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physio 3 last minute Flashcards

1
Q

myasthenia gravis

A

post synaptic autoimmune that blocks nicoitinic Ach

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2
Q

eaton-lambert syndrome

A

pre synaptic autoimmune on voltage gated Ca++ channels

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3
Q

botulinum toxin

A

pre synapic cleavage of SNAR proteins on synaptic vesicles

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4
Q

alpha bungarotoxin

A

post synaptic binding to nictonic Ach receptim

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5
Q

hemicholinium

A

inhibitss choline transport

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6
Q

what is the rate limiting step of catelones

A

tyrosine to DOPA

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7
Q

vesamicol

A

inhibits VAT

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8
Q

reseprine

A

inhibits VMAT

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9
Q

botulinum

A

inactiates VAMP fusion proteins

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10
Q

bretylium

A

inhibits VAMP

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11
Q

neostigmine

A

inhibits acetylcholinesterase

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12
Q

coacine and tricyclic antidepressent

A

inhibit NET

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13
Q

corticosterios

A

inhibit ENT

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14
Q

What are muscarinic recetpors

A

G protein coupled

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15
Q

M1 and M3

A

Gq proteins that increase Ca concen and activate PKC

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16
Q

M2

A

Gi protein that decreases cAMP concentration and PKA activity

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17
Q

nicotiniic recetpors

A

ACH dependent Na/K channels

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18
Q

alpha 1 receptor

A

activates phosphlipase C, increase IP3, DAG, PKC

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19
Q

alpha 2 receptor

A

inhibit adenylyl cyclan, decrease cAMP and PKA activity

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20
Q

beta recetpor

A

activat adenyly cyclase, increase cAMP and PKA

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21
Q

what does alpha 1 cause

A

constriction

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22
Q

what does alpha 2 cause

A

decrease insulin secretion, platete aggregation, transmitter release

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23
Q

What does beta 1 cause

A

increase HR (and other stuff in heart), increase renine release

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24
Q

What does beta 2 cause

A

dilation, relaxatino of uterus, insuline secretion, glycogenolysis

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25
Q

What is happening during P wave

A

atrial depolarization

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26
Q

What is happening during T wave

A

ventricular repolarization

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27
Q

What is happening during ST segment

A

plateau phase of ventricular AP

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28
Q

What is happening in QT interval

A

ventiruclar AP duration

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29
Q

What does long PR interval mean

A

blood in AV conductino, atrial hypertrophy

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30
Q

What does short PR interval mean

A

secondary pacemaker activity

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31
Q

What does very large and wide QRS in otherwise normal EKG

A

PVC

32
Q

What does P wave without subsequent QRS mean

A

secondary AV block

33
Q

What does QRS with no P mean

A

tertiary AV block

34
Q

How does a decreased bp affect ADH

A

increase ADH release, get renal retention of water

35
Q

How does a decreased bp affect ANP release

A

decrease release, decrease in water and Na loss

36
Q

How does low bp affect GFR

A

GFR decreases due to less blood flowing into golomerli, cause water retention

37
Q

How does low bp affect sympathetic tone

A

increase

38
Q

how does low bp affect angiotension aldosterone

A

increases angiotension II

39
Q

what does angiotensin II do

A

increase water resportion, thirt, and vasoconstriction

40
Q

Haptoglobin

A

binds free Hb that can enter the plasma after the lysis o ferthryocytes and trasport them to the liver for recycling of iron

41
Q

Where is TPO secreted from

A

liver and bone marrow

42
Q

Where is EPO produced by

A

kidneys

43
Q

What does carbonic anhydrase do

A

coverts CO2 and water into bicarb for transprot back to lungs

44
Q

MCV

A

average volume of RBCs in blood

45
Q

is erthropeiosis regulated

A

yes

46
Q

What are the componenets of the anticoagulation system

A

thrombin.thrombomodulin compelx, protein C, protein S, tissue factor inhibitor, antithrombin, and heparin sulphate

47
Q

heparin

A

binds to antithrombin, increases speed at which it degrades, inactivates thrombin.

48
Q

what does thrombin/thrombodulin complex reduce coagulation

A

these complexes bind to and activate protein C. APC interacts with prtoeitn S and this complex inactivates factors Va and VIIIa

49
Q

PAI

A

removal and deactivation of tPA to prevent removal of fibrin clots

50
Q

type II cell

A

produce surfant

51
Q

type I cell

A

cover 90-95% of slveolar surface

52
Q

equatino for laplace’s law

A

P = 2x surface tension/radius

53
Q

what is the consent for O2 binding capcity

A

1.34

54
Q

How do you calculat O2 content

A

1.34 x SaO2 + dissolved O2

55
Q

What is SaO2

A

% of heme groups bounds to O2

56
Q

How do you calculate O2 deilver

A

Cardic ouput x ((Hbx 1.34 x SaO2) + (PaO2 x 0.003))

57
Q

shift to the R

A

weaker binding, O2 lets go easilyu

58
Q

shift to L

A

tighter binding, O2 doesn’t let go

59
Q

What does fever cause

A

right shift

60
Q

what does decrease pH cause

A

right shift

61
Q

haldane effect

A

higher PO2 will shift the CO2 equilbrium down and to the right

62
Q

What are peripheral chemorecetpros most senstive to

A

O2

63
Q

What are central chemorecetpros most senstive to

A

CO2 and change in pH

64
Q

Pre bot

A

pacemaker

65
Q

DRG

A

acts on diaphragm and external intercostal

66
Q

pneumotax

A

inhibits DRG

67
Q

where is voluntary control

A

cererbral cortex

68
Q

spinal nerves

A

7, 9, 10, 11, 12

69
Q

kissmaul’s breathign

A

relentless, rapid, and deep breathing

70
Q

when is kussmauls breathing found

A

metabolic acidosis

71
Q

cheyne stokes breathin

A

ventilary oscillation with long cycle times

72
Q

when in sheyne stokes found

A

stroke, encephalopathy, heart failure

73
Q

biots breathing

A

groups of quick shallow inspirations folowed by apnea

74
Q

when is biots breathing found

A

medullary trauma, stroke

75
Q

what is ARDS assocaited with

A

sepsis, aspiration of gastric acid

76
Q

how do you diagnose ARDS

A

decrease in PaO2 that is refractory to supplemental O2 therapy

77
Q

key pathogolical feautres of ARDS

A

noncardiogenic pulomary edema
atelectsais
fibrosis

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