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PED 2006 brief Flashcards

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1
Q

where is the function of the gastrointestinal system major

A

metabolic and endocrine system

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2
Q

what is the pharmacological importance of the gastrointestinal system

A

gastric secretion
vomiting
bowel motility

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3
Q

which hormones are secreted in the endocrine

A

gastrin
cholecystokinin

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4
Q

which hormones are secreted in the pancreas

A

histamine
acetylcholine

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5
Q

what is the function of the parietal cells in the wall of the gastric gland

A

keep the pH between 6-7
within their structure the canaliculus releases Hcl
the tubulovesicles release hydrogen and potassium

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6
Q

what is the function of the canalicular membrane

A

contains a H+/K+ ATPase proton pump and is a Cl- co-transporter
pull potassium back in and hydrogen out - important to keep the pH isoelectrically neutral
this process required gastrin

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7
Q

what is gastrin

A

is a peptide hormone
stimulates acid secretion, pepsinogen secretion, blood flow and increases gastric motility
increases cytosolic ca2+

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8
Q

what is acetylcholine

A

a neurotransmitter
released from vagal neurons
increases cytosolic ca2+

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9
Q

what is histamine

A

hormone released from H2 receptors
increases cAMP

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10
Q

which diseases are associated with acid dysregulation

A

dyspepsia - upper abdominal pain, bloating and nausea
peptide ulceration - prolonged excess acid causes gastric and duodenal ulceration
reflux oesophagus - damage to oesophagus by excess acid secretion
Zollinger-Ellison syndrome - gastrin producing tumour

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11
Q

what is the therapeutic aim to treat diseases associated with acid dysregulation

A

to decrease secretion of gastric acid by
- reducing proton pump function (proton pump inhibitors)
- blocking histamine receptor function (H2 receptor antagonism)
- neutralising acid secretions with antacids

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12
Q

what are two examples of proton pump inhibitors

A

omeprazole
lansprazole

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13
Q

what is the mechanism of action of omeprazole and lansoprazole

A

irreversibly inhibit H+/K+ ATPase
can be used to treat peptide ulcers, reflux oesophagi’s and Zollinger-ellison

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14
Q

what are the pharmacokinetics of proton pump inhibitors

A

inactive at neutral pH
weak bases - allows accumulation in acidic environment
degrades rapidly at low pH
single dosing - 2-3 daily

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15
Q

what are the adverse effects of proton pump inhibitors

A

headache
diarrhoea
rash
masking the symptoms of gastric cancer
care should be taken with high risk groups e.g. liver failure and pregnancy

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16
Q

give two examples of histamine H2 receptor antagonists

A

cimetidine
ranitidine

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17
Q

what is the mechanism of action of histamine H2 receptor antagonists

A

competitive inhibits of H2 histamine receptors
used in peptic ulcers and reflux oesophagi’s

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18
Q

what are the adverse effects of H2 antagonists

A

diarrhoea
dizziness
muscle pain
cimetidine has androgenic action
reduction of metabolism of anticoagulants and tricyclic antidepressants - inhibit cytochrome P450s

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19
Q

give 2 examples of antacids

A

sodium bicarbonate
Mg2+/Al3+ hydroxide

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20
Q

what is the mechanism of action of antacids

A

bases that raise gastric luminal pH by neutralising gastric acid
used in dyspepsia and oesophageal reflux

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21
Q

what are the pharmacokinetics of antacids

A

relatively slow action
effects often short lived
acid rebound

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22
Q

what are the adverse effects of antacids

A

diarrhoea
constipation
belching
acid rebound
alkalosis
care must be taken with sodium content

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23
Q

what are helicobacter pylori infections

A

caused by gram negative bacteria
cause peptide ulcer formation that can lead to gastric cancer

