KYS already omg

Hypoglycemia

>70 mg/dL

Fasting BG goal

80 mg/dl to 130 mg/dL

post prandial BG goal

<180 mg/dL

A1c goal

> 7%

Blood glucose danger zone

> 50 mg/dL, >400 mg/dL

Digoxin therapeutic range

0.5 to 2 ng/mL

>2 ng/mL is toxic

Phenytoin therapeutic range

10 to 20 mcg/mL

>20 mcg/mL is toxic

Carbamazepine therapeutic range

4 to 12 mcg/mL

>12 mcg/mL is toxic

Lithium target serum concentration

Intiatation: 0.8 to 1.2 mEq/L

Maintenance: 0.8 to 1 mEq/L

>/= 2 meq/L is toxic

Pre-Analytical phase

Everything before tests is run

Exercise effects

Lowers cholesterol, lowers triglycerides, increases creatinine, and increases ALT

Diet Effects

Eating increases blood sugar, increases triglycerides

Protein Effect

Increase ammonia, increase urea

Analytical Phase

When the lab test is actually performed; running assays, measuring concentration, equipment accuracy

Sensitivity

Used for screening

Positive if disease is present

Specificity

Used for confirmation

Negative is disease absent

Testing reference intervals vary based on..

Age

Sex

Weight

Pregnancy

Menstrual Cycle

post analytical phase

Happens after results are generated

Clinical Chemistry lab methods

spectrophotometry: measures light absorption to determine concentration → glucose, electrolytes

Immunoassays: uses antigen-antibody binding → cancer biomarkers, infectious disease testing, drug screening

Mass Spectrometry: measures mass to charge ratio of molecules → TDM

TDM - Therapeutic drug monitoring

Monitors drug concentrations in blood to ensure levels are not sub-therapeutic (effective) or supra-therapeutic (toxic)

NTI - Narrow therapeutic index

Range between effective dosages and toxic dosages are narrow.

Drugs with NTI

Digoxin, phenytoin, phenobarbital, procainamide, carbamazepine, lithium, theophylline, methotrexate, vancomycin, and amikacin

Albumin

Binds to drug

High albumin → lower amount of free drug

Can cause toxicity in pts even when using normal dosages

Vancomycin monitor

TDM uses trough levels → 30 minutes before 4th dose

Target 15-20 mg/L

Amikacin Monitoring

Peak drawn: 1 hr after infusion

Trough drawn: 30 min before next dose

Toxicities: Nephrotoxicity, ototoxicity, vestibular damage

Thrombocytopenia (Low platelets)

> 150k per uL

Hgb levels in men with anemia

< 13.5 g/dL

Hgb levels in women with anemia

< 12 g/dL

Crockpot-Gault Equation

(140-Age) x (wt (kg) / Scr x 72 (Multiply all this by .85 if female

INR

Measures blood clotting time

Higher → thinner blood

<1.2 normal

Pancytopenia

decrease in RBCs, WBCs, and platelets

Leukocytosis and leukopenia

High and low WBCs

RBCs

Carries O2 and CO2

lifespan is 120 days

Production stimulated by kidney

Hgb

Carries O2

<13.5 anemia in males

<12 anemia in females

MCV

Helps determine the type of anemia

<80 → microcytic anemia (iron deficiency)

>100 → macrocytic anemia (B12 deficiency, folate deficiency)

RDW

Measures variation in RBC size

High → wide variation size (iron deficiency based anemia)

Reticulocyte count

Measures new RBC production

1% is normal

>2.5% suggests hemolysis or blood loss

ANC

A measure of the number of neutrophil cells in the blood, used to assess the immune system's ability to fight infections.

ANC = (segs + bands) / 100 x WBCs

ANC <1500

normal neutrophil levels

ANC <1500

mild neutropenia

ANC < 1000

Moderate neutropenia

ANC < 500

Low neutrophil count → High risk of infection

Anti-Xa

used when PK unpredictable

pregnant, obese, renal dysfunction

D-Dimer

Released when clots break down, used to assess thrombus formation and disintegration.

PT

Extrinsic clotting pathway test that measures the time it takes for blood to clot, typically used to evaluate the coagulation status and monitor anticoagulation therapy.

aPTT

Intrinsic clotting pathway test used to monitor heparin therapy and assess bleeding risk.

Cardiac Biomarkers

Substances released into he bloodstream when heart is stressed/damaged

Major Cardiac biomarkers

Troponin

Hs-CRP

Myoglobin

CK-MB

BNP/INT-ProBNP

Troponin

Golden standard for noticing myocardial injury however not just myocardial injury

Use levels plus ECG and symptoms to determine Myocardial injury

Rises with hours of injury

Troponin Timeline

Rise: 3-6 hours

Peak: 24 hours

Return to normal: 7-14 days

Long elevation days allow for it to be used to detect recent MI

High-sensitivity Troponin

Detect very small myocardial injury early

Used in rule-out myocardial injury protocol

CK-MB

older cardiac biomarker

less specific than troponin

CK-MB timeline

Rise: 3-6 hours

Peak: 24 hours

Return to normal: 48-72 hours

Faster return times allow it to be used to see repeated infarctions

Myoglobin

Rises very early after muscle injury

Not specific to heart

BNP

Heart Failure biomarker

Released when ventricles stretch too far signifying overload

100-400 score → possible HF; 400 high risk

INT-proBNP

Measure inactive fragment of BNP

often used clinically because long half-life

interpretation varies with age: <50 → >450 for HF; 50-75 → >900 for HF; >75 → >1800 for HF

