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Medicine > respiratory > Flashcards

respiratory Flashcards

1
Q

opiate overdose casues what to blood gas

A

respiratory acidosis

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2
Q

PE can casue what to blood gas

A

respiratory alkalosis- have low paO2 as well (unlike hyperventilation have norm,al or rasied PaO2)

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3
Q

what causes of respiratory alkalosis

A

PE
anxiety induced hyperventiulation
CNS disorderes= stroke, encephalitis, subarachnoid haemorrhage
altitude
pregnancy
salicylate poisoning (initial stages)

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4
Q

what causes respiratory acidosis

A

obesity hypoventilation syndrome
life threatening asthma (decompensated)
COPD - high co2
opiate overdose
benzodiazepines overdose
neuromuscular disease

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5
Q

whats the effects of salicylate overdose

A

salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis

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6
Q

whats the pathophysiology of salicylate overdose

A

In mild toxicity, salicylates directly irritate the gastric lining. They can also cause ototoxicity through a multifactorial process, involving reduced cochlear blood flow secondary to vasoconstriction and changes to cochlear cells.

In higher doses, the pharmacodynamics of salicylate poisoning leads to a mixed respiratory alkalosis and metabolic acidosis. In moderate/severe toxicity, salicylates stimulate the cerebral medulla, leading to hyperventilation and respiratory alkalosis.

Metabolisation of salicylates then causes uncoupling of oxidative phosphorylation, resulting in anaerobic metabolism. This causes heat production and pyrexia and increased lactic acid production, resulting in metabolic acidosis. The acidic effects of salicylates also contribute to the associated acidosis. Hyperventilation then worsens in response to the acidosis until the body can no longer compensate.

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7
Q

whats the signs and symptoms of a chest infection

A

sob
fatigue
fever
cough/productive
crackles on auscultation

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8
Q

whats the cuases of chest infection

A

streptococcus pneumoniae = most common
haemophilus influenzae

moraxella catarrhalis = immunocompromised/chronic lung disease

psudomonas aerguinsoa = CF/ bronchiectasis

staphylcoccus aureus = CF

atypical:
legionella pneumophila
chlamydia psittaci
mycoplasma pneumonia
chlamydia pneumonia
Q fever

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9
Q

whats the antibiotic of choice for chest infection

A

community = amoxicillin

or
doxycyline
or erythromycin or clarithromycin

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10
Q

what usually causes aPE

A

usually due to a dvt embolised

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11
Q

what risk factors for pe

A

recent surgery
imbolised
long haul flight
pregnacy
med involving oestrogen
cancer
polycythemia
thrombphilia
sle

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12
Q

what can you do for VTE prophylaxis

A

asses all pt admitted
LMWH- enoxaparin
antiembolic compression stokings

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13
Q

when are LMWH contradinicated

A

active bleeding
existing anticoagulant - warfarin doac

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14
Q

when are compression stockings contrainidcated

A

significant peripheral arterial disease

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15
Q

differentals of PE

A

MI
CAS
unstable angina
pneumonia
pneumothroax
acute exaserbation of asthma, copd
acute congestive heart failure
disecting/rupture of aortic anyeursm
acute bronchitits
pericardititS
GORD
any casue of collapse

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16
Q

presentation of PE

A

pleuritc chest pain
sob
cough with or without blood
hypoxia
tachycardia
tachypnoea
low grade fever
haemodynamiccaly unstable causing low bp
may have s and s of DVT= unilateral leg swelling and tenderness

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17
Q

pleurtic chest pains
sob
cough
what could this be

A

PE
other differnetials:
MI
CAS
unstable angina
pneumonia
pneumothroax
acute exaserbation of asthma, copd
acute congestive heart failure
disecting/rupture of aortic anyeursm
acute bronchitits
pericardititS
GORD
any casue of collapse

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18
Q

investigations for PE

A

wells score first

if score says likely pe= CTPA = if allergic to contrast or renal impairment do VQscan
if score says unlineky= d dimer and if positive do ctpa

can do cxr to exlcude other casues of symptoms

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19
Q

when would you not do a ctpa and what to use instead

A

ctpa require contrast
if renal impairmeent
contrast allergy
at risk from radiation

do vq scan= see mismatch= have well ventialted but not well perfused around area of pe

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20
Q

cause of respiratory alklalosis

A

pe= also have low pO2 - due to increase resp rate blowing off loads co2
hyperventialtion- have normal pO2

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21
Q

when will a d dimer be postive

A

pe - DVT
prengancy
cancer
surgery
pneumonia
heart failure

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22
Q

management of PE

A

supportive- analgesia, oxygen admit to hos[, monitor

intially give LMWH- enoxaparin/ dalteparin straight away before confriming diagnois if delay in the ctpa

long term anticoagulatn:
once diagnosed then need to either be on warfarin, doac or lmwh

warfarin: want inr 2-3
when switching from lwmh continue lmwh for 5 days or when inr 2-3 for 24 hrs (one takes longest)

or go on a doac that doesnt need monitorting = apixaban, rivaroxaban, dabigatran

or be on LMWH

stay on the anticoagulation for:
3 moths if cause is clear and reversible casue then review
or
more than 3 months if cause is unclear or ig cause isnt reversible or recurrent vte = usually 6 months
or
6 moths if active cancer then review

thrombolysis is massive PE with haemodyamic compromise = fibrinolytic medds = streptokinase, alteplase, tenecteplase

by iv cannula or catheter direct thrombosis

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23
Q

When is lmwh first line for long term coagulation for PE

A

pregfancy or cancer

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24
Q

whats enoxaparin and dalteparin

A

LMWH

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25
Q

whats apixaban , dabigatran, rivaroxaban

A

DOAC

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26
Q

whtas sarcoidosis

A

graulomatous inflammatory condition

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27
Q

presentation of sarcoidosis / organs it affects and how

A

typically involves chest symtpoms
young adults and 60s
woemn and black more

dry cough, fever and erythema nodosum eg. on shins most common presetation

restrictive pattern of lung fuction
lungs: 90%
pulmonary fibrosis
pulmonary nodules
mediastinal lymohadenopathy

systemic:
fever
weight loss
fatigue

skin: 15%
erythema nodosum
lupus pernio
granulomas can develop in scar tissue

heart:
heart block
bundle branch block
myocardial muscle involvement

cns:
nodules
pituitary involvemnt: diabetes insipidus
encephalopathy

pns:
bells palsy
mononeuritits multiplex

kidneys:
kidney stones= due to ince ca
nephrocalcinosis
interstitial nephritis

liver:20%
liver nodules
liver cirrhopsis
cholestasis

eyes: 20%
uveitis
conjunctivivtis
optic neuritits

bones:
arthritis
arthlagia
myopathy

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28
Q

erythema nodosum
polyarthralgia
bilateral mediastinal lymohadenopathy
what is this

