Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
43 Cards in this Set
- Front
- Back
|
Describe alkalosis.
|
Low [H+]
high pH |
|
|
What is respiratoy alkalosis?
|
Results from increased respiration and blowing off of CO2 (lose CO2)
|
|
|
What is metabolic alkalosis?
|
Results from other causes (not increased respiration)
ex: Bicarbonate ingestion with renal failure. Vomiting |
|
|
What is acidosis?
|
High [H+]
low pH |
|
|
What is respiratory acidosis?
|
Results from decreased respiration and a rise in CO2
|
|
|
What is metabolic acidosis?
|
Results from other causes
ex: Lactic acidosis, aspirin overdose |
|
|
What is the renal response to acidosis (high H+)? (only applies if the acidosis is due to the renal system)
|
1) Sufficient H+ secreted = reabsorb ALL filtered HCO3-
2) Still more H+ are secreted and this contributes new HCO3- to the plasma as these H+ are excreted bound to non-HCO3- buffer like HPO4 3) Tubular glutamine metabolism and ammonium excretion are enhanced, contributes also to new HCO3- in the plasma **Net result: More new HCO3- than usual are added to the plasma, .: compensating for the acidosis. Urine is highly acidic (lowest pH=4.4) |
|
|
What is the renal response to alkalosis (low [H+]/ high [HCO3-]?
|
1) Rate of H+ secretion is inadequate to erabsorb all the filtered HCO3-. sp extra HCO3- is SECRETED in the urine (incomplete reabsorption of HCO3 with H+)
2) Little or no H+ secretion of non-HCO3- urinary buffers (cuz don't want kidneys to make new HCO3-) 3) Tubular glutamine and ammonium excretion are decreased, so that little or no new HCO3- is contributed to the plasma from this source -->NET result: Plasma HCO3- will decrease, compensating for alkalosis. Urine will be highly alkaline (pH>7.4) |
|
|
What is the primary cause of HCO3 change in respiratory acidosis/alkalosis?
|
Renal compensation
|
|
|
What is the primary cause of CO2 change in respiratory acidosis/alkalosis?
|
Primary abnormality
|
|
|
What is the primary cause of HCO3 change in metabolic acidosis/alkalosis?
|
Primary abnormality
|
|
|
What is the primary cause of CO2 change in metabolic acidosis/alkalosis?
|
Reflex ventilatory compensation
|
|
|
What happens to H+, HCO3- and P(CO2) in resp acidosis?
|
H+: Inc
HCO3-: Inc CO2: Inc |
|
|
What happens to H+, HCO3- and P(CO2) in resp alkalosis?
|
H+: Dec
HCO3-: Dec CO2: Dec |
|
|
What happens to H+, HCO3- and P(CO2) in metabolic acidosis?
|
H+: Inc
HCO3-: Dec CO2: Dec |
|
|
What happens to H+, HCO3- and P(CO2) in metabolic alkalosis?
|
H+: Dec
HCO3-: Inc CO2: Inc |
|
|
Notes
Equation: CO2 + H2O <--> H2CO3 <--> HCO3- + H+ |
In respiration: initial change always in CO2, .: decide CO2 first after H+ (if H+ inc, shift equatio to the left, inc CO2. Then look at HCO3. If CO2 inc, the HCO3 must inc because equation now shifted to the right)
HCO3 always goes in same direction as CO2 |
|
|
What's a clinical example of respiratory acidosis?
|
Respiratory failure with CO2 retention
|
|
|
What's a clinical example of resp alkalosis?
|
Hyperventilation (high altitude)
|
|
|
What is a clinical example of metabolic acidosis?
|
Diarrhea (loss of HCO3-), renal failure (accumulation of inorganic acids), poisonings (aspirin, methanol)
|
|
|
What is a clinical example of metabolic alkalosis?
|
Vomiting (loss of H+), hyperaldosteronism (increased H+ secretion in DCT and CCD)
|
|
|
What are diuretics?
