Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Systems Pharmacology PED2006 > Flashcards

Systems Pharmacology PED2006 Flashcards

1
Q

What are the 2 main parts of the GI tract

A

Lower and upper part

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

Describe the upper tract of the GI tract

A

Mouth oesophagus stomach and duodenum
Aid in the ingestion and digestion offood

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

Describe the lower tract of the GI tract

A

Small and large intensities
Digestion is completed and absorption of nutrients

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

Describe the circular muscle of the gut

A

Between the inner and outer part of the gut
Circular structures that are able to narrow and restrict the lumen

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

Describe the longitudinal muscles

A

Muscles arranged lengthwise
Constriction causes of intestines

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

What are sphincters

A

Valves formed from circular muscle
Constriction determines the closure or natural opening of a passage

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

What causes peristaltic waves

A

The circular and longitudinal muscles constrict and release in coordinated waves

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

What factors are involved in peptic ulcer formation

A

Imbalance between aggressive and defensive factors
Breakdown of the mucosal barrier and excess acid secretion

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

What are the 3 major pathways for regulating acid secretion

A

Neural stimulation via vagus nerve
Endocrine stimulation via gastric release
Paracrine stimulating by histamine release

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

What are anatacids used for

A

Gastritis and duodenal ulcers

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

Describe antacid composition

A

Basic compounds composed of a metal ion and a base

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

What are the 3 principal secretagogues

A

Histamine
Acetylcholine
Gastrin

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

How is the action of the secretagogues synergistic

A

A small dose of one potentiates the response bought about by a small dose of another

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

What receptor does histamine activate in the parietal cells

A

H2 receptors

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

Why do H2 receptor antagonist do not interfere with other receptors in different tissues

A

Highly selective

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

What affect do H2 antagonists have on gastric secretion

A

Reduce gastric acid secretion
Decrease H+ concentration in gastric lumen
Decrease volume of acid secretion

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

Why do H2 antagonists in the gut develop rapid tolerance

A

Due to elevation of cAMP in parietal cells

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

how do the secretagogues increase acid within the stomach lumen

A

Activate by cAMP pathway (histamine)
Activate calcium sensitive pathways (muscarinic and gastrin receptors)
Triggers H+/K+ ATPase pump
Active transport of H+ into lumen

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

How do proton pump inhibitors work

A

Selectively block the action of the H+/K+ ATPase pump

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

How are PPIs specific

A

Requirement for an acidic condition in order to activate, trap and protonate the drug

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

How is acid secretion affected by PPIs

A

Inhibition is permanent and is only resumed after the insertion of new molecules

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

Why are PPIs better than H2 antagonists

A

More rapid in producing relief
Don’t develop tolerance as rapidly
No difference in inhibiting nocturnal vs day acid secretion

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

What is the 2 cell hypothesis

A

Ach and gastrin stimulate mast cells to make more histamine

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

What is the 1 cell hypothesis

A

Mast cells make more histamine
Lead to more proton pump stimulation

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

How its the frequency of stomach contractions controlled

A

Pacemaker cells in the fundus region
Critical in setting a slow depolarisation of the tissue to start contraction

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

How is the force of stomach contraction controlled

A

Increases vagal afferent activity to create stronger muscle contraction
Decreased by adrenergic activity

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

How does gastrin affect contraction of the stomach

A

Increases the force of contraction
Also increases the volume of HCL

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

Describe receptive relaxation

A

When the stretch receptors in the stomach turn off the afferent vagal nerve
Slows down smooth muscle contraction
Allows food to enter the large intestine

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

What is emesis

A

Forceful evacuation of stomach contents

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

What controls emesis

A

In the medulla:
Vomiting centre and chemoreceptor trigger zone (CTZ)

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

Why are alkaloids not the standard procedure to vomit when something toxic has been ingested

A

Patients can inhale the vomit as the sphincter that closes of the lungs doesn’t shut

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

What are H1 receptor antagonists effective in treating

A

Ocular issues e.g motion sickness
Not centrally active agents as they act on vestibular nuclei

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

Whats a side effect to H1 antagonists

A

Cause drowsiness and sedation
Helps with motion sickness and they don’t register the ocular disruption

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

Describe the use of muscarinic antagonists in treating emesis

A

Potential to interact w other systems
No CNS effects
Anti cholinergic affects e.g dry mouth, blurred vision and slight sedation

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

When are D2 receptor antagonist used to treat emesis

A

Severe forms of emesis
Given to only those who’s emesis is caused by the CTZ
Therefore CNS side effects

