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CPR > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Where do parasympathetic preganglionic neurons originate from

A

CNs 3,7,9 (dissectible) and 10 and S2, 3 and 4

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2
Q

where do sympathetic preganglionic neurons originate from

A

spinal cord segments T1 to L2/3

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3
Q

rami communicantes - part of what autonomic substystem, what kinds and functions

A

sympathetic
white = myelinated (carries preganglionic to sympathetic chain ganglion)
gray = unmyelinated (carries postganglionic to target organ)

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4
Q

BVs get what kind of innervation and have what kind of receptors

A

sympathetic
beta 2 in skeletal muscle responds to epi (vasodilation)
alpha 1 in rest of body responds to epi/NE (vasoconstriction)

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5
Q

Resistance in series equation

A

R = R1 + R2 + R3 + …

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6
Q

Resistance in parallel equation

A

1/R = 1/R1 + 1/R2 + 1/R3 + …

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7
Q

velocity equation (with regards to BVs)

A

V = Q/A (Q = flow rate, A = cross-sectional area)

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8
Q

what percentage of blood is in veins

A

2/3

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9
Q

large arteries have high ____

A

pressure

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10
Q

arterioles have high _____

A

resistance

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11
Q

veins have high ____

A

volume

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12
Q

compliance equation

A

change in volume/change in pressure

slope of pressure to volume is compliance - stress point = end of compliance of vessel

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13
Q

over 24 hours, how much plasma leaks from capillaries?

A

1 gallon

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14
Q

Ohm’s law

A

Q (flow) = change in pressure/ resistance

resistance = pressure/flow

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15
Q

Poiseuille’s law

A

Q = (pi x deltaP x radius^4) / (8 x L x viscosity)

think of straws

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16
Q

changing radius by 15% does what to flow

A

changes flow by 50%

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17
Q

is critical closing pressure higher or lower in dilated vessels (as compared to constricted ones)

A

lower in dilated (already stretched)

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18
Q

anemia and gas exchange

A

anemia, lower hematocrit, lower viscosity, faster flow, not enough time for diffusion in capillaries – increased Re because increased velocity

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19
Q

reynolds ratio

A

determines if you’ll get turbulence (over 1,000 when branching, over 2,000 otherwise)

Re = (diamater x density x velocity) / (viscosity)

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20
Q

when you decrease diameter 2 fold, what do you do to velocity and reynold’s number

A

increase velocity 4 fold, increase Re 2 fold

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21
Q

transmural pressure

A

pressure inside - outside vessel wall

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22
Q

LaPlace’s equation

A

wall stress = (transmural pressure x radius) / (wall thickness)

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23
Q

tension equation with respect to vessels

A

tension = wall stress x wall thickness = pressure x radius

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24
Q

active congestion

A

hyperemia with inflammation - arterial active congestion - tissue becomes redder, fills with oxygenated blood, inflammation, increased blood flow

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25
Q

passive congestion

A

venous, when you blocked the venous return to heart, increased blood volume in vascular spaces and increased hydrostatic pressure in capillaries. deoxygenated blood, becomes hypoxic

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26
Q

acute pulmonary congestion

A

lots of blood, result of MI, lots of RBCs, diestended capillaries, congestion and edema

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27
Q

chronic heart failure and lung pathology

A

increased pressure in capillaries which rupture into alveoli, macrophages take up RBVs and contain hemosiderin (heart failure cells)

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28
Q

liver congestion

A

seen with right heart failure because of blood flow from portal vein to liver. hepatocyts around central vein are last to be perfused and become degenerated

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29
Q

splenic congestion

A

due to backup from portal vein from liver leading to splenomegaly

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30
Q

signs of inflammatory edema

A

redness, warmth, swelling, protein rich exudate

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31
Q

non-inflammatory edema causes

A

increased capillary hydrostatic pressure, decreased plasma oncotic pressure, obstruction, hypervolemic state

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32
Q

how much of sudden blood volume loss will send you into shock

A

40%

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33
Q

muscarinic receptors - structure, coupling, response

A

G-protein coupled, respond to Ach, slow response via second messenger cascade (cAMP, phospholipase C

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34
Q

M2 and M4

A

contracts GI SM by inhibiting AC and decreasing cAMP through Ga(i)

slows heart rate in SA node by opening I channels via hyperpolarization through K+ channels

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35
Q

M1, M3 and M5

A

cause ciliary muscle contraction via stimulation of phospholipase C and increasing Ca2+

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36
Q

nicotinic Ach receptors

A

Nn - neuronal - permeable to Na+, K+ and Ca2+

Nm - skeletal muscle - only alpha1

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37
Q

muscarinic agonists (2) and uses

A
  • carbachol (eye drops only - nicotinic at high doses)
  • bethanechol

overcoming postoperative paralytic ileus, urinary retention and glaucoma

NOT metabolized by acetylcholinesterase

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38
Q

muscarinic antagonists (2) and uses

A

atropine (crosses BBB, preanesthetic for intubation)

ipratropium (NO BBB crossing, used for COPD bronchodilation)

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39
Q

nicotinic agonists (3) and uses

A

trimethaphan (use for acute dissecting aortic aneurysm to rapidly control BP)
vecuronium (skeletal muscle blocker - use in surgery, reversed by neostigmine)
succinylcholine (use for rapid sequence induction endotracheal intubation, causes fasciculations, metabolized by cholinesterase - no neostigmine)

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40
Q

indirect nicotinic agonists (5) and uses

A

edrophonium (diagnose myasthenia gravis)
neostigmine (treat myasthenia travis, give with atropine to reduce muscarinic receptor activation)
physostigmine (used for miotic glaucoma, crosses BBB, otherwise same as neostigmine)
donepezil (treatment for alzheimers)
sarin (nerve gas, irreversible anticholinesterase)

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41
Q

botulinum toxin mechanism

A

binds presynaptic membrane receptor, endocytoses, cleaves SNAP-25, which is required for release, and thus blocks Ach release from cholinergic nerve

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42
Q

catecholamines list (5)

A 
epinephrine
norepinephrine
isoproterenol
dopamine
dobutamine
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43
Q

alpha agonists

A

phenylephrine and ephedrine (Also beta agonist)

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44
Q

beta 2 agonists

A

terbutaline

albuterol

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45
Q

heart has what kind of adrenergic recetpors

A 
BETA 1 (be my number 1)
causes increased rate
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46
Q

BVs have what kind of receptors

A

all have alpha 1 for constriction, skeletal muscles have beta2 for dilation

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47
Q

what drug would you use for bronchial asthma

A

terbutaline (beta 2 agonist)

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48
Q

what drug would you use for cardiogenic shock

A

dopamine (catecholamine)

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49
Q

what drug would you use for heart failure

A

dobutamine (Catecholamine)

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50
Q

what drug would you use for rhinitis

A

phenylephrine (alpha agonist)

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51
Q

what drug would you use for hypertension

A

guanethidine (inverse agonist - looks like NE, gets stored in vessicles as NE gets eaten by MAO)

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52
Q

what drug would you use for angine pectoris

A

propranolol (Beta blocker)

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53
Q

what drug would you use for supraventricular arrhythmias

A

propranolol (Beta blocker)

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54
Q

feedback for NE

A
  • alpha 2 on presynaptic provides negative feedback
  • heteroreceptor PGE2 if released from another neuron will neg feedback NE release
  • angiotensin receptor gives boost to NE release
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55
Q

beta 1 receptors are coupled to…

A

Gs - stimulates AC, increases cAMP

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56
Q

alpha 2 receptors are coupled to…

A

Gi - inhibitory, decreases cAMP

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57
Q

alpha 1 receptors are coupled to…

A

Gq, causes Ca2+ increase and PKC

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58
Q

guanethidine

A

used for BP

looks like NE, gets stored in vessicle, MAO eats up NE, lowers bp because guanethidine doesn’t react with receptors

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59
Q

reserpine

A

used for BP, no transporter needed, binds to NE transporter that brings NE into vessicle, resulting in empty vessicles and no NE release

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60
Q

MAOI

A

inhibits MAO, gives NE more of a chance to get stored, dumps out more NE, only trying to elevate in the brain, but also raises BP

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61
Q

amphetamine

A

utilizes NE transporter, looks like NE, displaces NE, gets dumped outside, can result in hypertensive crisis (facilitated exchange diffusion)

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62
Q

tyramine

A

get it from diet (wine, cheese, fava beans), digested by MAO, displaces NE by getting into transporter, can get hypertensive crisis if on MAOI

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63
Q

cocaine

A

raises dopamine levels, but not specific for dopamine and also causes hypertensive crisis by raising NE levels by blocking NE transporter

