Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 1 > Pharmacology Resp > Flashcards

Pharmacology Resp Flashcards

1
Q

Fwhat class is clophenimine maleate

A

1st gen anti histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is usage of first gen anti histamine

A

Oral - symptomatic relief of hayfever and urticaria

IV - used as adjunt in the treatment of anaphylaxis & angioedema

Sedative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is chlorophenimine maleate binding site

A

H1 receptor anatgonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are all h1 receptors in relation to agonist/antagonist and competitive/uncomepetitive

A

Gq, competitive antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is chlorophenamine maleate MOA vs normal MOA

A
  1. Histamine is released from storage granules in mast cells as a result of antigen binding to the IgE receptor on the cell surface
  2. Histamine binds to the H1 receptor
  3. There is dissociation of the beta and gamma subunit. The Alpha unit will activate the 2nd messenger (PLC) by turning GDP to GTP
  4. This causes the degradation of PIP2 into DAG and IP3, DAG stays membrane bound while the IP3 becomes soluble
  5. IP3 activates smooth muscle contraction and induces the features of immediate type 1 hypersensitivity…
    a) Increased capillary permeability causing oedema formation (wheal)
    b) Vasodilation causing erythema (flare)
    c) Itching due to sensory nerve stimulation
    d) nasal irritation, sneezing, rhinorrhoea, congestion, conjunctivitis and itch (when histamine is released in the nasppharynx)

PKC is activated by DAG and it activates immune responses and transcription factors

DRUG MOA
Bind to H1 receptors and so prevent the activation of the second messenger system stated on the left. This results in reduced hypersecretion, pruritis & sneezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

chloraphenimine maleate

A

Drowsiness as first gen

Can’t see - blurred vision
Can’t pee - urinary retention
Can’t shit - constipation
Can’t spit - dry mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what class is promoethazine hydrochloride

A

1st gen anti histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is usage of promethazine hydrochloride

A

Oral - symptomatic relief of hayfever and urticaria

IV - used as adjunt in the treatment of anaphylaxis & angioedema

Sedative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is binding site of promoethazine hydrochloride

A

H1 receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what G receptor is promethazine hydrochloride and is it agonist/anatgonist

A

Gq competative antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is promethezine hydrochloride MOA and normal

A
  1. Histamine is released from storage granules in mast cells as a result of antigen binding to the IgE receptor on the cell surface
  2. Histamine binds to the H1 receptor
  3. There is dissociation of the beta and gamma subunit. The Alpha unit will activate the 2nd messenger (PLC) by turning GDP to GTP
  4. This causes the degradation of PIP2 into DAG and IP3, DAG stays membrane bound while the IP3 becomes soluble
  5. IP3 activates smooth muscle contraction and induces the features of immediate type 1 hypersensitivity…
    a) Increased capillary permeability causing oedema formation (wheal)
    b) Vasodilation causing erythema (flare)
    c) Itching due to sensory nerve stimulation
    d) nasal irritation, sneezing, rhinorrhoea, congestion, conjunctivitis and itch (when histamine is released in the nasppharynx)

PKC is activated by DAG and it activates immune responses and transcription factors

MOA
Bind to H1 receptors and so prevent the activation of the second messenger system stated on the left. This results in reduced hypersecretion, pruritis & sneezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are side effects of promoethezine hydrochloride

A

Drowsiness as first geb

Can’t see - blurred vision
Can’t pee - urinary retention
Can’t shit - constipation
Can’t spit - dry mout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what class are Ceritizine hydrochloride //
Loratidine

A

2nd gen antihistamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is usage of cetrizine hydrochloride//loratidine

A

Hypersensitivity reactions - hayfever, some drug allergies, insect bites, urticaria, puritis and rhinitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is binding side of cetrizine hydrochloride/loratidine

A

H1 receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what G protein does cetrizine hydrochloride/loratine bind to and it it antagonist/agonist

A

Gq anatagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is normal MOA of cetrizine hydrochloride/lorat

