1. History points a.

Cough - duration of cough - association w/ phlegm @ sputum - if yes, if the phlegm blood streaked or bloody @ haemoptysis - acute cough (infection - upper airway! sinusitis, tracheitis - lower airway! bronchitis, bronchiectasis - lung parenchyma! pneumonia - chronic cough (persisting more than " wks, assc. w/ obstructi#e lung disease, asthma, chronic bronchitis, nonrespiratory diseases like $%&', postnasal drip. -non producti#e cough (parenchymal lung disease, idiopathic pulmonary fibrosis. b. (hortness of breath - tempo, duration (acute, chronic , effect of position (orthopnea , infection, en#ironmental stimuli on dyspnea. - acute dyspnea - assc. w/ sudden physio changes (laryngeal edema, bronchospasm, myocardial infarc, pulmo embolism, pneumothora) - progressive dyspnea or episodic (C*+', idiopathic pulmonary fibrosis ha#e gradual dyspnea on e)ertion -chronic persistent (C*+', intersititial lung disease, chronic thrombo embolitic disease - orthopnea (dyspnea on lying flat , Congesti#e heart failure (CH- , diaphragm mechnicaly impaired assc. w/ obesity, asthma triggered by esophageal reflu) - e)ertion/trigger. asthma has specific trigger (allergen that cause sudden dyspnea. 'yspnea on e)ertion is an early symptom of lung or heart disease. -time, nocturnal dyspnea suggest CH- or asthma

- +ast medical history ie tra#elling a lot (./ , working w/ asbestos, smoking, 0nd hand smoker

0. /asic pathogenesis of symptoms 'yspnea,

Motor, efferent role in dyspnea, - 'isorders of #entilatory pump --1 l/t decreased compliance, discomfort (rasa sesak nafas - 2eak/fatigued muscles --1 greater effort needed to breathe, increased motor neural input result in release in corollary discharge, neural signals sent

to sensory corte) at the same time as the motor output increased. Sensory, afferent role in dyspnea, - chemoreceptors (carotid body, medulla acti#ated by hypo)emia, hypercapnia (inc. C*0 in blood , acidemia. --1 sensation of 3air hunger3 - mechanoreceptor --1 stimulated by bronchospasm l/t sensation of chest tightness - metaboreceptor --1 in skeletal muscle acti#ated by changes in the local biochemical milleu in tissue acti#e during e)ercise - 4-receptor (in between capillary and al#eoli --1 acti#ated by acute changes in pulmonary artery pressure. integratory mismatch such as in asthma or C*+'. an)iety dyspnea physical and lab work-up ,

COUGH PATHOGENESIS: refle) detected by ner#e fibres (myelinated sensory, unmyelinated c-fibres , send to 5.( in brainstem #ia #agus ner#e, causing the cough refle) cough refle)- adduction of #ocal cord l/t upper airway occulsion, e)piratory muscle contraction l/t increased intrathoracic pressure, sudden release of laryngeal contraction l/t batuk ---1 e)piratory blow as fast as 67mph enuff to dislodge mucus in the lungs

