4 Flashcards
What is the most accurate test for Wegener granulomatosis?
The most accurate test for WG is a biopsy of the kidney or lung looking for granulomas. Biopsy of the nasal septum is less sensitive and has more false negative results.
What is the treatment of Wegener’s granulomatosis?
Cyclophosphamide and steroids.
What is Churg–Strauss syndrome?
Characterized by lung involvement, neuropathy, skin lesions, GI, cardiac, and renal involvement.
What is the presentation of Churg–Strauss syndrome?
Fever, weight loss, malaise. Asthma, eosinophilia, atopic diseases. Elevated eosinophil, positive P–ANCA or antimyeloperoxidase. Most accurate test is lung biopsy: granulomas, eosinophils.
What is the treatment of Churg–Strauss syndrome?
Glucocorticoids and cyclophosphamide.
What is Goodpasture syndrome?
Idiopathic disorder of renal and lung disease characterized by a unique anti–basement membrane antibody. GP does not affect multiple organs or sites in the body other than the lung and the kidney.
What are the clinical signs of Goodpasture syndrome?
Hematuria, proteinuria, hemoptysis, cough, dyspnea. Best test is anti–basement membrane Ab to type IV collagen. Lung or kidney biopsy shows hemosiderin macrophages and linear deposits.
What is the treatment of Goodpasture syndrome?
Plasmapheresis and steroids. Cyclophosphamide.
What is polyarteritis nodosa?
Systemic vasculitis of small and medium arteries of every organ exception lung. Renal involvement manifests as HTN, renal insufficiency, and hemorrhage due to microaneurysms. Biopsy.
What is the treatment of polyarteritis nodosa?
Cyclophosphamide and steroids.
What are the symptoms of polyarteritis nodosa?
Fever, weight loss, malaise. Involvement of skin, eyes, muscles, GI, heart, kidneys, and neurologic system. Abdominal pain and joint pain. Anemia and an elevated sedimentation rate.
What is the treatment of polyarteritis nodosa?
Steroids and cyclophosphamide.
What is Henoch–Schönlein purpura?
Systemic deposition of IgA, resulting in renal insufficiency, skin lesions, GI symptoms.
What is the tetrad of Henoch–Schönlein purpura?
Tetrad of palpable purpura, arthralgias, abdominal pain, and renal disease. IgA deposited in walls of blood vessels. Biopsy is usually not performed. HSP most often resolves spontaneously.
What is the treatment of Henoch–Schönlein purpura?
Treatment is supportive. Steroids can be used.
What is IgA nephropathy (Berger disease)?
IgA nephropathy with mild hematuria that resolves spontaneously in 30%. About 40–50% of patients progress to end stage renal disease. Deposition of IgA only in kidney.
What are the signs of Berger disease?
HTN. Usually an Asian patient under 35 years of age who has had a recent viral illness or pharyngitis, then develops hematuria 1–2 days later.
How is Berger disease diagnosed?
The diagnosis is based on finding IgA deposited in the kidney on biopsy.
What is the treatment of Berger disease?
Proteinuria is treated with ACE inhibitors or angiotensin receptor blockers (ARB).
What are the causes of postinfectious glomerulonephritis?
Group A beta–hemolytic streptococci (S pyogenes) and other infections can cause postinfectious glomerulonephritis. Any infectious agent, including hepatitis B and C, CMV, staph endocarditis.
What type of infection can cause post–streptococcal glomerulonephritis?
Poststreptococcal glomerulonephritis can occur with throat or skin infection with S pyogenes. Rheumatic fever only occurs after pharyngitis in 10–15% of patients with GABS pharyngitis.
What are the signs of postinfectious glomerulonephritis?
Smoky, cola urine from hematuria, red cell casts, proteinuria. Periorbital edema and HTN. The best initial test is antistreptolysin (ASO) and the antihyaluronic acid. Complement low. Renal biopsy rarely.
What is the treatment of postinfectious glomerulonephritis?
Treatment is management of fluid overload and HTN with diuretics. Resolves spontaneously. Antibiotics should be given to eradicate the organism from the pharynx.
What are thrombotic thrombocytopenic purpura and hemolytic uremic syndrome?
TTP and HUS are two different varieties of the same disease of hemolytic anemia, uremia, and thrombocytopenia.
What are the causes of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome?
TTP is associated with HIV, but it is most often idiopathic. HUS is more common in children and with E. coli 0157:H7 food poisoning.
What is the triad of hemolytic uremic syndrome?
HUS is a triad of hemolytic anemia, uremia, and thrombocytopenia.
