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121 Cards in this Set

  • Front
  • Back

What is pneumonia?

Acute resp. illness with radiological pulm. shadowing (segmental / lobar / multilobar)

Pneumonia can be divided into?

1. community acquired pneumonia (CAP)


2. hospital acquired pneumonia (HAP) / nosocomial pneumonia


3. atypical pneumonia

CAP typically caused by?

Strep. pneumoniae

Other causes of CAP?

- H. influenza (rare)




- S. aureus




- G- rods


* E. coli


* Pseudomonas


* Klebsiella

Differences between CAP & nosocomial pneumonia?

1. CAP - NO contact with medical place


2. HAP - at least 2 days after admission



Patients with CAP may come with these symptoms?

- fever


- rigors / chills


- productive cough


- mucopurulent sputum


- pleuritic chest pain


- dyspnea


- vomit / LOA


- headache

Pleuritic chest pain is?

Pain that may occur on shoulder / anterior abdomen

On examinations, what can we obtain from the patients?

- fever / tachypnea / tachycardia




- PE


* crackles


* increase fremitus


* dull percussion


* bronchial breathing

How can we diagnose CAP?

1. CXR


- lobar consolidation




2. Sputum G stain + culture




3. CURB-65




4. PE

What is CURB-65?

To decide pt. admission




C - confusion


U - urea > 7mmol/L


R - RR > 30/min


B - BP <90 sBP, <60 dBP


65 - age >65y.o.

What can we decide from CURB-65?

1. if 1<,


- can be treated at home




2. if 2,


- treated at hospital




3. if >3


- treated at hospital as severe pneumonia

How can we manage CAP?

1. O2 - to make sure;


- PaO2 >8kPa


- SaO2 >92%




2. Fluid balance


- give IV fluid if dehydration / shock




3. ATB tx


- if uncomplicated = amoxicillin


- if allergic to PNC = clarithromycin, erythromycin




4. Tx pleural pain


- paracetamol


- NSAIDs


- opiates

Complications of CAP?

- pleural effusions


- pleural empyema


- acute resp. failure

What can we do for pleural effusions as complication of CAP?

1. Usually resolve as pneumonia is treated with ATB


2. If larger, may need pleural tap (culture of fluid as well)

Predisposing factor of CAP?

- smoking


- URTI


- alcohol


- CS therapy


- old age


- pre-existing lung dis.

Most common pathogens of HAP (nosocomial pneumonia)?

- G- rods


* Klebsiella


* E. coli


* Enterobacter


* Pseudomonas




- S. aureus (MRSA)

Clinical presentations of HAP?

- similar to CAP


- but may be complicated with comorbidities & drug-resistant

Predisposing factors of HAP?

- reduce host defence against bacteria


- aspiration of nasopharyngeal / gastric secretion


- bacteria to LRT


- bacteremia

What may differentiate CAP & HAP (other than contact with medical place)?

HAP


- worsening oxygenation


- increase tracheal secretion


- new radiology infiltration (than CXR on admission)

How can we treat HAP?

1. if NOT MRSA?


- ceftriaxone


- ciprofloxacin


- ampicillin




2. if YES MRSA?


- IV vancomycin


- cefepime


- ciprofloxacin / levofloxacin


- gentamicin

How about atypical pneumonia - it can be caused by?

- typically Mycoplasma pneumoniae


- can also be:


* Chlamydia pneumonia


* Legionella

Clinical presentations of atypical pneumonia - that may differentiate it with other pneumonia?

Presence of:


- headache


- pharyngitis


- fatigue (flu-like sx.)

What is COPD?

Chronic obstructive pulmonary disease


(or COAD - chronic obstructive airway disease)

Characteristics of COPD?


- COPD is combination of?

- chronic bronchitis


- emphysema




** usually coexist!

What can be seen roughly in patients with chronic bronchitis?

- chronic productive cough


- for at least 3months/year


- for at least 2 consecutive years



What happens in emphysema?

Permanent enlargement of air spaces distal to terminal bronchioles


- due to destruction of alveolar walls

What can trigger COPD?

- smoking (tobacco)


- alpha 1 antitrypsin deficiency


- environmental pollutants

How to differentiate etiology of COPD and types of emphysema?

