Preventing Iatrogenic Anemia-LABS Flashcards
Hemoglobin
-oxygen carrying component of a red blood cell
-Normal: 135.5-16.0 g/dl
High HGB
-Hypoxia (Smoking, OSA, Lung Dx, High Altitude, CO)
-Dehydration
-Polycythemia Vera (JAK2V617F)
-EPO producing tumors (Liver, Renal, Hemangioblastoma, Pheo, Uterine)
-PV is most common chronic myeloproliferative disorder
MCV
-way to differentiate anemia. -The higher the MCV is to be more likely it’s going to be B12 or folate.
-Normal: 85.2-95.1 fL
B12
-absorbed in the small bowel. If you have something that is rerouting past the small bowel or bacterial overgrowth, something inhibiting absorption, vegan, vegetarian’s-deficiency
-deficiency most likely Pernicious Anemia (decreased intrinsic factor).
Folate deficiency
-think about medications or alcohol. Alcoholics will have macrocytosis. People on methotrexate, chemotherapy, or on high doses of Bactrim for pcp prophylaxis or PCP pneumonia
Low HGB
-Nutritional Deficiency (Iron, B12, Folate)
-Blood Loss (Trauma, GI Tract, Hematoma)
-Hemodilution
-Hemolysis
-Renal Failure
-Chronic Disease
Macrocytosis
-B12 and Folate Deficiency (most common)
-Pernicious Anemia, Surgical Resection of ileum, sprue, fish tapeworm, bacterial overgrowth (B12)
-ETOH (folate)
-Hypothyroidism
-Drugs (AZT, MTX, Hydroxyurea, Bactrim, Valacyclovir, Triamterene, Phenytoin)
-Liver disease
-Pregnancy (Folic Acid)
-Myelodysplastic Syndromes
-Cold and Warm Agglutinins
-Hyperglycemia (>600)
-Extreme Leukocytosis (>50,000)
-Reticulocytosis
RDW
-RDW can differentiate Microcytic anemias. HIGH RDW= Iron deficiency LOW RDW= Thal
Microcytosis
-If you have ever had a normal MCV, you do not have Thalassemia
-Iron Deficiency (most common)-Ferritin
-Thalassemia (alpha or beta minor)-MCV always low
-Chronic Disease
-Lead Poisoning
-Sideroblastic Anemia
-Aluminum Toxicity
WBCs
3,500-10,000 x10^9
Leukocytosis
-High WBC count
-Infection (most common)
-Leukemia
-Steroids
-Stress
-Tumor Necrosis
-Drugs (Lithium, Digoxin)
-Platelet Clumping
-Cryoglobulins
–Large leukocytosis (pneumonococcus, staphylococcus, clostridium)
Leukopenia
-Low WBCs
-Leukopenia is low WBC and is different than neutropenia
–Medications
-Myeloproliferative Disorders
-Infections (Virus, Bacterial, Rickettsial)
-Gram Negative Sepsis
Neutrophils
3500-10000/L
-Most predominant white blood cell
Neutrophilia
-high neutrophil count
-Bacterial infection
-Smoking
-Inflammatory States
-Drugs (Lithium, Beta Agonists, Minocycline)
-Myeloproliferative Disorders
-Ethylene Glycol Intoxification
-Leukocytosis with a left shift is high neutrophil count
Neutropenia
-Low neutrophils
-Post Infectious (most common)
-Drug Induced (clozapine, sulfasalazine)
-Immune Disorders
-Hypersplenism
-Bacterial infections that cause neutropenia (salmonella, tularemia)
-Neutropenia (Influenza, measles, chickenpox, rubella, HIV, dengue fever, etc. Increased lymph)
Lymphocytosis
-High lymphocyte count
-Viral infections
-Leukemia
-Bacterial (TB, Brucella, Pertussis)
-Thymoma
Lymphopenia
-low lymphocyte count
-viral (HIV)
-Inflammatory (SLE)
Monocytes
-Bacterial (Listeria, TB, Rickettsia)
-CML
Eosinophilia
-Allergies/drug reaction
-Parasites
-Churg-Strauss
-Heme Malignancies
-Cancer patients-graft vs. host
Basophilia
-Heme malignancies
Platelets
-150,000-450,000/L
-30% of platelets found in normal size spleen. Anything that causes splenomegaly can cause decrease platelets.
