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48 Cards in this Set
- Front
- Back
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aplastic anemia
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bone marrow unable to produce RBC
causes for this are autoimmune, medication, radiation/chemo results in pancytopenia (wiping out of all blood cells) |
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hemolytic anemia
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if MCHC turns out normochromic then hemolytic anemia
premature destruction of RBC causes: infection, medication, autoimmue(sickle cell, G6PD, Bactrim) |
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megaloblastic anemia
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vitamin B12/folic acid deficiency
cells are macrocytic |
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microcytic
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small RBC size
due to iron deficiency anemia, thalessemia |
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hypochromic
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less color
due to iron deficiency anemia, thalessemia |
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thrombocytopenia
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decreased platelets
decreased production due to a decrease in vitamin B12/folic acid deficiency, leukemia, sepsis can be medication induced: heparin or chemo |
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thrombocytosis
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increase in platelets
inflammation severe iron deficinecy splenectomy |
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corticosteroids inc or dec WBC?
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increases
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anticonvulsants(phenytoin & carbamazepine) inc or dec WBC?
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decrease
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most abundant extracellular cation
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sodium
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when is aldosterone released?
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Aldosterone: released from adrenal gland when ↑K, ↓Na, ↓BP, or ↓BV =>↑Na reabsorption & K secretion at distal tubule. H2O follows Na at distal tubule if ↑ADH
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pseudohyponatremia (w/ hypertriglyceridemia) effect on edema?
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TBW & total body Na are unchanged. Excess proteins/lipids low serum Na, but normal effective osmolality no risk of cerebral edema
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hyponatremia (caused by hyperglycemia) effect on edema?
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TBW & total body Na are unchanged. In DM pt, excess glucose
↑osmolality in tissues ↑ risk of edema |
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hyponatremia effect on edema?
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low serum Na, ↓effective osmolality (H2O moves into cells)↑risk of cerebral edema
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hypernatremia effect on edema?
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high serum Na, ↑effective osmolality ↓risk of cerebral edema
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how should you treat hyponatremia
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give NS to replace....no more than 0.5mEq/L/hr of Na
fluid restriction, 3%saline, demeclocycline (chronic only), Li carbonate, phenytoin, vasopressin antagonist (Conivaptan) |
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how should you treat hypernatremia?
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tx dehydration w/ NS, then switch to lower Na solution (D5W or ½ NS)
-loop diuretics & D5W – excrete Na & restore body H2O -see DI tx ------ +nephrogenic: Na restriction, indomethacin +Hormone: aqueous vasopressin, desmopresin (DDAVP), lypressin, vasopressin tannate +Non-hormonal: chlorpropamide, clofibrate, carbamazepine, HCTZ/chlorthalidone w/ D5W |
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what is the predominant intracellular cation?
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potassium
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what can cause hypokalemia?
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alkalosis, insulin, B2-agonist (albuterol), caffeine, diuretics, licorice, vomiting, DIARRHEA, laxative abuse
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what do aldosterone and glucagon do to potassium levels in the kidney?
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↑K secretion at distal tubule & collecting ducts
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how should you treat hypokalemia?
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monitor for arrhythmia and give calicum gluconate 1st
then replace the potassium loss by giving potassium supplements |
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max infusion rate for IV potassium?
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no more than 40mEq/hr
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causes for hyperkalemia?
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-extracellular shift: acidosis (associated w/ renal dz – Tx w/ hemodialysis)
-↑ dietary intake -release of intracellular contents: hemolysis (malaria), rhabdomyolysis, muscle crush, or burn injuries -↓ elimination: acute/chronic renal failure, drugs (K sparing diuretics, ACEI/ARB for diabetes) -Heparin (in pt predisposed to hyperK – low salt intake, reduced GFR, salt subs) – inhibit enzymatic synthesis of aldosterone (↓aldosterone ↓K secretion) |
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how should you treat hyperkalemia/
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Prevent development of arrhythmia: Ca (raise threshold potential ↓excitability)
preferred Calcium Gluconate IV (release Ca slowly) than Calcium Chloride IV -Shift K intracellular: +insulin regular w/ 50% dextrose (prevent hypoglycemia) +B-agonist (albuterol – nebulized or IV) +NaHCO3: delayed effect & risk of hypernatremia / hypervolemic -↑ elimination: +Kayexalate (sodium polystyrene sulfonate): PO or rectal to exchange K for Na & eliminated in stool (risk of hypernatremia & diarrhea) +hemodialysis: tx of choice – most effective & permanent, esp. pt w/ renal dysfn |
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causes for hypomagnesemia?
