Pharmacology And Therapeutics Flashcards

1
Q

Compare the structure of the upper and lower airway structures

A

Upper airway: trachea and bronchi’s
- more cartilage, less smooth muscle

Lower airway: bronchioles and alveoli
- less cartilage, more smooth muscle

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2
Q

How does the autonomic n.s affect the respiratory system

A

SNS: fight or flight response
innervates blood vessels and glands > Release adrenaline and NA to b2R> > muscle relaxation, bronchodilation, decrease mucous secretion, increased clearance of mucous by inhibiting the de granulation of mast cells

PNS: rest and digest
- innervates smooth muscle > Ach on MR > bronchoconstriction, increase muscle secretion

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3
Q

How does the autonomic n.s affect the respiratory system

A

SNS: fight or flight response
innervates blood vessels and glands > Release adrenaline and NA to b2R> > muscle relaxation, bronchodilation, decrease mucous secretion, increased clearance of mucous by inhibiting the de granulation of mast cells

PNS: rest and digest
- innervates smooth muscle > Ach on MR > bronchoconstriction, increase mucous secretion

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4
Q

Asthma, COPD and fibrosis is a condition caused by what ?

A

Asthma and copd: Lower elasticity: lungs cannot recoil
Fibrosis: reduced compliance: lung cannot stretch fully and always recoil to original size

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5
Q

For a patient with COPD, what type of breathing pattern will be shown? Explain the FEC, FEV1, TLC and its ratio

A

Obstructive pattern ( reduced elasticity)
- FVC = reduced or normal
- FEV1 = reduced
- ratio = reduced
- TLC = normal

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6
Q

What does the body do during hyperventilation and how it overcomes it.

A

Loss of CO2 > alkalosis > body limits ventilation > CO2 contraction increase to normal

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7
Q

Diabetes patient could have metabolic acidosis. How does the body regulate this

A

Diabetic patients have insulin resistance, fat broken down incorrectly to form ketones leading to acidosis.

Drop in pH stimulates ventilation to expel CO2

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8
Q

Explain 5 difference between smooth and skeletal muscle

A

Smooth - Skm
Small spindle shape - large cylindrical fibre
Uni nucleate - multi nucleate
No striation and bands - banded
Actin attach to dense bodies - z bands
Energy efficient: maintain contraction for long time while using less energy) - short term contraction n requires more energy

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9
Q

Explain the sliding filament theory of smooth muscle

A
  1. Myosin head is bound to ATP in its low energy configuration
  2. Myosin head hydrolyses ATP into ADP and P. Myosin has high energy configuration.
  3. Myosin head attaches to actin filament to form cross bridge
  4. ADP and P is released returning it to is low energy configuration
  5. The actin filament is pulled and slide towards the centre of sacromere
  6. When ATP binds to myosin head, it releases the actin filament and a new cycle begins
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10
Q

What is the importance of smooth muscle latch phenomenon

A

Forms the cross bridge between myosin and actin. Allows contraction for hours while using less energy

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11
Q

What is the function of calmodulin

A
  1. Calcium ions binds to calmodulin to form calcium-calmodulin complex
  2. Activates MLCK (myosin light chain kinase)
  3. Adds phosphate group to myosin head
  4. Allows binding of myosin to actin
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12
Q

What drugs are able to induce relaxation of smooth muscle

A
  1. B-adrenoceptors: increase cAMP > inhibit MLCK > relaxation
  2. Nitric oxide: inhibits cGMP > increase MLCP > relaxation
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13
Q

How does Rho Kinase work

A

Inhibits MLCP and causes contraction

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14
Q

How can asthma be reversed?

A

B2 AR agonist
FEV1 increases > 200ml or 12%

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15
Q

A patient has a FEV1 of 49%. What is his diagnosis and its severity

A

Could be Asthma or severe COPD

COPD severity
- mild: 80% - smokers cough
- moderate: 50-79% - breathlessness with mild exertion
- severe: 30-49% - breathlessness while rest, cough and wheezing
- Very severe: <30%

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16
Q

What are the characteristics of airway in asthma patients

A
  • increased vascular permeability
  • smooth muscle hypertrophy
  • mucous glands hyperplasia: mucus buildup
  • ## desquamation of airway epithelial layer
17
Q

Explain what causes the early/ immediate phase of asthmatic attach

A

Allergen binds to IgE > the complex binds to mast cells receptor > mast cell degranulates and release histamine, prostaglandin, LTC4, LTD4 > bronchoconstrictions

18
Q

How does chemokines and cytokines cause the late phase of asthma

A

Activated mast cells secrete cytokines and chemokines that recruits leukocytes such as neutrophils and basophils.

