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Physiology > Review for test 3 > Flashcards

Review for test 3 Flashcards

1
Q

What is the effect of peptide YY?

A

Secreted from the ileum, and inhibits pancreatic secretions

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2
Q

What are the three actions of the stomach?

A

Relaxation
Churning
Emptying

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3
Q

What are the two neurotransmitters that stimulate neck cells of the stomach to secrete mucus?

A

Ach

PGs

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4
Q

What is pyloric stenosis the result of?

A

Lack of NO at pylorus

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5
Q

What is the primary controller of the cephalic phase of pancreatic secretion?

A

Vagovagal reflex

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6
Q

What is the primary controller of the gastric phase of pancreatic secretion?

A

Distension in the stomach

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7
Q

What is the primary controller of the intestinal phase of pancreatic secretion?

A

Fat on I cells, causing CCK release

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8
Q

What part of the intestines are Brunner’s glands found?

A

duodenum

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9
Q

What is the equation for TPR in the peripheral circulation?

A

TPR = dP/CO, where dP = (pressure at aorta - pressure at RA)

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10
Q

What is the equation for TPR in the pulmonary circulation?

A

TPR = dP/CO, where dP = (pressure at pulmonary artery - pressure at pulmonary vein)

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11
Q

What is the effect of NE/E on the afferent/efferent arterioles of the glomerulus?

A

Preferentially constricts afferent

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12
Q

What is the effect of adenosine on afferent/efferent arterioles?

A

Preferentially constricts afferent arteriole.

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13
Q

What stimulates FGF23 release, and what does it do?

A

high PO3 causes release. FGF23 causes increased secretion of PO3 via the kidneys, and decreases calcitriol production

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14
Q

What cells release FGF23?

A

osteoblasts

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15
Q

What is P2Y12?

A

G-protein coupled receptor that leads to platelet aggregation. –plavex inhibits this

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16
Q

What is the MOA of botulina toxin?

A

Inhibits SNAREs/SNAPs of acetylcholine release

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17
Q

What is the receptor located on sweat glands?

A

M3

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18
Q

What causes vasoconstriction of peripheral skin vessels?

A

Reduction in symp alpha2 activity

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19
Q

What is the effect of angiotensin on renal blood flow? What is the effect of ACE inhibitors?

A

Preferentially constricts efferent. Thus ACE inhibitors would decrease GFR if renal artery pressure falls below normal

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20
Q

Where are the juxtaglomerular cells found?

A

Afferent arteriole

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21
Q

What is effect of NSAIDs on GFR

A

Decreases because it inhibits prostaglandins at the afferent arteriole

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22
Q

What is FVC?

A

forced vital capacity (VC = total amount of air with inspiration)

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23
Q

What is FEV1?

A

The forced vital capacity after 1 second of maximal expiration

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24
Q

What is FEV1/FVC?

A

Amount of air that can be expelled after 1 second, as a percent of FVC

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25
Q

What happens to the TLC in obstructive lung disease? Peak flow? FEF25?

A

TLC Increases
Peak flow decreases slightly
FEF25 decreases markedly

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26
Q

What happens to the TLC in an upper airway obstruction? Peak flow? FEF25?

A

TLC remains the same
Flow reaches plateau
FEF25 decreases

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27
Q

What happens to the TLC in restrictive lung diseases? Peak flow? FEF25?

A

TLF decreases
Peak flow decreases
(everything gets smaller)

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28
Q

What is the main muscle of inspiration?

29
Q

What role does the diaphragm play in expiration?

A

Little–mostly relaxes

30
Q

How are the external intercostal arranged?

A

Superolaterally

31
Q

How are the internal intercostal arranged?

A

Inferolaterally

32
Q

Which are used for inspiration and which for expiration: internal and external intercostals?

A 
Inspiration = External intercostals
Expiration = Internal intercostals
33
Q

What are the accessory muscle of breathing? (3)

A

Scalenes/SCM
Abdominal muscles
External/internal intercostals

34
Q

What are the characteristics of asthma, in terms of reversibility, sputum production, and alveolar damage? (high, med, low).

