PANCE Topic List: Renal/GU
Terms in this set (305)
What is the role of the kidney?
Na balance/Circulatory volume
Ca/Phosphorus/Vit D metabolism
Urea/middle molecule clearance
What is Acute renal failure?
AKA acute kidney injury (AKI). It's a measurable reduction in GFR with accumulation of nitrogenous wastes (BUN, creatinine) which is called azotemia. AKI is SCr>1.5 or 50% increase in baseline SCr.
What is the criteria for AKI?
Clinical features of AKI?
Note: differs depending on underlying cause
Increased BUN/Cr ratio
Oliguria (<500cc a day)
Increased BP, differences in volume status, edema
SOB, angina, edema
Decreased mental status
Diagnostic labs for AKI?
Fractional excretion of Na (FENa)
Why is BUN not a reliable indicator of renal function?
Urea is reabsorbed in the nephron during stasis which causes false elevations of BUN. It is much more sensitive to dehydration, catabolism, diet, renal perfusion, and liver disease.
UA is best for detecting what causes of AKI?
Diagnostic imaging for AKI?
Renal US/CT - kidney smaller than 10cm is abnormal
What are the three types of AKI?
Pre-renal failure - inadequate delivery of blood to glomerulus
Intrinsic renal failure - tubular disease, glomerular disease, overlap
Post-renal failure - inability of urine to leave the body (obstruction)
What are the 2 overall most common causes for AKI?
Acute tubular necrosis (an intrinsic cause)
Pathophysiology of pre-renal AKI?
There is decreased effective circulating arterial volume, which leads to decreased renal perfusion and decreased GFR. The BUN to creatinine ratio will be elevated, and urinary casts are not commonly seen. Intrinsic renal damage may develop if hypoperfusion of the kidneys persists.
What are pre-renal causes of AKI?
Ineffective circulating volume (CHF, cirrhosis, nephrotic syndrome, early sepsis)
Renal artery stenosis
Tx of AKI due to pre-renal causes?
Isotonic IVF (NS or LR)
If due to CHF, optimize cardiac output and possibly use diuretics
What are postrenal causes of AKI?
Obstructive uropathy (urolithiasis, BPH, bladder outlet obstruction, cancer)
Clinical features of post-renal AKI?
Decreased urine output
Tx of AKI due to post-renal causes?
Relief of obstruction - stents, catheter
What are 4 categories of intrinsic AKI? What is the MC cause of intrinsic AKI?
Acute tubular necrosis (ATN) <---MC (85%)
Acute Interstitial Nephritis (AIN) (8%)
Acute Glomerulonephritis (5%)
What is ATN?
Death of tubular epithelial cells that form the renal tubules of the kidneys. It is typically seen in critically ill children with sepsis, hypotension, or exposure to nephrotoxic medications. Characterized by elevated creatinine and a urinalysis showing brown granular casts.
What are causes of ATN?
Ischemia (from progression from prerenal causes)
Toxins (drugs, pigments, proteins, crystals)
Contrast induced AKI
What will a UA look like with ATN?
Pigmented, granular, MUDDY BROWN CASTS
+/- RBCs and protein from tubular damage
Urine Na >20
Urine osmolality <350
What are causes of Acute interstitial nephritis (AIN)?
Drug induced allergy (NSAIDs, beta lactams, sulfa drugs, PPIs)
Infection (pyelo, legionella, Tb)
Infiltrative (sarcoid, lymphoma, leukemia)
Autoimmune (Sjogrens, IgG4, SLE)
Clinical features of AIN?
Presents 1-2 weeks following onset of an inciting agent (taking a medication, infection, autoimmune flare, etc), and may be associated with symptoms such as fever, rash, arthralgias, and eosinophilia
Urine output is preserved.
BUN to creatinine ratio is <15
Removal of the offending agent often leads to recovery
What will a UA look like with AIN?
+WBCs and WBC casts
Negative Urine cx
+Urine eosinophils with antibiotic induced
+Lymphocytes with NSAID induced
What is Glomerulonephritis?
AKA Nephritic syndrome. Type of intrinsic AKI. There is damage to the renal glomeruli due to inflammatory proteins in the glomerular membranes as the result of an immunologic response. 60% of cases are in children 2-12. Prognosis is excellent in children, worse in adults. Can be focal (affects <50%) or diffuse (affects >50%)
What are causes of GN? MC cause in adults?
Children: HUS, benign hematuria, Honoch-Schonlein purpura, mild postinfectious GN, IgA nephropathy, Hereditary nephritis, postinfectious GN, membranoproliferative GN
Adults: IgA nephropathy (MC cause), Lupus, hereditary nephritis, membranoproliferative GN, postinfectious GN, vasculitis
Clinical features of GN?
Tea/cola colored urine
Edema of face and eyes in morning, feet and ankles in the evening
Which urinary laboratory abnormality is most suggestive of the diagnosis of acute glomerulonephritis?
Diagnostic studies for GN?
Antistrepolysin-O titer (ASO titer)
UA - hematuria, RBC casts, proteinuria
Renal biopsy with immnofluroescence -determines extent of disease
Treatment for GN?
Methylprednisolone and immunosuppresive drugs
Dialysis if symptomatic azotemia is present
ACE-I for chronic GN
When is short term dialysis done for AKI?
Acid-base disturbance (acidosis)
Electrolyte disorder (usu. hyperkalemia, K>6.5)
Overload of volume
What is the MC cause of acute renal failure in children? What is it caused by?
