physio exam 2 Flashcards
Principal ECF electrolytes
Na, Cl, bicarbonate
Principal ICF electrolytes
K, phosphate, magnesium
calcium function
bone and teeth building; coagulations; muscle contraction
chloride function
formation of HCL in stomach; transmit nerve impulses
magnesium function
enzymes activation
potassium function
regulation of water and electrolyte content of ICF; acid-base balance
sodium function
regulation of fluid volume within ECF; increase membrane permeability; control water
distribution
effects of increased ADH
Stimulates water conservation at the kidneys, concentrating urine
Stimulates the thirst center to promote the drinking of fluid
where is aldosterone secreted
the adrenal cortex
T/F
The higher the plasma aldosterone concentration, the more efficiently the kidneys will conserve sodium
TRUE
Released by cardiac muscle cells in response to abnormal stretching of the atrial walls caused by elevated blood pressure or increase in blood volume
ANP
edema
presence of excess fluid in the tissues (mainly in the ECC)
list 4 causes of intracellular edema
o Hyponatremia
o Depression of metabolic systems of the cells
o Reduced nutrition of the cells (ischemia)
o Inflammation (increase membranes permeability)
list 3 causes of extracellular edema
o Abnormal leakage of fluid from plasma to interstitial spaces
o Failure of lymphatic vessels to return fluid from the tissues back into the blood
o Causes: increased capillary pressure, decreased plasma proteins, increased capillary
permeability, blockage of lymph return
thiazide
diuretics inhibit NaCl resorption in the DT
Potassium-sparing diuretics (amiloride) function
block sodium channels in the CD leading to a reduction
of potassium excretion
caused by a lack of ADH synthesis in posterior pituitary gland
Diabetes insipidus centralis
when ADH is produced but it cannot act in the kidney
Diabetes insipidus renalis
the testes determining gene (only in males) that causes the bipotential gonads to develop into testes
SRY gene
this hormone will cause the development of the external genitals
in males
Dihydrotestosterone
this will cause the degeneration of the mullerian ducts in
males (in females this is absent, allowing the development of mullerian ducts)
anti mullerian hormone
this will cause the wolffian duct to become seminal vesicles, vas deferens and epididymis
testosterone
Acts on anterior hypophysis to increase secretion of FSH and LH
GnRH
under FSH stimulation convert testosterone
to dihydrotestosterone
sertoli cells
Acts on sertoli cells to produce inhibin causing a negative feedback effect on pituitary release of FSH
FSH
Stimulates androgen production from leydig cells
LH
ensures a constant high intratubular concentration of testosterone essential for the function of the epididymis, and possibly other accessory glands
androgen binding protein
hormone produced by leydig cells
testosterone
This causes the androgen in males to be converted into estradiol
aromatase
produced by the follicular cells in the ovary
estradiol
produced by the CL
progesterone
mediates ovulatory surge of LH
estradiol
female hypothalamus – surge center
responsible for bursts of GnRH required to achieve preovulatory LH surge; female structure; in males this structure is regressed by the crossing of testosterone through the blood brain barrier
female hypothalamus – tonic center
frequency of GnRH pulses controlled by a pulse generator
T/F
hypothalamus is inherently female
TRUE
**testosterone during development defeminizes the brain
T/F
the surge center of the hypothalamus is also in men
FALSE
**Testosterone crosses blood brain barrier and converted to estradiol which causes defeminization of hypothalamus, eliminating the surge center in males