Pharmacology Resp Flashcards
Fwhat class is clophenimine maleate
1st gen anti histamine
what is usage of first gen anti histamine
Oral - symptomatic relief of hayfever and urticaria
IV - used as adjunt in the treatment of anaphylaxis & angioedema
Sedative
what is chlorophenimine maleate binding site
H1 receptor anatgonist
what are all h1 receptors in relation to agonist/antagonist and competitive/uncomepetitive
Gq, competitive antagonist
what is chlorophenamine maleate MOA vs normal MOA
- Histamine is released from storage granules in mast cells as a result of antigen binding to the IgE receptor on the cell surface
- Histamine binds to the H1 receptor
- There is dissociation of the beta and gamma subunit. The Alpha unit will activate the 2nd messenger (PLC) by turning GDP to GTP
- This causes the degradation of PIP2 into DAG and IP3, DAG stays membrane bound while the IP3 becomes soluble
- 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
chloraphenimine maleate
Drowsiness as first gen
Can’t see - blurred vision
Can’t pee - urinary retention
Can’t shit - constipation
Can’t spit - dry mouth
what class is promoethazine hydrochloride
1st gen anti histamine
what is usage of promethazine hydrochloride
Oral - symptomatic relief of hayfever and urticaria
IV - used as adjunt in the treatment of anaphylaxis & angioedema
Sedative
what is binding site of promoethazine hydrochloride
H1 receptor antagonist
what G receptor is promethazine hydrochloride and is it agonist/anatgonist
Gq competative antagonist
what is promethezine hydrochloride MOA and normal
- Histamine is released from storage granules in mast cells as a result of antigen binding to the IgE receptor on the cell surface
- Histamine binds to the H1 receptor
- There is dissociation of the beta and gamma subunit. The Alpha unit will activate the 2nd messenger (PLC) by turning GDP to GTP
- This causes the degradation of PIP2 into DAG and IP3, DAG stays membrane bound while the IP3 becomes soluble
- 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
what are side effects of promoethezine hydrochloride
Drowsiness as first geb
Can’t see - blurred vision
Can’t pee - urinary retention
Can’t shit - constipation
Can’t spit - dry mout
what class are Ceritizine hydrochloride //
Loratidine
2nd gen antihistamines
what is usage of cetrizine hydrochloride//loratidine
Hypersensitivity reactions - hayfever, some drug allergies, insect bites, urticaria, puritis and rhinitis
what is binding side of cetrizine hydrochloride/loratidine
H1 receptor antagonist
what G protein does cetrizine hydrochloride/loratine bind to and it it antagonist/agonist
Gq anatagonist
what is normal MOA of cetrizine hydrochloride/lorat
- Histamine is released from storage granules in mast cells as a result of antigen binding to the IgE receptor on the cell surface
- Histamine binds to the H1 receptor
- There is dissociation of the beta and gamma subunit. The Alpha unit will activate the 2nd messenger (PLC) by turning GDP to GTP
- This causes the degradation of PIP2 into DAG and IP3, DAG stays membrane bound while the IP3 becomes soluble
- 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
what are side effects Ceritizine hydrochloride /
Loratidine
Can’t see - blurred vision
Can’t pee - urinary retention
Can’t shit - constipation
Can’t spit - dry mouth
what class is cyclizine
1st gen antihistine
usage of cyclizine
Nausea, Vomitting, Vertigo, Labyrinthine disorders, motion sickness
what is bidning site of cyclizine
H1 receptor antagonist
what G protein receptor does cyclizine bind to and is it anatagonist/agonist
Gq, anatagonsit
side effects of cyclizine
Nausea,
Vomiting,
Vertigo,
Motion sickness,
Labyrinthine disorders
what is usage of injectable forumulation along w adrenaline
Severe hypersensitivity reactions and emergency treatment of anaphylaxis
what is usage if unjectable formaulation along w adrenaline
Severeq hypersensitivity reactions and emergency treatment of anaphylaxis
what is binding site of injectable formula along with adrenaline
H1 receptor anatgonist
what is side effects of injectable formula along with adrenaline
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.