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24
Q

how can helicobacter pylori infections be treated

A

combination therapy including PPI, antibacterial and cytoprotective agents

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25
what are cytoprotective agents
enhance mucosal protection mechanisms and form barriers over ulcer formations
26
what are some examples of cytoprotective agents
bismuth chelate sucralfate misoprotosol
27
what is bismuth chelate
toxic to bacillus they coat ulcer base, prostaglandins and bicarbonate synthesis
28
what is sucralfate
stimulate mucus production and prevent degradation increases prostaglandin and bicarbonate synthesis
29
what is misoprostol
is a prostaglandin analogue, has direct action on parietal cells
30
what are prostaglandins
synthesised by gastric muscosa they increase mucus and bicarbonate secretion decrease acid secretion
31
how do NSAIDs cause gastric ulcers
inhibit prostaglandin formation which causes gastric bleeds erosion ulcer formation specific COX2 inhibitors cause less GI damage
32
how is the frequency of gastric contractions controlled
pacemaker cells
33
what are pacemaker cells
found in smooth muscle cells in upper fungus rhythmic, autonomous, partial depolarisation depolarisation cause slow wave potentials that sweep down th stomach
34
how is the force of gastric contractions controlled
by neural and hormonal activity neural activity is increased by vagal activity and decreased by adrenergic activity hormonal activity is increased by gastrin and reduced by secretin
35
what happens when food is taken in
waves of peristaltic contractions throughout stomach forceful contractions and increased pressure in antrum retropulsion of food against close pylorus mixing and grinding of food
36
what happens to receptors when food is taken in
stretch receptors are activated vagal inhibitory neurones relaxation of smooth muscle little change in pressure
37
what is emesis
the forceful evacuation of stomach content. can be stimulated by pain, repulsive sights/smells, emotional factors, endogenous toxins.drugs, stimuli from pharynx/stomach, motion
38
how is emesis controlled
by the vomiting centre and chemoreceptor trigger zone it is sensitive to neurotransmitter stimulus such as acetylcholine, histamine, 5-HT and dopamine
39
how can we stimulate vomiting
ipecauaha are locally acting in stomach irritant effects of alkaloids emetine and cephaeline
40
what are the classes of anti emetics
H1 receptor antagonists muscarinic antagonists D2 antagonists 5-HT3 antagonists (cannabinoids, antipsychotics and steroid/neurokinin antagonists
41
what are the examples of H1 receptor antagonists
cyclizine promethazine
42
when are H1 receptor antagonists given
most effective for motion sickness when given before the onset of nausea and vomiting they act on vestibular nuclei
43
what are the adverse effects of H1 receptor antagonists
drowsiness sedation
44
example of muscarinic antagonists
hyoscine
45
when are muscarinic antagonists used
used for motion sickness effective against vestibular apparatus stimuli and local gut stimuli
46
what are the adverse effects of muscarinic antagonists
dry mouth blurred vision sedation
47
examples of D2 receptor antagonists
metoclopramide phenothiazines
48
when are D2 receptor antagonists used
used for vomiting caused by renal failure and radiotherapy they work in the chemoreceptor trigger zone
49
what are the adverse effects of D2 receptor antagonists
CNS effects (twitching and restlessness) prolactin stimulation = menstrual disorders
50
example of 5-HT3 antagonists
ondansetron
51
when are 5-HT3 antagonists used
in chemotherapy an post-surgery primarily act on CTZ 5-HT3 are released in gut following some endogenous toxins and chemotherapy drugs
52
what are the adverse effects of 5-HT3 antagonists
headache diarrhoea
53
what are the types of drugs used to treat bowel motility
anti-diarrhoea purgatives/laxatives
54
what are the causes of diarrhoea
viral - rotavirus bacterial - campylobacter systemic disease - inflammatory bowel disease drug induced - antibiotics e.g. erythromycin
55
how do antidiarrhoeals work
stimulate opiate receptors in the bowels increase tone of smooth muscle suppress propulsive peristalsis raise sphincter tone at oleo-caecal valve and anal sphincter reduced sensitivity to rectal distension
56
what is the effect of anti-diarrhoeals
delay in passage of faeces through the gut and increased water and electrolyte absorption in small intestine and colon
57
which opioid agonist can act as anti-diarrhoeals
codeine morphine
58
how do opioid agonists work as anti-diarrhoeals
