Brainscape's Knowledge GenomeTM

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


See full index

CM2001 > PED 2006 brief > Flashcards

PED 2006 brief Flashcards

1
Q

where is the function of the gastrointestinal system major

A

metabolic and endocrine system

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

what is the pharmacological importance of the gastrointestinal system

A

gastric secretion
vomiting
bowel motility

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

which hormones are secreted in the endocrine

A

gastrin
cholecystokinin

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

which hormones are secreted in the pancreas

A

histamine
acetylcholine

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

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

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

what is gastrin

A

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

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

what is acetylcholine

A

a neurotransmitter
released from vagal neurons
increases cytosolic ca2+

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

what is histamine

A

hormone released from H2 receptors
increases cAMP

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

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

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

what are two examples of proton pump inhibitors

A

omeprazole
lansprazole

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

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

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

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

give two examples of histamine H2 receptor antagonists

A

cimetidine
ranitidine

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

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

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

give 2 examples of antacids

A

sodium bicarbonate
Mg2+/Al3+ hydroxide

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

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

what are the pharmacokinetics of antacids

A

relatively slow action
effects often short lived
acid rebound

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

what are the adverse effects of antacids

A

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

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

what are helicobacter pylori infections

A

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

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

how can helicobacter pylori infections be treated

A

combination therapy including PPI, antibacterial and cytoprotective agents

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

what are cytoprotective agents

A

enhance mucosal protection mechanisms and form barriers over ulcer formations

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

what are some examples of cytoprotective agents

A

bismuth chelate
sucralfate
misoprotosol

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

what is bismuth chelate

A

toxic to bacillus
they coat ulcer base, prostaglandins and bicarbonate synthesis

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

what is sucralfate

A

stimulate mucus production and prevent degradation
increases prostaglandin and bicarbonate synthesis

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

what is misoprostol

A

is a prostaglandin analogue, has direct action on parietal cells

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

what are prostaglandins

A

synthesised by gastric muscosa
they increase mucus and bicarbonate secretion
decrease acid secretion

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

how do NSAIDs cause gastric ulcers

A

inhibit prostaglandin formation which causes gastric bleeds
erosion
ulcer formation
specific COX2 inhibitors cause less GI damage

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

how is the frequency of gastric contractions controlled

A

pacemaker cells

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

what are pacemaker cells

A

found in smooth muscle cells in upper fungus
rhythmic, autonomous, partial depolarisation
depolarisation cause slow wave potentials that sweep down th stomach

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

how is the force of gastric contractions controlled

A

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

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

what happens when food is taken in

A

waves of peristaltic contractions throughout stomach
forceful contractions and increased pressure in antrum
retropulsion of food against close pylorus
mixing and grinding of food

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

what happens to receptors when food is taken in

A

stretch receptors are activated
vagal inhibitory neurones
relaxation of smooth muscle
little change in pressure

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

what is emesis

A

the forceful evacuation of stomach content.
can be stimulated by pain, repulsive sights/smells, emotional factors, endogenous toxins.drugs, stimuli from pharynx/stomach, motion

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

how is emesis controlled

A

by the vomiting centre and chemoreceptor trigger zone
it is sensitive to neurotransmitter stimulus such as acetylcholine, histamine, 5-HT and dopamine

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

how can we stimulate vomiting

A

ipecauaha are locally acting in stomach
irritant effects of alkaloids emetine and cephaeline

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

what are the classes of anti emetics

A

H1 receptor antagonists
muscarinic antagonists
D2 antagonists
5-HT3 antagonists (cannabinoids, antipsychotics and steroid/neurokinin antagonists

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

what are the examples of H1 receptor antagonists

A

cyclizine
promethazine

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

when are H1 receptor antagonists given

A

most effective for motion sickness when given before the onset of nausea and vomiting
they act on vestibular nuclei

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

what are the adverse effects of H1 receptor antagonists

A

drowsiness
sedation

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

example of muscarinic antagonists

A

hyoscine

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

when are muscarinic antagonists used

A

used for motion sickness
effective against vestibular apparatus stimuli and local gut stimuli