A

lofgrens syndrome = triad of symtpoms
specific presentation of sarcoidosis

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29
Q

differentials for sarcoidosis

A

tb
lymphoma
hypersensitivity pneumonitits
HIV
toxoplasmosis
histoplasmosis

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30
Q

investigations for sarcoidosis

A

bloods:rasied serum ACE= screening test
raised ca
rasied serum soluble interleukin 2 receptor
rasied crp
raised immunglobulins

imagina:
cxr= hilar lymphadenopathy
high reoslution ct of thorax= hilar lymphadenopahty and pulmonary nodules
mri= may show cns involvmennt
pet scan = may show active inflammation in affected areas

hsitology= gold standard of diagnosis = bronchoscopy with ultra sound guided biopsy of mediastinal lymph nodes
= shows non caseating granulomas with epithelioid cells

others to see other organs ivlved=
u and e
lft
opthalmology
ecg, echo
acr - see if proteinuria - nephritits
us of abdo

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31
Q

screening test for sarcoidosis

A

serum ACE - rasied in sarcoidosis

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32
Q

definititve diagnosis of sarcoidosis

A

histology-
bronchoscopy with us guided biopsy of mediastinal lymph nodesshows non-caseating granulomas with epitheloid cells

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33
Q

treatment for mild/ no symotoks sarcoidoss

A

nothing
spontaneously resolve 6 months

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34
Q

treatment for symptoms of sarcoidosis

A

frist line: steroids 6-24 months with bisphosphonates to protect agaisnt osteoporosis
2nd line= methotraxate/ axathioprine
lung trasnplant if sevre

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35
Q

risk factors for sleep apnoea

A

obesity
smoking
males
middle age
alcohol

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36
Q

features of sleep apnoea

A

key feature is day time sleepiness
apnoea episides during sleep= reported by partner = not breathing for max mins during sleep
snoring
morning headache
waking up unrefreshed
concentration problems
reduced o sats during sleep

severe cases cuase hypertension and heart failure and increase risk of mi and stroke

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37
Q

management for obstructive sleep apnoea

A

initaly make sure know what occupation is = if requires fully alrt then need urgent referal ad amend work day duties till assesment

frist = refer to ent or sleep specialist
correct reversible factors= stop smoking, no alcohol, loose weight

second= cpap

sevre cases surgery to reconstruct soft palate and jaw= most common one is uvulopalatopharyngoplasty

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38
Q

whtas sleep apnoea

A

due to collapse of pahryngeal airway during sleep

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39
Q

pulmonary hypertension casues strain on which side of heart

A

right side of heart

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40
Q

causes of pulmonary hypertension

A

1- primary pulmonary hy/ connective tissue disease- sle

2- left heart fdailure due to MI / systemic hypertension

3- chronic lung disease- copd

4- pulmonary vascualr disease= PE

5- miscallaneous stuff- sarcoidosis, glycogen storage disorders, haematoglogical disorders

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41
Q

presentation of pulmoanry ht

A

sob
peripheral oedema
syncope
tachycardia
rasied jvp
hepatomegaly

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42
Q

investigations for pulmonary ht

A

ecg
chest x ray
NT- proBNP
echo

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43
Q

right ventricular hypertrophy
may occur when and what ecg changes show this

A

pulmoarny hypertension

large R wave in V1-V3= right chest leads

large S waves in V4-V6= left chest leads

right axis deviation
right bundle branch block

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44
Q

chest xray show in pulmoanry ht

A

dilated pulmonary arteries
right ventricular hypertrophy

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45
Q

whats the management for primary pulmoary ht

A

iv prostanoids = epoprostenol
endothelin receptor antagonist = macitentan
phosphodiesterase 5 inhibitor= sildenafil

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46
Q

treamtent for secondary pulmoanry ht

A

treat underlying cause eg pe, sle
supportive treatment for complcations too

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47
Q

what complciations are there of pulmoanry ht

A

heart failur
arythmias
resp failure

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48
Q

whats a pleural effusion

A

collection of fluid in the pleural cavity

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49
Q

whats exudative and whats transudative

A

exudative= high in protein- more then 3gtransudative= low in protien- less than 3

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50
Q

causes of pleural effusion thats exudative

A

related to inflammation
pneumonia
lung cancer
TB
rheumatoid arthritits

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51
Q

causes of pleural effusion thats transudative

A

related to fluid shift
congestive heart failure
hypoalbuminaemia
hypothryoidism
meigs syndrome = right sided pleural effusion and ovarian maligancy

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52
Q

whats right sided pleural effusion with ovarian malignacy

A

meigs sundrome

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53
Q

presentation of pleural effusion

A

sob
dullness to percussion over effusion
reduced breath sounnds over effusion
tracheal deviaiotion if bad

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54
Q

investigfation for pleural effusion

A

chest xray
sample fluids= aspiration / chest drain

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55
Q

what does pleural effusion look like on cxr

A

blunting of costophrenic angle
meniscus sign
deviation of trachea and mediastinum in massvie effusion
fluid in lung fissure