What are the signs of thrombotic thrombocytopenic purpura?
TTP has anemia, uremia, and thrombocytopenia, and is also associated with fever and headache, confusion, seizures, focal deficit.
What are the laboratory findings in hemolytic uremic syndrome and thrombotic thrombocytopenic purpura?
Anemia is intravascular, and the blood smear shows schistocytes, helmet cells, fragmented red cells. LDH and reticulocyte count will be elevated and the haptoglobin decreased.
What is the treatment of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome?
Plasmapheresis. Dipyridamole may preventing platelet aggregation in TTP. Antibiotics contraindicated in HUS; organism releases toxins. Administering platelets will worsen CNS and renal.
What is Alport syndrome?
Glomerular disease with anterior lenti conus (lens protrusion), and sensorineural hearing loss.
What is idiopathic rapidly progressive glomerulonephritis?
RPGN may occur with any glomerular disease. Idiopathic form is associated with crescent formation in the kidney, which is ANCA negative. Diagnosis is with renal biopsy.
What us the treatment of idiopathic rapidly progressive glomerulonephritis?
Treatment is with steroids and cyclophosphamide.
What is amyloid?
Amyloid is a proteinaceous material associated with chronic infectious or inflammatory conditions, such as rheumatoid arthritis, inflammatory bowel disease, or myeloma.
How does amyloidosis affect the organs?
Amyloid builds up in kidney, causing glomerulonephritis, accumulates in GI, nerves, muscles. Restrictive cardiomyopathy, rhythm disorders, heart block. Macroglossia, carpal tunnel, malabsorption.
How is amyloidosis diagnosed?
Biopsy of the involved organ, such as the kidney. Congo red testing shows green birefringence. Amyloidosis treatment consists of controlling the underlying disease. Melphalan and prednisone.
What is nephrotic syndrome?
Renal disease sufficient to cause proteinuria >3.5 gm/24 h, hyperlipidemia, edema, and a low serum albumin.
What are the causes of nephrotic syndrome?
1/3 nephrotic syndrome associated diabetes, HTN, myeloma. Glomerulonephritis becomes nephrotic syndrome if massive proteinuria, low albumin. Nephrotic syndrome describes severity, not etiology.
What are the signs of nephritic syndrome?
Hyperlipiduria with droplets in shape of Maltese crosses in urinalysis. Hypercoagulability from urinary loss of anticoagulant proteins. Arterial or venous thrombosis.
How is nephrotic syndrome diagnosed?
High protein in urine, low protein in blood, edema, hyperlipidemia. 24–hour urine protein >3.5 gm. A protein:creatinine ratio of >3.5 on a single urine. The most accurate test is a renal biopsy.
What is the treatment for nephrotic syndrome?
Control the underlying disease. Steroids, cyclophosphamide, mycophenolate, azathioprine. ACE inhibitors or ARBs are used for all patients with proteinuria.
What are the causes of proteinuria?
Microalbuminuria is 30–300 mg/24 h. Mild amounts of proteinuria
What are the causes of hematuria?
Nephrolithiasis, cancer, bleeding disorders, trauma, cyclophosphamide (hemorrhagic cystitis). Cystitis or prostatitis. The red cells become dysmorphic in glomerular disease.
What is the cause of nitrites on urinalysis?
Gram–negative bacteria reduce nitrate to nitrite.
What is the significance of asymptomatic bacteriuria?
The isolated finding of bacteria in the urine in pregnant women should be treated. About 30% of pregnant women with bacteriuria progress to pyelonephritis.
What is the significance of hyaline casts in the urinalysis?
Dehydration. These casts develop as an accumulation of the normal amount of tubular protein. Hyaline casts may occur in normal persons.
What is the significance of red cell casts on the urinalysis?
Glomerulonephritis
What is the significance of broad, waxy casts in the urinalysis?
Chronic renal failure
What is the significance of granular casts in the urinalysis?
Also called dirty or muddy. They are associated with acute tubular necrosis and represent accumulated epithelial cells.
What is the significance of white cell casts in the urinalysis?
Pyelonephritis, interstitial nephritis.
What are the most common causes of end stage renal disease that require dialysis?
Diabetes and HTN. Glomerulonephritis is the etiology of about 15%, with cystic disease and interstitial nephritis, causing 4–5% each.
What are the indications for dialysis?
Life–threatening abnormalities that cannot be corrected, such as fluid overload refractory to diuretics. Acidosis, pericarditis, encephalopathy, neuropathies, hyperkalemia, persistent nausea, vomiting, bleeding.
What type of dialysis is used most frequently?