what class is salbutamol
beonchodilator SABA
what is usage salbuatmol
asthma- first line, copd
what binding site for salbutamol
b2 receptor
what G protein does salbutamol bind to and it it anatgonist/agonist
Gs- stimulates adenyly cyclase. agonist
what is salbutamol MOA vs normal MOA
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
what are side effects salbutamol
trembling, headaches, palpitations, hypokalemia
what is formoteral//salmetoral class
Bronchodilator
LABA
what is formoterol/salmetarol usage
Asthma - third line (has to be given with ICS)
COPD (2nd line)
what is formetarol/salmetarol binding site
B2 receptor
what is formetarol/salmetarol binding site
B2 receptor
what G protein does salmeterol/formetarol bind to and is it antafonist/agonist
Gs- stimulates adenyl cyclase. agonist, saba
what is salmeterol/formetarol normal MOA, vs drug MOA
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
what is salmeterol/formetarol side effects
Uncommon at normal doses
High doses:
Tachycardia
Hyperglycaemia
Skeletal muscle tremors occur
what class is ipratropium bromide
bronchodilator SAMA
what is ipatropium bromide usage
Asthma - third line (has to be given with ICS)
COPD (2nd line)
what is binding side of ipratropium bromide
M2 receptor
what G protein does ipratropium brominde bind to and is it anatgonist/agonist
Gq, anatagonist
what is ipratropium bromide l normal vs drug MOA
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
what is ipratropium bromide side effects
can’t see, can’t pee, can’t spit, can’t sh*
what class is tiotropium
bronchodilator LAMA
what is usage of tiotropium
Chronic asthma - 5th line - adjunct to LABA
COPD - 1st line
what is tiotropium binding site
M2 receptor
what G protein does tiotropium bind to and it antagonist/agonist
Gq, antagonist
what is tiotropium normal MOA vs drug MOA
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
what are side effects of tiotropium
can’t see, can’t pee, can’t spit, can’t sh*t
what class is aminophylline
bronchodilators
what is aminophylinne usage
chronic asthma 5th line
what is binding site of aminophylline
a1 purinergenic receptors
what g protein does aminophyllien bind to and is it agonist/anatagonist
Gq, anatagonist
what is aminophylline moa vs normal moa
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
aminophylline side effects
Headache; nausea; palpitations; seizure (more common when given too rapidly by intravenous injection)
what class is theophylline and what does it inhibit
Bronchodilator
Phosphodiesterase enzyme inhibitor
what is theophylline usage
chronic asthma (t5th line)
what is theophylline binding site
phosphodiesterase enzyme. bind to albumin
what is theophylline receptor location
adenosine inhibitor, bith A1 and A2 receptors inhibited.
what is theophylline MOA vs normal MOA
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
what is theophylline side effects
GIT disturbances
Tachcardia
Anxeity
Insomnia
dysrythmia/ siezures - high levels of theophylline
what class is monteluklast
Bronchodilator
Leukotriene receptor antagonist
what is monteluklast usage
Asthma - 4th line (in adjunct to ICS and LABA)
Aspirin/exercise induced asthma
what is monteluklast binding site and is it antagonist/agonist
Cysteinyl leukotriene receptor anatgonist
what is monteluklast moa vs normal moa
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
what is monteluklast side effects
headaches, abdominal pain, URTI
what class is
Amoxicillin
Co-amoxiclav
Flucloxacillin
Piperacillin
beta lactams antiobiotics- penecillin
what is
Amoxicillin
Co-amoxiclav
Flucloxacillin
Piperacillin
usage
management and treatment of antibiotic infections
what is Amoxicillin
Co-amoxiclav
Flucloxacillin
Piperacillin
binding site
tripeptidase enzyme
what is Amoxicillin
Co-amoxiclav
Flucloxacillin
Piperacillin
normal MOA vs
MOA
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
what is Amoxicillin
Co-amoxiclav
Flucloxacillin
Piperacillin
side effects
diarrhea, nausea, rash, urticaria, superinfection (including candidiasis
what is Cefalexin
Cefotaxime
class
β-lactam antibiotics - Cephalosporins
what is Cefalexin
Cefotaxime usage
treatment of septicaemia, pneumonia, meningitis, biliary-tract infections, peritonitis, and urinary-tract infections.
