Chemistry 1 - Exam 1 Flashcards
What are the regulatory mechanisms of water balance?
Electrolytes (or the various cations and anions) trigger reabsorption and excretion of water.
The kidneys are responsible for reabsorption and exchange of electrolytes as fluid is filtered through the nephrons. If kidney is compromised, the glomerular filtration rate goes down. This can cause retention in things like sodium. Water follows sodium, and this will also trigger fluid retention.
The hypothalamus contains regulatory centers for water intake and water output in separate locations within the brain. Extracellular osmolarity (concentration of a solution expressed as the total number of solute particles in a given liter), intravascular volume, and angiotensin II can trigger responses in the neurons of these areas. Therefore, changes in the concentrations of solutes found in the extracellular water can trigger the neurons in the hypothalamus, leading to either water intake or water output. This can also affect the concentrations of solutes in turn.
ADH is a hormone that the hypothalamus can trigger the secretion of. When this happens, water intake or water output is the end result. In the event that the neurons controlling water output are stimulated, it can trigger the release of antidiuretic hormone (ADH) from the posterior pituitary gland. ADH will then trigger water reabsorption in the collecting ducts of the nephrons in the kidney. This means that less free water is leaving the body, and the urine is more concentrated with solutes in turn.
The renin-aldosterone system is a neurohormonal regulator of sodium, potassium, and water content. It also has some control over the blood pressure in the arteries. To begin, renin (enzyme) is secreted by juxtaglomerular cells in the kidney. Its secretion can be triggered by a few things such as low sodium concentration in the distal tubule. Renin turns angiotensinogen (globulin polypeptide produced in the liver) into angiotensin I (inactive decapeptide). As angiotensin I is an inactive form, it must be converted to angiotensin II (active octapeptide and a strong vasoconstrictor). This process happens in the lungs and kidney. Angiotensin II triggers the adrenal cortex in the brain to secrete aldosterone (causes thirst) and ADH (mentioned above). Aldosterone then, finally, triggers sodium reabsorption in the distal tubule of the nephrons in the kidney. Because water follows sodium, this means that more water will also be retained by the body.
Natriuretic peptides affect the renin-aldosterone system. When secretion of natriuretic peptides is increased it can trigger reduced blood pressure and plasma volume through a series of steps using the brain, kidneys, adrenal glands, and vasculature. There are about four different natriuretic peptides including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), and urodilatin.
What is the GFR?
Glomerulus filtration rate = 130 mL/minute
What is the function of the glomerulus?
- Filters blood to form the filtrate
- Consists of a capillary tuft surrounded by Bowman’s capsule.
- Supplied by an afferent arteriole and efferent arteriole.
What size molecules can be filtered by the kidney’s glomerulus?
What is fibro-cytosis?
The kidney’s glomerulus can filter any molecules smaller than 66 kD.
Anything bigger than 66 kD can’t be filtered.
During filtration of the kidney, fibrocytosis can be preformed if something exactly 66 kD in size tries to pass between the cells. This means they can absorb it, otherwise the filtration hole would be blocked.
What is the function of the proximal convoluted tubule? Describe it.
Located in the renal cortex.
- Reabsorbs major fractions of the filtrate.
> 75-80% of filtrate volume is H2O, HCO3-, Na+, & Cl-.
> All glucose up to renal threshold (180 mg/dL).
> Almost all amino acids, vitamins, proteins.
> Varying amounts of urea, uric acid.
> Varying amounts of ions: Mg+, Ca2+, P, K+.
- Secretes H+, K+, NH3, and drugs.
What is the primary function of the proximal tubule?
Reabsorption, but it can also secrete things.
What is the function of the loop of Henle?
What is the function of it’s ascending and descending limbs?
Loop of Henle - facilitates reabsorption of H2O, Na+, Cl-.
Descending limb - passive transport of H2O out of loop, so urine is highly concentrated at the bottom.
Ascending limb -active transport of electrolytes (Na+, Cl-) out of loop (reabsorption), so that urine is diluted in the tubular lumen.
*Note: Going downhill doesn’t require energy (ATP), but going uphill (ascending) does. Also osmolarity is high in descending limb and low in ascending limb.
What is the function of the distal convoluted tubule?
- Completes small adjustments to achieve electrolyte & acid-base homeostasis.
- Under the control of aldosterone & ADH (anti-diuretic hormone).
- Aldosterone is regulated by renin-angiotensin mechanism & ACTH.
Describe the different hormones of mentioned thus far?
Where, what, why, when, how?
Aldosterone - stimulates Na+ reabsorption and K+ excretion.
Renin - enzyme released by kidney in response to low Na+ or low blood volume. Converts angiotensinogen to angiotensin I.
Angiotensinogen - a protein released into the blood by the liver.
Angiotensin I - inactive form. Decapeptide.
ACE - angiotensin converting enzyme (in lungs).
Angiotensin II - vasoconstrictor. Converted from angiotensin I in lungs.
ADH - Anti-diuretic hormone. Increase aquaporin (water channel). Release triggered by hypothalamus, but it is secreted from posterior pituitary.
ACTH - made in anterior pituitary. Controlled by the sympathetic nervous system activity (biological activity). Adrenocorticotropic hormone.
Related Pathological conditions + Names + Causes.
Hypertension
Hypotension
Hypernatremia
Hyponatremia
Hyperaldosteronism
Hypoaldosteronism
Hypokalemia
Hyperkalemia
Respiratory alkalosis
Respiratory acidosis
Metabolic alkalosis
Metabolic acidosis
Sweat Chloride
Hypertension - high blood pressure
Hypotension - low blood pressure
Hypernatremia - high Na+
Hyponatremia - low Na+
Hyperaldosteronism - Cushing’s (aldosterone produced by adrenal cortex).
Hypoaldosteronism - Addison’s (aldosterone produced by adrenal cortex).
Hypokalemia - low K+.
Hyperkalemia - high K+.
Respiratory alkalosis - decreased pCO2
Respiratory acidosis - increased pCO2
Metabolic alkalosis - increased HCO3-
Metabolic acidosis - decreased HCO3-
Sweat Chloride - cystic fibrosis
What are the normal values of electrolytes?
Are they anions/cations?
Extracellular/Intracellular?
Na+: 135-145 mmol/L (extracellular cation)
K+: 3.5-5 mmol/L (intracellular cation)
Cl-: 98-106 mmol/L (extracellular anion)
HCO3-: 22-26 mmol/L or mEq/L (extracellular anion)
What is the anion gap? Describe it.
Measured cations: (Na+) + (K+)
Measured anions: (Cl-) + (HCO3-)
[(Na+) + (K+)] - [(Cl-) + (HCO3-)] = 15 mmol/L (10-20)
[(Na+)] - [(Cl-) + (HCO3-)] = 12 mmol/L (7-16)
Increased anion gap due to increase in unmeasured anions.
Decreased gap due to decrease in unmeasured anions.
What are the 4 Natriuretic Peptides discussed so far?
ANP - produced in the cardiac atria in response to stretching of atrial cavity. Increases GFR; inhibits salt appetite, water intake, and secretion of ADH and corticotropin.
BNP - produced in left cardiac ventricles in response to left ventricular pressure overload. Increased BNP = heart failure.
CNP - produced and secreted by vascular endothelial cells. BNP and ANP can trigger release of CNP. Most potent venous dilator.
Urodilatin - similar to ANP, but formed in kidney from same precursor protein. More potent effects than ANP.
What is the renal threshold for glucose? Describe the graph.
180 mg/dL
What are the effects of dehydration and overhydration on urine?
