that thing about the Carvallo’s sign. The increased murmur intensity with inspiration. And then sometimes we see that pulsatile liver. Because everything’s backing up on the right side, so, all that blood flow is going to the liver, and it’s causing it to kind of shake in a way. Sometimes we call it pulsatile.

So again, is everybody starting to understand this?

They’re not going to be nice to you and say, oh, it’s right or left because that gives you too much information.

So again, we’re just going to pull back, and we’re going to use Joe’s basic rules.

Murmur Question #9

[00:21:17] Next question. You have a healthy 24-year-old female sitting on your exam table who comes in with mild lightheaded and dizziness with very little exertion. On physical exam, you notice that she has a murmur when she performs standing and Valsalva; however, this murmur also goes away with squatting. The rest of her physical exams is essentially unremarkable.

[00:21:57] And when you have her perform handgrip, the murmur disappears. Who am I?

[00:22:05] Remember this murmur sounded louder with standing and Valsalva. It went away with squatting, and it went away with handgrip. So, wait a second. You’re going; it went away with squatting? Isn’t squatting a party, Joe, doesn’t that make everybody sound louder?

[00:22:22] It does. Wait a second. I’m back to my special needs murmurs, the ones that like low volume. So, this is either HOCM or mitral valve prolapse. Exactly! So, let me take this one step further. So, you’re telling me if I squat, what do I do again? I’m pushing all the blood flow back home. So, you’re taking the left ventricle and filling it with blood.

[00:22:47] So if I have HOCM, then all that blood will do what? It’s going to push the walls apart. But wait a second, the murmur is going to go away. That makes sense. Wait a second. It went away with hand grip as well? So let me think about this again. Hold on. Handgrip. What’d you do? Oh, that’s right, I increased my afterload. Joe said basically you’re just sitting here on the aorta. What did Frank say? You increase afterload; you increase preload. So, what’s the left ventricle going to do to fight that afterload? Fill it with more blood. And what are the walls going to do? Push apart. That’s HOCM.

You see what you have to remember is that HOCM is not a valve problem. Say to yourself, HOCM is not a valve problem. And if you didn’t get it the first two times, let’s say it a third time, HOCM is not a valve problem. It’s a wall problem. The left ventricle walls are hitting. And so now, does everybody understand, as they’re at rest, what do you want to do to make the murmur louder? You know you want the walls to hit. Just lightly tap, and you want them to hit. So, what’s in between the walls? Blood. So, what makes it sound louder? Oh, standing and Valsalva. Put blood in there, and what will we do with the walls? Push them apart. So how do you put blood in the left ventricle? Oh, I could squat, and I could do hand grip. Exactly. And that’s the whole point I’m trying to make about HOCM. The answer is HOCM.

Murmur Question #10

[00:24:10] Last question. You have a young, healthy 31-year-old female who comes into your clinic, and she’s been complaining of progressive, mild shortness of breath and palpitations. On physical exam, you notice this murmur increases in intensity with Valsalva and standing. You also notice that this murmur goes away with squatting and handgrip. You also note that this murmur sounds louder in mid-systole. Who am I?

[00:25:04] So, let’s think about the information we were given. We were given information that this murmur sounds louder with Valsalva and standing (our low volume maneuvers).

[00:25:13] We also know that this murmur goes away with squatting and handgrip (our high volume maneuvers, and then they give us this mid-systole. So who am I?

[00:25:25] You’re telling me that squatting makes it go away, which means it’s quite the opposite of what we would expect, which means it’s got to be a low volume lover, which is correct because it sounds louder with Valsalva and standing. Also, this murmur is a mid-systolic murmur.

[00:25:43] So wait a second, when I look at my “low volume lover” murmurs, you have to remember there’s really only one low volume murmur. That’s mitral valve prolapse because you remember HOCM has nothing to do with the valves. It has everything to do with the walls. So, you’re like, oh, they’re telling me that this thing sounds louder mid-systole.

[00:26:05] One more time, when is the left ventricular pressure highest? Mid systole. Then there is that redundant mitral valve that has prolapsed, and the valve can’t hold. And then what does it do? The blood blows right on through. And that’s the correct answer – this is mitral valve prolapse.

[00:26:24] All right, listen, I need you to replay this podcast until you get tired of me talking, OK?

[00:26:32] It’s like, oh my gosh, someone put Joe out of his misery, right? Tell him to stop talking to me. And I want you to keep replaying this and replaying this. But most importantly, stop memorizing!

[00:26:46] So let’s go over it again just as a recap.

[00:28:32] Hopefully, I’ve demystified the heart murmur issues for you, and I hope this makes more sense. Like I said, just replay this podcast episde.

Remember what I’ve been trying to teach about inspiration and expiration and squatting and handgrip and all these maneuvers we can do to make the murmur sound louder and disappear. And if you go with that approach, I promise you, no matter how the PANCE comes at you with a heart murmur question – You’re going to nail it.

[00:28:57] If you go at it from the memorization point of view, you will be in a boatload of trouble. Because all the buzzwords are gone and all those kinds of stuff. So listen, it’s been an honor. And it’s always a pleasure to speak with you out there in podcast land. And so right now, I got pixie.

[00:29:13] My rescue dog whose lying on my bed, sitting here, and she’s giving me that look like she wants to go outside for a walk. So it’s time to take my rescue dog out for a walk. All the best, and please, as you’re getting ready for the PANCE, like I said, in the previous podcast, make sure you take care of yourself, take care of your health and take care of your brain.

[00:29:32] All the best, Joe.

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Welcome to episode 96 of the Audio PANCE and PANRE PA board review podcast.

Today is part five of this fabulous five-part series with Joe Gilboy PA-C, all about cardiac murmurs. In this week’s episode of the Audio PANCE and PANRE podcast, we continue our discussion of cardiac murmurs with a focus on Mitral Valve Prolapse (MPV) and Hypertrophic Obstructive Cardiomyopathy (HOCM).

We’ll cover the ins and outs of these two NCCPA content blueprint murmurs and learn how to identify and differentiate them from other types of murmurs.

If you haven’t already, make sure to listen to our previous podcast episodes where we covered tricuspid stenosis, aortic valve murmurs, mitral valve murmurs, and pulmonic valve murmurs.

Hypertrophic Obstructive Cardiomyopathy (HOCM) is a cardiac abnormality that leads to the muscle in the wall of the heart growing and thickening to the point that it blocks blood flow exiting the heart.

The condition can be mild or severe, and it can lead to a variety of symptoms, including shortness of breath, chest pain, and irregular heartbeat. Complications may include heart failure, an irregular heartbeat, and sudden cardiac death.

HOCM is a hereditary condition, and it is usually diagnosed in adulthood. There is no cure for HOCM, but treatments are available to manage the symptoms and help reduce the risk of complications. With proper care, people with HOCM can live long and healthy lives.

*Hypertrophic cardiomyopathy is covered under the PANCE cardiology content blueprint -> cardiomyopathy -> hypertrophic cardiomyopathy

HOCM is also covered as part of the PAEA EOR pediatric rotation -> cardiovascular topic list -> hypertrophic cardiomyopathy

Mitral Valve Prolapse (MPV) is a condition in which the leaflets of the mitral valve bulge or prolapse back into the left atrium during systole. This may cause blood to flow backward into the left atrium, leading to a heart murmur.

In some cases, MPV may also cause symptoms such as fatigue, dizziness, chest pain, and shortness of breath.

While MPV is usually benign, it can occasionally lead to serious complications such as heart failure or stroke.

Treatment for MPV typically involves lifestyle modification and management of symptoms. In severe cases, surgery may be necessary to repair or replace the mitral valve.

*Miral valve prolapse is covered under the PANCE cardiology content blueprint -> valvular disorders -> mitral valve prolapse

Below is a transcription of this podcast episode edited for clarity.

Welcome back, everybody out there in the podcast world. This is Joe Gilboy, and I work with Stephen Pasquini at Smarty PANCE.

Today is part five of our five-part series covering heart murmurs – one of the most dreaded subjects in PA land.

Today we are going to cover what I call the low-volume lovers.

And who are the murmurs that like low blood volumes? In other words’ low blood volumes make these murmurs sound louder? That is Hypertrophic Obstructive Cardiomyopathy (HOCM) and mitral valve prolapse.

So, what is happening with HOCM? Let us go back and view this from a pathophysiology point of view. So what do you have with HOCM?

I have this young adult, and he is going to start exercising. So what is the left ventricle going to do on a typical day during exercise? You will stress out the left ventricle, which can lead to hypertrophy. 

I want everybody to look in the space you are in right now. Maybe you are in a room. Perhaps you are in a car. I want you to look at the volume of this room or car and look at the wall.

Now I want you to imagine that you start working out. You see, the wall will get thicker.

Now, what happens when those walls are thicker, my muscles get thicker. Thus, what is going to happen next? My stroke volume will go up, my cardiac output will increase, and my resting heart rate will decrease. And that is a nice normal day. That is the way it is supposed to work.

This is why aerobic exercise is so good. That’s what your Apple Watch or Fitbit is telling you. They are going, “Hey, we hit the target zone. You’re stressing out your left ventricle.” Your left ventricle will hypertrophy, which is a normal response to exercise.

Your wall will get thicker, but the volume of the room you are sitting in stays the same. Let this marinate for a second. I stress out my left ventricle, and it’s going to hypertrophy. The wall is going to get thicker, with more healthy tissue. My stroke volume will go up, my cardiac output will go up, my resting heart rate will go down, and my exercise tolerance will improve. That’s a nice normal day.

Hi, I have HOCM by genetics, no fault of my own. I was just born with this genetically. I will stress out my left ventricle, except instead of hypertrophying out, with HOCM, I am going to hypertrophy in. 

Okay, please stop and think about what I am saying. Now. See the room you are sitting in, that wall. It is coming in. Not out, but in. Look at the volume. You have in your room now. What have you done? You have decreased the volume (the size) of your room.

Now, since I have less volume, what is the last thing you want to take away from me? Volume? So what drug is contraindicated in HOCM? Diuretics!

The last thing I want to do is have these walls hit with low volume and a high pulse. That’s when bad things can happen. This is the VTACH and the VFIB that you see these young athletes with HOCM die from.

So, these walls get thick and come in and make my room smaller. So, the last thing I want to do is take volume away, and the last thing I want to do is give them a diuretic.

What is a lifestyle thing I can tell my patients with HCOM to do? Drink more water! This will increase the volume, and the walls to be pushed apart. Does everybody see that? 

Okay, my patient with HCOM is sitting at the edge of the bed at rest. He is not exercising, and he does not have an elevated pulse and low volume – that’s that nightmare scenario we were talking about where a patient with HOCM is exercising, and they have low volume. They are sweating, and their pulse is high. Now the walls hit, and this is when the bad things happen.

So, I have this patient sitting at the edge of the bed in an exam room at rest. Remember, HOCM is not a valvular issue. No valve is not functioning correctly here. These are walls that are enlarged (hypertrophied).