-(Ferritin, CRP, Sed Rate, Ceruloplasmin, Fibrinogen, alpha 1 antitrypsin, haptoglobin)
-Acute Phase Reactants… Body mobilizes for stress situation. Iron, fibrinogen, haptoglobin to handle bleeding.
Type 2 heparin induced thrombocytopenia (HIT)
is 3-5 days drop in plts after exposure-if large drop 5-10 days after exposure is something to be concerned about
Type 1 HIT
1 day after exposure to heparin
Thrombocytosis
-High Plt
–Infection (most common)
-Post Surgical Status
-Malignancy
-Splenectomy
-Acute blood loss
-Iron deficiency
-Inflammation (Acute Phase Reactant)
Thrombocytopenia
-Low plt
–Increased destruction (ITP, SLE, DIC, TTP, HUS, HELLP)
-Decreased production (Aplastic Anemia, ETOH, Viral infections)
-Splenomegaly
-Pseudo (RBC Transfusion)
-Drugs (Heparin, Quinine, Valproic Acid, Sulfonamide)
-Typically want to consider a peripheral smear
Sodium (Na)
-135-145mmol/L
–Primary extracellular cation and responsible for approx. half of the plasma osmolality
-Lasix (last 6 hours-works for 6 hours). If patient got a dose of Lasix I wont check a urine sodium for at least 6 hours.
-Correct sodium slowly
Hypernatremia
-Dehydration (Fever, sweating, vomiting, diarrhea, primary hypodipsia)
-Diabetes Insipidus (Neurogenic, Nephrogenic)
-Cushing’s Disease
-Osmotic Diuresis/Diarrhea (Hyperglycemia, Mannitol)
-Aggressive normal saline hydration
-Elevated Na = ADH secretion and thirst
-Serum sodium 1.6 for each 100 increase over 100.
-If you’re giving a lot of NS you can drive up hypernatremia and hyperchloremia creating metabolic acidosis (there are 9g of salt in a Liter bag NS)
What could happen if you give a patient with SIADH fluid such as NS
-hypotonic hyponatremic
-Could drive Na down
-A pt receiving a lot of free water or NS with SIADH could seize
-more volume equals more antidiuretic hormone with more free water retention creating lower sodium.
–Next step then is to check urine sodium <10-if serum sodium is low it will tell your body don’t pee out salt. So if that serum sodium is low but their urine sodium is high, that’s indicating SIADH and they’re on free water restriction
-100 cc of 3% hypertonic
Hyponatremia
-Overhydration
-Dehydration (Vomiting, Diarrhea, Diuretics)
-SIADH (Head trauma, Seizure, CNS disease, Neoplastic)
-Adrenal Failure
-Pseudo (Hyperglycemia) FOR EVERY 100 ABOVE 100 ADD 1.6
-Congestive Heart Failure, Cirrhosis
-Polydipsia
-Ecstasy
Potassium (Hyperkalemia) (3.6-5.2 mmol/L)
-Decreased excretion (renal dx)
-Tissue Catabolism (rhabdo, hemolysis, GI bleed)
-Cell shift (acidosis, lack of insulin)
-Excessive intake (IV, PO, KCl salt substitute)
-Blood transfusion
-Medications (ACE/ARB, K+ sparing, cyclosporine, NSAIDS)
-Pseudo (hemolysis, elevated WBC (> 50K) platelets (>1million))
-Heparin Induced Hypoaldosteronism (2-4d after admin)
Hypokalemia
-GI loss (Diarrhea, Ileostomy, Emesis, NGT)
-Cell shift/Redistribution (Increased insulin, albuterol, alkalosis)
-Hyperaldosteronism
-Poor intake
-Drugs (Diuretics, Prednisone)
-Geophagia
-40% of HypoK+ also HypoMg+2. replace Mg first.