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

what are the adverse effects of muscarinic antagonists

A

dry mouth
blurred vision
sedation

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

examples of D2 receptor antagonists

A

metoclopramide
phenothiazines

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

when are D2 receptor antagonists used

A

used for vomiting caused by renal failure and radiotherapy
they work in the chemoreceptor trigger zone

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

what are the adverse effects of D2 receptor antagonists

A

CNS effects (twitching and restlessness)
prolactin stimulation = menstrual disorders

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

example of 5-HT3 antagonists

A

ondansetron

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

when are 5-HT3 antagonists used

A

in chemotherapy an post-surgery
primarily act on CTZ
5-HT3 are released in gut following some endogenous toxins and chemotherapy drugs

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

what are the adverse effects of 5-HT3 antagonists

A

headache
diarrhoea

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

what are the types of drugs used to treat bowel motility

A

anti-diarrhoea
purgatives/laxatives

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

what are the causes of diarrhoea

A

viral - rotavirus
bacterial - campylobacter
systemic disease - inflammatory bowel disease
drug induced - antibiotics e.g. erythromycin

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

how do antidiarrhoeals work

A

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

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

what is the effect of anti-diarrhoeals

A

delay in passage of faeces through the gut and increased water and electrolyte absorption in small intestine and colon

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

which opioid agonist can act as anti-diarrhoeals

A

codeine
morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

how do opioid agonists work as anti-diarrhoeals

A

activate mow receptors on myenteric neurones
cause hyperpolarisation therefor inhibition of acetylcholine release
reduces bowel motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

why is codeine preferred to morphine

A

opiates are susceptible to misuse as they can cause tolerance and dependence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

two examples of synthetic opioid analogues

A

loperamide
diphenoxylate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is loperamide

A

binds to opiate receptors in gut wall and is relatively free of CNS side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what is diphenoxylate

A

marketed as a cophenotrope, atropine present to discourage abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what are the types of laxatives

A

bulk forming agents
osmotic laxatives
stimulants
faecal softeners

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what are the examples of bulk forming agents

A

ispaghula
methylcellulose
brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how do bulk forming agents work

A

contain polysaccharide and cellulose components
they are not digested and retain fluid, therefore increasing faecal bulk and stimulate peristalsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

side effects of bulk forming agents

A

flatulence
bloating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

examples of osmotic laxatives

A

magnesium salts
polyethylene glycol
phosphate enemas
lactulose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

how do osmotic laxatives work

A

act by osmosis to retain water in the bowel to produce a softer, bulkier stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

pharmacokinetics of osmotic laxatives

A

act in 30 mins
2-5hrs for magnesium salts
48hrs for lactulose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

side effects of osmotic laxatives

A

abdominal cramps
flatulence
electrolyte disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

examples of stimulant laxatives

A

Senna
bisacodyl
dantron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

how do stimulant laxatives work

A

directly stimulate colonic nerves
movement of faecl mass and reduce transit time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

side effects of stimulant laxatives

A

abdominal cramps
colonic atony

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

example of faecal softeners

A

docusate sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

how do faecal softeners work

A

they are non-ionic surfactant with stool softening properties
reduces surface tension
allows penetration of fluid into the faecal mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

examples of inflammatory bowel disease

A

crohns disease
ulcerative colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

characteristics of inflammatory bowel disease

A

cyclical bouts of diarrhoea
constipation
abdominal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

treatments for inflammatory bowel disease

A

glucocorticoids
aminosalicylates
sulfasalazine
immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what is asthma

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

major symptoms of asthma

A

wheezing
chest tightness
dyspnea
cough
hypoxemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what can be used to relax smooth muscle

A

beta blockers - SABA and LABA
PDE blockers - theophylline
LTRAs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what can be used to block inflammatory cascades

