Bethany's Flashcards
Questions to ask when a man presents with inability to conceive? (BD)
Normal potency, libido, ejaculation?
History of surgery, chemotherapy, radiation, heat exposure?
History of mumps, EtOH, tobacco, viral illness, environmental toxins, chronic illness?
(Previous children)
What are the key components of sexual history? (BD)
Personal: Gender identity, sexual orientation, age of sexual partner(s), relationship status, relationship duration, frequency of sexual activity
Sexual dysfunction: Severity, onset, rate of decline, nocturnal erections, ability to sustain erection, exacerbating or alleviating factors, previous treatments, degree of distress, goals of treatment
Social: Job, stress level, life changes, health changes associated with sexual dysfunction timing
Nitroglycerin and PDE5i (BD)
Serum half-life is relevant if a patient developed chest pain after a PDE5i is taken. Nitroglycerin must be withheld for: 24 hours with sildenafil and vardenafil 48 hours for tadalafil 12 hours for avanafil
PDE Metabolism (BD) + Drug Interactions
CYP4A4 system
Dose reduction when taking CYP450 inhibitors (ketoconazole, erythromycin, ritonavir, indinavir, grapefruit juice)
Dose should be increased (or these meds may increase the metabolism): rifampin, phenobarbitol, phenytoin, carbamazepine
Men with severe hepatic or renal dysfunction (GFR <30 mL/min) should start at the lowest dose
What is Bimix and why might it be used versus the others? (BD)
Bimix is papaverine (non-specific PDE inhibitor not used in monotherapy, metabolized by the liver and can rarely result in liver enzyme elevation) and phentolamine (alpha adrenergic receptor inhibitor not effective as a monotherapy, inhibits detumescence).
90% efficacy with NO penile pain
Alprostadil (only FDA approved medication) activates adenylate cyclase and increases intracellular cAMP but causes pain 37% of the time
DO NOT GIVE ICI WITH MAOIs
What is the differential diagnosis of an enlarging “boil” in the perineum/scrotum?
Fournier’s Gangrene
Furuncles and abscesses
Cellulitis
Balanitis or Balanoposthitis
Post-operative infections
Hidradenitis Suppurativa
Sexually Transmitted Infections -Certain sexually transmitted infections can present with cutaneous manifestations including: lymphogranuloma venereum, chancroid, granuloma inguinale, syphilis, herpes simplex, human papilloma virus, and molluscum contagiosum.
Intertrigo - A candidal infection of skin folds where the macerated skin becomes red and inflamed
Epididymo-orchitis
Non-infectious genital ulcers -Examples include fixed drug eruption and Behcet’s disease (inflammatory disorder that can result in oral and genital ulcerations, ocular disease, and skin lesions).
What questions should you ask if you are told a patient has hyperkalemia?
What are the vitals? Hyperkalemia can result in abnormalities in cardiac conduction which can predispose towards deadly arrhythmias.
What were some of the specifics of her operation? Long operations, especially those performed in flank position, can result in rhabdomyolysis and liberation of intracellular potassium.
What is her baseline renal function? There are two main mechanisms by which the body maintains potassium hemostasis: renal excretion and cellular shifts of potassium. Risk of hyperkalemia is inversely related to glomerular filtration rate, and increase perceptibly once the GFR is < 30 mL/min.
Was there a blood transfusion? Acute hemolytic transfusion reactions can occur due to use of incompatible red blood cells or large volume of incompatible plasma.
These reactions are rare but can cause release of large amount of intracellular potassium, which can cause hyperkalemia, especially in the setting of impaired renal function.
Differential diagnosis of hyperkalemia
Causes
Metabolic Acidosis
Mineral acidosis (NH4Cl or HCl) can directly result in potassium movement into extracellular fluid to maintain electroneutrality.