Hemolytic uremic syndrome caused by Shiga toxin-producing Escherichia coli O157:H7 (a GI illness). Causes intrinsic AKI.
What is the classic history of a patients with HUS?
A prodromal illness with bloody diarrhea following ingestion of hamburger meat contaminated with E. coli O157:H7
Clinical features of HUS?
Prodromal GI illness (abdominal pain or tenderness, nausea or vomiting, fever and anemia)
What should be monitored with HUS?
Renal function (BUN/creatinine levels)
Diagnosis and treatment of HUS?
Diagnosis is clinical
Treatment is supportive because HUS is a self-limiting disease with spontaneous recovery
What is chronic kidney disease (CKD)?
Progression of ongoing loss of kidney function. It's a GFR <60mL +/- the presence of kidney damage (proteinuria, glomerulonephritis, or structural damage) for more than 3 months. Patients with CKD progress to renal failure
What are the 5 stages of CKD?
1: GFR>90 with persistent albuminuria
2: GFR 60-89
3: GFR 30-59
4: GFR 15-29
5: GFR <15
What are causes of CKD? MC cause?
Hypertension <---2nd MC
Other: SLE, sickle cell, glomerular diseases, tubulointerstitial renal disease, chronic pyelonephritis, vascular disease, obstructive nephropathies
Signs and symptoms of CKD?
General: Fatigue/malaise/weakness, anorexia, metallic taste
Derm: Uremic frost (from urea crystals), pruritis, easy bruising
Neuro: AMS, seizures, Asterixis (flapping tremor), Sensory deficits
Cardio: Pericarditis, HTN, HLD, CHF
Metabolic: Hyperkalemia, hyperphophatemia, hypocalcemia
Diagnostic studies for CKD? What is the gold standard for staging?
GFR is gold standard for staging
Renal US - bilateral small kidneys indicates CKD
UA - proteinuria, microalbuminuria (appears early in disease)
What is the Cockcroft-Gault formula?
Uses patient age, body weight, and serum Cr to estimate GFR
Management of CKD?
Nephro referral once GRF <30
Treat Cardiac risk factors (smoking cessation, HTN, HLD, DM, weight loss)
Tight BP control (<130/80) - ACE/ARB slows progression of CKD however should not be used in renal failure
EPO for anemia
Antiplatelet therapy - dDAVP
Restriction of protein, Na, K intake
Consider transplant eval
What is Hydronephrosis?
A condition characterized by excess fluid in a kidney due to a backup of urine.
Pathophysiology of hydronephrosis?
Obstruction to urinary flow which may occur at any site in the urinary tract. Urinary tract obstruction (UTO) may be acute or chronic, partial or complete, and unilateral or bilateral. UTO is important to recognize since it is readily reversible if quickly corrected. If uncorrected, UTO may predispose to urinary tract infection (UTI) and urosepsis and eventually cause end-stage renal disease (ESRD).
Causes of hydronephrosis?
Kidney pelvis (Stones)
Ureter (intrinsic and extrinsic, vesicoureteral reflux)
Bladder (stones, tumors, neurogenic)
Prostate (BPH, cancer, prostatitis)
Clinical presentation of hydronephrosis?
Change in urine output
Increased Serum Cr
Urinary frequency, hesitancy
What is the preferred diagnostic study for hydronephrosis?
Can also do CT if stone is suspected
Voiding cystourethrography (VCUG) if reflux is suspected
Tx for hydronephrosis?
Treat underlying cause:
What is Nephrotic syndrome?
Excretion of >3.5g of protein in 24hrs. Albumin <3.5, edema, and elevated cholesterol. Prognosis depends on degree and specific cause.
Causes of primary nephrotic syndrome? MC?
Focal segmental glomerulosclerosis (FSGS) - 40%
Membranous glomerulonephritis (Focal GN) - 30%
Minimal change disease - 20% (MC cause in peds)
Membranoproliferative GN - 5%
Mesangial proliferative GN
Congenital nephrotic syndrome
Causes of secondary nephrotic syndrome? MC?
Diabetes --->glomerulosclerosis (Kimmelstiel-Wilson lesion) (MC)
Toxemia of pregnancy
Drugs and nephrotoxins
Lymphomas and leukemias
What can nephrotic syndrome predispose a patient to?
Clots due to loss of protein S and C and antithrombin III
Clinical features of nephrotic syndrome?
NO HEMATURIA, NO RBC CASTS!
Diagnostic studies for nephrotic syndrome?
24 hour urine - to measure proteinuria
UA - will show PROTEINURIA, lipiduria, glycosuria, FOAMY urine
Microscopic UA - Granular casts, hyaline casts, fatty casts. Key finding is OVAL FAT BODY - a tubular cell that has reabsorbed some of excess lipids in urine
BMP - hypoalbuminemia, azotemia
Tx for nephrotic syndrome?
ACEI/ARB <---first line to decrease proteinuria
Diuretics - used judiciously for edema
Dietary - low Na and fluid restriction
Treat infections aggressively
Anticoagulation if there are clots
What is Polycystic kidney disease?
Characterized by growth of numerous cysts on the kidneys made of epithelial cells from renal tubules and collecting system. Cysts replace renal parenchyma which reduces function and leads to kidney failure.
What are three types of PKD? Which is MC?
Autosomal dominant PKD (ADPKD) - MC. Always bilateral. Symptoms develop during 4th decade of life
Autosomal recessive PKD (ARPKD) - begins in utero and can lead to fetal and neonatal death. Surviving infants have significantly reduced life expectancy due to renal/hepatic failure.