activate mow receptors on myenteric neurones cause hyperpolarisation therefor inhibition of acetylcholine release reduces bowel motility
59
why is codeine preferred to morphine
opiates are susceptible to misuse as they can cause tolerance and dependence
60
two examples of synthetic opioid analogues
loperamide diphenoxylate
61
what is loperamide
binds to opiate receptors in gut wall and is relatively free of CNS side effects
62
what is diphenoxylate
marketed as a cophenotrope, atropine present to discourage abuse
63
what are the types of laxatives
bulk forming agents osmotic laxatives stimulants faecal softeners
64
what are the examples of bulk forming agents
ispaghula methylcellulose brain
65
how do bulk forming agents work
contain polysaccharide and cellulose components they are not digested and retain fluid, therefore increasing faecal bulk and stimulate peristalsis
66
side effects of bulk forming agents
flatulence bloating
67
examples of osmotic laxatives
magnesium salts polyethylene glycol phosphate enemas lactulose
68
how do osmotic laxatives work
act by osmosis to retain water in the bowel to produce a softer, bulkier stool
69
pharmacokinetics of osmotic laxatives
act in 30 mins 2-5hrs for magnesium salts 48hrs for lactulose
70
side effects of osmotic laxatives
abdominal cramps flatulence electrolyte disturbance
71
examples of stimulant laxatives
Senna bisacodyl dantron
72
how do stimulant laxatives work
directly stimulate colonic nerves movement of faecl mass and reduce transit time
73
side effects of stimulant laxatives
abdominal cramps colonic atony
74
example of faecal softeners
docusate sodium
75
how do faecal softeners work
they are non-ionic surfactant with stool softening properties reduces surface tension allows penetration of fluid into the faecal mass
76
examples of inflammatory bowel disease
crohns disease ulcerative colitis
77
characteristics of inflammatory bowel disease
cyclical bouts of diarrhoea constipation abdominal pain
78
treatments for inflammatory bowel disease
glucocorticoids aminosalicylates sulfasalazine immunosuppression
79
what is asthma
obstructive airway disease reversibly obstructs airflow due to airway stimulation and airway hyperresponsiveness obstruction can be cause by smooth muscle contractions, inflammation, oedema, muscus and airway structural changes
80
major symptoms of asthma
wheezing chest tightness dyspnea cough hypoxemia
81
what can be used to relax smooth muscle
beta blockers - SABA and LABA PDE blockers - theophylline LTRAs
82
what can be used to block inflammatory cascades
corticosteroids - ICS LTRAs PDE blockers targeted biologics
83
how do beta2 adrenoceptor agonists work
relaxation of smooth muscle by increasing cAMP through G proteins adrenaline has non-selective alpha, beta1 and beta2 effects isoprenaline is a selective beta agonist, causing bronchodilation and cardiac stimulation
84
how can beta 2 agonists be administered
aerosol inhalation inhalation of nebulised solution inhalation of powder oral administration
85
two examples of short acting beta 2 agonists
salbutamol terbutaline
86
when are short acting beta 2 agonists used
for acute episodes of asthma, inhalation relief within 5-10 mins Max effect within 30mins they last 3-5hours
87
examples of longer acting beta 2 agonists
salmeterol formoterol
88
mechanism of action of longer acting beta 2 agonists
give daily and last around 12 hours due to their lipophilic structures corticosteroids are used along side
89
side effects of beta2 adrenoceptor agonists
muscle tremor tachycardia cardiac dysrhythmias risk of paradoxical bronchospasm
90
how are leukotrienes linked with asthma
leukotrienes are synthesised and released during the acute response by mast cells, they are also produced by inflammatory cells
91
mechanism of action of cysteine leukotrienes LTC4 and LTD4
they increase vascular leakage and mucus production they can act as chemoattractants for eosinophils and basophils produced via cys-LT1 receptors coupled to Gq-Ca2+
92
what are LTB4
potent chemoattractants for neutrophils
93
two examples of leukotrienes receptor antagonists
zafirlukast and montelukast
94
how do leukotrienes receptor antagonists work
selective and are a high affinity competitive antagonist for cys-LT1 receptors they block the LTC4 and LTD4 effects on smooth muscle
95
what is zileuton
5-lipoxygenase inhibitors, so inhibits the formation of all 5-LOX products from LTA4 synthesis
96
when is montelukast used
acute prevent on exercise-induced bronchoconstriction used in cases of allergic and perennial rhinitis most commonly used leukotriene modulator