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64
Q

imipramine

A

does same thing as cocaine, it’s a tricyclic antidepressant

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65
Q

atomoxetine

A

ADD med. like cocaine

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66
Q

phenylephrine

A

for rhinitis, agonist, works directly at alpha receptor, causes downregulation

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67
Q

isoproterenol

A

beta agonist, downregulates receptor

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68
Q

propranolol

A

beta blocker, antagoinst, upregulates receptors

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69
Q

phentolamine

A

alpha blocker, antagonist, upregulates receptors

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70
Q

NE likes to bind to…

A

the 1’s - alpha 1 and beta 1

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71
Q

ISO likes to bind to…

A

Betas

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72
Q

E at low levels binds to…

A

betas

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73
Q

E at high levels binds to…

A

alpha 1 and betas

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74
Q

dopa at low levels binds to…

A

DA and beta1

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75
Q

dopa at high levels binds to…

A

everything

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76
Q

dobutamine at low levels binds to

A

beta 1 contractility

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77
Q

dobutamine at high levels binds to…

A

alpha 1 and beta 2

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78
Q

alpha stimulators do what and examples (2)

A

used for decongestion of mucous membranes, raise BP, dilate pupils, eye drops

phenylephrine and ephedrine

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79
Q

beta stimulators do what and examples (2)

A

stabilize mast cells, open airways (beta2), relax pregnant uterus

albuterol and terbutaline (selective beta2)

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80
Q

caffeine

A

resembles sympathetic receptors stimulation - accumulation of cAMP, keeps cAMP high, wakes you up (theophylline dilates bronchi)

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81
Q

where do you see lines of Zahn

A

large arterial and mural thrombi (white layers = platelets, dark lines = RBCs)

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82
Q

channels in SA node

A

I (f), Ca2+, TEA K

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83
Q

ventricular channels

A

voltage gated Na+, voltage gated Ca 2+, TEA K and K1

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84
Q

a type baroreceptors

A

react to both mean pressure increases AND rapid pressure changes

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85
Q

c type baroreceptors

A

react (slower) to mean pressure increases

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86
Q

trigeminal cardiac reflex

A

decreases HR by increasing para to heart and symp to BVs - preserve cardiac demand by slowing heart rate but constricting everywhere

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87
Q

cushing reflex

A

ischemia in brain - increase BP by withdrawing para, increasing symp

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88
Q

tracheal epithelium

A

PCC with goblet cells, brush cells with microvilli, APUD cells with basal granules, mixed serous and mucus glands

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89
Q

bronchial epithelium

A

same as trachael, but PCC are not as tall

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90
Q

bronchiole epithelium

A

have club cells (that secrete surface active materials and club cell secretory proteins that increase in blood and decrease in lavage during COPD) no cartilage, NO goblet cells, thin layer of SM

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91
Q

terminal bronchiole epithelium

A

less ciliated, more club, no alveoli yet

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92
Q

respiratory bronchiole epithelium

A

some alveoli - gas exchange can happen, ciliated cells are fewer and shorter

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93
Q

alveoli epithelium

A

squamous type 1 (95%) - thin, flattened, for gas exchange
cuboidal, septal type 2 cells, for synthesis and secretion of surfactant (5%)
tight junctions in between them

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94
Q

how much space is in between air space and blood?

A

0.1 micrometer

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95
Q

surfactant - compostiion

A

phospholipid protein with carbohydrate component,

made from type 2 cells combining amino acids, choline, glucose and fatty acids

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96
Q

type 2 cellular comonents

A

lots of SER, RER and gogli

contain multilamellar bodies - vessicles with surfactant in them that look like plasma membrane inside them

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97
Q

atelectasis

A

collapse of alveoli

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98
Q

what are the rudiments that form lungs

A 
respiratory diverticulum (foregut, endoderm)
splanchnic mesoderm

interact via reciprocal induction

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99
Q

what does splanchnic mesoderm become?

A

lamina propria, mural cartilate, SM, CT, BV and lymph

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100
Q

what does bone marrow make in the resp develpment

A

phagocytes

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101
Q

what does NCC make in resp development

A

APUD cells, but they may be endodermal

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102
Q

histogenesis stages of lung development

A
  1. pseudoglandular period (5-16 weeks)
  2. canalicular period (16-26 weeks)
  3. terminal sac period (26-term)
  4. alveolar period (32-childhood)
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103
Q

what happens in pseudoglandular period

A

between 5-16 weeks. terminal bronchioles, no respiratory bronchioles, no blood cell development, not viable at this age

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104
Q

what happens in canalicular period

A

16-26 weeks
some respiratory bronchioles, some alveolar ducts, have type 1 and type 2, possibility of gas exchange, but BVs are too far away - can’t survive well

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105
Q

what happens in terminal sac period

A

26-term
have type 2 and alveolar sacs
BVs are close, so babies can breathe, but might have RDS early on

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106
Q

what happens in alveolar period

A

32-childhood

BVs intimately related, many type 2

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107
Q

RDS - when does it happen

A

most common death in premature babies - severe prior to 28 weeks (Before type2 development and surfactant production)

AKA Hyaline Membrane Disease

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108
Q

presentation of babies with RDS

A
  • cyanotic (blue)
  • low pO2, high pCO2
  • tachycardic
  • grunting, difficulty breathing
  • clavicular depression
  • dense lungs on CXR
  • transudate layer on alveoli because of high blood flow but no surfactant - HYALINE membrane
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109
Q

what to do to prevent premature labor

A

bed rest and glucocordicoids

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110
Q

why test amniotic fluids in women who might give birth prematurely

A

can measure surfactant production by looking at lecitin and comparing it with sphingomyelin which remains at baseline - get a ratio of L/S - higher is better

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111
Q

what to give baby who was born prematurely

A

right level of O2 (not too much, causes blindness), artificial surfactant in aerosol

once air gets in, type 2 will differentiate (first couple days are dicey, gets better with time)

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112
Q

accessory muscles for inspiration

A

sternocliedomastoid
external intercostals
scalenes

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113
Q

accessory muscles for expiration

A

abdominal

internal intercostals

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114
Q

lung compliance equation

A

compliance = change in lung volume/ change in interpleural pressure

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115
Q

do stiff lungs have higher or lower compliance than normal

A

stiff lungs have reduced compliance because they take more pressure to fill a certain volume

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116
Q

hysteresis

A

difference seen in graphing lung inflation and deflation with air - not seen when lung is filled iwth saline - takes more pressure to inflate lung and keep it there, than it does to deflate it

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117
Q

at the beginning of inspiration - before any air enters - what is alveolar pressure and interplural pressure

A

alveolar pressure is atomospheric pressure, or zero, and interpleural is negative (example -5)

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118
Q

what is the transpulmonary pressure at rest

A

+5 –> alveolar minus pleural (0- -5 = +5)

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119
Q

what is transpulmonary pressure at the beginning of inspiration

A

+7.5 –> at first, alveolar dips with pleural, and creates drive for air to enter

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120
Q

what is alveolar pressure at the end of inspiration

A

0 again - because air has reached the alveoli

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121
Q

what happens to alveolar pressure at beginning of expiration

A

becomes positive, and pleural pressure becomes more postive (still negative). so pressure in alveoli is higher than in the mouth, so air moves out to equalize

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122
Q

diaphragm contraction does what to transpulmonary pressure

A

increases

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123
Q

diaphragm relaxation on expiration does what to transpulmonary pressure

A

decreases

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124
Q

what are the two factors that contribute to compliance factors of the lung

A
  1. tissue forces (elastic properties of CT) - area above the expiratory curve
  2. surface forces - area between expiratory and inspiratory curves
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125
Q

surfactant and surface tension

A

alters surface tension depending of volume of surface

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126
Q

pressure required to keep a sphere open

A

P = 2x surface T/ radius

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127
Q

surface tension in a small balloon is _____ than a large baloon

A

higher

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128
Q

functional residual capacity

A

point at which pressure from chest wall is the opposite but equal to lung pressure

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129
Q

relationship between elastic recoil and compliance

A

stiff rubberband has high elastance - high recoil, but low compliance

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130
Q

how many branch points before you see alveoli

A

16-18

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131
Q

flow equation

A

V = delta P/R

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132
Q

poiussel’s law solving for R

A

R = 8 L viscosity / pi r^4

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133
Q

is resistance higher in central airways than smaller airways? or lower?

A

higher, because surface area is larger in smaller - resistance in parallel instead of series

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134
Q

at which level is resistance the highest?

A

at 4th generation of airways in conducting zone

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135
Q

what does vital capacity mean

A

ventilatory reserve - what we can call upon for max ventilation of the lung

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136
Q

the lower the lung volume the ______ the airway resistance, why?

A

higher because radius of alveoli enlarges

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137
Q

people who have narrowing of airway, such as in asthma or COPD, is it harder to get air into lungs or out of lungs?