1. Smoking
- 90% of cases
- centrilobular emphysema

2. Alpha 1 antitrypsin deficiency


- panlobular emphysema

1. Smoking


- 90% of cases


- centrilobular emphysema




2. Alpha 1 antitrypsin deficiency


- panlobular emphysema





General pathophysiology of chronic bronchitis


What happens in chronic bronchitis?

Airways inflamed


→hypertrophy of mucous gl. & smooth m.


→ excess mucous production


→ airways obstruction

General pathophysiology of emphysema


What happens in emphysema?

Smoking irritates lungs


→ activate neutrophils, macrophages


→ release elastase


→ destruct alveolar walls

Functions of alpha 1 antitrypsin?

INHIBITS destruction of walls by elastase & free radicals

Patients with COPD may come with?




COMBINATION of manifestations of emphysema & chr. bronchitis

EMPHYSEMA


- dyspnea on exertion** / rest


- tachypnea


- barrel chest ('stuck' in inspiration phase)




CHR. BRONCHITIS


- cyanosis - due to respiratory insufficiency


- chronic productive cough**


- expiratory wheezing



How to diagnose COPD?

1. Pulm. Fx Test (spirometry)


- ↓ FEV1 (means obstructive pathways)


- ↑ TLC, RV (lots of air remained in lungs)


- ↓ VC vital capacity (less air in & out)




2. CXR


- hyperinflation


- flattened diaphragm


What need to add into diagnostic approach for children with sign of COPD?

Alpha 1 antitrypsin deficiency


- may need measurement

How to manage COPD?


(medications)

1. Inhaled B2 agonist


- albuterol, salmeterol


- as bronchodilator


** in MYS - seretide accuhaler




2. Inhaled anti-cholinergic drugs


- ipratropium bromide (muscarinic)


** in MYS - Spiriva




3. Mucolytic agents


- to relieve mucous secretion


- theophylline (↑ mucociliary clearance)


** in MYS - Bisolvon



Drugs used for COPD in MYS?

1. Neb Combivent (albuterol + ipra. bromide)


2. Bisolvon (mucolytic agent)

What can we ask the COPD to change about lifestyle?

- STOP smoking

When to use O2 therapy in COPD patients?

In pt. with advanced disease & hypoxemia


- to improve life quality & survival

If COPD is not well treated, it can lead to?


(complications)

1. Pulm. HTN & cor pulmonale


- ↑ pulm. resistance → affect RV → RVF




2. 2° polycythemia


- ↑ Ht, Hb, RBC




3. Acute exacerbation (AECOPD)



What is acute exacerbation of COPD?


(AECOPD)

COPD pt. have LOW resp. reserve


- we need to aware that small problem can lead to resp. failure


- eg:- pulm. infection (pneumonia)

How to manage AECOPD?

1. Bronchodilators / systemic CS


- hydrocortisone


- prednisolone


** to ↓ immunity for chr. bronchitis




2. Broad spectrum ATB


- IV unasyn (ampicillin + sulbactam)


- azithromycin


** to treat bronchitis




3. O2 supply


- for long standing hypoxia


- to keep SaO2 >90%


- if critical, may need CPAP / intubation




4. Monitor ABG


- PaO2 > 8kPa


- paCO2 < 6kPa

What is asthma bronchiale?


** BA

Chronic inflammation of airways


- assoc. with airway hyper-responsiveness




** known as BA (bronchial asthma)

Patients with bronchial asthma may come with?

Recurrent episodes of:


- wheezing


- dyspnea


- chest tightness


- coughing

What causes bronchial asthma?

- allergens (outdoor / indoor)


- air pollution


- resp. tract infection

What happens in BA?


(pathophysiology)

Narrowing of airways - how?


- constriction of bronchial m.


- edema of bronchial mucosa


- mucous hypersecretion & plug formation




** eventually airway wall re-modelling (irreversible!)

Patients with BA may complain?

1. Episodic dyspnea & wheezing


(not progressive)


- but worsen at night




2. Coughing during asthma attack




3. SOB on exertion




4. Chest tightness



What makes difficult to diagnose pt. with BA?

Clinical signs may appear ONLY during attacks


- PE is NORMAL between attacks

How can we diagnose BA?

1. Clinical signs




2. Spirometry


(but bronchial obstruction may absent)




3. Broncho-provocation test


- give histamine / metacholine to pt.


