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Chronic Obstructive Pulmonary Disease (COPD) (Symptoms (Sputum producion,…
Chronic Obstructive Pulmonary Disease (COPD)
Diagnosis
Chest X-ray
Pulmonary hyperexpansion (prominant hilar vascular shadows)
Flat diaphragm
Hyper expansion/ hyperinflamation
Spirometrey investigation
Pulse oxymetry check for O2 saturation
Full blood count (check for anemia)
Arterial blood gas (check pH)
ECG to rule out MI and heart failure)
Physical examinations
Prolonged expiatory phase
Pursed lips
Barrel chest
Use of accessory muscles
Decrease in breath sounds
Wheezing
Symptoms
Sputum producion
Wheezing
Chronic cough
Chest tighteness
Dyspnea
Ankle oedema
Orthopneu (shortness of breath when you lie dow)
Nocternal sleep apnea
Risk factors
Smoking
Recurrent lung infection
Low birth weight
Cannabis smoking
Airpolution
Low social economic status
Alpha-1 antitripsin
Job in/near factory (chemicals)
Chronic obstructive pulmonary DISEASES
Irreversible
Chronic Bronchitis (Blue bloaters)
Pathological changes
Increased goblet cell secretion and number
Excessive mucus production (hyper secretion) leads to productive cough in chronic bronchitis
Inflammatory changed
Muco-ssiliary dysfunction
Symptoms
Wheezing
Due to
Mucus hypersecretion
Air way obstruction (due to bronco constriction)
Productive cough
Due to
Mucus hypersecretion
Clubbing
Signs
Blotted due to dispnea and lack of exercise
Alveolar hypoxia (the oxygen isn't getting to the alveoli properly)
Leads to
V/Q mismatch
Leads to
Hypercapnea
(Elevated carbondioxide levels in the blood/ respiratory acidosis
Hypoxaemia
(low concentration of oxygen in the blood)
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Pulmonary vessel constriction
Leads to
Shunt of oxygen flow to healthy alveoli
Pulmonary hypertention
1 more item...
Due to
Obstruction
Sinosed causing a blue discoloration of the skin
Increased respiratory rate
Use of accessory muscles to breath
Clubbing
Warm temperture of skin
Dilated skin
Flapping due to CO2 retention
Risk factors
Heavy smokers
Emphysema (Pink Puffers)
Signs
Muscle wasting
Skinny
Flush skin (pink puffers)
Persed lip breathing (puffer)
Barrel shaped chest due to increased end expiatory volume (due to difficulty of getting rid of all the carbon dioxide in expiration, increased used of accessory muscles and increased force of breathing.
Pink discoloration due to CO2 retention
No cyanosis
Orthopneic (the patient is lying down forward to increase breathing capabilities)
Exertional dyspnea (use of accessory muscles)
Prolonged expiatory time
Speaks in short jerky sentences
Anxious
Pathological changes
Inflammatory response
Leads to
Destruction of alveolar wall
Loss of alveolar recoil
Elastic fiber breakdown
Decrease in ventilation
Neutrophils produce elastase which breakdown the elastic fibers in the alveoli causing less recoil to occur
Destruction of capillary beds leads to
decrease in perfusion
These 2 cause a decrease in V/Q deficit which causes hypoximea and hypercapnea
Onset (50-57)
Symptoms
Ineffective cough
Diagnosis
Hyperresonance on chest percussion
Reversible
Astham
Chronic Asthma
Chronic inflammatory disorder of the airway in which many cells and elements play a role. 3 things occur (Airflow obstruction, bronchial hyperresponsiveness (due to histamine release) and inflammation (due to increase of nutrophils)
Increase in Goblet cells
Increase in eosinophils in mucus and tissues
Increase in mucus production
Basement membrane thickens
Increase in mast cell numbers (causing an increase in histamine release
Increase in neutrophils during inflammation
Increase in T-helper cells
Smooth muscles cell hypertrophy
Columnar epithelial cells secret Thymic stromal Lymphocytes whikch will condition activated dendritic cells to produce chemokines to attract specifically T-helper 2. The activated TH2 promote humoral immunity
Symptoms (normally symptoms are worse in the morning)
Dyspnoea
Chest tightness
Dry rritatent Coughing
Shortness of breath
Is it nocturnal
Is it Episodic
Associated with other symptoms
Usage of Beta-agonist
Wheezing
Two types
Atopic
Inflammation mediated by systemic IgE production
Extrinisic asthma (triggered by environmental factors)
Allergic Rhinitis (symptoms affecting the nose)
Eczema (allergic affects causing
Hives
Nasal polips
Non-Atopic
Not caused by exposure to antige, the inflammation is mediated by local IgE production
Intrinsic asthma
Pathogenic change
IgE (bind to mast cells activating them by forming a mast cell IgE complex which recognize allergens and so release heaps of histamine)
Eosinophils
Dendritic cells
T-helper cells
T-helper 1 (normally found in the lungs) (promotes inflammation by causing cell mediated immunity)
T-helper 2 ( in asthma there's an up-regulation of this and the number of them increase in the lungs (where they're not normally found) (promotes inflammation by promoting humoral immunity causing increase in antibody production)
Increase in mucus secretion
Definition
It is a reversible intermittent airway obstruction associated with mucosal eosinophilic infiltration and inflammation.