97
examples of anti-muscarinics used in asthma
ipratropium and tiotropium
98
why are antimuscarinics used in asthma
cause bronchodilation and reduce mucus secretion commonly used with beta2 agonists and steroids increase mucociliary clearance through action on cilia of epithelial cells
99
how do muscarinic antagonists act as bronchodilators
they innervate all conducting airways from the trachea to the bronchioles the parasympathetic nerves synthesise and release acetylcholine and are the primarily source of acetylcholine in the lung
100
pharmacokinetics of ipratropium bromide
examples of a SAMA onset is low but can last 6-8hrs given 3-4 times a day
101
what are the examples of LAMAs
tiotropium bromide glycopyronium bromide umeclidinium bromide aclidinium bromide
102
side effects of non-selective muscarinic receptors blockage
systemic anticholinergic side effects e.g. dry mouth, gastrointestinal motility disorder, tachycardia and nausea
103
types of treatments for immunosuppression
ICS biologics
104
why can glucocorticoids be used as anti-inflammatories
inhibit inflammatory response to injury and allergic disease inhibit the synthesis of inflammatory mediators, cytokines, cell chemoattractants, vasoactive agents decrease inflammatory cell infiltration and proliferation, vascular permeability and mucus secretion
105
mechanism of action glucocorticoids
inhibit NFkB which is a major transcription factors for all inflammatory cytokines. this works as tranrepression of NFkB and major anti-immune effects of GCs SGR complex inhibits HAT and recruits HDAC2 HDAC2 deacetylates and represses the genes
106
examples of inhaled corticosteroids
beclomethasone budesonide
107
how do inhaled corticosteroids work
inhaled as a dry powder reducing transcription and decreased formation of Th2 cytokines, reduce action of eosinophils, reduce production of IgE, reduce production of leukotriene and PAD inhibit induction of cyclooxyrgenase
108
side effects of corticosteroids
adrenal suppression reduced bone mineral density oropharyngeal candidiasis may occur
109
examples of oral corticosteroids
prednisolone hydrocortisone
110
when are oral corticosteroids used
short term relief of severe episodes of acute asthma
111
what are the long term effects of corticoid steroids
suppression of immune response to infection Cushing syndrome oesteoporosis hyperglycaemia muscle wastage inhibition of growth
112
how are eosinophils involved in allergic asthma
main inflammatory cells in later/chronic allergic asthma activated by IL5 from Th2 cells
113
what do eosinophils secretes
Th2 cytokines ROS LTC4/LTD4
114
what can be used to decrease production of eosinophils
mepolizumab resilzumab they do this by binding to IL5a
115
mechanism of action of benralizumab
stops IL5 binding by binding to the IL5 receptor on eosinophils increase binding affinity for Fc RIII on natural killer cells causing apoptosis of eosinophils through ADCC
116
what is the innate immune system
non specific immediate first line of defence no memory
117
what is the adaptive immune system
specific slow second line of defence immunological memory
118
what is inflammation
protective reaction of vascularised living tissue of local injury brings cells and molecules of host defence from the circulation to the site where they are needed it serves to destroy, dilute or isolate the injurious agents, eliminating the necrotic cells and tissues
119
what are the steps of the inflammatory response (5 Rs)
recognition of the offending agent/injury recruitment of leukocytes removal of the offending substance regulation of the response
120
what is acute inflammation
rapid onset short duration involved neutrophils
121
what is chronic inflammation
slow onset long duration involved monocytes, macrophages and lymphocytes
122
what are the cardinal signs of inflammation
redness heat swelling pain loss of function
123
what causes acute vascular inflammation
dilation of small vessels, leading to slowed blood flow increased vascular permeability to the microvasculature, enabling plasma proteins and leukocytes to leave the circulation
124
what causes acute cellular inflammation
emigration of the leukocytes from the microcirculation, accumulating at the site of the injury before activating to eliminate the pathogen
125
what are the key inflammatory mediators
histamine plasma proteins prostaglanding leukotrienes cytokines chemokine
126
what are histamines
produced by mast cells/basophils cause vasodilation and increased permeability lead to leukocyte recruitment
127
what are plasma proteins