A

harder to get air out because airways are narrowing even more upon expiration, so you see increase in residual volume - air trapping, that can’t be pushed out at lower lung volumes

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138
Q

what controls airway smooth muscle tone

A

beta 2 adrenergic - dilation (helped by bronchodilator drugs)
vagus nerve cholinergic - background constriction tone
(can use anticholinergic to dilate airways)

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139
Q

equation of motion, solving for pressure

A

P = (volume / compliance) + (flow x resistance)

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140
Q

work of breathing equation

A

W = P x V

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141
Q

what is ventilation, where does it occur

A

bulk movement of flow of air through conducting airways. slows as it goes further down, and at terminal bronchioles, no longer bulk flow (pressure equalizes), but diffusion for gas exchange

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142
Q

what is the average tidal volume

A

500mL

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143
Q

what is normal breathing frequency

A

12-15 breaths per minute

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144
Q

what is dead space ventilation?

A

movement of air that never reaches repiratory airways - in anatomic dead space. first air that you expire thus has a high amount of O2 because it doesn’t participate in gas exchange

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145
Q

how large is the anatomical dead space

A

150mL

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146
Q

how much gas in in alveoli

A

3000mL - takes a couple minutes for all O2 in reservoir to be depleted - allows you to hold breath without dying

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147
Q

effective alveolar ventilation equation

A

ventilation = frequency x alveolar inspiration
= 15 breaths/min x 350mL — just over 5,000mL of effective alveolar ventilation each minute, which about mirrors cardiac output of 5,000mL flowing through the lung —- ventilation is matched to perfusion

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148
Q

how to estimate someone’s anatomical dead space

A

= lead body weight in pounds

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149
Q

tidal volume equation

A

VT = VD (anatomical dead space volume) + VA (alveolar volume)

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150
Q

minute ventilation equation

A

amount through the mouth each minute
VT x frequency = (VD x frequency) + (VA x frequency)
AKA
V(.)expired = V (.)D x V(.)A

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151
Q

what is physiological dead space, how to estimate

A

includes anatomical dead space plus alveoli that aren’t able to exchange gas (blocked by clot etc.)

can use CO2 in the blood to calculate physiological dead space:

VD = VT x (ParterialCO2 - PexpiredCO2) / ParterialCO2

REMEMBER - when measuring Pexpired, you can’t use first 150-200mL, you have to measure the alveolar expired air

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152
Q

Bohr’s equation, and normal value

A

measures physiological dead space

VD/VT = (ParterialCO2 - PexpiredCO2) / ParterialCO2

normal range: 0.2-0.35
higher is indicative of physiological dead space increase

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153
Q

stress

A

something that disrupts homeostasis, pressure to adapt

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154
Q

acute stress

A

fight/flight/freeze - automatic and autonomic survival response that can have pathogenic processes, especially if repeated

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155
Q

chronic stress

A

endocrine involvement - can get long term medical effects. what causes it? subordinate status, lacking control, (discriminatory status for poverty)

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156
Q

traumatic stress

A

threat to survival for self or close others, threat to things that give life meaning, mix of autonomic and neuroendocrine response

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157
Q

what happens in the cortical and limbic areas with regards to stress

A

cortex ascribe meaning to things, and can suppress or exaggerate the emotional (limbic) stress response

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158
Q

limbic structures and stress

A

amygdala - tiny cluster of cells, connects to hippocampus (where working memory forms) which connects to prefrontal cortical tissues. triggers hypothalmus reflexively

hypothalmus - secretes secretoryhormones that go to pituitary which secretes stimulating hormones to end organs, cortisol feeds back and shut it down

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159
Q

chronic stress and atherosclerosis

A

increased floating metabolites like glucose and cholesterol - clogs up arteries

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160
Q

systemic coritsol responses (4)

A

increases IL-6
increases white cell count
prevents storage and mobilizes nutrients
terminate adrenergic response

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161
Q

chronic cortisol effects and disease

A

autoimmunity, cancer, infections, metabolism disorders (obesity, diabetes)

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162
Q

physiologic changes with traumatic stress

A

amygdala gets big enough to image, hippocampus shrinks, can be reversed

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163
Q

U curve

A

certain amount of stress is necessary for development, overwhelming stress can impede development

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164
Q

cognitive distortion

A

making generalized comments personal, catastrophizing events, negative prediction, underestimation of ability to cope

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165
Q

3 levels of psychological defenses

A

1- primative (denial of reality)
2- immature (displacement)
3- mature (realistic)

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166
Q

is denial always bad?

A

no, patients with denial in ICU had better outcomes - only in certain contexts

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167
Q

stress and development

A

early stress can make permament changes genetically and physiologically (cns and endocrine)

can increase sucseptibility to disease later on

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168
Q

stress in the elderly

A

more memory but less reserve
more resilient but have more stressors (loss, pain, etc.)
frailty with existing disease
allostatic load - stress that leads to wear and tear

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169
Q

homeostenosis

A

reserve that helps maintain homeostasis in youth declines over time

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170
Q

what determines rate of homeostenosis

A 
genetics (telomer length)
environment
food
oxidative stress
aging
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171
Q

frailty and homeostenosis

A

frailty is point in homeostenosis decline at which someone becomes more at risk for illness and rapid decline

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172
Q

seratonin

A

modulator of NE and E and dopa in brain

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173
Q

common antidepressants

A

zoloft, prozac, paxil - used as antianxiety

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174
Q

functional residual capacity (FRC)

A

= expiratory reserve + residual volume (That can’t be expired)

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175
Q

inspiratory capacity

A

= tidal volume + inspiratory reserve

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176
Q

vital capacity

A

= expiratory reserve + inspiratory capacity

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177
Q

gas dilution method

A

indirectly measures residual volume by finding FRC: measures the total volume by measuring change in nitrogen (using 100% O2) or amount of helium (C1 x V1 = C2 (V1 +V2))

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178
Q

body plethsmography

A

indirectly measures residual volume by measuring FRC -
measure changes in pressure in a box in which the patient is sitting and panting – THIS IS more sensitive than gas dilution (Better for people with airways disease)

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179
Q

normal reserve volume percentage

A

25-35%

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180
Q

total lung capacity percentage in restrictive conditions (less compliance)

A

reduced below 80% normal lung capacity

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181
Q

flow thermister

A

can measure volume compartments, which shows you about compliance

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182
Q

forced vital capacity maneuver, why is it useful

A

volume vs time curve - measure volumes, the same as slow vital capacity maneuver, except for people with airways diseases, the added pressure of forced exhalation will cause collapse and decreased volume being exhaled as it would be in slow

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183
Q

what percentage of vital capacity will a normal person expire in 1 second doing forced vital capacity

A

at least 70%

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184
Q

what is midflow and what is its significance

A

FEF - forced expiratory flow -midflow = FEF slope measured between first quarter and 3rd quarter of forced expiration
if there’s a normal ratio, but low midflow, and then give bronchodilator and the midflow increases - indicative of small airways diseases and air trapping (asthma will correct, COPD will not)

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185
Q

volume time graph for obstructive disorders

A

decreased vital capacity, and proportionatly lower FEV1 - around 40%

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186
Q

volume time graph for restrictive (low compliance) disorders

A

deceased vital capacity, proportionaly higher FEV1 - around 90%

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187
Q

flow-volume loop

A

measures both inspiration (Can detect upper airways issues like tracheal tumor) and expiration.

shows that max flow is right at beginning of expiration when lung is near max inflation (resistance it as its lowest and driving pressure is highest - forced maneuver)

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188
Q

why does the flow-volume loop graph taper out linearly

A

there is limiting flow at low lung volumes - called equal pressure point. When you have increased intrapleural pressure (with forced expiration), when that pressure is equal to the pressure within the lungs, the airway narrows, and it does so at the same point regardless of the initial intrapleural pressure - as long as it’s positive with forced expiration.

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189
Q

what does flow-volume loop graph look like with obstructive disease

A

concavity in the taper - higher than normal resistance, airways collapse quickly (emphysema)

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190
Q

what does flow-volume loop graph look like with restrictive disease

A

compliance issue - like insterstitial lung disease - you see very rapid fluctuation of flow - relatively small peak and quick decline (tall steep mountain)

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191
Q

what qualifies as reversibility (asthma)

A

12% improvement of FEV1 and FVC and at least 200mL absolute change in these parameters

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192
Q

what is allowed deviation for normal lung volume fluctiation

A

20% on either direction - between 80% and 120% is okay.

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193
Q

examples of obstructive ventilitory diseases

A

asthma, COPD, chronic bronchitis, bronchiectasis, cystic fibrosis, emphysema

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194
Q

examples of restrictive ventilatory diseases

A

interstitial lung disease, chest wall disease, pleural disease, space occupying intrathoracic lesion, extra-thoracic conditions (obesity, pregnancy etc.)

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195
Q

what value is significant if obesity is the cause of the restriction?

