adv editor Flashcards

Question

what happens to gas exchange in restrictive lung disease, and why (O2 and CO2)

Answer 1

Diffusion - need integrity of AC membrane (thickness, surface area) Get a diffusion limitation of O2 transfer (usually is limited by ventilation) (the graph where blood stays in capillar .25 or .75 secs) Diffusion limitation for CO2 will occur with very severe abnormalities of AC membrane

Answer 2

low PaO2 - low inspired O2 - low ventilation - abnormal gas exchange (low V/Q, shunt, diffusion impairment) low PaCO2 - low ventilation (abnormal exchange only in VERY severe disease)

Answer 3

stiff lungs - increase elastic WOB - increase load on breathing

Answer 4

all lung volumes reduced both ↓FEV1 and FVC =\> ratio stays constant (can have both restrictive + obstructive =\> ↓FEV1/FVC + ↓FVC)

Answer 5

high frequency - rapid, shallow breaths

Answer 6

MV = 35 \* FEV1 FEV1↓ so ↓MV

Answer 7

all lung volumes are reduced ↓FVC ↓FEV1 normal FEV1/FVC

Answer 8

diffuse interstitial lung disease due to exposure to asbestos =\> restrictive pathophys * progressive, diffuse inflammation -\> over time drives fibrosis \> repair * abnormal fibrosis of lung parenchyma -\> disruption/destruction of AC membrane histo * areas of inflammation * fibrosis/scarring * asbestos bodies presentation = 3C's (clubbing, cyanosis, crepitations)

Answer 9

restrictive lung disease (interstitial) cause: unknown histo * interstitial inflammation * fibrosis at various stages of development prognosis * inevitable progression to end-stage lung * mean survival - 3 years

Answer 10

Normall - small amount of fluid leaks from capillary to interstitium (~5ml an hour) (capillary endothelium is highly permeable to water, ions, small molecules) =\> this is drained by lymphaticflow (~20ml/hr) if fluid leak \>20ml/hr =\> oedema - fluid accumulate in interstitium, then moves to alveoli

Answer 11

dry - epithelium actively pumps water back to intersitium

Answer 12

(1) increased capillary hydrostatic pressure (Starling's law) - increased pulmonary venous pressure, left heart pressure (2) Increased capillary permeability - toxins, sepsis, multiple trauma, aspiration of gastric acid etc. Theoretically: ↓colloid osmotic pressure, ↓lymp drainage = but these aggravate, not cause

Answer 13

CXR * Kerley B lines * dilated interlobular septa * dilated lymphatics * Perihilar alveolar opacities * ↑pulmonary vein size

Answer 14

Mechanical changes - small, stiff lungs Gas exhange abnormality - low V/Q units + shunt Pulmonary circulation - ↓vascular resistance Arterial blood gasses - type 1 resp initiall, then develop type 2

Answer 15

↓compliance, ↓lung vol, ↑airway resistance -fluid in airway, bronchioles are compressed, ↑wob

Answer 16

type 1 respiratory failure initially * ↓ PaO2 * ↓ PaCO2 * compensatory hyperventilation * ↑ pH * respiratory alkalosis - because of hyperventilation then develop type 2 respiratory failure * ↓ PaO2 * ↑ PaCO2 * ↓pH * metabolic and respiratory acidosis * metabolic: becaues of hypoxia - tissues start to produce lactic acid * respiratory: can't ventilate -\> ↑CO2

Answer 17

(1) Increased left atrium pressure (mitral stenosis, LVF) (2) Increased pulmonary blood flow (left-to-right shunts, high flow states, excess central vol) (3) Increased pulmonary vascular resistance (vasoconstriction, obstruction, obliteration)

Answer 18

Vasoconstriction - low alveolar O2, hypoxia, muscle spasm Obstruction - emobolism, primary pulmonary hypertension Obliteration = loss of capillary bed (interstitial lung disease - arteritis, emphysema, pulmonary fibrosis)