A

corticosteroids - ICS
LTRAs
PDE blockers
targeted biologics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

how do beta2 adrenoceptor agonists work

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

how can beta 2 agonists be administered

A

aerosol inhalation
inhalation of nebulised solution
inhalation of powder
oral administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

two examples of short acting beta 2 agonists

A

salbutamol
terbutaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

when are short acting beta 2 agonists used

A

for acute episodes of asthma, inhalation relief within 5-10 mins
Max effect within 30mins
they last 3-5hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

examples of longer acting beta 2 agonists

A

salmeterol
formoterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

mechanism of action of longer acting beta 2 agonists

A

give daily and last around 12 hours due to their lipophilic structures
corticosteroids are used along side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

side effects of beta2 adrenoceptor agonists

A

muscle tremor
tachycardia
cardiac dysrhythmias
risk of paradoxical bronchospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

how are leukotrienes linked with asthma

A

leukotrienes are synthesised and released during the acute response by mast cells, they are also produced by inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

mechanism of action of cysteine leukotrienes LTC4 and LTD4

A

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+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what are LTB4

A

potent chemoattractants for neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

two examples of leukotrienes receptor antagonists

A

zafirlukast and montelukast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

how do leukotrienes receptor antagonists work

A

selective and are a high affinity competitive antagonist for cys-LT1 receptors
they block the LTC4 and LTD4 effects on smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what is zileuton

A

5-lipoxygenase inhibitors, so inhibits the formation of all 5-LOX products from LTA4 synthesis

96
Q

when is montelukast used

A

acute prevent on exercise-induced bronchoconstriction
used in cases of allergic and perennial rhinitis
most commonly used leukotriene modulator

97
Q

examples of anti-muscarinics used in asthma

A

ipratropium and tiotropium

98
Q

why are antimuscarinics used in asthma

A

cause bronchodilation and reduce mucus secretion
commonly used with beta2 agonists and steroids
increase mucociliary clearance through action on cilia of epithelial cells

99
Q

how do muscarinic antagonists act as bronchodilators

A

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
Q

pharmacokinetics of ipratropium bromide

A

examples of a SAMA
onset is low but can last 6-8hrs
given 3-4 times a day

101
Q

what are the examples of LAMAs

A

tiotropium bromide
glycopyronium bromide
umeclidinium bromide
aclidinium bromide

102
Q

side effects of non-selective muscarinic receptors blockage

A

systemic anticholinergic side effects e.g. dry mouth, gastrointestinal motility disorder, tachycardia and nausea

103
Q

types of treatments for immunosuppression

A

ICS
biologics

104
Q

why can glucocorticoids be used as anti-inflammatories

A

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
Q

mechanism of action glucocorticoids

A

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
Q

examples of inhaled corticosteroids

A

beclomethasone
budesonide

107
Q

how do inhaled corticosteroids work

A

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
Q

side effects of corticosteroids

A

adrenal suppression
reduced bone mineral density
oropharyngeal candidiasis may occur

109
Q

examples of oral corticosteroids

A

prednisolone
hydrocortisone

110
Q

when are oral corticosteroids used

A

short term relief of severe episodes of acute asthma

111
Q

what are the long term effects of corticoid steroids

A

suppression of immune response to infection
Cushing syndrome
oesteoporosis
hyperglycaemia
muscle wastage
inhibition of growth

112
Q

how are eosinophils involved in allergic asthma

A

main inflammatory cells in later/chronic allergic asthma
activated by IL5 from Th2 cells

113
Q

what do eosinophils secretes

A

Th2 cytokines
ROS
LTC4/LTD4

114
Q

what can be used to decrease production of eosinophils

A

mepolizumab
resilzumab
they do this by binding to IL5a

115
Q

mechanism of action of benralizumab

A

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
Q

what is the innate immune system

A

non specific
immediate
first line of defence
no memory

117
Q

what is the adaptive immune system

A

specific
slow
second line of defence
immunological memory

118
Q

what is inflammation

A

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
Q

what are the steps of the inflammatory response (5 Rs)

A

recognition of the offending agent/injury
recruitment of leukocytes
removal of the offending substance
regulation of the response

120
Q

what is acute inflammation

A

rapid onset
short duration
involved neutrophils

121
Q

what is chronic inflammation

A

slow onset
long duration
involved monocytes, macrophages and lymphocytes

122
Q

what are the cardinal signs of inflammation

A

redness
heat
swelling
pain
loss of function

123
Q

what causes acute vascular inflammation

A

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
Q

what causes acute cellular inflammation

A

emigration of the leukocytes from the microcirculation, accumulating at the site of the injury before activating to eliminate the pathogen