Factors effecting BNP

HF, renal failure, pulmonary hypertension, sepsis increases BNP

Obesity decreases BNP

Hs-CRP

Inflammatory biomarker associated with CV risk

<1 low risk

2-3 moderate risk

>3 high risk

Key electrolyte ranges

calcium 8.5 to 10.5 mg/dL

Potassium 3.5 to 5.2 mEq/L

Magnesium 1.9 to 2.7 mg/dL

Sodium 136-145 mmol/L

Hyperkalemia

Mild: 5.2 to 5.4

Moderate: 5.5 to 6.5

Severe >6.5

Causes: fist clench during draw, hemolysis, delayed processing. high WBCs, high platelets

Hypokalemia

<3.5 mEq/L

Causes: Vomiting, diarrhea, poor intake, potassium wasting diuretics

Hypercalcemia

>10.5 mg/dL

Calcium binds to albumin → increases calcium serum concentration

Hypocalcemia

<8.5 mg/dL

Causes: Vitamin D deficiency, renal disease, hypoparathyroidism, high phosphorus

Phosphorus

Decreases bone mineralization by pulling calcium away from bones

ATP production

cell metabolism

Hyperphosphatemia

Often associated with hypocalcemia

Hypophosphatemia

Causes: starvation, alcohol abuse, burns, respiratory acidosis

Pseudohyponatremia

a laboratory artifact where measured sodium levels are falsely low due to high glucose levels which pulls water and dilutes sodium.

Normal blood pH

7.35 to 7.45

Acidemia

<7.35 blood pH

Alkalemia

>7.45 blood pH

Respiratory acidosis

A condition where blood pH decreases due to elevated carbon dioxide levels.

Causes: asthma, COPD, sleep apnea

Respiratory alkalosis

A condition where blood pH increases due to decreased carbon dioxide levels

Causes: hyperventilation

Metabolic acidosis

Non-anion gap → increased bicarbonate loss or acid gain in the body.

Caused by diarrhea, renal tubular acidosis, or pancreatic fistula.

Anion gap → increased acid production or reduced acid excretion

Caused by MUDPILES → methanol, uremia, diabetic ketoacidosis, propylene glycol, iron, lactic acidosis, ethylene glycol, salicylate

Anion gap formula

represents unmeasured anions in blood

Na - (Cl + HCO3)

>12 meq/L indicates metabolic acidosis

HbA1c

Measures average blood glucose over three months

Allowed because glucose binds to hemoglobin in RBCs which lives for 120 days

<5.7% normal, 5.7-6.4% pre diabetes, >6.5% diabetic

Inaccuracy comes from changes in life span of RBCs

Fasting plasma glucose

<100 mg/dL normal, 100-125 mg/dL prediabetic, >126 diabetic

Oral glucose tolerance

<140 normal, 140-199 pre diabetic, >200 diabetic

LDL

“Bad” cholesterol

Increase atherosclerosis CV risk

<100 optimal, >160 high to very high increased risk of cardiovascular disease

HDL

“good” cholesterol

Helps remove LDL from the bloodstream,

>/= 60 mg/dL optimal, <40 mg/dL increased CV risks

Triglycerides

A type of fat found in the blood that the body uses for energy.

<150 normal, >200 high to very high

Bone mineral density biomarkers

Calcium

Phosphorus

Magnesium

Vitamin D

Calcium

Bone mineralization

Magnesium

Bone structure

Vitamin D

Calcium absorption and maintains bone health.

Alkaline Phosphatase (ALP)

Indicates bone de-mineralization or liver disease; an enzyme found in several tissues.

Osteocalcin

Indicates bone formation activity

Lipid and Diabetes Connection

Diabetes often causes dyslipidemia → increase in triglycerides, small dense LDL, and decrease in HDL LEADING to increase in CV risk

Malnutrition indicators

Albumin → chronic nutrition status

Pre-albumin → short term nutrition

Transferrin → Protein status

Low levels suggest protein calorie malnutrition

Kidney function

Kidney ability to excrete waste

Processes of kidney excretion

Glomerular filtration

Tubular secretion

Tubular reabsorption

BUN

Blood urea nitrogen

Urea is filtered at glomerulus

50% is reabsorbed in the proximal tubule

Reabsorption increases when water is absorbed → dehydrated leads to increased water reabsorption → increased BUN

High levels indicate impaired kidney function or dehydration.

Serum Creatinine

Creatine → Muscle metabolism → creatinine

Levels fluctuates with muscle mass

Primarily eliminated by the kidneys. Elevated serum creatinine levels can indicate reduced kidney function or damage.

Misleading SCr

Very muscular pt → artificially high SCr

Low muscle mass → falsely low SCr

Malnutrition→ Low SCr

Spinal cord injury → low SCr

Elderly pt can appear normal in kidney function even when they don’t

Cystatin C

A protein that is produced by all nucleated cells and filtered by the kidneys,

Old marker for kidney function.

Not dependent on muscle mass

Limits: more expensive, slow lab turnaround, less accessible

eGFR vs CrCl

CrCl → for dosing

eGFR → for CKD staging, overall kidney function

IBW

50 + 2.3 x every inch over 5ft (male)

45.5 + 2.3 x every inch over 5ft (female)

Adjusted weight

IBW + 0.4 x (Actual - IBW)

Rules for which weight to use for CrCl

actual < IBW → pt is underweight, use actual

Actual </= 120% (x1.2) IBW → pt normal/slightly overweight, use IBW

Actual weight > 120% (x1.2) IBW → pt obese, use adjusted weight based on IBW

Modern eGRF guidelines

CKD-EPI 2021

Race-free

Acute kidney injury (AKI)

Sudden kidney dysfunction

If severe may require hemodialysis

Pre-renal cause → lack of blood flow to kidneys

Intrinsic renal → kidney directly damaged

Post renal → urinary obstruction