produced by the liver cause vasodilation and increased permeability leading to leukocyte recruitment
128
what are prostaglandins
produced by mast cells, basophils and neutrophils cause vasodilation and increase permeability
129
what are leukotrienes
produced by mast cells, basophils and neutrophils cause increase permeability and allow leukocyte recruitment
130
what are cytokines
produced by mast cells and macrophages cause vasodilation and increased permeability allow leukocyte recruitment
131
what are chemokine
produced by mast cells and macrophages allow leukocyte rectuiment
132
what are the two main cellular mediators for chronic inflammation
macrophages lymphocytes
133
what are macrophages
cause phagocytosis initiate tissue repair and secrete cytokines
134
what are lymphocytes
cause T cells to secrete chemokine and B cells to secrete antibodies activation is caused by antigen presentation
135
types of drugs that reduce inflammatory and immune response
non-steroidal anti inflammatory drugs steroidal anti-inflammatory drugs anti histamines immunosuppressant drugs immune check point inhibitors
136
what are the signalling pattern recognition receptors
PAMP binds to toll like receptors this activates transcription of NFkB and IRF3/7 leading to secretion of cytokines and inflammation
137
what is COX1
works as a housekeeper many unwanted responses are thought to be exerted mainly through COX-1 isoform inhibition
138
what is COX2
induced upon inflammatory cell activation anti-inflammatory, analgesic and antipyretic activity, antipyretic activation of NSAIDs thought to be exerted when COX2 isoforms are inhibits
139
what is the mechanism of NSAIDs
reversible competitive inhibition (ibuprofen), reversible non-competitive inhibition (paracetamol) and irreversible inhibition (aspirin
140
what causes the symptoms of inflammation
COX2
141
what causes the symptoms of non-selective NSAIDs
COX1
142
what causes fever from inflammation
caused by pyrogens caused by the secretion of cytokines into bloodstream, which migrate to the brain, bind to receptors on brain endothelial cells, activated prostaglandin E2 synthesis
143
what causes the side effects from NSAIDs
gastrointestinal problems - inhibitions of synthesis of stomach pge skin rashes renal effects - inhibition of synthesis of PGI2 and PGE brocnhospasms
144
side effects of COX2 inhibitors
increase the risk of thrombotic events such as heart attacks and stroke
145
side effects of NSAIDs
adverse cardiovascular effects as COX2 decrease platelet aggregation and vasodilation COX1 cause releases of platelet of thromboxane causing thrombotic vasoconstriction
146
what are lipocortins
is a GR agonists and is an examples of a steroid anti-inflammatory drugs blocks phospholipase A2
147
what causes the effects of cortisol anti-inflammatory
by the induction of lipocortin which inhibits phospholipase A2. causes decreased inflammatory mediators such as prostaglandin, leukotrienes and platelet activating factors decreased capillary permeability, decreased phagocytic action of leucocytes, decreased histamine release, decreased activity of mononuclear cells and proliferation of tissue
148
how can glucocorticoids cause Cushing syndrome
increase hyperglycaemia so they can lead to dysregulation of insulin
149
what are the 4 types of allergic reaction
reaction mediated by IgE antibodies cytotoxic reaction mediated by IgG or IgM antibodies reaction mediated by immune complexes delayed reaction mediated by cellular response
150
what causes type 1 hypersensitivity
caused by exposure to allergen APC processes antigen and presents it to Th2 cells released IL4 and IL12 which activates B cells B cells proliferate and differentiate into plasma cells that synthesise and secrete IgE antibody IgE binds to mast cells by Fc region, sensitising the mast cells
151
what can be cause by exposure to antigen
the release of histamine and other mediators increased smooth muscle contraction, peripheral vasodilation, increased vascular permeability causing bronchospasm, abdominal cramps and rhinitis extravasation of capillary blood causing erythema histamine release causes pruritic fluid shift into interstitial space causing oedema, swollen eyes
152
examples of localised type 1 hypersensitivity reaction
hay fever asthma hives angioedema
153
examples of systemic type 1 hypersensitivity
anaphylaxis
154
signs of allergic rhinitis
red, itchy, watery eyes sneezing congestion and runny nose sore throat fatigue
155
what causes allergic rhinitis
mediated by histamine binding to H1 receptors
156
how do anti-histamines work
by binding to the H1 receptor and reduce its activity they are inverse agonists
