CMP Flashcards
BUN: basics
- blood urea nitrogen
- amount of nitrogen in blood that comes from waste product urea
BUN: what makes it high?
if kidneys can’t remove urea from blood normally.
- heart failure
- dehydration
- diet high in protein
what makes BUN low?
liver disease or damage
2nd or 3rd trimester of pregnancy
BUN:creatinine ratio normal range
usually between 10:1 and 20:1
increased BUN:crt ratio
increased ratio may be due to condition that causes a decrease in blood flow to kidneys like:
-CHF
- dehydration
OR w/ increased protein from GI bleeding or increased protein in diet.
decreased BUN:Crt ratio
from liver disease (due to decrease in formation of urea
or malnutrition
what is urea?
waste product formed in liver when protein is metabolized into its component parts (amino acids). Process produces ammonia, which is then converted into the less toxic waste product urea.
two of the most common causes of high blood calcium are:
hyperparathyroidism cancer (breakdown of bone or makes hormone similar to PTH)
some causes of hypercalcemia:
hyperparathyroidism cancer hyperthyroidism sarcoidosis tuberculosis prolonged immobilization thiazide diuretics kidney transplant HIV/AIDS
causes of hypocalcemia
low blood protein levels, esp. low albumin (liver disease, malnutrition, alcoholism. w/ low albumin only bound calcium is low, ionized calcium remains normal and calcium metabolism is being regulated appropriately. **most common
hypoparathyroidism inherited resistance to effects of PTH extreme deficiency in dietary calcium decreased levels vitamin D magnesium deficiency incr. levels phosphorus acute inflammation of pancreas renal failure
Major causes of hyperkalemia
Increased potassium release from cells
Reduced urinary potassium excretion
What increases potassium release from cells?
pseudohyperkalemia metabolic acidosis insulin deficiency, hyperglycemia, and hyperosmolality increased tissue catabolism beta blockers exercise hyperkalemic periodic paralysis Other -overdose of digitalis or related digitalis glycosides - red cell transfusion - succinylcholine -arginine hydrochloride - activators of ATP-dependent potassium channels (eg, calcineurin inhibitors, diazoxide, minoxidil, and some volatile anesthetics)
What causes reduced urinary potassium excretion?
reduced aldosterone secretion reduced response to aldosterone reduced distal sodium and water delivery -effective arterial blood volume depletion acute and chronic kidney disease other -selective impairment in potassium secretion -gordon's syndrome -ureterojejunostomy
persistent hyperkalemia requires ____ ___ ___ ___.
impaired urinary potassium excretion.
what happens with k in metabolic acidosis?
as H enters the cells to be buffered, intracellular NA and K leave the cells and move into extracellular fluid, tending to raise plasma potassium concentration.
**doesn’t happen in lactic acidosis or keto acidosis bc of presence of sodium-organic anion cotransporter
what does insulin do to K?
promotes K entry INTO cells –> ingesting glucose minimizes rise in serum K conc induced by concurrent K intake, and glucoses ingest alone in pts w/o diabetes modestly lowers serum K.
what happens to K in uncontrolled diabetes setting?
insulin deficiency + hyperosmolality induced by hyperglycemia freq leads to hyperK even though there may be marked K depletion dt urinary losses caused by osmotic diuresis
two poss mech:
loss of cell water raises cell K conc –> gradient for K exit
friction forces bt solvent (water) and K (K gets dragged out of cell by water independent of electrochemical gradient)
what do beta blockers do to K?
increased beta-2-adrenergic activity drives K into cells and lowers serum K. –> beta blockers that interfere w/ this (mostly nonselective beta blockers like propranolol and labetalol) –> increase in serum K
what are major causes of hypoaldosteronism?
Reduced aldosterone production
Aldosterone resistance
What causes reduced aldosterone production?
Hyporeninemic hypoaldosteronism
Angiotensin inhibitors, such as ACE inhibitors, angiotensin II receptor blockers, and direct renin inhibitors
Chronic heparin therapy (impairs aldosterone synthesis)
Primary adrenal insufficiency
Severe illness
Inheritted disorders
What causes hyporeninemic hypoaldosteronism?
