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How to calculate anion gap
Na - (CL + HCO3)
difference between cations and anions
In what clinical state would you see increased albumin?
dehydration
in what clinical state would you see decreased albumin
liver disease, renal disease, malnutrition, malabsorption disorders (churns, whipples, sprue), muscle-eating disease
albumin
highest concentration in plasma
maintains appropriate fluid balance in tissues
functions as carrier protein
produced and secreted by liver
pre-albumin
carrier protein for thyroid hormones T3 and T4
transports vit A when complexed with retinol binding protein
sensitive marker of inadequate dietary protein intake
dec in hepatic diseases, acute inflammatory responses, tissue necrosis
AAT
majority component of alpha-1 globulin
acute-phase reactant
neutralizes elastase that damages structural proteins (released as part of immune process)
AFP
alpha-1 globulin
protects fetus from attack by mothers immune system
prenatal screening routinely performed between 15th and 20th week of gestation (protein freely crosses placenta)- triple screen (AFP, estradiol, HCG)
What is the clinical significance of alpha-1 antitrypsin? (AAT)
deficiency associated with sever, degenerative emphysematous pulmonary disease
a cause of emphysema in young people (20-40) who DO NOT smoke
high AFP during pregnancy
possible open neural tube defect in fetus
atresia of GI tract
fetal distress
Low afp in pregnancy
inc risk of downs syndrome and trisomy 18
high AFP not pregnant
liver cancer and adult gonadal cancers (testicular and ovarian)
tumor marker for these cancers
What is another setting AFP might be utilized besides pregnancy?
tumor marker for adult gonadal cancers
Acute-phase reactant
inc in response to trauma / inflammation to help prevent loss of hemoglobin from damaged RBCs
haptoglobnin
alpha-2 globulin; acute phase reactant
starts in liver
synthesized in hepatocytes and cells of reticuloendothelial (RE) system
binds free Hgb (RE removes complex)
prevents loss of Hgb and iron from kidneys
haptoglobin (alpha-2 globulin) is considered an acute phase reactant. describe a scenario it would be elevated.
infection or inflammation
ceruloplasmin
alpha-2 globulin
copper-containing protein with enzymatic activity (>90% total serum copper in it)
acute phase reactant
ceruloplasmin clinical significance; low levels
low levels seen in Wilson’s disease- inherited disease where copper is deposited in the liver, brain, and skin cause brain and neurologic damage (Kayser fleischer rings)
alpha-2 macroglobulin
alpha-2 globulin
large protein synthesized by hepatocytes
found in intravascular spaces
inhibit variety of protease enzymes (trypsin, Pepsin, plasmin)
elevated in renal disease
transferrin
synthesized by liver
major component of beta globulin fraction
transport iron and prevent loss
transferrin main function
transport iron and prevent loss of iron through the kidneys
transferrin clinical significance
decreased level in liver disease (dec synthesis)
TBIC- increase in iron deficiency anemia
What type of reactants are complement proteins?
proteins involved in immune and inflammatory responses; acute phase reactant
circulate blood as non-function precursors- activated when antigen-antibody (Ag-Ab) complexes are present (lysis of those cells);
opsonization- coat bacterial cells and increase likelihood of phagocytosis
what clinical scenarios would complement proteins be increased or decreased?
inc- inflammatory states
dec- systemic lupus erthematosis
fibrinogen
synthesized in liver
acute phase reactant
What is the function of fibrinogen?
formation of fibrin clot when activated by thrombin (removed during clotting process so not seen in serum)
clinical significance of dec fibrinogen?
severe liver disease
DIC (disseminated intravascular coagulation)
C-reactive protein (CRP)
acute phase reactant- one of the first inc in response to inflammation
non specific
can be used in place of ESR
commonly assayed as part of risk assessment for cardiovascular disease; indicates chronic inflammatory process ongoing in vascular system that enhances formation of atherosclerotic plaques, esp in coronary arteries
when is CRP elevated
significantly elevated in acute rheumatic fever, MI, viral infections, bacterial infections, rheumatoid arthritis
immunoglobulins synthesized by
plasma cells (B lymphocytes)
which is most abundant of immunoglobulins
IgG
elevated IgA levels
liver disease
autoimmune diseases
infections
elevated IgD
liver disease
infections
connective-tissue disorders
multiple myeloma
elevated IgE
asthma
allergic rhinitis
parasitic infections
elevated IgG
(infection is Gone)
liver disease
infecitons
collagen disease
multiple myeloma
elevated IgM
(need More first)
first to appear in immune response to foreign antigen
waldenstron’s macroglobunlinemia/lymphoplasmacytic lymphoma)
monoclonal gammopathies
dec immunoglobulins
inherited immunodeficiency disorders (faulty plasma cell function)
describe how there may be excessive protein loss from each system?
