USMLE Mistakes Deck

Question 1

Renal Artery Stenosis

Answer 1

• Unilateral kidney atrophy;
• Resistance to three anti-hypertensive medications
• High Plasma Renin Activity
  -Hypokalemia
• bilateral Carotid bruits.
• Increase in Cr following ACE inhibitor initiation
  Risk factors for RAS: Male sex, age greater than 45 years old, smoking history, DLD, PAD.

Decreased Renal perfusion in the renal artery stensosis activates the renin-aniotensin aldosterone system, which causes efferent arteriole constriction and increased Na/H2O retention ( leading to HTN) and increased aldosterone ( leading to HypoK)

Question 2

Isolated Systolic HTN

Answer 2

• decreased arterial compliance associated with aging;
• typically manifests with wide pulse pressure
• Pts have a risk of high risk of renal dysfunction and cardiovascular events ( e.x. MI and storke).

Question 3

Cholesterol Embolization Syndrome

Answer 3

• Complication of cardiac catheterization syndrome, vascular interventions, and anti-cogulant therapy. Choelsterol is released into circulation , where it travels to the kidneys ( receives large amount of blood supply). This patient presents with livedo reticularis, acute kidney failure, esoniphillia, and esophiliuria in setting of cholesterol embolism.
• Kidney biopsy show intravascular cholesterol vacuole deposits.

Question 4

Fat embolism Syndrome

Answer 4

Triad:

• Dyspnea
• Neurologic Deficits ( confusion)
• petechial rash

Question 5

Fibromuscular Dysplasia

Answer 5

• Elevated HTN
• Tinnitus
• Light-headedness
• cervical and abdominal bruits are caused by turbulent blood flow in the stenosed arteries due to fibromuscular dysplasia.
• HypoK

Proliferation of connective tissue and muscle fibres is associated with fibromuscular dysplasia–> RAS–>decreased renal perfusion–> increased renin-angiotension-aldosterone system, increasing the secretion of renin with subsequent re-absorbtion of Na and water leading to secondary HTN.

Question 6

Mitral Regurgitation

Answer 6

Holosystolic murmur at the apex of the heart; increases with hand grip. Handgrip, increases the afterload , as a result blood flow through the aortic valve is reduced, leading to increased retrograde blood flow through the incompetent mitral valve.

Question 7

Ventricular Septal Defect

Answer 7

Holosystolic murmur at the LLSB, that increases with handgrip. There is reduced blood flow through aortic valve, which leads to increased blood flow through the VSD.

Question 8

Aortic Regurgitation

Answer 8

Diastolic Murmur at the Right Sternal border that increases with rapid squatting is indicative of AR. AR in
children is very common and due to congenital bicuspid aortic valve.

Question 9

Patent Ductus Arteriosus

Answer 9

Machine like murmur at the left sternal border. Pts with patent ductus arteriosus are at increased risk of heart failure in infancy and pulmonary HTN in adolescence.

Question 10

Central Venous Hum

Answer 10

Continuous murmur at the RT supraclavicular region.
It’s a benign finding in children, as a result of turubulent blood flow in the internal jugular veins. The murmur disa ppears with the application of ipsilateral pressure to the ipsilateral jugular vein.

Question 11

Mitral Stenosis

Answer 11

Opening Snap + Diastolic Murmur. Usually happens as a result of incomplete treatment leading to rheumatic fever.

Mitral Stenosis leads to increased left atrial pressure, causing left atrial dilation ( which may result in a. fib) and an increase in pulmonary arterial pressure to overcome the increased left heart pressure. Overtime, this lead to pulmonary vascular remodelling with increased pulmonary vascular resistance, splitting of S2 and right ventricular hypertrophy. Right ventricular failure eventually mainfests with characterstic features such as JVP distension and pitting edema.