Now I want to hear the walls hit each other while my patient with HOCM is at rest. That’s all I want. I want the walls to hit. What is in the way between those two walls? Blood!

If I want the walls to hit, I have to get the blood out. I can do this with my low-volume maneuvers. What are my low-volume maneuvers? Standing and Valsalva. 

When I have HOCM, if I perform standing and Valsalva (the low volume maneuvers), I can get the blood out of the way so walls can get closer and hit. So, what makes the murmur of HOCM sound louder? Standing and Valsalva.

How do I push the walls of the ventricle apart? I can add more blood. How do I add more blood? If I squat! That is right; squatting is a party. If I go in there and squat and all this blood comes running back home, what will I do with the walls of the left ventricle? I am going to push them apart.

So, this is the opposite of all those murmurs I learned about! This is why I call HOCM and MVP the low volume lovers – because they like low volume. 

Let us take it one step further. Let’s do that one maneuver everybody hates out there in the podcast world: Handgrip.

Okay, think about it. Stop memorizing. Let’s make sense of this.

So, we perform handgrip. What am I doing? I am sitting on the aortic valve. You sat on the aortic valve and added more pressure to the valve by doing this. You have added more afterload.

What is the left ventricle going to do? Well, since I have more afterload, I need more preload. So, my ventricles are going to have to fill up more. With the increased volume, the walls will move apart from each other.

So, you are telling me that when I squat and put all that blood into the left ventricle, it will push the walls apart? Furthermore, when I do handgrip, it will also cause those walls to move apart because I must increase my preload and increase the volume. Exactly!

So, when I perform handgrip and have HOCM, the murmur goes away.

HOCM summary

This is everything you need to know about HOCM: It is not a valvular issue. To make HOCM louder, you want the volume out so the walls can hit. What are the low-volume maneuvers? Standing and Valsalva. How do you put volume (aka blood) in the room? Standing and handgrip? Exactly. That is precisely how this works.

The next murmur that likes low volume is the murmur of mitral valve prolapse. In comparison to HOCM, this one takes a bit more thought.

To demonstrate mitral valve prolapse put your two hands together like you are making the letter A. 

Okay, see how your fingertips are touching each other. This is how the mitral valve usually closes.

Now point your thumbs in the middle and view your thumbs as the chordae tendineae. They are pulling your fingers down. That is how it works on an average day.

To demonstrate mitral valve prolapse, take your right hand and place it where your metacarpals are – again, kind of like the letter A.

Do you see how your fingers are over the top of the other ones? They do not match up perfectly. This is what we sometimes call a redundant valve. In other words, there is extra tissue, and things are not lining up.

When the left atrium contracts on a normal day, the mitral valve comes down, and everything works as expected. However, we will run into trouble with MVP when the left ventricular pressure is highest. And when is the left ventricular pressure at its highest? Oh, that is right, I memorized that during PA school. It is highest during mid systole. That’s why we get a mid-systolic click – because the valve cannot hold the pressure below it during mid-systole.

That is because the connection is not very good. It is loose. So, the valve pops open during mid-systole, and we call that a mid-systolic click.

How can I crank that pressure up in the left ventricle? Oh, I could exercise. Exactly! This is why we often hear about people with mitral valve prolapse having palpitations with exercise.

Okay. I want the murmur of MVP to sound louder. Think about this. Let us go back to where my hands were in the example above. Remember how my fingers were coming together to form the letter A? Except when I have mitral valve prolapse, my right hand is touching my metacarpals, and I have these extra fingers on top of each other, creating a redundant valve.

So, I want this valve to collapse in on itself. I want it to fall in on itself.

What is down in the left ventricle? Blood. Now we need to get the blood out of there so the valve can fall down on itself. We will need to call in our low-volume maneuvers to do this.

What are our low-volume maneuvers? Standing and Valsalva! Standing and Valsalva are low volume maneuvers and will make the murmur associated with mitral valve prolapse sound louder. 

Now, if I put blood back in the ventricle, can that redundant valve fall down on itself? No, it cannot. So, squatting is a high-volume maneuver that puts blood back into the left ventricle, and it is not going to make the murmur of MVP sound louder because the valve is not going to fall in on itself. However, if I take the blood away, there is nothing down there in the left ventricle, and the valve will fall back down. So mitral valve prolapse is also a murmur that gets louder with low volume maneuvers.

Recap

There is just one more thing we need to cover. The ultimate apex question. Are you ready? Handgrip! With handgrip and HOCM, I could see how by increasing the volume of blood in the heart, the ventricle walls would get pushed apart, and the murmur goes away. Now we will cover handgrip and mitral valve prolapse.

Okay, handgrip, so what did I say? I am sitting on the aorta. Okay. So, what is the left ventricle going to do? I just increased my afterload. This means I also increased my preload.

So what did you do? You just put more blood in your left ventricle! Now you need to push that blood out, and you are pushing out more blood. The mitral valve is prolapsed and does not have a good connection. Is it going to be able to hold? No. So, will I hear the murmur of mitral valve prolapse if I do handgrip? Yes, the murmur of MVP will increase with handgrip.

How do I differentiate the low-volume lovers (MVP and HOCM)? By having the patient perform handgrip. With HOCM, when handgrip is applied, you push the walls of the ventricles apart. With mitral valve prolapse and handgrip, you increase left ventricular pressure, and what happens to the mid systolic click? Oh, it is still there, and if ff anything is louder. Because what did I do? I increased the pressure in my left ventricle.

Come back to this podcast and replay it again when you have a moment. This will make so much sense if you follow my physics, especially the laminar flow physics part.

Remember that HOCM and MVP are low volume lovers – meaning they like low volume – that is when the murmurs sound louder. They are the opposite of mitral stenosis, mitral regurgitation, aortic stenosis, and aortic regurgitation. Those usual players like more blood against the diseased valve.

Remember, in HOCM; it is not a valve issue; it is a wall issue. Mitral valve prolapse is a valve issue, but remember that the valve does not connect very well. It is still there. It works well, but the connection does not hold tight.

Next week we are going to start doing murmur questions.

We have covered aortic stenosis and aortic regurgitation, we went over mitral stenosis and mitral regurgitation, we covered pulmonic stenosis and pulmonic regurgitation, we have learned about tricuspid stenosis and tricuspid regurgitation, and in this episode, we covered what I call exceptions to the rule – which is HOCM, and mitral valve prolapse.

What is next? Test questions – where I will present these murmurs to you in a very ambiguous way, and you will have to figure out which murmur it is.

Take care of yourselves, and stay safe. I will see you soon.

Take care, Joe.

Follow this link to download your FREE copy of the PANCE/PANRE/EOR Content Blueprint Checklists.

Print it up and start crossing out the topics you understand, marking the ones you don’t, and making notes of key terms you should remember. The PDF version is interactive and linked directly to the individual lessons on Smarty PANCE.

Welcome to episode 95 of the Audio PANCE and PANRE Physician Assistant/Associate Board Review Podcast.

Join me as I cover ten PANCE, PANRE and EOR review questions from the Smarty PANCE Instagram/Facebook page and the smartypance.com board review website.

Special from today’s episode:

Below you will find an interactive exam to complement today’s podcast.

The Audio PANCE/PANRE and EOR PA Board Review Podcast

I hope you enjoy this free audio component to the examination portion of this site. The full board review course includes over 2,000 interactive board review questions and is available to all members of Smarty PANCE.

Listen Carefully Then Take the Practice Exam

If you can’t see the audio player, click here to listen to the full episode.

Podcast Episode 95: Ten PANCE/PANRE and EOR Topic Blueprint Questions

1. A 52-year-old patient is admitted with a lower gastrointestinal bleed. He is given 2 units of packed red blood cells. A few hours later the patient develops a fever but has no other symptoms or changes in vital signs. Lab studies reveal no significant changes. Which of the following is the most likely diagnosis?

A. Transfusion-associated circulatory overload
B. Acute immune-mediated hemolytic reaction
C. Transfusion-related acute lung injury
D. Febrile non-hemolytic transfusion reaction
E. None of the above

The answer is D. Febrile non-hemolytic transfusion reaction

The most common transfusion reaction is a febrile non-hemolytic transfusion reaction (FNHTR).

Patients with FNHTR may present with a fever a few hours after receiving packed red blood cells (PRBCs), which is caused by the small number of white blood cells and cytokines that can be found in each unit of PRBCs. Treatment consists of giving acetaminophen and ruling out other causes of fever (e.g., central line infection, urinary tract infection, etc).

Incorrect Answers:

Transfusion-associated circulatory overload (Choice A) occurs when the volume of the transfused component causes hypervolemia.

Acute immune-mediated hemolytic reaction (Choice B) occurs when there are antibodies presented to blood donor antigens. Patients may present with hypotension, fever, or coagulopathic lab abnormalities.

Transfusion-related acute lung injury (Choice C) is due to antibodies reacting with antigens leading to the release of mediators that causes edema in the lungs. Symptoms include fever, hypoxia, and dyspnea.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Hematology ⇒ Immunologic disorders ⇒ Transfusion reaction

2. Which of the following is not a side effect of lithium?

A. Hyperparathyroidism
B. Hypothyroidism
C. Cognitive fog
D. Tremors
E. All are side effects

The answer is E. All are side effects 

Lithium is the first-line treatment for bipolar disorder. It has many side effects that you should remember, such as hypothyroidism, hyperparathyroidism, nephrogenic diabetes insipidus, cognitive fog, and tremors. Lithium levels should be monitored to avoid toxicity.

Remember, bipolar disorder is characterized by the symptoms DIG FAST: Distractibility, Irritability, Grandiosity, Flight of ideas, Activity increased, Sleep deficits, and Talkativeness.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Psychiatry ⇒ Bipolar and related disorder

3. Which of the following best explains the pathophysiology of vasovagal syncope?

A. Increase in parasympathetic signals and withdrawal of sympathetic signals
B. Severe narrowing of the aortic valve
C. Drop in blood pressure upon standing due to inadequate peripheral vasoconstriction
D. Occlusion of the pulmonary artery leading to right ventricle dysfunction
E. Blood accumulation in the brain leading to compression of adjacent brain structures

The answer is A. Increase in parasympathetic signals and withdrawal of sympathetic signals

Vasovagal syncope is the most common cause of syncope. Syncope is essentially transient loss of consciousness due to the lack of cerebral perfusion. Vasovagal syncope is usually triggered by something, such as emotion or stress.

A leading hypothesis of vasovagal syncope is that it is due to an increase in parasympathetic signals and withdrawal of sympathetic nervous signals.

Incorrect Answers:

A drop in blood pressure upon standing due to inadequate vasoconstriction describes neurogenic orthostatic hypotension (Choice C).

Occlusion of the pulmonary artery leading to RV dysfunction is describing a pulmonary embolism, which can lead to syncope (Choice D).

Blood accumulation in the brain leading to compression of brain structures is describing an intracranial hemorrhage (Choice E), which is a (rare) cause of syncope.