Leads to airway remodelling and prolonged inflammation

19
Q

What are the function of cysteinyl leukotrienes

A
  • Inflammation mediator
  • contracts smooth muscle, increase vascular permeability, increase mucus and attract leukocyte

Two types: cytokines and chemokines

20
Q

IL 1 stimulates T cells while IL 8 attracts neutrophils
True or false

A

True

21
Q

Cytokines includes Interleukins and TNFalpha
True or false

A

True

22
Q

How does salbutamol work

A

It’s a b2 agonist

Salbutamol binds an activate B2 AR > Gs activates the ardenylyl cyclase which converts ATP to cAMP > increase protein kinase A > opens K+ channel for efflux > repolarisation > Ca channel closes > relaxation of airway smooth muscle

Increase protein kinase A will inhibit MLCP

23
Q

When will Salmeterol/ formoterol / indacaterol be given ?

A

Given for long term prevention.
Absorbed into lipid bilayer of cells

24
Q

How does PDEs inhibitor regulate cAMP and what are its effects on airway

A

Phosphodiesterase inhibitor inhibits it from breaking down cAMP into 5’AMP. More protein kinase A available for relaxation

25
Q

What is an example of PDE4 inhibitor

A

Roflumilast (DAXAS)
Cilomilast (Ariflo)

For COPD

26
Q

Example of Muscarinic R antagonist

A

Ipratropium
Tiotropium (longer acting)
Aclidinium (longer acting and new)

27
Q

What are xanthines (theophylline)

A

Bronchodilators (2nd line use)

28
Q

What is the use of aminophylline

A

Mix of theophylline and ethylenediamine

Improves water solubility and given as IV

29
Q

Explain the symptoms of allergic rhinitis

A

Nasal itching caused by histamine
Sneezing to remove allergens
Rhinorrhoea (runny nose)
Swollen eye due to oedema
Itchy, bilateral red eye due to vasodilations nd leaky blood vessels

30
Q

Why do some drugs have sedating effects . Give examples

A

They cross the bbb and have antimuscarinic effects

Chlorphenamine (piriton) - for kids above 1 year
Promethazine (Phenergan)
Alimenazine (Trimeprazine)

31
Q

What are some non sedating antihistamines

A

Acrivastine (Benadryl) given tds
Loratadine (Clarityn)
Cetrizine (Zirtek)
Fexofenadine (Telfast)

32
Q

What are cromones?

A

Sodium cromoglicate + nedocromil sodium

As nasal and eye administration OTC
Inhibits mast cell degranulation
Used 4-6 times daily
Eye drops are effective for conjunctival symptoms

33
Q

Compare intranasal antihistamine and intranasal corticosteroids

A

Antihistamine: corticosteroids
rhinitis : ✅ : ✅
Conjunctivitis: ❌: ✅
Onset of action: 15 mins : 12 hours (use for preventive measure)
Frequency: 2-4x a day : 1x a day

34
Q

How does decongestants work. Give examples of the drug

A

They are alpha AR agonists > vasoconstriction >reduce blood flow, mucus flow and swelling

Phenylephrine (alpha1)
Xylometazoline/ oxymetazoline (alpha2)

Overuse cause rebound conjestion

35
Q

How to treat anaphylaxis?

A

Adrenaline to allow bromchodilation
Salbutamol for wheezing
Hydrocortisone steroid IV

36
Q

What is the formula for concentration ratio?

A

CR = EC50 if agonist in the presence of antagonist / EC50 of agonist only

37
Q

Explain the Gaddum equation

A

CR = [Antagonist]/KD + 1

CR = concentration ratio
KD = Dissociation constant of antagonist