High Bicarbonate
-Metabolic Alkalosis (Volume Contraction)
-Respiratory Acidosis
-Can be an indicator for HF patients and those diuresing
Low Bicarbonate
-Metabolic Acidosis
-GI Loss
-Renal Loss
Normal creatinine level
0.6-1.1 mg/dL
-BUN/Creatinine ratio 20:1 =dehydrated
-When creatinine goes up GFR goes down
-Creatinine is a 24-hour delay
1) Kidney damage with normal or increased GFR90
2) Kidney damage with mild decrease in GFR 60-89
3) Moderate decrease in GFR 30-59
4) Severe decrease in GFR 15-29
5) Kidney failure <15 (or dialysis)
Elevated Creatinine
-Renal disease
-Drugs (Cimetidine, Trimethoprim)
Decreased Creatinine
-Minimal muscle mass
Hypercalcemia (8.9-10.1 mg/dL)
-Primary Hyperparathyroidism
-Malignancy (PTH peptide, Bone Mets)
-Sarcoidosis
-Drugs (HCTZ, Lithium, Theophylline)
-Vitamin D intoxification
-Hyperthyroidism
-Immobilization
-90% of cases of hypercalcemia are from Hyperparathyroid or Malignancy
-Elevated Ca and ALk Phos think bone.
Hypocalcemia
-Severe Pancreatitis
-Renal Failure
-Vitamin D Deficiency
-Post massive transfusion
-Hypoparathyroidism
-Pseudo (Hypoalbuminemia) ** Corrected Ca = Calcium + 0.8 x (4.0-Albumin) **
-Chelation secondary to use of citrate
Calcium
-8.9-10.1 mg/dL
–99% in the bone. 1% in serum.
-50% is bound to albumin, other ionized.
-Most prevalent catanion in the body.
-Body has approximately 2pounds of calcium. (99% in bone and 1% in extracellular fluid)
-Vital in coagulation and nerves.
Magnesium
-1.8-2.5 mmol/L
-Can’t replace K until mg is normal
-neuromuscular transmission, protein synthesis, enzyme activation
-4th most abundant cation (calcium, sodium, potassium)
-2nd most prevalent intracellular.
-Important in function of over 300 cellular enzymes.
-Usually iatrogenic.
-30% of magnesium bound to albumin
Hypermagnesemia
-Renal Failure
-Medications (Antacids, Laxatives, Infusion)
-Hemolysis
-Lithium Therapy
Hypomagnesemia
-Alcoholism (most common)
-Diarrhea (steatorrhea)
-Decreased absorption
-Excessive elimination (ETOH, NG suction, diuretics, vomiting)
-Refeeding
-Drugs (Cisplatin, Loop, Thiazides, Aminoglycosides, Cyclosporine)
Blood Urea Nitrogen (BUN)
-6-21 mmol/L
–Upper GI Bleed. If Hgb dropping with BUN going up somebody needs an EGD.
-Made in liver and final breakdown product of protein metabolism.
-If BUN only prerenal, if BUN and creatinine Kidney disease.
Azotemia
-High BUN
-Dehydration
-Rapid protein catabolism with decreased renal function
-CHF
-Shock
-MI
-High protein diet
-Anabolic effect of systemic corticosteroids
Low BUN
-Liver failure
-malnutrition
-nephrotic syndrome
Hyperglycemia
-Uncontrolled diabetes
-Stress (MI, CVA, Trauma, Anesthesia, Infection)
-Steroids
-Beta Blockers
Hypoglycemia
-Insulin
-Sulfonylureas
-Fasting
-Insulinoma
Hgb A1C
-HbA1c level reflects the mean glucose
concentration over the previous period (approximately 6-8 weeks) and provides a much better indication of long-term glycemic control than blood and urinary glucose determinations.
-A1C of >6.5 now equals Diabetes per ADA recommendations… Needed on two separate tests.
-The attachment of the hexose molecule occurs continually over the entire life span of the erythrocyte and is dependent on blood glucose concentration and the duration of exposure of the erythrocyte
ALT elevated (normal is 4-45U/L)
-Alcohol
-Viral Hepatitis
-Drugs (Tylenol, Statins, Antibiotics, anti epileptics, anti fungals)
-NASH
-Muscle Damage (Cardiac, Skeletal)
-Celiac Disease
-Elevated in destruction of hepatocytes
-Liver enzymes greater than 1,000 IU/L usually secondary to Tylenol, acute viral hepatitis, or ischemia.
-ALT more specific to liver than AST.