- renal disease, most often diabetic nephropathy
- NSAIDS
- calcineurin inhibitors
- volume expansion, as in acute glomerulonephritis
What inherited disorders reduce aldosterone production?
- congenital hypoaldosteronism (21-hydroxylase deficiency and isolated hypoaldosteronism)
- pseudohypoaldosteronism type 2 (Gordon’s syndrome)
what cause aldosterone resistance?
Inhibition of the epithelial sodium channel
Pseudohypoaldosteronism type 1
Voltage defects
what inhibits the epithelial sodium channel in aldosterone resistance?
- potassium-sparing diuretics, such as spironolactone, eplerenone, amiloride, and triamterene
- antibiotics, trimethoprim and pentamidine
what cause voltage defects in aldosterone resistance?
- markedly reduced distal Na delivery
- acquired or congenital defects in Na reabsorption by the distal tubule principal cells (obstructive uropathy), SLE, and sickle cell disease
What defines acute kidney injury (AKI) in adults?
Kidney Disease: Improving Global Outcomes (KDIGO) guidelines:
- increase in serum creatinine by >/= 0.3 mg/dL w/in 48 hrs OR
- increase in serum creatinine to >/= 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days,
OR
- Urine volume <0.5 mL/kg/hr for six hours
AKI stage 1
increase in serum crt to 1.5 to 1.9 times baseline
OR
increase in serum art by >/=0.3 mg/dL
OR
reduction in urine output to <0.5 mL/kg/hr for 6 to 12 hours
AKI stage 2
increase in serum creatinine to 2.0 to 2.9 times baseline
OR
reduction in urine output to <0.5 mL/kg/hour for >/= 12 hours
AKI stage 3
increase in serum creatinine to 3.0 times baseline
OR
increase in serum creatinine to >/=4.0 mg/dL
OR
reduction in UOP to <0.3 mL/kg/hr for >/= 24 hours
OR
anuria for >/= 12 hours
OR
initiation of renal replacement therapy
OR
in patients < 18yrs, dear in eGFR to <35 mL/min/1.73m^2
causes of prerenal disease
hypovolemic states alterations in renal vascular autoregulation angiotensin blockade (ACE or ARB meds)
what cause renal hypovolemic states?
- acute hemorrhage
- diarrhea
- unreplenished insensible losses
- low effective circulating (arterial) volume such as severe systolic heart failure w/ reduced EF (cardiorenal syndrome) or acutely decompensated liver disease with portal hypertension (hepatorenal syndrome)
what cause alterations in renal vasculature autoregulation?
afferent arteriole vasoconstriction caused by NSAIDS or iodinated radio contrast media
what are causes of intrinsic renal vascular disease?
small vessel vasculitides
diseases that cause microcangiopathy and hemolytic anemia
what diseases cause microangiopathy and hemolytic anemia (MAHA)?
- thrombotic thrombocytopenia purport - hemolytic uremic syndrome (TTP/HUS)
- scleroderma
- atheroembolic disease
- malignant hypertension
what diseases affect larger vessels and cause renal disease?
renal infarct from aortic dissection
systemic thromboembolism
renal artery abnormality (such as aneurysm)
acute renal vein thrombosis
causes of intrinsic glomerular disease: classification
primary (idiopathic, not assoc w/ systemic disease)
secondary (such paraneoplastic, drug induced, or part of a systemic rheumatologist disease)
patterns of intrinsic glomerular disease:
nephritic pattern (proliferative glomerulonephritis) nephrotic pattern (nonproliferation glomerulopathy)
what is produced in the nephritic pattern or glomerulopathy?
active urine sediment with dysmorphic red + white cells; granular, red cell, and other cellular casts; and a variable degree of proteinuria
what is seen in nephrotic pattern of glomerulopathy?
lots of protein
intrinsic tubular and interstitial disease causing AKI
most commonly is ATN from ischemia or a nephrotoxic exposure
–> may occur following concurrent use of ACEi/ARB medications with NSAIDs or radio contrast media
