Sweep 3 Flashcards
Xerostomia
Management
Stimulate muscarinic receptors
—–Pilocarpine—Ach agonist
Treat symptoms
Acetylcholine Primarily (some effect of Norepinephrine via α-adrenergic receptor)
Opening of Ca++ sensitive Cl- and K+ channels
Increased flow rate, lowered ductal modification
Norepinephrine
Protein rich saliva
PKA-mediated exocytosis
β-adrenergic receptor
Protein secretion by
PKA mediated exocytosis
Parasympathetic stimulation releases
ACh onto the acinar cells and results in a watery plasma-like secretion.
Secondary duct: Low flow rate=
Low rate=high [K]; high rate=high [Na]
Salivary fluid
Intracellular Na+
kept low
Salivary fluid
Intracellular K+
kept high
Salivary fluid
Intracellular Cl-
Cl- high
Salivary fluid
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-
Acinar Cellular Origin
Amylase, Lipase, Mucoproteins, Proline-rich proteins, Tyrosine-rich proteins (and many others)
Nonacinar Cell Origin
Lysozyme, immunoglobulin, growth factors, regulatory peptides (NGF)
Paracrine mediators
Produced by
local cells
Reach target cells via diffusion
CCK stimulated by
fatty acids
Pepsinogen—
Chief Cells
Body and Antrum (Oxyntic and Pyloric Gland Area)
Somatostatin is a potent inhibitor of —– secretion via 2 mechanisms
HCl
Effects on G Cell
Effects on Parietal Cell
when pH of chyme < 3, ——— produced
secretin
High H+, amino acids, and fatty acids stimulate ——, which——– production
CCK
↓HCl
trypsinogen to trypsin done by
membrane bound enterokinase.
3Increased HCl—->
———- ——>
HCO3
Secretin
Athetoid (dyskinetic) CP:
slow rate, dysrhythmia, inappropriate voice stoppages & reduced stress, more artic errors
Spastic CP:
breathy voice, monopitch, monoloudness, hypernasality, voice quality changes throughout utterance, better speech intelligibility with fewer artic errors
goblet cells secrete mucus which can trap airborne particles and pathogens; cilia on epithelial cells move mucus upwards to pharynx where it can be swallowed or expelled
this occurs in
conducting zone
Cystic fibrosis
mutation in genetic code for
Cl- channel reduces the amount of Na+ and Cl- secreted across the epithelium into mucus. This leads to there being less water in the mucus (due to osmosis)→ mucus is thick and dry
transpulmonary (Ptp) =
Palv - Pip
Patm is 0 by definition; Palv equal Patm between
breaths (no air is moving)
Between breaths:
Pip
below atmospheric pressure
Ptp = Palv – Pip;
lungs remain expanded
lungs tend to recoil inward –
chest wall tends to recoil outward –
net result is Pip is always subatmospheric
During inspiration –
diaphragm contracts → thorax expands
Pip becomes more negative
Ptp increases so lung volume increases and air flows in until Palv = Patm
During expiration -
diaphragm relaxes → thorax compresses
Pip becomes less negative
Ptp decreases so lung volume decreases and air flows out until Palv = Patm
Lung compliance
CL =
ΔVL/(Palv – Pip) = ΔVL/PTP
• for polar molecules like water, surface tension is created by
electrostatic force
Surfactant
production is regulated by ——— in Type II cells; —————— increases surfactant production
stretch receptors
deep breathing
Lung volumes and capacities
tidal volume (TV) – V entering lungs per breath; ~500 ml
inspiratory reserve volume (IRV) – max V inspired ; ~3000 ml
expiratory reserve volume (ERV) – V exhaled beyond TV; ~1500 ml
residual volume – V in lungs after maximum exhalation; ~1000 ml
Minute ventilation (ml per min) =
tidal V x respiratory rate
erythrocytes have a ————- transporter that moves HCO3- into plasma as it forms (see figure below).
HCO3- / Cl-
Hb affinity decreased by factors associated with metabolic activity –
curve shifts right
increased T due to production of metabolic heat
increased CO2 (Bohr effect) – CO2 binds to globin part of Hb (allosteric effect)
increased H+ (or decrease pH) – H+ also binds to globin part of Hb and has an allosteric effect
increased 2,3 diphosphoglycerate (2,3,DPG) – 2,3 DPG is a product of glycolysis in erythrocytes that enhances offloading/dissociation of O2 by allosteric modulation
↓ PO2 → increase Hb affinity for
CO2 as illustrated in difference in total CO2 in arterial vs venous blood
ESRD patients have a reduced ability to
eliminate nitrogenous wastes (urea) and excess nitrogen is converted to ammonium. The excess ammonium has direct effects on health – the blood is alkalized which leads to an increased pH in the oral cavity.
Contraindications for ESRD patients:
nephrotoxic drugs such as tetracycline, acyclovir, aspirin, NSAIDs
increased susceptibility to bleeding due to destruction of platelets
x % of plasma filtered in bowman’s capsule
15-20%
Filtration occurs due to pressure differences between the blood in the capillaries and the fluid in the capsule
(Starling forces).