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-GI tracts loss: diarrhea, dietary deficiency
-renal loss: renal tubular necrosis, diuretics -massive burns (acute) |
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treatment for hypomagnesemia?
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IV: take several days (large boluses ↑urine wasting & cardiac), careful w/ renal dysfn or preexist cardiac pt
-PO: antacids containing Mg, Milk of Mg, MgOx (monitor for diarrhea) |
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causes for hypermagnesemia?
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renal failure (most common)
-↑ intake: Mg containing laxatives & Epsom salt, IV fluids containing Mg |
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treatment for hypermagnesemia?
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-monitoring: cardiac monitor required for Mg >5mEq/L
-Prevent cardiac arrhythmia: preferred Calcium Chloride (fast release of Ca) than Calcium Gluconate -IV furosemide (loop diuretic) + IV fluids to dilute the blood -Dialysis (severe) |
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calcium binding to albumin inc/dec when acidosis?
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decreases
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calcium binding to albumin inc/dec when alkalosis?
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increase
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what are the actions of PTH?
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↑Ca level in blood (also activate vitamin D to D3 – Calcitrol)
+bone (w/ vit D): activate osteoclasts to break down bone matrix +small intestine (w/ vit D): ↑intestinal absorption of Ca (& of P) +kidney: ↑reabsorption of Ca from urine |
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what are the causes of hypocalcemia?
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decrease intake:
Hypoparathyroidism Magnesium Deficiency Vitamin D deficiency - increase output: Hyperphosphatemia (because it binds all Ca) osteoblast metastasis (b/c it concentrates Ca into the bone) |
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how should you treat hypocalcemia?
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-IV: preferred Calcium Gluconate than Calcium Chloride
-PO: Calcium carbonate (most common) Treat hyperphosphatemia Treat hypomagnesiema Forteo – SubQ Recombinant PTH Increase absorption of Ca from GI and distal renal tubules (by giving Vit D supplement) |
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what are the causes of hypercalcemia?
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cancer
- primary hyperthyroidism - primary, secondary and tertiary - thiazide diuretics, lithium and milk alkali syndrome |
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how should you treat hypercalcemia?
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bone: inhibit Ca release (Calcitonin, bisphophanates)
-intestine: ↓Ca absorption (oral phosphate – caution w/ diarrhea and corticosteroids) -kidney:↑Ca excretion (loop diuretics & IV fluids) -remove Ca from circulation by DIALYSIS -control underlying disease Medications: Calcitonin (Miacalcin) Bisphosphonates: Pamidronate, Etidronate Zoledronic Acid Ibandronate Sensipar |
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what is the major intracellular anion?
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phosphate
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what are the causes of hypophosphatemia?
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decreased intestinal absorption
- excessive renal excretion: Hyperparathyroidism - redistribution from extracellular to intracellular |
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how should you treat hypophosphatemia?
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correct hypocalcemia first
- oral if phos 1.5 to 2.5 - Fleet phosphor-soda - IV NaPhos or KPhos if severe |
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How should you treat hyperphosphatemia?
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IV calcium if tetany or seizure
- volume expansion to pee out phosphate - phosphate binders - Fosrenol (lanthanum carbonate) chewable - Phoslo (calcium acetate) binds 45mg – don’t give to pt w/ high Ca - Renagel (sevelamer)– first line in pt w/ hypercalcemia Also lowers LDL - (calcium carbonate) Tums, Oscal and Caltrate binds 39mg)(don’t give to pt with High Ca levels) - hemodialysis |
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what receptor does aldosterone work on?
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Na/K/ATPase in the distal convoluted tubule
also in collecting duct |
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what receptor do loops work on?
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Na/K/2Cl in the ascending loop of Henle
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what receptor do thiazides work on?
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Na/Cl cotransporter in the distal convoluted tubule
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what receptor do carbonic anhydrase inhibitors work on?
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none they block carbonic anhydrase's actions!
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what are the causes of hyperphosphatemia?
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- impaired glomercular filtration (renal damage)
- hemolysis of cells - medications (sodium phosphate and vitamin D) |
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How should you treat metabolic acidosis?
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sodium bicarb
sodium acetate THAM |
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how should you treat metabolic alkalosis?
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give acid via KCL, NaCl or arginine HCl or ammonium chloride
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how do you know if there is respiratory compensation in metabolic acidosis?
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low pH, low pCO2
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how do you know if there is respiratory compensation in metabolic alkalosis?
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high pH, high HCO3, high pCO2
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