Tissue Injury: 1) Xanthine Derivatives (-Phylline)

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DISORDERS OF THE RESPIRATORY SYSTEM BRONCHODILATORS ARE GIVEN FIRST THAN OXYGEN

PART A – COPD BECAUSE WE NEED TO DILATE THE LUNGS FIRST SO


THAT THE OXYGEN CAN ENTER PROPERLY
A.) COPD (Chronic Obstructive Pulmonary Disorder) - MANAGEMENT: (ABCD)
 Aka CAL – Chronic Airway Limitation A – Airway  O2 needed (Low flow; 2-
“Chronic” 3L/min)
- > 6months; progressive B – Bronchodilators
“Obstruction” Types:
- Bronchoconstriction 1) XANTHINE DERIVATIVES (-PHYLLINE)
“Pulmonary” – MOA: relaxes the smooth muscle
- Referring to lungs of the bronchioles
 COPD – there is inflammation (vasodilation), – ‘Caffeine’ containing
therefore there’s tissue injury – CI  coffee
TISSUE INJURY  Arachydonic Acid  becomes – S/E: Palpitations
Leukotriene by means of lipoxygenase; Leukotriene – Example: Aminophylline;
causes bronchoconstriction Theophylline
----Arachydonic acid by means of COX-2
Agonist – promoter
(cyclooxygenase)becomes prostaglandin  causes
Antagonist –
Pain.
blocker/inhibitor
a) CHRONIC BRONCHITIS
B1 – Heart (increase HR)
- Aka “blue bloaters”
B2 – Lungs (bronchodilation)
- Definition: productive cough (mucus) for 3 2) B2 AGONIST
months in 2 consecutive years (thus, total 6 – Example: ventolin
months) – No Specificity (meaning it affects
- Causes: ALL beta-receptors!!)
1. Smoking (main cause) – S/E: Tachycardia
2. Environmental Pollutants 3) LEUKOTRIENE ANTAGONIST
- PATHOPHYSIOLOGY – Example: Zafirkulast
SMOKING 4) ANTICHOLINERGIC BRONCHODILATOR
Irritation of the Respiratory tract – Example: Ipratopium
Inflammation C – Chest Physiotherapy
1. Bronchoconstriction S (1) Mucus (2) Able
 DOB due to a decrease in O2 When? (1) Upon awakening (2) Morning
 Diaphragm will push the lungs  Use of *Location? best way to locate  CXR
accessory muscles (diaphragm)  Fatigue Common way  Ausculation
 less appetite  Anorexia  WEIGHT *Effective? If there is clear breath sounds,
LOSS it is effective
2. Hypertrophy of Goblet Cells (produces *AUSCULTATE WHEN?
mucus)  Before – YES (TO KNOW
 Increase of mucus secretion therefore LOCATION)
productive cough  During – NO
 Cyanosis can occur due to a decrease in O2  After - YES
PHASES OF CHEST PHYSIOTHERAPY:
**NOTE: A.) Percussion:
- Aka clapping
- Hands: cupped
- When? Exhalation
- Cx: breast, liver, abdomen, kidney,
heart
B.) Vibration:
- FLAT hands
- Performed during EXHALATION as
well
C.) Postural Drainage:
- Aka bronchial segment drainage
- Position + Gravity
- Duration: 30 mins
- Secretions in higher lobe  HIGH E – exhalation, ERV – expiratory reserve volume, RV –
FOWLER’S residual volume (needed to prevent lung collapse)
- Secretions in lower lobe  **NOT EVERYTHING IS EXPELLED THEREFORE, THE
TRENDELENBURG (using gravity to ALVEOLI CONTINUES TO EXPAND, IT PUSHES THE
make secretions go to the upper WHOLE THORAX, THIS CAUSES THE PATIENT TO
lobe DEVELOP “BARREL CHEST”
D – Drugs - Due to Hyperinflation, it is possible for the
1) MUCOLYTIC alveoli to RUPTURE.
*MOA: liquefies mucus to make them - Alveoli is VASCULAR meaning it contains
soft blood, so what happens when alveoli
*Example: Carbocisteine hyper-inflates, it can rupture.
2) EXPECTORANT - Therefore when the patient coughs, there
*MOA: to cough out secretions will be blood (HEMOPTYSIS, LATE SIGN) =>
*Example: Guiatenesin MABULA/BUBBLY SALIVA w blood =>
b) EMPHYSEMA FROTHY SPUTUM (CO2 IS IN SALIVA)
- Pink Puffers - S/SX:
- Definition: overdistention/hyperinflation 1. NO COUGH is present
