Res Drugs Flashcards

1
Q

explain DF , Complains , Predesposing factors , pathophysiology

A

-DF : its chronic inflammatory disease reversible episodes of airway obstruction, with symptoms of broncho spasm, mucosal edema , increase bronchial mucosa secretion,
-Complains :
1-wheezing 2-coughing 3-shortness of breath
-pre disposing factors:
1-genetical factors
2-environmental factors
3-Drugs thats induced BA such as : B blocker , cholinimaitics , PGF2A , Morphine > vigal stimulation

-pathophysiology: Frequent exposer to allergic stimulate, Cause infiltration of the bronchial wall by activating inflammatory substance such as : PGS , LTs , adenosine , histamine all of these getting out from Mast cells
> which lead to :
1-hypertrophy of air way smooth muscles
2-increase muscos secretion

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2
Q

explain the Classification of Drugs for BA

A

-there are 4 types : 1 and 2 is the primary way
1-bronchodilator : B2 agonist, muscranic blockers
2-Antiiflmatory drugs : Glucocorticoids
3-Prophylactic drugs
4- Antitussive , mucolitic , Expectoran
————

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3
Q

Explain the B2 Agonist for treating BA

A

— Drugs :
1- short acting
1.1Salbutamol tab, aears
1.2 Fenoterol
2- long acting :
2.1 Formoterol Caps
2.2 Salmeterol Aers
— mechanism: by activating the B2 receptor it will increase the CAMP which lead to broncho dilation , and suppress of inflammatory mast cells , mediators secretion and reducing of Ach reales from Nerve Ending
—uses : Quick relief , long term controlling of BA in combaination with Glucocorticoids
-side effect :
1- tolerance
2-tremors
3-hypoglycemia

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4
Q

explain the Methylxanthines

A

-Drugs :
1-Theophylline Tab
2-Aminophylline Amp
-mechanism:
1- Adenosine ( A1) receptor: these drugs blocks A1 receptor which lead ti broncho dilation , CNS stimulate , decrease mediator’s that secreted by Mast cells , Increase AV conductivity,
2- they inhibit Phosphodiesterase PDE3 and PDE4 which lead to accumulation of CAMP leading to :
1-B.D
2- increase cardiac conductivity, relaxation of most smooth muscle
-pharmocokintics :
1- absorption : full absorption 90-100%
2-metabolism: in the liver Cyp450 ~ CYP1A2 and metabolite to Cafien
3- cleared by smoking bcs its microsomal inducer
4- decrease cleared by microsomal inhibitor ~ Erythromycin
-side effect : nausea, vomiting , dyspepsia , durisis stimulation
-uses : Chronic BA theophylline
Acute BA aminophylline Amp

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5
Q

explain The glucocorticoids For BA

A
  • Drugs :
  • there is two types
    1-local effect drugs :
    1.1 Beclomethasone
    1.2 budesonide
    1.3 Fluticasone all aresol
    2-systematic effect :
    2.1 Prednisolone Tab , Amp
    —mechanism: bind to cell surface receptors to the cytoplasm receptor carrier then transferred to nucleus where it interacts with DNA then transcription which results of RNA which lead to

—systemic Pharmacological effect :
1-metabolic effect :
1-1 Carbohydrates metabolism: decrease the peripheral glucose utilization which lead to hyperglycemia
1-2 Protein metabolism: increase the proteolysis which lead to decrease muscle mass and then limbs
1-3 Fat metabolism: Increase lipolysis with redistribution of fat which lead to moon face with buffalo hump ( cushing syndrome )
1-4 salt and water retention: which lead to hypoklamia
2- immunological effect :
-Anti inflammtory , anti immunological
2-1 they inhibt B cells function : which lead to decrease Antigen-Antibody reaction
2-2 they inhibit T cell function : which lead to decrease inflammatory mediators and cytokines
2-3 inhibit macrophages activity and stabilize lysosomes membrane
2-4 inhibit mast cells : which lead to decrease Histamine release and capillary permeability
2-5 they inhibit PLsA2 enzyme: which lead to decrease synthesis PGs and LTs
3-CVS :
3-1 hypertension: duo to
salt and water retention and increase sensitivity pf BV and heart to circulating catecholamines
3-2 Antishock : duo to hypertensive and CVS effect , and anti inflammatory action
4- haematological effect :
4-1 increase RBCs and neutrophils and decrease lymphocytes and eosinophils
4-2 increase coagulation factors and plasma lipids
5- CNS effect : initial euphoria followed by depression
6- Eye effect : increase IOP
7- effect on bone : decrease bone matrix bcs the bone has proteins and the glucocorticoids are catabolic of protein
8- effect of growth : growth retardation bcs bones and , decreasing the growth hormone
— local pharmacological effect :
1-reducing the inflammation and hyper reactivity of bronchi
2-reducing frequency and severity of BA
—uses :
-local drugs : BA inflammatory
-systematic drugs : Sever asthma ~ asthmatic status IV

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6
Q

explain the prophylactic drugs

A
  • we have 3 families of these drugs
    1-Luktraines
    2-Mast cells stabilizer
    3-MABs
    ———
    1- Leukoutraines inhibitors
    -Drugs :
    1-Zafirlukast tab
    2-Montelukast tab
    -mechanism: they inhibit LTD4 receptor which is responsible for :
    1-plasma exudation
    2-mucous secretion
    3-Esionphilis recurmnet
    4- B. C
    -uses : as adjuvant drugs For BA, and ita a replacement for Glucocorticoids in children bcs the glucocorticoids cause growth retardation
    ———-
    2-Mast cells stebiliazer
    -Drug : Cromoglicic acid ~ Caps for inhalation
    -mechanism: they block Ca2+ entry to the mast cell which lead to membrane stiblazation and inhibit the degranulation
    -Pharmacokinetics: poorly absorbed in GIT
    -uses : only for pervntation
  • side effect : Res tract irritation
    ——
    3- MABs
    -Drugs : benralizumab Amp S.c
    -mechanism: Via its Fab fragments, the humanized monoclonal antibody benralizumab specifically binds to IL-5Rα, thereby preventing the interaction between IL-5 and its receptor
  • Uses : As adjuvant drug For BA
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