A

ERV will be more reduced than others

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196
Q

diffusion of the lung test measures what

A

if alveolar membrane is intact or compromised (anemia can also affect these values)

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197
Q

what pO2 do you want to keep your patients above

A

60 - above pO2 of 60, the curve flattens out (correlates to a pulseox (hem saturation) of 90%)

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198
Q

what is the pO2 at 100% hem saturation

A

120

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199
Q

what is pO2 at 50% hem sat

A

27

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200
Q

altitude and symptoms related to hypoxia at 90% O2 sat

A

corresponds to altitude of 10,000ft

decreased night vision, high altitude pulmonary edema

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201
Q

altitude and symptoms related to hypoxia at 80-89% O2 sat

A

10,000-15,000 ft

drowsiness, poor judgement, impaired coordination and efficiency

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202
Q

altitude and symptoms related to hypoxia at 70-79% O2 sat

A

15,000-20,000 ft

impaired handwriting, speech, vision, memory, judgement, intellect, pain sensation

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203
Q

altitude and symptoms related to hypoxia at below 69% O2 sat

A

over 20,000 ft

circulatory failure, CNS failure, convulsions, cardiovascular collapse and death

204
Q

what is pO2 change as you go from arterial side after lungs, to venous side normally (AKA after unloading in tissues)

A

40 (corresponds to 75% hem sat - loss of one O2 molecule into tissue)

205
Q

left shift and O2 affinity (what are the surrounding environmental factors - pH, pCO2, temp, 2,3 DPG)

A

left shift = higher affinity (good in lung)

higher pH, decreased temp, less pCO2, less 2,3 DPG

206
Q

right shift and O2 affinity (what are the surrounding environmental factors - pH, pCO2, temp, 2,3 DPG)

A

right shift = lower affinity (good in tissue)

decreased pH, increased temp, increased pCO2, increased 2,3 DPG

207
Q

2,3 DPG changes slowly or fast?

A

slowly - has to do with altitude

208
Q

what else moves the curve to the left (pathological)

A

carbon monoxide and

methemoglobin

209
Q

does fetal hemoglobin have higher or lower affinity - right or left shift?

A

left shift = higher affinity

210
Q

acute respiratory distress syndrome - what do you see on CXR and labs

A

white stuff in lungs, lungs aren’t efficient - right shift

pO2 is 40 (should be 90-100) in arteries is 48, pCO2 (should be around 40) pH is low

211
Q

what should you do for this patient with ARDS immediately

A

give him bicarb to bring back his pH to 7.40 (is 7.20 now)

212
Q

difference between ARDS and climbing mount everest

A

pO2 was 28 on top of mount everest, but pH was 7.70 (difference between ARDS is here pH is higher, left shift)

213
Q

oxygen carrying capacity (bound to hemoglobin)

A

how many mL of O2 per gram of hemoglobin — 1.39 mL

214
Q

what is O2 solubility coefficient (dissolved in plasma)

A

0.0031

215
Q

arterial O2 content equation

A

= (1.39[Hb] x SarterialO2) + (0.0031 x ParterialO2)

216
Q

venous O2 content equation

A

= (1.39[Hb] x SvenouslO2) + (0.0031 x PvenousO2)

217
Q

systemic oxygen delivery equation

A

= arterial O2 content x cardiac output x 10

218
Q

Fick’s principle for tissue O2 consumption

A

= cardiac output x (arterial O2 content - venous O2 content)

219
Q

does it matter where you measure arterial O2 content?

A

no

220
Q

does it matter where you measure venous O2 content?

A

yes - different organs require different amounts of O2, or during exercise etc.

so we measure mixed venous blood in pulmonary artery

221
Q

what are usual values for PO2 and PCO2 in arteries

A 
pO2 = 100
PCO2 = 40
222
Q

what are normal values for pO2 and pCO2 in mixed venous blood

A 
pO2 = 40
pCO2 = 45
223
Q

extraction ratio

A

= O2 consumption/ O2 delivery

at rest around 20%
may rise to about 80% during exercise

224
Q

what determines how much O2 gets exchanged in capillaries?

A

PO2 in cappilaries

225
Q

what is the effect of anemia on the oxygen dissociation curve

A

no effect

226
Q

what curve does anemia effect?

A

oxygen CONTENT curve

227
Q

how are the anemia content curve and CO content curve similar

A

both start at half arterial O2 content and both have high or normal pO2

228
Q

how are the anemia and CO content curves different

A

difference in how they fall - CO ends up with much lower mixed venous pO2 - CO doesn’t have enough pressure to get O2 from capillary into tissue, but anemia does (not as efficient, but possible)

229
Q

what cell does not produce CO2

A

RBC - no TCA cycle

230
Q

what are the two sources of CO2?

A

aerobic metabolism (glucose, TCA, oxygen transport etc)

anaerobic metabolism (lactate and bicarb)

231
Q

mechanisms of CO2 transport

A
  1. dissolved in plasma (5%)
  2. bicarbonate buffer system (85%)
    - fast process in RBC (chloride shift), slow in plasma
  3. bound to Hb as carbamino-Hb (10%)
232
Q

CO2 content curve (not used clinically)

A

extra CO2 is released in the lungs - causes the curve to drop more than expected

233
Q

greater the ventilation the ____ the pCO2

A

lower

234
Q

an acute change of PCO2 by 10mm Hg results in reciprocal change in blood pH of _____

A

0.08 units

235
Q

what’s the ideal atmospheric oxygen partial pressure

A

160 mmHg (at sea level)

236
Q

what’s the partial pressure of water vapor in the air

A

47 mmHg

237
Q

what’s the real atmospheric oxygen partial pressure in DC

A

150 mmHg
=O2% x (Patm - Pwater)
=0.21 x (760 - 47)

238
Q

alveolar air equation

A

alveolar PO2 = %O2 x (Patm - Pwater) - ParterialCO2/0.8

in DC,
= 150 - (ParterialCO2/0.8)
= 150 - (40/0.8)
= 100 mmHg

239
Q

diffusion capacity for O2 (From alveoli to BV) equation

A

DLO2 = rate of O2 uptake / (PalveolarO2 - ParterialO2)

240
Q

alveolar arterial oxygen gradient equation

A

alveolarPO2 - arterialPO2

241
Q

what’s an abnormal value for alveolar arterial oxygen gradient

A

1/2 patient’s age

if larger, it’s abnormal

if gradient is more than 30 it’s abnormal

242
Q

what is the ideal ratio of alveolar air ventilation to lung blood perfusion

A

1:1

243
Q

what does “shunted” mean in terms ventilation/perfusion ratio

A

V = 0, so V/Q = 0 (will be the same as venous blood)

244
Q

what is normal ventilation/perfusion rate

A

1 (because alveolar ventilaion is around 5,000, and so is cardiac output)

245
Q

what is ventilation/perfusion rate in trachae

A

happens in physiological dead space. infitinty, because as much as V increases, there is no Q

246
Q

3 zones of the lung

A 
zone 1 (doens't exist in normal lung - very top, no blood flow, V/Q >>1)
zone 2 (flow depends on pressure difference between artery and arteriole, V/Q >1)
zone 3 (bottom of lung, flow depends on the difference between the artery and the vein, V/Q
247
Q

most blood goes to areas of the lung with what V/Q ration

A

1:1

248
Q

in what disease do you see shunting

A

ARDS (everything else is considered V/Q mismatch)

249
Q

in people with lots of shunting, when you increase FiO2, what happens to the PO2

A

only increases a little bit

250
Q

which has more shunting, pneumonia in lower lung, or upper lung

A

lower lung, because have more blood flow - more perfusion, but no ventilation because there’s fluid in the way

251
Q

how far does blood have to traverse through the alveolar capillary to exchange most of O2 and CO2

A

1/3

252
Q

what pathologies do you see for asthma on histology

A
  1. airway inflammation (eosinophils, mast cells)
  2. goblet cell metaplasia
  3. mucous gland hyperplasia (increase sterile, eosinophilic “allergic” mucus)
  4. airway muscular hypertrophy
253
Q

hypoxemia vs hypoxia

A

hypoxemia is low O2 in blood, hypoxia is low oxygenation in alveolar spaces

254
Q

how to quantitate SM hyperresponsiveness

A

methylcholine challenge - increase doses, repeat spirometry, high enough methylcholine will cause SM contraction. so for asthmatics, the reaction will be super early (greater than 20% fall) because already primed

255
Q

atopic asthma presentation/characteristics

A
  • childhood onset
  • family history
  • preceded by allergic rhinitis, urticaria or eczema
  • triggered by environmental antigens
  • positive prick skin tests
256
Q

intrinsic asthma presentation/characteristics

A
  • mechanism less clear (maybe viral or air pollutants)
  • more severe hyperresponsiveness and sustained
  • no family history, allergic prick skin tests, normal IgE
257
Q

respiratory viruses leading to hyperreactivity and inflammation - characteristcs of presentation

A

RSV and rhinovirus

  • last 4 weeks
  • neutrophilic response
  • increased IL8, GM-CSF, RANTES
  • potentiates eosinophilic airway inflammation
258
Q

confounding conditions to asthma

A

sleep apnea, GERD, sinusitis, ABPA (allergic bronchopulmonary aspergillosis)

259
Q

why are symptoms worse at night

A

more constricting tone at night because of circulating bronchodilators (adrenergics) are low

260
Q

4 key symptom expressions of asthma

A
  • daytime asthma symptoms
  • how frequently you wake up at night because of symptoms
  • frequency of use of short acting beta agonist
  • if it’s limiting daily activity
261
Q

how long should an albuterol inhaler last?