Narrowing of the aortic valve aka aortic stenosis (Choice B) can lead to syncope, but again, this is not vasovagal syncope.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Neurology ⇒ Vascular Disorders ⇒ Syncope

Also covered as part of the Internal Medicine EOR, Family Medicine EOR, Emergency Medicine EOR, Pediatric EOR, and General Surgery PAEA EOR topic list

4. A 71-year-old male smoker with prostate cancer presents to your clinic complaining of unilateral leg swelling and pain. Vital signs are unremarkable. On a physical exam, the entire leg is swollen with localized tenderness along the venous system. Which of the following is the next best step?

A. Order a d-dimer
B. Order a duplex ultrasound
C. Admit to the hospital immediately
D. Reassurance and follow-up in 6 months
E. Order a CT angiogram

The answer is B. Order a duplex ultrasound

This patient needs an ultrasound because he has a high pre-test probability for thrombosis. Ordering a d-dimer, in this case, would be inappropriate. Lots of things (e.g., cancer, trauma, etc) can elevate d-dimer.

Well’s Score helps us determine a patient’s risk for DVT based on these criteria: active cancer, surgery or bedridden, calf swelling, collateral veins presence, entire leg swollen, localized tenderness along deep venous system, pitting edema, previous DVT, recent immobilization, & alternative diagnosis more likely.

The main idea: d-dimer should be ordered in low-risk patients, and a venous duplex US should be ordered for high-risk patients.

VIEW BLUEPRINT LESSON

Covered under ⇒ PANCE Blueprint Cardiology ⇒ Vascular Disease ⇒ Venous thrombosis

Also covered as part of the General Surgery PAEA EOR topic list

5. Which of the following individuals would be considered to have a positive purified protein derivative test at 6 millimeters of induration?

A. 31-year-old who was in contact with a person who has active TB
B. 65-year-old intravenous drug user
C. 53-year-old who lives in a prison
D. 90-year-old with hypertension
E. None of the above

The answer is A. 31-year-old who was in contact with a person who has active TB

Tuberculosis (TB) is a worldwide health concern and is deadly. A purified protein derivative (PPD) test can be used to screen for TB. A PPD test is considered positive depending on the patient’s risk factors. Remember, we measure induration, NOT erythema. See below for a high-yield list of positive PPD tests (not exhaustive):

>5 mm: HIV, immunosuppressive condition, or recent contact with active TB case

>10 mm: IVDU, came from a country with a high TB prevalence (<5 y prior), health care worker, resident/employee in a high-risk congregate setting

>15 mm: everyone else

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Pulmonary ⇒ Infectious Pulmonary Disorders ⇒ Tuberculosis

Also covered as part of the Internal Medicine EOR, Emergency Medicine EOR, and Family Medicine PAEA EOR topic list

6. A 48-year-old male presents with headaches, vision loss, enlarged jaw, and enlarged hands. Which of the following laboratory studies is the preferred initial diagnostic test?

A. Beta glycoprotein 2a
B. Growth hormone
C. Prolactin
D. Calcitonin
E. Insulin growth factor 1

The answer is E. Insulin growth factor 1

The patient has acromegaly, which is an endocrine disorder characterized by excess secretion of growth hormone after epiphyseal closure. The most common cause is a pituitary adenoma. Clinical manifestations include coarsening of facial features, enlarged hands/feet, macrognathia, bitemporal hemianopsia, sleep apnea, and headaches.

Insulin growth factor-1 is the best initial diagnostic test to screen for acromegaly. A CT or MRI can help confirm the presence of a pituitary adenoma. A glucose suppression can also be ordered. Definitive treatment is transsphenoidal resection of the pituitary adenoma.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Endocrinology ⇒ Pituitary Disorders ⇒ Acromegaly/gigantism

Also covered as part of the Internal Medicine PAEA EOR topic list

7. A 14-year-old obese male presents to the ER complaining of dull pain in the right hip and thigh for the past few weeks. No history of trauma. On physical exam, the affected leg is held in an externally rotated position and is shorter than the left leg. What is the most likely diagnosis?

A. Legg Calve Perthes
B. Septic arthritis
C. Slipped capital femoral epiphysis
D. Transient synovitis
E. Pelvic stress fracture

The answer is C. Slipped capital femoral epiphysis

The patient most likely has slipped capital femoral epiphysis (SCPE), which is defined as displacement of the capital femoral epiphysis from the femoral neck (through the physeal plate). The classic clinical presentation is hip pain in an obese, adolescent male. Remember, it can be bilateral (~20-40%)!

On physical exam, the affected leg may be externally rotated and shorter than the other leg. Cases are diagnosed via plain radiographs (AP view and lateral views of both hips). Once diagnosed with SCPE, most patients should be made non-weight-bearing and referred to an orthopedic surgeon.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Musculoskeletal ⇒ Lower extremity disorders ⇒ Disorders of the hip ⇒ Slipped capital femoral epiphysis

Also covered as part of the Pediatric Rotation PAEA EOR topic list

8. A 32-year-old male with sarcoidosis presents to the clinic complaining of shortness of breath, fatigue, and palpitations for a few months. His in-office EKG reveals QRS prolongation and some premature ventricular beats. A chest radiograph shows cephalization of the pulmonary vessels and cardiomegaly. Which of the following is the most likely diagnosis?

A. Cryptogenic organizing pneumonia
B. Hypertensive encephalopathy
C. Cardiac sarcoidosis
D. Acute coronary syndrome
E. Pneumoconiosis

The answer is C. Cardiac sarcoidosis

Sarcoidosis is a multisystem granulomatous disorder; it impacts the lungs, eyes, lymph nodes, heart, skin, and nervous system. Cardiac sarcoidosis (CS) is often under-recognized and can occur as a clinical feature of sarcoidosis. Presenting symptoms may include palpitations, syncope, fatigue, & dyspnea.

CS happens because granulomas infiltrate the heart, leading to conduction issues, tachyarrhythmias, cardiomyopathies, & heart failure. Holter monitoring and echocardiography are two helpful tests. The gold standard would be a heart biopsy (not routinely done because it is so invasive; cardiac MRI is preferred). Treatment is steroid therapy and anti-arrhythmic drugs.

Incorrect Answers:

Cryptogenic organizing pneumonia (Choice A) is a type of diffuse interstitial lung disease that typically presents with cough, fever, dyspnea, and malaise.

Hypertensive encephalopathy (Choice B) manifests as headaches, vomiting, confusion, and neurological symptoms. The patient has none of these.

Acute coronary syndrome (Choice D) is more likely to present with diaphoresis and crushing chest pain.

Pneumoconiosis (Choice E) is a fancy word that means the accumulation of dust (e.g., coal, asbestos, etc) within the lungs. This patient has absolutely nothing in his history that suggests this.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Pulmonary ⇒ Restrictive Pulmonary Disease ⇒ Sarcoidosis

Also covered as part of the Internal Medicine PAEA EOR topic list

9. A 64-year-old male presents with tremors in both of his hands. He says the tremors worsen with movement and caffeine. The tremors improve with alcohol use. Which of the following is the best initial treatment option for his likely diagnosis?

A. Dopamine agonist
B. Beta-blocker
C. Alpha antagonist
D. NMDA antagonist
E. None of the above

The answer is B. Beta-blocker

The patient likely has an essential tremor (ET) which is the most common cause of action tremor in adults. It occurs bilaterally in both hands, commonly worsens with anxiety, and improves with alcohol use. The tremor becomes more noticeable when the hands are outstretched or during goal-directed movement (e.g., writing with a pencil).

ET is a clinical diagnosis. Treatment includes beta blockers (propranolol), anticonvulsants (primidone, gabapentin, topiramate) and benzodiazepines. Propranolol and primidone are the most effective treatment options. Remember there is often a strong genetic component (family history is present 30-70% of the time).

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Neurology ⇒ Movement Disorders ⇒ Essential tremor

Also covered as part of the Family Medicine and Internal Medicine PAEA EOR topic list

10. Which of the following is the most common cause of infective lactational mastitis?

A. Escherichia coli
B. Staphylococcus aureus
C. Bacteroides species
D. Staphylococcus epidermidis

The answer is B. Staphylococcus aureus 

Lactational mastitis presents as a red, painful, swollen breast usually during the first three months of breastfeeding. It commonly results from poor drainage. The most common cause is Staphylococcus aureus. If it develops over 24 hours, patients may also have flu-like symptoms and a fever — this is considered “infective” lactational mastitis.

Treatment includes cold compresses and complete emptying of the breasts. For infective lactational mastitis, antibiotics (e.g., clindamycin, cephalexin, dicloxacillin) should be given. Remember, patients should NOT stop breastfeeding.

VIEW BLUEPRINT LESSON

Smarty PANCE Content Blueprint Review:

Covered under ⇒ PANCE Blueprint Reproductive System ⇒ Breast Disorders ⇒ Mastitis 

Also covered as part of the Women’s Health EOR and Emergency Medicine PAEA EOR topic list

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Follow this link to download your FREE copy of the PANCE/PANRE/EOR Content Blueprint Checklists

Print it up and start crossing out the topics you understand, marking the ones you don’t, and making notes of key terms you should remember. The PDF version is interactive and linked directly to the individual lessons on Smarty PANCE.

Welcome to episode 94 of the Audio PANCE and PANRE PA board review podcast.

Today is part four of this fabulous five-part series with Joe Gilboy PA-C, all about cardiac murmurs. In this week’s episode of the Audio PANCE and PANRE podcast, we continue our discussion of cardiac murmurs with a focus on the tricuspid valve.

We’ll cover the ins and outs of tricuspid valve stenosis and learn how to identify it and differentiate it from other types of murmurs.

If you haven’t already, make sure to listen to our previous podcast episode where we covered aortic valve murmurs and mitral valve murmurs, and pulmonic valve murmurs.

The tricuspid valve, or right atrioventricular valve, is a one-way valve that sits between the right atrium and right ventricle of the heart. It is essential for right ventricular filling and for preventing the backflow of blood from the right ventricle into the right atrium when the right ventricle contracts during systole.

When functioning properly, the tricuspid valve is a passive structure that opens and closes in response to the pressure of the blood flowing through the heart.

The right atrium receives deoxygenated blood from the superior and inferior vena cava. The tricuspid valve which separates the right atrium from the right ventricle opens during ventricular diastole, allowing the deoxygenated blood to flow from the right atrium into the right ventricle, and closes during ventricular systole preventing the backflow of blood from the right ventricle into the right atrium as the right ventricle contracts to pump blood into the lungs out through the pulmonary artery.

Tricuspid stenosis is a narrowing of the tricuspid valve or one of its three leaflets.

If the tricuspid valve is narrowed or stenotic, it will not open properly during diastole, increasing the volume of blood in the right atrium. When the right ventricle contracts the stiffened tricuspid valve also fails to close completely and tricuspid regurgitation develops.

Nearly all cases are caused by rheumatic fever.