157
examples of 1st generation antihistamines
chlorophenamies diphenhydramine
158
side effects of 1st generation antihistamines
caused by anticholinergic activity drowsiness difficulty to urinate
159
examples of second generation antihistamines
certizine loratadine less likely to have side effects as they don't pass the blood brain barrier
160
what is anaphylaxis
sudden and rapid onset of allergic symptoms can be life threatening due to breathing and circulation problems can lead to skin and/or mucosal changes
161
what is used to treat anaphylaxis
adrenaline as it prevents and relieves airway obstruction this promotes cardiac output and increases total peripheral resistance to increased blood pressure
162
when is hydrocortisone used
to prevent biphasic late responses
163
what is immunosuppression
block T cell mediated immune response primarily by blocking the expression and activity of the T cell growth factors activating cytokine interleukin 2
164
what can be used to treat immunosuppression
prednisolone (glucocorticoid) tacrolimus or cyclosporin (calcineurine inhibitors) sirolimus (dual calcineurin/mTOR inhibitors) daclizumab/basiliximab (IL2 receptor antagonists) mycophenolate (nucleic acid synthesis antagonists)
165
how does antibody opsonisation benefit the immune system
enhances phagocytosis (agglutination and chemoattraction) neutralisation natural killer cell activation and increasing components of the classical component cascade
166
how to prevent NFkB activation of inflammatory genes
T cells and B cells are activated when GR complexes directly bind to the p65 subunit of NFkB and this prevent NFkB activation of inflammatory genes including il2 GR promotes IkBa synthesis, which prevents p50/p65 nuclear translocation
167
how do daclizumab and basiliximab cause immunosuppression
they prevent IL2 binding to the receptor and thus IL2 mediated T cell activation daclizumab is a humanised monoclonal antibody to the alpha subunit of the IL2 receptors of T cells basiliximab is a chimeric mouse - human monoclonal to the IL2-Ra of T cells
168
what is OKT3
TCR receptor antagonist is a murine monoclonal antibody against the chain of CD3 complex. OKT3 acts in 2 phases, firstly causes increased T cell depletion from the circulation by the liver secondary it promotes the removal of an important activator domain of the T cell receptor from cytotoxic T cells and helper T cells
169
what is immunotherapy
involves the stimulation of immune cells by a range of immune cell checkpoint protein interaction this can also be inhibited by PDL/PD1
170
when is immunotherapy used
in cancer treatment by activating the bodies own immune system to recognise and kill cancer cels PD1 receptor antagonists are a novel group of checkpoint inhibits for the treatment of multiple solid cancer
171
how can immune cells cause cancer
when PD1 receptor on T cells binds to PD-L1 antigen on tumour cells, the T cell is deactivated, allowing the cancer cell to evade immune attack PD1 immune checkpoint inhibitors MOA can prevent tumour cells from binding to the inactivating antigen PDL1, enabling the T cells to remain active
172
what are antibiotics
inhibit the growth or destroys bacteria. bacteriostatic inhibit multiplication bactericidal kill bacteria
173
how do antibiotics work
target cell wall synthesis, membrane synthesis, protein synthesis, metabolic pathways and nucleic acid synthesis
174
what is flucloxacillin
beta-lactase resistant penicillin that targets gram positive and beta-lactamase resistant bacteria
175
what is benzylpenicillin
natural penicillin that targets gram positive bacteria
176
what is amoxicillin
broad-spectrum penicillin that targets gram positive and negative bacteria
177
what is mecillinam
reverse spectrum penicillin that targets gram negative bacteria
178
what is mezlocillin
extended spectrum penicillin that targets gram positive, gram negative and pseudomonas aerginose bacteria
179
what is cephalosporins
used to treat septicaemia, pneumonia and meningitis effects is exerted through penicillin binding protein given parentally, IM or IV excreted in the kidney
180
examples of cephalosporin
cefaclor cephalexin cefotaxime
181
how do cells become resistant to penicillin
producing beta-lactamases and modifying penicillin binding proteins
182
what can inhibit protein synthesis
chloramphenicol erythromycin tetracycline streptomycin
183
how do chloramphenicol work
binds to 50S portion and inhibits formation of peptide bonds
184
how does erythromycin work
binds to 50S portion, prevents translocation - movement of ribosomes along mRNA