A

Reversibility = high
Sputum production = low
Alveolar damage = low

35
Q

What are the characteristics of chronic bronchitis, in terms of reversibility, sputum production, and alveolar damage? (high, med, low).

A

Reversibility = med
Sputum production = high
Alveolar damage = med

36
Q

What are the characteristics of emphysema, in terms of reversibility, sputum production, and alveolar damage? (high, med, low).

A

Reversibility = low
Sputum production = low
Alveolar damage = high

37
Q

What are the two types of asthma?

A

Allergic

Non-allergic

38
Q

What is the one treatment that can be offered for allergic asthma, that cannot be offered for non-allergic asthma?

A

Immunotherapy

39
Q

Which is genetically acquired, allergic or nonallergic asthma

40
Q

What are the three characteristics of asthma?

A
  1. Contraction of airway smooth muscle
  2. Airway wall thickening
  3. Accumulation of secretions
41
Q

What are the two therapeutic options in treating asthma (think sympathetic and parasympathetic responses)?

A
  1. B2 stimulators (bronchodilators)

2. Anticholinergics (inhibit M3)

42
Q

What is the MOA of corticosteroids in the treatment of asthma?

A

Block leukotriene synthesis, (which cause smooth muscle contraction)

43
Q

What is the MOA of cocaine?

A

Inhibits dopamine reuptake proteins (NET)

44
Q

What is the blocker of Tyrosine hydroxylase?

A

Metyrosine

45
Q

What is the protein that stores dopamine? What inhibits this?

A

VMAT, reserpine

46
Q

What is the chemical that inhibits dopamine release?

47
Q

Long presynapse, short post = ?

Equal = ?

A

Long pre, short post = para

Equal = symp

48
Q

All presynaptic ganglia use what neurotransmitter?

49
Q

What is the neurotransmitter and receptor utilized for all somatic nerves?

A

Ach, nicotinic

50
Q

What is the neurotransmitter and receptor utilized for all presynaptic nerves?

A

Ach, Nicotinic

51
Q

What is the neurotransmitter and receptor utilized for all parasympathetic nerves?

A

Ach, muscarinic

52
Q

What is the neurotransmitter and receptor utilized for sympathetic nerves?

A

NE/E, D, alpha, or beta adrenergic receptors

53
Q

What is the neurotransmitter and receptor for sweat glands?

A

Ach, Muscarinic

54
Q

What is the MOA of alpha bungarotoxin?

A

irreversible blocking of nicotinic receptors

55
Q

What is the precursor molecule for ACh?

56
Q

What is the transporter for choline? What blocks this?

A

CHT, hemicholine

57
Q

What is the storage protein for Ach? What inhibits this?

A

VAT, vesamicol

58
Q

What is the chemical that inhibits the release of ACh?

A

Botulinum toxin

59
Q

What is the pathophysiology behind Eaton lambert syndrome?

A

Autoimmune against PREsynaptic Ca channels on motor end plate

60
Q

Stimulation of what part of the brain leads to sweating?

A

Hypothalamic-preoptic area

61
Q

What is the normal value of FEV1?

62
Q

What happens to the FEV1/FVC ratio in obstructive lung diseases?

A

Decreases because FEV1 decreases more than FVC

63
Q

What happens to the FEV1/FVC ratio in restrictive lung diseases?

A

Increases because both FEV1 and FVC decrease, but FVC decreases more

64
Q

What are the two parts of the hypothalamus that regulate body heat? What does each do?

A
  1. Pre-optic area (main body core sensor

2. Posterior hypothalamus (integrating center)

65
Q

What is the MOA of GLP1 analogues in treating DM?

A

GLP1 is normally release with insulin, and promotes it activity. Thus increase GLP1 promote insulin action

66
Q

What is the MOA of DPP4 inhibitors?

A

DPP4 normally degrades GLP1. GLP1 increases insulin action. Thus more GLP1

67
Q

What is the MOA of thiazolidinediones?

A

Increases the expression of GLUT1 and GLUT4

68
Q

What is the MOA of Sulfonylureas and meglitinides?

A

Inactivates the K pump on beta cells of the pancreas. This causes depolarization, influx of Ca, and release of insulin

Physiology (75 decks)

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