Acquired cystic kidney disease (ACKD) - occurs in individuals with long term CKD
Clinical features of PKD?
Back and flank pain
Nocturia <----early sign
Diagnostic labs for PKD?
CBC - anemia (decreased EPO)
UA - proteinuria, hematuria, pyruria, bacteriuria
Diagnostic imaging for PKD? Study of choice?
US <----study of choice
Excretory infusion urography
Tx for PKD?
No cure - treatment is supportive
Fluids and low protein diet
Treat infections aggressively
What are 4 types of renal vascular disease? What is MC cause?
Atherosclerosis ---> renal artery stenosis (90%)
Fibromuscular dysplasia (FMD) - 10%, seen in young women
Polyarteritis nodosa (PAN)
What are suggestive findings of renal vascular disease?
Acute renal failure induced by ACEI/ARB
Recurrent flash pulm edema
Initial workup for renal vascular disease? What is the initial study and the best study?
MRA <---best study
Renal duplex US <---initial test
Tx for renovascular disease?
Control BP with diuretic + ACEI/ARB or CCB
Treat atherosclerosis risk factors (diet, exercise, smoking cessation, glucose control, etc)
Stenting, revascularization for stenosis
FMD - percutaneous tranluminal angioplasty (PTA)
What is the most common type of renal malignancy?
Renal cell carcinoma (RCC). AKA hypernephroma or renal adenocarcinoma. It originates from the epithelial cells of the proximal convoluted tubule.
Risk factors for RCC?
American Indian/Alaskan race
What are two hereditary forms of RCC?
von Hippel-Lindau disease
Hereditary papillary renal carcinoma
Clinical features of RCC? What is the MC symptom? What is the classic triad?
Wide range of symptoms:
Gross or microscopic hematuria <----MC symptom
Classic triad - hematuria, flank pain, palpable mass
Diagnostic studies for RCC? What is the study of choice?
US - to rule out stones
CT with and without contrast - study of choice
MRI with contrast
What is the tx for RCC with localized disease?
What is tx for RCC wth dissemeniated disease?
Hormone therapy and chemo have no effect
Interferon a and interleukin have been successful in reducing growth of some RCCs, including some with mets
What is a Wilms tumor?
AKA Nephroblastoma. It is the MC abdominal malignancy in children. It is caused by alterations in the genes responsible for genitourinary development.
Clinical features of a Wilms tumor? MC symptom?
Asymptomatic unilateral abdominal mass (80% of cases)
Abdominal pain (25% of cases
Work up for Wilms tumor?
Coagulation studies and cytogenetic studies for 1p and 16q chromosomal deletions
Renal US <----initial study
CXR, abdominal CT, abdominal MRI
Treatment for Wilms tumor?
Nephrectomy followed by chemotherapy, with or without post-operative radiotherapy
What are congenital abnormalities commonly associated with Wilms tumor?
Horseshoe kidney, duplicate collecting system, hypospadia and cryptorchidism.
What is vesicouretal reflex?
The retrograde passage of urine from the bladder into the upper urinary tract. It is the most common urologic finding in children
Clinical features of VUR?
Complications from VUR?
Acute pyelonephritis which may lead to loss of renal parenchyma (renal scarring) and CKD
Diagnostic studies for VUR?
Postnatal renal US <---initial test
VCUG is performed only in patients who have abnormalities on US, who develop a UTI during observation, or who have a family history of VUR
What is a Hydrocele?
Mass of fluid-filled congenital remnants of the tunica vaginalis, usually resulting from a patent processus vaginalis.
Clinical features of a hydrocele?
SOFT, non-tender fullness of the hemiscrotum that TRANSILLUMINATES
May wax and wane in size
What is a Varicocele?
Formation of a venous varicosity within the spermatic vein (pampinform plexus).
Which spermatic vein tends to have an increased incidence of varicosity?
L>R because it's longer and joins the left renal vein at right angles
Diagnostic study of choice for varicocele?
Clinical features of varicocele?
NONTENDER "BAG OF WORMS" consistency
Increases in size with Valsalva
Decreases in size with elevation of the scrotum or supine position
Feeling of scrotal heaviness
Chronic in duration
Does not transilluminate
Can be primary (idiopathic) or secondary
Tx for varicocele?
Surgical repair (left spermatic vein ligation) if painful or there is infertility
Tx for hydrocele?
Causes of secondary varicocele?
Abdominal mass that compresses the renal veins (more common with right sided varicocele)
Superior mesenteric artery compression of the left renal vein (aka "Nutcracker Syndrome"; most commonly due to renal cell carcinoma and retroperitoneal fibrosis/adhesions)
What are 5 types of urinary incontinecne?
Characterization of urge incontinence?
Feeling of urgency and frequency, day or night. Caused by detrusor overactivity (AKA overactive bladder)
Causes of urge incontinence?
BPH with overflow
Treatment for urge incontinence?
Characterization of stress incontinence?
Small volumes of urine lost with coughing or sneezing. Due to outlet incompetence often from urologic procedures or multiple pregnancies
Treatment for stress incontinence?
Characterization of overflow incontinence?
Unpredictable dribbling of urine or weak urine stream
Treatment of acute urinary retention?
Acute urinary retention and acontractile bladders require indwelling or intermittent catheterization
What is atonic bladder incontinence?
Incontinence due to severe diabetic neuropathy or stroke. Tx is intermittent caths.