- may evoke asthmatic pathogenesis


- then, measure FEV1 (>20% ↓ is +ve)

How to differentiate obstructive & restrictive problems from FEV1?

1. If FEV1 ↓


- obstruction


* air cannot escape the lungs




2. If FEV1 = FVC


- restrictive


* fibrosis / lung pathology


(↓ compliance to inspire / expire)

How to differentiate COPD & BA?

COPD


- neutrophils (CD8)


- onset > 40 y.o.


- smoking




BA


- eosinophils (CD4)


- onset < 20 y.o.


- atopy

Why do we need to treat BA?

- to control symptoms


- to ↓ exacerbations


- to ↓ SE

How can we manage BA?


* depends on severity

1. Inhaled bronchodilator (SABA)


2. Low dose inhaled CS (ICS)


3. Low dose ICS + LABA


4. Medium / high dose ICS + LABA


5. Systemic CS

Functions of medications in BA?


- Beta agonist


- CS

Beta agonist


- bronchodilator




CS


- to reduce inflammation

Dyspnea is also known as?


* define

Shortness of breath (SOB)


- unpleasant breathing


- worsened with exercise

SOB can be caused by?

1. Heart disease


2. Airway obstruction


3. Diffuse parenchymal lung disease


4. Pulmonary embolism


5. Disease of chest wall / resp. muscles

How dyspnea / SOB may occur?

- due to ↑ pulm. capillary pressure


- can also be due to fatigue of resp. m.


- ↓ vital capacity & lung compliance


- ↑ airway resistance


How is appearance of SOB in heart disease?

1. Exertional breathlessness


→ orthopnea


→ PND + dyspnea at rest




2. Need to check heart diseases



Symptoms that may appear with dyspnea in heart disease?

- hx of MI (ECG changes)


- presence of S3 / S4


- murmurs


- cardiomegaly


- JV distention


- hepatomegaly


- peripheral edema

How to diagnose heart diseases with dyspnea?

1. Clinical signs


- symptoms WORSEN gradually




2. ECG


- to check conduction in heart




3. ECHO


- to check ventricular fx

In which parts of airways may be obstructed in pt. with dyspnea (WITHOUT heart symptoms)?

ANYWHERE


- from extrathoracic airways


- to lung periphery

How to differentiate acute vs chronic dyspnea (with airway obstruction)?

ACUTE


- difficulty inhaling (URT obstruction)


- intermittent with expiratory wheezing (asthma)




CHRONIC


- slowly progressive exertional dyspnea (emphysema, CHF)


- chronic cough with sputum (chr. bronchitis & bronchiectasis)

How to differentiate upper tract obstruction and asthma?

Upper tract obstruction


- difficulty inhaling




Asthma


- intermittent with expiratory wheezing

How to diagnose dyspnea with pulm. embolism?

Sudden SOB with chest pain


- tachypnea


- inspiratory rales


- may check D-dimers

Examples of diseases of chest wall & resp. m. than can cause dyspnea?

- kyphoscoliosis


- bilateral diaphragmatic palsy



Diagnostic approaches of dyspnea?


- with suspection of...

1. General appearance


- can speak in complete sentences


- use of accessory m.




2. Vital signs (VS)


- RR


- O2




3. Chest exam


- wheeze, rales


- ↓ breath sounds


- barrel chest


- CXR




4. Heart exam


- ECG


- JVP


- murmurs




5. Limbs


- edema, cyanosis

What need to be noted on CXR with pt. with dyspnea?

- cardiac size (cardiomegaly)


- evidence of CHF


- pneumonia


- intersititial / diffuse parenchymal lung dis.


- pleural effusions

What is orthopnea?

Dyspnea when lying flat


- need more pillows / sit on chair

How to differentiate cardiac dyspnea VS pulmonary dyspnea?

HEART


- less gradual onset


- nocturnal exacerbation


- dyspnea on exertion


- ↑ BNP


- ↓ LV ejection fraction at rest/exertion




LUNG


- more gradual onset


- nocturnal exacerbation


- normal BNP


- ↓ FEV1, FEV1/FVC, TLC


- dyspnea on exertion

What is pleural effusion?

Excess fluid accumulated in pleural space

What is normal value of pleural fluid?