Question 12

Pulmonary Arterial HTN ( PAH)

Answer 12

Mean arterial pressure is greater than 20 mmHg at rest, and there is no evidence of underlying pulmonary and left hear conditions (e.g. valvular heart disease, systolic dysfunction, diastolic dysfunction). While PAH is often idiopathic, amphetamine and cocaine have been associated with PAH. The pt has evidence of Rt-sided heart strain.

Question 13

Hypertensive Nephrosclerosis

Answer 13

Happens as a result of renal vascular injury secondary to long standing arterial HTN.

Kidney biopsy show findings of sclerosis in the capillary tufts and arterial hyalinosis which is caused by chronic damage from increased capillary hydrostatic pressure in the glomeruli as well as ischemic damage as renal arterioles progressively narrow.

Clinical features:

• Elevated BP
• Impaired renal function, elevated BUN/Cr, proteinuria, and microangiopathic hemolytic anemia, hyperkalemia.

Question 14

Splitting of the S2

Answer 14

Splitting of the second heart sound (S2) during inspiration is a normal finding, especially among young individuals. During inspiration, the intrathoracic pressure falls, and there is increased venous return to the right side of the heart, resulting in a prolonged right ventricular systole and delayed closure of the pulmonic valve (P2). Inspiration leads to decreased blood flow to the left side of the heart due to pooling in the pulmonary vasculature, which results in early closure of the aortic valve (A2). Therefore, auscultation of variable splitting of S2 that becomes more pronounced during inspiration is considered a physiologic finding and does not necessitate further workup.

Question 15

Renal Artery Stenosis

Answer 15

• hypertension, hypokalemia, increased creatinine, elevated BUN/Cr ratio, and history of atherosclerotic disease raise suspicion for renal artery stenosis.
• Abdominal duplex ultrasonography is the first-line imaging modality for diagnosing suspected renal artery stenosis because it is noninvasive, low-cost, and has relatively high sensitivity and specificity for this condition. Typical findings in renal artery stenosis include a reduction in the diameter of the renal artery, increased systolic flow velocity in the renal artery, and a decrease in kidney size on the affected side. Alternative noninvasive diagnostic tests are CT angiography and MR angiography. The choice of test is based on the test’s availability, patient factors, and the clinician’s expertise.

Renal artery stenosis is most commonly caused by either atherosclerosis (∼90% of cases) or fibromuscular dysplasia (10% of cases). While atherosclerotic plaques resulting in stenosis are typically found in the proximal ⅓ of the renal artery, fibromuscular dysplasia affects the distal ⅔.

Question 16

Murmurs requires TTE

Answer 16

• Diastolic murmurs
• Systolic murmurs are often physiologic, however, you need to cognizant of holosystolic murmurs, late systolic, murmurs with added sounds such as clicks and radiating murmurs, continuous murmurs, and any murmur that is symptomatic.

Question 17

High Output Heart Failure

Answer 17

May happen as a result of AV fistula;

AV fistulas cause a decrease in the peripheral vascular resistance because they allow shunting of blood from the high pressure arterial circulation to the low pressure venous circulation.

Shunting leads to decreased systemic vascular resistance, which results in elevated HR, and decreased effective circulating volume, thereby triggering RAAS. RASS activation causes retenion of water and sodium, resulting in increaed cardiac filling pressurewith elevated cardiac ouptut ( which may culminate in a state of high output heart failure); high output CHF
Ttt: surgical division of the fistula to reverse the current symptoms and prevent irreversible myocardial damage.
Other common causes of high output CHF include pregnancy, anemia, hyperthyroidism, and wet beriberi.