what is Cefalexin
Cefotaxime binding side
transpeptidase enzyme
what is cefelaxin, cefotaxime normal MOA vs drug MOA
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
what is cefelaxin, cefotaxime side effects
nausea, vomiting, lack of appetite, and abdominal pain.
what is vancomycin class
glycopeptides
what is vancomyocin usage
treatment of gram positive bacterial infections
what is vancomycin binding site
amino acids
what is vancomycin normal moa vs drug moa
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
what is vancomyosin side effects
nausea.
vomiting.
stomach pain.
diarrhea.
gas.
headache.
back pain.
what is ciproflaxin class
quinolone
what is ciproflaxin usage
Broad spectrum:
Anthrax infections
Complicated UTIs
GIT infections
Pseudomonal infection in CF patients
Typhoid fever
where is ciproflaxin binding site
topoisomerase II
what is cirproflaxin MOA
DNA transcription inhibitor - bactericidal
- Interact with topoisomerase II (enzyme that changes the configuration of DNA)
- This causes interference with its strand cutting + resealing function
- This then leaves breaks in the DNA, meaning that it can’t be transcribed or translated
- Without the ability to replicate or produce protein, the cell dies
what is ciproflaxin side effects
GI disturbances due to altered gut flora - nausea, vomiting, discomfort, diarrhoea
Phototoxicity
CNS problems - dizziness & headache
what is metronidazole class
nitroimizadole class
what is metronidazole usage
Bacterial vaginosis
C.difficile
Dracunculus
E.histolytica
Gairdiasos
H.pylori
Trichomoniasi
what is metronidazole MOA
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
what is metronidazole side effects
GI disturbances - nausea & vomitting
Oral disorders - Dry mouth & metallic bitter taste
Myalgia - drig induced muscle pain
what is chloramphenicol usage
eye infections
what is chloamphenicol normal MOA vs MOA
normal MOA
Protein synthesis inhibitor (50s) - bacteriostatic
- Binds reversibly to the 50s subunit of the bacterial ribosome near site A
- Inhibits peptidyltransferase reaction - peptide bond formation between the newly attatched AA and polypeptide chain.
- This prevents continuation of protein synthesis
drug MOA
Grey baby syndrome - rare but ocurs in newborwn with the accumulation of chloramphenicol
what class is
Erythromycin, roxithromycin, azithromycin and clarithromycin
class
macrolides
what is Erythromycin, roxithromycin, azithromycin and clarithromycin usage
Legionnaires disease
Syphilis
Mycoplasma pneumonia
Chlamydial infection - during pregnancy
Diphtheria
what is Erythromycin, roxithromycin, azithromycin and clarithromycin moa
drug moa
Protein Synthesis Inhibitor (50s) - bacteriostatic
- Reversibly binds to the 50s subunit of the bacterial ribosome in site P
- 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
- 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.
- The macrolides also promote the premature dissociation of the peptidal-tRNA from the A-site
what is Erythromycin, roxithromycin, azithromycin and clarithromycin side effects
Motility receptor stimulation - GI disturbance
Allergy
Cholestasis
Rashes
Ototoxicity
what is gentamicin class
Aminoglycosides
what is gentamicin usage
Aerobic gram negative bacteria
e.g. P.aeruginosa
Bronchitis common 2
what is gentamicin MOA
Protein Synthesis Inhibitor (30s) - bactericidal
- Binds irreversibly to the 30s portion of the bacterial ribosome PRIOR to ribosome formation
- This inhibits the formation of the ribosome unit and thus impairs its function
- This non functioning ribosome unit causes the wrong closely associated amino acid to be incorporated into the amino acid chain
what is gentamicin side effects
Neurotoxicity
Allergic reactions
Nephrotoxicity
Ototoxicity
what is tetracycline, doxycycline, minocycline, tigecycline class
tetracyclines
what is tetracycline, doxycycline, minocycline, tigecycline usage
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.
what is tetracycline, doxycycline, minocycline, tigecycline binding site
tetricylane chelate with 2+ ions and inactivate antibiotic.
tetracycline, doxycycline, minocycline, tigecycline drug mechanism of acion
Protein synthesis inhibitor (30s) - bacteriostatic
- Bind to the 30s subunit of the ribsome at the A-site
- During protein biosynthesis, the new t-RNA with the amino acid attempts to bind to A-site of the ribosome.