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56
Q

what look for in pleural effusio naspirationsample

A

protein count
cell count
pH
glucose
lactate dehydrogenase = LDH
microbio testing

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57
Q

treatment for pleural effusio n

A

if small then conservativr = trwt underlying cause if larger the aspiration, cehst drain

aspiration temporay relieves pressure but they can recur

chest drain= prevent reccurence

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58
Q

whats empyema

A

infected pleural effusion

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59
Q

penummonia is improving but pt has ew or ongoing fever

what is this

A

empyema

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60
Q

aspiration of fluid in pleural cavity if pt has empyema shpws what

A

pus
acidic ph
low glcuose
high LDH

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61
Q

treamtent of empyema

A

chest drain to remove pus
antibitocs

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62
Q

whats pneumothorax

A

air in pleural space = seperates lung from chest wall

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63
Q

causes of pneumothroax

A

iatrogenci - lung biopsy, mechanical ventilation , central line insertion
spontaneous
lung pathology- infection, astha, copd

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64
Q

presentation of pneumothroax

A

sudden sob
pleuritc pain - can radiate
cyanosiis
ipislateral reduced breath sounds
ipsilateral hyperresonance on percussion and hyperinflation

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65
Q

typical person to present with pneumothorax

A

tall young thin male presenting with breathlessness and pleuritic chest pain possibly while playing sport

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66
Q

investigations for pneumothorax

A

cxr
bloods
consider ct chest if too small to see on cxr

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67
Q

what does no lung markings show on cxr

A

pneumothroax

also measure the size of lung edge to iside chest wall at level of hilum

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68
Q

management of penumothorax

A

no sob
and less than 2cm of air on cxr = no treatment and will resolve, folow up in 2-4 weeks

if sob and or more than 2cm air = aspiration and reasess

if aspiration fails 2 times chest drain

if unstable / bilateral / secondary oneumothroax then chest drain

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69
Q

where chest drain go

A

triangle of safety
5th intercostal spacce mid axillarly line and anterior axillary line

needle above rib to avoid neurovascular bundle at bottom of ribcxr to cehck in postion after inserttion

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70
Q

whats tnesions pneumothroax and cause

A

trauma to chest wall creating a one way valve
air comes in each breath but non can go out so increase pressure each breath psushes mediastium across= kinks big vessels and causes cardiorespiratior arrest

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71
Q

signs of tension pneumothroax

A

tracheal deviation away from pneumothroax= air pushing it away
decreased air entry in affected side
increase respnance on percussion on affected side
tachycarida
hypotension

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72
Q

management of tension oneumothorax

A

insert a large bore cannula in secind intercostal space in midclavicular line
then once pressure relieved insert chest drain

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73
Q

whats sarcoidosis

A
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74
Q

whats pneumonia

A

infection of lung tissue
casues inflammation of lung tissue and produciton of sputum that fills airways and alveoli

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75
Q

presentation of pneumonia

A

sob
cough - producitve
haemoptysis
fever
pleuritic chest pain- inspiratory pain
delerium
sepsis
bronchial breath sounds - harsh breath sounds in and out due to consolidation
focal course crackles
dullness to percussion- consolidation/lung tissue collapse

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76
Q

signs of sepsis secondary to pneumoni a

A

fver
confusion
tachycardia
tachypnoea
hhypoxia
hypotension

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77
Q

how to asses severity of pneumonia

A

CURB 65
dont use urea in cap

confusion
urea over 7
resp rate 30 or over
bp systolic under 90 or diastolic 60 or less

65 or over

if 2 or more then consider hosp admission

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78
Q

casues of pneumonia - common ones

A

streptoccus pneumonia - most common cap in healthy
haemophilus influenxa- also v common casue cap in healthy

moraxella aeurginsoa = immunocompromised/ chronic lung condition
pseudomonas aeurginosa = CF/brocnhiectasis = common hap casue
staphylcoccus aureus = cf and durg users - needles

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79
Q

casues of penumonia atypical

A

atypical- not treated by pencillins wont work

legions of pscitatti mcq

legionella pneumophila = infected water/ac - think if been on holiday
casues hyponatraemia due to casuing SIADH

mycoplasma pneumoniae = rash- eythmeatous multiform- pink ring with pale centre - children can get neuro symtpoms

chlamydophila pneumoniae= mild to moderate pneumonia - school age - chronic pneumonia and wheeze

coxiella burnetti- Q fever = exposrue to animals and their bodily fluids

chlamydia psittaci = contact with infected birds

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80
Q

farmer got sob and productive cough and fever casue ?

A

Q fever= coxiella burneti
causes pneumonia
exposure to animals and their bodily fluids

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81
Q

man has fever and productive cough and pleuritic chest pain
owns a bird

A

chlymaydia psittaci
= contact with infected birds

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82
Q

fungal casue of pneumonia that seen in immunoscompromised pts. esp those with new hiv/ low cd4 count

A

PCP= pneumocystis jiroveci

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83
Q

investigfations for pneumonia

A

if crb 65 is 0-1 no need

if in hosp do
cxr= see consolidaiton
fbc- raised wbc
u and e - urea
crp- rasied
if moderate to severe also do:
sputum culture
blood culuture
legionella and pneumococccal urinary antigens

if immunocomprosied may not have raised inflammatory markers as they may not ahve any inflammatory response

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84
Q

treatment of pneumonia if atypical casue

A

macrolides(clarithromycin)
or fluroquines (levofloxacin)
or tetracyclines (doxycycline)

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85
Q

treatment for pcp

A

co-triomoxazole

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86
Q

patient siwth low cd4 are prescribed what to protect agaisnt pcp

A

oral co-triomoxazole as prophylaxis

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87
Q

treament for pneumonia if mild cap

A

5 day course- amoxicillin/ macrolide = oral

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88
Q

treatment dor mod-severe cap

A

7-days course- amoxicillin and macrolide

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89
Q

complications of pneumonia

A

sepsis
empyema
pleural effusion
lung absess
death

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90
Q

whats fev1

A

forced expiration volume in one second

measures how easily air can flow luot of lungs

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91
Q

FEV1 is low means

A

obstructive
air struggling to flow out

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92
Q

whats fvc

A

forced vital capaicty
total maount of air can be exhaled after full inspiration
measures to total volume of air a person can take into the lungs

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93
Q

FVC low means

A

restrictive - restriction of filling the lungs up

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94
Q

FEV1:FVC ratio less than 75%

A

obstructive

fvc normal but cant blow air out quick cus obstructing but can get air into the lungs and out but its just slow but still has the full capcaity of lungs