Hemodialysis is used in 85% of patients and peritoneal dialysis in 15%. The most common complication of peritoneal dialysis is peritonitis.
What is the cause of anemia in end–stage renal disease?
Decreased erythropoietin from the kidney. Treated with replacement of erythropoietin. The anemia of ESRD is normochromic and normocytic.
What is the cause of hypocalcemia/hyperphosphatemia in end–stage renal disease?
Loss of 1,25–dihydroxyvitamin D. Hyperphosphatemia is from inability of kidneys to excrete PO4. High PO4 contributes to low Ca by precipitating out in tissues in combination with the calcium.
What is the treatment of hyperphosphatemia in renal disease?
High phosphate levels are treated with phosphate binders, such as calcium carbonate or calcium acetate.
What is the treatment of hyperphosphatemia with hypercalcemia?
Sevelamer and lanthanum are phosphate binders. Used when calcium is high because of vitamin D. Aluminum–containing binders should not be used because associated with dementia and bone abnormalities.
What is osteodystrophy of end–stage renal disease?
Osteitis fibrosa cystica occurs because kidneys fail to produce 1,25 vitamin D. Low Ca leads to hyperparathyroidism, which removes Ca from bones. Controlled by increasing calcium levels.
What is the treatment of hypermagnesemia in renal insufficiency?
Magnesium accumulates because of decreased renal excretion. Treatment is restriction of magnesium intake.
What is the effect of end–stage renal disease on the cardiovascular system?
HTN, accelerated atherosclerosis, coronary artery disease. This is the most common cause of death for patients on dialysis. Goal BP is
What is the effect of end–stage renal disease on the immune system?
Increased infection because WBCs do not function in uremia. Infection is the second most common cause of death in dialysis patients. Most common organism is Staphylococcus.
What is the effect of end–stage renal disease on the coagulation system?
Bleeding occurs because uremic platelet dysfunction. Bleeding treated with desmopressin, which releases subendothelial von Willebrand factor and factor VIII, which increases platelet adherence.
What is the dietary treatment for severe renal disease?
Diet restricted in potassium, sodium, protein, magnesium, and phosphate.
What is hyponatremia?
Hyponatremia is defined as a low serum sodium
What is the formula for serum osmolality?
Serum osmolality is largely a function of the serum sodium level. Serum osmolality = (2 x sodium) + BUN/2.8 + glucose/18. When the glucose and BUN are normal, this equation becomes 2 x sodium + 10.
What is the presentation of hyponatremia?
Neurologic symptoms range from mild confusion and memory loss to disorientation and obtundation to seizure or coma, depending on the severity.
What factor is associated with hyponatremic seizures?
Symptoms depend on rate of decline. Acute 15–20 point drop can result in a seizure or coma. If the level drops gradually, the patient can sustain an extremely low sodium. There should be no symptoms unless below 125.
What is the treatment of mild hyponatremia?
Mild asymptomatic hyponatremia should resolve with fluid restriction.
What is the treatment of moderate hyponatremia?
Moderate hyponatremia can be managed with normal saline administration combined with a loop diuretic such as furosemide. The saline provides sodium, and the loop diuretic causes a net free water loss.
What is the treatment of severe hyponatremia?
3% hypertonic saline. Severe symptoms do not occur unless Na
What is the maximum rate of correction of severe hyponatremia?
Hyponatremia can be corrected as rapidly as 2 mEq per hour if the patient is having seizures. Fludrocortisone is given for cerebral salt wasting disease.
What is pseudohyponatremia?
Na level is artificially low because of hyperglycemia. Na is decreased by 1.6 mEq/L for every 100 increase in glucose. Glucose load causes a transcellular shift of water. Hyperlipidemia causes low Na.
What hypervolemic states (increased ECF) are associated with hyponatremia?
There is a decrease in intravascular volume resulting in an increase in ADH secretion from the posterior pituitary in congestive heart failure; nephrotic syndrome and low albumin states; and cirrhosis
What is the cause of hyponatremia in renal insufficiency?
When renal failure becomes advanced, the impaired free water excretion will reduce the sodium level and result in hypervolemia.
What is the cause of hyponatremia in hypovolemic states?
Loss of sodium through body fluids and replacement with free water. Sweating and replacement only with free water causes the sodium level to drop.
What are the gastrointestinal causes of hyponatremia?
Vomiting, diarrhea, gastric suction; hypovolemia.
What are the causes of sodium loss through the skin?
Skin loss: burns, sweating with replacement with free water, cystic fibrosis.
How does renal failure cause renal sodium loss?