Question 18

Beri-Beri Syndrome

Answer 18

Beriberi: inadequate thiamine uptake due to malnutrition, heavy drinking, or increased demand (e.g., hyperthyroidism, pregnancy)
Dry beriberi
- Symmetrical peripheral neuropathy (sensory and motor)
Progressive muscle wasting
Paralysis
Confusion
Wet beriberi
Cardiomegaly
Edema
High-output cardiac failure (dilated cardiomyopathy)
Infantile beriberi: cardiomegaly, tachycardia, cyanosis, aseptic meningitis (vomiting and seizures)
Wernicke encephalopathy
Leigh syndrome
Diagnostics: vitamin B1 administration → ↑ RBC transketolase activity

Question 19

Typical Angina vs. Atypical Angina

Answer 19

Typical angina fulfills all of the following criteria:
- Retrosternal chest pain of characteristic nature and duration (e.g., transient retrosternal pressure)
- Provoked by exertion or emotional stress
- Relieved by rest and/or nitroglycerin
Atypical angina: fulfills only two of the aforementioned criteria

Question 20

Beta blocker OD

Answer 20

Sx of Beta-blocker OD: bradycardia, hypotension, wheezing, hypoglycemia, and prolonged PR interval.

• intravenous glucagon should be administered when blood pressure and heart rate do not respond sufficiently to IV fluids and atropine alone.
• Glucagon increases intracellular cAMP by activating adenylate cyclase, which improves cardiac contractility and heart rate while bypassing the beta receptors. It also improves hypoglycemia.

Question 21

Stable Angina

Answer 21

• Exertion chest pain and ST-segment changes during stress testing
• Mngmt of Stable Angina:
  1. Metoprolol - β1-selective adrenergic receptor blocker - reduce anginal episodes and improve exercise tolerance in patients with stable ischemic heart disease. Like other β-blockers, metoprolol relieves anginal pain by decreasing heart rate and cardiac contractility, which reduces myocardial oxygen demand.
  2. Antiplatelet therapy, lipid-lowering therapy, and management of hypertension and diabetes, risk-reducing strategies include weight loss, smoking cessation, and aerobic exercise.

In select patients, revascularization ( not routinely recommended for stable CAD techniques):

• Percutaneous coronary intervention (PCI)
• Coronary artery bypass grafting (CABG)

Question 22

NSTEMI

Answer 22

• acute non-ST-segment elevation myocardial infarction (NSTEMI) and elevated Troponin
• underwent percutaneous transluminal coronary angioplasty (PTCA) with stent placement. His discharge medication regimen should be directed at reducing the risk of subsequent ischemic events and mortality.
• Long term dual antiplatelet therapy ( DAPT) with aspirin and a P2Y12 receptor inhibitor (e.g., clopidogrel, prasugrel, ticagrelor) is the recommended regimen for all patients after reperfusion therapy. After PCI with stent placement, DAPT is recommended for 12 month.
• Long-term management for secondary prevention after ACS include ACE inhibitor, beta blocker, nitrate, and high dose statin therapy. Low dose ASA is continued lifelong.

Question 23

Postive HJR

Answer 23

• indicative of cardiac disease ( but may help distinguish b/w liver disease)
• A positive HJR indicates impaired relaxation of the right ventricle and consequently inability to accomodate an increased venous return to the heart.
  The most common causes of positive HJR: restrictive cardiomyopathy, constrictive pericarditis, and RV HF ( due to MI)

Question 24

Hemochromatosis

Answer 24

• Arthritis: arthropathy of 2nd and 3rd MCP joint
• Fatigue, abdominal pain, and hepatomegaly
• Restrictive CM: iron deposition in the heart, which ultimately causes congestive hepatopathy ( cardiac cirrhosis)

Question 25

Hemochromatosis

Answer 25

• Arthritis: arthropathy of 2nd and 3rd MCP joint
• Fatigue, abdominal pain, and hepatomegaly
• Restrictive CM: iron deposition in the heart, which ultimately causes congestive hepatopathy ( cardiac cirrhosis)

Question 26

PCP

Answer 26

Sx: generalized malaise, fatigue, a non-productive cough, and a low-grade fever along with symmetrical, diffuse interstitial infiltrates on the chest x-ray, which suggests Pneumocystis pneumonia (PCP) related to a suspected AIDS infection (sexually active with several partners; inconsistent use of condoms; HIV wasting syndrome over the past 6 months; white plaques on the lateral side of the tongue, which are likely oral hairy leukoplakia; positive HIV testing).

