USMLE #wizard

High yield topics for Step 1 and Step 2 explored. Sharing my notes that will help you excel on the USMLE exams! Please feel free to request material you'd like to cover!

[theplaguemd-deactivated20220116]

You wont ever have trouble remembering this: Modified Duke Criteria for diagnosis of endocarditis. Have fun! #cardiology #infectiousdiseases #medicine #postitpearls #doctors20 #FOAMed #FOAM #MedEd #FOOAMcc #FOAMus #FOAMEMS #illustration #USMLE #medicalstudent #medicalschool #education #art #drawing #anatomy #physiology #pathophysiology #emergencymedicine #criticalcare #nursingstudent #medicalillustration (at Spain)

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Do YOU know your Abdominal Pain?

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Ischemia

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I matched into General Surgery!!!

Officially going to become a surgeon. #dreamcometrue

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Hyperbilirubinemias

% Conjugated Bilirubin (CB) = CB / Total bilirubin Unconjugated bilirubin (UCB)

All hereditary hyperbilirubinemias are Autosomal Recessive.

Not included - posthepatic cause of jaundice: Galactosemia

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Trimethoprim/Sulfamethoxazole (Bactrim)

*DOC = drug of choice

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Staphylococcus Aureus

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Ebstein Barr Virus

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Nephritic Syndrome Overview

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Visual Pathway Lesions Practice

I put this together and it really helps to practice this worksheet!

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Hemodynamics in Shock

Notes:

Distributive Shock ・↑CO: rapid blood flow through dilated arterioles ・↓SVR: arteriolar vasodilation ・↑MvO₂: blood flowing too fast ➝ tissues can't extract O₂

Cardiogenic Shock 1. LV Dysfunction    ・↑LVEDP: pulmonary edema 2. RVMI     ・↓LVEDP: clear lungs     ・↓RV SV ➝ ↓LV filling & CO ➝ ↓BP unresponsive to IV fluids

Obstructive Shock 1. Pulmonary Vascular     ・↓LVEDP: Right ventricle fails because it is unable to generate enough pressure to overcome the high pulmonary vascular resistance associated with PE or PH 2. Mechanical     ・↑CVP: JVD     ・↑LVEDP: ↑RV filling pressure ➝ ↓LV filling ➝ no pulmonary edema

Pericardial Tamponade ・Persistent JVD, tachycardia, & hypotension despite IV fluid resuscitation ・Equalization of right atrial, right ventricular end-diastolic and pulmonary artery wedge pressures is classic in pericardial tamponade and distinguishes it from primary cardiogenic shock ・RAP = RVEDP = PCWP

Addisonian crisis ・Adrenal failure due to mineralocorticoid deficiency ・In states of mineralocorticoid deficiency, vasodilatation can occur due to altered vascular tone and aldosterone-deficiency-mediated hypovolemia

Terminology: RAP/CVP: right atrial pressure/central venous pressure PCWP/LVEDP: pulmonary capillary wedge pressure/left ventricular end diastolic pressure SVR/TPR: systemic vascular resistance/total peripheral resistance MvO₂: mixed venous oxygen content LAD: left anterior descending artery RVMI: right ventricular myocardial infarction RCA: right coronary artery SV: stroke volume PE: pulmonary embolism PH: pulmonary hypertension

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Changes after Myocardial Infarction

This chart is a compilation of material taken from UWorld, Pathoma, and Goljan.

Terminology: MCC: most common cause NՓ: neutrophils MՓ: macrophages SCD: sudden cardiac death EF: ejection fraction LHF: left heart failure FRs: free radicals LAD: left anterior descending artery RCA: right circumflex artery

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Calcium Homeostasis

M-CSF (monocyte colony stimulating factor) and RANKL (look up the acronym if you want) are the most important factors for osteoclast differentiation.

Osteoprotegerin (OPG aka osteoclastogenesis inhibitory factor) is a physiologic decoy receptor for RANKL and is upregulated by estrogen. This is important because of pharmacology: ・Denosumab acts like osteoprotegerin and is used in the treatment of osteoporosis and bone metastasis.

Low OPG : RANKL ratio ➝ osteoclast fusion, activation, survival

High OPG : RANKL ratio ➝ decreased osteoclast formation and survival

Vitamin D₃ is hydroxylated in the liver by the CYP-450 system, so two notable causes of Vitamin D deficiency are: ・Chronic liver disease: Decreased synthesis of 25-(OH)-D in the CYP-450 system. ・Induction of the liver cytochrome P-450 enzyme system (e.g., alcohol): Increased metabolism of 25-(OH)-D into an inactive metabolite. Know your pharmacology most common inducers!

**drawing inspired by @Armando71021105

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Stages of Inflammation

It’s important to know the normal, especially when it ties into pathology.

Leukocyte Adhesion Deficiency (LAD) Disorders

(AR inheritance pattern)

LAD type 1 ・Absence of CD18 subunit of β2-integrin ・Impaired leukocyte adherence & transmigration LAD type 2 ・Impaired fucosylation of sialyl Lewis X on leukocytes → defeciency of endothelial cell selectin binding LAD type 3 ・Impaired cytokine signaling prevents integrin activation

Clinical features: ・Recurrent skin infections → celulitis, abscess, omphalitis (superficial cellulitis around umbilical stump) ・Recurrent mucosal infections → severe periodontitis ・Inflammation with notable lack of purulence (no PMNs) ・♥︎ Delayed separation of umbilical cord (>21 days) ・Poor wound healing ・Peripheral blood neutrophilic leukocytosis (loss of marginating pool) with neutrophilia

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Summary of Cardiac Electrical Activity

Note: An increase in U-wave amplitude is frequently associated with hypokalemia.

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Glycogen Storage Diseases

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Congenital Adrenal Hyperplasia

My strongest advice.... PRACTICE DRAWING THIS YOURSELF! 💪

In case you’re wondering, I don’t include 17-Hydroxylase deficiency because it is rare, and I consider it low yield.

Use the screening and urine tests to narrow down your answer choices quickly. In my opinion, these diseases will all present similarly on an exam. You might get tripped up when they give you non-classical 21-OHase deficiency vs. 11-OHase deficiency. Use these two labs to guide you in the right direction.