The kidney can lose the ability to reabsorb sodium in the proximal convoluted tubule as the kidney is damaged. Damaged tubules cannot reabsorb sodium and hypovolemia results.
How does adrenal insufficiency (Addison disease) cause hyponatremia?
Aldosterone reabsorbs sodium from the kidney. Without aldosterone, sodium is lost.
What are the causes of hypovolemic hyponatremia with a urine sodium
Dehydration, vomiting, diarrhea, sweating
What are the causes of hypovolemic hyponatremia with a urine sodium >10?
Diuretics, ACE inhibitors, renal salt wasting, Addison disease, cerebral sodium wasting
What are the causes of euvolemic hyponatremia?
Psychogenic polydipsia with >15–20 liters/d. Hypothyroidism. Diuretics: can be both hypovolemic and euvolemic. ACE inhibitors. Endurance exercise. Syndrome of inappropriate secretion of ADH.
What are the causes of syndrome of inappropriate secretion of ADH (SIADH)?
CNS infections, stroke, tumor, trauma, vasculitis, pain, pneumonia, TB, PE, asthma. Lung CA, pancreas CA. SSRIs, tricyclics, haloperidol, cyclophosphamide, vincristine, carbamazepine.
How is syndrome of inappropriate secretin of antidiuretic hormone diagnosed?
Neurologic symptoms; elevated urine osmolality and elevated urine sodium. If the urine osmolality is >100 Osm/L in the presence of hyponatremia, the person has SIADH. Elevated ADH level.
What is the treatment of SIADH?
Restrict fluids. Give hypertonic saline for severe disease. Normal saline with a loop diuretic. For chronic disease, demeclocycline or lithium to inhibit the effect of ADH on the kidney tubule.
What are the insensible causes of hypernatremia?
Insensible losses: extrarenal loss of water without intake of hypotonic fluids; increased skin loss of water (sweating, burns, fever, exercise) or respiratory infections
What are the gastrointestinal causes of hypernatremia?
Osmotic diarrhea (e.g., lactulose, malabsorption), infectious diarrhea. Transcellular shift caused by Rhabdomyolysis or seizures can cause muscles to take up water and Na.
What are the renal causes of hypernatremia?
Nephrogenic diabetes insipidus (NDI), causing by renal disease, increased calcium, decreased potassium, lithium, demeclocycline, sickle cell disease, and others
What are the causes of central diabetes insipidus?
Idiopathic, trauma, infectious, tumor, granulomatous, hypoxic brain damage or neurosurgical brain injury. Idiopathic most common.
What types of osmotic diuresis can cause hypernatremia?
Osmotic diuresis: diabetic ketoacidosis (DKA), nonketotic hyperosmolar coma, mannitol, diuretics.
What are the signs of hypernatremia?
Lethargy, weakness, irritability, seizures, and coma are present with severe hypernatremia of any cause. Diabetes insipidus causes a dilute diuresis of 3–20 L per day.
How is central diabetes insipidus distinguished from nephrogenic diabetes insipidus?
Decrease in urine volume after administering ADH distinguishes central diabetes insipidus from NDI.
What is the treatment of acute hypernatremia?
IV isotonic saline. Correction should not be >1 mEq every 2 h or 12 mEq/d. 1 mEq/h is acceptable if the patient is having seizures.
What are the complications of overly rapid correction of hypernatremia?
Complications of overly rapid correction include cerebral edema, permanent neurologic damage, or seizures.
What is the treatment of central diabetes insipidus?
Correct the underlying cause. Give vasopressin (ADH) subcutaneously, intravenously, intramuscularly, or by nasal spray.
What is the treatment of nephrogenic diabetes insipidus?
Correct underlying cause if possible. Diuretic or NSAIDs. NSAIDs function by inhibiting prostaglandins, which impair concentrating ability. NSAIDs will increase the action of ADH at the kidney.
What are the gastrointestinal causes of hypokalemia?
Gastrointestinal losses can be from vomiting, diarrhea, or tube drainage.
What types of transcellular shift can cause hypokalemia?
Increased entry into cells can be from alkalosis, increased levels of insulin, beta adrenergic, and the replacement of B12. Trauma causes increased beta adrenergic activity.
What are the causes of urinary potassium losses?
Diuretics. Increased aldosterone states, such as Conn, licorice, Bartter, or Cushing. Aldosterone is the most important regulator of potassium. Renal artery stenosis. Hypomagnesemia will cause potassium loss.
What is the presentation of hypokalemia?
Affects muscles and the heart. Weakness, paralysis, fatal arrhythmias, rhabdomyolysis. Potassium is necessary for ADH effect on the kidney, and hypokalemia causes nephrogenic diabetes insipidus.
What are the ECG signs of hypokalemia?
T–wave flattening and U–waves. A U–wave is an extra wave after the T–wave caused by Purkinje fiber repolarization.
What is the treatment of hypokalemia?
Correct the underlying cause. IV potassium maximum 10–20 mEq/h; do not use dextrose containing fluids, because dextrose causes increase insulin release and lower potassium.
What are the complications of excessively rapid repletion of potassium?
Fatal arrhythmia. Idioventricular rhythm, asystole.
How many mEq of potassium is needed to raise the potassium level by one point?
Very large amounts of potassium may be necessary to raise the body potassium level by 1 or 2 points. The total body requirement is to give 4–5 mEq per kg per point.
What are the causes of hyperkalemia related to movement of K+ from cells to extracellular fluid?
Pseudohyperkalemia: venipuncture, platelets >1,000,000, WBC >100,000. Acidosis. Insulin deficiency. Rhabdomyolysis, tumor lysis, seizures, exercise. Periodic paralysis: weakness, hyperK, family history.
What is the relationship between pH and potassium level?
H+ moves into cells, K+ out. For every 0.1–point decrease in the pH, the potassium level will increase by 0.7 points because of the transcellular shift.
What are the renal causes of hyperkalemia?
Renal failure. Hypoaldosteronism: ACE inhibitors, type IV RTA, adrenal enzyme deficiency; heparin. Primary adrenal insufficiency (Addison) or adrenalectomy. K–sparing diuretics. NSAIDs.
What is the presentation of hyperkalemia?
Muscular weakness can begin usually with K+ levels >6.5.Abnormal cardiac conduction is the most common cause of death, hypoventilation.
How is hyperkalemia diagnosed?
ECG findings: peaked T waves, widened QRS, short QT, or prolonged PR interval.
What is the acute treatment of hyperkalemia?
Calcium chloride one ampule for membrane stabilization. Effect is immediate and short lived. Bicarbonate one ampule. Do not give in same IV line as calcium. Glucose one ampule and insulin, takes 30 min.
What is the non–acute treatment of hyperkalemia?
Furosemide, beta agonists. Cation exchange resin (Kayexalate) absorbs 1 mEq K+/gm. Given with sorbitol. Kayexalate can also be given as a retention enema. Dialysis.
What are the causes of distal renal tubular acidosis (type I)?
Sporadic. Also caused by Sjögren, SLE. Amphotericin, lithium, analgesics, cyclophosphamide. Nephrocalcinosis, sickle cell, chronic infection. Familial, chronic hepatitis.
What is the presentation of distal renal tubular acidosis (type I)?
Inability to concentrate H+ in urine. Urine pH is >5.4. Secondary hyperaldosteronism and hypokalemia. Nephrocalcinosis and nephrolithiasis.
How is distal renal tubular acidosis (type I) diagnosed?
Acid load test; give ammonium, which should lower urine pH. With type I RTA, urine pH remains elevated. Bicarbonate
What is the treatment of distal renal tubular acidosis (type I)?
Oral bicarbonate is the treatment because bicarbonate reabsorption in the proximal tubule remains intact; potassium replacement.
What are the causes proximal (type II) renal tubular acidosis?
Fanconi, Wilson, amyloidosis, myeloma, acetazolamide, vitamin D deficiency, secondary hyperparathyroidism, hypocalcemia, heavy metals, hepatitis, SLE and Sjögren syndrome.
What is the presentation of proximal (type II) renal tubular acidosis?
Inability to absorb bicarbonate. Urine pH is basic. Hypokalemia and bicarbonate of 18–20, and malabsorption of glucose, phosphate, urate, amino acids. Bone lesions (osteomalacia and rickets).
How is proximal (type II) renal tubular acidosis diagnosed?
Patients are have a basic urine in the presence of acidemia.
What is the treatment of proximal (type II) renal tubular acidosis?
Give potassium; mild volume depletion will enhance proximal bicarbonate reabsorption. Thiazide diuretics and very large amounts of bicarbonates.
What are the causes of hyporeninemic/hypoaldosteronism (type IV renal tubular acidosis)?
An aldosterone deficiency of any cause or adrenal insensitivity to angiotensin II, diabetes (50%), Addison disease, sickle cell disease, renal insufficiency.
What is the presentation of hyporeninemic/hypoaldosteronism (type IV renal tubular acidosis)?
Usually asymptomatic hyperkalemia. Mild to moderate renal insufficiency. Hyperchloremic metabolic acidosis (nonanion gap).
