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pharm Flashcards

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1
Q

defintion of asthma

A

chronic inflammatory disorder of the airways causing reversible airflow obstruction

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2
Q

key features of asthma

A

airway hyperresponsiveness
bronchoconstriction
mucus hypersecretion

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3
Q

triggers of asthma

A

allergens
infections
cold air
irritants

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4
Q

what are the two phases of asthma airway inflammation

A

early phase
late phase

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5
Q

describe the early phase of airway inflammation in asthma

A

Allergen exposure –> activation of mast cells which release histamine, leukotrienes –> bronchoconstriction

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6
Q

describe the late phase airway inflammation in asthma

A

Eosinophils, T-helper cells 2 cells –> chronic inflammation

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7
Q

what is bronchial hyperesponsiveness

A

increased smooth muscle contraction

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8
Q

desrcibe airway remodelling in asthma

A

in severe cases goblet cell hyperplasia, fibrosis- thickened basement membrane, smooth muscle hypertrophy

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9
Q

define COPD

A

a progressive and chronic obstruction of airways

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10
Q

risk factors of COPD

A

smoking –> most important
age –>. loss of FEV1 as we age
genetic factors–> a1 anti-trypsin deficiency

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11
Q

describe the pathophys of COPD

A

Pollutants and toxins cause an inflammation response in the lung (neutrophils cause sig damage)
narrowing of airways
goblet cell hypertrophy

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12
Q

how do short acting beta agonists work

A

stimulates beta-2 adrenoreceptors to relieve symptoms via airway smooth muscle relaxation( rapid bronchodilation)

-increase cAMP –> less intracellular Ca release –> less muscle contraction

-increased mucocilliary clearance

-mild anti-inflame effects

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13
Q

onset of sulbutamol and preferred route

A

onset of action= 5-15 minutes, 4-6 hour duration

inhaled route, preferred –> faster onset fewer systemic side effects

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14
Q

side effects of salbutamol(core drug Ventolin)

A

tachycardia and palpations–> B1 simulation

tremor –> B2 activation

hypokalaemia –> increased K+ uptake

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15
Q

what can Ventolin not protect against n what can it protect against

A

-protective against exercise induced asthma

-NOT protective against attacks at night

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16
Q

what is the target for LABAs(long acting beta agonists)

A

late chronic phase of asthma
reduce inflammation

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17
Q

out of Salmeterol and Eformoterol which has a faster onset

A

eformoterol

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18
Q

what do LABAS protect against

A

protects against excersize induced and nocturnal asthma( due to longer duration of action)

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19
Q

inhaled corticosteroids role

A

USED FOR ANT-INFLAM THERAPY
reduces inflammation and prevents airway spasm via phospholipase, A2, COX-2 and IgE inhibition

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20
Q

side effects of inhaled corticosteroids

A

oral candidiasis(thrush)