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95
Q

whats obstrucitve picture in fev1:fvc ratio

A

less than 75%

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96
Q

how to see if ashtma or copd on lung function test

A

test for reversibility - asthma is copd isnt

give bronchodilator - salbutamol- then do spirometry again
if fev1:fvc improve then asthma

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97
Q

if FEV1:FVC ratio is normal / rasied measn

A

restrictive
they are either both equally reduced so normal or can even be raised becasue the FEV1 can be raied becasue tight lungs so push air out

fvc be reduced becasue cant ge tthe air into the lungs

98
Q

restrictive pattern in spirometry

A

FEV1:FVC ratio normal or rasied

both are euqally reduced
ott fev1 can be normal / raised
fvc reduced

99
Q

causes of restrictive pattern

A

anythig that restricts chest wall and lung expansion to draw air in
interstitial lung disease- pulmonary fibrosis
sarcoidosis
scoliosis
obesity
MND

100
Q

whats peak flow and how to use and when to use

A

= fastest point (peak) of a persons expiratory flow of air
use to see obstrutive lung disease and esp how asthma controlled - obstructive air can fill all lungs but does so slowliy in and out

it demonstrates how much obstruction there is to the outflow in pts lungs

stand tall
from good tight seal
deep breath in
blow fast and hard as can
x3 and take best number

compare what shuld be of sex age ehight etc
and gives perceetnage of predicted

101
Q

whats asthma

A

reverisble airway obstruciton

102
Q

pathology of ashtma

A

chronic inflammatory condtion that causes episodic exaserbations of bronchoconstction

inflammation casues excess mucus secretion = cough and further blockage

constriction casued by hypersensitivity and can be triggered by enviromental factors

103
Q

trigers of ashtma

A

infection
night and early morning
allergens
cold air
damp/dusty air
animals
exercise
strong emotions
after nsaids, beta blockers
occupational

104
Q

what meds exaserbate asthma

A

nsaids
beta blockers

105
Q

presentation of asthma

A

episodic
diurnal variability - worse at night
cough with wheeze and sob
hx of atopy- eczema, hayfever, food allergy
fam hist
bilateral widespread polyphonic wheeze

106
Q

diangosis nice of asthma

A

do investigations before treatment
1st line= FeNO - above 40 postive
spiroemtry with bronchodilator reversibilty - improve fev1 by 12 % or more and increase volume by 200ml or more

if uncertain after that:
peak flow - PEFR - 2-4 weeks if 20% variable
direct bronchial challenge test with histamine/ mathacholine

107
Q

managment of asthma according to nice

A

1= saba = salbutamol/ terbutaline
2= add ICS = beclometasone/ butesonice/ flucticasone/ mometasone
3= add oral leukotriente receptor antagonist = monteleukast
4= add LABA inhaler - only contrinue if good repsonse - review 4-8 weeks = salmeterol
5= consider changing to MART
6= increase ICS dose to medium
7= consider increase ics to high dose/ oral theophylline / inhlaed LAMA
8= refer to specialst

108
Q

what mart options are there and what is mart

A

fast acting LABA and ICS
use 1/2 in morn and eve and then when needed

fostair= formoterol + beclasmetasone
symbicort = formoterol + budenoside
seretide= salmeterol + fluticasone

109
Q

whats saba and action and options

A

salbutamol
terbutaline

short acting beta 2 agonsit
relacion of smooth muscle

110
Q

what ics are there and side effects

A

beclometasone
butsenonide
fluticasone
mometasone
maitence/prevernter - take regualry

se= thrush, hoarse voice, osteoporosis- ensure ca intake and exercise

111
Q

se of saba/laba

A

tremor- excess use measn not controlled

tachycardia, headaches, hypokaleamia = causes blood potassium to move into cells

112
Q

what laba options are ther

A

salmeterol
formoterol

113
Q

lama
name and mechanism

A

tiotropium
blocks ach r
ach - pns activates to casue contraction so blcok this casues bronchodilation

114
Q

leukotriene receptor antagonist
name and mechasnim

A

monteleukast
leukotrienes are produced by immune system
cause inflammation, bronchoconstriction, mucus secretion
anatagonist so block leukotrienes so block allthis

115
Q

theophylline
action

A

relax bronchial smooth muscle and reduce inflammation

has a narrow therpaeutic index so needs monitoring blood levels as can then be toxic

monitor after 5 days starting and then after 3 days for each dose change

116
Q

which asthma drug do you need to monitor blood for

A

theophylline

117
Q

what is a low, med. high ics dose

A

400micrograms or less = low
400-800 micrograms= med
over 800 high dose

118
Q

theophylline toxicty/ posioning symtoms

A

vomiting
agitation
restlessness
dialted pupils
sinus tachycardia
hyperglycemia

serious:
haemetemesis
convulsion-seizures
supraventriocular and ventricular aryhtmias
severe hypokalameia

119
Q

presentation of acute asthma

A

progressively worseing sob
use of accesory msucles
symmetrical wheeze on asucultation
tachypnoea
chest sound tight and reduced air entry

120
Q

what moderate acute asthma attack

A

pefr 50-75% predicted

121
Q

whats severe acute asthma attack

A

PEFR 33-75%
or
resp rate more than 25
or
hr over 110
or
unable to complete snetnece

122
Q

whats life threatening acute asthma attack

A

PEFR less than 33%
or
sats less than 92%
or
tired
or
no wheeze- silent cehst
or
cyanotic
or
haemodynamically unstbale.- low bp
or
confusion

123
Q

abg of person initally acute asthma attack

A

repsiratory alkalsos- breathing wuick so blow off co2

124
Q

abg of lifethreatening acute asthma attack

A

normal pco2
/ hypoxia
concerning as patient is then tiring ans not breathing as much