What is functional incontinence?
Inability to get to bathroom due to immobility, impaired cognition, etc
Causes of overflow incontinence
Underactive bladder - meds (e.g. CCBs, anticholinergics), detrusor denervation or injury.
Outlet obstruction - BPH, tumors, urethral stricture, or chronic constipation.
Treatment for overflow incontinence?
discontinuation of medications that promote urinary retention.
Alpha blockers (Prazosin, trazosin)
5-alpha reductase inhibitors (Finasteride)
It's important to rule out what with any intial complaint of incontinence
What is the cause of urolithiasis?
Increased saturation of urine with stone-forming salts or a lack of inhibitors (citrate) in the urine to prevent crystal formation. Can form in the kidney, ureter, or bladder
Risk factors for urolithiasis?
High animal protein, sugar, salt, Vit. C intake
Low K, Ca, fluid, fruits/veggies intake
Abnormal urinary tract anatomy
What are 4 kinds of stones that cause urolithiasis and which is most common?
Calcium oxalate/phosphate - 80%
Uric acid - 5-10%
What condition predisposes a patient to form uric acid crystals?
Acidic urine with or without hyperuricemia
Classic kidney stone findings?
Severe renal pain, flank pain (asymptomatic until inflammation or obstruction occurs)
Stone on AXR
Irritative voiding symptoms
Fever/chills, pyuria (if stone is obstructing)
What is the cause of each type of stone?
Ca oxalate: Formed by precipitation of Ca crystals
Struvite: Formed by combination of Ca, ammonium, Mg. Due to urease producing bacteria (infection stones)
Uric acid: Formed by precipitation of uric acid
Cystine: Due to impairment of tubular cystine reabsorption due to autosomal recessive trait
Where is the MC site of stone obstruction?
Initial diagnostic studies for nephrolithiasis?
Noncontrast helical CT <---study of choice
24 hour urine x2
Strain urine to analyze stone
UA with culture
Additional workup for kidney stones?
Labs: CBC, CMP, PTH, BUN/Cr, oxalate, citrate, pH
Intravenous pyelogram (IVP) <-- rarely indicated
Which renal calculi are radioopaque? Which are radiolucent?
Ca oxalate and struvite are radiopaque
Uric acid and cysteine stones are radiolucent
Medical tx for all types and sizes of kidney stones?
Analgesia is most important first step (narcotics +/- NSAIDs)
All stones should be chemically analyzed with metabolic workup
Surgical tx options for kidney stones
Extracorporeal shock wave lithotripsy (ESWL)
Treatment for nephrolithiasis when stone is <5mm?
<5mm: stone is likely to pass on its own. Fluids, analgesia, strain urine, alpha blocker or CCB to help stone pass. Most pass in 2-4 weeks.
Treatment for nephrolithiasis when stone is 5-10mm?
Elective lithotripsy or ureteroscopy with stone basket extraction
Treatment for nephrolithiasis when stone is >10mm
Ureteral stent or percutaneous nephrostomy <---- gold standard
Chronic treatment for kidney stones
Increase fluid intake
Ca stones - Decrease Na and animal protein intake. D/c thiazides.
Uric acid - Allopurinol, urine alkalinization
Struvite - Antibiotics
Cystine - urine alkalinization
What is the MC cause of bladder calculi?
The MC cause is infection of residual bladder urine with urea-splitting organisms. Bladder stones are much less common than renal or ureteral calculi. In the United States, bladder stones occur almost exclusively in elderly men, often as a complication of other urologic disease. They are usually associated with urinary stasis.
What is Paraphimosis?
Occurs when the foreskin cannot be returned to its anatomic position covering the glans penis. Subsequent venous congestion can lead to arterial compression, penile necrosis and gangrene.
Cause of paraphimosis?
Infection, trauma or hair tourniquets
Clinical features of paraphimosis?
Erythema and engorgement of the penis distal to the obstruction and proximal flaccidity
Initial management of paraphimosis?
Manual reduction should be attempted: Circumferential compression should be held starting at the glans to reduce edema. This should be followed by manual reduction by placing steady pressure on the glans with both thumbs while holding the shaft straight
Urology consult for dorsal slit procedure if reduction doesn't work
What is Phimosis?
Phimosis is the inability to retract foreskin over the glans penis. About 50% of boys typically are able to retract their foreskin by 1 year of age and 80% by age 3.
Treatment for phimosis?
Low-potency topical steroid therapy combined with daily prepuce retraction
Circumcision is definitive treatment
What is Testicular torsion?
Testis is abnormally twisted on its spermatic cord which compromises arterial supply and venous drainage leading to ischemia. Surgical emergency!
Risk factors for testicular torsion?
Postpubertal boys ages 12-18, especially with a history of cryptorchidism
What is a bell-clapper deformity?
Bilateral nonattachement of the testicles by the gubernaculum to the scrotum
Diagnostic studies for testicular torsion?
Doppler U/S demonstrates decreased blood flow
Tx for testicular torsion?
Immediate urologic consultation
Manual detorsion (medial to lateral/opening a book) if delays expected
Surgical detorsion and orchiopexy are definitive therapies
Elective orchiopexy for contralateral testis is recommended
Clinical features of testicular torsion?
Sudden onset of severe unilateral pain and scrotal swelling
Testes are painful to palpation
Negative Phren's sign
No cremasteric reflex
What is the most common congenital abnormality of the genitourinary tract
What is cryptorchidism? Who is at highest risk?