! "A# TESTS$IMAGING %O& COUGH AN' '(SPNEA: CH&ONIC COUGH: chest ra)iograph *a+norma, ,ist o- )isease is ,ong ie. ho)g/ins.,ung cancer. etc0 sputum e1amination (purulent appearing for bacterial culture, sometimes mycobacterial culture ( mucoid appearing sputum shd be check for cytology to check for malignancy and to distinguish eosinophilic/neutrophilic bronchitis . +,oo) in sputum 2arrants specia, investigation! '(SPNEA: physica, e1amination (in C(C , e1ercise test (walk under obser#ation in order to reproduce symptom, e)amine o0 saturation 8 new findings , chest ra)iograph a! (obser#e lung #olume, hyperinflation indicating *+', low lung #olume indicate edema/fibrosis/diaphragm rosak/ chest wall motion problem +! (obser#e lung parenchyma for interstitial disease, emphysema . c! (obser#e #asculature. kalau upper 9one #asculature prominent indicate pulmonary #enous hypertnsion, central 9one, pulmonary arteries, shadow 4antung besar suggest dilated cardiomyopathy @ #al#e problem . )! (check for effusion which shd be dark, bilateral effusion are typical of CH-/collagen #ascular disease, unilateral maybe carcinoma or pulmonary embolism 3! 'I%%E&ENTIA" 'IAGNOSIS %O& COUGH$'(SPNEA: COUGH: CAUSES O% COUGH chronic +ronchitis 4 in longterm cig smokers acute cough *5 2/s04 respiratory tract infection, aspiration e#ent, smoke/no)ious chemical inhalation su+acute cough * 46 2/s04 tracheobronchitis such as in pertussis chronic cough *76 2/s04 wide. ie, cardiopulmonary disease including those w/ inflammatory, infectious, neoplastic, cardiopulmonary etiology ! 8hen chronic cough present 2$ norma, chest e1am an) ra)iograph: cough-#ariant asthma, $%&', nasopharyngeal disease, medication (;C% inhbitors '(SPNEA: &ESPI&ATO&( CAUSE' '(SPNEA "$T A"TE&E' MECHANICA" P&OPE&TIES O% "UNGS$CHEST 8A"". CA&'IO9ASCU"A& CAUSE' '(SPNEA "$T GAS E:CHANGE A#NO&MA"IT(. STIMU"ATION O% PU"MONA&($9ASCU"A& &ECEPTO& '(SPNEA OCCU&S IN air2ay )iseases (asthma, C*+' . both are obstructive (e)piratory airflow obstructed l/t hyperinflation of lungs and chest . both also lead to hypo)emia

and hypercapnia --1 increased work to breathe. chest 2a,, )isease (kyphoscolosis- stiffening of chest wall , (myasthenia gra#is, guillain-barre both weaken wall muscles , pleural effusion --1 increased work in breathing, receptor acti#ation if atelectasis (closure of lung occur. ,ung parenchyma )isease *interstitial lung disease d/t infection, occupational e)posure, smoking, autoimmune disorder all results in decreased lung compliance d/t increased stiffness . destruction of al#eolarcapillary interface ,e-t heart )isease such as in myocardial diseases d/t coronary artery disease, non-ischemic myopathies l/t higher left-#entricle %'< (e)cess blood ---1 inc. capillary pressure, edema, dyspnea. in diastolic dysfunction, left #entricle too stiff ---1 dyspnea )iseases o- pu,monary vascu,ature pulmonary thrombo/embolic disease, primary disease of pulmnary circu (pulmonary hypertension, pulmonary #asculitis cause dyspnea d/t increased pressure l/t receptor acti#ation. gi#ing *0 does not reduce se#erity of dyspnea d/t these causes. pericar)ia, )isease constricti#e pericarditis, cardiac tamponade (fluid buildup in pericardial sac l/t increased intracardiac pressure 8 pulmonary blood #essel pressure --1 receptor acti#ated. cardiac output also decrease in these conditions, l/t lactic acid buildup which trigger chemo and metabo receptor.

;! P&INCIP"ES O% MANAGEMENT O% COUGH$'(SPNEA PTS '(SPNEA: CO&&ECT UN'E&"(ING P&O#"EM &ESPONSI#"E %O& S(MPTOM! if not possible , reduce symptom intensity such as gi#ing supplemental o0 when saturation = ">?

COUGH: T&EAT UN'E&"(ING CAUSES! for chronic idiopathic (tak tau punca cough, cough suppresant such as co)eine *narcotic0 bt l/t constipation, drowsiness, additction. )e1tromethorphan. o#er the counter, less side effect, can be used in con4c. w/ narcotic as different site of action (narc in brainstem cough center . +en<onatate inhibit sensory ner#es in cough pathway