A
  1. Histamine is released from storage granules in mast cells as a result of antigen binding to the IgE receptor on the cell surface
  2. Histamine binds to the H1 receptor
  3. There is dissociation of the beta and gamma subunit. The Alpha unit will activate the 2nd messenger (PLC) by turning GDP to GTP
  4. This causes the degradation of PIP2 into DAG and IP3, DAG stays membrane bound while the IP3 becomes soluble
  5. IP3 activates smooth muscle contraction and induces the features of immediate type 1 hypersensitivity…
    a) Increased capillary permeability causing oedema formation (wheal)
    b) Vasodilation causing erythema (flare)
    c) Itching due to sensory nerve stimulation
    d) nasal irritation, sneezing, rhinorrhoea, congestion, conjunctivitis and itch (when histamine is released in the nasppharynx)

PKC is activated by DAG and it activates immune responses and transcription factors
DRUG MOA
Bind to H1 receptors and so prevent the activation of the second messenger system stated on the left. This results in reduced hypersecretion, pruritis & sneezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are side effects Ceritizine hydrochloride /
Loratidine

A

Can’t see - blurred vision
Can’t pee - urinary retention
Can’t shit - constipation
Can’t spit - dry mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what class is cyclizine

A

1st gen antihistine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

usage of cyclizine

A

Nausea, Vomitting, Vertigo, Labyrinthine disorders, motion sickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is bidning site of cyclizine

A

H1 receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what G protein receptor does cyclizine bind to and is it anatagonist/agonist

A

Gq, anatagonsit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

side effects of cyclizine

A

Nausea,
Vomiting,
Vertigo,
Motion sickness,
Labyrinthine disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is usage of injectable forumulation along w adrenaline

A

Severe hypersensitivity reactions and emergency treatment of anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is usage if unjectable formaulation along w adrenaline

A

Severeq hypersensitivity reactions and emergency treatment of anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is binding site of injectable formula along with adrenaline

A

H1 receptor anatgonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is side effects of injectable formula along with adrenaline

A

Dry mouth, Reduced appetite, nausea, vomiting, hypersalivation. Difficulty in micturition, urinary retention. Sweating, weakness. Repeated injections of Adrenaline can cause local ischaemic necrosis as a result of vascular constriction at the injection site.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what class is salbutamol

A

beonchodilator SABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is usage salbuatmol

A

asthma- first line, copd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what binding site for salbutamol

A

b2 receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what G protein does salbutamol bind to and it it anatgonist/agonist

A

Gs- stimulates adenyly cyclase. agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is salbutamol MOA vs normal MOA

A

normal MOA
1. The B2 receptor is activated this causes the beta and gamma subunits dissociate
2. GDP is transferred to GTP
3. The alpha subunit activates adenyl cyclase - this causes the increase of cAMP – a signalling molecule
4. cAMP activates protein kinase A (PKA)
5. PKA causes phosphorylation of proteins this reduces the amount of cytosolic Ca2+.
6. This causes smooth muscle relaxation

drug MOA1. Binds to B2 adrenoreceptor - agonist effect
2. Activates adenyl cyclase
3. Causes ↑cAMP
4. ↑PKA activation
5. Reduces cytosolic Ca2+
6. Causes bronchial smooth muscle relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are side effects salbutamol

A

trembling, headaches, palpitations, hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is formoteral//salmetoral class

A

Bronchodilator
LABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is formoterol/salmetarol usage

A

Asthma - third line (has to be given with ICS)

COPD (2nd line)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is formetarol/salmetarol binding site

A

B2 receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is formetarol/salmetarol binding site

A

B2 receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what G protein does salmeterol/formetarol bind to and is it antafonist/agonist

A

Gs- stimulates adenyl cyclase. agonist, saba

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is salmeterol/formetarol normal MOA, vs drug MOA

A

normal moa
1. The B2 receptor is activated this causes the beta and gamma subunits dissociate
2. GDP is transferred to GTP
3. The alpha subunit activates adenyl cyclase - this causes the increase of cAMP – a signalling molecule
4. cAMP activates protein kinase A (PKA)
5. PKA causes phosphorylation of proteins this reduces the amount of cytosolic Ca2+.
6. This causes smooth muscle relaxation

drug moa
1.. Binds to B2 adrenoreceptor - agonist effect
2. Activates adenyl cyclase
3. Causes ↑cAMP
4. ↑PKA activation
5. Reduces cytosolic Ca2+
6. Causes bronchial smooth muscle relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is salmeterol/formetarol side effects