Below is a transcription of this podcast episode edited for clarity.

Welcome everybody, this is Joe Gilboy PA-C and I work with Stephen Pasquini at Smarty PANCE. Today, we will continue this series on heart murmurs. Today’s topic is tricuspid stenosis.

So, sit back, listen to my voice, and try not to take notes. Don’t do anything other than just listen and follow my logic. I promise you, when this is all said and done, you’ll be looking at heart murmurs and more specifically, tricuspid stenosis in a vastly different light. I want you to view the tricuspid valve. Just think about it. There you are the right atria. The tricuspid valve opens during diastole and closes during systole.

There’s all your blood in the right ventricle, and it goes out through the pulmonary valve to get oxygenated out in the lungs.

So now, I want you to think about this for a second. I have a tricuspid valve that is stenotic. It’s stiff and hard to open.

When are you going to have problems opening this valve? During diastole? Or during systole?

You are going to have problems with this during diastole because that’s when the tricuspid valve is supposed to open up. Because it’s supposed to be closed during systole.

So, it’s a diastolic murmur, it’s considered a mid-diastolic murmur.

Now give this some more thought. Okay, so you’re in the right atria – Is it easier or harder to push through this stenotic valve?

Oh, it’s a lot harder. And so, where’s the blood flow going to back up to? Into the right atrium and now that right atrium, it’s going to have all this increased pressure going into it. So now what are you going to get? You are going to get right atrial enlargement!

Here is another question – If the right atrium is having a tough time pushing blood through the stenotic valve then where’s this extra blood going to back up to? The right side of the body. Exactly! So, I’m going to have JVD and I’m going to get pedal edema? You are going to get right-sided heart failure with tricuspid stenosis.

Can I ask another question? How’s your blood flow to your right ventricle? It is diminished. Well, then how’s your blood flow to the pulmonary area? That’s diminished! How’s your oxygenation? That’s also diminished. So how are you feeling? I’m short of breath. Exactly. And you are short of breath not because you’re in heart failure. You’re short of breath because you’re just not getting blood to oxygenate. Exactly.

So, tricuspid stenosis is on the right side. One more time – Inspiration right. Expiration left. Inspiration right. Expiration left that if you didn’t get it the first two times. Let’s try the third time. Inspiration right. Expiration left.

Hi, I’m tricuspid stenosis, which side of the heart am I on the right or left? I’m on the right. So, tricuspid stenosis is going to sound louder with inspiration. Exactly.

What’s the party maneuver where all the blood flow comes back home and everybody’s just partying as you get more blood flow back home – squatting. What else could make tricuspid stenosis sound louder? Squatting! Exactly!

Squatting is a high-volume maneuver and will make the murmur of tricuspid stenosis sound louder. 

What are my low-volume maneuvers? What are the maneuvers that take blood out of my heart? Standing in Valsalva!

So, what would make tricuspid stenosis go away? Standing and Valsalva are low volume maneuvers and will decrease the sound of tricuspid valve stenosis.

So, I have a right-sided heart murmur. It’s diastolic and is considered mid-diastolic. Where am I going to put my stethoscope?

You see, there’s only one thing on the right – that’s the aortic valve at the right second intercostal space, right that we all memorized in school. So, everybody’s on the left.

The left upper sternal space – that’d be pulmonic. But what is on the left – everybody else?

So hi, you’re the tricuspid valve, where are you? I’m on the left… Exactly! You’re going to be on the left at the lower sternal border.

So now I have this mid-diastolic murmur. Left sternal border that sounds louder with inspiration => goes away with expiration => left. It’s going to sound louder with squatting and is going to go away with standing and Valsalva – these are my low volume maneuvers.

And how did you get this? Usually, the most common cause of tricuspid stenosis is rheumatic fever, is it not?

So now, let’s pull back, and let’s look at this from 30,000 feet.

When you get to the boards (on your PANCE or PANRE) I want you to forget about brute memorization and all these buzzwords.

Just pull back and try to make sense of this from a laminar flow physics point of view.  If you do it this way, you’ll always do great.

In the real world when we hear a heart murmur what’s the first thing we do? We order an echocardiogram to figure it out. But what I’m really trying to get you ready for is your boards.

So, on the boards, they give you a patient with a murmur at the left sternal border murmur and they’re going to talk about how it gets louder with inspiration, which means okay, it’s going to be on the right.

Or they say the murmur gets louder with expiration so it’s going to be on the left.

I want you to start viewing it this way. Not the way that you memorized it in school with all the PowerPoints and all the other mnemonics. I’ve seen every mnemonic known to man in my 30 years of teaching, so I don’t want to go down that rabbit hole.

So now that we understand the physics hopefully this makes more sense and I hope this helps you better understand the murmur of tricuspid stenosis better.

And next week, what are we going to do guys? Oh is going to be tricuspid regurgitation. And don’t worry about the following week. Oh, that’s going to be a fun day. That’s when I start asking you test questions and we start trying to pull this all together.

So once again, it’s an honor. It’s an absolute pleasure to speak to all of you. Be safe out there, be healthy, and most importantly take care of yourself. I will talk to you soon.

Joe Gilboy PA-C

This episode was transcribed for your reading pleasure by Stephen Pasquini PA-C

Why is it all in there

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Follow this link to download your FREE copy of the PANCE/PANRE/EOR Content Blueprint Checklists.

Print it up and start crossing out the topics you understand, marking the ones you don’t, and making notes of key terms you should remember. The PDF version is interactive and linked directly to the individual lessons on Smarty PANCE.

Welcome to episode 93 of the Audio PANCE and PANRE physician assistant/associate board review podcast.

Today is part three of this extraordinary five-part series with Joe Gilboy PA-C, all about cardiac murmurs. In this week’s episode of the Audio PANCE and PANRE podcast, we continue our discussion of cardiac murmurs with a focus on the pulmonic valve.

We’ll talk about the different types of murmurs (stenosis and regurgitation) that can occur with the pulmonic valve and how to differentiate them from other types of murmurs. If you haven’t already, make sure to listen to our previous podcast episode where we covered the aortic valve murmurs and mitral valve murmurs.

Pulmonic valve stenosis (PVS) and pulmonic valve regurgitation (PVR) are two common heart valve diseases. PVS is a narrowing of the pulmonic valve, while PVR is leakage of blood back through the pulmonic valve. Both conditions can lead to significant heart problems if left untreated.

PVS is the most common congenital heart disease, affecting approximately 1 in 1000 people. It can lead to right heart failure and/or pulmonary hypertension (high blood pressure in the lung arteries). PVS is caused by an abnormally thickened pulmonic valve or localized stenosis which means that it has a narrowing of the valve. Pulmonic valve stenosis has several different causes including:

Symptoms of PVS can vary depending on the type of stenosis that is present and how much it has advanced. Mild cases may not cause any symptoms at all; however, it is common for patients to experience breathlessness, fatigue, chest pain, and palpitations.

Heart sounds include increased splitting of S2 and a harsh crescendo-decrescendo ejection murmur heard best at the left parasternal 2nd or 4th intercostal space when the patient leans forward; the murmur grows louder immediately with Valsalva release and with inspiration.

People with PVS may need to take some medication to ease their symptoms. For example, diuretics can help remove excess fluid; beta-blockers reduce the workload on the heart and therefore lower blood pressure and heart rate, and long-acting calcium channel blockers can reduce the force of contraction of the heart’s left ventricle.

Pulmonary valve replacement is an effective treatment for severe PVS, which involves surgically implanting a new pulmonary valve to replace the defective one. Because the valve only affects the blood flow through one part of the heart, this surgery can often be carried out using minimally invasive techniques.

For milder cases of PVS that do not cause symptoms then medication or exercise may be prescribed instead. Regular exercise helps to strengthen the left ventricle (the main pumping chamber) which is important for people with PVS. For more information, view our lesson on pulmonary stenosis.

Pulmonic valve regurgitation is leakage of blood back through the pulmonic valve.

It can lead to right-sided heart failure and/or pulmonary hypertension (high blood pressure in the lung arteries). This means that it has a leakage of the valve.

It can be caused by any condition that impairs cardiac function, including pulmonary hypertension (the most common cause), chronic obstructive pulmonary disease (COPD), left ventricular hypertrophy (LVH), and heart failure (HF).

Although 5-8% of the general population has PVR, it is more common in COPD and other respiratory diseases, such as bronchiectasis.

Pulmonary valve regurgitation is an important determinant of functional class and quality of life among patients with chronic obstructive pulmonary disease (COPD), who have a higher incidence of this valvular disease than the general population. It appears to be more frequent than traditionally thought and its impact on patient survival is greater than previously estimated.

Heart sounds when PR is due to pulmonary hypertension include a high-pitched, early diastolic decrescendo murmur that begins with P2 and ends before S1 and that radiates toward the mid-right sternal edge; it is heard best at the left upper sternal border while the patient holds the breath at end-expiration and sits upright.

The murmur of PR without pulmonary hypertension is shorter, lower-pitched, and begins after P2.

Treatment is directed at the cause; valve replacement is usually not needed.

Below is a transcription of this podcast episode edited for clarity.

Click here if you are unable to view the audio player.

Welcome back, everybody. This is Joe Gilboy PA-C, and I work with Stephen Pasquini PA-C at Smarty PANCE. Today, we will cover the dreaded two words that all PA students hate. What are these dreaded words?

We’ve covered the aortic valve. We’ve covered the mitral valve. Who’s the next one up?

Okay. So, let’s erase everything we memorized in school.

Most of you are chuckling right now and saying Joe, it’s already erased, right? I’m sure it is.

So, let’s do it my way. I want you to pull back and forget everything you already know.

What’s the pulmonary valve supposed to do on a typical day? Let’s think about this. The right ventricle contracts and the pulmonic valve is supposed to open up. Then, that deoxygenated blood goes out to the pulmonary vasculature.

And then, on a normal day, the pulmonic valve closes during diastole to keep the blood out in the pulmonary area, and then that deoxygenated blood becomes oxygenated.

So, that diagram that you see in the books where the blood is blue, deoxygenated, then becomes oxygenated and red. And then it comes back to the pulmonary vein and back to the left atria, left ventricle, and up to the rest of the body, it goes. So that’s a nice normal day.

And where is the pulmonic valve located? Well, there’s only one valve on the right. That’s the aortic valve. Everybody else is on the left. So, where is the pulmonic valve? The left upper sternal border.

Pulmonary Stenosis

Okay, I want you to stop and just pull back and think, just think, and stop memorizing.

So, I have this stenotic pulmonary valve, and it’s hard to open up.

When am I supposed to open up? During systole. Does a stenotic pulmonic valve open up easily during systole? No, it has a hard time. So, when are you having difficulty with this valve? During systole. Because during diastole, it’s supposed to close. That’s what it wants to do. It wants to stay closed.

So, I don’t have a problem during diastole. I have a problem with systole. So, pulmonary stenosis is going to be a systolic ejection murmur.

