Sweep 1 Flashcards

1
Q

Enteric Nervous System

A

submucosal and myenteric nerve plexuses

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2
Q

e.g., CCK stimulated by ———, stimulates ——— by pancreas, which will reduce CCK and reduce pancreas activation.

A

fatty acids

enzyme production

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3
Q

e.g., CCK can stimulate pancreas, liver, gallbladder, and inhibit ——–

A

stomach emptying

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4
Q

Cephalic Phase

A

(parasympathetic nerve fibers affecting ENS)

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5
Q

Gastric Phase

A

(short and long neural reflexes and gastrin)

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6
Q

Intestinal

A

(short and long neural reflexes, secretin, CCK, and GIP)

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7
Q

Gastrin—G Cells

A

Antrum (Pyloric Gland Area)

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8
Q

Somatostatin—D cells

A

Throughout the stomach at the base of the gastric glands

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9
Q

Histamine is the strongest

A

HCl stimulant.

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10
Q

Histamine release can be triggered by

A

gastrin or Ach

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11
Q

Gastrin and Ach can have direct effects on

A

parietal cells.

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12
Q

Somatostatin is a potent inhibitor of HCl secretion via 2 mechanisms

A

Effects on G Cell

Effects on Parietal Cell

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13
Q

Enterogastrone is a hormone produced by ——- that inhibit the ——– in the stomach. Secretin, and CCK are enterogastrones.

A

intestinal cells

secretion or motility

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14
Q

Parasympathetic stimulation releases —— onto the —— and results in a ————-.

A

ACh

acinar cells

watery plasma-like secretion

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15
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
Muscarinic or α-adrenergic

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16
Q

Norepinephrine

A

Protein rich saliva
PKA-mediated exocytosis
β-adrenergic receptor

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17
Q

Lungs

e.g. convert

A

angiotensin I to angiotensin II

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18
Q

Cystic fibrosis is a disease that

A

impairs the normal function of the conducting zone

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19
Q

Cystic fibrosis

mutation in genetic code for

A

Cl- channel reduces the amount of Na+ and Cl- secreted across the epithelium into mucus.

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20
Q

Cystic fibrosis

This leads to there being

A

less water in the mucus (due to osmosis)→ mucus is thick and dry

21
Q

Between breaths:

Pip —— atmospheric pressure

A

below

22
Q

Between breaths:

Ptp =

A

Palv – Pip; lungs remain expanded
lungs tend to recoil inward –

chest wall tends to recoil outward –

net result is Pip is always subatmospheric

23
Q

During inspiration

Pip becomes

A

more negative

24
Q

During inspiration

Ptp increases so

A

lung volume increases and air flows in until Palv = Patm

25
Q

During expiration -

Pip becomes

A

less negative

26
Q

During expiration -

Ptp decreases so

A

lung volume decreases and air flows out until Palv = Patm

27
Q

Closed pneumothorax

A

pleural cavity pressure less than atm

28
Q

open pneumothorax

A

pleural cavity pressure is atm

29
Q

tension pneumothorax

A

pleural cavity pressure greater than atm

30
Q

Compliance is the inverse of

A

stiffness, and is indicative of the amount of muscle force needed to ventilate the lung.

31
Q

Forces are strong on the ——, but weak on the —— side.

A

liquid side

air

32
Q

Surface tension (ST) in bubbles cause the liquid lining to be

A

pulled toward the center (note that in a bubble there are two air/liquid interfaces).

33
Q

Surfactant is an

A

amphipathic phospholipid + protein molecule that forms a monolayer between air and water.

34
Q

Reduces surface tension by

decreasing

A

density of H2O molecules

35
Q

Surfactant does not create

A

additional surface tension and will increase compliance.

36
Q

transpulmonary pressure – dilates

A

bronchioles during inspiration

37
Q

increase R

breathe

A

more deeply (to increase ΔP)

38
Q

Increase R

breathe more slowly because

A

airflow during expiration is limited

39
Q

decrease compliance

breath shallowly to decrease

A

muscle involvement

40
Q

inspiratory reserve volume (IRV) –

A

max V inspired ; ~3000 ml

41
Q

tidal volume (TV) –

A

V entering lungs per breath; ~500 ml

42
Q

expiratory reserve volume (ERV) –

A

V exhaled beyond TV; ~1500 ml

43
Q

obstructive lung disease:

A

↓ FEV1; normal VC

44
Q

restrictive lung disease:

A

↓VC, normal FEV1

45
Q

Alveolar dead space exists when there is a mismatch between

A

ventilation and bloodflow

46
Q

Alveolar dead space is always

A

greater than zero, even in normal lungs, due to the effects of gravity on bloodflow

47
Q

Hypoventilation – ventilation

A

decreased relative to metabolism

decrease alveolar PO2
increase alveolar PCO2

48
Q

Hyperventilation – ventilation

A

increased relative to metabolism

increase alveolar PO2
decrease alveolar PCO2