Undescended testes or absence of one or both testes from the scrotum. Highest risk is in premies.
What percent of boys with undescended testes when they are born will still have undescended testes after a year?
Treatment for cryptorchidism?
Observation until 6 months
Orchiopexy - treatment of choice
What is the MC malignancy in young men?
What are types of testicular cancer? MC?
Germ cell tumors (95%)
What are two major types of of germ cell testicular tumors?
How does a patient with a testicular tumor present?
Painless unilateral scrotal mass
Risk factors for testicular cancer?
Diagnostic tests for testicular cancer?
Scrotal US <---initial test of choice
CXR and CT of chest, abdomen, and pelvis to rule out metastasis
What are the two tumors markers for testicular cancer?
Beta Human chorionic gonadotropin (B-HCG)
A nonseminoma testicular tumor is most likely when there is an elevated serum concentration of which markers?
Beta Human chorionic gonadotropin
How do you treat a nonseminomatous tumor?
Inguinal orchiectomy - removal of testis with spermatic cord up to inguinal ring
Chemo for stage II and III
A seminoma testicular tumor is most likely when there is an elevated serum concentration of which marker?
Placental alkaline phosphatase (PLAP)
Rarely is AFP or B-HCG elevated
How do you treat a seminomatous tumor?
What is cystitis?
AKA Bladder infection or UTI. Affects F>M
What are the the MC bacteria that cause UTIs?
E. coli (80% of uncomplicated cystitis)
Risk factors for UTI?
Elderly of both sexes
(Males <50 usually have urethritis due to STD)
Uncomplicated vs complicated UTI?
Uncomplicated: Seen in healthy, nonpregnant women
Complicated: Ascending infection in women, any UTI in a male or pregnant woman, or UTI with underlying structural disease or immunosuppression
What are clinical features of a UTI?
Irritative voiding symptoms (frequency, dysuria, urgency)
Diagnostic studies for UTI?
UA shows +WBCs, +Nitrites, +RBCs, bacteria
What is first line for uncomplicated cystitis?
Nitrofurantoin 100mg PO BID for 5 days
TMP/SMX 160/80mg 1 DS (double strength) PO BID x 3 days
Cipro (second line but used often 1st line)
Antibiotics for treatment of UTI in pregnancy?
Symptomatic tx for UTI?
Phenazopyridine (Pyridium) <----will turn urine orange and stain
What is pyelonephritis?
Infectious inflammatory process involving the kidney parenchyma and renal pelvis. Often due to ascending infection and is MC in young adult women.
What are clinical features of acute pyelonephritis?
Irritative voiding symptoms
Labs for pyelonephritis?
UA: Will show Pyruria, bacteriuria, RBCs, WBC CASTS!
UA Culture - start abx empirically
Antibiotic and duration of tx for outpatient treatment of pyelo?
Cipro 500mg PO BID for 7-14 days
When do you admit for pyelo?
Inability to tolerate oral meds
Signs of obstruction
Antibiotic and duration of tx for inpatient treatment of pyelo?
Ceftriaxone or ampicillin/sulbactam (Unasyn) or aminoglycoside for 14 days (change from IV to PO once improved and afebrile)
What is the MC cause of urethritis in men?
STIs - Neisseria gonorrhoeae is the cause of gonoccocal urethritis. Causes of nongonoccocal urethritis include Mycoplasma genitalium, Ureaplasma, Trichomonas, HSV, and adenovirus.
Clinical features of urethritis?
Diagnostic testing for urethritis?
Usually clinical diagnosis. Can do:
Nucleic acid hybridization or nucleic acid amplification testing
Treatment of urethritis?
Empiric treatment with IM ceftriaxone and oral doxycycline
What is Orchitis?
Inflammation of the testes. MC in prepubertal boys
What is the MC pathogen that causes orchitis?
Clinical features of orchitis?
Diagnostic studies for orchitis?
UA - will show pyuria and bacteruria
Cultures - positive if bacterial
Scrotal US - useful if abscess or tumor is suspected and to rule out testicular torsion
Tx for orchitis?
If mumps is cause - symptomatic with ice and analgesia
If bacterial - antibiotics (ceftriaxone 250mg IM plus Doxy or Azithromycin for 7 days)
What is Balanitis?
Inflammation of the glans penis or clitoris. More commonly refers to males. Can occur at any age.
What are causes of balanitis?
MC risk factor for balanitis?
What are clinical features of balanitis?
Symptoms evolve in 3-7 days
Pain, TTP, or pruritus associated with small erythematous lesions which can be ulcerated or scaly
Tx of balanitis?
Topical clotrimazole if due to Candida
What is Epididymitis?
Infection of epididymis acquired by spread of organisms through the vas deferens.
What is the common cause of epididymitis in men <35? >35?
<35: Chlamydia and Gonorrhea
>35: E. coli
What are clinical features of epididymitis?
Heavy, dull, aching discomfort of testes
Swollen epididymis which is TTP
Warm, erythematous scrotal mass
Fever and chills
Irritative voiding symptoms
+ Prehn's sign <---classic sign but not sensitive
How do you differentiate epididymitis from torsion?
Onset - testicular torsion is abrupt
US - torsion blood flow is decreased
Diagnostic studies for epididymitis?
UA - will show pyuria and bacteriuria
Cultures are positive
Scrotal US - enlarged heterogeneous testis with increased color flow
Treatment for epididymitis?
<35 yo: Ceftriaxone 250mg IM + Doxy or Azithromycin for 7 days. Should be brought back for test of cure.