Can cause
Adverse asthma parameters
Adverse behavior/psychosocial features
Death
Signs
Speech
The way the patient is sitting in order to breath easier
Accessory msucles
Respiratory distress
Tachypneamic
Tachcardia
Diagnostic
Chest X-ray
Arterial blood gas (normal value 80-100ml (PaCO2 35-45ml)
Pulse oximetry
Full blood count
Peak flow meter
If peak flow is above 75 the patient can leave but keep under observation. If the peak flow is between 75 and 50 give another nabuliser. If peak flow is below 50 the patient must stay
Uric acid & Electrolytes
Exercise testing
Spirometry
Histamine challange test
DO NOT GIVE TO ASTHMATICS
Beta blockers
NSAID
Asprin
Treatment
Muscarinic antagonist
Drugs
Ipratropium
Leukotriene antagonists
Oxygen therapy
Oral Steroids
Hydrocortisone
Side effects
Bruising
Peptic ulcer disease
Osteoporosis
Glaucoma
Myopathy
Striae
Obesity
Diabetes
Beta agonist
Drugs
Terbutaline
Salbutamol (Bronchodilator due to activation of adenyl cyclase)
Side effects
Tremor
Palpitation
Muscle cramps
ICU ventilation
Nebulized therapy
Antibiotic usage
Corticosteroids
Prednisolone
Side effects
Glucose intolerance
Change in voice
Increase in BMI
Oral candidiasis
Magnesium sulphate (decreases smooth muscle intracellular calcium by blocking its entry by activating sodium calcium pumps. The decrease in interaction of calcium interaction with myosin results in muscle cell relaxation)(inhibits mast cell degranulation leading to reduction in inflammation)
Acute Asthama
Treatment
Oxygen (must get blood O2 to above 95%)
Salbutamol
Complications
Pulse paradox (the systolic pressure decreases by 10mmHg during inspiration)
When to give ventilation
When FEV1 is below 50%
If PCO2 is above 42mm Hg
When O2 is less than 90%
Increased distress and agitation
Confusion(Low O2)/Drowsiness (increased CO2)/exhaustion
Alpha 1 anitripsin deficiency (emphysema), bronchiectasis, asper
4 hallmark causes of COPD
Squamous cell hyperplasia
Increse mucus secretion
Classification
Stage 3
FEV1/FVC less than 70%
FEV1 between 30%-%0%
Severe severety
Stage 4
FEV1/FVC less than 70%
FEV1 less than 30% or FEV1 less than 50% with chronic respiratory failure
Very severe
Stage 2
FEV/FVC less than 70%
FEV1 50%-80%
Moderate severity
Stage 1
FEV1/FVC less then 70%
Mild severety
FEV1 more than 80%
Management
Vaccination
Influenza vaccine
Pneumococcal vaccine
Bronchodilators
Anticholinergic
Methotrexate
Beta 2 agonists
Short acting
Salbutamol
Albuterol
Long acting
Smoking sesation
Steroids
Pulmonary rehabilitation
Nutrition (30% of COPD patients have protein deficiency)
Smoking cessation
Exercise
Education of their condition
Breathing exercises (pursed lips)
Oxygen therapy
Surgical intervention
Lung volume reduction surgery (removing parts of the lungs that don't work)
Lung transplantation