Sweep 2 Flashcards
Sublingual
Lesser sublingual
(Rivinus’s) ducts anterior floor
Mostly mucous
Salivary Fluid Secretion
Intracellular Na+ kept low
Intracellular K+ kept high
Intracellular Cl- high
In unstimulated cells, Ca2+ levels are low, and Ca2+ activated K+ and Cl- channels are closed.
Upon stimulation, Ca2+ opens the Cl- and K+ channels.
Na+ leaks through tight junctions to follow Cl-
Mucin
Predominately produced by
sublingual & submandibular glands
Parasympathetic Synapse in
Trigeminal
Solitary Nucleus
Big Picture of salivation
Muscarinic or Alpha-adrenergic receptor activation
Intracellular calcium release
Calcium activated K+ and Cl- channels
Increase luminal Cl- concentration
Intercellular sodium follow
Water follows
Protein secretion by PKA mediated exocytosis
Acetylcholine
Primarily (some effect of Norepinephrine via α-adrenergic receptor)
Opening of Ca++ sensitive Cl- and K+ channels
Increased flow rate, lowered ductal modification
Muscarinic or α-adrenergic
Norepinephrine
Protein rich saliva
—PKA-mediated exocytosis
β-adrenergic receptor
Trypsin is an essential protease for
cleavage of proteins
Trypsinogen cleaved by
enteropeptidase
Intrinsic factor
needed for b12 absorption
Secretin, and CCK are
enterogastrones
Membrane bound enterokinase
converts trypsinogen to trypsin
Increased HCl—->Secretin—->
HCO3
Also, bicarbonate secretion is coupled to
Cl- ion absorption.
transpulmonary (Ptp) =
Palv - Pip
Interpulmonary pressure
sine wave
IP
smile face
P =
2 x surface tension / radius
Therefore, increase ST → increase pressure
decrease radius → increase pressure
`
Emphysema - alveolar tissues damaged or destroyed, perhaps due to overproduction of
proteolytic enzymes
obstructive lung disease:
↓ FEV1; normal VC
restrictive lung disease:
↓VC, normal FEV1
Acclimatization to high altitude depends on delayed responses that take days or weeks
increased erythropoiesis which results in polycytothemia; stimulated by erythropoietin (EPO), a hormone from the kidney
increased 2,3 DPG synthesis which will shift the Hb-O2 curve to the right
increased synthesis of other components of O2 delivery and consumption
capillary density –
mitochondria –
myoglobin -
The effects of natriuretic peptides include
vasodilation of afferent arterioles
vasoconstriction of efferent arterioles
inhibition of renin (and aldosterone)
inhibition of ADH secretion
Excrete sodium and water***
NH4+ substitutes for——- in the ——–r and enters the interstitial fluid in the medulla where it is in equilibrium with NH3
K+
Na+K+2Cl- symporter
• parathyroid hormone (PTH)
released in response to
hypocalcaemia
• parathyroid hormone (PTH)
increases
bone resorption, increases renal Ca+ reabsorption, and stimulates calcitriol production
• calcitriol (1,25 dihydroxyvitamin D)
metabolism of vitamin D to calcitriol is stimulated by
hypocalcaemia and/or hypophosphatemia (and further stimulated by PTH, see above)
• calcitonin
released in response to
hypercalcaemia
increases bone deposition
in distal tubule – ——— reabsorption of calcium
transcellular
Osmotic diuretics - retain water by increasing osmotic pressure; act in water-permeable segments of the nephron
(PT & descending loop of Henle)
CA inhibitors – reduce Na+ reabsorption; ———- is major site of action
proximal tubule
Thiazides – block
Na+Cl- symporter in early distal tubule
- aldosterone antagonists, e.g. spironolactone
block aldosterone’s ability to
increase Na+ transporters in principal cells
- ENaC blockers, e.g. amiloride
block
Na+ reabsorption across the apical membrane
these act on a membrane protein so can gain access by secretion into the proximal tubule
aldosterone stimulates —- secretion
K+
Loop and thiazide diuretics —-> reduced ECV ——> metabolic
alkalosis
potassium-sparing diuretics —-> metabolic ———– because H+ secretion in distal tubule and cortical collecting duct is inhibited
acidosis
Loop diuretics increase calcium excretion by affecting the
transepithelial voltage that normally provides the driving force for paracellular transport of calcium.