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

When are 5-HT3 antagonists used to treat emesis

A

Very severe forms of sickness

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

What is the mechanism of opiates in anti-diarrhoeals

A

Increase activity of receptors
Hyperpolarisation = inhibition of ACH release
No stimulation and contractility
Reduced bowel motility

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

What are the cons of using opiates in treatments

A

Can be misused and are a class of drug where you have to take more each time to be bale to stimulate the receptor the next time

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

How can the abuse potential of opiates be reduced in anti-diarrhoeals

A

The use of synthetic analogues e.g codeine
Less likely to cause dependent and no CNS effects
Use atropine to discourage base to make the patient feel queasy

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

Describe bulk forming laxatives

A

Contain undigestable cellulose components
Therefore retain fluid and increase fecal bulk
Stimulate stretch receptors = peristalsis

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

How do osmotic laxatives work

A

Salt present in gut lumen
Osmosis sucks in water into fecal matter
Softer bulkier stool

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

How do stimulant laxatives work

A

Stimulate the intramural plexus i.e neuronal firing

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

What is the downfall of using stimulant laxatives

A

Degree of colonic atrophy over time
If nervous system stimulated too often it can’t stimulate on its own

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

How doe fecal softners work

A

Coats the stool in non ionic surfactant
Reduces surface tension of stol
Allows the penetration of fluid in the stool

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

Describe dopamine

A

Inhibitory neurotransmitter
2 dopamine receptors: D1 and D2

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

Describe noradrenaline

A

Endogenous catecholamine
Excitatory: A1 and B1
Inhibitory: A2 and B2

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

Describe 5-HT

A

Strong inhibitory action in most CNS areas

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

What are benzodiazepines

A

Widely used anxiolytics
Relatively safe and effective
See for: anxiety and insomnia

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

What receptors do benzodiazepines target

A

GABA receptors

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

Describe the mechanism of action for benzodiazepines

A

Binding of GABA = opening of ion channel allowing Cl- through the pore
Influx of Cl- causes hyperpolarisation decreasing neurotransmission
BZs increase frequency of channel opening

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

Describe barbiturates

A

Used to sedate patients or to induce and maintain sleep
Replaced by benzodiazepines

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

Why are barbiturates controlled substances

A

Induce tolerance and physical dependence
Associated with very severe withdrawal symptoms

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

What is the mechanism of action for barbiturates

A

Enhances GABAergic transmission
Prolongs to duration of pore channel opening
Decreases neuronal activity

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

Describe SSRIs

A

Group of antidepressants that inhibit serotonin reuptake

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

What are SNRIs

A

Antidepressants that inhibit NA and serotonin uptake

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

What are TCAs

A

Antidepressants that block NA and serotonin reuptake into the presynaptic neurone

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

What is the mechanism of action for TCAs

A

Inhibit neurotransmitter reuptake
Blocking of receptors

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

What are MAOIs

A

Antidepressants that ir/reversibly inactivate the MAO enzyme
Permits neurotransmitters to accumulate within the presynaptic neurone

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

What are the 2 types of depression

A

Unipolar
Bipolar

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

Describe unipolar depression

A

Depression with no evidence for genetic cause
Older at first occurrence in response to distressing circumstances

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

Describe bipolar depression

A

Depression and mania
Evidence for genetic cause
Biochemical disorder
Apathetic and inert

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

What is the monoamine hypothesis for depression

A

That it is a result of under activity of monoamines
Especially 5-HT

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

What is the evidence for the monoamine theory

A

Antidepressants such as TXA and MAOI facilities monoaminergic transmission
Urinalysis and CSF concs of MOPEG is reduced in depressed patients

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

What is the evidence against monoamine theory

A

Amphetamine and cocaine has no affect in depressed patients despite causing a release of NA and inhibits its re-uptake

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

What is a theory for the 2-3 week delay in effectiveness

A

Quick increase in [5-HT] which inhibits 5-HT firing
Autoreceptors become desensitised after exposure

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

What are the advantages of SSRIs over TCA and MAOI

A

Lack of anticholinergic and cardiovascular side effects
No weight gain
Low acute toxicity
No food reaction

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

What are the symptoms of schizophrenia

A

Hallucinations/delusions
Blurred emotions/ lack of feeling
Loss of motivation
Social withdrawal

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

Describe the dopamine hypothesis of schizophrenia for positive symptoms

A

Too much dopamine in the subcortical and limbic regions of the brain may cause positive schizophrenic symptoms