A

1 year

262
Q

what clinical findings present with pneumonia (4)

A
  • fever
  • tachypnea
  • tachycardia
  • consolidation on chest exam
263
Q

what would you give for pneumonia?

A

oral azithromycin

264
Q

besides CXR, what would you do for pneumo in hospitalized patients

A
  • blood culture
  • sputum gram stain and culture
  • urine antigen test for pneumococcus and legionella
265
Q

what bacterial pathogens commonly cause community acquierd pneumo (6)

A
  • strep pneumo
  • h flu
  • mycoplasma pneumo
  • chlamidophila pneumo
  • legionella
  • stauph aureas
266
Q

what bacterial pathogens would you see in COPD patient causing pneumonia (2)

A
  • moraxella

- gram negative rods

267
Q

what viruses cause penumonia

A
  • influenza
  • adenovirus
  • RSV
  • parainfluenza
  • MERS/SARS
268
Q

prognosis for community acquired pneumonia

A 
C - confusion
U - BUN>19 mg/dL
R - RR >30/min
B - BP <90/60
65 - over 65y/o

score >1 = hospitalized

269
Q

for someone who has comorbitidies or use of antibiotics in past 3 months, what do you give for pneumonia

A

beta lactam + macrolide (amox/clavulanate)

or respiratory quinolone

or ceftriaxone, cefotaxime or cefuroxime

270
Q

how long do you treat community acquired pneumonia for?

A

7-10 days

271
Q

reasons for lack of response to CAP treatment

A

resistance
wrong drug/wrong dx
comorbidities
spread to empyema or lung abcess

272
Q

causes of acute bronchitis

A

viral (influenza, parainfluenza, RSV, corona, rhino, adenovirus)

nonviral (mycoplasma pneumo, chlamydophila pneumo, bordatella)

273
Q

what can cause pharyngitis (in adult) - 5

A 
group A strep
adenovirus
EBV
CMV
neisseria gonorrhoeae
diptheria
274
Q

tx for antrhax

A

cipro and clinda

PLUS mAb

275
Q

what are the central rhythm generators

A

pons and medulla

276
Q

what can supercede central rhythm generators

A

cortical influence (like in exercise, or conscious influence)

277
Q

periperhal chemoreceptors sense mainly ____ central sense _____

A

O2, CO2

278
Q

GROUPS in the medulla

A

dorsal and ventral respiratory group

279
Q

dorsal group is responsible for____ and what are the outputs

A

inspiration

output 12-15/min (RR) for 1-2 sec each and then ceases - to diphragm and external intercostals

280
Q

ventral group is reponsible for ____ and what are the outputs

A

expiration

output is normally silent, active during stress and heavy exercise - to abdominal and internal intercostal muscles

281
Q

dorsal is also commonly referred to as

A

pacesetting center

282
Q

apneusic center is caused by a cut at what level in brainstem/medulla/pons and is responsible for what

A

cut at level 2 in mid pons and vagus cut too
apneustic breathing - deep inspiration until stretch receptor -
without check by pneumotaxic center

283
Q

what suppresses rhythmic activity in medulla

A
  1. drugs (alchohol, benzons)
  2. increased intracranial pressure
  3. acute poliomyelitis
284
Q

where are central chemoreceptors located

A

in retrotrapezoid nucleus (RTN) in ventral medulla

285
Q

arterial pCO2 control over medullary respiratory center (2 varieties)

A

normal increase (45 mmHg) causes activation of medullary respiratory center

high increase (when pCO2 > 70-80 mmHg) in inhibits

286
Q

relationship between O2 levels on pCO2 and ventilation curve

A

when hypoxic, the slope is steeper and left shifted - lowering threshold and more sensitive response

287
Q

other factors that left-shift CO2 response curve (2)

A

acidosis and exercise - although those are only threshold changes, not stronger response as in hypoxia - just a left shift, no change in slope

288
Q

factors that right-shift CO2 response curve (4)

A

sleep
morphine
COPD
anesthesia

289
Q

peripheral chemoreceptors

A

carotid and aortic

O2 content feedback goes through glossopharyngeal nerve (CN9) to brain

290
Q

what are thresholds for O2 and ventilation increase

A

around 60mmHg

at around 30mmHg, lower response threshold

291
Q

effect of PCO2 on O2 ventilation curve

A

at increased CO2, there’s a right shift - now sensative to smaller drop in O2 (instead of 60, now you start hyperventillating at 70 if you have a PCO2 of 45 instead of 40)

292
Q

do peripheral chemoreceptors respond to partial pressure or total content of O2

A

Partial pressure - so they don’t respond to CO poisoning or anemia - because partial pressure is the same

293
Q

Hering-Breuer reflex

A

AKA inflation reflex
generated by stretch receptors in walls of bronchi and visceral pleura

protects against hyperinflation (more significant for newborns)

294
Q

Juxtapulmonary-capillary receptrors respond to what and cause what

A

between alveolar wall and capilarry - C-fibers,

respond to alveolar inflammation, congestion and edema, seratonin/bradykinin or PE

activation causes rapid shallow breathing

295
Q

peripheral proprioceptors

A

joints/muscles/tendons – response to sudden pain causes apnea (also sudden cold)
– response to prolonged pain causes hyperventilation

296
Q

phase 1 of exercise

A

rapid increase - thinking about excercise - anticipation, caused by cortical input

297
Q

what receptors does nicotine bind to

A

alpha4beta2

alpha7

298
Q

what controls addiction and craving

A

addiction – activation of the MIDBRAIN REWARD PATHWAY causes increased release of DA in NUCLEUS ACCUMBENS -

craving - many centers

299
Q

midbrain reward pathway

A

GLU (with presynaptic ALPHA7 receptors) input to DA neurons (with ALPHA4BETA2 receptors) in ventral tegmental area which synapses in nucleus accumbens (with ALPHA4BETA2 prsynaptic) releases DA (more release with nicotine). nucleus accumbens has pathways to prefrontal cortex - pleasure reward sensations

300
Q

varenicline (mechanism, use, adverse)

A

AKA Chantix
binds to alpha4beta2 as a PARTIAL AGONIST so even at its best it’s not as strong an activator as nicotine BUT it blocks nicotine’s access to these receptors

success rates are the best

start 1 week prior to quit attempt

not as much craving.

but get suicidal ideation, depression, contraindicated in pregnancy and lactation

301
Q

5 A’s approach to quitting

A 
ask
advise
assess
assist
arrange follow-up
302
Q

beta 2 agonists

A

short acting = albuterol

long acting = salmeterol

303
Q

muscarinic agonists

A

short acting = ipratropium bromide

long acting = tiotroprium

304
Q

ideal size for particles for inhalation

A

2-5 micrometers

305
Q

inhaled corticosteroids have what affect on asthma

A

suppress the inflammatory process - DO NOT CURE disease. don’t raise the level because you can have systemic affects, add a beta2 agonist

306
Q

mechanism of action for cotricosteroids

A

1) transrepression of NFkB
2) decrease production of prostaglandin/leukotriene products by inhibiting phospholipaseA2 and COX2 synthesis
3) inhibit monocyte proliferationa nd antigen presentation
4) decrease synthesis of pro-inflammaotry cytokines (IL-1, -6, TNFalpha)

307
Q

adverse systemic effects of corticosteroids

A
  • bone resoprtion
  • skin thinning
  • growth retardation
308
Q

systemic gucocorticoids for asthma

A
  • prednisone - short term use for asthma exacerbations not controlled by other methods
  • prednisolone IV for status asthmaticus in ER

REDUCE INFLAMMATION, DO NOT BRONCHODILATE

309
Q

3 classes of bronchodilators

A
  • beta agonists
  • muscarinic antagonists
  • theophylline
310
Q

theophyline mechanism

A

inhibits PDE which is the enzyme which degrades cAMP

311
Q

what does cAMP do to airway smooth muscle

A

relaxes airway smooth muscle

312
Q

what action do beta2 adrenergic agonists have? (3)

A

1) raise cAMP levels - relaxing SM
2) inhibit release of mast cell mediators - inhibiting leakage and improving mucociliary transport
3) increase glucocorticoid receptor nuclear transport

313
Q

can you take LABA alone for asthma?

A

NO! needs to be used with corticosteroid (sometimes used alone for copd)

314
Q

what are the SABA and LABA protptyles

A

albuterol and salmeterol

315
Q

how long to SABA and LABAs last?

A

SABA works within 3-5 minutes and lasts 3-6 hours

LABA lasts over 12 hours

316
Q

mechanism of action for Beta2 agonists

A

bind to Beta adrenergic receptor (G protein) coupled to AC, which increases cAMP causing smooth muscle relaxation

317
Q

systemic adverse effects of beta agonists

A

tremors, hyperkalemia, tachycardia

318
Q

if SABA is used more than 2 times a week, is this controlled?