A

Uncommon at normal doses

High doses:
Tachycardia
Hyperglycaemia
Skeletal muscle tremors occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what class is ipratropium bromide

A

bronchodilator SAMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is ipatropium bromide usage

A

Asthma - third line (has to be given with ICS)

COPD (2nd line)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is binding side of ipratropium bromide

A

M2 receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what G protein does ipratropium brominde bind to and is it anatgonist/agonist

A

Gq, anatagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is ipratropium bromide l normal vs drug MOA

A

normal
1. Acetylcholine binds to the receptor
2. Beta and gamma units dissociate
3. GDP turns into GTP
4. Alpha subunit activates PLC

drug moa

antagonist inhibits the binding of acetylcholine - causing bronchial smooth muscle relaxation + decrease mucus secretion

Works in immediate phase of an asthma attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is ipratropium bromide side effects

A

can’t see, can’t pee, can’t spit, can’t sh*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what class is tiotropium

A

bronchodilator LAMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is usage of tiotropium

A

Chronic asthma - 5th line - adjunct to LABA
COPD - 1st line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is tiotropium binding site

A

M2 receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what G protein does tiotropium bind to and it antagonist/agonist

A

Gq, antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is tiotropium normal MOA vs drug MOA

A

normal moa
1. Acetylcholine binds to the receptor
2. Beta and gamma units dissociate
3. GDP turns into GTP
4. Alpha subunit activates PLC
5. PLC degrades PIP2 into DAG and IP3
6. IP3 causes bronchoconstriction

drug moa
Muscarinic antagonist inhibits the binding of acetylcholine - causing bronchial smooth muscle relaxation + decrease mucus secretion

Works in immediate phase of an asthma attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are side effects of tiotropium

A

can’t see, can’t pee, can’t spit, can’t sh*t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what class is aminophylline

A

bronchodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is aminophylinne usage

A

chronic asthma 5th line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is binding site of aminophylline

A

a1 purinergenic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what g protein does aminophyllien bind to and is it agonist/anatagonist

A

Gq, anatagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what is aminophylline moa vs normal moa

A

binds to adenosine receptors and blocks adenosine-mediated bronchoconstriction

Theophylline also binds to the adenosine A2B receptor and blocks adenosine-mediated bronchoconstrictio

drug moa
compelx of theophyllien and ethylendediamine

58
Q

aminophylline side effects

A

Headache; nausea; palpitations; seizure (more common when given too rapidly by intravenous injection)

59
Q

what class is theophylline and what does it inhibit

A

Bronchodilator
Phosphodiesterase enzyme inhibitor

60
Q

what is theophylline usage

A

chronic asthma (t5th line)

61
Q

what is theophylline binding site

A

phosphodiesterase enzyme. bind to albumin

62
Q

what is theophylline receptor location

A

adenosine inhibitor, bith A1 and A2 receptors inhibited.

63
Q

what is theophylline MOA vs normal MOA

A

normal MOA
1. The B2 receptor is activated this causes the beta and gamma subunits dissociate
2. GDP is transferred to GTP
3. The alpha subunit activates adenyl cyclase - this causes the increase of cAMP – a signalling molecule
4. cAMP activates protein kinase A (PKA)
5. PKA causes phosphorylation of proteins this reduces the amount of cytosolic Ca2+.
6. This causes smooth muscle relaxation

moa
1. Inhibition of phosphodiesterase enzymes
2. Decreases the breakdown of cAMP to AMP
3. Leaves cAMP levels high for longer than normal - prolongs the action of these second messengers -↑cAMP - ↓Ca2+ - smooth muscle relaxation

Works in the immedite phase of an asthma attack to cause bronchodilation

64
Q

what is theophylline side effects

A

GIT disturbances
Tachcardia
Anxeity
Insomnia
dysrythmia/ siezures - high levels of theophylline