125
Q

abg of near fatal acute ashtma attack

A

repsiratory acidosis due to high co2 - vvv bad

126
Q

patient has respiratory acidosis in acute asthma attack
how bad is this

A

near fata

127
Q

pt has normal pco2/ hypoxia in acute astham attack
how bad is this

A

life threathening
means not brehting much as pt is tiring

128
Q

treatment for acute ashtma attack

A

if moderate :
nebulsised SABA - salbutamol 5mg and repeat every 30 mins
if no imporvemnt add nebulised ipratroium bromide

give steroids- iv hydrocortisone or oral prednisolone - contiunue for 5 dys
abx if bacterial infection casue

if severe aslo give :
oxygen so sats maintained 94-98%
aminophylline iv - senior dp
consider iv salbutamol

life threatening:
add
iv magensium sulphate - senior
hdu/icu
intubation- need consider early as intubating when severe bronchoconscrition is hard

129
Q

monitor acute asthma attack

A

o2 sats - below 92% life threatning - aim for 94-98%
resp rate
resp effort
peak flow
chest asucultation
monitor serum potassium as salbutamol can casue hypokalameia as casue k to go into cells
onitor hr as salbutamol will also casue tachycardia

130
Q

pt has pneumonia but no acute exaserbation of copd (no wheeze, no dysponea)
pt has copd
should give steroids??

A

yes
give steroids to copd pts with pneumonia even if no sign of acute exaserbation

131
Q

gynaecomastia is associated with what lung cacner - paraneoplastic syndrome

A

adenocarcinoma

132
Q

paraneoplastic syndromes asscoaited with small cell lung cancer

A

SIADH-> hyponatraemia
ectopic ACTH= cushings syndrome
lambert - eaton myasthenic syndrome - diff walking and muscle tenderness. weakness worsens as use increases

133
Q

FVC and FEV1 in restrictive pattern

A

both equally reduce so that the ratio is then normal or can be raised becasue the FEV1 can be okish becasue the restricted lngs can push the air out as they restricted anyway

134
Q

obstructive spirometry and casues

A

FEV1 - significantly reduced - air slow to move out
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced - less than 0.75 (0.7)
Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans

135
Q

restrictive pattern and casues in spirometry

A

FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased

Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis e.g. ankylosing spondylitis
Neuromuscular disorders
Severe obesity

136
Q

casue of copd

A

smoking
air pollution
alpha 1 anti trypsin deficiency
work place dust and fumes

137
Q

pathology of copd

A

empysema = alveolar walls damaged and so air trapped in them = pink puffers = hyper inflated and barrel cehst as air trapped in them . increased resp rate and purse lips

chronic bronchitits= chronic inflammaation - thick sticky mucus blocks airways and inflammation and swelling makes worse = blue bloaters

138
Q

presentation of copd

A

wheeze
cough- often productive
recurretn resp infections
barell chest
chronic sob

139
Q

cxr findings and oxamination for copd

A

barrel chest
bullae may be there in empysema
hyperresonance percussion

140
Q

differentials for copd

A

lung cancer
fibrosisi
heart failure
asthma- see reversibility
unusual to have haemoptysis, finger and chest pain in copd
no finger clubbing

141
Q

hyper resonance percussion occurs in what

A

asthmna
severe empysema
pneumothorax

142
Q

how to diangose copd

A

clinical and spirometry
obstructive picture - FEV1/FVC ratio less than 0.7 (70%)
no dramatic reversibility with b2 agonist

143
Q

whats the severity stages of copd

A

all have fev1/fvc ratio less than 0.7
stage 1: FEV1 more then 80% predicted
stage 2: FEV1 50-79% predicted
stage 3 : FEV1 30-49% predicted
stage 4: FEV1 less than 30%

144
Q

other investigatins for copd can be done

A

cxr to rule out other patholgoies
gbc = see if polycythameia (if chronic hypoxic then increase hb) and anemia
bmi
sputum culutre- asses for chronic infection
ecg and echo- asses heart function
ct thorax- lung cancer , fibrosis, bronchiectasis
serum alpha 1 antitrypsin - of deficiency empysema is worse and early onset
TLCO is low in copd (asthma its raised)

145
Q

managemnt of copd

A

stop smoking
pneumococcal and flu vaccone
stage 1: SABA/SAMA(ipratropium bromide)
stae 2 if no response to steroids or asthma like features) = LABA + LAMA (anoro ellipta, ultrobreehaler, dualar genuair)

stage 2 if athmatic features/response to steroids= LABA + ICS

stage 3= LABA + LAMA + ICS= trimbo/ trelelg elipta

severe:
oral theorphylline
nebulsisers
home oxygen therpay if hypoxic at rest (no smoking though) , polycythamia, cyanosis, heart failure secondary to pulmonary ht= cor pulmonale
prophylactic abx= azithromycin
oral mucolytic= carbocisteine

146
Q

exaserbation of copd

A

= acute worsening of symptoms
cough
wheeze
spututm
sob
fever
inc rr/ hr

147
Q

most common casue of copd infective exaserbations

A

haemiphilus influenza

148
Q

investigations for copd exaserbatin

A

cxr - pneumonia etc
fbc - wbc
abg - see what co2 levels are
ecg - arhtmia and heart strain
u and e check electrolytes
sputum culutre
blood culture if septic

149
Q

treamten tof copd exaerbation

A

at home:
increase doses / take regular of inhaler/ nebulsier (what normally use)
prednisolone 30mg od for 5 days
abx may be needed= amoxicillin/ doxycylicn / clarithromycin

in hosp:
oygen= venturin mask if retianing co2 keep sats 88-92%
if not retaining co2 then can aim for normal sats of 94-98
nebulised bronchodilators- saba/sama = salbutamol/ipatropium
steroids - 200mg hydrocortison (possibly iv), 30-40mg oral prednisolone
abx
physio

severe:
iv aminophylline
niv
intubation
doxapram if no niv/intubation appropriate

150
Q

how many times pt with copd exaserbations with steroids need consider for prophylaxis for …

A

3-4 cases per year of exaserbations using steroids to treat then consider prophylaxis for osteoporisis

151
Q

ABG has high co2 and high bicarb and normal ph

A

retaing co2 but chronic as kidneys able to compensate

152
Q

pt abg got copd
high co2
relaitvely high bicarb
ph acidodic

A

copd exaserbation

normally high levels bicarb to compensate for retaining co2 but kidneys cant keep up wth the incerase co2 as acute exaeerbation cant get it out