Glucose and amino acids are rebsorbed with
Na+ using symporters
Ascending /descending limbs
Reabsorption in these segments is
passive
There are two cell types in the collecting duct and late distal tubule
principal cells have epithelial sodium channels (ENaC) that reabsorb Na+ and secrete K+
Na+ reabsorption drives paracellular Cl- reabsorption
K+ secreted due to Na+ K+ ATPase activity in basal membrane
Tubular fluid becomes positive when
Cl- reabsorbed so cations diffuse along an electrical gradient
—– is the opposite of ADH
natriuretic peptides
Increase volume sees —— in sodium reabsorption
decrease at all places except ATL, DT
Factors affecting excretion of potassium include
plasma [K+] - increased K+ stimulates aldosterone release, and aldosterone increases Na+ K+ ATPases in principal cells
The are three options for renal regulation of body pH that will produce urine with different pH
- decrease body pH by not reabsorbing all HCO3- ; produces an alkaline urine and acidifies body fluids
- no effect on body pH by reabsorbing all HCO3- ; urine has a neutral pH
- increase body pH by reabsorbing all and producing more HCO3- (typical); produces an acidic urine and alkalinizes body fluids
Intercalated cells
H+ is secreted via an
H+ ATPase pumps and an H+/K+ ATPase pump (not illustrated)
Ascending loop NH4+ substitutes for K+ in the
Na+K+2Cl- symporter and enters the interstitial fluid in the medulla where it is in equilibrium with NH3
Because it is a polar molecule, NH4+ is
“trapped” in the interstitial fluid, but NH3 (being nonpolar) can diffuse into the lumen of nearby collecting ducts
hyperventilaite
increase pH
Note that a decrease in plasma pH will increase the amount of
free Ca2+ which can be filtered and excreted, so alkalosis can lead to hypocalcemia.
Calcium is regulated by three hormones all of which are regulated by a calcium sensing receptor (CaSR)
found in
plasma membrane of cells in parathyroid gland, thyroid parafollicular cells, and cells of the proximal tubule.
• parathyroid hormone (PTH)
released in response to hypocalcaemia
increases bone resorption, increases renal Ca+ reabsorption, and stimulates calcitriol production
try to keep calcium up
in distal tubule – transcellular reabsorption of calcium
transport here can be regulated because expression of
Ca2+ transporters is regulated by PTH
Thiazides – block
Na+Cl- symporter in early distal tubule
K+ - sparing – two classes that both act in late
distal tubule and cortical collecting duct to inhibit sodium reabsorption AND potassium secretion
- aldosterone antagonists
- ENaC blockers
↓ water reabsorption → ↓
Ca2+ reabsorption by solvent drag
Loop diuretics are the most powerful of all diuretics;
they inhibit Na+ reabsorption in the ascending limb of the loop of Henle. Furosemide (lasix) is an example of a loop diuretic.
Inhibit Na+K+2Cl- symporter in the thick ascending limb which inhibits Na+ reabsorption
urine leaving loop is not dilute
no osmotic gradient established in the medulla interstitium so water is not reabsorbed along collecting duct → urine is dilute (500 mOsm instead of 1400 mOsm)
Thiazide diuretics like chlorothiazide are secreted into the
proximal tubules, and they act in the early distal tubule to block the Na+Cl- transporter
- aldosterone antagonists, e.g. spironolactone
block
aldosterone’s ability to increase Na+ transporters in principal cells
must get inside tubular cells to block aldosterone receptors
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
3increase aldosterone —->
stimulate K+ secretion
Loop and thiazide diuretics —>
reduced ECV à metabolic alkalosis
potassium-sparing diuretics —>
metabolic acidosis because H+ secretion in distal tubule and cortical collecting duct is inhibited
Loop diuretics increase calcium excretion by affecting the
transepithelial voltage that normally provides the driving force for paracellular transport of calcium.
Thiazide diuretics stimulate
calcium reabsorption in the distal tubule and thus reduce excretion.
Normally, distal tubule reabsorbs 9% of filtered calcium via active transport.
Intercalated cells are
ciliated i guess?
- Which of the following conditions WILL NOT shift the O2-hemoglobin dissociation curve to the right?
C. metabolic alkalosis.
- Hypoxic vasoconstriction of pulmonary blood vessels
A. minimizes ventilation-perfusion inequality.
Temp increases as
O2 is used up - metabolic activity will raise temp.
15. Contraction of the diaphragm during inspiration results in an increase in A. alveolar pressure. B. intrapleural pressure. C. transpulmonary pressure. D. atmospheric pressure. E. All of the above are true.
C. transpulmonary pressure.
- Patients with severe, uncontrolled diabetes mellitus produce large quantities of organic acids. Which of the following will be observed in these patients?
A. hyperventilation and renal excretion of ammonium
- Chronic diarrhea could result in
A. metabolic acidosis.
- Erythropoietin is
A. regulated by hypoxia-sensitive transcription factors.
HIF
- Which of the following would increase systemic blood pressure?
D. a drug that enhances the activity of the angiotensin-converting enzyme (ACE)
- Which of the following does NOT occur in the proximal tubule?
C. potassium secretion
- Aldosterone
C. stimulates the synthesis of Na+-K+ ATPase proteins in the distal tubule.