65
Q

what class is monteluklast

A

Bronchodilator
Leukotriene receptor antagonist

66
Q

what is monteluklast usage

A

Asthma - 4th line (in adjunct to ICS and LABA)
Aspirin/exercise induced asthma

67
Q

what is monteluklast binding site and is it antagonist/agonist

A

Cysteinyl leukotriene receptor anatgonist

68
Q

what is monteluklast moa vs normal moa

A

normal moa
1. Archadonic acid forms leukotrienes and prostaglandins (asthma mediators)
2. Leukotrienes cause bronchoconstriction, promotes mucus secretion, recruits immune cells to enhance airway inflammation

moa
1. Montelukast binds to the cysteinyl leukotriene receptors CysLT1 receptors) on which bronchospasmic mediators act on
2. This works on the immediate phase of the asthma attack and causes bronchodilation which can decrease the delayed phase of the asthma attack to reduce inflammation

69
Q

what is monteluklast side effects

A

headaches, abdominal pain, URTI

70
Q

what class is
Amoxicillin
Co-amoxiclav
Flucloxacillin
Piperacillin

A

beta lactams antiobiotics- penecillin

71
Q

what is
Amoxicillin
Co-amoxiclav
Flucloxacillin
Piperacillin

usage

A

management and treatment of antibiotic infections

72
Q

what is Amoxicillin
Co-amoxiclav
Flucloxacillin
Piperacillin
binding site

A

tripeptidase enzyme

73
Q

what is Amoxicillin
Co-amoxiclav
Flucloxacillin
Piperacillin
normal MOA vs
MOA

A

normal MOA
In the cell wall there are NAG and NAM units, which are cross-linked by amino acid chains. The amino acid chains are linked by transpeptidase enzymes.

drug MOA

Penicillins contain a beta-lactam ring. This structure binds to the transpeptidase enzyme that cross links peptidoglycans and so prevents cell wall synthesis in bacteria. This leads to the destruction of the cell wall which exposes the bacterial membrane

They also stimulate the release of autolysins that digest the bacterial cell wall

74
Q

what is Amoxicillin
Co-amoxiclav
Flucloxacillin
Piperacillin
side effects

A

diarrhea, nausea, rash, urticaria, superinfection (including candidiasis

75
Q

what is Cefalexin
Cefotaxime

class

A

β-lactam antibiotics - Cephalosporins

76
Q

what is Cefalexin
Cefotaxime usage

A

treatment of septicaemia, pneumonia, meningitis, biliary-tract infections, peritonitis, and urinary-tract infections.

77
Q

what is Cefalexin
Cefotaxime binding side

A

transpeptidase enzyme

78
Q

what is cefelaxin, cefotaxime normal MOA vs drug MOA

A

normal MOA
In the cell wall there are NAG and NAM units, which are cross-linked by amino acid chains. The amino acid chains are linked by transpeptidase enzym

drug MOA
Cephalosporins contain a beta-lactam ring. This structure binds to the transpeptidase enzyme that cross links peptidoglycans and so prevents cell wall synthesis in bacteria. This leads to the destruction of the cell wall which exposes the bacterial membrane

They also stimulate the release of autolysins that digest the bacterial cell wall

79
Q

what is cefelaxin, cefotaxime side effects

A

nausea, vomiting, lack of appetite, and abdominal pain.

80
Q

what is vancomycin class

A

glycopeptides

81
Q

what is vancomyocin usage

A

treatment of gram positive bacterial infections

82
Q

what is vancomycin binding site

A

amino acids

83
Q

what is vancomycin normal moa vs drug moa

A

normal- In the cell wall there are NAG and NAM units, which are cross-linked by amino acid chains. The amino acid chains are linked by transpeptidase enzymes
drug- Binds to the amino acids that form the cross links between peptidoglycans in bacterial cell walls and so prevent the amino acid chains binding, therefore inhibiting cell wall synthesis

84
Q

what is vancomyosin side effects

A

nausea.
vomiting.
stomach pain.
diarrhea.
gas.
headache.
back pain.

