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IHP respiratory & cardiac syst. > respiratory > Flashcards

respiratory Flashcards

1
Q

PsyNS do NOT innervate wht?

A

blood vessels & heart ventricles ( so decr contractility by decr SyNS) Blood vessels & heart ventricles r not dual innervated

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2
Q

Bronchiconstriction process?

A

PsyNS: muscarinic ACh rec.: active MLCK: bronchiconstriction

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3
Q

way of air in resp syst? Pharynx (yutak)- - - - bronchioles

A

Pharynx (yutak) -larynx (girtlak)- trachea ( soluk borusu) - Bronchus - Bronchioles

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4
Q

Airways split- conducting & respiratory zones. What’s dif?

A

Conducting : No alveoli, no gaseous exchange Respiratory zone: have alveoli, Yes gaseous exchange

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5
Q

All respiratory muscles — muscles.(e.g. diaphram, intercostal muscles , accessory musc.)

A

SKELETAL ( somatic) have conrol over!

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6
Q

Pip is what?

A

P. btwn visceral & parietal pleura = intrapleural pressure

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7
Q

Pip is already —–.Why?

A

Pip is already -ve. BC of counter recoil of chest wall(out) & alveoli ( in: buzusur, gets smaller). So incr in V intrapelural space: P decr

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8
Q

What is Ptp?

A

Transpulmonary P = Palv - Pip = Alveolar distension

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9
Q

How Ptp & Pip changes during insp & exp.?

A
  • Insp: Ptp(alveolar ditension) inc, Pip decr
  • Exp: Ptp decr, Pip inc
  • Rmmbr tips- Pip & Ptp change dif.ly
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10
Q

Pneumothrax is wht?

A

Pleural seal broken, lung collapses ( buzulur gibi hany), Ventilation (breathing) ineffective, tracheal shift

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11
Q

PsyNS : using mAChr: ACh or histamine: 4 bronchiconstriction. Pathway is similar to wht?

A

SyNS : a adr. rec. using IP3: Ca2+ released fr ER/SR: Ca2+ Calmodulin complex : activates MLCK : vasoconstriction here tho

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12
Q

IgE

A

Emmunity, allergic reactions

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13
Q

Bronchodilation wht rec.?

A

rmmbr: Salbutamol: B2 agonist: b=B2 adr. rec.

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14
Q

B2 adr rec. result in bronchodilation how? (process)

A

B2 adr. rec.: Gas: adenylyl cyclase: cAMP: PKA P-s: MLCK so P-ed inactive MLCK; bronchodilation

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15
Q

Asthma (obstructive)Type 1 hypersensitivity?

A

histamine & chemokines & other vasoreactive elements result in asthamatic: hi resistance in bronchioles: bronchiconstriction by using mAChr: PsyNS

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16
Q

We all want — lung when it comes to compliance.

A

Emphysema-tic(barrel chest)

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17
Q

Emphysema bc of air trapping so wht changes happen?

A

Air trapping: lose alveoli: lose surface area: gaseous exchange decr.: 02 dif. decr.: 02 in blood decr.

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18
Q

Surfactant?

A

girl in the middle so H20 in alveoli not attrctd to other H20 anymore: surface tension decr.(less opposing force for expanding): compliance incr

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19
Q

Perfusion (blood supply) & Ventilation(getting air in) well matched. How?

A

BOTH Greater perfusion(blood supply/flo) & ventilation at the base/bottom of lungs.

20
Q

Extreme V/Q(perf.) abnormalities? ( 2 exmpls)

A
  • Shunt: whn NO ventilation (whn alveoli bronchi entrance is SHUT)
  • Alveoli dead space: NO perfusion (blood supply): so air in alveoli same as room air bc no blood flo no gaseous exchange e.g. bc: blood clot
21
Q

Asthma: expiratory probl. bc hi resist: diameter of bronchi small. PEFR (peak expiratory flo rate) ..?

A

PEFR is low fro asthmatic

22
Q

How FVC (forced vital capacity) & FEV1 (Forced expiratory volume in 1 sec: rate) &FEV1/FVC changes depending on obstructive or restrictive disease?

A
  • obstructive: e.g. asthma: whn resistance inc.: FEV1 decr= expiration rate decr., FVC stay same : FEV1/FVC decr.
  • Restrictive: e.g. fibrosis: FEV1 decr. : FVC decr. :FEV1/FVC same
23
Q

FVC is what?

A

Forced vital capacity: max air you can get into ur lungs whn restrictive it decr.

24
Q

FEV1 is what?

A

Forced expiratory vol. in 1 sec= rate : decr whn obstructive: e.g. asthma

25
Q

HCO3- makes ur blood?

A

basic

26
Q

If you have more CO2 in blood ur blood will become more – & pH will —.(e.g whn you hold your breath inc.ed arterial pCO2 as well as inc.ed alveoli pCO2)

A

CO2 will form carbonic acid so: blood bcms acidic: pH decr.