So, here’s my question to you. Where’s the blood flow supposed to go? It’s supposed to go to the pulmonary area. Alright, stop and think about this for a second.

I’ve got a lack of blood flow to my pulmonary area. Lack of it. How is your oxygenation now? It’s pretty poor. So how are you going to present? I will be short of breath.

Imagine I go to walk up a flight of steps.  I’m walking down the aisle in Costco. I’m completely tanked out. I am short of breath – I lack so much oxygenation I become syncopal; maybe I lack so much oxygen to my heart I have angina. You’ve got a lack of oxygenated blood because the right ventricle can’t get that blood past that valve.

And now, let’s pull back. Remember from the last podcast that S1 is the date between the mitral and the tricuspid valve, and S2is the date with the aorta and pulmonary valve.

Hi, I’m pulmonary stenosis, and I’m taking longer to open up. How’s your S2?

Well, I’m kind of late to the date. Yes, you are because you’re taking longer to open up. So how is your S2 in pulmonic stenosis? It’s split!

Do you now see what the split S2 means? Either I’m aortic stenosis or pulmonic stenosis – someone’s late to the date because it’s taking longer to open up.

Now that I know I have a split S2, I need more information to determine if this is aortic or pulmonic stenosis. But imagine (on the exam) they give you a split S2, and I’m on the right side – that’s aortic.

Now imagine having a split S2, and I’m on the left? Oh, that’s pulmonic. And now give this some thought. Okay, you’ve got this stenotic pulmonic valve, and I can’t get blood out. So, of course, I’m short of breath.

Can I ask you a question? Just give this some thought. Ready?

Hi, you have a stenotic pulmonic valve. Where’s the blood flow back up to? The right ventricle!

OK, so you’re the right ventricle. What are you going to do with all this extra blood? I’m going to dilate, and I’m going to get right ventricular hypertrophy.

And now imagine, if you can, that right ventricle gets bigger and bigger and bigger – stretching, stretching, stretching, stretching, stretching, stretching your right ventricle wall. Can I ask you a question? Can I bust those wires in the right ventricular wall? Yes, I can!

Welcome to right bundle branch block. So, could I get a right bundle branch block with pulmonary stenosis? Yes, I can.

And that’s precisely what we see with pulmonary stenosis.

So, pulmonary stenosis.

Imagine you are given a question, and the patient has a systolic ejection murmur on the left side of the sternal border. There is a split S2, and the patient is short of breath. Maybe they are lacking so much blood flow they get syncopal.

What’s the diagnosis? You have all the information you need. It’s pulmonic stenosis!

Now let’s make the murmur sound louder.

Okay, back to our first podcast on murmurs. What’s the maneuver that makes all the blood flow go back home? Squatting, squatting is a party. So, if I bring more blood flow back home, just laminar flow physics, the more blood flow I have against the murmur, the louder it sounds – so squatting. That’s a party, and squatting makes the murmur of pulmonic stenosis sound louder.

Remember this: Inspiration, right = Louder and Expiration, left = louder. Inspiration right => Expiration => left

The pulmonic valve is on the right side, so inspiration will make the murmur of pulmonic stenosis sound louder, and the murmur of pulmonic stenosis would go away with expiration.

What are low-volume maneuvers? Standing and Valsalva. So, if I stand or Valsalva, the murmur of pulmonic stenosis goes away.  

So, let’s recap once again:

Okay, so let’s just stop and think about this for a second.

Regurgitation – come and get goes you please, I could care less, my doors are always open. I’ve got regurgitation, and I have an open door, and I can come and go as I please.

So now think about it. During systole, should I be open? Yeah. But diastole, am I supposed to be closed? Oh, yes, I am.

But remember, in pulmonary regurgitation, you’re coming and going as you please. You’re supposed to be closed, but you’re not. So, this is a diastolic murmur, and it’s going to go from the left upper sternal border down to the apex. That’s just physics.

Can I ask you a question? That blood flow, where was it? Well, Joe, it was out in the lungs. Exactly. And so now what are you doing? I’m taking blood flow away from our lungs.

Is anybody late to the date? No, not at all. So that’s going to be okay.

So, it will be a diastolic murmur, and it will decrease. It will be loud in the beginning, and then, of course, as the right ventricle fills up, it’s going to sound less. So, it’s going to be considered a diastolic, decrescendo murmur.

But now I want you to stop and think about this because this is where a lot of the test questions come from.

Okay, so I have to blow through the pulmonic valve, right? Yeah. Okay, so let me think about this.

So, I have to push so hard push against the pulmonic valve that it blows open. So, I could see how right ventricular hypertrophy could cause that.

What does your right ventricle push against? It’s the pulmonary vascular.

I’m going to get pulmonary hypertension. See it? Who’s going to push hard against pulmonary hypertension? You’re like, oh, it’s the pulmonary valve on the right side. Is it built for high blood pressures? Yes, or no? And the answer is no.

So, you tell me if I get right ventricular hypertrophy due to pulmonary hypertension, I may blow my pulmonic valve? That’s precisely what’s going to occur.

What’s the most common cause of pulmonary regurgitation? Pulmonary hypertension because my right ventricle will hypertrophy, and I have to push harder. Exactly. The most common cause of pulmonary regurgitation is pulmonary hypertension.

Now, we can get to this argument of what causes pulmonary hypertension. CHF is a common cause.

Everybody’s on Adderall. What’s one of the side effects of Adderall? Pulmonary hypertension. And then here you are the pulmonary valve fighting, Adderall, and you’re like, Dude, that’s pulmonary hypertension out there. I have to push harder. Then you get right ventricular hypertrophy. And then what could I eventually get blowing through the valve? Pulmonary regurgitation!

What are the most common things that we see in people on Adderall? Pulmonary hypertension and pulmonary regurgitation.

So, when I start to fill in that right ventricular, and it hypertrophies due to all that pulmonary hypertension, I will push hard against your pulmonary valve. I can push so hard that I push right through it. Then what do you get? Pulmonary regulation.

Who was pulmonary stenosis? That was a systolic ejection murmur left upper sternal border, right ventricular hypertrophy, right bundle branch block.

This could be congenital. We see with tetralogy of Fallot.

And then we saw pulmonary regurgitation. What was that? It was a diastolic crescendo/decrescendo murmur. As the right ventricle filled up, it started tailing off, henceforth the word decrescendo.

Remember, what caused me to blow through my pulmonary valve? The right ventricle got so big that it just blew through because the pressure was so high. And remember, I’m the pulmonary valve. I’m not built for high blood pressure.

What was my right ventricle fighting the whole time? Pulmonary Hypertension. So, who was that? Well, that could be the Adderall. That could be the Fen-Phen. And then here’s the point. I don’t want you to forget.

Can I ask you a question? Who’s the vasoconstrictor everywhere?

What is nicotine? Nicotine is a drug. What is it? A vasoconstrictor? Where does it vasoconstrict? Everywhere! Who has the highest incidence of hypertension? Smokers!

What is the most common cause of coronary disease? Vasoconstricting and smoking.

What is a risk factor for peripheral vascular disease? Smoking.

I lack blood flow to my fingers and now my toes so much that they lack blood flow. They lack blood flow so much that they can’t grow. What’s clubbing, smoking! And now who saw the vasoconstriction? First, folks?

Your lungs? Yeah. What do you think you have as a smoker with COPD, and you’re going to go, oh, wait a second, Joe? I have pulmonary hypertension! Entirely correct.

Wait a second, Joe; then you’re telling me I get right into ventricular hypertrophy smoking? That’s exactly right. Then I can stretch my walls and get right bundle branch block? 100% correct. Then I can blow through my tricuspid and pulmonic valve with my pulmonary hypertension. Exactly.

What is the most common cause for pulmonic regurgitation or tricuspid regurgitation? Regurgitation blew through because the right ventricle got so big? Hmm. Smoking, COPD! Now, does everybody see the bigger picture?

So, imagine the exam question where a patient presents with a murmur at the right upper sternal border?  There’s only one person up there at the right upper sternal border, and that’s the aortic valve.

Now, if they tell you the murmur is at the left sternal border, that’s everybody else. Now I need some more information.

Try to make sense of this, and if you do, you will always answer heart murmur questions the best way.

I still remember being in PA school at Duke, and I still remember memorizing all the buzzwords and all this stuff. And I remember my first year in the ER. I couldn’t tell you what murmur I was hearing on the physical exam.

And now that I have stepped back and taken the time to learn the pathophysiology, I can appreciate how the cardiologist calls this a two, or three, or four, five, or six systolic ejection murmur. I really can understand where they’re coming from. I hope one day that you too can appreciate that as well.

So once again, it’s been an honor and, as always, a pleasure to speak to everybody out there in the PA podcast world.

Please be healthy, please be good, and whatever you guys do. Try to make sense of things.

Take care, Joe.

Transcribed for your reading enjoyment by https://otter.ai and Stephen Pasquini PA-C

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Image attribution: LadyofHats, Public domain, via Wikimedia Commons

Welcome to episode 92 of the Audio PANCE and PANRE physician assistant/associate board review podcast.

Today is part two of this extraordinary five-part series with Joe Gilboy PA-C, all about cardiac murmurs. In this week’s episode of the Audio PANCE and PANRE podcast, we continue our discussion of cardiac murmurs with a focus on the mitral valve.

We’ll talk about the different types of murmurs (stenosis and regurgitation) that can occur with this valve and how to differentiate them from other types of murmurs. If you haven’t already, make sure to listen to our previous podcast episode where we covered the aortic valve murmurs.

The mitral valve is located between the left atrium and the left ventricle in the heart. It consists of two leaflets (or cusps) and is responsible for preventing blood from flowing back into the atrium when the ventricle contracts.

The mitral valve can have two types of murmurs: stenosis and regurgitation.

In addition to auscultation, you can also look for certain signs and symptoms that may indicate mitral stenosis or regurgitation. For example, if a patient presents with chest pain (angina pectoris), this could be from decreased oxygen supply due to poor cardiac output in cases of significant stenosis. On the other hand, if a patient presents with an irregular heart rate (arrhythmia), this could be from increased electrical conduction velocity in cases of significant regurgitation.

Also, keep in mind that mitral valve disease can also occur secondary to rheumatic fever or endocarditis, so you may need to consider these diagnoses if a patient has any of the aforementioned signs and symptoms.

Below is a transcription of this podcast episode edited for clarity.

Welcome, everybody. This is Joe Gilboy, and I work with Stephen Pasquini at Smarty PANCE.

Today we’re back to the heart murmur podcast, and we just finished the aortic valve. The next one up is the mitral valve.

Let’s just look at this my way. In school, you memorize a bunch of facts, then someone asks a question about mitral stenosis or mitral regurgitation, and you are completely lost. It’s time to change that. Now, we are going to do it my way. Are you ready? Here we go.

Let’s look at the mitral valve on a normal day. What’s the mitral valve doing?

Let’s start with the first heart murmur, mitral stenosis. Think about it. Slow down and give this some thought.

