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Flashcards in Pharmacology and Therapeutics Deck (50)
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State some of the abnormal treatments for COPD

Mucolytics --> N-acetyl cyteine and DNAse


In terms of arachiodonic acid metabolism, what bad effect can be caused as a result of aspirin/ibuprofen?

Aspirin/Ibuprofen inhibit COX (prostaglandin formation)


This causes more arachiodonic acid to be converted to leukotrienes via 5-lipoxygenase


How do glucocortiocids work?


And how do LTRAs (eg, Zileutin and Montelukast) work differently?

By inhibiting PLA2, and so the formation of arachidonic acids


LTRAs inhibit 5-lipoxygenase (zileutin) and leuktotrienes (montelukast)


What is so good about Aclidinium?

Its a muscarinic antagonist that has a fast 'off' time at M2 the negative feedback loop is preserved


What's the difference between homotropic and heterotropic inhibition?

Homotropic --> Acts on the same cell type

Heterotropic --> Acts on different types of cell This is usually inhibiton using ACh and NA


What does sodium cromoglycate do?

Reduces the activity of airway sensory nerves


What does PEFR and FEV1 stand for?


And what do they mean in terms of asthma sufferers?

PEFR = Peak Expiratory Flow Rate

FEV1 = Forced Expiratory Volume in 1 second


These will be low in asthma sufferers, with FEV1 having a bigger drop in correlation with the severity of the asthma


What are the functions of the subtypes of (A) and (B) adrenoceptors?


How do these work?

A1 --> Constricts smooth muscle (relaxes GI smooth muscle) - Work through GPCRs (Gq) --> Phospholipase

A2 --> Presynaptic inhibition of neurotransmitters - Work through GPCRs (Gi) --> Adenylyl Cyclase


B1 --> Increases HR and force of contraction

B2 --> Dialates/relaxes smooth muscle

B3 --> Thermogenesis in skeletal muscle - These 3 act through GPCRs (Gs) --> Adenylyl Cyclase


How would you diagnose active and latent tuberculosis?

Active --> Chest X-ray, sputum tests and molecular assays

Latent --> Tuberculin skin test (forms a skin lesion) and molecular tests


How do the 4 anti-TB drugs work?

Rifampicin --> Inhibits RNA polymerase

Isoniazid --> A pro-drug that decreases the synthesis of mycolic acid

Pyrazinamide --> Same as Isoniazid

Ethambutol --> Increases the permeability of M.TB


What are liposomal sprays?

Soy lecithin (a phospholipid) that is encapsulated within microscopic liposomal vesicles

Sprayed onto the eye-lid (eg, Optrex ActiMist)


They mimic what happens naturally when lipids are secreted from the meibomian glands


What can oxidant stress cause? In terms of histone decacetylase (HDAT)?

Glucocorticoid inflmmatory transcription will carry on


What is a cough?

A motor reflex in response to sensing chemicals, particulates and airway excessive mucus


What specificity does Rofluimase have?


And what does this cause?

Its a PDE inhibitor that is selective to PDE IV


PDE IV is present only in leukocytes, and so inhibitors increase cAMP levels, inhibit respiratory burst, and inhibit TNF(a) release


What is the main reason for a drop in FEV1 in COPD patients?


How could we stop this?

Mucus blockage


Muscarinic antagonists (eg, tiotropium)

Neurokinin antagonists


Explain the 4 stages of primary tuburculosis progression

Stage 1 --> Bacilli are inhaled by droplets, which settle in the alveoli and start to grow. They are phagocytosed by macrophages, but not killed!!

Stage 2 --> Multiplies in inside the macrophages. The macrophage then bursts, potentially with the patient asymptomatic for 1 month

Stage 3 --> Immune cells surround the macrophages, forming tubercules. Symptoms start, and collagen fibres are formed

Stage 4 --> Uncontrolled lysis of the macrophage. This can cause enzymes to be released, forming lesions and destroying local tissue


Explain Histone acetyltransferase (HAT) and Histone Deacetylase, and their effects in inflammation

Histone acetyltransferase (HAT) --> Unpacks chromatin, allowing transcription to occur....allowing more inflammation gene expression

This is inhibited by glucocorticoids --> which promotes inflammation!!


Histone Deacetylase --> Wraps DNA closely, not allowing transcription

We need more of this as it will prevent transcription of inflammation markers..... but cigarrete


What treatments would you give for the following.....


Plaque Psoriasis (trunk and limbs)

Scalp Psoriasis

Face/Flexural/Genital Psoriasis

Plaque Psoriasis (trunk and limbs) - An emolient and potent topical corticosteroid


Scale Psoriasis - Potent topical corticosteroid (and maybe coal-tar shampoo)


Face/Flexural/Genital Psoriasis - An emolient and mild corticosteroid


What is dry eye syndrome? (ketoconjunctivitis sicca)

A lack of tear production, or too much tear evaporation


Caused by a problem with the tear film


Main complications = Keratitis and conjunctivitis


What are some of the actions of IL-13 and IL-4?

Increased eosinophil adhesion and migration

Increased mucous secretion

Tissue remodelling

Increases airway smooth muscle contractibility


Anti IL-13 and IL-13 receptor antibodies avaliable (but not in the UK)


Define Difficult Asthma

Asthma with symptoms despite being on step 4/5 plus....


An event of acute severe asthma which is life threatening, requiring invasive ventilation within the last 10 years OR


Requirement for oral corticosteroids for at least 6 months at a dose of 7.5mg prednisolone daily OR


2 hospitilisations in the last 12 months OR


Fixed airflow obstruction with a post bronchodilator FEV of less than 70% of predicted normal


How does normal cholinergic signalling work and with what feedback loops?

ACh leaves the parasympathetic nerve, binding to M3 receptors (on the cellullar target), which causes Ca2+ to be formed

Other ACh binds to the M2 receptor on the parasympathetic nerve, causing a negative feedback loop....decreasing the amount of ACh that is made and released


What is the difference between Hyperplasia and Hypertrophy of muscle cells?

Hyperplasia = More muscle cells

Hypertrophy = Bigger muscle cells These are both stimulated by inflammation


What does Theophylline do?

Inhibits phosphodiesterase so cAMP is not broken down --> bronchodialation


How does Omalizumab work?

Binds to the Fc part of IgEs, so they cant bind to mast no degranulation can occur

Only recommended if glucocortiocids dont work first


What is the main cause of emphysema?

Lung elastases that degrade elastin, the basement membrane and connective tissue

These are derived from neutrophils and macrophages

Increased after smoking



Describe Muscarinic receptors

Postganglionic receptors --> GPCRs


M1 --> Create slow EPSP due to closing K+ channels, so does cause depolarisation eventually

M2 --> Increases K+ conductance, so causes hyperpolarisation via a slow IPSP


How can some people with COPD get respiratory acidosis?

CO2 levels increase to a very high level during an exacberation, which normally would increase breathing rate.....


However if given high oxygen levels then this stimuli is suppressed as the patients suddenly have loads of oxygen!!


So the CO2 is kept in...caused respiratory acidosis


Name 4 steroid sparing agents





Gold (oral)


Terbutaline (IV)


These all have a lot of side effects


Exactly how does ipratropium (M3 antagonists) work?


How would an agonist of M3 work differently?

Bind to  and block M3 (muscarinic) receptor


Usually an agonist would acivate M3, causing Gq to upregulate PLC --> which increases calcium levels. This stimulates MLCK which causes vasoconstriction