renal- diseases that damage glomerulus of nephron (proteinuria)- nephrotic syndrome
gi- protein leakage into GI tract due to protein-losing enteropathy (PLE)
skin- severe skin diseases- extensive burns
blood- bleeding- large loss of proteins with the blood
liver is the site of all ______ protein synthesis
non-immune
(all proteins synthesized in liver except gamma globulins)
describe the levels of all proteins in state of liver disease
inc: gamma globulin proteins
dec: plasma protein, albumin
what is the most commonly used screening test for serum protein abnormalities? what are the five protein fractions identified?
serum protein electrophoresis- separating proteins based on electric charge properties
albumin
alpha 1 globulin
alpha 2 globulin
beta
gamma
AAT deficiency SPE
dec alpha-1
chronic inflammation SPE
elevated alpha 1, alpha 2, beta, and gamma
nephrotic syndrome SPE
alpha 2 elevated
albumin dec / lost in urine
severe cirrhosis SPE
dec albumin and alpha 2
inc beta and gamma
glycolysis
breakdown/oxidation of glucose to be used as energy
glycogenesis
buildup/glucose converted to glycogen for storage
glygogenolysis
breakdown/glycogen converted to glucose from storage
gluconeogenesis
build up/ new glucose formed from amino acids ( when there is nothing left in glycogen stores)
what role do insulin and glucagon play in control of plasma glucose
insulin- dec plasma glucose, bring down blood sugar, promote glycogenesis and inc cellular uptake
glucagon- inc plasma glucose in times of need, stimulate glycogenolysis and gluconeogenesis
diagnostic criteria for diabetes
fasting plasma glucose 126 mg/dl or more
symptoms and random plasma glucose 200 mg/dl or more
hemoglobin A1C 6.5% or more
2 hr plasma glucose 200 mg/dl or more during oral glucose tolerance test
one of these confirmed on repeated testing on different day
glucosuria
glucose in urine
generally when blood glucose level exceeds about 160-180 mg/dl
epinephrine _____ plasma glucose
increases
GH, ACTH, Cortisol, thyroid hormones ______ plasma glucose
increases
symptoms of hyperglycemia
nausea/vomiting, malaise, diarrhea
high and dry
symptoms of hypoglycemia
nausea, trembling/sweating, rapid pulses, lightheadedness, CNS symptoms (altered mental status)
cold and clammy gets them candy
type 1 DM
insulin dependent
caused by autoimmune destruction of pancreatic beta cells → absence of insulin production
pts usually less than 20 yrs
labs: hyperglycemia, hyperkalemia, glucose and ketones in urine
type 2 DM
non-insulin dependent
caused by insulin resistance - insulin levels high but not effective at maintaining normal glucose levels
insulin produced by beta islet cells, but target cells unresponsive; insulin levels increased, however, target cells are resistant to the insulin
dec number of insulin receptors caused by obesity receptors destroyed by antibodies
genetically determined insulin receptor insensitivity
patients usually older than 40 and obese
majority of DM
beta cells produce ______ and alpha cells produce _______
insulin, glucagon
DKA (diabetic ketoacidosis)
type 1 diabetics (type 2 has enough insulin to prevent accumulation of ketones)
missed insulin dose causes:
inc fat breakdown and fatty acid metabolism → inc ketones → metabolic acidosis (high anion gap) → hyperkalemia
hyperglycemia (500 msg/dl) → osmotic diuresis → dehydration
relative increase in glucagon which enhances problems
insulin dose is taken but insufficient for new stress or infection
What is the hallmark for DKA?
positive plasma ketone level (urine ketones not specific, may be detected in healthy fasting people)
lab diagnosis of DKA
positive plasma ketone level
hyperglycemia
Hgb A1C reflect glucose control over how long?
8-12 weeks, 3 months
pre diabetic A1C range
5.6-6.4 %
diabetic A1c range
6.5% or more
normal A1c range
4.8-5.5%
What test is most appropriate gestational diabetes?