185
how do tetracyclines work
interfere with attachment of tRNA to mRNA-ribosome complex. they are bacteriostatic and bind competitively to the A site. resistance to this antibiotic is growing used to treat borrelia, chlamydia and rickettsia
186
how do streptomycin work
changes shape of 30S portion and causes code on mRNA to be read incorrectly
187
how do amunoglycosides work
inhibit protein synthesis by interfering with mRNA translation, this is enhanced by penicillin. they can cause ototoxicity and nephrotoxicity
188
mechanism of action of macrolides
inhibit protein synthesis by binding to 50S subunit and preventing translocation they are metabolised by demethylation in liver CYP3A4
189
when are macrolides used
to treat legionella, chlamydia and mycoplasma and effective against gram positive bacteria
190
side effects of macrolides
heart arrhythmias a GI disturbance
191
action of sulphonamides
inhibit dihydropteroate well distributed and cross BBB
192
action of trimethoprim
inhibits dihydrofolate reductase given oral and used to treat UTI and respiratory tract infection
193
action of fluoroquinolone
inhibits DNA gyrase taken orally and well absorbed but don't cross BBB inhibits CYP1A2
194
use of fluoroquinolone
kill gram positive and negative bacteria and enterobacter
195
side effects of fluoroquinolone
GI problems prolongation of QT interval
196
what is mycobacteria
causes tuberculosis and leprosy non-motile, slow growing bacteria with very thick, waxy, lipid-rich hydrophobic cell wall this cell wall contains mycotic acid so can survive in macrophages
197
what is rifampicin
semisynthetic derivative of rifamycin used against gram positive, negative and mycobacteria induces CYP3A4 so increased degradation of glucocorticoids and warfarin inhibits prokaryotic DNA-dependent RNA polymerase given orally and crosses BBB
198
what is daptomycin
a lipopeptides and inserts into the membrane leading to cell death attacks gram positive bacteria including MRSA and VRSA poorly absorbed so given orally it is eliminated from the body by renal excretion can cause damage to musculoskeletal system, eosinophilic pneumonia and peripheral neuropathy
199
types of DNA viruses
adenovirus herpesvirus papillomavirus
200
types of RNA viruses
paramyxovirus rhabdovirus togavirus influenza virus retrovirus
201
stages in the viral replication cycle
attachment to host cells uncoating of virus control of DNA, RNA and protein porduction this leads to the production of viral subunits causing the assembly and release of visions
202
action of antiviral drugs
penetrate infected cells by targeting unique enzymes and metabolic pathways interfere with viral nucleic acid synthesis and/or regulation some specific targets include viral cell binding, interrupting virus un-coatin or stimulating the host cell immune system
203
what is viral latency
the recurrence of an infection due to non-replicating cells, joint replication process and limited immune detection no antiviral agents eliminate viral latency
204
which types of acute infections are associated with viral latency
rhinovirus rotavirus influenza virus
205
which types of persistent infections are associated with viral latency
lymphocytic choriomeningitis virus
206
which types of latent, reactivating infections are associated with viral latency
herpes simplex
207
which types of slow viral infections are associated with viral latency
measles HIV
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how does antiviral resistance occur
by rapid replication rates and high mutation rates mutations prevent binding of drug to active sites of key enzymes such as protease and reverse transcriptase
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what does herpes virus cause
cold sores - simplex chicken pox - varicella zoster glandular fever - epstein barr
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what are the symptoms of herpes virus
flu-like symptoms blister/ulcer stage
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where does herpesvirus resides
herpes virus infects sensory ganglia where it becomes latent this latency can become stimulated again from external infection
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action of acyclovir
antiviral action utilises virus specific thymidine kinase and then undergoes conversion to di and triphosphate forms via host cells kinases, when it triphosphate form it has antiviral action inhibits viral DNA polymerase by being a DNA chain terminators
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characteristics of HIV infections
