8 Flashcards
High osmolarity causes:
Thirst increased water intake
ADH release water reabsorbed from urine
Low osmolarity causes:
Lack of thirst decreased water intake
Decreased ADH release water lost in urine
Capillary pressure - pushes
water out of cap, perssure goes up water gos out
Capillary colloidal osmotic pressure pulls
water back into capillaries
interstitial fluid pressure -
stops movement of fluid from capillary
tissue colloidal pressure pulls
water from capillary into tissue spaces
Hydrostatic pressure can be thought of as………. and osmotic pressure can be thought of as ……pressure.
.. “pushing pressure,”.., ….“pulling”
Edema-
is fluid in the interstitial space
Pedal edema-
sweeling of the feet
dec capillary colloidal osmotic pressure –
loss of proteins - albumin is the smallest, decreased proteins control *decreased permeability *
inc capillary permeability -
increase pores
- lymphedema
obstruction of lymph flow
Sodium (Na+) - controls
ECF(Extracellular) osmolality
most abundant cation - enters in GI - leaves by kidney
Why would “retaining sodium” cause high blood pressure?
Sodium bonds to water
When you have sodium and water being retain when it goes in the veins.
Hypodipsia –
drink less elderly
Polydipsia-
True
False
Psychogentic
True, symptomatic- hypothalamus tell you to drink cuz your need water you truly need it.
False, secondary(causes by something else), inappropriate(false), heart is holding water, fluid is not going out to the body hypothalmas thinks you need water.
Kidney-filters , kidney flails , ie excrete all fluids
Psychogenic, compulsive- psychological, SZ Sx drink a lot
First response of a fluid hormone is to
retain fuild!
ADH – anti diuretic hormone –
Vasopressin, we should be 70% water! (will also retain Sodium) retains sodium(Na) kick potassium(k). Happens when pain trauma stress
Vasopressin- contracts vessels
Increase ADH - caused by
pain, trauma, nausea, surgery, narcotics, nicotine
alcohol lowers
ADH- thus why we pee more when we drink
diabetes insipidus-(has nothing to glusoce) –
frequent peeing unable to concentrate urine - does not respond to ADH usually deficiently
syndrome of inappropriate ADH (SIADH) -
failure of negative feedback system, pee too much
Aldosterone supports…. secretion and suports … retention
Supports K+ secretion
supports Na+ and H2 retention
stress, trauma inc cortisol which increases aldosterone so increase transfer of
IntraCellFluid K+ to ECF –results in hypokalemia (excreted)
Addison’s)
deficiency in aldosterone effect – (Addison’s)
prevents K+ excretion
treat with glucose to move K+ back to ICF
hypovolemia
dec in ECF
inc in ECF
retention (na and h20 resorbed)
Renal failure, heart failure
Hyponatremia - < 135 mEq/l – Chart 31-6
if inc h2o, then dec Na+
Muscle cramps, weakness
hypernatremia - > 145 mEq/l – Chart 31-7
if inc sodium in serum, then cell dehydration results
Second most abundant cation - major in ICF
K+(Potassium)
hypokalemia -
cardiac sx, but not serious Ch 31-8 not usally ACUTE
Slowing down heart rate, less O more tired.
hyperkalemia -
if cardiac sx, potentially fatal stops performing – Chart 31-9. too much K HR to much heart contractility. Will have Heart firing in other spots. Cardiac arrhythmia abnormal heart beat.
Hyperkalemia raises
resting potential toward threshold
Cells fire more easily
When resting potential reaches threshold, Na+ gates open and won’t close
Calcium
absorbed from GI (intestine) - stored in bone - excreted by kidney
Calcium, controls (stable)
neural messages
Hypocalcemia
to much firing
Hypomagnesemia
(Helps with Calcium nerve controlling) - symptoms only if severe malnutrition, malabsorption, laxative abuse usually hypo Ca, hypo K diuretics sx inc neuro excitability
hypermagnesemia -
rare
renal failure, elderly
hyporeflexia, dullness
Acid (H+) Blocks Controls Byproducts of “Food”
Blocks Na+ gates
Controls respiratory rate
Individual acids have different functions:
Byproducts of energy metabolism (carbonic acid, lactic acid)
Digestion (hydrochloric acid)
“Food” for brain (ketoacids)
Acidosis -
alkalosis -
DEC in pH
increase pH
metabolic - alt bicarb (base) in ECF
dec pH, dec bicarb =
inc pH, inc bicarb =
=acidosis
=alkalosis
respiratory - alt CO2 (acid)
dec pH, inc CO2 =
inc pH, dec CO2 =
=acidosis
=alkalosis
Metabolic acidosis
Increased levels of
ketoacids, lactic acid, etc.
Decreased bicarbonate levels
Metabolic alkalosis
Decreased
H+ levels Increased bicarbonate level
Co2is toxin in
is toxic to brain
Dec pH, dec bicarb
inc respiratory rate to release CO2
Metabolic Acidosis
lactic acidosis
-inadequate oxygen,ketoacidosis
unavailable carbs so fatty acids mobilized - become ketones if excess
lactic acidosis
-inadequate oxygen
,ketoacidosis
unavailable carbs so fatty acids mobilized - become ketones if excess
CO2 + H2O H2CO3 H+ + HCO3-
get money
work with and explain action potential thresholds and if you have less NA orK+
get money
Dec pCO2, dec H2CO3, Inc pH hyperventilation lightheaded, dizzy paresthesias short periods of apnea treat with rebreather
Respiratory alkalosis
Byproducts of energy metabolism
Digestion
“Food” for brain
Byproducts of energy metabolism (carbonic acid, lactic acid)
Digestion (hydrochloric acid)
“Food” for brain (ketoacids)
Respiratory acidosis
Inc pCO2, H2CO3, dec pH acute - narcotic overdose, lung injury chronic - emphysema HA, blurred vision, inc HR and BP - flushed - irritable, muscle twitching ventilation
Dec pCO2, dec H2CO3, Inc pH hyperventilation lightheaded, dizzy paresthesias short periods of apnea treat with rebreather
Respiratory alkalosis
Byproducts of energy metabolism
Digestion
“Food” for brain
Byproducts of energy metabolism (carbonic acid, lactic acid)
Digestion (hydrochloric acid)
“Food” for brain (ketoacids)
Respiratory acidosis
Inc pCO2, H2CO3, dec pH acute - narcotic overdose, lung injury chronic - emphysema HA, blurred vision, inc HR and BP - flushed - irritable, muscle twitching ventilation
