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Physio Exam 3 > Sweep 3 > Flashcards

Sweep 3 Flashcards

1
Q

Xerostomia

Management

A

Stimulate muscarinic receptors
—–Pilocarpine—Ach agonist
Treat symptoms

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2
Q

Acetylcholine Primarily (some effect of Norepinephrine via α-adrenergic receptor)

A

Opening of Ca++ sensitive Cl- and K+ channels

Increased flow rate, lowered ductal modification

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3
Q

Norepinephrine

A

Protein rich saliva
PKA-mediated exocytosis
β-adrenergic receptor

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4
Q

Protein secretion by

A

PKA mediated exocytosis

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5
Q

Parasympathetic stimulation releases

A

ACh onto the acinar cells and results in a watery plasma-like secretion.

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6
Q

Secondary duct: Low flow rate=

A

Low rate=high [K]; high rate=high [Na]

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7
Q

Salivary fluid

Intracellular Na+

A

kept low

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8
Q

Salivary fluid

Intracellular K+

A

kept high

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9
Q

Salivary fluid

Intracellular Cl-

A

Cl- high

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10
Q

Salivary fluid

In unstimulated cells, Ca2+ levels are

A

low, and Ca2+ activated K+ and Cl- channels are closed.

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11
Q

Upon stimulation, Ca2+ opens the

A

Cl- and K+ channels.

Na+ leaks through tight junctions to follow Cl-

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12
Q

Acinar Cellular Origin

A

Amylase, Lipase, Mucoproteins, Proline-rich proteins, Tyrosine-rich proteins (and many others)

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13
Q

Nonacinar Cell Origin

A

Lysozyme, immunoglobulin, growth factors, regulatory peptides (NGF)

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14
Q

Paracrine mediators

Produced by

A

local cells

Reach target cells via diffusion

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15
Q

CCK stimulated by

A

fatty acids

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16
Q

Pepsinogen—

A

Chief Cells

Body and Antrum (Oxyntic and Pyloric Gland Area)

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17
Q

Somatostatin is a potent inhibitor of —– secretion via 2 mechanisms

A

HCl

Effects on G Cell
Effects on Parietal Cell

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18
Q

when pH of chyme < 3, ——— produced

A

secretin

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19
Q

High H+, amino acids, and fatty acids stimulate ——, which——– production

A

CCK

↓HCl

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20
Q

trypsinogen to trypsin done by

A

membrane bound enterokinase.

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21
Q

3Increased HCl—->
———- ——>
HCO3

A

Secretin

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22
Q

Athetoid (dyskinetic) CP:

A

slow rate, dysrhythmia, inappropriate voice stoppages & reduced stress, more artic errors

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23
Q

Spastic CP:

A

breathy voice, monopitch, monoloudness, hypernasality, voice quality changes throughout utterance, better speech intelligibility with fewer artic errors

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24
Q

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

A

conducting zone

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25
Q

Cystic fibrosis

mutation in genetic code for

A

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

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26
Q

transpulmonary (Ptp) =

A

Palv - Pip

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27
Q

Patm is 0 by definition; Palv equal Patm between

A

breaths (no air is moving)

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28
Q

Between breaths:

Pip

A

below atmospheric pressure

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29
Q

Ptp = Palv – Pip;

A

lungs remain expanded

lungs tend to recoil inward –

chest wall tends to recoil outward –

net result is Pip is always subatmospheric

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30
Q

During inspiration –

A

diaphragm contracts → thorax expands

Pip becomes more negative

Ptp increases so lung volume increases and air flows in until Palv = Patm

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31
Q

During expiration -

A

diaphragm relaxes → thorax compresses
Pip becomes less negative

Ptp decreases so lung volume decreases and air flows out until Palv = Patm

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32
Q

Lung compliance

CL =

A

ΔVL/(Palv – Pip) = ΔVL/PTP

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33
Q

• for polar molecules like water, surface tension is created by

A

electrostatic force

34
Q

Surfactant

production is regulated by ——— in Type II cells; —————— increases surfactant production

A

stretch receptors

deep breathing

35
Q

Lung volumes and capacities

A

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

36
Q

Minute ventilation (ml per min) =

A

tidal V x respiratory rate

37
Q

erythrocytes have a ————- transporter that moves HCO3- into plasma as it forms (see figure below).

A

HCO3- / Cl-

38
Q

Hb affinity decreased by factors associated with metabolic activity –

A

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

39
Q

↓ PO2 → increase Hb affinity for

A

CO2 as illustrated in difference in total CO2 in arterial vs venous blood

40
Q

ESRD patients have a reduced ability to

A

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.

41
Q

Contraindications for ESRD patients:

A

nephrotoxic drugs such as tetracycline, acyclovir, aspirin, NSAIDs

increased susceptibility to bleeding due to destruction of platelets

42
Q

x % of plasma filtered in bowman’s capsule

A

15-20%

43
Q

Filtration occurs due to pressure differences between the blood in the capillaries and the fluid in the capsule

A

(Starling forces).