85
Q

what is ciproflaxin class

A

quinolone

86
Q

what is ciproflaxin usage

A

Broad spectrum:
Anthrax infections
Complicated UTIs
GIT infections
Pseudomonal infection in CF patients
Typhoid fever

87
Q

where is ciproflaxin binding site

A

topoisomerase II

88
Q

what is cirproflaxin MOA

A

DNA transcription inhibitor - bactericidal

  1. Interact with topoisomerase II (enzyme that changes the configuration of DNA)
  2. This causes interference with its strand cutting + resealing function
  3. This then leaves breaks in the DNA, meaning that it can’t be transcribed or translated
  4. Without the ability to replicate or produce protein, the cell dies
89
Q

what is ciproflaxin side effects

A

GI disturbances due to altered gut flora - nausea, vomiting, discomfort, diarrhoea
Phototoxicity
CNS problems - dizziness & headache

90
Q

what is metronidazole class

A

nitroimizadole class

91
Q

what is metronidazole usage

A

Bacterial vaginosis
C.difficile
Dracunculus
E.histolytica
Gairdiasos
H.pylori
Trichomoniasi

92
Q

what is metronidazole MOA

A

DNA transcription inhibitor - bactericidal

Metabolized to an intermediate that inhibits bacterial DNA synthesis and degrades existing DNA

Inhibits nucleic acid synthesis by disrupting the DNA of microbial cells

This only occurs when metronidazole is reduced and because this reduction usually happens only in anaerobic cells, it has little effect upon human cells or aerobic cells - since intermediate toxic metabolite won’t be produced in mammalian cells

93
Q

what is metronidazole side effects

A

GI disturbances - nausea & vomitting
Oral disorders - Dry mouth & metallic bitter taste
Myalgia - drig induced muscle pain

94
Q

what is chloramphenicol usage

A

eye infections

95
Q

what is chloamphenicol normal MOA vs MOA

A

normal MOA
Protein synthesis inhibitor (50s) - bacteriostatic

  1. Binds reversibly to the 50s subunit of the bacterial ribosome near site A
  2. Inhibits peptidyltransferase reaction - peptide bond formation between the newly attatched AA and polypeptide chain.
  3. This prevents continuation of protein synthesis

drug MOA
Grey baby syndrome - rare but ocurs in newborwn with the accumulation of chloramphenicol

96
Q

what class is
Erythromycin, roxithromycin, azithromycin and clarithromycin
class

A

macrolides

97
Q

what is Erythromycin, roxithromycin, azithromycin and clarithromycin usage

A

Legionnaires disease
Syphilis
Mycoplasma pneumonia
Chlamydial infection - during pregnancy
Diphtheria

98
Q

what is Erythromycin, roxithromycin, azithromycin and clarithromycin moa

A

drug moa
Protein Synthesis Inhibitor (50s) - bacteriostatic

  1. Reversibly binds to the 50s subunit of the bacterial ribosome in site P
  2. When t-RNA attatched with the peptide chain tries to move, it can’t because the site is blocked by the macrolide, thus the tRNA is thrown away by the ribosome thinking it is faulty
  3. This process also prevents the transfer of the peptidyl tRNA from the A-site to the P-site and blocks the protein synthesis due to the inhibition of the translocation of the nascent peptide chain.
  4. The macrolides also promote the premature dissociation of the peptidal-tRNA from the A-site
99
Q

what is Erythromycin, roxithromycin, azithromycin and clarithromycin side effects

A

Motility receptor stimulation - GI disturbance
Allergy
Cholestasis
Rashes
Ototoxicity

100
Q

what is gentamicin class

A

Aminoglycosides

101
Q

what is gentamicin usage

A

Aerobic gram negative bacteria
e.g. P.aeruginosa

Bronchitis common 2

102
Q

what is gentamicin MOA

A

Protein Synthesis Inhibitor (30s) - bactericidal

  1. Binds irreversibly to the 30s portion of the bacterial ribosome PRIOR to ribosome formation
  2. This inhibits the formation of the ribosome unit and thus impairs its function
  3. This non functioning ribosome unit causes the wrong closely associated amino acid to be incorporated into the amino acid chain
103
Q

what is gentamicin side effects

A

Neurotoxicity
Allergic reactions
Nephrotoxicity
Ototoxicity

104
Q

what is tetracycline, doxycycline, minocycline, tigecycline class

A

tetracyclines

105
Q

what is tetracycline, doxycycline, minocycline, tigecycline usage

A

used to treat infections caused by bacteria including pneumonia and other respiratory tract infections; ; certain infections of skin, eye, lymphatic, intestinal, genital and urinary systems; and certain other infections that are spread by ticks, lice, mites, and infected animals.

