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Henderson Hasslebach
equation measures blood pH from bicarc:carbonic acid ratio
dec
inc/dec SHBG inc free testosterone
inc
inc/dec SHBG dec free testosterone
inc, dec, dec
pCO2, pH, pO2 when blood gas testing is prolonged or not on ice (glycolysis not inhibited)
dec, inc, inc
pCO2, pH, pO2 when blood gas testing exposed to air (bubbles, tube uncapped)
FP depression
colligative property used to measure osmolality
SLUMPED
conditions cause increased osmolal gap (>15)
Na, glucose, BUN
particles included in calculation of osmolality
ADH, thirst, ICF
ways to restore ECF osmolality (inc bp) with low H2O/bp
albumin
protein that makes up majority of anion gap
dec (inc)
inc/dec unmeasured cations (inc/dec measured) with increased anion gap
inc (dec)
inc/dec unmeasured anions (inc/dec measured) with increased anion gap
inc
anion gap inc/dec with SLUMPED
dec
anion gap inc/dec with
-nephrotic syndrome (low albumin)
-liver disease (low albumin)
-hypercalcemia
-Li therapy
dec (inc)
inc/dec unmeasured anions (inc/dec measured) with decreased anion gap
inc (dec)
inc/dec unmeasured cations (inc/dec measured) with decreased anion gap
Na, K
cations measured in anion gap eq
Cl, HCO3
anions measured in antion gap eq
dec
CO2 is inc/dec in
-metabolic acidosis
-diabeteic ketoacidosis
-salicylate pois
inc
CO2 is inc/dec in
-metabolic alkalosis
-emphysema
-severe emesis
blood
buffer system that HCO3 is part of
Ca
regulates
-skeletal, smooth, cardiac musc contraction
-nerve impulse transmission
-enzyme activity
-coag
regulated by
-PTH
-vitD
-calcitonin
acid
acid/basic environment leads to more free Ca (less bound)
basic
acid/basic environment leads to less free Ca (more bound)
inc
Ca is inc/dec with
-primary hyperparathyroidism
-bone malignancy
-renal failure
dec
Ca is inc/dec with
-hypoparathyroidism
-dec albumin
-chronic renal failure
-Mg deficiency
-vitD deficiency
dec
hypocalcemia occurs with inc/dec albumin
phosphate
-important for carb metab
regulated by
-PTH
-vitD
-FGF23
inc
phosphate is inc/dec with
-hypoparathyroidism
-neoplastic diseases
-renal failure
-intense exercise
-lymphoblastic leukemia
dec
phosphate is inc/dec wtih
-diabetic ketoacidosis
-hyperparathyroidism
-asthma
-alcoholism
-malabsorption
parathyroid (PTH)
regulates Ca and phosphate levels with kidneys, bones, and intestines
FGF23
-hormone from kidneys
-inhibits phosphate excretion, Ca absorption, and 1a hydroxylase activation by kidneys
-released with high Ca and low phosphate
inc, dec, inc, dec
serum Ca, phosphate and urine Ca, phosphate with primary hyperparathyroidism
dec, inc, inc, dec
serum Ca, phosphate and urine Ca, phosphate with secondary hyperparathyroidism
all inc
serum Ca, phosphate and urine Ca, phosphate with tertiary hyperparathyroidism
dec, inc, inc, dec
serum Ca, phosphate and urine Ca, phosphate with hypoparathyroidism (autoimmune, inborn error, accidental removal)
EDTA, citrate, oxalate
tube additives that should not be used to collect sample for Mg masurement
-chelate Mg and Ca
magnesium (Mg)
-regulated by kidneys
-inc reabs with inc PTH
inc
Mg inc/dec with
-renal failure
-antacid overuse
dec
Mg inc/dec with
-hyperparathyroidism (high Ca)
-GI disorders
-DM
-alcoholism with dietary insuff
chlorine (Cl)
maintains
-blood osmolality
-blood vol
-electrical neutrality
chloride shift
term describes Cl into cell with HCO3 into plasma
pilocarpine iontophoretic (>60)
CF sweat test
inc
inc/dec chlorine with
-prolonged diarrhea
-renal tubular disease
-dehydration
-excess loss of HCO3
dec
inc/dec chlorine with
-excess vomiting
-diuretic overuse
-burns
-low aldosterone
potassium (K)
-intracellular cation
-cardiac and skeletal muscle contraction
-imbalances cause arrythmias
-released during PLT clotting
-released with hemolysis
plasma
serum/plasma has lower K during clotting
inc
potassium is inc/dec in
