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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
Origin beta waves
Same as alpha Sensory input disrupts the oscillation to some extent Thalamus to frontal
26
Gamma waves
30-80 HZ Occur when aroused or focused on something Replaced by even more irregular activity if plan a motor response May require hippocampus
27
Theta waves
;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
28
Origin theta
Probably hippocampus
29
Delta waves
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”
30
Origin delta wave
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
31
Alpha
Awake, eyes closed
32
Beta
Wake, eyes open High freq low amplitude Frontal parietal
33
Gamma
Slower | Associated with attention.motor planning
34
Theta
Slower higher amplitude, frustration sleep
35
Delta
Slow large | Dissociation cortex and hypothalamus
36
Increased mental and neural activity
Increased EEG activity
37
Infant
Fast bets like activity, but over the occipital region there is slow .5-2 HZ activity Babies delta wave can be normal
38
Occipital region slow was in infancy willl increase in childhood
Alpha wave patten will appear during adolescence
39
Alpha decreased
Hypoglycemia(brain activity dec) Low body temp Low adrenal glucocorticoids High paCO2
40
Age
Infant-generally slower waves predominance even in wakefulness Adolescence is when EEG topical adult pattern
41
52 yo female with insomnia and day time sleepiness but cant fall asleep at night , HTN, obesity, type I diabetes,
1. Risk of dying in sleep or falling asleep at wheel
42
The hypothalamus controls both the circadian rhythm and sleep induction.arousal ___
Separately
43
Sleep
Cycle of deep to shallow sleep Common to wake up briefly at end of cycles !!
44
Non rem sleep
Grey areas - Earlier in night
45
Deeper sleep
Slow and bigger wave
46
Stages non rem
1(N1), 2(N2), deep sleep
47
Rem sleep
Black areas-top of bars eeg looks like away Come into and out as go through the cycles
48
Nonrem
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
Non rem dreams
Consolidation of short to long term memory occurs at night | Consolidate what need to remember activate papez circuit
50
REM
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
Non rem
Bulk, slow rolling eye movements, eeg slow and increases in amp, dreams mundane but starting to consolidate to long term memory,
52
Rem sleep
Cycle through 90 mins, epoch is is longer into sleep more time EEG eye movements dreams memorable(vivid and bizarre)
53
How prevent ourselves from acting out dreams in sleep
Ok
54
Inducing sleep
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
What drives rem sleep
Circadian clock
56
What drives non rem
Sleep homeostasis need for sleep
57
Ventral preoptic ares homeostatic need for sleep
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
Caffeine
Weak blocker of adenosine receptors keeps you awake
59
PGD2
Binds leptomeninges which secretes adenosine which binds A2a in VPO start sleep Caffeine blocks this-caffeine 7 hour
60
What else causes sleep
IL1b and TNF-a Cytokines-when sick, inflammation sick people are sleepy NFKB->NO synthase->NO
61
When else do you sleep a lot
During growth, Teens don’t get up!! Can sleep in till noon GHRH NF-Kb->NO synthase, NO
62
VPO neurons
Inhibit ascending reticular activating system and reduce sleep
63
That was all induction of NREM sleep
First o bed , nap
64
REM sleep
Initiated independently and separate mechanism
65
REM sleep structures
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
Muscle paralysis in REM sleep
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
Sleep normal induction
PGD2 accumulation in periphery Adenosine accumulation in CSF (triggered by PGD2) Adenosine receptor activation in VPI Leads to inhibition of ARAS
68
During special circumstance
Growth -GnRH and GH secretagogue receptors Illness -TNF of IL1b Any of these trigger NFKB
69
Induction of REM
Ach from lateral pontine tegmentum, release in geniculate body Large muscle paralysis requires locus cerulean
70
When wake up
From REM
71
How wake up
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
Orexin
Makes you eat from lateral hypothalamus
73
Hypocretin
Hypothalamic for secretin | Triggers pancreatic secretions
74
Orexin
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
REM sleep controlled by what
Circadian clock more active as more into night so stopping rem sleep
76
First cycle
70-100 minutes | Then moves to short REM and back to deep sleep
77
Later into night
Hardly in deep sleep, in shallow and rem | 90 minute cycle
78
Children
Sleep a lot in deep and rem More total sleep
79
Older elderly
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
Slow wave sleep
N1-N3 | Slow eeg
81
REM sleep
RAM and eeg picks up high frequency Paralysis of large muscles
82
N1
Drowsiness/earliest stage of sleeo Physical-slow, rolling motions of eyes, EMG show muscle activity, EEG-low voltage , slowing frequency
83
N2
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
Sleep spindles
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
N3
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
REM
Rapid side to side movements —DEFLECT IN OPPOSITE DIRECTIONS ``` EMG suppressed (locus ceruleus) Vivid dreams ``` EEG-rapid low voltage
87
Out patient
Obstructive sleep apnea Increased sleep latency
88
Thorax bigger abdomen smaller
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
Expiration
Internal inter coastal and abdominal recti
90
Upper middle lower zone
-10 top -2.5 bottom Lowest ventilation top bigger at bottom
91
Insp to ex aVL and intrapleural pressure
-5, -8, -5 intrapleural 0, -1, 0, +1 alveolar pressure
92
Anatomic dead space
Respiratory bronchiole-has alveoli, anything with alveoli are not anatomic dead space Trachea, right main, terminal bronchioles
93
Physiologic dead space
Anatomic+alveolar dead space=total
94
Total dead space
Usually same as
95
Pulmonary flow
Low resistance, high compliance
96
Hypoxia effect
Vasoconstriction
97
Hypocapnea what happens
Ok
98
Hypercapnea what happens
Ok
99
Acid base of respiratory system
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
Central vs peripheral chemoreceptors *low O2 can trigger increased external respiration
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
Rapidly adapting stretch receptors
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
J receptors what stimulates central
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
Changes in compliance on response system
Increased compliance-filling easy, exhalation hard | Change in v/change in p=compliance
104
Chances on respiratory system
Ok
105
Equation flux
SAxDiffusion coefficient (P1-P2)/diffusion distance
106
Westmarkers sign reduced blood flow to an area what is blood like leaving that area
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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