Raymond Parker Flashcards
Strategies for smoking cessation
- Nicotine replacement therapy
- NICE- long and short acting product, titrate dose down
- Prescription meds- nicotine receptor agonists
- Understand consequences
- Motivational interviewing
what is polycythemia?
- Percentage of blood that’s made of RBC
* >48% in women, >52% in men is abnormal
symptoms of polycythaemia
o Headaches o Blurred vision o Fatigue o HT o Dizziness o Confusion
causes of polycythaemia
o Dehydration o COPD o Sleep apnoea o Tumour o Reduced blood flow to kidneys
complications of polycythaemia
o Increased risk of clots
o AML
what is cricosternal distance?
The distance between the inferior border of the cricoid cartilage and the suprasternal notch. Should be 3-4 fingers long. A distance of less than 3 fingers suggest underlying lung hyperinflation e.g. asthma and COPD.
define cor pulmonale
right sided heart failure
RFs for cor pulmonale
PE, tobacco use, occupational exposure to toxins, hypercoagulable state, obesity, age, chest wall or ventilatory abnormalities.
DDx for cor pulmonale
: mitral stenosis, left to right cardiac shunt, primary pulmonary hypertension, pulmonary valve stenosis, congestive cardiac failure, congenital right sided cardiac impairment, RS heart failure due to MI, ventricular septal defect
Aetiology of cor pulmonale
COPD, emphysema, pneumoconiosis, CF, polio, MG, MND, obstructive or central sleep apnoea, thoracic deformities e.g. kyphoscoliosis, bronchopulmonary dysplasia in neonates.
clinical presentation of cor pulmonale
retrosternal chest pain, cough, dyspnea, fatigue, sputum production, tachycardia, cyanosis, finger clubbing, Kussmaul’s sign- distension of neck veins on inspiration, hepatomegaly, ascites, oedema
Basic pathophys of cor pulmonale
COPD causes hypoxia, acidosis and hypercapnia. this leads to increased pulmonary vascular resistance which causes pulm HT, RV hypertrophy which leads to cor pulmonale
Mx of cor pulmonale
pulmonary therapies e.g. bronchodilators, oxygen, Abx when indicated, low sodium diet, diuretics, digoxin, anticoagulation
Ix for cor pulmonale
FBC, ECG, pulmonary function tests e.g. spirometry, ABG, CXR, echocardiogram, VQ scan (ventilation and perfusion scan)
why does compliance increase in COPD
destruction of elastic tissue, alveoli lose shape and elasticity
give 5 diseases you would use long term oxygen therapy for
COPD
advanced CF
• severe non-cystic fibrosis bronchiectasis
• severe kyphoscoliosis or severe ankylosing spondylitis
• severe lung scarring caused by tuberculosis
• musculoskeletal disorders with respiratory weakness, especially if on home ventilation
MICA of salbutamol
- MOA: beta 2 adrenoceptor agonist. Csuses bronchodilation via Gas receptors leading to increased adenylyl cyclase, signaling pathway lowers intracellular calcium, resulting in SM relaxation. Also in heart, so salbutamol might have cardiac effects.
- Indications: asthma, chronic bronchitis and reversible obstructive disease
- CIs: with beta blockers, can induce angina and arrhythmias
- Adverse effects: tachycardia, palpitations, anxiety and tremors, increased serum lactate
definition of COPD
progressive, non reversible disease that is characterized by airway obstruction and includes chronic bronchitis and emphysema
RFs for COPD
smoking, breathing second hand smoke, air pollution, working with chemicals, genetic e.g. alpha 1 tryptase deficiency, hx of childhood respiratory infection
DDx for COPD
asthma, congestive heart failure, bronchiectasis, TB, GORD, lung cancer
aetiology of COPD
environmental e.g. smoking (90%), genetics- alpha 1 antitrypsin deficiency, antibody deficiency e.g. IgA def
clinical presentation of COPD
chronic cough, sputum production, dyspnea, fatigue, wheeze, tachypnoea, usage of accessory muscles- decreased cricosternal distance, decreased chest expansion, hyperresonance on percussion, cyanosis, barrel chest, peripheral oedema
Pathophys of COPD
repetitive damage to airways and lings, chemicals and ROS cause tissue damage, causing remodeling. Thickening of airways and metaplasia of epithelial cells. Impaired mucocilliary clearance and mucous plugging.
Ix for COPD
FBC, CXR, CT, ECG, ABG, spirometry
MICA of ultibro breezhaler
M: Bronchodilators.
LAMA - Bind to muscarinic receptors and act as a competitive inhibitor of acetylcholine. Muscarinic ACh receptors are G-protein coupled receptors that act through 2nd messengers. M3 muscarinic receptors found on smooth muscle cells in airway and when activated, they cause bronchoconstriction. By blocking this pathway, the LAMAs reduce smooth muscle tone and act as bronchodilators.
LABA - B2 receptors found in smooth muscle in bronchi. They are Gs-protein coupled receptors which inhibit myosin light chain kinase and lead to smooth muscle relaxation. Long acting beta 2 agonists relax smooth muscles in lungs increasing airway diameter for up to 12 hours (salbutamol a SABA only works for up to 3 hours)
I -
LAMA helps prevent breathlessness and exacerbations in COPD. LAMAs can be added to high dose inhaled corticosteroids and LABAs as maintenance treatment in pts who have had one or more severe asthma exacerbations in the past year.
LABA used as treatment combined with corticosteroids for chronic asthma when corticosteroids alone are insufficient. Second line therapy for COPD to improve symptoms and reduce exacerbations.
C -
LAMA - Should be used with caution in pts with angle-closure glaucoma, arrhythmias & urinary retention (but most pts can take them as long as its by inhalation and not oral/IV)
LABA - Associated with increased asthma deaths when not used alongside corticosteroids in chronic asthma. Care should be taken for pts with cardiovascular disease, in whom tachycardia may provoke angina or arrhythmia.
A -
LAMA - Irritation of respiratory tract with nasopharyngitis, sinusitis and cough; GI disturbance including dry mouth, constipation, urinary retention, blurred vision and headaches.
LABA - Activation of Beta receptors in other tissues results in tachycardia, palpitations, anxiety and tremor. LABAs also can cause muscle cramps.
MICA doxycycline
MOA: tetracyclines such as doxycycline are thought to inhibit translation by binding to the 16S rRNA portion of the ribosome, preventing binding of tRNA to the RNA-30S bacterial ribosomal subunit, which is necessary for the delivery of amino acids for protein synthesis. As a result of the above actions, the initiation of protein synthesis by polyribosome formation is blocked. This stops the replication of bacteria and produces a bacteriostatic effect
Indications: infections such as chlamydia and mycoplasma, severe infections including refractory UTI, acute sinusitis, acute cough, pneumonia,acute exacerbation of bronchiectasis and COPD, mild diabetic foot infection, cellulitis, acne, leg ulcer infection, rosacea, syphilis, PID, lyme disease, prophylaxis of malaria
CIs: pregnancy and breast feeding due to teratogenicity. Cautions include alcoholism and children 8-11 (only use when no alternative)
Adverse effects: Dyspnoea, hypotension, peripheral oedema, tachycardia, GI discomfort
MICA prednisolone
M:
The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation.4 Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.
Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10
I: acute exacerbation of COPD, croup, mild to moderate acute asthma, suppression if inflammation and allergic disorders, ITP, UC
C: bowel perforation, extensive fistulas, recent intestinal anastamosis
A: diarrhoea, dizziness, hiccups, hypoT, malaise
MICA benzyl penicillin
M:
By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, penicillin G inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that penicillin G interferes with an autolysin inhibitor
I: infection, endocarditis, anthrax, meningitis
C: allergy
A: fever, Diarrhoea; hypersensitivity; nausea; skin reactions; thrombocytopenia; vomiting
MICA clarithromycin
Mechanism of action:
it inhibits bacterial protein synthesis by binding to the bacterial 50s ribosomal subunit. Binding inhibits peptidyl transferase activity and interferes with amino acid translocation during the translation and protein assembly process. Clarithromycin may be bacteriostatic (stops bacterial growth) or bactericical depending on the organism and drug concentration
Indications:
1) Treatment of respiratory, skin and soft tissue infections as an alternative to penicillin when use is contraindicated.
2) In severe pneumonia added to a penicillin to cover atypical organisms including Legionella pneumophila and Mycoplasma pneumoniae
3) Eradication of H.pylori in combination with a proton pump inhibitor and either amoxicillin or metronidazole
Contraindications
- Avoid in people who are allergic to macrolides or inactive ingredient in tablets
- People with a history of cholestatic jaundice and/or liver dysfunction associated with prior clarithromycin use.
- Renal impairment
Adverse effects:
- Nausea, vomiting, diarrhoea, and abdominal pain when taken orally
- Allergy
- Antibiotic associated colitis
- Ototoxicity at high doses
what controls the basic pattern of breathing
central pattern generator (CPG), sometimes also referred to as the ‘respiratory pattern generator’ (RPG).
what conditions affect V/Q ratio
Chronic bronchitis (a type of COPD) • Asthma • Pulmonary edema • Airway obstruction, such as aspiration (e.g., choking on food, swallowing a toy) • Pneumonia • Sleep apnea • COPD Pulm HT