-Elevations in ALT remain up longer than AST
-Tylenol, Amio, Augmentin, anti seizures, anti fungals, Statins
AST elevated (normal 8-43 U/L)
-Alcohol
-Viral Hepatitis
-Shock Liver
-Drugs
-NASH
-Muscle Damage (Cardiac, Skeletal)
-Celiac Disease
*AST/ALT Ratio >2:1 think ETOH (Pyridoxal-5’-phosphate)
–Also involved with heart, skeletal muscle, kidney, and some involvement in brain and pancreas
Alkaline Phosphatase elevated (normal 37-98U/L)
-Biliary stasis (most common)
-Bone disorders (Paget’s, Rickets, Osteomalacia, Fractures, Metastatic Tumor)
-Pregnancy (Typically third trimester)
-Chronic renal failure
-Drugs (Cephalosporins)
-Right Sided Heart Failure (congest the liver)
-Ulcerative Colitis
-Hyperparathyroidism
–The higher the Alk Phos, the more likely its extra hepatic obstruction vs intrahepatic.
Elevated Bilirubin (0.1-1.0 mg/dL)
-Indirect will start with bowels
-Direct-conjugated
-Choledocholithiasis (most common)
-Liver Disease
-Hemolysis (Indirect)
-Recent transfusion
-Gram Negative Sepsis
-TPN
-Obstruction (Tumor, Mass, Stone)
-Gilberts Disease
-Derived from degradation of hemoglobin released from RBC’s (85% from dead blood, 15% from RBC precursors destroyed in bone marrow)
-Direct-hepatocellular dysfunction or cholestasis
-Indirect (unconjugated) increased production (hemolysis) or defects in hepatic uptake or conjugation
Elevated Amylase (26-102U/L)
-Pancreatitis (most common)
-Pseudocysts
-Iatrogenic (ERCP)
-Cystic Fibrosis
-Salivary Gland Disease
-Macroamylase (Celiac disease, HIV infection, lymphoma, ulcerative colitis, rheumatoid arthritis, monoclonal gammopathy)
-Drugs (Macrobid, Flagyl, Valproic Acid)
-Renal Disease
-Ectopic Pregnancy
Amylase
-Cleared by kidneys.
-Carbohydrate digestion. (Pancreas, Salivary)
-Rise within 2-12 hours of insult, clear 48-72hrs.
-Macroamylase-see above. Molecules too big to pass through kidneys.
-Really high amylase doesn’t necessarily mean really bad pancreatitis.
Elevated Lipase (normal is 10-73U/L)
-Pancreatitis (most common)
-Pseudocysts
-Iatrogenic (ERCP)
-Macrolipases (Celiac disease, HIV infection, lymphoma, ulcerative colitis, rheumatoid arthritis, monoclonal gammopathy)
-Drugs (Macrobid, Flagyl, Valproic Acid)
-ESRD on Dialysis
Ammonia
-normal <50ug N/L
-Waste product of Amino and nucleic acid metabolism.
-Like amylase, higher level does not mean higher mental status changes.
-Arterial levels correlate better with encephalopathy
-Eat protein, broken down by bacteria in small bowel to glutamine, absorbed into portal system, removed as urea.
Elevated Ammonia
-Liver Congestion/Failure
-Urea Cycle Enzyme Dysfunction
-Increased protein intake
-Lactulose treatment
-Increasing diarrhea/stooling takes the bad bacteria from the gut that increases that ammonia. Rifaxin helps wipe out the bacteria in the gut
Albumin
-Most common protein in body (2/3)
-Major protein produced by liver
-average adult synthesized 15g/day
-Half life is 20 days (takes weeks to increase or decrease)
-Carries Ca, Mg, Bili, Coumadin
-Nephrotic syndrome you pee out the protein
Hyperalbuminemia
-Dehydration
-Gammopathies
-Lupus, RA
Hypoalbuminemia
-Inverse Acute Phase Reactant
-Poor nutrition
-Liver disease
-Nephrotic Syndrome
-Burns
-Increased catabolism (Cancer)
-Protein losing Gastropathies
Prothrombin Time
-10-13 seconds
-Produced by the liver.
-Vitamin K dependent
-Vitamin K factors 2,7,9,10 extrinsic pathway
-INR standardized from lab to lab
Elevated Prothrombin Time
-Iatrogenic (Coumadin)
-Liver Failure
-Fat Malabsorption
-DIC
C Reactive Protein (general marker-if normal can usually indicate no cellulitis & abx not necessarily needed)
-Inflammatory markers
-<8.0 mg/dL
-Infection
-Trauma
-Infarction
-Inflammation
-Neoplasm
-Obesity
-OCP’s
-CRP is synthesized by liver. More sensitive to inflammation and infection. Goes up fast and comes down fast compared to Sed rate
Sed Rate
-Inflammatory Markers
-ESR (explain method). More acute phase protein, the faster and further the blood falls in capillary tube.