- AS the A-site is blocked, the aminoacyl-tRNA cannot bind to it.
- Without tRNA attatchment at the A-site protein biosynthesis cannot occur.
- This cause cell death of the bacterial cell.
what is tetracycline, doxycycline, minocycline, tigecycline side effects
DEVILS CAP
Dentition
Epigastric pain, nausea, vomitting, diarrhoea
Vestibular toxicity
Insipidus diabetes
Liver damage
Superinfections
[C] Kidney damage
Anti-anabolic effect
Phototoxicity
what is sulfadiazine class
sulfonamides
what is sulfadiazine usage
prevention of rheumatic fever
what is sulfadiazine MOA
Inhibits folate synthesis - bacteriostatic
Suladiazine inhibits dihydropteroate synthase
- Sulfadiazine is structularly similar to PABA (intermediate in formation of DNA bases)
- Sulfadiazine competes with PABA for the active site of the enzyme dihydropteroate synthase
- This inhibits enzyme activity on PABA and reduces the formation of dihydrofolate from PABA.
what is sulfadiazine side effects
SULFA
Steven-johnson syndrome/skin rashes
Urticaria/Urine precipitation
Leucopoenia
Folic acid deficiency
Aplastic Anaemia
what is trimethoprim usage
Prophylaxis recurrent UTI
what is trimethropin MOA
Inhibits folate synthesis - bacteriostatic
Trimethoprim inhibits dihydrofolate reductase
This inhibition reduces the production of tetrahydrofolate, which is required for DNA nucleotides to be formed
what is co-trimoxazole class
sulfonamides
what is co-trimoxazole usage
Taxoplasmosis
Pneumonia caused by pneumocystis jirovecii
what is co-trimoxazole MOA
Inhibits folate synthesis - bacteriostatic
what is co-trimoxazole side effects
Diarrhoea; electrolyte imbalance; fungal overgrowth; headache; nausea; skin reactions
what is hydrocortisone class
corticosteroid
what is hydrocortisone usage
Treatment
Acute hypersensitivty reactions - where angioedema of URT & anaphylaxis are present
Severe acute/life-threatening asthma
Thyrid storm
IBD/UC
IBD/ Ulcerative colitis
what is hydrocortisone MOA
(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
what is hydrocortisone side effects
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
what is beclomethasone class
Corticosteroid
what is beclomethasone usage
Prophylaxis of asthma
Prophylaxis and treatment of allergic & vasomoto
what is beclomethasome MOA
(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
what is beclomethasone side effects
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
what is prednisolone class
corticosteroid
what is prednisolone usage
Acute exacerbations of COPD
Moderate/severe/life-threatening asthma
Severe croup
Suppression of inflammatory & allergic disorders
what is prednisolone MOA
(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
what is prednisolone side effects
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
what is prednisolone side effects
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
what is dexamethasone class
corticosteroid
what si dexamethasone usage
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
what is dexamethasone drug MOA
(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
what is dexamethasome side effect
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
what is hydrocortisone usage
-acute hypersensitivity reactions, angioodeama of the upper resp tract + anaphylaxis
-severe acute asthma
-thyroid storm
-IBD
- 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
what is beclamethasone used for
-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
what do glucorocosteroids do
-protein catabolism
-glucoeogenesis
-glycogenesiss
-enhanced fight or flight response
-CNS stimulation
describe how endogenous release glucorticosteroids
. hypothalamus stimulated by sypathetic input - releases (corticotropic release hormone CRH)
- release of glucocosterouds negative feedback for further release
2.1 from hypothalamis (release CRH) -> anterior pituitary (release ATCH) ->adrenal cortex (release cortisol) - also negative feedback on throid stimulating hormone (TSH)
what is hydrocortisone used for
acute hypersensitivity reactions, angioodeama of the upper resp tract + anaphylaxis
-severe acute asthma
-thyroid storm
-IBD
- 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
what are the firts gen histamines
SEDATING- crosses blood brain barrier
-chlorophenamine maleate
-promoethazine chloride
-cyclizine
what are the second gen histamines
SECOND GEN - non sedating- no cns activity
-cetrizine hydrochloride
-loratidine
* CYP450 inhibition with grapefuit juice
**shows some cardiac toxicity
