DRUGS BLOCK 13 Flashcards

1
Q

ISONIAZID

A
  • In order to covert when given isoniazid is first converted by a mycobacterial enzyme called peroxidase, into its active metabolite: IPRONIAZID
  • Iproniazid inactivates enzymes associated with MYCOLIC ACID synthesis, and mycolic acid is needed to build bacterial cell walls
  • It also INHIBITS MYCOBACTERIAL PEROXIDASE preventing the bacteria from metabolizing hydrogen peroxide, which accumulates inside the cell causing serious damage.
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2
Q

PACLITAXAL

A

Interfering with the formation of microtubules will cause mitosis to fail and the cell will eventually die without replicating.​

All anticancer microtubule inhibitors are given intravenously.​

DRUG CLASS: TAXANE – microtubule inhibitor​

INDICATION: lung cancer (metastatic– small cell lung cancer), breast and ovarian cancer.​

MOA: So they act like cement that overstablizes the microtubules and prevents them from depolymerizing and breaking down.This is a problem because the microtubules need to break down during anaphase so the cell can divide​

Impaired degradation of the polymerised microtubules

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3
Q

CISPLATIN

A

DRUG CLASS: Chemotherapy drug​

INDICATION: testicular tumours, ovarian tumours and bladder cancer​

MOA: DNA Alkylating agent > DNA crosslinking > decrease DNA replication

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4
Q

RIFAMPICIN

A

DRUG CLASS: Antibiotic​

INDICATION: Myobacterial infections including latent or active TB​

MOA: ​
Rifampin acts via the inhibition of DNA-dependent RNA polymerase, leading to a suppression of RNA synthesis and cell death.​

Side Effects: Rifampicin can cause red/orange discolouration of secretions, such as urine and tears.

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5
Q

ISONIAZID

A

Indication: active or latent TB​

MOA: Isoniazid > Iproniazid. ​

  1. Iproniazid prevents the formation of mycolic acid which is needed to build the bacterial cell walls.​
  2. Also inhibits myobacterial peroxidase which would usually metabolise hydrogen peroxidase so it doesn’t harm the bacteria. By preventing it from metabolising we are allowing it to accumulate and cause serious cell damage.​

Side effect: Isoniazid can cause peripheral neuropathy. Pyridoxine (vitamin B6) is co-prescribed to reduce the risk.

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6
Q

ETHAMBUTOL

A

DRUG CLASS: TB med​

Indication: Treatment and prophylaxis of TB​

MOA: blocking arabinosyltransferase, which synthesizes the arabinogalactan that’s used in the bacterial cell wall.​

SIDE EFFECT: ​

optic neuritis, which decreases visual acuity and the ability to differentiate between red and green ( colour blindness)​

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7
Q

PYRAZINAMIDE

A

INDICATION: TB​

MOA: converted to its active form PYRAZINOIC ACID.​

This medication inhibits mycobacterial fatty acid synthase which is an enzyme that also participates in the synthesis of mycolic acid.​

SIDE EFFECT:​

Decreases the renal excretion of uric acid - HYPERURICEMIA- gout​

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8
Q

CIPROFLOXACIN

A

Drug class: second generation fluoroquinolone. It is an antibiotic ​

Indication: bacterial infections including resp infections and UTI​

Mechanism of action:​
- acts on bacterial topoisomerase II ( DNA gyrase) and topoisomerase IV​
- Ciprofloxacin’s targeting of the alpha subunits of DNA gyrase prevents it from supercoiling the bacterial DNA which prevents DNA replication

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9
Q

SALBUTOMOL

A

Drug class: Beta 2 agonist ​

Indication: Asthma, Bronchitis, COPD​

MOA: ​

Bind to b2 receptors on the lungs ​

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10
Q

SALMETEROL

A

Drug Class: B2 agonist​

​Indication: Asthma and COPD​

​MOA: ​
- is a long-acting beta-2 adrenergic receptor agonist used to treat asthma and COPD.

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11
Q

BUDESONIDE

A

Drug Class: Steroid​

Indication: Asthma, Crohn’s disease, ulcerative collitis, COPD​

MOA:​

  • decreased leukocyte migration to sites of inflammation​

Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days​

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12
Q

MONTELUKAST

A

Drug Class: Leukotriene receptor antagonist ​

Indication: as part of asthma regime, ASTHMA PROPHYLAXIS especially really good at preventing exercise induced bronchoconstriction and also relieve seasonal allergic rhinitis ​

ONLY TAKEN ORALLY ​

MOA:

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13
Q

IPRATROPIUM

A

Drug Class: Anticholinergic drug ​

Indication: severe asthma flares​

Usually given with b2 agonist in an inhaler​

MOA:​

muscarinic acetylcholine receptor antagonist​

The function of the parasympathetic system in the airway is to generate bronchial secretions and constriction and hence, the inhibition of this action can lead to bronchodilation and fewer secretions.​

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14
Q

Leukotrine Antagonists

A

Leukotriene receptor antagonists like montelukast and zafirlukast are peroral medications that bind to the leukotriene receptors in the smooth muscles of the respiratory airways and prevent leukotriene from binding.

This weakens smooth muscle contraction in the respiratory tract, decreases mucus secretion, and reduces inflammation

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15
Q

HOW leukotrines cause inflammation

A

Allergens from environmental triggers, like air pollutants or cigarette smoke, are picked up by dendritic cells which present them to a type 2 helper T cell or Th2 cell in the lamina propria. These cells then produce cytokines like IL-4 and IL-5 which causes the inflammatory response.

