Flashcards in Damjanov - Chapter 1 - Laboratory Medicine Deck (54)
what are acute phase proteins?
positive and negative
+ appear in increased concentration in blood in response to inflammation (C-reactive PRO, transferrin, ceruloplasmin, fibrinogen, alpha1-antitrypsin)
- concentrations decrease in response to inflammation (albumin)
what is alkaline phosphatase? when is it elevated?
hydrolyzes orthophosphoric esters in many cells of the body and in serum
-elevated in biliary obstruction, growing bones, remodeling bones (Paget's), osteoblastic metastases, and bone-forming tumors
what is aminotransverase/transaminase? what are two important ones?
a group of enzymes transferring amino groups from one AA to another
-ALT and ASP are important in liver function tests
what is BUN for?
blood nitrogen present as urea
-elevated in renal failure (but less specific than elevated creatinine), but falls rapidly after renal dialysis b/c highly diffusible
-increased in heart failure, shock, dehydration
-doesn't measure N included in proteins (18% of total blood N)
what forms the most powerful of body's buffer systems?
CO2 and HCO3-
what is the creatinine level in renal failure (azotemia)?
why is lactate dehydrogenase important?
ubiquitous enzyme involved in removing H from lactate
-elevated in conditions with widespread cell destruction
sensitivity VS specificity
-when do you want them to be high?
sensitivity: correctly identify who has the disease (positivity in health; "true positives, false negatives")
-high in screening tests
specificity: correctly identify who doesn't have the disease (negativity in health; "true negatives, false positives")
-high in final diagnosis
what is serum best defined as?
-does not clot, can't be used for study ofcoagulation factors and substances entrapped in fibrin meshwork of clot
under what 4 things is Na+ balance under control of? how do they work?
1. thirst (increases if one ingests too much Na or loses too much water; osmoreceptors in hypothalamus increase osmolality of plasma to activate thirst)
2. ADH (increased osmolality releases ADH from hypothalamus to resorb water in kidney)
3. aldosterone (loss of ECV decreases GFR,, releasing renin to act on angiotensinogen to increase aldosterone from ZG of adrenal cortex, to promote exchange of Na+ for K+ or H+ in distal renal tubules to retain Na+)
4. ANP (stimulates kidneys to increase excretion of Na+ in urine)
what is the primary determinant of serum osmolality?
when does dilutional hyponatremia happen?
1. increased water intake
2. infusion of water
3. decreased excretion of water (water retained in ECS)
4. hypoproteinemia (inadequate production of serum PRO in cirrhosis; loss of PRO in nephrotic syndrome or gastroenteropathy)
5. shift of water from cells into the ECV (hyperglycemia of DM, paraproteinemia, hyperlipidemia has osmotically active substances in blood)
6. SIADH (water poisoning when tumor secretes ADH)
when does depletional hyponatremia happen?
1. gastrointestinal loss (vomit, diarrhea, sequestration of fluid in intestine, GI fistulas)
2. renal loss (glycosuria of DM, hypercalcemia, salt-wasting kidney disease, diuretics, Addison's)
3. dermal loss (burns)
what is the most common cause of hyponatremia?
combined loss of Na+ and water, where lost Na+ is not adequately replaced
how can there be renal loss of water?
-central and nephrogenic diabetes insipidus
-renal tubular necrosis (postsurgical period)
-loop and osmotic diuretics
explain the difference between central and nephrogenic diabetes insipidus
C: primary (related to injury of hypothalamus or posterior pituitary) or secondary (drug treatment)
N: consequence of end-stage renal disease
both lead to renal loss of water and hypernatremia
when does sodium retention occur? (3)
1. adrenal cortical lesions (most common)
-hypercorisolism due to benign or malignant adrenal cortical tumors
2. corticosteroids (esp. long-term use)
3. infusion of Na-rich solutions
what are signs of dehydration?
explain hyperchloremic metabolic acidosis?
depletion of HCO3- in metabolic acidosis is usually accompanied by formation of organic anions to replace lost HCO3-
-if this doesn't occur, the gap is filled with Cl-
-NOT accompanied by hypernatremia
explain hypochloremic metabolic acidosis
metabolic alkalosis caused by loss of Cl- in GIT is associated with anion gap filled with HCO3-
-Na+ concentration is normal
what does insulin do for potassium?
insulin promotes K+ flux across cell membrane into cells
-no insulin = efflux of K+ from cells
what is hypokalemia usually caused by?
increased loss of K+ in urine, GIT, or skin
-also may be due to redistribution of K+ from ECF to ICF compartment
-rarely reduced intake (unless starvation or alcoholics)
explain increased GI loss of K+
all GI secretions have K+, so vomit/diarrhea causes K+ and Na+ loss
-prolonged laxative use has same effect
-increased mucus production in inflammed mucosa or villous adenomas
how does prolonged loss of Na+ cause K+ loss?
prolonged Na+ loss causes secondary hyperaldosteronism and increased loss of K+ in urine
explain increased renal loss of K+
occurs most in patients treated with diuretics or those who have osmotic polyuria (diabetes)
-rare cases are mineralcorticoid excess in primary hyperaldosteronism, or secondary hyperaldosteronism (in end-stage kidney disease or cirrhosis)
explain redistribution of K+ and how it causes K+ loss
occurs during alkalosis, which favors entry of K+ into cells, replacing H+ that entered ICF
-insulin administration promotes entry of K+ into cells
-familial periodic muscle paralysis: rare condition where hypokalemia develops b/c of entry of K+ into muscle cells
what are cardiac symptoms of hypokalemia?
arrhythmias and abnormal cardiac contractinos associated with EKG changes
-flattening/inversion of T-waves
-ST segment depression
-appearance of U waves
-digitalis toxicity increases
what are neuromuscular symptoms of hypokalemia?
generalized muscle weakness and hypotonia
-lethargy, depression, and confusion
what are GI symptoms of hypokalemia?
slow peristalsis, constipation, ileus