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BMS235 > Gene Mutations and Drug Treatments > Flashcards

Gene Mutations and Drug Treatments Flashcards

1
Q

Na+/K+ ATPase inhibitors

A

Cardiac Glycosides

Oubain and Digoxin

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2
Q

NHE1 inhibitors

A

Amiloride (affects Na channels)

EIPA (no effect on Na channels)

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3
Q

Short lasting Beta2 Adrenergic agonist

A

Salbutamol

- Activates Gs pathway to relax Airway Smooth muscle

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4
Q

Long lasting Beta2 Adrenergic agonist

A

Salmeterol

- Reduces inflammation

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5
Q

Anti-cholinergics for Asthma

A

Tiotropium Bromide

- Acts on M3 receptors to decrease Gq pathway to relax Airway Smooth muscle

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6
Q

Glucocorticoids for Asthma

A

Beclametasone

- Inhibits expression of inflammatory genes by decreased stability of mRNA

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7
Q

Advantages + Disadvantages of 3H radiolabel

A

+ Effective for achieving high specific activities
+ Long half-life
- Expensive
- Dangerous and requires specialist labs

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8
Q

Advantages + Disadvantages of 125I radiolabel

A

+ Cheap and easy

- Short half-life

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9
Q

LQT1 (KCNQ1 mutation)

A
  • Gene codes for voltage-gated K+ mutation (Kv7.1a)
  • Loss of function mutation (high density in TMDs)
  • Also causes hearing loss as Kv7.1a pumps K+ into endolymph so loss of function causes Reissner’s Membrane to collapse = deafness
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10
Q

MinK

A
  • Accessory ion channel protein (Kv7.1a) that regulates function
  • Loss of function also causes loss of ion channel function and results in symptoms of Long QT syndrome
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11
Q

Long QT Syndrome Treatment

A
  • Beta blockers (Class 2 anti-dysrhythmic drug)
  • Atenolol - Beta1 selective antagonist
  • Has negative ionotropic (force of contraction) and chronotropic (rate of contraction) effects
  • Contra-indiciation - causes bronchoconstriction in patients with obstructive lung disease
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12
Q

Short QT Syndrome Treatment

A
  • Implant a defibrillator to control heart rate in event of fibrillation
  • Quinidine (K+ channel blocker) may slow down repolarisation
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13
Q

Sildenafil

A

Inhibits cGMP breakdown in muscles to increase vasodilation to to increase blood flow to penis

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14
Q

Nitroglycerate

A

Increases Nitric Oxide production to cause vasodilation and increase blood flow and O2 supply for Angina

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15
Q

Thiazide

A

Diuretic - Increases Na+/Cl- excretion to increase urine production and lower blood volume

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16
Q

Clonidine

A

Alpha blocker - decreases sympathetic output

17
Q

Prazosin

A

Alpha blocker - decreases TPR by relaxing smooth muscle

18
Q

Propanolol

A

Beta blocker - decreases heart rate and contractility

19
Q

Minoxidil

A

Ca2+ channel blocker - decreases contractility and vascular muscle tone

20
Q

ACE Inhibitor

A

Decreases production of AGII so decreases TPR

21
Q

AGII Receptor Blocker

A

Decreases TPR

22
Q

First Degree Heartblock Consequence

A

Benign

23
Q

Second Degree Heartblock Consequences

A

Type 1 - Benign

Type 2 - Requires pacing

24
Q

Third Degree Heartblock Consequences

A

Requires pacing

  • Atrial Ventricular dissociation
  • Atrial contraction against closed tricuspid valve when out of synchrony
  • Results in cannon wave in Jugular vein as right atrium and ventricle contract at same time and blood pushed back into Jugular vein
  • Results in reduced perfusion
25
Q

Atrial Fibrillation treatments

A
  • Beta-blocker to decrease heart rate

- Warfarin to prevent clot formation when blood pools in atria during fibrillation

26
Q

Cystic Fibrosis Current Treatments

A
  • Physiotherapy to loosen mucous to be coughed up
  • Bronchodilator to increase flow of air in the lungs
  • Steroid to reduce inflammation
  • Dnase to break down mucous
27
Q

Cystic Fibrosis Gene Therapy + Complications

A
  • Delivery of CFTR DNA to target cells
  • Production of CFTR mRNA
  • Production of fully functioning CFTR protein
  • Poor succes rate due to renewal of airway cells
  • Expensive
28
Q

Cystic Fibrosis Read Through Agent

A

Force production of full length CFTR if there is a premature stop mutation

29
Q

Cystic Fibrosis Correctors

A

Force mutant CFTR protein to cell membrane, if mutant CFTR functions then restore CL- secretion

30
Q

Cystic Fibrosis Potentiatiors

A

Increase the open probability of CFTR proteins, requires them to be trafficked normally

31
Q

Example of CF Potentiator and its effects

A

Ivacaftor

  • Increases CFTR function so increase in periciliary layer thickness
  • Increases lung function
  • Decreases occurrence of respiratory infections

BMS235 (1 decks)

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