125
Q

what are the key inflammatory mediators

A

histamine
plasma proteins
prostaglanding
leukotrienes
cytokines
chemokine

126
Q

what are histamines

A

produced by mast cells/basophils
cause vasodilation and increased permeability
lead to leukocyte recruitment

127
Q

what are plasma proteins

A

produced by the liver
cause vasodilation and increased permeability
leading to leukocyte recruitment

128
Q

what are prostaglandins

A

produced by mast cells, basophils and neutrophils
cause vasodilation and increase permeability

129
Q

what are leukotrienes

A

produced by mast cells, basophils and neutrophils
cause increase permeability and allow leukocyte recruitment

130
Q

what are cytokines

A

produced by mast cells and macrophages
cause vasodilation and increased permeability
allow leukocyte recruitment

131
Q

what are chemokine

A

produced by mast cells and macrophages
allow leukocyte rectuiment

132
Q

what are the two main cellular mediators for chronic inflammation

A

macrophages
lymphocytes

133
Q

what are macrophages

A

cause phagocytosis
initiate tissue repair and secrete cytokines

134
Q

what are lymphocytes

A

cause T cells to secrete chemokine and B cells to secrete antibodies
activation is caused by antigen presentation

135
Q

types of drugs that reduce inflammatory and immune response

A

non-steroidal anti inflammatory drugs
steroidal anti-inflammatory drugs
anti histamines
immunosuppressant drugs
immune check point inhibitors

136
Q

what are the signalling pattern recognition receptors

A

PAMP binds to toll like receptors
this activates transcription of NFkB and IRF3/7 leading to secretion of cytokines and inflammation

137
Q

what is COX1

A

works as a housekeeper
many unwanted responses are thought to be exerted mainly through COX-1 isoform inhibition

138
Q

what is COX2

A

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
Q

what is the mechanism of NSAIDs

A

reversible competitive inhibition (ibuprofen), reversible non-competitive inhibition (paracetamol) and irreversible inhibition (aspirin

140
Q

what causes the symptoms of inflammation

A

COX2

141
Q

what causes the symptoms of non-selective NSAIDs

A

COX1

142
Q

what causes fever from inflammation

A

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
Q

what causes the side effects from NSAIDs

A

gastrointestinal problems - inhibitions of synthesis of stomach pge
skin rashes
renal effects - inhibition of synthesis of PGI2 and PGE
brocnhospasms

144
Q

side effects of COX2 inhibitors

A

increase the risk of thrombotic events such as heart attacks and stroke

145
Q

side effects of NSAIDs

A

adverse cardiovascular effects as COX2 decrease platelet aggregation and vasodilation
COX1 cause releases of platelet of thromboxane causing thrombotic vasoconstriction

146
Q

what are lipocortins

A

is a GR agonists and is an examples of a steroid anti-inflammatory drugs
blocks phospholipase A2

147
Q

what causes the effects of cortisol anti-inflammatory

A

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
Q

how can glucocorticoids cause Cushing syndrome

A

increase hyperglycaemia so they can lead to dysregulation of insulin

149
Q

what are the 4 types of allergic reaction

A

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
Q

what causes type 1 hypersensitivity

A

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
Q

what can be cause by exposure to antigen

A

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
Q

examples of localised type 1 hypersensitivity reaction

A

hay fever
asthma
hives
angioedema

153
Q

examples of systemic type 1 hypersensitivity

A

anaphylaxis

154
Q

signs of allergic rhinitis

A

red, itchy, watery eyes
sneezing
congestion and runny nose
sore throat
fatigue

155
Q

what causes allergic rhinitis

A

mediated by histamine binding to H1 receptors

156
Q

how do anti-histamines work

A

by binding to the H1 receptor and reduce its activity
they are inverse agonists

157
Q

examples of 1st generation antihistamines

A

chlorophenamies
diphenhydramine

158
Q

side effects of 1st generation antihistamines

A

caused by anticholinergic activity
drowsiness
difficulty to urinate

159
Q

examples of second generation antihistamines

A

certizine
loratadine
less likely to have side effects as they don’t pass the blood brain barrier

