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Physiology > Lung > Flashcards

Lung Flashcards

1
Q

Describe the indications/contraindications for PFT

A

Evaluate signs of lung disease

Assess progression of lung disease

Monitor the effectiveness of therapy

Evaluate preoperative patients in selected situations

Screen t risk of pulmonary disease such as smokers of occupational exposure

Monitor toxic effects of drugs (amiodarone, beryllium)

-NOT in others without symptoms-may be confusing when nonpulmonary diseases effect pulmonary system

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2
Q

Describe the components of pulmonary function test

A

Ok

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3
Q

Compare and contract obstructive and restrictive PFT

A

Obstructive-decreased to normal FVC, decreased FEV1, decreased FEV1/FVC ration

TLC normal or increased

Restrictive-decreased FVC, decreased or normal FEV1, normal FEV1/FVC, decreased total lung capacity

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4
Q

What is the body’s clock

A

Suprachiasmatic nucleus of the hypothalamus

Neurons discharge rates wax and wan as days go on

Genes control this

-strong genetic component

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5
Q

How set time in nucleus of SCN neuron (no circadian rhythm on its own)

A

Clock (CLK) on own no circadian rhythm with BMAL19has circadian rhythm increases at night (protein products are transcription factors->increase transcription/translation of:
Period genes:Per1, Per2, Per3 and cryptochrome genes: Cry1, Cry2

Also come back and inhibit Clocka Nd BAL 1 gene products,

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6
Q

Night

A

Increasing BMAL and CLOCK

Phase shift of CRY.PER bc made by them —-as accumulate at night get negative feedback on BMAL and CLOCK which triggers CRY and PER to fall off

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7
Q

Day

A

Decrease BMAL and CLOCK

Phase shift Cry/PER just a little behind bc caused by BAL and CLOCK

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8
Q

In nucleus

A

Two set of neurons fire at day break and another set active at dusk

Tell morning vs night

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9
Q

Morning vs night people

A

Genetically controlled

Ppl fall asleep at 7—-mutation in clock genes if homozygous had to fall asleep at 7 and wake up at 4

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10
Q

Genetic day

A

Longer than 24 days..genetic day longer than circadian

We match out active/inactive periods to the day.night cycle of the external env

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11
Q

Younger

A

Longer genetic day

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12
Q

Older

A

Shorter day

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13
Q

How long is genetic day

A

35 hours

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14
Q

How we do this

A

Retinal hypothalamic tract.. photoreceptors in retina that axons through ganglion travel directly to the SCN in hypothalamus, retino hypothalamic tract is separate from vision tract and it relays light and dark to SCN using 2 neurotransmitters

Glutatme (light
Melatonin (dark)

So SCN gets signal of light (glutamate)
Dark (melatonin)

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15
Q

How generate circadian rhythm, including genetic components

A

The circadian rhythm is set by the activity of clock, BMAL, Per and CRY gene products in neurons and SCN
Our natural circadian clock seems to be 25 hours long

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16
Q

Describe how entrainment of the genetically determined circadian rhythm to the env occurs

A

Our circadian clock is synchronized to physical day/night by the action of the retinohypothalamic pathway (glutamate) for day and melatonin for night

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17
Q

Action potential brain

A

By millions of neurons int he human brain create the EEG

Put electrodes on skull, eye monitors and EKG

*activity is not as regular as EKG-lower volatile
<200 microV

Frequency<1Hz->50 HZ

Differs over different parts of the brain

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18
Q

EEG changes

A

Degree of activity in brain

Arousal/awareness

Sensory input

Most of time no distinct astern
Clear patterns associated with pathology (epilepsy)

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19
Q

Normal EEG wave

A 
Alpha waves 
Beta waves
Gamma waves 
Theta waves
Delta waves
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20
Q

Alpha waves

A

8-13 Hz
50 microvolts

Occurs during quiet wakefulness (thinking) when eyes are CLOSED

Over occipital cortex

Disappear during sleep

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21
Q

Origin alpha waves

A

Requires connection between thalamus and cortex

GABAergic neurons force coordination of neuronal activity (activated by thalamalcortical neurons)