Ttt:

1. IV TMP- SMX
2. If allergic to sulfa, consider IV clindamycin and oral primaquine.

Question 27

Noromoplactinemic Galactorrhea

Answer 27

• Bilateral, nonbloody nipple discharge in a nonpregnant, nonbreastfeeding patient with normal serum prolactin levels.
• Noroprolactinemic galactorrhea is a type of nonpathological nipple discharge due to chronic nipple stimulation ( due to piercing or ill fitting clthes)
• Galactorrhea typically manifests with bilateraly milky nipple discharge that is typically white, but maybe green or yellow.
• If the D/C is unilateral and/or bloody, imaging studies ( sub-areolar U/S or mammography) are indicated to evaluate for lactinferous duct abnormalities.
• If hyper-prolactinemia is suspected, work up include B-HCG ( to exclude pregnancy), serum Cr levels to exclude CKD, and serum TSH levels ( as uncontrolled hypotherism can lead to hyperprolactinemia).
• MRI of pituitary gland may be indicated if pituitary adenoma is suspected.

Question 28

Hyperprolactinoma Sx in males vs. Females

Answer 28

• In M: hypogonadotropic hypogonadism because prolactin inhibits the synthesis and release of GnRH, which results in decreased secretion of FSH and LH. In men, decreased concentrations of LH result in decreased production of testosterone in testicular Leydig cells. The resulting manifestations include erectile dysfunction, decreased libido, reduced testicular volume, infertility, gynecomastia, and loss of axillary hair.
• In F ( especially post-menopausal F): you may have galactorrhea.

Question 29

Venous Hum

Answer 29

• High-velocity flow of blood through blood vessels.
• Venous Hum is common benign finding on auscultation in children. It is most likely due to due turbulent flow in the internal juguar vein ( when the blood enters the thoracic intlet)
• It is typically a continuous murmur that occur on either side of the neck ( It is more common on the RT side, and it tends to be louder during diastole)
• The murmur disappears or becomes softer when the pt compresses the internal jugular vein, lie in the supine position or flex their head ( which helps differentiate from the PDA).

Question 30

Mitral Regurgitation

Answer 30

• Rupture of a papillary muscle would result in acute mitral regurgitation (MR), a complication associated with myocardial infarction (MI).
• Holosystolic, blowing murmur of MR, which is best heard in the apex.

Question 31

Aortic Regurgitation

Answer 31

• Bounding pulses of peripheral arteries (water hammer pulse) occur in patients with aortic regurgitation (AR) and are caused by the hemodynamic changes caused by the regurgitant aortic valve.
• Decrescendo, early diastolic murmur of AR, which is best heard in the left third and fourth intercostal spaces along the left sternal border.

Question 32

Heart Failure

Answer 32

• Elevated levels of brain natriuretic peptide (BNP) and the presence of an S3 gallop both indicate increased ventricular filling pressures, which is seen in congestive heart failure (CHF).
• High levels of BNP (> 400 pg/mL) in patients with classic symptoms of CHF have a high positive predictive value and are associated with a worse prognosis, while low values (< 100 pg/mL) in patients with dyspnea have a high negative predictive value for CHF.

Question 33

Aortic Stenosis

Answer 33

• usually due to the calcification of the aortic valve is the most common cause of aortic stenosis (AS).
• The resulting left ventricular outflow tract obstruction causes left ventricular hypertrophy, which manifests with an S4 gallop, not an S3 gallop.
• a systolic, crescendo-decrescendo murmur heard loudest at the upper right sternal border.

Question 34

Left heart failure Sx

Answer 34

• PND
• frothy cough
• S4
• bibasilar crackles
• EF less than 60%
• Hyperventilation, which will show respiratory alkalosis on ABG.