44
Q

Glucose and amino acids are rebsorbed with

A

Na+ using symporters

45
Q

Ascending /descending limbs

Reabsorption in these segments is

A

passive

46
Q

There are two cell types in the collecting duct and late distal tubule

A

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

47
Q

Tubular fluid becomes positive when

A

Cl- reabsorbed so cations diffuse along an electrical gradient

48
Q

—– is the opposite of ADH

A

natriuretic peptides

49
Q

Increase volume sees —— in sodium reabsorption

A

decrease at all places except ATL, DT

50
Q

Factors affecting excretion of potassium include

A

plasma [K+] - increased K+ stimulates aldosterone release, and aldosterone increases Na+ K+ ATPases in principal cells

51
Q

The are three options for renal regulation of body pH that will produce urine with different pH

A
  1. decrease body pH by not reabsorbing all HCO3- ; produces an alkaline urine and acidifies body fluids
  2. no effect on body pH by reabsorbing all HCO3- ; urine has a neutral pH
  3. increase body pH by reabsorbing all and producing more HCO3- (typical); produces an acidic urine and alkalinizes body fluids
52
Q

Intercalated cells

H+ is secreted via an

A

H+ ATPase pumps and an H+/K+ ATPase pump (not illustrated)

53
Q

Ascending loop NH4+ substitutes for K+ in the

A

Na+K+2Cl- symporter and enters the interstitial fluid in the medulla where it is in equilibrium with NH3

54
Q

Because it is a polar molecule, NH4+ is

A

“trapped” in the interstitial fluid, but NH3 (being nonpolar) can diffuse into the lumen of nearby collecting ducts

55
Q

hyperventilaite

A

increase pH

56
Q

Note that a decrease in plasma pH will increase the amount of

A

free Ca2+ which can be filtered and excreted, so alkalosis can lead to hypocalcemia.

57
Q

Calcium is regulated by three hormones all of which are regulated by a calcium sensing receptor (CaSR)
found in

A

plasma membrane of cells in parathyroid gland, thyroid parafollicular cells, and cells of the proximal tubule.

58
Q

• parathyroid hormone (PTH)

A

released in response to hypocalcaemia

increases bone resorption, increases renal Ca+ reabsorption, and stimulates calcitriol production

try to keep calcium up

59
Q

in distal tubule – transcellular reabsorption of calcium

transport here can be regulated because expression of

A

Ca2+ transporters is regulated by PTH

60
Q

Thiazides – block

A

Na+Cl- symporter in early distal tubule

61
Q

K+ - sparing – two classes that both act in late

A

distal tubule and cortical collecting duct to inhibit sodium reabsorption AND potassium secretion

  1. aldosterone antagonists
  2. ENaC blockers
62
Q

↓ water reabsorption → ↓

A

Ca2+ reabsorption by solvent drag

63
Q

Loop diuretics are the most powerful of all diuretics;

A

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)

64
Q

Thiazide diuretics like chlorothiazide are secreted into the

A

proximal tubules, and they act in the early distal tubule to block the Na+Cl- transporter

65
Q
  1. aldosterone antagonists, e.g. spironolactone

block

A

aldosterone’s ability to increase Na+ transporters in principal cells

must get inside tubular cells to block aldosterone receptors

66
Q

ENaC blockers, e.g. amiloride

block

A

Na+ reabsorption across the apical membrane

these act on a membrane protein so can gain access by secretion into the proximal tubule

67
Q

3increase aldosterone —->

A

stimulate K+ secretion

68
Q

Loop and thiazide diuretics —>

A

reduced ECV à metabolic alkalosis

69
Q

potassium-sparing diuretics —>

A

metabolic acidosis because H+ secretion in distal tubule and cortical collecting duct is inhibited

70
Q

Loop diuretics increase calcium excretion by affecting the

A

transepithelial voltage that normally provides the driving force for paracellular transport of calcium.

71
Q

Thiazide diuretics stimulate

A

calcium reabsorption in the distal tubule and thus reduce excretion.
Normally, distal tubule reabsorbs 9% of filtered calcium via active transport.

72
Q

Intercalated cells are

A

ciliated i guess?

73
Q
  1. Which of the following conditions WILL NOT shift the O2-hemoglobin dissociation curve to the right?
A

C. metabolic alkalosis.

74
Q
  1. Hypoxic vasoconstriction of pulmonary blood vessels
A

A. minimizes ventilation-perfusion inequality.

75
Q

Temp increases as

A

O2 is used up - metabolic activity will raise temp.

76
Q 
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.
A

C. transpulmonary pressure.

77
Q
  1. Patients with severe, uncontrolled diabetes mellitus produce large quantities of organic acids. Which of the following will be observed in these patients?
A

A. hyperventilation and renal excretion of ammonium

78
Q
  1. Chronic diarrhea could result in
A

A. metabolic acidosis.

79
Q
  1. Erythropoietin is
A

A. regulated by hypoxia-sensitive transcription factors.

HIF

80
Q
  1. Which of the following would increase systemic blood pressure?
A

D. a drug that enhances the activity of the angiotensin-converting enzyme (ACE)

81
Q
  1. Which of the following does NOT occur in the proximal tubule?
A

C. potassium secretion

82
Q
  1. Aldosterone
A

C. stimulates the synthesis of Na+-K+ ATPase proteins in the distal tubule.

Physio Exam 3 (19 decks)

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