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22
Q

Beta waves

A

14-80Hz
<50 microV

Awake and alert with eyes open

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23
Q

Alpha block

A

Eyes closed but awake

Open eyes show more beta waves

Open eyes prevents alpha waves

With sensor input alpha waves cease
-alpha block or alerting response

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24
Q

Where are beta waves

A 
Frontal cortex (thinking’s)
Parietal cortex too

But can occur elsewhere

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25
Q

Origin beta waves

A

Same as alpha
Sensory input disrupts the oscillation to some extent

Thalamus to frontal

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26
Q

Gamma waves

A

30-80 HZ
Occur when aroused or focused on something

Replaced by even more irregular activity if plan a motor response

May require hippocampus

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27
Q

Theta waves

A

;rage slow
4-7 HZ
100 microvolts

Normal in kids, particularly over parietal and frontal cortex
Adults frustration or disappointment if awake
-pathologic if not frustrated or disappointed if awake

See in sleeed

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28
Q

Origin theta

A

Probably hippocampus

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29
Q

Delta waves

A

Big slow
<3.5Hz
100-200 micro V

Deep sleep in adults
Infants awake and asleep

If in awake it is “serious organic brain disease”

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30
Q

Origin delta wave

A

Does not require connection between thalamus and cortex
-disconnection during sleep

If see when awake substantial dearangement

Feedback oscillation within cortex creates waves

Taken to indicate that the cortex is no longer connected to thalamus

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31
Q

Alpha

A

Awake, eyes closed

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32
Q

Beta

A

Wake, eyes open
High freq low amplitude

Frontal parietal

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33
Q

Gamma

A

Slower

Associated with attention.motor planning

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34
Q

Theta

A

Slower higher amplitude, frustration sleep

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35
Q

Delta

A

Slow large

Dissociation cortex and hypothalamus

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36
Q

Increased mental and neural activity

A

Increased EEG activity

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37
Q

Infant

A

Fast bets like activity, but over the occipital region there is slow .5-2 HZ activity

Babies delta wave can be normal

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38
Q

Occipital region slow was in infancy willl increase in childhood

A

Alpha wave patten will appear during adolescence

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39
Q

Alpha decreased

A

Hypoglycemia(brain activity dec)
Low body temp

Low adrenal glucocorticoids

High paCO2

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40
Q

Age

A

Infant-generally slower waves predominance even in wakefulness

Adolescence is when EEG topical adult pattern

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41
Q

52 yo female with insomnia and day time sleepiness but cant fall asleep at night , HTN, obesity, type I diabetes,

A
  1. Risk of dying in sleep or falling asleep at wheel
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42
Q

The hypothalamus controls both the circadian rhythm and sleep induction.arousal ___

A

Separately

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43
Q

Sleep

A

Cycle of deep to shallow sleep

Common to wake up briefly at end of cycles !!

44
Q

Non rem sleep

A

Grey areas -

Earlier in night

45
Q

Deeper sleep

A

Slow and bigger wave

46
Q

Stages non rem

A

1(N1), 2(N2), deep sleep

47
Q

Rem sleep

A

Black areas-top of bars eeg looks like away

Come into and out as go through the cycles

48
Q

Nonrem

A

Msot time asleep
Three stages-1, 2, and deep

Slower and bigger EEG waves the deeper and less sensitive you are to external stimuli bc of the thalamus

Dreams do occur in non rem, but they are generally rehashing of days evens (boring)

49
Q

Non rem dreams

A

Consolidation of short to long term memory occurs at night

Consolidate what need to remember activate papez circuit

50
Q

REM

A

Rapid eye movement

Low amplitude high frequency

Eyes move rapidly l to r

Vivid dreams that you remember
-memory consolidation, brain is sifting through new things you learn and match to old things

51
Q

Non rem

A

Bulk, slow rolling eye movements, eeg slow and increases in amp, dreams mundane but starting to consolidate to long term memory,

52
Q

Rem sleep

A

Cycle through 90 mins, epoch is is longer into sleep more time

EEG eye movements dreams memorable(vivid and bizarre)

53
Q

How prevent ourselves from acting out dreams in sleep

A

Ok

54
Q

Inducing sleep

A

Circadian clock entrained to physical reality day and night drives part of need to sleep

1.sleep homeostasis “need for sleep”-loosely tied to circadian clock , gets stronger as night time approaches
NREM sleep

Alertness-tied to circadian clock
Circadian clock drives rem sleep

55
Q

What drives rem sleep

A

Circadian clock

56
Q

What drives non rem

A

Sleep homeostasis need for sleep

57
Q

Ventral preoptic ares homeostatic need for sleep

A

Ventral Preoptic area of hypothalamus gets signals fromt he body
Daylight PGD2 made and released bind to cells of leptomeninges using DP receptor, leads to release of adenosine into CSF , adenosine bind cells in ventral preoptic region , VPO express adenosine 2a receptors which trigger you falling asleep,