106
Q

what is tetracycline, doxycycline, minocycline, tigecycline binding site

A

tetricylane chelate with 2+ ions and inactivate antibiotic.

107
Q

tetracycline, doxycycline, minocycline, tigecycline drug mechanism of acion

A

Protein synthesis inhibitor (30s) - bacteriostatic

  1. Bind to the 30s subunit of the ribsome at the A-site
  2. During protein biosynthesis, the new t-RNA with the amino acid attempts to bind to A-site of the ribosome.
  3. AS the A-site is blocked, the aminoacyl-tRNA cannot bind to it.
  4. Without tRNA attatchment at the A-site protein biosynthesis cannot occur.
  5. This cause cell death of the bacterial cell.
108
Q

what is tetracycline, doxycycline, minocycline, tigecycline side effects

A

DEVILS CAP
Dentition
Epigastric pain, nausea, vomitting, diarrhoea
Vestibular toxicity
Insipidus diabetes
Liver damage
Superinfections
[C] Kidney damage
Anti-anabolic effect
Phototoxicity

109
Q

what is sulfadiazine class

A

sulfonamides

110
Q

what is sulfadiazine usage

A

prevention of rheumatic fever

111
Q

what is sulfadiazine MOA

A

Inhibits folate synthesis - bacteriostatic

Suladiazine inhibits dihydropteroate synthase

  1. Sulfadiazine is structularly similar to PABA (intermediate in formation of DNA bases)
  2. Sulfadiazine competes with PABA for the active site of the enzyme dihydropteroate synthase
  3. This inhibits enzyme activity on PABA and reduces the formation of dihydrofolate from PABA.
112
Q

what is sulfadiazine side effects

A

SULFA
Steven-johnson syndrome/skin rashes
Urticaria/Urine precipitation
Leucopoenia
Folic acid deficiency
Aplastic Anaemia

113
Q

what is trimethoprim usage

A

Prophylaxis recurrent UTI

114
Q

what is trimethropin MOA

A

Inhibits folate synthesis - bacteriostatic

Trimethoprim inhibits dihydrofolate reductase

This inhibition reduces the production of tetrahydrofolate, which is required for DNA nucleotides to be formed

115
Q

what is co-trimoxazole class

A

sulfonamides

116
Q

what is co-trimoxazole usage

A

Taxoplasmosis

Pneumonia caused by pneumocystis jirovecii

117
Q

what is co-trimoxazole MOA

A

Inhibits folate synthesis - bacteriostatic

118
Q

what is co-trimoxazole side effects

A

Diarrhoea; electrolyte imbalance; fungal overgrowth; headache; nausea; skin reactions

119
Q

what is hydrocortisone class

A

corticosteroid

120
Q

what is hydrocortisone usage

A

Treatment
Acute hypersensitivty reactions - where angioedema of URT & anaphylaxis are present
Severe acute/life-threatening asthma
Thyrid storm
IBD/UC
IBD/ Ulcerative colitis

121
Q

what is hydrocortisone MOA

A

(all drugs are glucocorticosteroids I think)

Glucocorticosteroid MOA 1:
1. Corticosteroid binds to corticosteroid receptor in the cytoplasm
2. This induces a conformational change in the receptor
3 The corticosteroid-receptor complex dimerises and is transported to the nucleus
4. Complex binds to steroid responsive elements on DNA to cause up regulation or down regulation of transcription of mRNA
5. Downstream altered protein synthesis
6. Biological effect

(up-regulation of anti-inflammatory proteins or down-regulation of pro-inflammatory proteins caused by binding of complex to DNA)

Glucocorticosteroid MOA 2:
They can also inhibit the enzymes phospholipase A2 & cyclo-oxygenase which can inhibit the release of inflammatory mediators and bronchoconstrictors.