Question 35

Lt heart failure with preserved EF

Answer 35

• Usually as a result of chronic uncontrolled hypertension is the most common cause of HFpEF.
• Chronic hypertension increases the afterload against which the left ventricle (LV) contracts. As a compensatory mechanism, the myocardium undergoes concentric hypertrophy to maintain cardiac output. This leads to LV thickening with a consequent increase in LV stiffness and impaired myocardial relaxation. As a result, patients develop an increase in left ventricular filling pressures and reduced ventricular filling (i.e., diastolic heart failure) with normal ventricular contraction.

Question 36

LT heart failure with reduced EF

Answer 36

usually happens post MI

Usually due to reduced cardiac contractility

Question 37

Lt heart failure with pEF TTt

Answer 37

1. O2 and ventillatory support
2. IV furosmedie ( monitory for hypoK, and HypoNa, as well as weight changes, and volume status).
3. IV nitroprusside and NG can be used as an adjunct ttt, which may cause peripheral vasodilation, resulting in pooling of blood in the venous system, which reduce ventricular filling pressure and improve cardiac function/

Question 38

Hypothermia

Answer 38

Classification

1. Mild: 32-35 C (90-95 F)

Tachycardia, tachypnea
Ataxia, dysarthria, increased shivering
2. Moderate: 28-32 C (82-90 F)

Bradycardia, lethargy, hypoventilation, decreased shivering, atrial arrhythmias
3. Severe: <28 C (82 F)

Coma, cardiovascular collapse, ventricular arrhythmias
Treatment

Management:

1. Warmed (42 C [107 F]) crystalloid for hypotension
2. Endotracheal intubation in comatose patients
3. Rewarming techniques

Mild hypothermia: passive external warming (remove wet clothing, cover with blankets)
Moderate hypothermia: active external warming (warm blankets, heating pads, warm baths)
Severe hypothermia: active internal rewarming (warmed pleural or peritoneal irrigation, warmed humidified oxygen)

Question 39

Hypothermia Management

Answer 39

Most patients with mild hypothermia will respond to conservative measures, including fluid resuscitation and passive warming (ie, removing wet clothes and covering with blankets). Treatment should target a warming rate of approximately 1-2 C/hr. Core temperature may initially fall slightly due to increased return of blood from cold extremities. Once patients are euthermic and hemodynamically stable, they may be transitioned to oral fluids and nutrition

• Dopamine may be necessary for hypothermic patients if intravenous fluids and rewarming measures are ineffective in restoring normal blood pressure.
• Active internal rewarming with pleural or peritoneal irrigation may occasionally be needed for patients with severe hypothermia (core temperature <28 C [82 F]). External warming is more appropriate for patients with mild to moderate hypothermia.
• Endurance athletes are at risk for thermal illness, both hyper- and hypothermia. Mild hypothermia is generally managed with passive rewarming. More severe hypothermia requires aggressive treatment, including active external (heated blankets) and internal (heated peritoneal irrigation) rewarming.

Question 40

Caustic Alkali Ingestion

Answer 40

Caustic ingestion

Clinical features

Chemical burn or liquefaction necrosis resulting in:

Laryngeal damage: hoarseness, stridor
Esophageal damage: dysphagia, odynophagia
Gastric damage: epigastric pain, bleeding
Management

Secure airway, breathing, circulation
Decontamination: remove contaminated clothing & visible chemicals; irrigate exposed skin
Chest x-ray if respiratory symptoms
Endoscopy within 24 hr
Complications

Upper airway compromise
Perforation
Strictures/stenosis (2-3 weeks)
Ulcers
Cancer