>35 yo: Cipro 500mg for 10-14 days
Supportive care: Analgesics, Scrotal elevation, Bed rest
What causes acute bacterial prostatitis?
Ascending infection of Gram neg rods in the prostatic ducts
What organism usually causes acute bacterial prostatitis?
E. coli - up to 80% of cases
What are clinical features of acute bacterial prostatitis?
Sudden onset of high fever, chills, low back pain, and perineal pain
Irritative voiding symptoms
Prostate is swollen and tender
Clinical features of chronic prostatitis?
More variable symptoms
Irritative voiding symptoms
What will prostatitis feel like on DRE?
Slightly enlarged, unchanged, or smaller.
Swollen, boggy, and tender
Flattened longitudinal furrow
What will a UA show with acute bacterial prostatitis?
Culture is positive (usually for E. coli)
How do you treat acute prostatitis?
Cipro or Levo for 2-6 weeks
Bactrim for 6 weeks
Culture urine 1 week after therapy
NSAIDs and alpha 1 blockers for symptomatic tx
What is benign prostatic hypertrophy (BPH)?
Growth of prostatic tissue in transition zone. It compresses the urethra. BPH is the most common benign tumor in men, with the incidence estimated at 50% of men by 60 years.
What percent of men will develop BPH? When?
80% - usually starting in the 5th decade of life. 50% will need treatment
What are signs/symptoms of BPH?
Urinary frequency, urgency, nocturia
Stream hesitancy and poor flow, intermittency, straining, dribbling
What will BPH feel like on DRE?
Smooth, firm enlargement
How do you diagnose BPH?
How do you decide whether or not to treat a patient with BPH?
American Urological Association (AUA) scoring index
Patient's perception of severity of condition and the degree to which the condition interferes with patient's lifestyle and causes embarrassment are the most influential factors when deciding to treat
What are non-pharm options for treatment for BPH? What is the most effective treatment?
Lifestyle/behavioral management (fluid restriction)
Surgery - most effective
What is the gold standard for prostate surgery due to BPH?
Transurethral resection of prostate (TURP) - Visualize prostate through urethra, remove tissue by electrocautery or sharp dissection.
How do you medically treat BPH?
Alpha adrenergic blockers (Tamsulosin, doxazosin, etc)
5 alpha-reductase inhibitors (Finasteride)
MOA of alpha-blockers?
Improve urine flow at the bladder neck by inducing internal sphincter relaxation
MOA of 5 alpha-reductase inhibitors?
Interrupts the processing of testosterone and can actually decrease the size of the prostate and improve symptoms. Six months are required to see improvement.
General characteristics of prostate cancer?
MC cancer in men. 2nd MC cause of cancer related death in men. Slow growing malignant neoplasm of the adenomatous cells which leads to urinary obstruction and metastatic disease. It is a disease of aging. Rarely seen in men <45.
Where do the majority of Prostate cancers originate?
Peripheral zone (75%) - the outer portion
Transitional zone (20%)
Central zone (5%)
What is the MC type of prostate cancer?
Risk factors for prostate cancer?
Clinical features of prostate cancer?
Obstructive or irritative voiding symptoms
Advanced disease: bone pain, spinal cord impingement
Prostate feels enlarged, nodular, and asymmetric on DRE
Screening for Prostate cancer
PSA (controversial). >4 is high
Reasons PSA can be elevated other than prostate cancer?
Post biopsy or TURP
Diagnostic studies for prostate cancer?
Transrectal US (TRUS) guided biopsy - shows hyperechoic lesions
CT/MRI for staging
What is the histology grading system for prostate cancer?
Gleason grading system - provides prognostic information
Tx for stage I or II prostate cancer
Radical prostatectomy +/- radiation
Hormonal therapy - Flutamide
Tx for stage III prostate cancer?
(Tumor with local invasion)
Radiation with androgen deprivation (leuprolide - a GnRH agonist, Flutamide)
Tx for stage IV prostate cancer?
Hormonal manipulation using orchiectomy, antiandrogens, LH-releasing hormone agonists, or estrogens
What is Erectile dysfunction?
Consistent inability to maintain an erect penis with sufficient rigidity to allow sexual intercourse. It affects millions of men and incidence is age related.
Risk factors for ED?
What should be examined in the history for ED?
Diagnostic labs for ED?
How do you differentiate primary organic ED from psychogenic ED?
Nocturnal penile tumescence testing - patients with psychogenic impotence have normal nocturnal erections of adequate frequency and rigidity
Diagnostic imaging for ED?
Tx for ED?
Phosphodiesterase-5 inhibitor therapy (PDE-5) is mainstay of treatment
Vacuum constriction device
Psychogenic should be treated with behaviorally oriented sex therapy
SE of PDE-5 inhibitors?
What is contraindicated with PDE-5 inhibitors?
Nitrates within 24 hours - may cause significant drop in BP
What are causes of bladder cancer?
Smoking <---#1 risk factor
Occupational exposures (rubber, dye, printing, chemicals)
Exposure to cyclophosphamide
What kind of uroepithelial tumors account for 98% of bladder cancers?
Transitional cell carcinomas
Diagnostic studies for bladder cancer? Which test makes the definitive diagnosis?
Cystoscopy with biopsy <----definitive diagnosis
IV urogram, pelvic and abdominal CT
Clinical features of bladder cancer?
Painless hematuria!! <---MC symptom
Tx for bladder cancer with superficial lesions?