Causes up regulation of anti inflammation

Down reg of pro inflammation

122
Q

what is hydrocortisone side effects

A

Side effects are seen due to Cushings syndrome or cushings disease

Cushings disease is a specific type of cushings syndrome

Cushings syndrome occurs when your body makes too much of a glucocotricosteroid called cortisol.

The side effects associated with this are:

Weight gain
Round moon face
Buffalo hump - fat build up between the shoulders
Easily bruising & poor wound healing
Muscle atrophy
Wide purple stretch marks - mainly on the abdomen, breasts, hips & under the arms
Red scar tissue

123
Q

what is beclomethasone class

A

Corticosteroid

124
Q

what is beclomethasone usage

A

Prophylaxis of asthma
Prophylaxis and treatment of allergic & vasomoto

125
Q

what is beclomethasome MOA

A

(all drugs are glucocorticosteroids I think)

Glucocorticosteroid MOA 1:
1. Corticosteroid binds to corticosteroid receptor in the cytoplasm
2. This induces a conformational change in the receptor
3 The corticosteroid-receptor complex dimerises and is transported to the nucleus
4. Complex binds to steroid responsive elements on DNA to cause up regulation or down regulation of transcription of mRNA
5. Downstream altered protein synthesis
6. Biological effect

(up-regulation of anti-inflammatory proteins or down-regulation of pro-inflammatory proteins caused by binding of complex to DNA)

Glucocorticosteroid MOA 2:
They can also inhibit the enzymes phospholipase A2 & cyclo-oxygenase which can inhibit the release of inflammatory mediators and bronchoconstrictors.

Causes up regulation of anti inflammation

Down reg of pro inflammation

126
Q

what is beclomethasone side effects

A

Side effects are seen due to Cushings syndrome or cushings disease

Cushings disease is a specific type of cushings syndrome

Cushings syndrome occurs when your body makes too much of a glucocotricosteroid called cortisol.

The side effects associated with this are:

Weight gain
Round moon face
Buffalo hump - fat build up between the shoulders
Easily bruising & poor wound healing
Muscle atrophy
Wide purple stretch marks - mainly on the abdomen, breasts, hips & under the arms
Red scar tissue

127
Q

what is prednisolone class

A

corticosteroid

128
Q

what is prednisolone usage

A

Acute exacerbations of COPD
Moderate/severe/life-threatening asthma
Severe croup
Suppression of inflammatory & allergic disorders

129
Q

what is prednisolone MOA

A

(all drugs are glucocorticosteroids I think)

Glucocorticosteroid MOA 1:
1. Corticosteroid binds to corticosteroid receptor in the cytoplasm
2. This induces a conformational change in the receptor
3 The corticosteroid-receptor complex dimerises and is transported to the nucleus
4. Complex binds to steroid responsive elements on DNA to cause up regulation or down regulation of transcription of mRNA
5. Downstream altered protein synthesis
6. Biological effect

(up-regulation of anti-inflammatory proteins or down-regulation of pro-inflammatory proteins caused by binding of complex to DNA)

Glucocorticosteroid MOA 2:
They can also inhibit the enzymes phospholipase A2 & cyclo-oxygenase which can inhibit the release of inflammatory mediators and bronchoconstrictors.

Causes up regulation of anti inflammation

Down reg of pro inflammation

130
Q

what is prednisolone side effects

A

Side effects are seen due to Cushings syndrome or cushings disease

Cushings disease is a specific type of cushings syndrome

Cushings syndrome occurs when your body makes too much of a glucocotricosteroid called cortisol.

The side effects associated with this are:

Weight gain
Round moon face
Buffalo hump - fat build up between the shoulders
Easily bruising & poor wound healing
Muscle atrophy
Wide purple stretch marks - mainly on the abdomen, breasts, hips & under the arms
Red scar tissu

131
Q

what is prednisolone side effects

A

Side effects are seen due to Cushings syndrome or cushings disease

Cushings disease is a specific type of cushings syndrome

Cushings syndrome occurs when your body makes too much of a glucocotricosteroid called cortisol.