dysphonia

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21
Q

SAMA/LAMA

A

short/long acting muscarinic antagonists

block M3 receptors in airway–>bronchodilation and reduced secretion

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22
Q

core SAMA drug

A

ipratropium

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23
Q

core LAMA drug

A

tiotropium

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24
Q

side effects of LAMA/SAMA

A

dry mouth, urinary retention, blurred vision

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25
Luekotriene Receptor Antagonists MOA
block cysLT1 receptors, preventing leukotriene-induced bronchoconstriction inflammation and mucus production
26
side effects of Leukotriene receptor antagonists
mood changes headache GI upset (not as effective for bronchodilation as beta 1 agonists)
27
penicillin MOA and A/E
inhibit cell wall synthesis -nausea,diarrhoea, allergies
28
penicillin examples
amoxicillin benzylpenicillin
29
cephalosporins MOA and A/E
inhibits cell wall synthesis -nausea -vomiting -diarrhoea -neurotoxicity
30
cephalosporins examples
cefuroxime, ceftriaxone, cefalexin
31
tetracyclines MOA + A/E
inhibits protein translation -GI, calcium chelation, photosensitivity, nephrology/hepatotoxic
32
tetracycline examples
doxycycline
33
macrolides MOA + A/E
inhibit protein synthesis GI, cardiac/ototoxicity
34
macrolides example
azithromycin, erythromycin
35
what are the URTI's
rhino sinusitis, tonsilitis, otitis media
36
treatment for rhino sinusitis
NSAIDs, decongestants, ICS, amoxicillin, or cefruxime, doxycycline
37
treatment for tonsillitis
narrow spectrum penicillin cefalexin/azithromycin if allergic
38
treatment for otitis media
paracetamol amoxicillin cefuroxime if allergic
39
LRTIS
bronchitis influenza pneumonia
40
bronchitis treatment
azithromycin/ erythromycin
41
influenza treatment
oseltmaivir, zanamivir
42
mild pneumonia treatment
amoxicillin or doxycycline
43
moderate pneumonia treatment
benzylpencillin + doxycycline
44
severe pneumonia treatment
ceftriaxone + azithromycin
45
TB treatment plan
RIPE Rifampicin:inhibt RNA synthesis+ causes red urine Isoniazid: inhibits mycobacterial cell call synthesis Pyrazinamide: G, fever,malaise Ethambutol: inhibits mycobacterial cell wall synthesis optic neuritis
46
what are the 4 constipation drugs
bulk laxative osmotic laxative stimulant laxative faecel softness
47
bulk laxatives eg. + MOA
absorbs water from gut--> increase stool size---> peristalsis metamucil
48
osmotic laxative
absorbs water from surrounding --> increase stool --> peristalsis lactulose
49
stimulant laxative
stimulate secretion of electrolytes--> water follows --> stool softens senna
49
faecal softeners
allows water to mix with fat in stool--> softens stool docusate
50
types of diarrhoea
anti-cholenergic opioids muscarinic antagonists
51
opioids MOA + eg. for diarrhoea
act on u receptors in the gut--> decrease Ach - decrease muscle contraction -peristalsis loperamide
52
muscarinic antagonists for diarrhoea
block M3 receptorsss --> increased motility atropine anti-cholinergic
53
what are the 4 vomiting drugs
anti-muscarinic antihistamine anti-serotonin anti-dopamine
54
anti-muscarinic vomiting drug
block M1 receptors in vestibular nulcei --> no transmission to vomit centre hyoscine. anti-cholinergic
55
anti-histamine vomiting drug
block H1 receptors in vestibular nuclei --> no transmission to vomit centre promethazine sedation
56
anti serotonin vomiting drug
block 5-HT3 receptors in CTZ --> no transmission to vomit centre ondansterone constipation
57
anti dopamine vomiting drugs
block D2 receptors in CTZ --> no transmission to vomit centre metoxlopramide
58
what are the motion sickness vomiting drugs
hyoscine, promethazine
59
what are the "chemotherapy and other drugs" for vomiting
ondansterone and metoxlopramide
60
What is the Anti-NK1
-new drug -competitively binds to NK1 receptors and blocks substance P -works on both CTZ and the vomiting centre itself -hence, very effective -used primarily for chemo
61
what are the ABCD's for hypertension
ACE-Inhibitors/ ARBs Beta Blockers Calcium Channel Blockers Diuretics
62
flowchart of RAAS physiology
decrease BP --> increase RAAS--> 1) AgII= vasoconstriction 2) aldosterone= Na+ reabsorption 3) ADH= H2O reabsorption
63
3 steps in the RAAS system with ACE inhibitor
DETECTION: 1)macula densa(Na+) or baroreceptor stretch @ aortic arch/ corticoids PATHWAY Angiotensinogen ----( renin)--> AGI----> AGII final pathway blocked by ACE inhibitors EFFECT blocks vasoconstriction
64
ACE inhibitor mode of action
Blocks the action of (ARB) or conversion to (ACEi) Angiotensin II, a potent vasoconstrictor Blocks pro-fibrotic effects of ATII (good for heart failure (HFrEF)) Increase renal perfusion (good for CKD) in the long-run
65
side effects of ace inhibitor
cough hypotension hyperkalemia hypersensitivity
66
what to be aware of with administrating ACE inhibitors
triple whammy:NSAID,ACE, DIURETIC potassium sparing drugs NO PREGNANT
67
what is a diuretic
increases the production of urine
68

med 2100/ 2200 (8 decks)

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