by destruction of host immune systems they are opportunistic infection, rare neoplasm and can cause death
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how is HIV transmitted
congenitally parentally sexual contact
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what are the 2 forms of HIV
HIV1 is responsible for human aids HIV2 is less virulent form of immune suppression
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what is primary HIV infection
asymptomatic there is seroconversion which is negative to positive HIV antibody detection increase viral load
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stages of AIDs
asymptomatic - 25-35% develop persistent generalised lymphadenopathy progression to severe infection - weight loss and increased opportunistic infections such as bronchitis and sinusitis greater weight loss - oral candidiasis, hairy leukoplakia and mycobacterium tuberculosis is developed HIV wasting syndrome, kaposis sarcoma, DNA toxoplasmosis, HIV encephalopathy
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mechanism of action of HIV
viral DNA RNA translation into viral components viral assembly host cell death the immune target cells involves cytotoxic/helper T lymphocytes. reverse transcriptase converts DNA to viral RNA
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How to inhibit HIV life cycle
fusion inhibitors CCR5 inhibitors NRTIs NNRTI protease inhibitors
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examples of fusion inhibitors
enfurviritde
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action of fusion inhibitors
inhibits the fusion of cellular and viral membranes usually given by subcutaneous injections and most effective as combination therapy
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examples of CCR5 inhibitor
maraviroc
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action of CCR5 inhibitors
it binds to the CCR5 receptor on the membrane of human CD4 cells. this binding prevents the interaction of HIV1 GP120 and human CCR5 receptor which is necessary for entry into the cells
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examples of a nucleoside reverse transcriptase inhibitor
zidovudine
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action of NRTI
prevents HIV replactions active when phosphorylated intracellularly to its triphosphate and then inhibits reverse transcriptase. this causes premature termination of viral DNA elongation
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further action of zidovudine
inhibits mammalian lambda and beta DNA polymerase, so increases toxicity in man
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side effects of NRTIs
headache nausea anemia leucopenia neutropenia
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examples of non-nucleoside reverse transcriptase inhibitors
nevirapine delaviridine efavirenz
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action of NNRTIs
bind to reverse transcriptase causing denaturation induce cytochrome p450
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examples of protease inhibitors
saquinavir ritonavir
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action of protease inhibitors
targeting virus specific protease enzyme which is required for post translational processing of gag and gag-pol poly proteins into functional proteins inhibition of protease interrupts viral spread
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examples of highly active anti-retroviral therapy
NRTI + NNRTI or PI
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what is a combination pill for HIV treatment
Atripla contain emtricitabine tenofovir efavirenz
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what is raltegravir
an integrase inhibitors and inhibits integration of transcribed viral DNA into host cell chromosomes
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categories of neuro drugs
sedatives - exert calming effect hypnotics - sleep inducing anticonvulsant - inhibit seizures anxiolytics and antidepressatns - reduce anxiety and stress antipsychotics - treatment for psychotic disorders mood stabilisers - anti-manic agents
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why target GABA receptors
inhibit neurotransmission sedatives and hypnotics directly hyperpolarize muscle relaxants such as baclofen indirectly hyperpolarize by inhibiting K+ channel
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what are GABA A receptors
ligand gated chloride permeable ion channels

CM2001 (13 decks)

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