Answer 19

if very severe - right ventricular dilatation + hypertrophy (afterload) =\> ↑systemic venous pressure (extravasation of fluid in tissues) - oedema, ascities =\> poor cardiac output (breathlessness)

Answer 20

* right ventricular heave - feel beat of RV (just next to sternum) * loud P2 and 4th heart sound * pulmonary systolic ejection murmur * right heart is dilated - cusps can't come together, don't have functional tricuspid anymore * tricuspid pansystolic murmur -\> incompetence * sinus tachycardia - get decreased SV, so have to increase rate * hepatomegaly * ascites

Answer 21

* inhibits muco-ciliary escalator * increases mucous (direct trigger) * inhibits leukocyte function * direct damage to epithelial layer

Answer 22

* **Reduced respiratory centre activity ** * reduced drive (eg low CO2, high pH) * suppression of activity (drugs, trauma, vascular accidents etc ) * **Neuromuscular disease ** * nerve paralysis (drugs, polio, Guillian-Barre, trauma..) * muscle weakness (drugs, motor neurone disease, muscular dystrophy ) * **Chest wall deformity** (gross) * respiratory pump becomes inefficient * **Obesity** (gross) * respiratory pump becomes inefficient * **Sleep disordered breathing **

Answer 23

(1) Obstructive sleep apnoea - most common * upper airway (2) Central sleep apnoea * main abnormality: brain stem * several forms: eg Cheye Stokes breathing - delayed stimulus to brainstem * management: manage underlying problem +/- CPAP/BiPAP (3) Obesity hypoventilation syndrome * combo: particularly diaphragm * usually presents as ventilatory failure +/- RHF * "sensitive" to supplemental O2 * manage: BiPAP, weight reduction

Answer 24

Must sleep During sleep - you get hypoventilation (resetting of resp centre) - patient keeps waking due to inadequate stimulation (↓O2, ↑CO2) brain "decides" that LR sleep deprivation is not tenable -\> brain starts to accept a higher C O2 and lower O2 so that sleep can continue this spills over into daytime -\> **day-time hypoventilation =\> hypercapnoea**

Answer 25

day time hypoventilation (chronic severe sleep apnoea, severe COPD, severe pulm fibrosis, neuromusc disease) =\> chronic hypoxia, chronic hypercapnoea, compensated resp acidosis

Answer 26

become dependent on hypoxic drive (not stimulated to ventilate by CO2) - O2 is low because of chronic hypoventiliation ventilation also stimulated by exercise, metabolic acidosis

Answer 27

If someone has had chronic hypercapnoea - their drive to breathe will have swtiched from CO2 to O2 =\> supplemental O2 brings PaO2 back up - can develop acute hypoventilation only give enough O2 to bring them back to "their normal" - ~90-ish don't aim for 100 ish - then will dev acute hypoventilation

Answer 28

1. Snoring in light sleep 2. Complete obstruction (apnoea) in deep sleep 1. some people have narrowing such that this occurs with light sleep 3. Reduced blood O2, increased CO2 other stimuli 1. trying to breathe against obstruction 2. increasingly forceful breaths - icn WOB is another stimulus 4. Brain "wakes" to lighter sleep (arousal) 1. this takes some compared to while awake - sensing by brain is also depressed during sleep 5. Muscles contract, airways opens, breathing recommences 1. muscles regain tone, obstruction clears (at least partially) 6. Back into deep sleep -\> obstruct again Often 60x per hour throughout sleep

Answer 29

* Nasal CPAP - continuous positive airway pressure * applies positive pressure to upper airway during sleep * pressure acts as splint to keep soft tissues apart - stops their collapse * 85% compliance for moderate+ OSA * Mandibular advancement splint - mouthguard * brings jaw forward, base of tongue brought bwd, tends to stop it flopping back * Surgery * Lie on side

Answer 30

Transient obstruction of the throat during sleep preventing breathing, and disturbing sleep Obstruction occurs during sleep because of * relaxed airway muscles - floppy throat (esp REM) * throat already arrowed (obesity, tonsils etc) * tongue falls backward (esp if supine)