1 hour oral GTT (50 mg glucose)- routine screening beginning of 3rd trimester (24-28 weeks)- confirmed with 3 hr
3 hr oral GTT (100 mg glucose)
4 blood draws- 0 hrs, 1 hr, 2 hr, 3 hr
if at least 2 out of 4 samples at or above cutoff values, test is positive
oral glucose tolerance test
unrestricted diet 3 days before (at least 150 gm carb daily)
10-16 hour fast before test (may drink water)
oral glucose ingested within 5 min
patient must remain seated until 2 hour blood sample drawn
specimen must be frozen or analyzed within 4 hours to determine plasma glucose
microalbumin testing
very sensitive
reveals earliest, reversible renal disease
albuminuria may precede other signs of renal disease by 10-15 years: slow progression of microalbuminuria → macroalbuminuria
What is role of microalbuminuria testing in patients with diabetes? what findings become more concerning?
reveal early, reversible renal disease (high blood sugar damage blood vessels in kidneys)
- microalbuminuria- 30-300 mg/day
macroalbuminuria- more than 300 mg/day - concerning
which electrolytes are inside cell?
K and HCO3
which electrolytes are outside cell
Na and Cl
what regulates Na
kidneys - ADH and aldosterone
what regulates K
kidneys- proximal tubules
aldosterone regulates Na/k exchange in kidney
what regulates Cl
aldosterone- excess sweating stimulates aldosterone which conserves Na and Cl
kidneys
what regulates HCO3
kidneys
aldosterone
Na retaining hormone
increases Na and water with K loss
manages Na/K exchange in kidneys
hyponatremia
ratio between Na and H20; H20 greater than Na
hypo hypo- low H20, lower Na
normo hypo- high H20, normal Na (looks dilute)
hyper hypo- higher H20, high Na
hypovolemic hyponatremia
(low H20, lower Na)
water and sodium both lost from body, but sodium loss is greater
causes: loss of fluid (GI, burns) with hypotonic fluid replacement
thiazide diuretics- inc Na and K loss
K depletion in cells- causes Na movement into cells
aldosterone deficient - inc Na and water loss
normovolemic hyponatremia
(high H20, normal Na)
total body water increases, but body’s sodium content stays the same
causes: SIADH- body hangs on to water, diluting Na
severe hyperglycemia (polyuria)- water moves into plasma to normalize osmolality
polydipsia- inc thirst
diuretics
hypothyroidism
hypervolemic hyponatremia
(higher H20, high Na)
both sodium and water content increase, but water gain is greater
causes: CHF
hepatic cirrhosis
overhydration
nephrotic syndrome
renal failure - inability to excrete water
hyponatremia symptoms
nausea
generalized weakness
mental confusion
hypernatremia symptoms
tremors
irritability
ataxia- loss of coordinated muscle movement
confusion
coma
hypovolemic hypernatremia
(lower H20, low Na)
lose more H20 than Na
most common cause of hypernatremia
causes: dehydration
profuse sweating
vomiting or diarrhea
normovolemic hypernatremia
low H20, normal Na
causes: skin/lung loss
DI- water loss with Na retention
hypervolemic hypernatremia
high H20, higher Na
causes: hypertonic saline treatment
hyperaldosteronism
causes of hypokalemia
diuretics (most common)
decreased dietary intake
excessive insulin
alkalosis
hypomagnesemia - enhances aldosterone secretion
hyperaldosteronism
causes of hyperkalemia
excess intake - diet
acidosis
insulin deficiency- loss of cellular K+
drugs (heparin, digoxin, cyclosporine)
Ace inhibitors, K sparing diuretics
dec excretion- renal failure, hypoaldosteronism
loop and thiazide diuretics
inc Na deliver to distal segment of distal tubule → inc K loss
this stimulates aldosterone-sensitive Na pump to inc Na reabsorption in exchange for K and H (lost in urine)
What other electrolyte does Cl parallel?
Na
hyperchloremia
parallels hypernatremia
causes: hyperventilation (respiratory alkalosis)
dehydration
excess loss of bicarb (gi loss / diarrhea leading to metabolic acidosis, rental tubular acidosis)
hypochloremia
parallels hyponatremia
causes: prolonged vomiting
metabolic alkalosis
pylonephritis - sodium losing renal disease
what is considered an indirect measure of HCO3 anion
CO2
Low AG associated with
multiple myeloma
instrument error
(rare)
normal blood pH
7.35-7.45
volatile acids
derived from CO2 (can be exhaled)
respiration allows volatile acid/CO2 to be removed by lungs and the remaining byproduct is H20 (neutral)
acid base balance is maintained by
lungs and kidneys
bicarb buffer system formula
CO2 + H2O → H2CO3 → HCO3- + H+
nonvolatile sources
derived from sources other than CO2 (can’t be exhaled)
keto acids, lactic acid, sulfur and phosphorus containing compounds
excreted by kidneys
values are more accurate from _____ than ______
arterial blood than venous blood
metabolic acidosis
decrease in plasma HCO3-, dec pH, kidney
dec bicarb due to inc accumulation of nonvolatile acids or loss of bicarb from kidney or GI tract (diarrhea, vomiting)