A

no

319
Q

muscarinic antagonist action (1)

A

1) decrease bronchial muscle tone and mucus secretion by blocking Ach receptor

320
Q

do you use muscarinic agoinists in asmtha?

A

not usually, unless they’re intolerant of beta2 agnosits

  • use SAMA Ipratropium or LAMA triotropium for maintenance
321
Q

do you use muscarinic agonists in copd

A

yes, blocking tone is effective

322
Q

adverse effects of muscarinic agonists

A

1) dry mouth

2) caution in older men with prostatic hyperplasia - urinary retention (systemic effect)

323
Q

methyxantine prototype

A

theophylline

324
Q

is theophylline inhaled?

A

no it’s oral

325
Q

use of theophylline in COPD

A

can increase diaphragm muscle contractility

326
Q

adverse effects of theophylline

A

oral, so narrow therapeutic window

  • cardiovascular effects (Vasodilation, tachycardia, arrhythmias)
  • CNS stim (nervousness, anxiety, tremor)
  • GI (nausea, vomiting)
327
Q

leukotriene pathway inhibitor prototype

A

montelukast

328
Q

leukotriene inhibitor action

A

1) inhibit bronchoconstriction - effective for aspirin-sensitive asthmatics

329
Q

do leukotriene inhibitors help COPD

A

no

330
Q

mechanism of action for montelukast

A

inhibit the binding of leukotrienes to target receptors

331
Q

adverese effects

A

not so much for montelukast

332
Q

anti IgE prototype

A

Omalizumab

333
Q

mechanism of action for IgE inhibitor

A

binds to Fc receptor of IgE (block allergen binding site)

334
Q

adverse effects of IgE inhibitors

A
  • $$$
  • maybe anaphylaxis
  • only helpful in allergic asthma
335
Q

COPD treatments

A

LAMA or LABA for maintenance, inhaled corticosteroids when FEV is really low (below 50)

336
Q

amygdala controls

A

fight and flight - amygdala and below control resp.

337
Q

acidemia and alkalemia values

A

arterial pH <7.35 = acidemia
arterial pH >7.45 = alkalemia

acidosis in the process that will cause decrease in pH

338
Q

primary buffers in body (4)

A

bicarbonates
proteins (lactate, pyruvate)
phosphates
hemoglobin

339
Q

henderson equation

A

{H+} = 24 x (PaCO2/HCO3)

340
Q

when pH changes by 0.5, how much does [H+] change

A

by 5 in the opposite direction

341
Q

PaCO2 alterations are caused by _____ disturbances

bicarbonate concentration alterations are caused by _____ disturbances

and how does pH change

A

PaCO2 – respiratory disturbances (pH changes in opposite direction)

bicarb concentrations – metabolic disturbances (pH changes in same direction)

342
Q

causes of acute respiratory acidosis (4)

A
  • airway obstruction
  • respiratory center depression
  • neuromuscular disorder
  • pulmonary disorder
343
Q

how much does pH change with pCO2 in acute processes

A

with a rise of 10 pCO2, your pH decreases by 0.08

344
Q

in chronic respiratory acidosis, how does HCO3- change with changing PaCO2

A

HCO3- increases 3.5 for each increase of 10 PaCO2

345
Q

in chronic respiratory acidosis, how does pH change with PaCO2

A

pH decreases by 0.03 with each increase of 10 PaCO2

346
Q

in acute respiratory alkalosis, how does HCO3- change with PaCO2

A

HCO3- decreases 2 for each decrease of 10 PaCO2

347
Q

causes of respiratory alkalosis

A
  • hypoxemic respiratory drive
  • mechanical overventilation
  • respiratory center stimulation
  • fever/infection
  • pregnancy
  • pain
348
Q

when can you have a normal pH with abnormal blood gas situation

A

chronic respratory alkalosis (like pregnancy)

349
Q

in chronic respiratory alkalosis, how does HCO3- change with PaCO2

A

HCO3- decreases 5 with each decrease of 10 PaCO2

350
Q

what causes acute metabolic acidosis (5)

A 
ketoacidosis
lactic acidosis
starvation
toxins
GI issues
351
Q

winter’s formula

A

for metabolic acidosis expected respiratory compensation

expected pCO2 = [1.5 x (HCO3)] + 8 +/- 2

352
Q

formula for expected respiratory compensation for metabolic alkalosis

A

(not as common)

increase in PaCO2 = 0.6 - (0.7 x delta[HCO3])

353
Q

3 signs that there is a complex disorder

A
  1. normal pH (except in respiratory alkalosis)
  2. PaCO2 and HCO3 deviate in opposite directions
  3. pH changes in opposite direction for KNOWN primary disorder
354
Q

is CF AR or AD?

A

AR - most common AR disease (35,000 in US every year)

355
Q

what is the main mutatioin in cf?

A

CFTR gene, deltaF508 on long arm of chromosome 7 (7q31)

356
Q

different classes of CF mutations

A

class 1 - no protein at all, class4 - functioning but not fully

357
Q

how to diagnose CF (3)

A

chloride test - testing concentration of sodium or chloride in sweat (>60mmol/L)

newborn screening - immunoreactive trysinogen on Guthrie Card

genetic confirmation

358
Q

how does CF effect exocrine gland function

A

nasal, sweat, sinusitis, bonchitis, pancreatitis, diabetes, intestinal blockage, reduced fertility portal hypertension etc.

359
Q

daily treatment routine for CF

A
  1. neubluizers: (albuterol, hypertonic saline, pulmozyme, tobramycin)
  2. percussive physiotherapy to dislodge mucus
  3. pills 3x day for pancreatic enzymes, vitamins (ADKE), and antibiotics
  4. oxygen and feeding tube at night
360
Q

new treatments for CF

A
  • Ivacoftor

- Ivacoftor/Luvacoftor

361
Q

genetic risk factor for COPD

A

alpha1-antitrypsin deficiency

362
Q

characteristics of COPD inflammation

A
  • neutrophilic
  • macrophages
  • oxidative stress
  • IL-8 and CD8 and TNFa
  • protease/antiprotease imbalance
  • loss of elastic recoil
363
Q

definition of chronic bronchitis

A

cough productive of sputum most days during at least 3 consecutive months for more than 2 successive years

leads to hypoxemia - more obstruction in small airways, small V/Q ratio – leads to right heart failure (blue and bloated)

364
Q

parameters for qualifying COPD (ABCD rating scale)

A

1) FEV1
2) how short of breath are you
3) how often are exacerbations

365
Q

treatment for acute COPD exacerbation

A
  • SABA and SAMA
  • systemic oral glucocorticoids (prednisone 40 mg per day for 5 days)
  • oxygen admistration if SpO2 <88 (with venturi principle face mask)
366
Q

emphysema characteristics

A
  • breakdown of surface area - distal (alveolar sacs) decreased O2 exchange, sensed as dyspnea
  • NO scarring, more like atrophy
367
Q

types of emphysema

A
  • central lobular - associated with smoking
  • panacinar with alpha1-antitrypsin deficiency (can save lives)
  • paraseptal - very distal, associated with pneumothorax
368
Q

clinical emphysema picture

A
  • no/little sputum (more dyspnea over cough)
  • fewer exacerbations or infections
  • loss of elastic recoil
  • low DLCO
369
Q

Chronic bronchitis characteristics

A
  • persistent cough with sputum
  • inflmmatory leads to change in architecture
  • acute exacerbations
  • more proximal
  • cor pulmonale (right ventricular failure)
370
Q

Reid index

A

mucus glands/entire mucosal length

normal is 0.4

371
Q

BODE index

A 
systemic disease factor
B - body mass
O - obstruction of flow
D - dyspnea
E - exercise capacity
372
Q

bronchiectasis

A

abnormally dilated airways
cycle of obstruction inflammation damage mucus secretions obstruction etc.

leads to mucus plugs and abscesses - hemoptysis

373
Q

bronchogenic cancers

A 
non small cell lung cancers (85%)
- adenocarcinoma
- scc
- large cell ca
small cell lung cancers (15%)
374
Q

common caracinogens in tobacco

A
  • tobacco specific N-nitrosamine
  • Polycyclic aromatic hydrocarbons

induces modulation of oncogenes (Ras, onc) and tumor suppressor genes (p53)

375
Q

genetic risk factors for developing lung cancers

A

mutations in RB and p53 or EGFR (nonsmokers) KRAS (smokers)

376
Q

size of environmental pollutants that cause problems

A

less than 2.5 micro meters

377
Q

how to identify early lung cancer

A

CT

378
Q

which lung cancer has most metastesis

A

small cell (95%) (see weight loss, skeletal pain, CNS complaints)

379
Q

paraneoplastic syndrome

A

1) hypercalcemia (ectopic PTH) primarily with squamous cell carcinoma - stones bones abdominal groans and psych
2) hypernatremia (SIADH) - small cell
3) clubbing - non small cell lung cancers