-renal failure
-low aldosterone (Addisons)
-metabolic acidosis
-hemolysis
-leukemia/chemo
dec
potassium is inc/dec in
-high aldosterone (Conns, Cushings)
-diuretic/laxative overuse
-excess insulin
-diarrhea/vom
kidneys
where renin is secreted
low
high/low bp signals to kidneys to secrete renin
vasoconstriction, aldosterone
RAAS action to inc bp
retention
aldosterone promotes retention/secretion of Na and H2O by kidneys
secretion
aldosterone promotes retention/secretion of K and H by kidneys
inc
inc/dec aldosterone with
-primary: Conn’s, adrenal adenoma/disease
-secondary: renin-angiotensin disorder, renin-secreting tumor
dec
inc/dec aldosterone with
-Addison’s disease
-adrenal atrophy
-21 a hydroxylase CAH
HVA, VMA, metanephrine
catecholamine metabolism end products
MAO, COMT
enzymes in catecholamine metabolism
dopamine, norepinephrine, epinephrine
catecholamines
dopamine
HVA precursor catecholamine
norepinephrine (normeta)
VMA precursor catecholamine
epinephrine
metanephrine precursor catecholamine
cortisol
-adrenal gland hormone
-stim by CRH and ACTH
-dec immune system, inc glucose, protein, lipolysis metabolism
Addison’s disease
-adrenal hypofunction due to glucocorticoid use, autoimmunity (atrophy), TB
-test: ACTH stim → no response
Cushing’s syndrome
-adrenal hyperfunction due to exogenous cortisol admin, adrenal malignancy, ACTH secreting tumor
-test: high dose dexameth → no response
Cushing’s disease
-adrenal hyperfunction due to ACTH hypersecretion (pituitary or hypo)
-test: high dose dexameth → suppressed
Conn’s
-adrenal hyperfunction due to adrenal adenoma in zona glomerulosa cells
-screen: aldosterone:renin ratio → high
K
Na/K is elevated in Addison’s disease
syndrome
Cushing’s disease/syndrome is a result of a problem at the adrenal glands
disease
Cushing’s disease/syndrome is a result of a pituitary tumor
inc
aldosterone is inc/dec in Conn’s
21
CAH hydroxylase enzyme that results in inc testosterone, low aldosterone (low bp)
17
CAH hydroxylase enzyme that results in dec testosterone, inc aldosterone (high bp)
11
CAH hydroxylase enzyme that results in inc testosterone, inc bp (not aldosterone → 11 deoxycortisol)
AFP
elevated in neural tube defect
AFP
elevated in trisomy 13 (Patau’s)
uE3, hCG
decreased in trisomy 18 (Edward’s)
dec
uE3 and hCG are inc/dec in trisomy 18 (Edward’s)
AFP, uE3
decreased in trisomy 21 (Down’s) and Turner’s
hCG, inhibin A
elevated in trisomy 21 (Down’s) and Turner’s
inc
hCG and inhibin A are inc/dec in trisomy 21 (Down’s) and Turner’s
dec
AFP and uE3 are inc/dec in trisomy 21 (Down’s) and Turner’s
dec/n, dec
FSH/LH, testosterone with pre-testicular infertility (hypo/pit lesions)
inc, dec
FSH/LH, testosterone with testicular infertility (congenital - Kleinfelter’s xxy, acquired - chemo, tumor)
n
FSH/LH, testosterone with mechanical infertility
dec, inc
FSH/LH, estradiol with hypo/pituitary issues due to tumors, stress, illness, drugs, prolactinoma
inc, dec
FSH/LH, estradiol with ovarian issue (tumor, infection, PCOS, Turner’s)
n
FSH/LH, estradiol with uterine/fallopian issue (tumors, endometrial damage, infection)
hypo
GHRH is released from hypo/pit
pit
GH is released from hypo/pit
liver (IGF-1)
GH target
glucose suppression
-acromegaly/gigantism test
-will not change GH
dec
glucose administration suppression should inc/dec GH if normal, but does not change if adenoma
hypo
CRH released from hypo/pit
pit
ACTH released from hypo/pit
adrenal glands (cortisol)
ACTH target
high dose dexamethasone suppression (HDDS)
test for Cushing’s syndrome/disease → change in ACTH?
disease
HDDS test dec cortisol in Cushing’s syndrome/disease
Arg, L-dopa, insulin (stimulation)
test for dwarfism (low GH)
-no change in GH if adenoma (inc if normal or if primary (IGF receptor issue))
ACTH (stimulation)
test to differentiate primary vs secondary/tertiary cortisol deficiency