Clin Lab Med Exam II Study Guide

What clinical states increase albumin?

dehydration

What clinical states decrease albumin?

liver disease, renal disease, malnutrition, malabsorption (Chron's, Whipples, Sprue), and muscle-wasting diseases

What is the clinical significance of AAT?

decreases with severe, degenerative emphysematous pulmonary disease

-associated with chronic smokers or genetic link

What is a scenario where an acute-phase reactant would be elevated?

inflammation or stress

What is the significance of high AFP levels during pregnancy?

open neural tube defect in the fetus, atresia of the GI tract, and fetal distress

What is the significance of low AFP levels during pregnancy?

down's syndrome and trisomy 18

What is another clinical setting (besides pregnancy) that AFP would be utilized?

liver cancer and adult gonad cancer

-tumor marker

What disease is associated with low ceruloplasmin levels?

wilson's disease

-causes copper to be present in the whole body

What is the major function of transferrin?

transport iron and prevents loss of iron through the kidneys

-made in the liver

What types of reactants are complement proteins?

acute phase reactants

What clinical scenarios would acute phase reactants be elevated?

inflammation

What clinical scenarios would acute phase reactants be decreased?

systemic lupus erythematosis

What is the function of fibrinogen?

formation of fibrin clot when activated with thrombin

What happens to the fibrinogen level in the presence of DIC?

decreases

-also decreases with severe liver disease

What is the clinical significance of CRP in an acute setting (ED or inpatient)?

elevated with MI, viral infections, bacterial infections, and RA

-CVD marker

What is the downfall to drawing a CRP?

one of the first proteins to increase with inflammation, so it is non-specific

When would you see elevated IgA levels?

liver disease, autoimmune disease, and infections

When would you see elevated IgD levels?

liver disease, infections, connective tissue disorders, and multiple myeloma

When would you see elevated IgE levels?

asthma, allergic rhinitis, and parasitic infections

When would you see elevated IgG levels?

liver disease, infections, and collagen disease

When would you see elevated IgM levels?

immune response (1st to arrive) and waldenstrom's macroglobulinemia (lymphoplasmacytic lymphoma)

How would there be excessive protein loss from the renal system?

damage to the glomerulus of the nephron which results in proteinuria

How would there be excessive protein loss from the GI tract?

protein leaking into GI tract due to protein losing enteropathy (PLE)

How would there be excessive protein loss from the skin?

extensive burns

How would there be excessive protein loss from the blood?

large loss of proteins with blood loss

What are the levels of proteins in liver disease?

-decreased plasma protein and albumin

-increased gamma globulin

What is the most commonly used screening test for serum protein abnormalities?

total protein and albumin assay

What are the 5 protein fractions that are identified in a total protein and albumin assay?

1. albumin

2. alpha-1 globulin

3. alpha-2 globulin

4. beta globulin

5. gamma globulin

Label the SPE scan

see picture

What would alpha-1 antitrypsin deficiency look like on an SPE?

no alpha 1 bump

What would chronic inflammation look like on an SPE?

spikes in alpha 1, alpha 2, beta, and gamma (all globulins)

What would nephrotic syndrome look like on an SPE?

decreased albumin and increased alpha-2 bump

What would severe cirrhosis look like on an SPE?

decreased albumin and increased gamma bump

Glycolysis

oxidation of glucose to use as energy

Glycogenesis

glucose to glycogen for storage

Glycogenolysis

glycogen to glucose from storage

Gluconeogenesis

new glucose made from amino acids

What role does insulin play in the control of plasma glucose?

decreases

What role does glucagon play in the control of plasma glucose?

increases

What are the diagnostic criteria for diabetes?

-hyperglycemia with a fasting blood sugar level > 126 mg/dl

-symptoms and a random plasma glucose > 200 mg/dl

-A1c > 6.5%

-2 hour OGTT > 200 mg/dl

What is the pathology of type I diabetes?

-insulin dependent (no insulin production)

-autoimmune destruction of pancreatic beta cells

*diagnosed in juvenile patients

What is the pathology of type II diabetes?

-high insulin production but target cells are unresponsive

-decreased insulin receptors cause by obesity receptors destroyed by antibodies

*diagnosed in obese, adult patients

If a 7 yo patient came in with complaints of polyuria and polydipsia with a high glucose level based on her UA, what would the diagnosis most likely be?

type I diabetes mellitus

What is the pathophysiology behind DKA?

diabetic ketoacidosis occurs from a missed insulin dose (type I diabetes) and leads to increased ketoacids (ketones) and hyperkalemia

What is the hallmark finding for DKA?

postive plasma ketone level

How many weeks does HgbA1c reflect glucose control?

8-12 weeks

What are the HgbA1c ranges for prediabetes?

5.6-6.4%

What are the HgbA1c ranges for diabetes?

>6.5%

What test is most appropriate for gestational diabetes?

oral glucose tolerance test (OGTT)

What happens during a gestational OGTT?