Caustic Esophageal injury
This patient who ingested sodium hydroxide (a strongly caustic alkaline solution) now has pain, dysphagia, and erythema of the oropharynx, which is concerning for caustic esophageal injury. This injury can be caused by ingestion of:

acidic substances, which cause coagulation necrosis (eg, protein denaturation) that results in an eschar, thereby preventing further acid penetration and injury.
alkaline substances (eg, many cleaning supplies), which cause liquefactive necrosis (eg, cell membrane dissolution) that often leads to deeper penetration of tissues and therefore more severe injuries.
Mucosal injury results from contact with the caustic substance (rather than from systemic absorption); therefore, patients often have immediate oropharyngeal, retrosternal, or epigastric pain as well as dysphagia and hypersalivation (eg, drooling). Vomiting and hematemesis may also occur. Patients should initially undergo assessment and stabilization of the airway, breathing, and circulation. Serial chest and abdominal x-rays should be obtained to identify any signs of perforation, such as pneumomediastinum, pleural effusions, or subdiaphragmatic air (none of which are seen in this patient). An upper gastrointestinal x-ray study with water-soluble contrast should be performed in patients with suspected perforation.

The severity of esophageal injury cannot be predicted by either clinical symptoms or the extent of oral injury seen on physical examination. Therefore, in the absence of perforation or severe respiratory distress, endoscopic evaluation within the first 24 hours is recommended to assess the severity of esophageal damage.

• Corticosteroid therapy has been hypothesized to reduce the risk of late complications (eg, stricture) but has not been shown to be effective. In addition, it may increase the risk of secondary infections.
• Because esophageal damage occurs instantaneously, neutralizing agents are not effective. In addition, acid-base reactions are exothermic and could cause further injury.

Caustic alkali ingestion causes immediate esophageal injury with liquefactive necrosis. In stable patients with no evidence of perforation, endoscopy should be performed within the first 24 hours to assess the severity of the injury and guide further management.

Question 41

Opioid Intoxication

Answer 41

Opioid Intoxication

Clinical Features of Opioid Intoxication:
AMS, Somnolence
Pinpoint pupils ( less than 2 mm), but it could be sometime absent
shallow breathing or decreased respiratory rate
bradycardia, hypothermia, and decreased bowel sounds
respiratory acidosis on ABG.

Risk Factors for Opioid Intoxication:
Substance Abuse
Chronic Opioid Use
Hospitalized pt ( especially post-operative)
hepatic or renal insufficiency

Management:
Naloxone
Airway management and ventilation
Exclude other causes of altered mental status ( ex. hypoglycaemia)

Question 42

Signs of Opioid Intoxication

Answer 42

Signs of Opioid Intoxication:

AMS, respiratory depression, hypotension, hypothermia, decreased bowel sounds

Naloxone ( early administration) decreases the need for invasive interventions(ex. intubation)

Question 43

Allergic Reactions

Answer 43

Local allergic reaction is swelling and erythema contiguous to the site of the sting to the multiple stings form fire ant bites or wasps or bees

Wheal and flare reactions: occur within a few mins of the encounter and are accompanied by a burning and stinging pain. Sterile pustules develop within 24 hours due to venom alkaloids. They should be left intact and they resolve within a week. These minor reactions don’t require treatment
Large local reactions- exaggerated, local IgE mediated response, characterized by erythema, warmth and swelling. Large local reactions develop within the first 24 hours and extend to ~10 ccm or more contiguously from the site of the sting. Swelling can be significant enough to cause vascular compromise  ( absent in this pt with normal perfusion and sensation), but this rare.  The lesions contain fibrin, eosinophils, neutrophils and lymphocytes. They are treated with topical high potency corticosteroids ( ex. Clobatesol 0.05% ointment and oral anti-histamines)
In pts with severe local symptoms, a short course of oral prednisone can be prescribed. 
Systemic Reactions ( e.x. vomiting, urticaria, swelling of the airway, bronchospasm, shock ( hypotension) should be treated with anaphylaxis with IM or IV epinephrine. This patient’s localized swelling in the feet with no systemic manifestations of anaphylaxis ( ex. normal vital signs, clear lungs, normal oropharyngeal exam) makes a systemic reaction unlikely.