160
Q

what is anaphylaxis

A

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
Q

what is used to treat anaphylaxis

A

adrenaline as it prevents and relieves airway obstruction
this promotes cardiac output and increases total peripheral resistance to increased blood pressure

162
Q

when is hydrocortisone used

A

to prevent biphasic late responses

163
Q

what is immunosuppression

A

block T cell mediated immune response
primarily by blocking the expression and activity of the T cell growth factors activating cytokine interleukin 2

164
Q

what can be used to treat immunosuppression

A

prednisolone (glucocorticoid)
tacrolimus or cyclosporin (calcineurine inhibitors)
sirolimus (dual calcineurin/mTOR inhibitors)
daclizumab/basiliximab (IL2 receptor antagonists)
mycophenolate (nucleic acid synthesis antagonists)

165
Q

how does antibody opsonisation benefit the immune system

A

enhances phagocytosis (agglutination and chemoattraction)
neutralisation
natural killer cell activation and increasing components of the classical component cascade

166
Q

how to prevent NFkB activation of inflammatory genes

A

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
Q

how do daclizumab and basiliximab cause immunosuppression

A

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
Q

what is OKT3

A

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
Q

what is immunotherapy

A

involves the stimulation of immune cells by a range of immune cell checkpoint protein interaction
this can also be inhibited by PDL/PD1

170
Q

when is immunotherapy used

A

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
Q

how can immune cells cause cancer

A

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
Q

what are antibiotics

A

inhibit the growth or destroys bacteria.
bacteriostatic inhibit multiplication
bactericidal kill bacteria

173
Q

how do antibiotics work

A

target cell wall synthesis, membrane synthesis, protein synthesis, metabolic pathways and nucleic acid synthesis

174
Q

what is flucloxacillin

A

beta-lactase resistant penicillin that targets gram positive and beta-lactamase resistant bacteria

175
Q

what is benzylpenicillin

A

natural penicillin that targets gram positive bacteria

176
Q

what is amoxicillin

A

broad-spectrum penicillin that targets gram positive and negative bacteria

177
Q

what is mecillinam

A

reverse spectrum penicillin that targets gram negative bacteria

178
Q

what is mezlocillin

A

extended spectrum penicillin that targets gram positive, gram negative and pseudomonas aerginose bacteria

179
Q

what is cephalosporins

A

used to treat septicaemia, pneumonia and meningitis
effects is exerted through penicillin binding protein
given parentally, IM or IV
excreted in the kidney

180
Q

examples of cephalosporin

A

cefaclor
cephalexin
cefotaxime

181
Q

how do cells become resistant to penicillin

A

producing beta-lactamases and modifying penicillin binding proteins

182
Q

what can inhibit protein synthesis

A

chloramphenicol
erythromycin
tetracycline
streptomycin

183
Q

how do chloramphenicol work

A

binds to 50S portion and inhibits formation of peptide bonds

184
Q

how does erythromycin work

A

binds to 50S portion, prevents translocation - movement of ribosomes along mRNA

185
Q

how do tetracyclines work

A

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
Q

how do streptomycin work

A

changes shape of 30S portion and causes code on mRNA to be read incorrectly

187
Q

how do amunoglycosides work

A

inhibit protein synthesis by interfering with mRNA translation, this is enhanced by penicillin. they can cause ototoxicity and nephrotoxicity

188
Q

mechanism of action of macrolides

A

inhibit protein synthesis by binding to 50S subunit and preventing translocation
they are metabolised by demethylation in liver CYP3A4

189
Q

when are macrolides used

A

to treat legionella, chlamydia and mycoplasma and effective against gram positive bacteria

190
Q

side effects of macrolides

A

heart arrhythmias a
GI disturbance

191
Q

action of sulphonamides

A

inhibit dihydropteroate
well distributed and cross BBB

192
Q

action of trimethoprim

A

inhibits dihydrofolate reductase
given oral and used to treat UTI and respiratory tract infection

193
Q

action of fluoroquinolone

A

inhibits DNA gyrase
taken orally and well absorbed but don’t cross BBB
inhibits CYP1A2