I’ve got the stenotic mitral valve. See it? It can barely open. It’s like, man; you’ve got to push hard to open this door. So, you are the left atrium, and you’re pushing down on this stenotic mitral valve. It’s like, man; this is hard to open up! I have to push harder. Yes, you do!

Wait for a second; then I’m going to put more blood flow back against my left atrium? Completely correct. So, my left atrium might hypertrophy? Yes, that’s correct!

So, you’re telling me I might get left atrial hypertrophy with mitral stenosis? Exactly!

Now, think about it. There you are in the left atrium pushing against the mitral valve during stenosis that’s supposed to open during diastole. You’re just taking longer to open up. You see, in school, what you memorize is an opening snap. Remember that ridiculous graph where you saw it had S1, S2 on all those bar graphs? You thought you were reading a musical sheet. Do you remember that thing? Or you’re like oh, S1 S2 ……….!? You were looking at it thinking, ” I have no fricking idea what I’m looking at.” Let’s erase that.

Think about this for a second; if the left atrium is pushing on a stenotic valve, it’s going to have trouble during diastole. Because during systole, it has to be closed. It’s going to close without a problem.  The problem is opening it up. You can see the left atrium hypertrophy. Then blood flow may back up into the lungs and causes pulmonary hypertension.

Oh, wait for a second, I get pulmonary hypertension? Yes, you do!

Then maybe I have some fluid backed up in the lungs, and I might have a little shortness of breath and CHF. Exactly! Yes, that’s exactly how they’re going to present.

So, I have this diastolic murmur. It’s a diastolic ejection murmur to open that valve up. So, it’s not going to be an accentuated S1. But that’s not what they’re going to say on your boards, are they? No, that’s just a buzzword.

What they’re going to say is, “I have this diastolic rumbling murmur.” Rumbling means I’m trying to open up, and I’m going to radiate down towards the apex. That just makes logical sense.

So, I have this diastolic murmur radiating to the apex. Let’s take a closer look at the mitral valve. Remember, your heart doesn’t sit flat. It sits tilted and towards the back. So, I need this mitral valve to get towards the front. Okay, well, then tilt yourself to the left and lay down. Oh! That’s that left lateral to decubitus position they keep talking about. I’m going to bring it closer to the front.

Oh, that makes sense. I totally see that. So, I have a diastolic murmur that radiates to the apex. I can hear it better if I lay down on the left lateral decubitus position because that will bring the valve closer to the chest. Let’s make it sound louder now.

Okay, one more time back to how we were in the beginning with the aortic valve. Okay, what’s your party maneuver? Oh, I want to party, and I want to bring all the blood flow back home. How do you party? Oh, I squat. Squatting is a party. So, what are you going to do if I squat? How’s mitral stenosis sound? Louder! I get more blood flow pushing against the stenotic valve.

If I perform low-volume maneuvers, which are standing and Valsalva, I get less blood to the heart. Hi, standing and Valsalva, what’s going to happen to mitral valve stenosis. Yes, it’s going to go away!

Inspiration right (louder), and expiration left (louder). Repeat: inspiration right and expiration left. Hi, I have mitral stenosis! Oh, he’s on the left. What’s going to make him sound louder? Expiration? Yes, exactly!

Now, does everyone see this? So, you see, they’re not going to give you that “opening snap” buzzword.  All the buzzwords on the PANCE are gone, guys, so just throw them away. What they’re going to give you is some person with a heart murmur, who maybe has a little CHF, has a diastolic murmur, and that’s it. That’s all they’re going to give you now. What you have to think is diastolic: left side, going back to the lungs = stenosis. That makes perfect sense. And that’s mitral stenosis. So, the “open snap,” those buzzwords are gone.

Let’s review one more time:

There you go, that’s mitral stenosis.

Then there’s mitral valve regurgitation. I want you to view mitral regurgitation as “come and go as you please.”

This is a valve that won’t close. Repeat, “come and go as you please.” Let’s review the mitral valve again. “Hi, I’m diastole, I’m the left atria, and I’m coming through a valve that doesn’t care. Do you have any problems? No, I’m supposed to be open. So, I’m coming through during diastole not a problem.”

Now, let’s compare that to systole: “Hi, I’m systole and that mitral valve is supposed to be closed.” But is it going to be closed? Nooo. In systole, blood is coming and going as it pleases. So, wait for a second, then I’m going to be a systolic murmur. 100% correct. And are you having any resistance? Zero.

That’s why we call it a holosystolic murmur. Understand? And now I’m going from the apex at the bottom of the heart, and I’m radiating to the axilla. So, you’re going back up to the left atrium? Exactly.

So how is your blood flow out to the rest of the world? Not that good. Not good at all. So how are you feeling? I’m feeling a bit lightheaded (syncope) and short of breath.

Now let’s go one step further. Remember that LAD, the Windowmaker? Okay, if you look at the left anterior descending artery, it bifurcates into the left anterior descending and septal branches. Both these guys feed the chordae tendineae. It’s that octopus-looking muscle that pulls the mitral valve down. So now think about this for a second. Just give us some thought. Ready?

You just had a LAD MI. You’re in the hospital. The cardiologist has just put down a stent. You’re on the heparin drip. You are getting ready to go home, maybe on Xarelto or Eliquis. Right.

So, there you are, on a blood thinner. Can I ask you a question? Just give it a thought. You know, your chordae tendineae? You know, during the MI, remember that? Yes, your lacking blood flow to the left ventricle, weren’t you? Yes. How was your blood flow to your chordae tendineae? Yes, it was diminished.

Let’s review. The patient is in the hospital and on an IV beta-blocker (you want to rest the heart). Well, they’re going home and back to activities like walking through Costco or Walgreens, or CVS. He’s no longer on a beta-blocker, folks. His heart rates back up.

Is this chordae tendineae ready for normal heart rate? Yes, or no? No, not at all. He’s on the injured reserve list as well. And guess what? His chordae tendineae is not going to hold very well. He says, “Oh my god, I’m so weak. I can’t hold the mitral valve down”. Which means it is going to open back up.

That’s the test question you will see about post the MI patient who comes in two to four weeks later. The patient who’s got a new-onset murmur. What does he have? He’s got mitral regurgitation because his chordae tendineae got hypoxic during the MI, and now he’s got the murmur. So that’s a question that you see on Rosh Review, Hippo, Smarty PANCE, UWorld, and Kaplan. You’ll see this question rear its head, but the root of what they’re really after is something else. They want you to understand that the chordae tendineae itself was actually lacking blood flow during the LAD or ischemic event. So, it’s weakened. As soon as the patient goes to stress it out, it’s not going to work very well. It’s going to give way, and the chordae tendineae will rupture. What you have is mitral valve regurgitation. Does everybody see this?

This is the test question you’re going to get. An immigrant comes in with a diastolic murmur and shortness of breath. We don’t have the best testing for strep. Remember rheumatic fever? They are in their 30s and 40, and they’ve had rheumatic fever in the past, with mitral stenosis, and now the fluid is backing up to the lungs. That’s why they have shortness of breath.

And that’s the point I’m trying to make about the mitral valve. Does everybody see that now?

When you get the test questions, stop and think. You’re going to laugh because one of the things I tell all my students to do all the time is to try to make sense of it. See, what you guys do is memorize these things, and you run into your, what I call your data closet. I call it a closet full of data.

You get into this data closet, and what happens is you get lost in the closet. You say to yourself, “Okay, diastolic murmur, axilla blah, blah, blah, what did I memorize? Let me write down my little mnemonic. Yes, yes. Oh, man, I can’t Oh, man.” Next, you’re just panicking. And you just choose A, B, C, or D.

You say to yourself, “oh my god, I think I got the question wrong.” Exactly.

So next time, just try making sense of it.

So, we did the aortic valve, and we did the mitral valve. So, we did everything on the left. Next week, we are going to the right folks. We’re going to go to the pulmonic valve and the tricuspid valve.

So, one more time, guys. Inspiration right, expiration left. Inspiration right, expiration left. To make the right side of your heart murmur sound better, what are you going to do? Inspiration, so pulmonic and tricuspid sound louder with inspiration.

Expiration left. Who sounds better on the left? Aortic and mitral!

It’s been an honor and a pleasure talking with you today. I hope this makes more sense. Next week we’ll do the pulmonic valve. Till then, be good to yourself and take care.

Joe Gilboy PA-C

You can download and listen to past FREE episodes here, on iTunes, Spotify, Google Podcasts, Stitcher, Amazon Music, and all podcasting apps.

Follow this link to download your FREE copy of the PANCE/PANRE/EOR Content Blueprint Checklists.

Print it up and start crossing out the topics you understand, marking the ones you don’t, and making notes of key terms you should remember. The PDF version is interactive and linked directly to the individual lessons on Smarty PANCE.

Featured Image attribution (aortic stenosis and regurgitation): Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014“. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. Crop by Stephen Pasquini PA-C, CC BY 3.0

Welcome to episode 91 of the Audio PANCE and PANRE Physician Assistant/Associate Board Review Podcast.

Today is part one of an extraordinary five-part series with Joe Gilboy PA-C, all about cardiac murmurs.

It’s time to throw away everything you have ever learned that made you hate cardiac murmurs (you know those crazy line diagrams) and let Joe hard-wire your brain for success.

I promise you that by the end of this podcast, you will no longer be afraid of murmurs, but you will welcome them into your brain with a whole heart, open arms, and the need to share this podcast with all your classmates.

Below is a transcription of this podcast episode slightly edited for clarity.

Welcome, everybody. This is Joe Gilboy PA-C, and today is part one of a five-part series on the two most dreaded words that every pa student and recert PA hates. Are you ready for the two words?

Today we’re going to start talking about heart murmurs, and we are going to break this down into a five-part series:

We’re going to cover each valve one at a time. We will look at it and try to really make sense of it all.

Because I know what you did in PA school, you had that little diagram that you made, you know, systolic or diastolic murmurs. You’ve memorized certain things. And then you get to that test question, and you’re completely clueless on it, you’re like, “I have no idea what they just said, Joe, I have no idea.”

And then you’re back to scrambling, looking for some word that’s going to trigger you. And that’s the key point- all the trigger words, all those high-value trigger words, they’re gone. That’s what the creators of the PANCE did about two to three years ago. They took all the trigger words out.

Key point:

So now, let’s look at this differently. You did it your way. How did it work out? Probably not so well. So, guess what, we’re going to do it my way. And that’s what I want to do here.

So, think about it for a second. I want you to picture the aortic valve.

Opening during systole, closing during diastole. That’s really what it’s supposed to do.

Go ahead and picture that in your head. And for those who are in a safe place, close your eyes because it makes more sense.

The valve is going to be open during systole and is going to be closed during diastole.

Now, who gets fed right after the aortic valve? Well, that’d be the coronary arteries.

If I’m lacking blood flow to my coronary arteries, how’s that feel? I’ve got chest pain.