How is hyporeninemic/hypoaldosteronism (type IV) diagnosed?
Presence of high urine sodium with oral salt restriction establishes the diagnosis.
What is the treatment of hyporeninemic/hypoaldosteronism (type IV)?
Administration of fludrocortisone. Fludrocortisone has a high degree of mineralocorticoid effect and is similar to administering aldosterone.
What is the relationship of serum bicarbonate and pCO2?
For every 1–point increase in the level of serum bicarbonate, there is a 0.7–point increase in pCO2. Dehydration results in increased aldosterone, which leads to metabolic alkalosis.
What are the causes of alkalosis from H+ ion loss?
Exogenous steroids. GI loss (vomiting, nasogastric suction). Renal loss (Conn syndrome, Cushing, ACTH overproduction, licorice, Bartter syndrome). Decreased chloride intake. Diuretics.
What are the causes of alkalosis from HCO3 retention?
Bicarbonate administration. Contraction alkalosis. Milk–alkali syndrome?
What is the cause of alkalosis from H+ movement into cells?
Hypokalemia.
What are the respiratory causes of alkalosis?
Hyperventilation, pulmonary embolus, sarcoid, anxiety, pain. Progesterone, catecholamines, hypoxia, cirrhosis, pregnancy, and salicylates.
What are the causes of acidosis (low pH) with a low anion gap?
Myeloma, low albumin level, lithium.
What is the formula for anion gap?
Anion gap = (Na + K) – (HCO3 + Cl) Normal: 8–14. Na+ and cations = HCO3– and Cl– and anions
What are the causes of a normal anion gap acidosis?
Diarrhea, renal tubular acidosis, ureterosigmoidostomy.
What are the causes of an increased anion gap acidosis?
Lactate (sepsis, ischemia). Aspirin. Methanol. Uremia. Diabetic ketoacidosis. Paraldehyde, Propylene glycol. Isopropyl alcohol, INH. Ethylene glycol (antifreeze), low calcium.
What are the causes of respiratory acidosis?
Hypoventilation, chronic obstructive pulmonary disease (COPD), Pickwickian, obesity, suffocation, opiates, sleep apnea, kyphoscoliosis, myopathies, neuropathy, effusion, aspiration.
What are the causes of nephrolithiasis?
1–5% of the population. Calcium oxalate stones in 70%. Calcium phosphate in 10%. Mg/Aluminum/phosphate (Struvite) 5%. Uric acid 5%. Cysteine 1%. Indinavir.
What are the causes of hypercalciuria?
Vitamin D intoxication with sarcoid and granulomatous disease. Familial. Idiopathic renal hypercalciuria. Hyperparathyroidism (10%). Multiple myeloma, metastatic disease to bone, hypercalcemia of malignancy.
What are the causes of hyperoxaluria?
Primary familial, enteric hyperoxaluria (chronic diarrhea causes excessive absorption of oxalate).
What complication may result from hypocitraturia?
Citrate binds calcium and prevents calcium absorption. Low citrate leads to increase in calcium absorption and kidney stones. Causes of hypocitraturia: renal tubular acidosis; chronic diarrhea, thiazides.
What are the causes of uric acid stones?
Uric acid stones are associated with diseases like gout, hematologic malignancies, and Crohn disease. Radiolucent on x–rays.
Infection with which organisms can cause struvite kidney stones?
Urinary infection with urease–producing organisms like Proteus, Staphylococcus, Pseudomonas, and Klebsiella causes a highly alkaline urine that produces struvite stones.
What is the presentation of nephrolithiasis?
Constant flank pain (not colicky), hematuria, and pain radiating to groin. Stones
How is nephrolithiasis diagnosed?
Ultrasound. Strain the urine. Serum and urine calcium. Helical (spiral) CT scan is the best test. No contrast needed for stones. Plain x–ray (80% yield) is rarely used. Intravenous pyelogram is not done.
What is the treatment of nephrolithiasis?
Analgesia, hydration, and bed rest. Shockwave lithotripsy for stones
What is the presentation of adult polycystic kidney disease?
Flank pain, hematuria (micro and gross), infections, and calculi. Genetic. Hepatic cysts (40–60%), colonic diverticula, HTN (50%), intracranial aneurysm (10–20%), mitral valve prolapse (25%).
How is adult polycystic kidney disease diagnosed?
Ultrasound and CT scan.
What is the treatment of adult polycystic kidney disease?
Management of complications (UTI, calculi, and hypertension).
What are simple renal cysts?
Very common; if smooth–walled with no debris in cyst, no treatment necessary. Cysts with irregular walls or debris inside should be aspirated to exclude malignancy. Dialysis causes cysts.