380
Q

when do you get false positive pET scans

A

in inflammatory processes related to infections or recent surgeries

381
Q

when do you get false negative PET scans

A

small lesions or hyperglycemia

382
Q

ceptral vs peripheral lung cancers

A

central - squamous and small (can use sputum or bronchoscopy)
periperhal - adeno and large (can use CT biopsy)

383
Q

EGFR mutations seen in

A

adenocarcinoma, young, women, non smoking asian

384
Q

Stage 1a

A

only in lung, less than 3cm

385
Q

stage 1b

A

only in lung, gibber than 3cm, not bigger than 4

sx as first line

386
Q

stage 2a

A

only in lung, less than 5cm

sx with chemo as first line

387
Q

stage 2b

A

partial collapse, involve visceral pleural

sx with chemo as first line

388
Q

stage 3

A

lymph, airways, trachea etc

sx with chemo as first line if resectable, if not, chemo

389
Q

stage 4

A

metastesis outside thorax

chemo first line, look for mutations

390
Q

who can tolerate a pneumonectomy

A

FEV greater than 2

391
Q

who can tolerate lobectomy

A

FEV greater than 1.5

392
Q

recent MI and thoracic surgery

A

contraindicated

393
Q

small lung cancer treatment

A

mostly advanced, surgery not an option

limited disease = one hemithorax, treat with chemo and radiotherapy

extensive disease (and malignant pleural effusion) = outside hemithorax, treat with chemo alone

394
Q

solitary pulmonary nodule characteristics and evaluation

A

single opacity up to 3cm surrounded by normal lung (more than 3 is lung mass)

majority are not cancer, have to look at probability (history, growth over 2 years, pattern of calcification (stippling or eccentric - bad), margin regularity)

395
Q

neuroendocrine lung tumors

A

carcinoid, atypical carcinoid
small (same as scc) and large NE carcinoma

cause paraneoplastic syndromes

396
Q

anatomical vs phyiological staging

A

TNM - is the tumor ressectible

physiological - is the patient operable

397
Q

lepidic

A

growth along the alveolar surface of the lung - excellent survival

adenocarcinoma in situ (make serous or mucin) AKA minimally invasive adenocarcinoma (MIA)

398
Q

diagnostic features of squamous cell carcinoma (3)

A
  • squamous pattern with intercellular bridges (on EM)
  • squamous keratin pearls
  • cytologic keratin production
399
Q

small cell carcinoma histological criteria (2)

A
  • neuroendocrine markers - dense core neurosecretory granules
  • mitoses and tumor necrosis
400
Q

large cell carcinoma histological criteria

A
  • no distinctive differentiation - diagnosis by exclusion
401
Q

diagnostic features of adenocarcinoma (2)

A
  • glandular (Acinar, papillary, solid)

- mucin production and vacuoles

402
Q

neuroendocrine carcinoma - typical carcinoid characteristics

A

well differentiated- good prognosis, low grade, NO mitoses NO necrosis NO LN mets

403
Q

diffuse mesothelioma characteristics

A
  • thick collagen
  • tubularpapulary pattern
    looks like adenocarcinoma BUT:
  • keratin positive
  • CEA negative
  • calretinin positive
  • mucin negative
404
Q

immunotherapy in lung malignancies

A

block PD-1/PD-L1 to upregulate immune response to tumor cells

405
Q

penumococcal vaccine

A

first give conjugate and then follow with polysaccharide (for those over 50)

406
Q

pleural fluid characteristics in empyema

A

low pH
low glucose
pus in pleural space
thick rind

staph aureas, legionella, strep pneumo, anaerobe

407
Q

mycosplasma pneumonia dx and treatment

A

no culture - clinical dx

treat with macrolides (azithro)

408
Q

legionella pneumonia, characteristics, dx, tx

A 
cavitation
fevers
GI symptoms and headache
temp-pulse dissociation
hyponatremia

dx with urinary antigen, sputum on charcoal

tx fluoroquin

409
Q

klebsiella pneumonia, characteristics, tx

A

necrotizing pneumonia
associated with alcoholism
bulging fissure - really mucoid

tx - pennicilin with beta lactamase inhibitor

410
Q

H. flu

A

have to use beta lactamase inhibitor

411
Q

MRSA, characteristics, tx

A

follows viral infection, hematogenous dissemination with peripheral nodules, cavitation

tx with linezolid

412
Q

strep pyogenes pneumo characteristics

A

rapidly progressive, associated with preceding viral illness, can cause empyemas

413
Q

invasive pulmonary aspergillosis, characteristics, dx, tx

A

long term steroid treatment or advanced immunosuppression

nodular infiltrates with halp sign, requires biopsy

usually fatal if no neutrophil recovery

tx. voriconazole

414
Q

PCP, characteristics, dx, tx

A

diffuse pneumonia, ground glass appearance

T cell autoimmunity, chronic steroid, chemo

sick for weeks

dx - silver save sputum or lavage

tx - oral bactrim

415
Q

pulmonary tuberculosis in children vs adults

A

children - primary

adults - apical infiltrates with cavitation without adenopathy, with monocytosis

416
Q

primary localized TB

A

granulomatous, Ghon lesion, drain into hilar LN with caseous necrosis

417
Q

primary disseminated TB

A

immunocompromised individuals with caviation and miliary pattern

418
Q

secondary TB

A

reactivation who develop immunodeficiency

419
Q

lung abcesses mostly caused by

A

staph aureus or klebsiella

destruction and pus with outer organization of fibroblasts

420
Q

what do you look for in neutropenic patients

A

gram pos neg and fungus

421
Q

what do you look for in B abnormalities

A

encapsulated

422
Q

what do you look for in T abnormalities

A

pcp cmv and fungal (histo, cocciodio, crytpto)

423
Q

aspergillus presentations (3)

A
  • aspergilloma (non-invasive)
  • mycetoma (round/oval mass -
    occupying cystic cavity)
    hypersensitivity
424
Q

coccidio

A

spherules
SW united states
no budding
purulent AND granulomatous response (to spherules and endospores)

425
Q

crypto

A

budding
immunocompromized
patients with birds

426
Q

histo

A 
middle america
localized primary pneumonia
disseminated with HIV
dimorphic
budding yeast
427
Q

what kind of inclusions does CMV have?

A

nuclear AND cytoplasmic

428
Q

lipid pneumonia

A

sterile
seen with obstruction
macrophages

429
Q

do you see wheezing with diffuse parenchymal lung disease?

A

no

430
Q

diffuse parenchymal lung disease of konwn causes:

A
  • drugs (chemo, biologics)
  • inhaled particles (inorganic - pneumocomyoses, small organic particles, paraquat)
  • associated with collagen vascular disease
431
Q

DPLD of unknown etiology (5)

A
  • most common is idiopathic pulmonary fibrosis (IPF), idiopathic interstitial pneumonia
  • non-specific interstitial pneumonia
  • cryptogenic organizing pneumonia (airway filling)
  • DIP and RBILD (tobacco related)
  • sarcoidosis
432
Q

neutrophilic DPLD

A

IPF, inorganic

433
Q

lymphocytic DPLD

A

sarcoid, hypersensitivity pneumo (lower ratio of CD4 compared to sarcoid)

434
Q

presence of adenopathy with intersitital ilfiltrates (2)

A

sarcoidosis, silicosis

435
Q

presence of pleural effusions and interstitial infiltrates (3)

A

collagen vascular disease, drug hyperesnsitivity, asbestos

436
Q

IPF clinical presentation

A 
50-70y/o
progressive dyspnea
nonproductive cough
mid/late crackles
clubbing
heterogeneous histology
requires lung transplantation
437
Q

NSIP

A 
temporally uniform histology
no fibroblasts
some have connective tissue underlying
younger (40-50)
no association with cigarette
no clubbing
ground glass opacity with fine reticulation
438
Q

RB-ILD

A

related to cig smoking
pigmented macrophages in first and second resp bronchioles
obstruction and reduction in DLCO

439
Q

DIP

A

smoking
mean age 42
good response to corticosteroids

440
Q

sarcoidosis

A
  • young and middle-aged adults
  • presents with BILATERAL symmetrical hilar (inside pleura) and mediastinal lymphadenopathy, ocular, skin lesions, infiltration
  • liver, spleen, salivary glands, heart, muscle, CNS involvement
  • non caseating granulomas orchestrated by CD4
441
Q

hypersensitivity pneumonias

A
  • immune mediated - IgG antibodies and lymphocytes
  • combined type 3/4: immune complex (type 3) and type 4 (cell medatied)
  • fungi in farmer’s lung
  • chronic exposure leads to progressive lung disease
  • INTERSTITIAL, not intra-alveolar
  • bronchiolitis with granulomas
442
Q

pneumoconiosis

A

inorganic
occupational history (sandblasting, coal, asbestos)
silicosis

443
Q

fine silicosis

A

asymptomatic

fine pinpoint CXR

444
Q

complicated

A

dyspnea, sputum
can lead to Right Heart Failures
masses at apeces - no pleural involvement
mycobacterial disease