27
Q

PEFR ( peak expiratory flo rate) is – for asthmatic. ( the one you used during LSRC with smaller diametered tube)

A

low bc resistance hi, bronchi diameter small

28
Q

Probs with resistance: — disorder Probs with compliance: — disorder

A

have 1 ‘RES’ in each whn resistance hi : obstructive (e.g. asthma) compliance probs: restrictive (e.g. fibrosis or emphysema)

29
Q
  • whn compliance probs: restrictive disorder: ——
  • whn resistance probs: obstructive disorder:——
A
  • restrictive: change in vol (thts y FVC decr.. FEV1 decr. too)
  • obstructive: change in expiration rate & flo (FEV1 decr, FVC same)
30
Q

Obst. & rest. disease exmaples?

A
  • Obst: asthma, bronchitis
  • Restr: fibrosis, emphesema
  • both obst & restr: COPD = Chronic Obstructive Pulmonary Disease
31
Q

as you go up (e.g climbing mountain) wht happens in terms of pressure and ventilation?

A

Patm decr, PO2 decr (partial pres.), gaseous exchange decr. bc partial P gradient btwn alveoli & pulmonary circulation decr.

32
Q

intrapleural P = P btwn visceral & parietal pleura =?

A
  • can put visceral pleura= lungs
  • parietal pleura= intercostal muscles, thoracic cavity, ribcage (gogus kafesi), chestwall
33
Q
  1. vasoconstriction 2. vasodilation& bronchidilation 3. bronchiconst. by wht nerv. syst & rec?
A
  1. a adr. rec.= SyNS 2. B adr. rec. = SyNS 3. PsyNS
34
Q

Inspiration: all P changes?

A
  1. Palv ↓ :bc Valveoli ↑
  2. Alveolar wall distension=Ptp↑ = Palv-Pip
  3. if Ptp ↑: Pip ↓
  4. Inspi. musc.contract: Vthoracic cavity/chest wall ↑
  5. Palv smaller than Patm so get air into lungs
35
Q

P changes during expiration?

A
  1. Palv inc. bc Valv decr.
  2. Alveolar wall distension= Ptp decr = Palv-Pip
  3. Pip incr
  4. Insp Musc relax= Vthoracic cavity/ chest wall decr.
  5. Palv bigger than Patm = air out
36
Q

Alveolar interdependence?

A

Alveolar connected to each other and to intrapleural pressure (Pip): If inspire: Thoracic cavity out - extends parietal pleura- parietal pleura pulls visceral pleura- visceral pleura connects& extends alveoli then next one —connectivity

37
Q

hi resistance: obstr disorder: asthma: diameter change?

Hi resistance results in —- respiratry rate?

A

airway narrowing, diamter decr.

inc respiratory rate

38
Q

Fibrosis: – increases:

:—-compliance (expandability)

:—– Vair into lungs

A

thickness incr

low compliance= cannot expand the lung

less Vair into lungs

restrictive disorder

39
Q

compliance = —y of lungs & chest wall

A

expandability

40
Q

low compliance =?

High compliance= ?

A

fibrosis

emphysema

41
Q

Smooth muscle dif than skeletal muscles how?

A

Ca2+ entry fr both SR & thru L-TYPE CA2+ CHANNELS SO EXTRACELLULAR CA2+

42
Q

bronchial smooth muscle contraction, process?

A

Histamine(type1 hypersentvty) or ACh binds to mAChr:

PLC: IP3: binds to SR IP3rec. : Ca2+ out fr SR: also thru L-type channel extracellular Ca2+ gets in: Ca2+ bound active calmodulin: active MLCK (kinase): Ps MLC : P-ed MLC bronchicontraction

to relax: MLCP-ase: removs P fr MLC & Ca2+ into SR

43
Q

Bronchiodilation by B2 adr rec. process?

A

B2 agonist (e.g. salbutamol):Adenyly cyclase: cAMP: PKA: p-es MLCK: P-ed MLCK inactive:bronchiodilation

44
Q

in compliance disease curve

Fibrosis?

A

lower line bc fibrosis: with same Ptp you get less air in bc low compliance

y: vol of air into lungs
x: Ptp :alveolar wall distension : Palv-Pip

45
Q

Obstructive disorder Volume- t graph

FVC & FEV1 & FEV1/FVC changes ?

A

e.g. asthma : Resstnce hi

FVC- stays same: same amount of air out but takes longer

FEV1: expiration takes longer: flo rate low

FEV1/FVC= decr

46
Q

Restrictive disease V- t graph FVC & FEV1 & FEV1/FVC changes?

A

e.g. fibrosis: lo compliance

FVC decr: overall vol you expire decr/bc inspired less too & air trapping ..

thus FEV1 (rate) decr

FEV1/FVC same

like- paralel line below the normal compliant lungs

IHP respiratory & cardiac syst. (2 decks)

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