Don’t order both unless you have to… ESR
-Infection
-Trauma
-Infarction
-Inflammation
-Neoplasm
-Obesity
-Monoclonal Gammopathies
-Age
BNP
-Differential Diagnosis of Dyspnea.
-Normal BNP essentially rules out cardiac.
-Released from Ventricles.
-Obesity causes lower BNP levels.
-Normal <200pg/mL
Elevated BNP
-Heart Failure
-Atrial Fibrillation/Flutter/Stretch
-Cor Pulmonale
-Pulmonary Hypertension
-Pulmonary Embolism
-Renal dysfunction
Lactate
-normal 0.6-2.3 mmol/L
-End product of anaerobic carbohydrate metabolism.
-Metabolized by the liver and therefore concentration depends on rate of production and rate of liver clearance.
Elevated Lactate
-Tissue hypoxemia (most common)
-Seizures
-Exercise
-Leukemia
-Liver and kidney disease
-Medications (metformin)
-Short Bowel Syndrome
-Ethanol, Methanol, Salicylates
D-Dimer
-<250ng/mL
-Degradation product of cross-linked fibrin
negative predictive value of -
-D-dimer assays of 94 percent
-Can get an elevated D-Dimer from checking a D-Dimer.
-Take into consideration the age for d-dimer level
Elevated D-Dimer
- Venous thromboembolic disease
- Arterial thromboembolic disease
- Myocardial infarction
- Stroke
- Acute limb ischemia
- Atrial fibrillation
- Disseminated intravascular coagulation
- Preeclampsia and eclampsia
- Severe infection/sepsis/inflammation
- Surgery/trauma (eg, tissue ischemia, necrosis)
- Systemic inflammatory response syndrome
- Severe liver disease (decreased clearance)
- Malignancy
- Renal disease
- Nephrotic syndrome
Macrocytosis, ast/alt 2:1, hypomagnesemia, thrombocytopenia, elevated lactate
-Alcohol withdrawal
-Liver is shot and agitated is produced higher lactate and takes a lot longer to come down
Procalcitonin
<0.15ng/mL
-can differentiate if its bacterial
Balancing Potassium
-Acidemia: drive K to shift to blood > Hyperkalemia
-Alkalemia: drive K inside cell-Hypokalemia
-Factors present for kidney to excrete K: Aldosterone, Flow of urine, amount of Na in urine
Medications that risk Hyperkalemia
-K supplements
-Penicillin
-Digoxin
-NSAIDS
-ACEI/ARBs
-BB
-Heparin
-Trimethoprim/pentamidine
Patiromer (Veltassa)
-Ion exchange binding resin (exchanges K for Calcium)
-Mean decrease in K was 0.5-1mEq/L
-a single dose of 25.2 g of oral patiromer reduced serum potassium within 2 hours but did not show a difference at 6 hours
Initial Regimen of Hypernatremia
-D5W at rate of 3-6 mL/kg/hr
-Free water
-Rate of infusion should decrease to 1mL/kg/hr until normonatremia (140)
Low Plasma Sodium Concentration
-<137 meq/L
-low urine osmolality usually indicative of water overload due to primary polydipsia
High-normal plasma sodium concentration
->142 meq/L
-d/t water loss
-points towards DI, particularly if the urine osmolality is less than the plasma osmolality
Normal plasma sodium concentration
-not helpful in dx but if associated with urine osmolality >600 mosmol/kg, excludes a dx of DI
Each of three causes of polyuria
-Primary polydipsia
-Central DI
-nephrogenic DI
TSH
0.5-5.0
Low in hyperthyroidism
High in hypothyroidism
HCT
Women: 37-47%
Men: 40-54%
RBC concentration
MCHC
32-36%
Hypochromic <
Hyperchromic >
Serum Iron
50-150
TIBC
250-450 ug/dl
Ferritin
Women 12-150 ng/mL
Men 15-300 ng/mL
Low in IDA