Endoscopic resection and fulguration followed by cystoscopy every three months
Tx for bladder cancer with multiple/recurrent lesions?
Intravesical instillation of thiotepa
Bacillus Calmette-Guierin (BCG)
Tx for recurrent bladder cancer, diffuse TCC in situ, and for tumors that have invaded the muscle?
Radical cystectomy with pelvic lymphadenopathy
What causes Lymphogranuloma venereum (LGV)?
Lymphogranuloma venereum (LGV) is a STI caused by Chlamydia trachomatis, a gram negative intracellular bacteria.
Risk factors for LGV?
Clinical features of LGV?
Incubation lasts for 3-21 days
Small, painless genital ulcer appears and spontaneously resolves after 2-3 days <---first sign
The secondary stage is characterized by regional lymphadenopathy and progresses to BUBOES which are painful, firm fluctuant lymph nodes which form a "GROOVE SIGN" in which the adenopathy that extends above and below the inguinal ligament
Treatment of LGV?
Doxycycline is DOC
What is Chancroid?
STI caused by Haemophilus ducreyi
Clinical features of chancroid?
Small pustule at the site of inoculation which progresses to multiple PAINFUL genital ulcers with sharply demarcated purulent bases
Unilateral, large, painful and fluctuant node (bubo)
Treatment of chancroid?
Azithromycin 1 g PO
Ceftriaxone 250 mg IM
Clinical features of HSV 2?
Initially presents as grouped small painful vesicles after a viral prodrome.
Localized tingling, burning, and pain at the site where the vesicles eventually develop. These vesicles eventually deroof and become painful ulcers.
Tender bilateral lymphadenopathy may develop, but does not progress to large fluctuant nodes and will not develop above and below the inguinal ligament
What is the main intracellular cation? Extracellular?
Intracellular - K
Extracellular - Na
What ions balance K? Na?
K is balanced by PO4
Na is balanced by Cl
What regulates the body's volume status and electrolyte composition? How?
The kidneys - by modulating how much free water and Na+ is reabsorbed from the renal filtrate. Antidiuretic hormone (ADH), also known as arginine vasopressin, is the chief regulator of osmolality.
What is osmolality?
The concentration of a solution. If serum osmolality is high, solution is more concentrated and ADH will go up to cause water retention to dilute the serum. Normal is 275-295
What hormone regulates Na levels?
Aldosterone - increased levels causes increased retention of Na
What are some assessments to determine volume status? What is the #1 assessment?
Blood pressure - #1
Skin turgor - (less useful in elderly)
Mucous membranes - (less useful in elderly)
Fractional excretion of Na
BUN/Cr ratio (>20)
How do patients clinically present with hypovolemia?
Decreased urinary output
If severe: ischemia, shock, lethargy, AMS
What labs confirm hypovolemia? (4)
Hct - will be high
Serum albumin - high
Urinary Na - decreased
Urea - increased
How do you treat hypovolemia?
IV isotonic fluid (NS or LR). Coexistent electrolyte abnormalities should be addressed simultaneously.
What is do changes in Na reflect in the body?
Hypo- and hypernatremia reflect excessive gain or loss of TBW, respectively
What is hypernatremia?
Serum Na of >145 mEq/L. A water deficit relative to solute AKA "boiling down the soup".
What causes hypernatremia?
Usually caused by inadequate intake or excess water loss (dehydration).
Deficit of thirst
Hypotonic fluid loss
GI loss (vomiting, diarrhea)
DI (Central and nephrogenic)
What is the difference between hypernatremia and volume depletion?
Hypernatremia is a loss of free water alone with high Na
Volume depletion is loss of water and Na.
What are signs/symptoms of hypernatremia?
Similar to hypovolemia
Dry mucous membranes
Lack of salivation, lacrimation, urination
How do you treat hypernatremia?
Identify underlying cause
Calculate water deficit
Free water administered orally (or IV D5). Replace 50% in first 24 hours then the rest over 48 hours.
How to calculate water deficit?
0.6 x premorbid weight x [1-(140/Na)]
What do you have to be cautious of when treating hypernatremia?
Replacing water too quickly - can cause cerebral or pulmonary edema.
What is hyponatremia?
Water in excess of Na (Serum is too dilute). Plasma Na is <135. Severe is <120
Causes of hyponatremia?
Due to increased free water retention or urinary Na loss:
What are signs/symptoms of hyponatremia?
Often asymptomatic if chronic/mild
Subtle mental status changes
Increased risk for falls in elderly
Lab findings with hyponatremia?
Serum Na is low
Serum osmolality is low (<270)
Urine Na can be low or high
What are three types of hyponatremia? Causes of each?
Hypovolemic - dehydration from N/V/D, diuretics, sweating
Euvolemic - Hypothyroidism, SIADH, Addison's
Hypervolemic - Renal failure, CHF, cirrhosis, nephrotic syndrome
How do you treat euvolemic and hypervolemic hyponatremia?
Treat undelying cause
Free water restriction
How do you treat hypovolemic hyponatremia?
0.9% NaCl 500 cc bolus
If there are neurologic symptoms present or Na is <120 give 3% NaCl and repeat Q10 min for up to 3 times until symptoms resolve
What can occur if you correct hyponatremia too quickly?
Central pontine myelinolysis - demyelination of axons causing neurologic damage
What is SIADH?
Syndrome of Inappropriate Antidiuretic Hormone Secretion from the posterior pituitary. High ADH causes free water retention.