Acute or Chronic Renal
Renal failure is a significant risk factor for the development of hyperkalemia and can occur whether acute or chronic. Decreased renal function results in impairment of potassium excretion
Decompensated Heart failure
can exacerbate hyperkalemia due to decreased renal perfusion
Medications
Renin angiotensin aldosterone system (RAAS) inhibitors
angiotenisin-concerning enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), aldosterone receptor antagonists
Calcineurein inhibitors
decrease aldosterone synthesis and the activity of the sodium-potassium ATPase pump
Nonsteroidal anti-inflammatory drugs
decrease prostaglandin-mediated renin release, renal blood flow, and glomerular filtration
Heparin
blocks the biosynthesis of aldosterone in the adrenal gland
Ketoconazole
Interferes with biosynthesis of adrenal steroids and can cause aldosterone deficiency
Potassium-sparing diuretics
spironolactone, eplerenone, amiloride, triamterene
Trimethoprim
blocks luminal sodium channels
Pentamide
blocks luminal sodium channels
Nonselective beta blockers
(i.e. propranolol, carvedilol, labetalol, nadolol)
High potassium diet
Tissue Injury
rhabdomyolysis, hemolysis, tumor lysis
Insulin Deficiency: insulin promotes potassium entry into cells
Diabetic Ketoacidosis or Hyperosmolar Hyperglycemic State
Although patients generally have a potassium deficit in these conditions, some patients may develop hyperkalemia. The increased serum osmolality can result in water shift from intracellular into extracellular space, which results in potassium also following out of the cells by solvent drag and redistribution11
Hyperkalemic Periodic Paralysis
Exercise
potassium increases during exercise, but rarely important clinically
Use of jejunum as urinary diversion
Reduced aldosterone secretion hyporeninemic aldosteronism (e.g. diabetic nephropathy, medications), primary adrenal insufficiency, severe illness, congenital hypoaldosteronism, pseudohypoaldosteronism type 2 Aldosterone resistance medications, pseudohypoaldosteronism type 1, reduced sodium delivery to distal tubule, defects in the sodium resorptive capacity of distal tubule (i.e. obstructive uropathy)
‘Pseudohyperkalemia’
Spurious elevations in measured serum potassium levels can occur with hemolysis during venipuncture (fist clenching during phlebotomy, application of tourniquets, use of small-bore needles) or handling/processing of blood, thrombocytosis, familial pseudohyperkalemia, or polyctemia14
A 68-year-old man with a history of muscle-invasive bladder cancer treated by radical cystectomy and urinary diversion 6 years ago presents to your office complaining of weakness, fatigue, and weight loss.
What are your first questions?
What are the patient’s vitals?
Weakness and fatigue should first prompt a consideration of infection and fluid status.
What was the patient’s pathology, treatment, and disease status?
In a patient with advanced bladder cancer, disease recurrence should also be considered as a possibility.
What type of urinary diversion did the patient have?
Urinary diversions are associated with metabolic abnormalities. The typical pattern of metabolic abnormality seen is dependent on the segment of bowel used for urinary diversion, and is typically more severe with continent vs. incontinent urinary diversions, as well as with the length of bowel resected. When ileum and colon are used, the typical pattern of electrolyte abnormality is hyperchloremic metabolic acidosis, with the possibility of hypokalemia. Less commonly, when jejunum is used, this can result in hyponatremic, hyperkalemic, hypochloremic metabolic acidosis. When stomach is used, this can result in a hypochrloremic, metabolic alkalosis with the possibility of hypokalemia.
How is he emptying his urinary diversion?
If he has a continent urinary diversion, then there is a greater contact time between the urine and intestinal mucosa.
What is the patient’s baseline and current renal function?
Patients with poor renal function are less capable of compensating for an increased acid load and more likely to exhibit metabolic acidosis.
What is the patient’s baseline liver function? Patients with poor liver function can experience sequelae of elevated ammonia levels.
What medications is the patient taking?
How are the patient’s bowel movements? Chronic diarrhea and steatorrhea can occur after urinary diversion.
A 68-year-old man with a history of muscle-invasive bladder cancer treated by radical cystectomy and urinary diversion 6 years ago presents to your office complaining of weakness, fatigue, and weight loss.
What is the differential diagnosis?
