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Ascites - Diagnostic Approach and Differential Diagnosis
The most common causes: cirrhosis, malignancy and heart failure. Approx
Ascites - Diagnostic Approach and Differential Diagnosis The most common causes: cirrhosis, malignancy and heart failure. Approx 5% of patients w/ ascites have more than one cause (e.g. cirrhosis + TB, peritonitis, peritoneal carcinomatosis, HF, etc.). Physical Exam: 1) Most relevant findings: Fluid wave (LR 5.3), peripheral edema (LR 3.8) / absence of edema (LR 0.17), shifting dullness (LR 2.1) - fluid wave/shifting dullness detect > 1 litre of ascites. 2) Other findings: bulging flanks, flank dullness, puddle sign, auscultatory percussion, abdominal wall hernias (umbilical, inguinal, incisional). 3) Signs of underlying disease: Cirrhosis, Malignancy, Heart Failure Labs + Ascitic Fluid Analysis: 1) General appearance: Uncomplicated ascites: clear, pale straw-colored yellow, infection: hazy, cloudy or bloody fluid; hemorrhagic: frank blood; chylous: milky fluid; brown: elevated bilirubin 2) Routine tests: Cell count and differential, albumin and total protein concentration 3) Optional tests: Culture in blood culture bottles (infection, bowel perforation), glucose concentration (malignancy, infection, bowel perforation), LDH (malignancy, infection, bowel perforation), gram stain (suspected bowel perforation), amylase concentration (pancreatic ascites or bowel perforation), TB smear/culture/ADA (TB peritonitis), cytology/CEA antigen (malignancy), triglyceride (chylous ascites), bilirubin concentration (bowel or biliary perforation), Serum pro-brain natriuretic peptide (heart failure) Dr. Jorge Cortés @Jcortesizaguirr #Ascites #workup #Differential #Diagnosis #hepatology
Benign Prostatic Hyperplasia: Pathogenesis and Medications
Aging
 -> Increased Testosterone -> Testosterone metabolized into DHT by type
Benign Prostatic Hyperplasia: Pathogenesis and Medications Aging -> Increased Testosterone -> Testosterone metabolized into DHT by type II 5-a-reductase in prostate -> DHT binds to androgen receptor in prostate cell nuclei -> Hyperplasia of the prostate -> Prostate encapsulated by fibromuscular tissue, therefore grows inwards -> Prostatic urethral compression and bladder outlet obstruction -> Increased Bladder pressures -> Bladder smooth-muscle hyperplasia (detrusor thickening) -> Increased Sensitivity (i.e. overactive detrusor) -> Decreased Volume to first detrusor contractio -> LUTS - alpha-1 blockers (e.g. tamsulosin) -> Bladder and prostate smooth-muscle alpha-1 receptor antagonism Relaxation of bladder outlet and prostate smooth-muscle -> Improved urinary outflow - PDE-5 inhibitors (e.g. tadalafil) -> Decr PDE-5-mediated cGMP degradation in prostate smooth-muscle and associated vascular supply -> Relaxation of prostate smooth-muscle -> Improved urinary outflow - 5-ARIs (e.g. dutasteride) -> Decr 5-a-reductase activity -> Decr Conversion of testosterone into DHT -> Decr Progression of LUTS - LHRH receptor antagonists (e.g. cetrorelix) -> GnRH antagonism -> Decr LH secretion from pituitary -> Decr Testosterone secretion from testicular Leydig cells -> Decr DHT production -> Decr progression of LUTS - ß3-adrenergic agonists (e.g. mirabegron) -> Relaxation of detrusor muscle -> Incr Bladder capacity -> Improved LUTS - anticholinergics (e.g. oxybutynin) -> Acetylcholine antagonism at muscarinic receptors -> Relaxation of bladder outlet smooth-muscle -> Incr volume to first detrusor contraction -> Improved LUTS - NSAlDs -> Decr COX activity -> Decr Prostaglandin release -> Analgesia and Decreased Prostatic inflammation #BPH #Benign #Prostatic #Hyperplasia #Prostate #Pathophysiology #Medications #Pharmacology #Urology
Benign Prostatic Hyperplasia: Pathogenesis and Clinical Findings

Hormonal alterations (result of aging process)
    ->
Benign Prostatic Hyperplasia: Pathogenesis and Clinical Findings Hormonal alterations (result of aging process) -> Incr testosterone to DHT conversion via 5-alpha-reductase -> DHT binds to AR within prostate cells, especially in transitional zone -> Incr aromatization of androgens to estrogens via enzyme P450 aromatase -> Estrogen binds to ERs in the prostate -> altered gene expression -> Initiation of ER and AR -dependent production & secretion of peptide growth factors (IGF-1, EGF, FGF-related proteins) Inflammation & immune dysregulation -> Bacterial infection, diet, hormones, urine reflux, autoimmune response, or combination -> Incr proliferation of immunocompetent cells (lymphocytes, macrophages, granulocytes) -> Prostate Inflammation: Incr tissue injury and activation of inflammatory cytokines (IL-2, IL-15, IL-17) -> Chronic process of tissue remodeling activates hyper-proliferative programs via Incr growth factors and Decr apoptosis -> Stromal proliferation, transdifferentiation, and extracellular matrix production -> Bladder outlet obstruction due to mass effect (static component) - Postmicturition: Dribbling, incomplete emptying - Voiding Symptoms: Hesitancy, weak steam, intermittency, straining - Storage Symptoms: Urgency, nocturia, incontinence, frequency Chronic retention of urine & inability to completely empty the bladder -> Hydronephrosis, Acute or chronic renal injury, Hematuria, Urinary retention, UTIs & bladder stones #BPH #Benign #Prostatic #Hyperplasia #Prostate #Pathophysiology #Urology #Signs #Symptoms #Diagnosis
Types of Renal Calculi