The side effects associated with this are:

Weight gain
Round moon face
Buffalo hump - fat build up between the shoulders
Easily bruising & poor wound healing
Muscle atrophy
Wide purple stretch marks - mainly on the abdomen, breasts, hips & under the arms
Red scar tissu

132
Q

what is dexamethasone class

A

corticosteroid

133
Q

what si dexamethasone usage

A

Eye drops for local treatment of inflammation
Localised joint & soft tissue inflammation

Palliative care for
Anorexia
Dysphagia due to bronchospasm or partial obstruction
Nausea and vomiting
Headache due to raise intracranial pressure Pain due to nerve compression
Cerebral oedema with or without malignancy

134
Q

what is dexamethasone drug MOA

A

(all drugs are glucocorticosteroids I think)

Glucocorticosteroid MOA 1:
1. Corticosteroid binds to corticosteroid receptor in the cytoplasm
2. This induces a conformational change in the receptor
3 The corticosteroid-receptor complex dimerises and is transported to the nucleus
4. Complex binds to steroid responsive elements on DNA to cause up regulation or down regulation of transcription of mRNA
5. Downstream altered protein synthesis
6. Biological effect

(up-regulation of anti-inflammatory proteins or down-regulation of pro-inflammatory proteins caused by binding of complex to DNA)

Glucocorticosteroid MOA 2:
They can also inhibit the enzymes phospholipase A2 & cyclo-oxygenase which can inhibit the release of inflammatory mediators and bronchoconstrictors.

Causes up regulation of anti inflammation

Down reg of pro inflammation

135
Q

what is dexamethasome side effect

A

Side effects are seen due to Cushings syndrome or cushings disease

Cushings disease is a specific type of cushings syndrome

Cushings syndrome occurs when your body makes too much of a glucocotricosteroid called cortisol.

The side effects associated with this are:

Weight gain
Round moon face
Buffalo hump - fat build up between the shoulders
Easily bruising & poor wound healing
Muscle atrophy
Wide purple stretch marks - mainly on the abdomen, breasts, hips & under the arms
Red scar tissu

136
Q

what is hydrocortisone usage

A

-acute hypersensitivity reactions, angioodeama of the upper resp tract + anaphylaxis
-severe acute asthma
-thyroid storm
-IBD

  1. replacement therapy
    2.1 addison’s disease, septic shock:insufficient endogenous corticosteroids
    2.2. if taken out 3 gand, >10mg prednisolone for 3 months after surgery
137
Q

what is beclamethasone used for

A

-prophylaxis of asthma
-prophylaxis and treatment of allegic and vasomotor rhitis
-acute exacerbations of COPD
-moderate, severe, life threatning asthma
-severe crouo
-suppresion of inflammatory and allergic disorders

138
Q

what do glucorocosteroids do

A

-protein catabolism
-glucoeogenesis
-glycogenesiss
-enhanced fight or flight response
-CNS stimulation

139
Q

describe how endogenous release glucorticosteroids

A

. hypothalamus stimulated by sypathetic input - releases (corticotropic release hormone CRH)

  1. release of glucocosterouds negative feedback for further release
    2.1 from hypothalamis (release CRH) -> anterior pituitary (release ATCH) ->adrenal cortex (release cortisol)
  2. also negative feedback on throid stimulating hormone (TSH)
140
Q

what is hydrocortisone used for

A

acute hypersensitivity reactions, angioodeama of the upper resp tract + anaphylaxis
-severe acute asthma
-thyroid storm
-IBD

  1. replacement therapy
    2.1 addison’s disease, septic shock:insufficient endogenous corticosteroids
    2.2. if taken out 3 gand, >10mg prednisolone for 3 months after surgery
141
Q

what are the firts gen histamines

A

SEDATING- crosses blood brain barrier
-chlorophenamine maleate
-promoethazine chloride
-cyclizine

142
Q

what are the second gen histamines

A

SECOND GEN - non sedating- no cns activity
-cetrizine hydrochloride
-loratidine
* CYP450 inhibition with grapefuit juice
**shows some cardiac toxicity

Year 1 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions