UW - Med/Renal Flashcards
What is membranous nephropathy and what are its major clinical associations?
Nephrotic syndrome (2nd most common)
AdenoCA, NSAIDs, Hep B, SLE
What is focal segmental glomerulosclerosis and its major clinical associations?
1 nephrotic syndrome
African Americans, HIspanics, Obesity, HIV, Heroin use
What symptoms are characteristics of mixed cryoglobulinemia?
Palpable purpura, proteinuria, hematuria, arthralgias, hepatosplenomegaly, decreased complement
Older patients, most have HCV infection
What are the causes of normal anion gap metabolic acidosis?
HARDUP Hyperalimentation; hyperchloremic acidosis, Hypoaldosteronism Acetazolamide, Argenine Renal tubular acidosis Diarrhea Ureteral diversion Pancreatico-duodenal fistula
What are the etiologies of primary adrenal insufficiency?
HIMA
Hemorrhagic infarct (meningococcemia, anticoagulants)
Infections (TB, HIV, disseminated fungal)
Metastatic cancer (lung)
Autoimmune
What are the main symptoms in acute and chronic primary adrenal insufficiency?
Acute - SHOCK, Ab tenderness w/ deep palp, FEVER, N/V/Wt loss/Anorex, HypoNa, HyperK, HyperCa, Eosinophilia
Chronic - Fatigue, WEAK, anorex, GI (n/v/ab pain), Weight loss, HyperPIGMENT/VITILIGO, LOW BP, same ion imbalance, Eosinophilia, ANEMIA
Where does aldosterone primarily act and what does it do? What can happen if it gets blocked?
Distal renal tubules, “saves sodium”, secretes K+ and H+
If blocked, K+ and H+ are saved –> Normal AG Met Acid
What is the treatment for uric acid stone?
Hydration, Alkalization of urine (to 6-6.5 w/ potassium citrate), low purine diet,
Add allopurinol for recurrent symptoms
What is the risk of calcium restriction, or decreased Ca in renal tubules for patients with kidney stones (Ca or Uric acid)?
Ca restriction in diet –> Negative calcium –> Hyperoxaluria from increased GI absorption of oxalate
What is the effect of Furosemide on urine Ca?
Increased excretion (because action of Na/K/Cl transport brings Ca in)
What is the treatment for severe hypernatremic hypovolemia? Less severe?
Severe = 0.9% saline which gradually corrects hyperosmolality while normalizing patient’s volume status then switch to 0.45% saline to replace free water deficit
Less = 5% dextrose in .45% saline
What is D5W (5% dextrose in water) used in the treatment of?
Euvolemic and hypervolemic hypernatremia (oral free water in stable patients)
What possible medication in diabetics should be removed during acute kidney injury and/or sepsis and why?
Metformin -> can cause lactic acidosis, withhold until renal function improves
What is the target blood glucose level in patients who are acutely ill and have hyperglycemia? What treatment can facilitate this?
140-180 mg/dL, use short acting insulin
What should always be considered in patients getting CT scan w/ contrast? What alternatives are available?
Pts w/ renal insufficiency (Cr >1.5) or history of diabetes are increased risk of contrast induced nephropathy
Use non-ionic contrast agents
What is the most common cause of AA amyloidosis and what can result from this?
Rheumatoid arthritis -> amyloidosis can lead to Nephropathy via glomerular amyloid deposits (congo red staining etc.)
What are linear glomerular deposits seen with immunoflorescence staining characteristic of? Granular deposits?
Linear = Antiglomerular basement membrane disease (Goodpasture’s)
Granular = immune complex glomerulonephritis (Lupus nephritis, IgA nephropathy, postinfection glomerulonephritis)
What are common causes of nephrogenic DI?
HyperCa, severe HypoK+, tubulointerstitial renal disease, and medication (lithium, cidofivir, foscarnet, demeclocycline, amphotericin)
What is detrusor sphincter dyssnergia?
Neurological disease where detrusor contracts while urethral spinchter contracts –> difficult voiding/interruption of urine stream
What are the causes of hypervolemic hypernatremia?
CHF, cirrhosis, chornic kidney disease or nephrotic syndrome
What are the causes of euvolemic and hypovolemic hypoNa+?
Euvol = SIADH, primary psycho polydipsia, Hypothyroid, secondary adrenal insufficiency
Hypovol = Volume loss (hemorrhage), Primary adrenal insufficiency, GI loss (diarrhea, vomit), Renal loss (diuretics)
How do you calculate serum osmolality and osmolar gap?
Serum Osm = [2Na + Glu/18 + BUN/2.8]
Osm Gap = Observed Osm - Calculated Osm
What causes omsolar gap met acidosis?
Methanol, ehtylene glycol, ethanol poisoning
How do you treat patients with sever hyperK+ with major EKG changes?
- Emergent administration of IV calcium gluconate to stabilize cardiac membrane
- Lower serum K+ by driving into cell w/ insulin and glucose, sodium bicarb, and beta 2 agonists
- Lower total body K+ –> loop diuretic
What does hyponatremia in the setting of serum Osm > 290 mOsm/kg suggest?
Marked hyperglycemia, Advanced renal failure
When should bicarb be used for the treatment of lactic acidsosis?
Only very severe cases where pH
How do you manage severe hypercalcemia?
Short term: NS hydration + Calcitonin (avoid loop diuretics, only use in small doses for HF pts)
Long term: bisphosphonates,
What are common meds that can cause hyperkalemia?
Nonselective beta blockers, potassium sparing diuretics (esp triamterene), ACE inhibitors, ATII-R blockers, NSAIDs
What are some features of cyanide toxicity?
Skin flushing (cherry red), AMS/seizures/coma, Arrhythmias, Tachypnea then resp depression/pulm edema/cyanosis, Ab pain/N/V, Metabolic acidosis (lactic acid) and renal failure
What is the presentation for patients with acute nephritic syndrome + fluid overload?
Anasarca, pulmonary + facial edema, HTN, proteinuria and micro hematuria (>50 rbcs, rbc casts)
What acid/base disorder can result with aspirin toxicity (give abg) and how does this occur?
Direct stimulation of medullary respiratory centers -> Tachypnea -> Resp alkalosis
Anion gap metabolic acidosis from increased production and decreased renal excretion of organic acids
Normal pH, low PaCO2 and bicarbonate
What is the etiology of Familial Hypocalciuric Hypercalcemia?
PT gland and renal tubule cell receptors resistant to Ca –> secrete excess PTH (can be high or high normal)
What is renal tubular acidosis?
Normal Anion Gap Met Acidosis w/ preserved renal fxn (usually elderly w/ poorly controlled DM
Resistance to or deficiency of Aldosterone –> K+/H+ retention
What is the cause in 70% of cases of interstitial nephritis?
Drugs like cephalosporins, penicillins, sulfonamides, sulfonamide containing diuretic, NSAIDs, rifampin, phenytoin and allopurinol