Calcium oxalate
 - Interstitial apatite plaque, Low urine volume, Increased urinary calcium excretion,
Types of Renal Calculi Calcium oxalate - Interstitial apatite plaque, Low urine volume, Increased urinary calcium excretion, Increased urinary oxalate (dietary) - Idiopathic hypercalciuria, Hypercalcemia, Renal tubular acidosis (type 1) Calcium phosphate - Inner medullary collecting duct plaque, Low urine volume, Increased urinary calcium excretion - Idiopathic hypercalciuria, Hypercalcemia Calcium carbonate - Hypercalciuria, Hypercarbonaturia - Ingestion of calcium carbonate as calcium supplement (>2000 mg/day) Cystine - Cystinuria, Defective transport of cysteine and di-basic amino acids in kidney and intestine, Low urinary citrate - Autosomal recessive genetic disease (incidence 1/10,000) Struvite - Magnesium, ammonium and phosphate: alkaline urine - Infection with ammonia-producing organisms: Proteus, Pseudomonas, Klebsiella, Staphylococcus and Mycoplasma infections, High dietary magnesium Uric acid - Hyperuricemia - Hyperuricemia, Renal tubular acidosis (types 1 and 2) Drugs - Acyclovir, indinavir, atazanavir, triamterene - Antiviral treatment for herpes virus or HIV/AIDS, diuretics to treat heart failure #Calculi #Types #Renal #stones #differential #diagnosis #causes #calculus
Causes of Nephrolithiasis - Differential Diagnosis Algorithm
Radio-opaque - Calcium-containing - 90% of stones
Radiolucent - Non-calcium 10%
Causes of Nephrolithiasis - Differential Diagnosis Algorithm Radio-opaque - Calcium-containing - 90% of stones Radiolucent - Non-calcium 10% of stones Uric Acid Stones: • Hyperuricosuria • High protein intake Soft Stones - Struvite Stones - 10% of stones: • Urinary tract infection Cysteine Stones - Non Calcium containing, but opaque: • Cystinuria Hypercalciuria: • Increased PTH • High salt intake • High protein intake Hyperoxaluria: • Enteric overproduction • Low calcium intake • Dietary • Ethylene glycol ingestion Stones with decreased solubility: • Low urine volume • Hypocitraturia • RTA Type I • High protein intake Anatomical problem: • Medullary sponge kidney #RenalStones #Nephrolithiasis #Nephrology #Differential #Diagnosis #Algorithm #Causes
Approach to Therapy for Idiopathic Urolithiasis

#Management #Algorithm #Treatment #Idiopathic #Urolithiasis #Nephrolithiasis
Approach to Therapy for Idiopathic Urolithiasis #Management #Algorithm #Treatment #Idiopathic #Urolithiasis #Nephrolithiasis
Algorithm and Differential Diagnosis of Macroscopic Hematuria
Important Historical Elements:
- Painless: suggests malignancy
- Painful: suggests calculi/infection
- Urinalysis:
Algorithm and Differential Diagnosis of Macroscopic Hematuria Important Historical Elements: - Painless: suggests malignancy - Painful: suggests calculi/infection - Urinalysis: presence of dysmorphic RBC’s, RBC/WBC casts, proteinuria suggest intrinsic renal disease - Timing: early (distal urethra), throughout (upper urinary tract), terminal (bladder neck, prostatic) #Diagnosis #EM #IM #Urology #Hematuria #Macroscopic #Differential #Algorithm #Ddxof
Basic preoperative airway assessment conducted by anesthesiologists to assess intubation difficulty, along with the two commonly
Basic preoperative airway assessment conducted by anesthesiologists to assess intubation difficulty, along with the two commonly used methods to do so based on airway class. #clinical #management #anesthesia #anesthesiology #airway #intubation References: Lamberg, J. J. (2019, November 9). Mallampati Classification: Mallampati Classification. https://emedicine.medscape.com/article/2172419-overview.
Nephritic vs Nephrotic Syndrome

Step 1: If the patient has hematuria and/or proteinuria, think about nephrotic/nephritic syndromes.
Step
Nephritic vs Nephrotic Syndrome Step 1: If the patient has hematuria and/or proteinuria, think about nephrotic/nephritic syndromes. Step 2: Does the patient have glomerular hematuria (RBC casts or dysmorphic RBCs in urine)? #Nephritic #Nephrotic #Syndrome #Comparison #Algorithm #Nephrology #Diagnosis
Approach to an Eye Exam

1. History
2. Obvious Physical Trauma
3. Initial Assessment
  A. Visual Acuity
Approach to an Eye Exam 1. History 2. Obvious Physical Trauma 3. Initial Assessment A. Visual Acuity B. Pupils a. Light Reflex, Accommodation, RAPD C. Ocular Movements (CN 3, 4, 6) D. Visual Fields by Confrontation 4. Slit Lamp Exam (SLE) A. Lids / Lashes/ Lacrimal B. Sclera/ Conjunctiva C. Cornea D. Anterior Chamber E. Iris F. Lens G. Vitreous Humor 5. Fundoscopy A. Retina B. Optic Nerve / Disc / Cup: Disc Ratio C. Macula D. Fovea E. Blood Vessels #Ocular #EyeExamination #Approach #Ophthalmology #PhysicalExam