58
Q

Caffeine

A

Weak blocker of adenosine receptors keeps you awake

59
Q

PGD2

A

Binds leptomeninges which secretes adenosine which binds A2a in VPO start sleep

Caffeine blocks this-caffeine 7 hour

60
Q

What else causes sleep

A

IL1b and TNF-a

Cytokines-when sick, inflammation sick people are sleepy
NFKB->NO synthase->NO

61
Q

When else do you sleep a lot

A

During growth,
Teens don’t get up!! Can sleep in till noon
GHRH

NF-Kb->NO synthase, NO

62
Q

VPO neurons

A

Inhibit ascending reticular activating system and reduce sleep

63
Q

That was all induction of NREM sleep

A

First o bed , nap

64
Q

REM sleep

A

Initiated independently and separate mechanism

65
Q

REM sleep structures

A

Cholinergic neurons in the lateral pontine tegmentum, release Ach in the geniculate body
Which then sends input to the occipital cortex

Lateral pontine tegmentum is also part of the brainstem arousal mechanism-the use f Ach to induce REM sleep as

66
Q

Muscle paralysis in REM sleep

A

Anhistamines-drowsiness

Promotes induction of sleep into NREM , interfere with REM sleep bc of two different mechanisms

*mucsle paralysis
-crucial to prevent muscle activation during dreams 9if not we would act out, rem behavioral disorder ppl act out dream)
By inhibiting motor neurons
Locus cerulean: inhiibtory input to a motorneurons down spinal cord to paralyze large msucles (not small bc cant do harm)-spares diaphragms and respiratory

67
Q

Sleep normal induction

A

PGD2 accumulation in periphery
Adenosine accumulation in CSF (triggered by PGD2)
Adenosine receptor activation in VPI
Leads to inhibition of ARAS

68
Q

During special circumstance

A

Growth -GnRH and GH secretagogue receptors

Illness -TNF of IL1b

Any of these trigger NFKB

69
Q

Induction of REM

A

Ach from lateral pontine tegmentum, release in geniculate body
Large muscle paralysis requires locus cerulean

70
Q

When wake up

A

From REM

71
Q

How wake up

A

Hypothalamus

Lateral hypothalamus controls appetite , and releases orexins which make you hungry (orexin a and b) (aka hypocretin 1 and 2) int he brain

72
Q

Orexin

A

Makes you eat from lateral hypothalamus

73
Q

Hypocretin

A

Hypothalamic for secretin

Triggers pancreatic secretions

74
Q

Orexin

A

From lateral hypothalamic axons to tubulomamillary nucleus in hypothalamus, release histamine from tubulomamillary sent to locus ceruleus bind to H1 receipts and thesis neurons release NE and suppress sleep

_whi anti histamine makes you sleeps

75
Q

REM sleep controlled by what

A

Circadian clock more active as more into night so stopping rem sleep

76
Q

First cycle

A

70-100 minutes

Then moves to short REM and back to deep sleep

77
Q

Later into night

A

Hardly in deep sleep, in shallow and rem

90 minute cycle

78
Q

Children

A

Sleep a lot in deep and rem

More total sleep

79
Q

Older elderly

A

Disruption of cycle
-fewer REM epochs(but they can be long)

Same amount of REM but different sequence

No deep sleep-where brain clears adenosine, so older feel increased need for sleep by not going through deep sleep adenosine not cleared

More frequent awakenings from different sleep stages (not just rem)

Less total sleep (more likely to nap)

80
Q

Slow wave sleep

A

N1-N3

Slow eeg

81
Q

REM sleep

A

RAM and eeg picks up high frequency

Paralysis of large muscles

82
Q

N1

A

Drowsiness/earliest stage of sleeo
Physical-slow, rolling motions of eyes, EMG show muscle activity,

EEG-low voltage , slowing frequency

83
Q

N2

A

Slower and bigger
“True sleep”
Physical-EMG show msucle activity, but relatively quiet

EEG-increasing voltage, slowing free, SLEEP SPINDLES(bring interruption with very fast activity)

84
Q

Sleep spindles

A

Being in N1, but are most prominent in N2

Bursts of alpha like activity interrupting the slower EEG of sleeo

May be preceded by a sharp wave (K complex) BIG SHARP may preceded

85
Q

N3

A

Deep
Large amplitude, slow, delta waves
———-disaccociation between thalamus and cortex, thalamocortical neurons are hypopolarized, cortex is free wheeling