153
Q

retaining co2 acutely abg

A

resp acidosis

154
Q

whatrs NIV

A

alternative to full intubation and ventilation
mid point
full face/tight fitting nasal mask to blow air frocefully into lungs

155
Q

whats BiPAP and when used

A

bilevle postivie airway pressure
cycle high and low pressure correspondong to breathing in and out
higher pressure inspiration
used in t2 resp faulure- typically copd

ipap= pressure during inspiration
epap= pressure during expiration = less but still some to stop airways collapsing

the pressures are based off body. ass
average male starts ipap= 16-20cm H2O
epap= 4-6cm H2O

then can increase ipap by 2-5cm increments until acodisis is resovled

156
Q

criteria for bipap

A

respiratory acidosis:
pH less than 7.35
paco2 more than 6
despure adequate med treatment

157
Q

contraindications for bipap

A

pneumothroax untreated
structural/ patholgy abnormalities affecting face, gi tract and airway

do cxr prior to starting if this can be done

158
Q

when to monitor abg in bipap

A

1 ahr after ever change
and
every 4 hrs until stable

159
Q

whats cpap and when used

A

continuous possitive pressure
keeps airways expanded all time so air can travel in and out

uses: in airways prone to collapse
obstructive sleep apnoea
congestive cardiac failure
acute pulmonary oedema

160
Q

whats. interstitial lung disease

A

conditions that affect the lung parenchyma casuing inflammation and fibrosis= replacment of normal elastic tissue and lung function with scar tissues thats stiff and not function effectviely

161
Q

types of interstital lung disease= fibrosis

A

idiopathic pulmonary fibrosis
secondary pulmonary fibrosis
asbestosis
cryptogenic organsisng pneumonia
hypersenstivitiy pneumonitit s(extrinsic allergic alvelolitis)
drug induced
can get from infection eg. pneumonia ]can be focal or can be diffuse (extrnisic allergic alveolitits/idiopathic pulmoanry fibrosis)

162
Q

diangsos of pulmonary fibrosis

A

HRCT- ground glass apperance
and with clinical features

if unclear do lung biopsy

163
Q

managment of pulmoanry fibrosis / interstial lung disease

A

generally poor progniosis and limited rx
damage is irreveersibl
rmeove andtreat the underlying cause
home o2 if hypoxic at rest
stop smoking
physio and rehab
penumoccoal and flu vaccine
advanced care planning
lung transplant

164
Q

presentation of pulmonary fibrosis

A

persistant sob and dry cough for over 3 months
50 and over
bibasal fine crackles inspiratory
finger clubbing
can have a restricitve pattern on spirometry

165
Q

whats idiopathic pulmonary fibrosis

A

progressive pulmonary fibrosis with no clear casue

166
Q

treatment idiopathic oulmonary fibrosis

A

pirfenidone = anti fibrotic and anti inflammatiory

nintendanib= monocolonal ab targetting tyrosine kinase

167
Q

whats drugs can induce pulmoanry fibrosis

A

amiodarone
methotrexate
nitrofurantoin
cyclophosphamide

168
Q

what casues are there of secodnary pulmonary fibrosis

A

rheumatoid arthritis
alpah 1 anti trypsin deficieny
skorgrens syndrome
sle
systemic sclerosis

169
Q

what type of hyersenstivity rxn is hypersenstivity pneumonitits (extrinsic allergic alveolitits)

A

type 3 hypersentitivty rnx to enviroemntal allergen

170
Q

causes of hypersenstivity pneumonitits (extrinsic allergic alveolitits)

A

farmers lung= rxn to mouldy spores in hay
bird fanciers lung= rxn to bird droppings
mushroom wokrers lung= rxn to specfic mushroom antigen
malt workers lung = rxn to mould on barley

171
Q

investigatios for hypersenstivity pneumonitits (extrinsic allergic alveolitits)

A

bronchoalveolar lavage=> increased lymphocytes and mast cells

172
Q

treat hypersenstivity pneumonitits (extrinsic allergic alveolitits)

A

remove allergen
oxygen and steroids where needed

173
Q

whats cryptogenic organising pneumonia

A

focal area of inlammation of lung tissue- leads to focal areas of pulmoanry foibrosis

174
Q

cayses of cryptogenic organising pneumonia

A

idiopathic
triggered by infection
inflamm disorder
radiation
meds
envromental toxins
allergens

175
Q

presentation of cryptogenic organising pneumonia

A

fevr
sob
cough
lethargy
- like pneumonia

176
Q

cryptogenic organising pneumonia cxr

A

focal consolidation- look like pneumonia

177
Q

definitive investigation for cryptogenic organising pneumonia

A

lung biopsy is definitive

178
Q

treamtne tof cryptogenic organising pneumonia

A

systemic corticosteroids

179
Q

what irritants can casue pulmoanry fibrosis/ interstial lung disease

A

silica
coal dust
asbestotis

180
Q

whats asbesosis

A

lung fibrosis related to inhallation of asbetso

181
Q

whats asbestots

A

fibrogenic and oncogenic
takes decades to develop

182
Q

inhalation of asbestos can casue what probelms

A

adenocarcinoma
mesothelioma
pulmonary fibrosis
pleural thickening and pleural plaques

pts with heslth conditions reated to exposure (exceptnplaques) can get compensation

183
Q

if pt dies with known asbestos exposure hwat needs be done

A

refer to coroner

184
Q

whats cystic fibrosis

A

autosomal recessive condition affecting the mucus glands => thick and stcky

185
Q

what gene is afected in CF and whats most comon mutation

A

CFTR gene on chr 7
delta F508

186
Q

key consequences of CF

A

thick pancreatic and bilary secretion=>
blockage of ducts
lack digestive enzymes to get to the system as blocked = pancreatic liipase esp

low volume and thick airway secretions=>
decresed airway celarance-> bacterial colonisation and suseptible to airway infections

congenital bilateral absence of vas deferens =? male infertility- have ehalthy sperm but sperm cant ge tout