445
Q

asbestos related diseases

A

pleural plaques
parenchymal fibrosis
pleural effusions
malignancies

446
Q

marker of interstitial lung disease

A

fibrotic foci

447
Q

Hamman-Rich syndrome

A

RAPIDLY progression
diffuse isterstitial infiltrates
fibrosing alveolitis
pulmonary fibrosis

448
Q

usual interstitial pneumonia

A

chronic, insidious 2-5 years, poor survival
confined to lung
fibroblasts
60+
idiopathic
DIFFERENT IN TIME AND SPACE (heterogenous) - old and new in same area, different stages of lesions (some quicker than other)

449
Q

nonspecific interstitial pneumonia

A

similar, but homogenous rather than patchy, uniform rick lymphoplasmacytic infiltrate termporally
steroid responsive
idopathic

450
Q

RBILD/DIP

A 
ground glass (alveolar filling)
macrophages
hemosiderin
intra-alveolar
give steroids
451
Q

beryliosis

A 
type 4 pneumoconiosis
hypersensitivie
see in urine
can do lymphocyte stimulation test
non-caseous necrosis
452
Q

where do you see fibrosis and macrophages in pneumoconiosis

A

in bifurcations

453
Q

differences between visceral and parietal pleura

A

visceral = thick, mesothelial cells and dense CT, supplied by bronchial arteirs and pulmonary veins

parietal = thin, mesothelial and loose CT, supplied by systemic capillaries and intercostal nerves, has lymphatic lacunae that remove large particles (proteins and RBCs)

454
Q

low thick is pleural space

A

20 microns

455
Q

pleural fluid comp

A

protein ratio less than 0.5
no neutrophils or eos
mostly macros (75%), lympho (23%)
alkaline

456
Q

symptoms with pleural effusions

A

dyspnea, chest pain, chest pressure, tachycardia, tachypnea, sometimes asymptomatic

457
Q

what does white pleural fluid suggest

A

chylothorax

458
Q

what does yellow/green pleural fluid suggest

A

rheumatoid arthritis

459
Q

what does black pleural fluid suggest

A

old blod or aspergillosus nigra

460
Q

light’s criteria

A

PF/serum protein ratio >0.5
PF/serum LDH ratio >0.6
PF LDH >2/3 normal value LDH

IF ONE of the above is true it’s an exudate

461
Q

most common cause of exudative effusion and types

A

para pneumonic effusion (3 types):

  • uncomplicated (from pneumonia, inflammation, tap is alkaline and no bacteria)
  • complicated (more acidodic, bacteria)
  • empyema (pus, low ph <7.2, low glucose <60, positive smear, need chest tube or sx. phases are exudative to fibroproliferative to organization phases - more fibrinous)
462
Q

common causes of malignant effusion

A
  • breast
  • lung
  • lymphoma

para-malignant (non malignant effusion with known malignancy) due to lymphatic obstruction

463
Q

PE causing pleural effusion

A

always exudative, serosanginous, see PE on CT scan

464
Q

TB causing pleural effusion

A

due to hypersensitivity to tuberculous protein
primary TB
fluid culture, smear, PCR, ADA>40 is likely

465
Q

chylothorax

A

milky white exudate
due to trauma
needs to be drained

466
Q

masses in anterior mediastinum

A
  • thymoma
  • teratoma
  • lymphoma
  • thyroid masses
467
Q

masses in meddle mediastinum

A
  • vascular masses
  • enlarged lymph nodes
  • pleural or pericardial cysts
468
Q

masses in posterior mediastinum

A
  • neurogenic tumors

- meningocele

469
Q

acute mediastinitis

A

fever and chest pain
due to esophageal perforation due to mediastinal surgery
need surgery

470
Q

chronic mediastinis

A

TB, histoplasmosis cause

symptoms related to compression of other ograns

471
Q

pneumomediastinum

A

gas in mediastinal space, causes substernal chest pain

472
Q

pulmonary edema - transudate and exudative causes

A

henodynamic (Starlings) forces caused by CHF, LV dysfunction cause transudate

alveolar injury causes exudate

473
Q

ARDS - what do you see in exudate

A
  • intra alveolar exudative effusion
  • rule out cardiogenic pulmonary edema
  • increased permeability of plasma proteins and inflammatory cells into alveolus
  • see HYALINE FIBRINOUS MEMBRANE and CELLULAR (fibrinous) EXUDATE
474
Q

ARDS - characteristcs

A

arterial hypoxemia refractory to oxygen therapy due to shunting - perfusion mismatch marked V/Q, stiff lung

475
Q

ARDS - caused by

A

sepsis, shock, inhaled toxic injuries, trauma, drowning, burn injuries etc.
cause acute respiratory insufficiency

476
Q

ARDS phases

A
  • hyaline membrane within a few days, refractive hypoxemia with shunt
  • exudative phase, now see angioblasts and fibroblasts (week)
  • organizing (fibrosing) phase - interstitial fibrosis (few weeks)
  • resolution or progression to pulmonary fibrosis
477
Q

clinical features of ARDS

A 
low PaO22/FiO2 -- (200-300)
pulmonary arterial wedge pressure <18
no L heart failure
arterial hypoxemia
rapid onset tachypnea and dyspnea
stiffness
shunt and dead space
478
Q

what do you do for acute cardiogenic pulmonary edema therapy

A 
LMNOP
Lasix
Morphine
Nitroglycerine
Oxygen
Positive pressure ventilation (pushes fluid back so that lymph can drain)
479
Q

what do you hear iwth cardiogenic pulmonary edema and cause is fixable

A

wheeze, crackle cough

480
Q

what do you hear with acute lung injury (ards)

A

cough crackle death

481
Q

ARDS - 3 definite findings

A
  • rapid onset
  • bilateral infiltrates
  • PaO2/FiO2 ratio under 300 on oxygenation (refractory to treatment), bilateral infiltrates, wedge pressure under 18 (this is not the heart causing this)
482
Q

common direct insults causing ARDS

A
  • aspiration pneumonitis (vomiting and aspirating)

- pneumonia

483
Q

common indirect insults causing ARDS

A
  • sepsis
  • shock
  • trauma
484
Q

treatment for ARDS

A
  • low tidal volume ventilation

ARMA

485
Q

stridor

A

stridor is large airways (larynx and trachea)

high pitched inspiratory sound

486
Q

are crackles musical?

A

no. they are discontinuous. fine or coars, and at the end of inspiration

487
Q

pleural friction rub description

A

continuous inspiratory AND expiratory rhythmic sounds

488
Q

Hamman’s sign

A

mediatsinal cruch with pneumomediastinum

489
Q

ronchi

A

low pitched wheezes

sound more like snoring, not musical

490
Q

wheezing

A

small airways - hear over peripheral lung fields

bernoulli’s principle - increased velocity, low pressure, airway walls collapse and vibrate

491
Q

what causes stridor

A

infections:
croup, RSV, flu, pertussis, tracheitis, epiglottitis, retropharyngeal abcess

inhalation, aspiration, burns, or foreign bodies

492
Q

what causes wheezing

A 
asthma
acute bronchitis with bronchiolitis
COPD
CHF
PE
obstruction
vocal cord dysfunction
493
Q

inspiratory stridor caused by internal or external problem

A

external

494
Q

expiratory stridor caused by

A

internal (foreign bodies, compression by intrathroacic things- LNs)

495
Q

bronchiolitis

A

inflammation in bronchioles, expiratory wheezing, viral cause (RSV)

496
Q

bronchiectasis

A

purulent chronic sputum, destruction of bronchi, chronic inflammation, caused by TB or MAI, or CF
wheezes, sqeaks and focal crackles

cycle of nastyiness causing scarring and damage

497
Q

PE is how common cause of death in in-patient

A

3rd and most common preventable cause of in-patient death

498
Q

Virchow’s triad

A
  • stasis
  • hypercoagulability
  • vascular injury
499
Q

most common cause of acquired thrombophilia

A

antiphospholipid antibody syndrome

500
Q

Wells criteria for PE

A
  • previous PE, tachycardia, SX, hemoptysis, cancer, DVT (1 or less, not suspicious)
501
Q

D-Dimer

A

measures cross-linked fibrin derivatives - elevated in presence of acute thrombosis (activation of coag and fibrinolysis at same time)

also high in pregnancy, trauma etc.

502
Q

best imaging for PE

A

Chest CT

503
Q

westermark

A

no vascularity

504
Q

hapton’s hump

A

transudate/exudate on pleura for pulmonary infarction

505
Q

McConnell’s sign

A

echocardigram

if you see free wall RV not doing much, while th eapex is moving a lot, then you see pE

506
Q

when do you do IVC filter

A

if low risk PE

507
Q

what is IVC filter

A

placed in inferior vena cava, take it out later. if you can’t do anticoag treatment

CPR (3 decks)

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