Deep sleep

Quiet EMG,
EEG large slow,

86
Q

REM

A

Rapid side to side movements
—DEFLECT IN OPPOSITE DIRECTIONS

EMG suppressed (locus ceruleus)
Vivid dreams

EEG-rapid low voltage

87
Q

Out patient

A

Obstructive sleep apnea

Increased sleep latency

88
Q

Thorax bigger abdomen smaller

A

Paradoxical motion of thorax and abdomen no airflow in or out

Upper airway collapses-suppression of muscle during REM spares diaphragm and not other muscles of respiration collapse and negative pressure in trachea collapses, this person not moving air but moving muscles O sat falls, SNORING

89
Q

Expiration

A

Internal inter coastal and abdominal recti

90
Q

Upper middle lower zone

A

-10 top -2.5 bottom

Lowest ventilation top bigger at bottom

91
Q

Insp to ex aVL and intrapleural pressure

A

-5, -8, -5 intrapleural

0, -1, 0, +1 alveolar pressure

92
Q

Anatomic dead space

A

Respiratory bronchiole-has alveoli, anything with alveoli are not anatomic dead space

Trachea, right main, terminal bronchioles

93
Q

Physiologic dead space

A

Anatomic+alveolar dead space=total

94
Q

Total dead space

A

Usually same as

95
Q

Pulmonary flow

A

Low resistance, high compliance

96
Q

Hypoxia effect

A

Vasoconstriction

97
Q

Hypocapnea what happens

A

Ok

98
Q

Hypercapnea what happens

A

Ok

99
Q

Acid base of respiratory system

A

PHa=7.48, PaO2 51, PaCO@ 27, HCO3

Acute respiratory alkalosis

Normal ph 7.4, PaO2 95-100, CO2 40, HCO3, 24

PH first 7.4 acid or alk

Cause?resp(CO2 down) or metabolic (HCO3 up)

CO2+H2O=H2CO2=H+HCO2

Decrease CO2 get less product

100
Q

Central vs peripheral chemoreceptors *low O2 can trigger increased external respiration

A

Central-medullary neurons

Peripheral-carotid and aortic bodies

Arterial PO2<60, increase peripheral chemoreceptors and decrease central and medullary respiration center, peripheral chemoreceptors increase medullary respiratory center and central has no effect

Increases ventilation, increases arterial PO2

Peripheral chemoreceptors-decrease O2, increase CO2, increase H…very sensitive to reduction in partial pressure of oxygen. Send impulses to inspiration center to stimulate, increase rate and force of respiration and rectifies tha lack of oxygen

Central chemoreceptors increase CO2, increase H+, sensitive to increase in H, H cant cross BBB CO2 crosses and forms carbonic acid, as carbonic acid is unstable it dissociates to H and bicarbonate, , stimulates central which stimulate dorsal group of respiratory center and increase rate and force of breathing …need CO2 in , DONT CHANGE AS OXYGEN CHANES IN BLOOD. H not allowed into CSF so CO2 cross make cabinoc acid then H

101
Q

Rapidly adapting stretch receptors

A

Nerve endings between airway epithelial close to the mucosal surface
Myelinated afferent fibers

Stimulated by a host of irritates: cigarette, gases

Depending not he stimulus may result in cough, rapid shallow breathing or mucus secretion

State dependent: reflex cough in awake state versus apnea when asleep/anesthetize

102
Q

J receptors what stimulates central

A

In alveolar walls in juxtaposition to the pulmonary capillaries

Stimulated espicially when the pulmonary capillaries become engaged with blood
*pulmonary edema , microembolism

Excitation may give feeling of dyspnea

C fiber sensory nerve endings located within he alveolar walls in juxtaposition to the pulmonary capillaries of lung and innervated by vagus

Stimualtion of these receptors leads to inhibition of the skeletal muscles

103
Q

Changes in compliance on response system

A

Increased compliance-filling easy, exhalation hard

Change in v/change in p=compliance

104
Q

Chances on respiratory system

A

Ok

105
Q

Equation flux

A

SAxDiffusion coefficient (P1-P2)/diffusion distance

106
Q

Westmarkers sign reduced blood flow to an area what is blood like leaving that area

A

110, 30

V/q left lung 1.2 (.8 normal) Q down

V/q healthy lung= =.5 Q up!

High V/Q=alveoli with lots of O2, not getting in
PaO2 and PAO2 climb bc not removing O2 , decrease flow,

Bringing low CO2 bc little blood…decrease bc not delivering any.

Physiology (7 decks)

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