187
Q

presentation of cf

A

normally picked up at birth
meconium ileus = not pass meconium in frst 24 hrs as thick and sticky in cf=, abdo distention and vomiting

recurrent LRTI
failure to thrive
pacnreatitis
chronic cough
thick sputum production
parent says child is salty to kiss
steathorrea- loose ad greasy
nasal polyps
finger clubbing
crackles and wheeze on asucultation
abdo distenition

188
Q

dianosis of CF

A

most picked up with blood spot testing newborn
sweat test- gold standard- chloride levels over 60mmol/l is positive
genetic test for CFTR gene - amniocentesis, chorionic vilus, bloood test

189
Q

common microbial colonisiers for CF

A

staphlycoccus aureus -> can give long term prophylaxis flucloxacillin
haemophilus influenza
klebsiella pneumonia
e coli
burkhodhena capacia
psuedomonas aeurginosa- hard to treat and worsesn cf prognosis - avoid cf pts seeing eachother as risk colonsiers passing it on - treat colonisation with long term nebulised abx = tobramycin. oral ciprofloxacin

190
Q

maangemnt of cf

A

physio
high calorie intake- physio, coughing, malunutrition, increase resp effort, infections
creon- for replacement of lipase if needed
prophylactic flucloxacillin (staph aureus)
treat chest infections
bronchodilators- salbutamol
nebulised DNase= break down resp secretions
nebulsied hypertonic saline
vaccination - pneumoncoccal influenza, varicella

other:
liver tranplant and lung trasnplant in end stage failure
feritlitt rx= sperm extraction
genetic counselling

191
Q

number of carriers of cf

A

1 in 25

192
Q

both parents are healthy, one sibling has cystic fibrosis and a second child does not have the disease, what is the likelihood of the second child being a carrier?

A

2 in 3 chances

know they dint have it
and both parents must be carriers so got two xaxA and so dont have xaa cus know they dont have it. left have got xaxA and xaxA and xAxA. so 2 in 3 chance of carrying

193
Q

when to monitor cf patients and monitoring for what

A

every 6 months
sputum colonsidation for psuedomonas
diabetes
osteporosis
vit d deefciecny
liver failure

194
Q

what can cf patietns develop

A

90% develop pancreatic insufficnecy
50% cf related diabetes and and require insulin
30% develop liver disease
most males infertile due to absent vas deferens

195
Q

whats bronciectasis

A

chronic resp disease characterised by permantne t bronchial dialtion due to irreversible damage to broncial wall

196
Q

caues of bronciectasis

A

previous severe lrti = most common casue
eg. oenumonia, pertussis, pulmonarry tb, mycoplasma, influenza etc
pulmonary disease- copd, asthma= frequent exaserbations

ongenital- CF, primary cilairy dyskinesia , alpha 1 anti tryppsin deficiency - empysema
connetive tissue disease- rhemuatoid arthritis, sle, sarcoidosis

idiopathic- 40%

IBD - more common in UC

197
Q

presnetation of bronchectasis

A

persitant couch with mucuopurulent sputum - 8 weeks or more
hameotpysis
exertional dynspnoea and gets worse pregresdively so then at rest sob
fatigue
rhinosinututs symptoms - nasal discahrge, obstruction,
histroy of a trigger
weight loss
course crackles esp on lower zones
wheeze
high pitch inspiratory squeaks
large airay rhonci
finger clubbing

198
Q

investigations for bronciectasis

A

sputum culute - see if colonising pathogen
cxr- may be normal. may see tram lines and ring shadows
spirometry- obstruction
o2 sats
HRCT= broncial dialtion,
test fpr a casue- anti ccp, ana, anca, ige, ciliary dyskinesa, RA etc
crp rasied in acute exaserbation

199
Q

differentiels for brocniectasis - presitant cough with sputum, haemptysis, sob, fatigue, tiger, weight loss, course crackles, wheeze, high putch inspiratory squeak, rhinositits sympotoms

A

asthma= have diurnal variaiton, history of atopy, bronchodilation reversibility

copd= have decreased breath sounds, no high pitch sqeak, ct may be normal

penumonia- more acute onset, day not months to years
cxr show consolidation

chronic sinusitis= vesicular breath sounds, radiology invetigations normal

200
Q

pathology of bronciectasis

A

inital insul eg, infection activates immune cells
immune cells reasle cystokines and proteases
inflamamtio casues damage to muscle and elastin casuing dilation
but in bronciectasis this cant be reveresed eg. due to impaired mucociliary clearnace, dysregulated immunuty

dilaition then predisposes to microbial colonisation and then all hapens again so get more and more dialted

201
Q

treatment for bronchestasis

A

stop smoking
follow up in secindary care if had 3 or more exaserbaions in a year, chronic psudomonas, mrsa, deteroiring,allergic oulpnary aspergillos, asscoatedwith RA, ibd, priamry cilairy dyskinesia, immune deficient

pulmoanry rehab
anual vacines
mucoactie agents- carbocistein/nebulsied saline
long term abx if 3 or more exaserbation in a year= azithromycin 3 /7
bronchodilator- laba
treat underlying condition
long termo2 if sats below 88% on room air
lung resection of localsied
lung trasnplant if under 65 depsite med rx no better

202
Q

complications of broncoectasis

A

infective exaserbations and chornic colonisation
haemoptysis
pneumothorax
resp failure
cor pulmonale due to pulmonary ht
chest pain
corary heart disease
anxiety and depression
nutirtional deficnect ]fatigue
lung transplant comlications
macrolides (axithromycin) = long QT , tinnutus, hearing loss

203
Q

se of long term use of macrolides - azithromycin which is used in long term abx if 3 or more exaserbation in 1 year of bronciectasis, copd

A

long QT
tinnitus
hearing loss

204
Q

whats TB

A

mycobacterium tuberculsos
acid fast baccili that stain red with zihel neelsen staining

205
Q

acid fast baccilli that stain red with ziehl neelsen staining

A

TB

206
Q

what stating use for TB

A

zeihl neelsen- stain red

207
Q

disease course of TB

A

v slow divding and need lots oxygen- hence often in lungs
trasmoission via saliva droplets
spreads through body in blood and lymph
granulomas form containg the baceria
most cases can celar and kill infection

latent tb= immune system encapsulates site of infection to stop progression bt can reactivate
seocndary tb = latent tb reactivated