What is essential hypertension?
A systolic blood pressure of 140 mm Hg or a diastolic >90 on multiple readings in the absence of a specific, identifiable underlying cause.
What is the criteria for hypertension in patients with diabetes or renal disease?
Any blood pressure above 130/80 mm Hg is defined as hypertension.
What is the treatment of stage 2 hypertension?
Patients with stage 2 hypertension (blood pressure >160/100 mm Hg), should receive initial therapy with two medications.
What is the criteria for normal BP?
120/80 mm Hg.
What is the criteria for pre–hypertension?
Systolic 120–139. Diastolic 80–89 mm Hg.
What is the criteria for stage 1 hypertension?
Systolic 140–159. Diastolic 90–99 mm Hg?
What is the criteria for stage 2 hypertension?
Systolic >160. Diastolic >100 mm Hg.
What is a hypertensive emergency?
HTN with stroke, subarachnoid hemorrhage, encephalopathy, myocardial ischemia, retinopathy. Requires substantial reduction of blood pressure within one hour.
What are the symptoms of a hypertensive emergency?
Headache, dizziness, chest pain, dyspnea, blurred vision, and palpitations. Malignant HTN is defined as encephalopathy or nephropathy.
What are the long–term cardiac complications of hypertension?
Myocardial ischemia or infarction, congestive heart failure, left ventricular hypertrophy, aortic aneurysm, and dissection. S4 gallop, accentuated A2 heart sound, and prominent left ventricular impulse.
What are the long–term cerebrovascular complications of hypertension?
Transient ischemic attack (TIA) and stroke.
What are the long–term renal complications of hypertension?
Proteinuria, microscopic hematuria, and elevation of BUN/creatinine.
What are the long–term ocular complications of hypertension?
Retinopathy: Hemorrhages, exudates, arteriolar narrowing, and papilledema. Blurred vision, scotomata, and blindness.
What are the signs of secondary hypertension?
How is hypertension diagnosed?
Allow the patient to sit 5 min before BP measured. Should not diagnose HTN after only a single reading. Repeat the reading 3–6 times over several months before confirming diagnosis and initiating therapy.
What basic studies are obtained in the evaluation of hypertension?
Urinalysis for protein, glucose, and red blood cells. Hematocrit. Potassium to exclude hyperaldosteronism. Serum creatinine and BUN. ECG to evaluate for left ventricular hypertrophy. Glucose and lipid analysis.
What is the lifestyle modification for essential hypertension?
Weight reduction, sodium restriction, aerobic exercise, avoid alcohol. Low–fat, increased fiber. Severe HTN (diastolic >100 mm Hg) should be start drug therapy with 2 medications.
What is the drug treatment of essential hypertension?
If DBP >90 despite a 3–months nonpharmacologic, start antihypertensive. Diuretics are initial treatment. For stage 2 HTN, BP >160/100, use a diuretic with an ACE/ARB/calcium–blocker or beta–blocker.
What medication should be added if a diuretic dose not control the patient’s blood pressure?
If diuretics do not control BP, then add a beta–blocker, calcium–blocker, ACE inhibitor, or angiotensin–receptor blocker. beta–Blockers avoided in asthma, COPD, heart block, or depression.
What is the initial antihypertensive for diabetics?
Diabetics should be treated with ACEI or ARBs, which prevent nephropathy. BP goal in a diabetic is lower, at
What is the initial antihypertensive for patients who have ischemic heart disease?
After a myocardial infarction (ischemic heart disease), beta–blockers should be started.
What is the initial antihypertensive for patients with decreased left–ventricular systolic function?
Decreased left–ventricular systolic function (congestive heart failure or postmyocardial infarction) should receive ACE inhibitors and beta blockers.
Which antihypertensive should be avoided in African American patients?
African American patients are least effectively treated with ACE inhibitors.
What are the initial antihypertensive choices for pregnant patients?
Alpha–methyldopa, labetalol, hydralazine, or calcium blockers. ACE inhibitors and angiotensin–receptor blockers are contraindicated in pregnancy. Diuretics are relatively contraindicated.
What is a hypertensive emergency?
The acute onset of severe hypertension with severe and rapidly worsening symptoms of end–organ damage. This usually happens with a diastolic pressure >120–130 mm Hg.
What are the neurologic manifestations of hypertensive emergencies?
Encephalopathy, headache, confusion, seizures, and subarachnoid or intracerebral hemorrhage.
What are the cardiac manifestations of hypertensive emergencies?