** anatomy?


** composition?

10-20ml of pleural fluid
- between parietal & visceral pleura


- similar composition with plasma


(but ↓ protein, <1.5g/dL)

How pleural fluid may accumulate more than normal?

- ↑ formation of pleural fluid


- ↓ fluid removal by pleural lymphatics




** in 25% cases - unknown causes (maybe viral etiology)

How to classify pleural effusions?

EXUDATES
- effusions due to pleural diseases


- resemble plasma




TRANSUDATES


- effusions with normal pleura


- ultrafiltrates of plasma



Symptoms of pleural effusions?

May be ASYMPTOMATIC




But, if symptomatic:


- pleuritic chest pain


- dry, nonproductive cough


- dyspnea


- orthopnea

On physical exams, pleural effusions may appear as?

- ↓ chest expansion at affected side


- flat percussion


- ↓ vesicular breathing


- presence of rubs


- ↓ fremitus



How to diagnose pleural effusions?

- PEx


- CXR


- pleural tap


- pleural fluid analysis



How CXR of pleural effusions look like?

- loss of sharp costophrenic angle
- loss of hemidiaphragm

- loss of sharp costophrenic angle


- loss of hemidiaphragm

Functions of pleural fluid analysis?

- to check if pleural effusions are exudates OR transudates


- to see etiology is due to pleural disease OR others

Criteria of exudates?

At least one of these:


- high total fluid / serum protein ratio (>0.5)


- pleural fluid LDH >2/3 of normal


- pleural / serum LDH ratio (>0.6)

Mechanism of formation of exudates & transudates?

EXUDATES
- ↑ capillary permeability


- exudation of fluid, protein, cells, others




TRANSUDATES


- ↑ hydrostatic pressure


- ↓ plasma oncotic pressure

Which of exudates & transudates usually occur unilateral / bilateral?

Exudates


- unilateral




Transudates


- bilateral

How to differentiate exudates & transudates based on lab test?

Check:
- RBC- WBC + differential
- pH
- glucose
- amylase
- specific protein

Check:


- RBC
- WBC + differential


- pH


- glucose


- amylase


- specific protein



Etiology of transudates?

Transudates


- congestive HF (most common)


- liver cirrhosis (with ascites)


- nephrotic sy. (hypoalbuminemia)


- pulm. embolism


- SVC obstruction


- peritoneal dialysis

Etiology of exudates?

Exudates


- pneumonia


- cancer / malignancy


- pulm. embolism


- viral inf.


- TB (pleuritis)


- rheumatoid arthritis


- chylothorax / hemothorax

In pneumonia, when tube thoracostomy with drainage of all fluid is indicated?

- G+ stained


- presence of gross pus


- ↓ pleural fluid glucose

Why ↓ pleural fluid glucose in exudates?

Inflammation


- glucose is taken by bacteria

Which cancers can cause pleural effusions (exudates)?

- lung cancer


- breast cancer


- lymphoma

In pulmonary embolism, effusions can be?

Either exudates or transudates

What can be seen in effusion of TB pleuritis?

Exudates


- predominant lymphycytosis

How to confirm TB pleuritis?

- PCR for TB


- Mycobacterium TB (MTB) culture from fluid

How chylothorax may cause pleural effusions?

Due to trauma to thoracic duct / mediastinal tumor


- lymphomatous damage


- SVC syndrome

How hemothorax may occur?

- trauma


- malignancy

Other signs of malignancy related to pleural effusions?

- cachexia


- clubbing


- lymphadenopathy


- radiation marks


- mastectomy scars

How to manage pleural effusions?

Depends on underlying causes




1. Drainage


2. Pleurodesis

How to remove / drainage pleural effusions?

- best removed slowly (<2L/24h)




- insertion of chest drain


* safe triangle


* 4th-6th ICS, ant. to mid axillary line

What is pleurodesis?

- with TTC, bleomycin, talc


- for recurrent pleural effusions

Which management is good for:


- malignant effusions?


- empyema?

Malignant effusions


- thoracoscopic talc pleurodesis




Empyema


- drainage with chest drain

Which diagnostic markers may show empyema / TB in pleural effusions?

- glucose < 3.3mmol/L


- pH < 7.2


- LDH ↑



Which diagnostic markers may show rheumatoid arthritis in pleural effusions?