208
Q

diseminated tb

A

immune system cant control the disease - severe- mililary TB

209
Q

site of infection of mycobacterium tuberculosis

A

lungs most common
extrapulmoanry:
bones and joints
cutaneous tb
GI
genitourinary
pleura
CNS
pericardium

210
Q

vaccin for TB

A

BCG
live atenuated- cehck not got hiv . immunosupressed before giving it

before vaccine do mantoux test and give vaccine if test is negatve
give vaccine:
BCG vaccine is offered to patients that are at higher risk of contact with TB:

Neonates born in areas of the UK with high rates of TB
Neonates with relatives from countries with a high rate of TB
Neonates with a family history of TB
Unvaccinated older children and young adults (< 35) who have close contact with TB
Unvaccinated children or young adults that recently arrived from a country with a high rate of TB
Healthcare workers

211
Q

risk factors tb

A

known contact with active TB
immirants from area of high rate tb
peoplewith close relative.close contat from countires of hogh rate tb
immunocompreommsied
homeless, drug users, alcoholics

212
Q

presentation TB

A

fever
chronic gradual worsening of symtoms
most pulmoary tb
lethargey
weight loss
haemoptyisis
cough
lymphadenomapthy
erythema nodosum
spinal pain in spine TB =potts disease

213
Q

investigations TB

A

mantoux test to see if got tb= used tuberculin into skin, wait 72hrs and if induration 5mm or more postive. then do interferon gamma realease assay to see if active - this test confirms latent tb

ziehle neelsen stain- bright red
cxr

214
Q

see on cxr for primary tb

A

pathcy consolidation
pleural effusions
hilary lymphadenopathy

215
Q

see on cxr for reactivated tb

A

patchy / nodular consolidation with cavitations esp inthe upper zones

216
Q

see on cxr in diseminated TB

A

millet seeds throughput lung fields

217
Q

managment of latent tb

A

if ehalthy do nothing
if at risk of reactivation (immuncompsormised etc)
:
rifampacin and isonazid = 3 months
or
isonazid 6 months

218
Q

managemnt of acute pulmoaryTB

A

ripe
rifampacin 6 months
isonazid 6 months
pyrazinamide 2 months
ethambutol 2 months

test for other disease- hiv, hep b and c
contact test tb
notify public health
isolate for 2 weeks once started rx
extrapulmoarny disease= corticosteroids

219
Q

se of rifampacin

A

hepatoxocity
red/ orange disolcouration of secretion- tears and urine
induced cyp450 enxyme so drugs metabolsied by this less effective- COCP

(red and orange pissin)

220
Q

se of isonazid

A

peripheral neuropathy
hepatoxicity
(im so numb a szid)

221
Q

isonazid what other med take too

A

pyrixodine - b6 to prevent peripheral neuropahty

222
Q

pyrazinamide se

A

hepatoxicity
hyperuricaemia = gout

223
Q

se ethambutol

A

colour blindess adn reduced visual acuity
(eye thambutol)

224
Q

which tb meds can casue hepatoxocitiy

A

rip
rifampacin
isonazid
pyrazinamide

225
Q

tb rx
orange urine and red tears
which meds causes

A

rifamacin

226
Q

tb rx
difficulty recognising coliurs
which med

A

ethambutol

227
Q

tb rx
painful elbows
whioch med

A

pyrazinamide
casues hyperuricaemia - gout

228
Q

tb rx
feels numbness in toes and unusual sensation
ned casues

A

isoniazid

229
Q

arterial blood gas
first look at what

A

oxygen
PaO2= are they hypoxic - if hypoxic then respiratory failure

then look at FiO2- fraction of inhaled 02
room air= 21%
venturi mask can control FiO2
pther masks can only give approximate FiO2

230
Q

types of resp failure

A

type 1= normal CO2, low O2

type 2- rasied CO2, low O2

231
Q

once looked at co2 and oxygen look at what

A

pH
acidoitic, alkaltoic or noral
full compensation? partial compensation?

eg. COPD have full metabolic compensation chronic high CO2 and so kidneys have tome and make bicarb high so balance sout the high co2

232
Q

repsiratory acidosis whats this

A

high PaCO2
low pH high CO2
acutely retaining co2- unable to blow it off

233
Q

where bicarb come from

A

produced by kidneys
take time to be produced
if bicarb high then chirnically retaitning CO2 (if the co2 is high this is)
eh. copd

acute resp acidosis the bicarb be low cus isnt fast enough to keep up with rising co2

234
Q

acute exaserbation COPD ABG

A

acidotic
rasied CO2
raised bicarb
- kidneys cant keep up. norally the bicarb is rasied to compensate for the high co2 but now the co2 risijg too fast in the exaserbation so acidotic despite higher bicarb than normal

235
Q

respiratory alkalsosi

A

rasied resp rate- blowing off too much CO2
high pH
low PaCO2

236
Q

casues of resp alklasosis

A

hyperventialtion
PE

237
Q

high pH
low PaCO2
normal/ high O2

A

hyperventilation
resp alklaisis with normal / high o2
= hyperventialtion

238
Q

high oH
low PaCO2
low PaO2

A

PE
resp alkalosis with low po2= PE

239
Q

metabolic acidosis causes

A

low pH
low bicarb

casues:
rasied lactate- anerobic resp= tissue hypoxia - damge
raised ketones= DKA
increased H ions = renal failure (cant excrete them), type 1 renal tubular necorisis, rhambomyolysisi (casues aki cus myoglobuin )

reduced bicarb= renal fialure, diarhoea (stool contains bicarb), type 2 acute tubular necorisis

240
Q

metbaolic alkalsosis casues

A

hgih pH
high bicarb

casues:
loss H ions = Gi tract (vomiting)
loose H ions from kidneys= too much aldosterone (aldosterone enoucarges excretion h ions and k ions and reabsorbtion na and water)
high aldosterone=
heart failure (trying inc bp cus heart not pumping enough around so inc Bp by inc aldosterone)
conns synrome = priamry hyperaldosteronism
liver cirrhosis
loop diruetic
thiazide diuretics

Medicine (11 decks)

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