|
Drugs used clinically to increase the volume of urine excreted
|
|
|
How do diuretics act?
|
Acton tubules to INHIBIT reabsorption of sodium (along with Cl and HCO3-) so that there is increased excretion of these ions
->Water excretion aso increass |
|
|
Why are diuretics used?
|
Get rid of excess volume (furosemide in heart failure)
Control BP ((hydrochlorothiazide) |
|
|
Describe loop diuretics.
|
Act on TAL
Inhibit cotransport of Na, Cl and K+ (Na+-K+-2Cl cotransporter) (if Na is not absorbed in the loop, it goes all the way to the collecting duct) |
|
|
What are the side effects of loop diuretics?
|
Lowers K+ because of increased distal flow of Na (as Na flows by and in, K+ leaves)
|
|
|
What are the 5 areas that are worked on by diuretics?
|
Proximal tubule
TAL DT CCD IMCD |
|
|
What does furosemide do?
|
Blocks reabsorption at the TAL
|
|
|
What do K+-sparing diuretics do?
|
Inhibit Na+ reabsorption at the CCD and inhibit K+ secretion there (.: plasma [K+] doesn't decrease)
|
|
|
How do K+-sparing diuretics work?
|
Block action of aldosterone (get less Na channels) or block the epithelial Na channel in the CCD
ex: Ailoride: blocks Na channel Spironolactone: competes with aldosterone |
|
|
what happens if there is no ldosterone?
|
In CCD:
-> Blocks Na+ reabsorption -> Blocks K+ secretion |
|
|
What is the clinical use of diuretics?
|
If a person has renal retention of salt and water: abnnormal expansion of the extracellular fluid (edema)
|
|
|
What happens with congestive heart failure?
|
Cardiac failure--> get less Cardiac output, can get pulmonary edema
Heart not pumping effectively, not enough volume oing around ->Baroreceptors sense this, activate AG system, send signal to kidneys to retain water |
|
|
What happens in hypertension?
|
Renal retention of salt and water contribut to high BP
|
|
|
What are common features of kidney disease/failure?
|
1) Proteinuria: ptn in the urine cuz the glomerulus can't properly hold back ptn in the blood (barrier fct impaired)
2) Accumulation of waste products in the blood (urea, creatinine, phosphate, sulfate) 3) High [K+] in the blood 4) Metabolic acidosis 5) Anemia (decreased secretion of erythropoietin) 6) Decreased secretion of 1,25- vit D (leads to hypoacemia) |
|
|
When is there kidney failure?
|
When more than 90% of the nephrons stop working
->Can lose 50% of nephrons (1 kidney) and be fine -> Can live normally with more than 10% of nephrons |
|
|
How is kidney failure treated?
|
Renal replacement therapy
1) Hemodialysis 2) Peritoneal dialysis 3) Kidney transplantation (best method) |
|
|
What happens in hemodialysis?
|
Put 2 needles in the arm
Remove blood Put in pump and add anticoagulants Goes through dializer (has hollow fibers) Run dialysate from bottom to top, surrounding the hollow fibers that have blood in them Get exchange between the blood and dialysate of waste, nutrients, etc some things in low [ ] go back into the blood (Ca2+ etc) Blood returned to patient |
|
|
What is the problem with hemodialysis?
|
Have to go to the hospital ~3 times/week for several hours
Can never miss a session |
|
|
What is peritoneal dialysis?
|
Use the lining og the patient's own abdominal cavity (peritoneum) as the dialysis mb
Fluid (dialysate) is injected into the cavity via a tube inserted through the abdominal wall Solutes diffuse into the fluid from the person's blood Fluid is exchanged several times/day -> can be done at home |
|
|
How is kidney transplantation accomplished?
|
Get a kidney fom recently deceased person (cadaveric transplant) or living donor
|
|
|
Why is kidney transplantation getting better?
|
Anti-rejection treatments have improved
|
|
|
What is the main problem with transplants?
|
Not enough donors
|