of the alveoli 2. Barrel Chest
- Cause: Smoking  10k packs of cigarettes 3. Hyper-resonance  determined
consumed (1pack =20 sticks)
during PERCUSSION
- NORMAL PHYSIOLOGY: 4. Increase in RESIDUAL VOLUME
INHALE IN O2 Lungs expands 5. Orthopnea is present (DO NOT
Lungs recoils  alpha 1-
EXHAL CONFUSE WITH ORTHOPNEIC
OUT CO2 antitrypsin is responsible for
E POSITION)
the recoiling.
-Orthopneic position -> management
- PROBLEM  alpha 1 antitrypsin is
by nurse
decreased  decrease in recoil  CO2 is
-Orthopnea -> symptom, the pt can
retained
breathe only when leaning forward
- PATHOPHYSIOLOGY
6. Hemoptysis (LATE SIGN)
Smoking  Decrease in alpha 1 antitrypsin
- MANAGEMENT:
Decrease in recoiling Air trapping
1) Avoid smoking
CO2 retentionHyperinflation of ALVEOLI
2) DIET:
 BARREL CHEST
*decrease carbohydrates because they
will increase CO2 if consumed)
*increase CHON (muscles build)
*increase calories (for energy) *Prostaglandin  minor hormone
3) Purse Lip Breathing (found in stomach & kidneys) 
*Inhale  NOSE NO PROSTAGLANDIN  NO PAIN.
*Exhale  MOUTH (gradually to make *You should take steroids AFTER A
sure that the air doesn’t bounce back MEAL ONLY
and cause atelactasis!!!) *Route  metered dose inhaler
c) BRONCHIAL ASTHMA (1.3shake, 1-3 buga, 1-10 buga)
- Not curable *S/E: (1) water retention, (2)
- Treatable/manageable decreases immune system, (3)
- Definition: irreversible lung condition candidiasis  ORAL CARE NEEDED
caused by hypersensitivity leading to TO PREVENT THIS!!
smaller airways. 2) OXYGEN  AFTER
- Types: 3) BROWN PAPER BAG  DURING
1) INTRINSIC ASTHMA MEDULLA OBLONGATA  stimulated by CO2
*aka primary asthma O2 & CO2  INVERSELY PROPORTIONAL!!
*non-allergic asthma Medulla oblongata wants decrease in oxygen and
*Meds: Aspirin, Penicillin increase in CO2
*Due to change in temperature, stress - WOF: Status Asthmaticus (life-threatening
2) EXTRINSIC ASTHMA type of asthma!!  complete obstruction);
*secondary asthma sign of this is NO MORE WHEEZING
*Allergic asthma (dust, pollen grains, SOUNDS
perfume) d) BRONCHIECTASIS
3) COMBINATION/MIXED TYPE OF - Definition: permanent dilation of the
ASTHMA bronchioles due to recurrent respiratory
- PATHOPHYSIOLOGY: infection.
Antigen vs Antibody  if you are exposed - Cause:
to foreign antigens, it will cause 1. Respiratory Infection (most common)
inflammation  severe 2. Tumor
bronchoconstriction  wheezing  DOB - PATHOPHYSIOLOGY:
 use accessory muscles  fatigue  RESPIRATORY INFECTION  inflammation
anorexia  weight loss of bronchioles (bronchoconstriction)
- MANAGEMENT hypertrophy of goblet cells  increase in
1) MEDICATIONS (because affects on mucus secretion  PUS formation 
bronchioles) HALITOSIS
a. Mucolytics *DILATION  LATE STAGE, happens
b. Expectorants because eof recurrent infections
c. Bronchodilators - S/Sx:
d. Steroids 1. Pus: Sputum
*anti-inflammatory; hence 2. Fever
bronchoconstriction! 3. Halitosis
*MOA: blocks COX and 4. Productive Cough
arachydonic acid (so - MANAGEMENT:
prostaglandins and leukotriene 1) INCREASE ORAL FLUID INTAKE (to
won’t be produced) liquefy mucus secretions)
2) MEDICATIONS:
*Mucolytics
*Expectorants
*Bronchodilator (ONLY IF ITS STILL
CONTRICTED)
*Antibiotics (BECAUSE THERE IS
INFECTION)
3) CHEST PHYSIOTHERAPY
4) STEAM INHALATION (SUOB)
*to administer medications
*liquefy mucus
*relaxes smooth muscles (bronchioles)
*FUNCTION: DEPENDENT
*CX: BURNS
*SHIELD: towel on chest to prevent
burns
*DISTANCE: 12-18 inches
*DURATION: 30 mins

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