Causes of SIADH?
Clinical features of SIADH?
No edema or HTN
Euvolemic hyponatremia (Low serum Na, high urine Na)
Treatment of SIADH?
How is DI and SIADH different?
DI you either don't make ADH or your kidneys are insensitive to ADH which causes a loss of water and thus hypernatremia. No ADH=peeing a lot.
SIADH is too much production of ADH causing retention of water and hyponatremia
What are two factors that determine K concentration?
1. Acid-base homeostasis. H and K+ are exchanged between the intracellular and extracellular spaces, thus disturbances of acid-base balance tend to cause disturbances in serum K+
2. Size of the total body K+ pool. Intracellular stores of K+ are large, but may be exhausted, especially in the setting of prolonged
Acidosis and hyperglycemia cause K to do what?
Shift out of the cells
What drugs enhance excretion of K?
What is hyperkalemia? At what level does it become symptomatic?
K >5.0 mEq/L. Usually has to be >6.5 to show symptoms.
What are causes of hyperkalemia?
Crush injuries, burns and other catabolism-inducing events (Rhabdomyolysis)
Excessive K+ administration
What are signs/symptoms of hyperkalemia?
Arrthymias - heart block, V tach, peaked T waves, flattened P waves, widened QRS, sine wave pattern (seen with cardiac arrest)
EKG changes with hyperkalemia
Tall, peaked T wave
Flat P wave
Prolonged PR interval
Widened QRS complex
How do you treat hyperkalemia?
IV Calcium gluconate to stabilize heart <----first line!
IV administration of D50, 10 units of insulin
Stop offending drugs and start low K diet
Dialysis - if all of the above fails
What drugs excrete K? Redistribute K?
Excretes K+: kayexalate, furosemide, dialysis
Redistributes K+: Insulin, bicarbonate, albuterol
What is hypokalemia defined as?
K <3.5 mEq/L. MC electrolyte abnormality seen in clinical practice.
What causes hypokalemia?
GI losses (Emesis, diarrhea)
Excessive diuretic administration <---MC cause
Prolonged malnutrition, particularly in alcoholic patients
How does hypokalemia clinically present?
Decreased muscle contactility leading to diaphragmatic paralysis
EKG changes with hypokalemia
Depressed ST segment
Flat or inverted T wave
Prominent U wave
How do you treat hypokalemia?
Oral K therapy is preferred for non-emergent cases.
If severe (K is <2.5), IV replacement is indicated (limit to 10 mEq/hr).
RAAS agents and K sparing diuretics can be used as well.
What other electrolyte do you want to check with low K?
Mg - hypomagnesemia may cause hypokalemia refractory to parenteral adminstration. Therefore Mg should be corrected with K.
What is the role of Mg in the body?
Mg is an essential cofactor in many of the most important biochemical reactions in the body. ATP must be bound to Mg2+ to be biologically active. Mg2+ is required for every step of DNA transcription and translation, nerve conduction, ion transport and Ca2+ channel activity
What two organs regulate pH?
How do the lungs regulate pH?
By eliminating or replenishing H+ in the body by altering CO2 elimination
How do the kidneys regulate pH?
By eliminating or replenishing H+ by altering plasma HCO3 (bicarb) concentrations
What is normal pH? CO2? Bicarb?
CO2: 35-45 mmHg
Bicarb: 22 to 26 mEq/liter
Arterial blood gas interpretation
What are causes of respiratory acidosis (retention of CO2)?
Hypoventilation <---MC cause
What are signs/symptoms of respiratory acidosis?
Hypercapnic encephalopathy: HA, drowsiness, hypoxemia
What is pH, CO2, and bicarb for respiratory alkalosis?
pH - high
CO2 - low
Bicarb - normal or low (if compensated)
What causes respiratory alkalosis (loss of CO2)? Which is MC?
What are signs/symptoms of respiratory alkalosis?
What are signs/symptoms of metabolic acidosis?
Neurologic symptoms - lethargy to coma
What do you have to calculate with metabolic acidosis?
Anion gap: Na - (Cl + HCO3). If >12, there is a gap
What is pH, CO2, and bicarb for metabolic acidosis?
CO2: Normal or low (if compensated)
If the anion gap is >14, what could be the cause of metabolic acidosis (loss of bicarb)?
If there is no anion gap, what could be the cause of metabolic acidosis?
Actezolamide (carbonic anhydrase inhibitor), Addison's
Renal tubular acidosis
Diarrhea - MC cause
Spironolactone/Small bowel fistula
What formula is used to calculate compensation with metabolic acidosis?
Winter's formula: If PCO2 = (1.5x bicarb) +8 +/-2 then it's compensated
PCO2 < Winter's formula calculation = respiratory alkalosis
PCO2 > Winter's formula calculation = respiratory acidosis
What is pH, CO2, and bicarb for metabolic alkalosis?
pH - high
CO2 - normal or high (if compensated)
Bicarb - high
What causes metabolic alkalosis (retention of bicarb)?
NG tube suctioning
Excess bicarb therapy
What are signs/symptoms of metabolic alkalosis?
Neurologic abnormalities - paresthesias, spasms, light headedness
Which acid-base disturbance has neuro symptoms, tachypnea, and ventricular arrhythmias?
Which acid-base disturbance has frequent, deep, sighing respirations and a tetany-like syndrome?
Which acid-base disturbance has HA and drowsiness?
Which acid-base disturbance has frequent, deep, sighing respirations and a tetany-like syndrome?
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