Metabolic Acidosis: Most urinary diversions can lead to electrolyte abnormalities. The most common bowel segments used are ileum and colon are generally lead to a hypercholeremic, hypokalemic, metabolic acidosis
Hypokalemia: Signs of hypokalemia include fatigue, constipation, weakness, muscle spasms
Renal Failure: Following urinary diversion, patients have multiple sources of developing renal failure including age, utero-enteric anastomosis stricture, recurrent infections, nephrolithiasis, and reabsorption of creatinine through the intestinal epithelium (pseudoazotemia)
Urinary tract infection: Common occurrence following urinary diversion
Hyperammonemic encephalopathy: In urinary diversions, ammonia is re-absorbed through the bowel wall. Patients with normal liver function can typically deal with the increased ammonia load, however infections with urea-splitting bacteria, urinary tract obstruction, and poor liver function can lead to hyperammonemic encephalopathy and even coma
Chronic Diarrhea: Following urinary diversion, patients may experience chologenic (bile acid) diarrhea due to loss of bile acids. Normally, the ileum will resorb most conjugated bile acids, however resection of longer segments can produce a malabsorption of bile acids and these enter the colon with resultant loss of bile acids, water, and sodium.4 Depletion of bile acids can also result in malabsorption of fatty acids and the development of steatorrhea
Disease recurrence: Metastatic disease can produce the constitutional symptoms the patient is complaining of
What kind of stones do diabetic get more often than the general population?
Uric acid stones are over-represented among diabetic patients compared to the general population. Low urine pH in patients with type 2 DM and insulin resistance is thought to be the result of both impaired renal ammonium excretion and increased net acid excretion, leading to reduced urinary buffering capacity and acidic urine.
Uric acid stone formation has been linked to the metabolic syndrome, sharing a number of features including hypertension, obesity, hypertriglyceridemia and hyperglycemia.
When performing 24 hour urinalysis, it is important to note that in the setting of low urine pH (<5.5), uric acid can precipitate out in the collection jug and may not be properly measured. Rechecking uric acid levels after the urine has been adequately alkalinized may reveal a significant increase in uric acid levels due to resolublization.
Cystine Stones
Cystinuria is an autosomal recessive disorder which leads to defective renal proximal tubule and intestinal epithelium transport of the four dibasic amino acids: cystine, ornithine, lysine and arginine (COLA).
Cystinurics excrete abnormally high levels of all four, but only cystine (cysteine-cysteine) is poorly soluble and uniquely forms stones.
Cystine is a dimeric amino acid formed by two oxidized cysteine monomers linked ay a disulfide bond (cysteine-cysteine).
Cystine solubility is highly pH dependent and increases exponentially with increasing urinary pH.
Sodium enhances cystine excretion and methionine is a precursor in cystine synthesis.
Therefore, dietary management for cystinurics includes high fluid consumption, sodium restriction, and low methionine diet which most practically means decreased animal protein intake.
Medical management is primarily urinary alkalinization with an oral agent such as potassium citrate or sodium bicarbonate.
Thiol therapy is given to select patients and works by forming a cysteine-drug complex, which is 50 times more soluble than cystine (cysteine-cysteine).
Bacteria that raise concern for struvite stones
Urine culture should be obtained in patients with recurrent urinary tract infections or in those with a urinalysis suspicious for infection. Infection with a urease-splitting organism should raise concern for struvite (magnesium ammonium phosphate) stones.
Common Urease-Producing Bacteria
Gram Negative Bacteria Gram Positive Bacteria
Proteus mirabilis Corynebacterium sp
Klebsiella Pneumoniae Staphylococcus aureus
Pseudomonas sp Staphylococcus epidermidis
Indications for 24 hour urine evaluation
Recurrent calcium stone former Family history of stone disease Intestinal or malabsorptive disease Pathologic skeletal fracture Osteoporosis Gout Young age of onset of stone disease Uric acid nephrolithiasis Cystine stones Patient-specific risk factors (Solitary kidney, chronic kidney disease, vocation, infirm health)
Side effects of Thiazides
↑’s calcium reabsorption in distal renal tubule (direct mxn) and through extracellular volume depletion in the proximal tubule (indirect mxn)
Decreases urinary calcium
Thiazide use may be accompanied by hypokalemia, hyperglycemia, hyperuricemia, dyslipidemia and hypocitraturia, and therefore monitoring of these levels is indicated.
To prevent thiazide-induced hypokalemia and hypocitraturia, potassium supplementation is recommended. Potassium citrate has the advantage of enhancing urinary citrate and further reducing the risk of stone formation.