IL-4 is especially important because it leads to the production of IgE antibodies by B cells, and these antibodies bind to FcεR1 receptors on mast cells to activate them.

These mast cells use an enzyme called phospholipase A2 to take membrane phospholipids and make a 20 carbon polyunsaturated fatty acid called arachidonic acid.

Arachidonic acid is then metabolized by two important enzymes: one is cyclooxygenase-2 or COX-2, which makes prostaglandins, another one is 5-lipoxygenase or 5-LOX, which makes leukotrienes.

Now, IL-5 on the other hand, activates eosinophils, which promote an immune response by releasing more cytokines and leukotrienes.

Minutes after exposure to the allergen, phospholipase A2 gets activated inside the mast cells, which results in the synthesis and release of leukotrienes and the prostaglandins.

Leukotrienes bind with the leukotriene receptors on the bronchial smooth muscles and cause them to contract. They also bind to receptors on the mucous glands to increase mucus secretion.

Similarly, prostaglandins also bind to their receptors in smooth muscles and mucus glands to cause a similar effect. These mediators also increase the vascular permeability in the airways and attract more immune cells to the area.

The combination of inflammation and bronchospasm cause obstruction of the airway which leads to symptoms like coughing, chest tightness, dyspnea, or difficulty breathing, and wheezing, which is a high-pitched whistling sound during exhalation.

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16
Q

DIGOXIN

A

Drug Class: Sodium Potassium ATPase inhibitor

Indicated:
- Heart Failure
- Supraventricular fibrillation
- Atrial flutter

MOA:
-Inhibits Na/K ATPase

-Which means there is more intracellular NA+

-Which means there is more intracellular Ca+

-Which increases the force of myocardial infraction.

Contraindications:
- Recent MI (myocardial infraction)
- thyroid disease
- severe respiratory disease
- hypoxia
- ventricular tachycardia
- myocarditis

Side effects:
arrhythmias
anorexia
nausea
vomiting
diarrhea
intoxication

17
Q

VERAPAMIL

A

Drug Class: Calcium Channel Blocker

Indicated:
- angina
- unstable angina
- hypertension
- arrythmia

MOA:
Angina and hypertension:
- Inhibition of calcium influx prevents the contraction of vascular smooth muscle, causing relaxation/dilation of blood vessels throughout the peripheral circulation - this lowers systemic vascular resistance (i.e. afterload) and thus blood pressure.

Arrhythmia:
- Electrical activity through the AV node is responsible for determining heart rate, and this activity is dependent upon calcium influx through L-type calcium channels.

By inhibiting these channels and decreasing the influx of calcium, verapamil prolongs the refractory period of the AV node and slows conduction, thereby slowing and controlling the heart rate in patients with arrhythmia

18
Q

DILTIAZEM

A

Drug Class: a nondihydropyridine calcium channel blocker

Indication:
- hypertension
- angina
- heart arrhythmias

MOA:
- watch osmosis

19
Q

ATROPINE

A

Drug Class: Muscarinic Receptor Antagonist

Indication:

  • to increase bradycardia, so it increases the heart rate ad improves atrioventricular conduction
20
Q

AMIADRONE

A

Drug Class: Potassium Channel Blocker

Indicated:
- Tachycardia
- Supraventricular and ventricular tachyarrhythmias.

MOA:
- Act by slowing repolarisation and prolonging action potential and refractory period in all cardiac tissues.

  • Amiodarone has blocking actions on several channels (potassium ion and inactivated sodium ion channels) and beta adrenoceptors.
21
Q

ADENOSINE

A

Indicated:
- myocardial perfusion scintigraphy and to treat supraventricular tachycardia

22
Q

Adenosine

A

Adenosine injection is used in combination with Thallium-201 as a pharmacologic stress agent for myocardial perfusion scintigraphy in patients unable to undergo adequate exercise stress. This medicine works by dilating the arteries of the heart and increase blood flow to help identify coronary artery disease.

This medicine is to be given only by or under the direct supervision of a doctor.

23
Q

LIDOCAINE

A
24
Q

ATENOLOL

A

Class: selective β-1 receptor antagonist

Indication: Hypertension, angina, cardiac arrhythmias, heart failure and glaucoma.

Mechanism of action:
Selective to Beta 1 adrenoceptors, Atenolol acts as an antagonist. It does not pass the blood-brain barrier, resulting in no CNS side effects.

Contraindications:
Asthma, uncontrolled heart failure, hypotension, metabolic acidosis.

Side effects:
Abdominal discomfort, bradycardia, peripheral coldness, dyspnoea, gou

25
Q

GTN SPRAY

A

Drug Class: nitrate vasodilator

Indicated:
- used to treat or prevent angina, heart failure, hypertension, and anal fissures.

MOA:

itroglycerin is converted by mitochondrial aldehyde dehydrogenase in smooth muscle cells to nitric oxide (NO), a potent vasodilator. NO activates the enzyme guanylate cyclase, which converts guanosine triphosphate (GTP) to cyclic guanosine 3’,5’-monophosphate (cGMP) in vascular smooth muscle and other tissues.1,2,10 cGMP is an endogenous vasodilator of vascular smooth muscle:3 it causes protein kinase-dependent phosphorylation and activates downstream cascades that promote relaxation and increased blood flow in veins, arteries and cardiac tissue.3,1

Watch osmosis

26
Q

FUROSEMIDE

A

Drug Class: Diuretic

27
Q
A