194
Q

use of fluoroquinolone

A

kill gram positive and negative bacteria and enterobacter

195
Q

side effects of fluoroquinolone

A

GI problems
prolongation of QT interval

196
Q

what is mycobacteria

A

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
Q

what is rifampicin

A

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
Q

what is daptomycin

A

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
Q

types of DNA viruses

A

adenovirus
herpesvirus
papillomavirus

200
Q

types of RNA viruses

A

paramyxovirus
rhabdovirus
togavirus
influenza virus
retrovirus

201
Q

stages in the viral replication cycle

A

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
Q

action of antiviral drugs

A

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
Q

what is viral latency

A

the recurrence of an infection due to non-replicating cells, joint replication process and limited immune detection
no antiviral agents eliminate viral latency

204
Q

which types of acute infections are associated with viral latency

A

rhinovirus
rotavirus
influenza virus

205
Q

which types of persistent infections are associated with viral latency

A

lymphocytic choriomeningitis virus

206
Q

which types of latent, reactivating infections are associated with viral latency

A

herpes simplex

207
Q

which types of slow viral infections are associated with viral latency

A

measles
HIV

208
Q

how does antiviral resistance occur

A

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

209
Q

what does herpes virus cause

A

cold sores - simplex
chicken pox - varicella zoster
glandular fever - epstein barr

210
Q

what are the symptoms of herpes virus

A

flu-like symptoms
blister/ulcer stage

211
Q

where does herpesvirus resides

A

herpes virus infects sensory ganglia where it becomes latent
this latency can become stimulated again from external infection

212
Q

action of acyclovir

A

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

213
Q

characteristics of HIV infections

A

by destruction of host immune systems
they are opportunistic infection, rare neoplasm and can cause death

214
Q

how is HIV transmitted

A

congenitally
parentally
sexual contact

215
Q

what are the 2 forms of HIV

A

HIV1 is responsible for human aids
HIV2 is less virulent form of immune suppression

216
Q

what is primary HIV infection

A

asymptomatic
there is seroconversion which is negative to positive HIV antibody detection
increase viral load

217
Q

stages of AIDs

A

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

218
Q

mechanism of action of HIV

A

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

219
Q

How to inhibit HIV life cycle

A

fusion inhibitors
CCR5 inhibitors
NRTIs
NNRTI
protease inhibitors

220
Q

examples of fusion inhibitors

A

enfurviritde

221
Q

action of fusion inhibitors

A

inhibits the fusion of cellular and viral membranes
usually given by subcutaneous injections and most effective as combination therapy

222
Q

examples of CCR5 inhibitor

A

maraviroc

223
Q

action of CCR5 inhibitors

A

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

224
Q

examples of a nucleoside reverse transcriptase inhibitor

A

zidovudine

225
Q

action of NRTI

A

prevents HIV replactions
active when phosphorylated intracellularly to its triphosphate and then inhibits reverse transcriptase. this causes premature termination of viral DNA elongation

226
Q

further action of zidovudine

A

inhibits mammalian lambda and beta DNA polymerase, so increases toxicity in man

227
Q

side effects of NRTIs

A

headache
nausea
anemia
leucopenia
neutropenia

228
Q

examples of non-nucleoside reverse transcriptase inhibitors

A

nevirapine
delaviridine
efavirenz

229
Q

action of NNRTIs

A

bind to reverse transcriptase causing denaturation
induce cytochrome p450

230
Q

examples of protease inhibitors

A

saquinavir
ritonavir

231
Q

action of protease inhibitors

A

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

232
Q

examples of highly active anti-retroviral therapy

A

NRTI + NNRTI or PI

233
Q

what is a combination pill for HIV treatment

A

Atripla
contain emtricitabine
tenofovir
efavirenz

234
Q

what is raltegravir

A

an integrase inhibitors and inhibits integration of transcribed viral DNA into host cell chromosomes

235
Q

categories of neuro drugs

A

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

236
Q

why target GABA receptors

A

inhibit neurotransmission
sedatives and hypnotics directly hyperpolarize
muscle relaxants such as baclofen indirectly hyperpolarize by inhibiting K+ channel

237
Q

what are GABA A receptors

A

ligand gated
chloride permeable ion channels

CM2001 (13 decks)

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