1. patient performs 1 hour OGTT

2. patient will perform a confirmatory 3 hour OGTT

-measured in 4 increments : 0, 1, 2, 3 hours

*if 2/4 or more are above cutoff values: positive result

What is the role of microalbumin testing in patients with diabetes?

reveals early, reversible renal disease

What findings become more concerning in microalbumin testing?

albuminuria can suggest early onset of macroalbinuria

Where is Na found?

outside the cell

What regulates Na?

kidneys: ADH and aldosterone

Where is K found?

inside the cell

What regulates K?

kidneys: aldosterone

Where is Cl found?

outside the cell

What regulates Cl?

excretion in sweat/urine

-increased sweat -> aldosterone secretion -> conserve Cl and Na

Where is HCO3 found?

inside the cell (maintains buffer system)

What regulates HCO3?

kidneys

What is hypovolemic hyponatremia?

water and Na lost but Na loss is greater

What causes hypovolemic hyponatremia?

-loss of fluid (GI, burns) with hypotonic replacement

-thiazide diuretics

-hypokalemia

-hypoaldosteronism

What is normovolemic hyponatremia?

increased water but Na stays the same

What causes normovolemic hyponatremia?

-SIADH

-severe hyperglycemia (polyuria)

-polydipsia

-diuretics

-hypothyroidism

What is hypervolemic hyponatremia?

water and Na are elevated but water is greater

What causes hypervolemic hyponatremia?

-CHF

-hepatic cirrhosis

-overhydration

-nephrotic syndrome

-renal failure

What is hypovolemic hypernatremia?

decreased water and increased Na

What causes hypovolemic hypernatremia?

-dehydration

-excessive sweating

-vomiting

-diarrhea

What is normovolemic hypernatremia?

increased Na and same water

What causes normovolemic hypernatremia?

-skin/lung loss

-diabetes insipitus (DI)

What is hypervolemic hypernatremia?

increased Na and water

What causes hypervolemic hypernatremia?

-hypertonic saline treatment

-hyperaldosteronism

What are the causes of hypokalemia?

-decreased dietary intake

-diuretics

-increased insulin tx

-alkalosis

-hypomagnesia

-hyperaldosteronism

What are the causes of hyperkalemia?

-increased dietary intake

-acidosis

-decreased insulin

-drugs

-ACE inhibitors

-decreased excretion

What other electrolyte does chloride parallel?

Na

How do you calculate anion gap? (will be on exam)

AG = Na - (Cl + HCO3)

No K

Metabolic Acidosis

-in kidney

-acid

-decrease HCO3

Metabolic Alkalosis

-in kidney

-basic

-increase HCO3

Respiratory Acidosis

-in lung

-acid

-increase CO2

Respiratory Alkalosis

-in lung

-basic

-decrease CO2

What are the causes of high anion gap metabolic acid?

Methanol ingestion

Uremia (increased BUN)

Diabetic ketoacidosis

Polyethylene glycol

Iron and isonizaiades

Lactic acidosis

Ethanol and ethylene glycol

Salicyclates and starvation

What are the causes of normal anion gap?

Hyperalimentation

Acetolamide

Renal tubular acidosis

Diarrhea

Ureto-pelvic shunt

Post-hypocapnia

Spironolactone

Causes of metabolic alkalosis

-loss of HCl (vomiting and nasogastric suction)

-renal loss of H+ (some diuretics)

-increased aldosterone (conn's disease)

-increased cortisol (cushing's disease)

Causes of respiratory acidosis

-hypoventilation

-COPD

-neuromuscular disease

Causes of respiratory alkalosis

-hyperventilation

-stimulation of brainstem response center (stress, pregnancy)

-cardiac disease

-mechanical over-ventilation

What is the compensation mechanism for metabolic acidosis?

decreased CO2

What is the compensation mechanism for metabolic alkalosis?

increased CO2

What is the compensation mechanism for respiratory acidosis?

increased HCO3

What is the compensation mechanism for respiratory alkalosis?

decreased HCO3

What are the steps to determining states of acid-base disorders?

1. look at pH (high: basic and low: acidic)

2. look at pHCO3 (same direction as pH)

3. look at pCO2 (opposite pH)

What lab is associated with azotemia?

BUN/Creatinine ratio

What is the cause of an increased BUN/Cr ratio?

pre-renal

What is the cause of a decreased BUN/Cr ratio?

-acute tubular necrosis (kidney disease)

-decreased protein intake/starvation

-liver disease

What is the cause of an increased BUN and Creatinine?

-post-renal obstruction

-pre-renal azotemia superimposed on kidney disease

What lab value is needed to calculate GFR?

Creatinine

What will the BUN and Cr levels look like for pre-renal azotemia?

increased BUN and decreased Cr

What will the BUN and Cr levels look like for post-renal azotemia?

increased BUN and Cr

What lab is associated with gout?

uric acid

What is the relationship between Ca2+ and PTH?

proportional (Ca2+ is regulated by PTH)

What happens to PTH in hypercalcemia?

increases