Answer 31

Thromboembolus lodges in pulmonary circulation Effects depend on: size of embolus, presence/absence of underlying lung and cardiovascular disease Embolus leads to development of: * hypoxaemia * local pulmonary artery obstruction + widespread reflex vasoconstriction * increases pressure in system * RV stress -\> dilation and contractile dysfunction * platelets in thrombi can release TXa -\> lead to vasoconstriction * Constriction of airways distal to bronchi * decreased pulmonary compliance * haemorrhage, loss of surfactant * VQ mismatch -\> acute pulmonary hypertension

Answer 32

Depends on the size Large/numerous * if \>60% of vascular bed is occluded - sudden collapse + death * acute cor pulmonale - dyspnoea, hypotension (↓LV output), cyanosis * pulmonary hypertension in setting of underlying lung problem Medium sized * Dyspnoea, cough, acute cor pulmonale * Pulmonary infarction (relatively uncommon - blood supply of lung ) Small sized * may be clinically silent * pulmonary infarction * recurrent * many small emboli over time -\> chronic pulmonary hypertension + cor pulmonale

Answer 33

rare - dual blood supply: * O2 comes in via bronchial arteries and pulmonary arteries (even though deox blood) more common if there is pre-existing lung and/or cardiovascular disease (eg heart failure - bronchial supply is sluggish; COPD - already hypoxaemic) typically seen as peripheral, wedge-shaped, haemorrhagic tissue dies because there is not enough O2, but there is still blood there -\> red infarct Signs * haemoptysis * pleuritic chest pain (acute inflammation -\> fibrous exudate -\> chest pain) * pleural friction run (from associated inflammation) * pleural effusion (because of inflammation)

Answer 34

Pulmonary trunk + both R&L pulm arteries

Answer 35

Early - coagulative necrosis + inflammation Heals same as MI - acute inflammation, granulation tissue, fibrosis + scar formation

Answer 36

* Smoke irritant -\> epithelium undergoes squamous metaplasia * stem cells -\> stratified squamous cells instead of respiratory epithelium * Carcinogens in smoke cause mutations in proto-oncogees and tumour suppressor genes -\> **dysplasia ** * get increased nuclei at surface compared to normal squamous epithelium * bit more disorganised * **carcinoma in situ** - more atypical and disorganised * these cells invade into underlying stroma -\> **invasive carcinoma **

Answer 37

Typically: * pale mass, irregular, often arising from bronchus * often necrotic (left) - form cavities * especially squamous cell carcinoma * adeno: tend to be more peripheral * enlarged hilar lymph nodes

Answer 38

if bronchus is blocked -\> can develop * pneumonia - mucus is obstructed - good place for bacteria to grow * collapse or bronchiectasis of distal lung

Answer 39

Squamous cell carcinoma =\> squamous proliferation Adenocarcinoma =\> glandular stem cells Large cell undiff =\> undiff cells, but of epithelial type (ep'm proteins) Small cell carcinoma =\> neuroendocrine origin

Answer 40

normally seen in the form of rounded centre of keratin in centre of tumour islands joined by intercellular bridges often a lot of eosinophilic cytoplasm (squamous cells - lots of cytoplasm)

Answer 41

shows glandular differentiation usual feature: malignant cells that try to form a lumen sometimes no cells - see accumulation of mucous (with special stain)

Answer 42

lots of large cells large pleomorphic nuclei - usually sheets of these larger atypical cells undifferentiated - no glands, mucous, intercellular bridges, keratin

Answer 43

cells are small - not that big compared to RBC don't show typical features of malignancy * small * small nuclei * not that pleomorphic * fine chromatin but have a "characteristic look"

Answer 44

Adenocarcinoma Smokers: squamous, small-cell, large-cell

Answer 45

Mutations in adenocarcinoma: EGFR (tyrosine kinase), ALK, K-RAS, B-RAF Gefitinim, Erlotinib - inhibit EGFR tyrosine kinase (different mutations in diff tumors - have to genotype)

adv editor Flashcards

(69 cards)