What’s the second thing that gets fed after the aortic valve? Well, that’d be my internal and external carotid arteries.

If I lack blood flow to my internal or external carotids, how will I feel? Lightheaded with syncope and dizziness.

Where does blood flow third? That would be my left subclavian artery, and if I lack blood flow, then I get left arm pain. And then, of course, everything down south after that.

Okay, so let’s start with the first one—aortic stenosis.

So, think about this for a second. Stop memorizing. Start thinking. I have this stenotic aortic valve, and it can’t open up. So that’s my question to you. When are you going to have problems with this valve? During systole or diastole?

It is supposed to open during systole. And it won’t. It’s too stenotic.

The aortic valve is supposed to be closed during diastole, and it will close. Oh, then I see your point, then that is a systolic murmur. Right? Aortic stenosis is a systolic murmur!

Where’s the aortic valve located? The right second intercostal space. And where does it radiate to? The neck.

I want you to understand something. Who’s got to work harder to push against this stenotic aortic valve. Who’s got to work harder to open the door? It’s the left ventricle.

Okay, you’re the body. Are you going to take this, or are you going to fight back? I’m going to fight back a little bit, Joe.

So, what’s going to happen to the left ventricle? The left ventricle is going to hypertrophy.

And then go and stretch and stretch and stretch and stretch and stretch and stretch and stretch that left ventricle and you’re going to rupture the wires in there. And you’re going to get left bundle branch block.

And for those of you thinking, ahead of the game, will right ventricular hypertrophy, unopposed cause right bundle branch block? The answer is yes.

Back to aortic stenosis – I see the left ventricular hypertrophy because it’s backing up. I can even see the left bundle branch block. That makes sense.

So, aortic stenosis is a systolic ejection murmur. Oh, I see it because it’s supposed to be open during systole. But it’s a tight valve, and it won’t open up. I get it!

Let’s go one step further. It’s the most commonly acquired valvular stenosis, and usually, it’s congenital or from a bicuspid valve. But that’s not what they’re going to ask. That’s too easy. So, how would aortic stenosis present? That’s the right question.

Let’s say you have a stenotic aortic valve; it’s not opening during systole. “Hi, I have aortic stenosis, and I’m walking through Costco.”

So, you are walking through Costco, looking at the Christmas decorations or whatever they have. And how is your valve? Is it opening up? Yes, or no? No, it’s not Joe. And are you demanding more of it? You’re walking through Costco. How’s the blood flow to your coronary arteries? Oh, it’s diminished. Exactly.

Then I get chest pain with exertion – exactly. I could be walking up steps – and that’s the test question you see rear its ugly head – it’s going about the person with chest pain who’s walking up steps or exerting himself.

And then how’s your blood flow to your head? I get lightheaded and dizzy because of a lack of blood flow there. Get it? Do you see this picture?

I have this murmur in the right second intercostal space. It’s going to be systolic. The person is going to complain of chest pain and lightheadedness, and dizziness with exertion.

I can see the left ventricular hypertrophy. I can even see the left bundle branch block. Oh, that all fits.

So, they have chest pain. What do you give them? What do you give to people with chest pain? You give nitroglycerin.

And now the question is this. Well, what’s nitroglycerin? It’s a vasodilator. Where does it vasodilate? Everywhere. That’s right. I always love how people treat nitroglycerin like it’s intelligent, but it’s not. Nitroglycerin is going to vasodilate everywhere – including the left ventricle.

Wait for a second, hold on here. You just vasodilated my left ventricle, and I can’t get through the valve. Then the blood flow to my valve is not increased, but it’s decreased. And now you have less blood flow through that stenotic aortic valve. How’s your blood through the coronary arteries and in your internal and external carotids? It is incredibly diminished.

And what happens to these patients with aortic stenosis who are treated with nitroglycerine? They get syncope. See it now? It makes sense, doesn’t it?

Now, I have this systolic ejection murmur. It’s going to radiate to my neck because that’s how it’s pointing, and it’s going to be in that right second intercostal space.

And now comes the questions about inspiration, expiration, squatting, standing, and handgrip! You’re like, I just can’t believe you’re going there, Joe. Yes, we’re going there. But we’re doing it my way, which is a lot more fun.

So now let’s think about this. I want you to imagine that S1 is a date with the mitral and tricuspid valve.

So, there they are, a cute little couple, the mitral and tricuspid valve come together, and they’re the S1. And now I want you to imagine S2 as a date between the aortic and pulmonic valve – so S2 is the combination of the two sounds, and S1 is a combination of the two sounds.

Key points:

Okay. Imagine I have aortic stenosis – does my valve take shorter or longer to open up? It’s taking longer to open up.

Your pulmonic valve opened on time, but your aortic valve is late to the date!

That’s right. You took longer to get ready to open up. So, guess what happens to my S2 – It becomes split.

So, you see, a split means that someone’s late to the date. Now I need more information to figure out whether it’s pulmonic stenosis or aortic stenosis.

Key point:

Do you remember that ridiculous bar graph that you saw in PA school? You’re like, I have no idea what I’m looking at! What they’re trying to show you is the timing of the valves. Someone is late to the date.

So, I want you to erase what you memorized in PA school. If I have a split S2, someone’s late to the date. Is it pulmonic or aortic? I need more information, but someone’s late to the date.

Okay. One more step. Can we all agree just from a laminar flow physics point of view that the more blood flow I put across the valve, the louder it sounds?

Think about this for a second. The more blood flow I put across the valve, the louder it sounds.

So, to make aortic stenosis sound louder? What do I need to do? Put more blood flow across the valve!

Key point:

Okay, so there is a party, and everybody’s showing up – Your mom, your dad, your cousins, your second cousins, the neighbors, the neighbors, friends. I mean, everybody’s showing up. Everybody’s coming back to the heart. Who’s the party maneuver? Squatting – squatting is a party!

So, what are you doing? I’m shoving all the blood flow back home. Who showed up? The entire neighborhood – and my cousins and my second cousins everybody’s showing up. So, when I squat, you know what I get? More blood flow in the heart. Guess which murmur sounds louder? All of them – mitral stenosis, mitral regurgitation, tricuspid stenosis, tricuspid regurgitation, pulmonic stenosis, pulmonic regurgitation, aortic stenosis, and aortic regurgitation – all sound louder with more blood flow back home. Who’s the maneuver? Squatting!

So, squatting really doesn’t help me much because everybody sounds louder.

Key point:

And then who’s your low volume maneuvers? Who makes blood flow go away from the heart? Well, that would be standing – when you stand up, that takes blood flow away from the heart. So, all the blood flows to your legs. How are all your murmurs? They go away. So, standing is a lack of blood flow, and all the murmurs are diminished.

Key point:

And then Valsalva. When you grunt, what you’re doing is Valsalva or if you have a bowel movement – what you’re doing is you’re squeezing the inferior and superior vena cava, and you’re stopping blood flow from going to the right side of the heart.

You’ve got less blood flow in the heart. So, do you have any blood flow to put on my murmurs? No, it went away. So, standing and Valsalva make murmurs go away.

Squatting sounds louder. Standing and Valsalva – these are my low volume maneuvers, and the murmur goes away.

Key point:

Inspiration right. Expiration left. Inspiration right. Expiration left – and for the third time. Inspiration right expiration left – to make right-sided heart murmur sound louder, you breathe in (inspiration). What do you do to make left-sided heart murmurs sound louder? Expiration!

When you inhale, you breathe air in – imagine your inferior and superior vena cava are pushing blood into your right side. So, you get more blood flow on to the right – increasing the laminar flow on the right and increasing the sound of right heart murmurs.

When you exhale and blow air out, you are decreasing that pressure in the chest. So now the blood on the left can get out easier – increasing the laminar flow across the valve and increasing the sound of the murmur on the left.

So, one more time, inspiration right and expiration left. Hi, I’m aortic stenosis – am I on the left or the right? I’m on the left.

So, what’s it going to make it louder? Expiration!

Key point:

You learned that handgrip increases peripheral vascular resistance.

Okay. Let’s translate that to more layperson terms. When I increase my peripheral vascular resistance, I’m sitting on your aortic valve. What is your only exit valve? Yes, that’s right – it’s the aortic valve. So, if I increase your peripheral vascular resistance AKA, I’m pushing all the blood against your aortic valve AKA I’m sitting on your aortic valve.

So, I want you to get this, I want this visualization of handgrip and sitting on the aortic valve. So, I’m sitting on your aortic valve, and we’re just sitting on it. Got it?

Grab your hands and squeeze them – see how your muscles are tight? Can you visualize the blood flow getting harder to come out? So, you’re pushing it against the exit valve, which is your aortic valve. And now I want you to visualize this as sitting on the valve.

Okay, hi, I’m aortic stenosis, and I can barely open up – squeak, squeak, squeak, squeak, squeak. I can barely open the valve. I’m stenotic, and you did what? You did hand grip. You just sat on my aortic valve, and I can barely open up. Do you think I can open it up anymore?

The answer is no. Exactly. So, guess what murmur is in the right second intercostal space and goes away with handgrip? Aortic stenosis!

Key point:

And then, of course, how do we diagnose it? Echocardiogram!

The aortic valve is the one valve that requires an emergent replacement.  So, when somebody has aortic stenosis, what is the end game? It’s going to be an aortic valve replacement.

Now, let’s discuss aortic regurgitation. Okay, with all these new tools, it’s going to be easy.

With aortic regurgitation, the valve is just flapping in the breeze, come and go as you please. I could care less – come and go as you please.

Are you going to have problems with this valve during systole? Yes, or no? No, because the valve is supposed to be open during systole.

So, when do you have problems with the regurgitating aortic valve? During diastole, when the valve is supposed to be closed!

Key point:

It’s going to travel from my right-second intercostal space down to my apex.

Anything split? Is anybody late? No, not at all.

So, aortic regurgitation will be a diastolic murmur, and there is a wide arterial pulse pressure. They call this a water-hammer pulse. To understand this, imagine your pulse as a series of train cars. So, imagine a train, and there’s your aortic valve—pulse, pulse, pulse, pulse, pulse, pulse, pulse. But imagine if you’ve got aortic regurgitation – What do you do?

Well, I threw a pulse out there. But did you hold it out there? No, because my valve was open. So, what happened to some of that blood that you threw out there? It sneaks back home!

They call that wide arterial pulse pressure. I want you to view the arteries like this PVC pipe. You threw blood out there, didn’t you? So, it kept it full. But during diastole, I didn’t close the door. So, it all rushed back home, and the pipe collapsed. Exactly. That’s what we call a wide arterial pulse pressure, and this is what’s called a water hammer pulse.

So, I have this diastolic murmur. Right second intercostal space. Radiates to the apex. Okay. Let’s make it sound louder. What do you want to do? Oh, let’s squat – that’s a party!

To make it go away. I could stand or Valsalva. These are my low-volume maneuvers. Does inspiration or expiration make it louder? This is on the left, so expiration makes it louder.