Chest pain, myocardial infarction, palpitations, dyspnea, pulmonary edema, jugular venous distension, and gallops.
What are the renal manifestations of hypertensive emergencies?
Nephropathy: Acutely progressive hematuria, proteinuria, and renal dysfunction.
What are the retinal manifestations of hypertensive emergencies?
Retinopathy: Papilledema, hemorrhages, and blurred vision.
What is the laboratory evaluation for hypertensive emergencies?
The laboratory evaluation is the same as with essential hypertension. CT scan of the head to exclude hemorrhage. ECG is as an initial test to exclude myocardial infarction.
What is the treatment of hypertensive emergencies?
Intravenous nitroprusside and labetalol are the two best agents. Nitroglycerin if myocardial ischemia. Enalaprilat is IV ACEI. Initial goal is to reduce BP by no more than 25% within the first 1 to 2 hours.
What is secondary hypertension?
HTN with underlying cause. 5% of cases of HTN are caused by an identifiable underlying cause. Renal artery stenosis is the most common of these causes.
Which patients should be screened for secondary hypertension?
Hypertension in the very young or very old (55)
What is the cause of renal artery stenosis?
Caused by arthrosclerotic disease in elderly persons and fibromuscular dysplasia in young women. Upper abdominal bruit is present in 50–70% of patients.
How is renal artery stenosis diagnosed?
Screening ultrasound. Captopril renogram measures the uptake of radioisotope before and after captopril. Positive test is decreased uptake (decreased GFR) after captopril. Arteriogram is the best method of diagnosis.
What is the treatment of renal artery stenosis?
Percutaneous transluminal angioplasty. If stenosis recurs, then the procedure should be repeated. If angioplasty fails, surgical resection. ACE inhibitors if angioplasty or surgery is not possible.
What is the cause of primary hyperaldosteronism (Conn Syndrome)?
Conn Syndrome is most commonly due to a unilateral adrenal adenoma. Bilateral adrenal hyperplasia is less common. Cancer is rare as a cause of hyperaldosteronism.
What are the symptoms of primary hyperadosteronism?
Hypertension in association with hypokalemia. Symptoms of hypokalemia such as muscular weakness and polyuria and/or polydipsia from a nephrogenic diabetes insipidus.
How is primary hyperaldosteronism diagnosed?
Elevated aldosterone levels in urine and blood.
What is the treatment of Conn syndrome?
Surgical resection of adenoma. Potassium sparing diuretics such as spironolactone in adrenal hyperplasia.
What is pheochromocytoma?
Pheochromocytoma is most often due to a benign tumor of the adrenal gland; 10% are bilateral, 10% are malignant, and 10% are extra–adrenal.
What is the presentation of pheochromocytoma?
Episodic hypertension with headaches, sweating, palpitations, and tachycardia. Pallor or flushing may also occur.
How is pheochromocytoma diagnosed?
Initial test is urinary vanillylmandelic acid (VMA), metanephrines, and free urinary catecholamines. Plasma catecholamine evaluation. CT and MRI scanning is used to localize tumor.
What is the treatment of pheochromocytoma?
Alpha–adrenergic blockade with phentolamine or phenoxybenzamine, followed by surgical removal.
What is the most common cause of Cushing disease?
Cushing Disease is commonly caused by ACTH hypersecretion by a pituitary adenoma. HTN in association with cushingoid truncal obesity, buffalo hump, menstrual abnormalities, striae.
How is Cushing disease diagnosed?
Dexamethasone suppression testing and 24–hour urine cortisol are the best initial tests.
What is the treatment of Cushing disease?
Surgical resection of the pituitary adenoma.
What is the clinical sign of coarctation of the aorta?
Hypertension greater in the upper extremities compared with the lower extremities.
What are the endocrinologic and renal causes of secondary hypertension?
Oral contraceptives, acromegaly, congenital adrenal enzyme deficiencies, glomerulonephritis, polycystic disease, diabetic nephropathy, pyelonephritis.
What are the commonly used thiazide diuretics?
Hydrochlorothiazide, chlorthalidone, metolazone, indapamide.
What are the names of the potassium sparing diuretics?
Spironolactone, amiloride, triamterene.
What are the indications for diuretics in hypertension?
Congestive heart failure, edematous states, African–American patients; least expensive.
What are the major side effects of diuretics?
Decreases in potassium and magnesium; increases in calcium, uric acid, glucose, LDL–cholesterol; gynecomastia.
What are the relative contraindications to diuretics?
Diabetes, gout, hyperlipidemia.
What are the two most commonly used beta–blockers for hypertension?
Metoprolol and atenolol are the most commonly used.