- glucose < 3.3mmol/L


- pH < 7.2


- LDH ↑


- rheumatoid factors


- ↓ complement levels

Which diagnostic markers may show SLE in pleural effusions?

- glucose < 3.3mmol/L


- pH < 7.2


- LDH ↑


- antinuclear Ab


- ↓ complement levels

What is pneumothorax?


(PNTX)

Free air in pleural space

Pneumothorax can be classified into?

1. Traumatic PNTX




2. Spontaneous PNTX


- primary


- secondary

1° spontaneous PNTX may occur in which patients?

- pt. w/out any u/l lung disease


- tall, lean young men

What causes 1° spontaneous PNTX?

Spontaneous rupture of subpleural blebs at apex of lungs


→ air from lung escape into pleural space


→ lung collapse

Why there is NO respiratory distress in1° spontaneous PNTX?

There is sufficient respiratory reserve

Can 1° spontaneous PNTX reoccur?

Yes


- 50% in 2 years

2° spontaneous PNTX occur due to?

- COPD


- interstitial lung dis.


- CF


- TB

Why 2° spontaneous PNTX may be potentially life-threatening?

Due to lack of respiratory reserve


- may lead to resp. distress

Clinical signs of spontaneous PNTX?

Usually ASYMPTOMATIC




But, if symptomatic;


- dyspnea


- pleuritic chest pain (ipsilateral)


* usually sudden onset



How to diagnose spontaneous PNTX?

1. PEx (on affected side)


- ↓ chest expansion


- ↓ breath sound


- hyperresonance percussion




2. CXR


- to confirm dx.


- in tension PNTX = mediastinal shifted away from PNTX

Difference between spontaneous VS tension PNTX?

SPONTANEOUS
- no mediastinal shift
- means air is not accumulated in pleural space 

TENSION
- air accumulated and cannot escape from pleura

SPONTANEOUS


- no mediastinal shift


- means air is not accumulated in pleural space




TENSION


- air accumulated and cannot escape from pleura

What causes tension PNTX?

- barotrauma 2° to mechanical ventilation (changes in air pressure)


- CPR


- chest trauma

How tension PNTX occur?

Injury to pleural layer:


→causes entry to pleural cavity as one-way valve


→ it allows air to enter BUT not to leave cavity


→air accumulated under +ve pressure in cavity


ipsilateral lung collapse


→ mediastinal shift to healthy side

How tension PNTX manifestations may different than spontaneous PNTX?

In tension PNTX, pt. may have:


- hypotension, tachycardia


- JV distension


- resp. distress




On chest exam:


- ↓ breath sound


- hyperresonance percussion over PNTX side





Do we need CXR of pt. with tension PNTX?

NO!


- tension PNTX needs IMMEDIATE relief!




* make use of clinical signs of tension PNTX?

Why tension PNTX need immediate relief?

Air accumulated in pleural space cannot leave the cavity


- mediastinum is pushed to opposite hemithorax → kinking & compressing great veins


- if air is not removed, may cause cardioresp. arrest

How to diagnose tension PNTX?

Same as in spontaneous PNTX




1. PEx (on affected side)


- ↓ chest expansion


- ↓ breath sound


- hyperresonance percussion




2. CXR


- to confirm dx.


- mediastinal shifted away from PNTX

How to manage 1° spontaneous PNTX?

Check if pt. SOB & rim of air > 2cm on CXR


- if no, consider discharge


- if yes, try aspiration


- consider aspiration 2x before proceed with chest drain


- if aspiration success, may discharge pt.

How to manage 2° spontaneous PNTX?

Check if pt. SOB, age > 50 & rim of air > 2cm on CXR


- if no, try aspiration → if success, admit for 24h


- if yes, proceed with chest drain

How to remove air in tension PNTX?

1. Insert large-bore needle with syringe


- partially filled with 0.9% saline into 2nd ICS in midclavicular line of affected side




2. Remove plunger


- allow trapped air to bubble through syringe


(with saline as water seal)




3. Then, insert chest drainage tube

Why management of PNTX is done during;


- expiration


- Valsalva manoeuvre?

To make sure high pressure in thorax outwards(?)

What should we do in case of persistent air leak?

1. Ask specialist advice




2. May need suction (high volume, low pressure systems)


** -10 to -20cmH2O




3. Or surgical intervention