So, I’m sitting on your aorta valve, and what’s the problem? You can come and go as you please. So, what will happen when we perform handgrip with aortic regurgitation is that blood flow is going to go against your valve, and it’s wide open. Blood is going to go right through it!

So now, does everybody see this question rearing its ugly head?

Instead of going for the knee-jerk answers that you’ve memorized (I call this the data closet in a student’s head), try to make sense of the question instead of going for your data closet. Think laminar flow physics.

And now, do you see the test question? They’re not going to tell you if it’s systolic or diastolic. That’s too easy. They’re going to tell you about some murmur in the right second intercostal space that either gets louder with handgrip (aortic regurgitation) or goes away with handgrip (aortic stenosis).

And now you will get the answer right every time!

Now go back and re-listen to this podcast episode a couple of times. I always tell people if they get a chance to listen to this podcast, do yourself a favor and find a quiet room and turn off all the lights.

And then just listen. Keep your eyes closed and visualize this in your head… and that’s just money!

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Welcome to episode 90 of the Audio PANCE and PANRE Physician Assistant/Associate Board Review Podcast.

Join me as I cover ten PANCE, PANRE and EOR review questions from the Smarty PANCE Instagram/Facebook page and the smartypance.com board review website.

Special from today’s episode:

Below you will find an interactive exam to complement today’s podcast.

I hope you enjoy this free audio component to the examination portion of this site. The full board review course includes over 2,000 interactive board review questions and is available to all members of Smarty PANCE.

If you can’t see the audio player, click here to listen to the full episode.

1. A 32-year-old male presents with acute ascending symmetrical paralysis and diminished reflexes in his bilateral lower extremities. He has a history of bloody diarrhea a few days ago. What did he likely eat that led to his symptoms?

A. Uncooked rice

B. Mayonnaise

C. Uncooked chicken

D. Soft unpasteurized cheese

E. None of the above

C. Uncooked Chicken

This patient has Guillain-Barré Syndrome (GBS), an acute immune-mediated polyneuropathic disorder. Clinical features include ascending symmetrical paralysis, diminished tendon reflexes, and respiratory muscle weakness.

GBS is typically precipitated by an infection. Campylobacter jejuni infection is the most common precipitant of GBS. It is commonly found in uncooked poultry.

Cerebrospinal fluid analysis helps confirm the diagnosis. Treatment includes plasmapheresis and IV immune globulin.

View lesson: Guillain-Barré Syndrome

2. Which of the following disorders is characterized by a scaly, rough erythematous patch that appears on sun-exposed areas?

A. Seborrheic keratosis

B. Keratosis pilaris

C. Actinic keratosis

D. Lichen planus

E. Pityriasis rosea

Answer: C. Actinic keratosis

Actinic keratosis (AK) is a skin lesion that results from atypical keratinocyte proliferation. Risk factors include UV radiation, fair skin, and sunburns.

AK can present in various ways, but classically you will see an erythematous, scaly macule, papule, or plaque. A shave or punch biopsy can confirm the diagnosis. However, AK is often diagnosed clinically.

Treatment depends on the location and extent of the condition. Options include cryotherapy, fluorouracil, and imiquimod. It is important to remember that AK can develop into SCC.

View Lesson: Actinic keratosis (AK)

3. A 42-year-old male is admitted for typical pneumonia. He is given IV azithromycin and ceftriaxone. His QT interval becomes prolonged and he develops a polymorphic ventricular tachycardia. Which of the following is the most appropriate pharmacological management?

A. Intravenous calcium gluconate

B. Intravenous magnesium sulfate

C. Intramuscular epinephrine

D. Oral amiodarone

E. Oral procainamide

B. Intravenous magnesium sulfate

The patient developed torsades de pointes (Tdp), which is a specific type of polymorphic ventricular tachycardia in patients with a long QT interval. It is a ventricular dysrhythmia characterized by rapid (>100 bpm), irregular, wide QRS complexes that vary in size and shape. Diagnosis is made via EKG.

Examples of meds that prolong the QT interval include antiarrhythmics (amiodarone, sotalol), antimicrobials (fluoroquinolones, macrolides), antidepressants (fluoxetine, sertraline), and antipsychotics (haloperidol, quetiapine).

Treatment is usually IV magnesium sulfate.

View lesson: torsades de pointes (Tdp)

4. Which of the following is true about an indirect inguinal hernia?

A. It does not usually enter the scrotum

B. It is caused by a patent processus vaginalis

C. The strangulation risk is lower than a direct inguinal hernia

D. It is the least common type of inguinal hernia overall

E. It is medial to the inferior epigastric vessels

Answer: B. It is caused by a patent processus vaginalis

A hernia is a protrusion or projection of an organ through the body wall that typically contains it. An indirect inguinal hernia is specifically a protrusion of the abdominal organ into a patent processus vaginalis that extends into the inguinal canal.

Indirect inguinal hernias are the most common type of inguinal hernia. An indirect inguinal hernia is found lateral to the inferior epigastric vessels and it usually enters the scrotum. The strangulation risk is actually higher in indirect inguinal hernias. Definitive treatment is surgery.

View lesson: Indirect inguinal hernias

5. Which of the following is the most common cause of death in hemochromatosis?

A. Hepatocellular carcinoma

B. Diabetic-related complications

C. Acute respiratory failure

D. Left ventricular failure

E. Pancreatic cancer

Answer: A. Hepatocellular carcinoma

Hemochromatosis is an autosomal recessive disorder defined by excessive iron deposition in the liver, pancreas, and heart. It is often caused by a mutation in the HFE gene. Clinical features include skin hyperpigmentation, weakness, hepatomegaly, liver function abnormality, and diabetes mellitus.

Lab findings will show elevated serum iron, elevated ferritin, elevated transferrin saturation percentage, and decreased transferrin. Diagnostic tests include genetic testing and liver biopsy (gold standard, not always needed). Treatment consists of life-long phlebotomy. The most common cause of death in these patients is hepatocellular carcinoma.

View lesson: Hemochromatosis

6. A 15-year-old female with no medical history presents to the ER with altered mental status. She is tachycardic. Labs reveal a glucose level of 900 mg/dL and elevated beta-hydroxybutyric acid. Which of the following acid-base issues would you expect to see?

A. Normal anion gap metabolic acidosis

B. High anion gap metabolic acidosis

C. Metabolic alkalosis

D. Respiratory alkalosis

E. Respiratory acidosis

Answer: B. High anion gap metabolic acidosis

The patient most likely has diabetic ketoacidosis (DKA), a life-threatening emergency defined by insulin insufficiency, along with an elevation in counter-regulatory hormones. Patients in DKA will usually have a high-anion gap metabolic acidosis (HAGMA).

An anion gap is calculated by subtracting anions (HCO3- and Cl-) from a cation (Na+). It is normally 8 to 12. The gap is elevated in DKA because unmeasured anions (ketones) are giving off H+, which interacts with bicarbonate. Bicarbonate becomes depleted, thus increasing the gap.

Other causes of HAGMA include acute kidney injury, lactic acidosis, and toxins.

View lesson: Acid-Base Disorders

7. Which of the following is the first-line treatment for nasal polyps in patients with chronic rhinosinusitis?

A. Anti-histamines

B. Intranasal steroids

C. Leukotriene inhibitors

D. Beta-agonists

E. None of the above

Answer: B. Intranasal steroids

Nasal polyps are grayish masses filled with inflammatory mediators in the nasal cavity or sinuses. They are associated with aspirin sensitivity, chronic rhinosinusitis, asthma, allergies, and cystic fibrosis. Symptoms include increased nasal drainage, congestion, anosmia.

Nasal examination via nasal endoscopy can help confirm the diagnosis. The first-line treatment for nasal polyps is typically nasal corticosteroid spray. Surgery may be needed if the nasal polyp obstructs the cavity/airway.

View lesson: Nasal polyps

8. A 52-year-old female with a history of mitral valve regurgitation presents with exertional dyspnea. On physical exam, you notice abdominal swelling and lower extremity edema. You suspect pulmonary hypertension (PH). Which of the following is the gold standard for diagnosing PH?

A. Right heart catheterization

B. Chest radiograph

C. Computed tomography angiography

D. Echocardiogram

E. Polysomnography

Answer: A. Right heart catheterization

Pulmonary hypertension (PH) is defined by a mean pulmonary arterial pressure > 25 mmHg. The World Health Organization lists 5 broad etiologies of PH: pulmonary arterial hypertension (Group 1), left heart disease (Group 2), lung disease (Group 3), chronic thromboembolism (Group 4), and unknown causes (Group 5).

Symptoms are usually related to right ventricle failure and include “body congestion” signs: pitting edema, abdominal swelling, hepatomegaly, etc. A transthoracic echocardiogram is the best initial diagnostic test. A right heart catheterization is the gold standard for diagnosing PH.

View lesson: Pulmonary hypertension (PH)

9. A 72-year-old female smoker with a history of atrial fibrillation presents to the ER with severe abdominal pain for a few hours. Vitals are unremarkable. Physical exam reveals nothing significant. Which of the following is the gold standard diagnostic modality for the most likely diagnosis?

A. Computer tomography scan

B. Right upper quadrant ultrasound

C. Abdominal radiographs

D. Mesenteric angiography

E. None of the above

Answer: D. Mesenteric angiography

The patient most likely has acute mesenteric ischemia, which is the sudden onset of small intestinal hypoperfusion. The most common cause is emboli from the heart (usually from atrial fibrillation). Other causes include thrombosis and atherosclerotic disease. The most common artery occluded is the superior mesenteric artery.

Clinical features include acute onset of abdominal pain out of proportion of exam findings, abdominal distention, and elevated lactate. A good initial diagnostic test for a stable patient is an abdominal CT scan. The gold standard test is mesenteric angiography. Treatment is surgical revascularization and antibiotics.

View lesson: acute mesenteric ischemia

10. Orbital cellulitis most commonly occurs when an infection spreads into the orbit from which sinus?

A. Maxillary sinus

B. Frontal sinus

C. Sphenoid sinus

D. Ethmoid sinus

E. Temporal sinus

Answer: D. Ethmoid sinus

Orbital cellulitis is an ophthalmic emergency, as it can lead to vision loss. Clinical features include diplopia, decreased vision, pain during eye movement, proptosis, fever, and an erythematous, edematous eyelid. The most common bacterial culprits are Staphylococcus aureus and Streptococcus species. The ethmoid sinus is the most common origin of infection (90%).

The best diagnostic test is a high-resolution CT scan. Treatment is intravenous antibiotics, like IV vancomycin and ceftriaxone.

View lesson: Orbital cellulitis

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I will be releasing new episodes every few weeks. Smarty PANCE is now discounted, so sign up now before it’s too late!

Follow this link to download your FREE copy of the PANCE/PANRE/EOR Content Blueprint Checklists

Print it up and start crossing out the topics you understand, marking the ones you don’t, and making notes of key terms you should remember. The PDF version is interactive and linked directly to the individual lessons on Smarty PANCE.