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

Describe the dopamine hypothesis of schizophrenia for negative symptoms

A

Negative symptoms are associated with less dopamine in the prefrontal cortex

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

What is a evidence for the dopamine theory of schizophrenia

A

Amphetamines that release of DA produce a syndrome that mimics the +tive symptoms of schizophrenia

Abnormally high DA content in post morgen amygdala

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

What is the serotonin hypothesis for schizophrenia

A

5-HT dysfunction is involved in the pathophysiology of the disease

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

What are the 3 types of phenothiazines derivatives

A

Aliphatics
Piperazines
Piperidines

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

What is the role of phenothiazines

A

First generation antipsychotic mediations
Used in the treatment of schizophrenia, bipolar disorders and other psychotic disorders

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

What os the mechanism of action for neuroleptics

A

Inhibit dopaminergic neurotransmission
Antipsychotic effects due to blockade of D2 receptors

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

What are the limitation of conventional antipsychotics

A

1/3 of patients fail to respons
Limited efficacy against negative and affective symptoms
High proportion of relapse

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

Name a few atypical antipsychotics

A

MARTA (multi acting receptor targeted agents)
SDA (serotonin-dopamine antagonists)
Selective D2/D3 antagonists

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

What is excitotoxicity

A

Release of excitatory neurotransmitters that can damage nerve cells e.g glutamate

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

How does excitotoxicity happen

A

When NMDA and AMPA receptors are over activated
Allows high level of Ca2+ to enter the cell
Activates proteases
Impaired mitochondrial function
Produces free radials

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

What diseased could excitotoxicity be involved in

A

Stroke
Parkinson’s Disease
Alzheimer’s Disease

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

What is a defence mechanism against excitotoxicity

A

Mitochondrial energy metabolism
ATP production sustains membrane potential an Ca2+ uptake by ER

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

What is oxidative stress

A

When products of oxidative phosphorylation create free radicals
They damage certain cellular components

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

How does a mutation in a gene cause Parkinson’s

A

Causes excessive production of A-synuclein that aggregates to form Lewy bodies
Clearance of the plaques is reduced as well

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

Describe the effect on the brain due to Parkinson’s

A

Degeneration of the basal ganglia and the substantia nigra
Reduced amount of DA
Correlated with a loss of cell bodies of dopaminergic neurons

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

What are the different treatments of Parkinson’s

A

Drugs that replace dopamine
Drugs that mimic the action of dopamine
MAO-B inhibitors
Drugs that release dopamine
Acetylcholine antagonists

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

What is the need for pain with short latency

A

Warn the organism that it is in danger so it will alter the situation

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

What is the need for pain with long latency

A

Immobilise the organism so that recover from injury can occur

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

What is nociception

A

The process whereby noxious peripheral stimulation are transmitted to the CNS

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

What are polymodal nociceptors

A

Main peripheral sense organs that respond to noxious stimuli
Majority are non-myelinated C fibres
Respond to thermal, mechanical and chemical stimuli

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

What happens when there has been an injury to tissue

A

Release of chemicals that sensitive or activate receptors
Neurone release substance P which stimulates mast cells and blood vessels
Histamines released from mast cells and bradykinin released from blood vessels add to pain stimulus

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

What is an opioid

A

Any substance which produces morphine-like effects that are antagonised by naloxone
Not necessarily similar to morphine

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

What is an opiate

A

Chemical compounds that are extracted from natural plant manner
Has a close structural similarity to morphine

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

What are endogenous opioids

A

Opioid peptides and their receptors
Involved in central and peripheral nervous systems
Involved in pain modulation, reward and response to stress

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

What are the 4 major opioid peptides

A

Leucine enkephalin
Methionine enkephalin
Dynorphins A
Dynorphins B

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

What are the 3 types of opioid receptor that mediate the main pharmacological effects of opiates

A

Mu
Delta
Kappa

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

How do the opioid receptors mediate the effects of opiates

A

GCPR that inhibit ardently cyclase = inhibit cAMP production
Bind to g-protein on ion channels to promote K+ channel opening = inhibitory effects
Bind to Ca2+ channel to inhibit ca2+ channel opening = reduces neurotransmitter release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What opioid receptor subtype accounts for the dysphoric effects

A

Sigma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What opioid receptor are most analgesic opioids agonists for

A

Mu

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What does tolerance to opioids mean

A

An increase in the dose needed to reduce a given pharmacological effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Describe tolerance in opioids

A

Develops rapidly
Extends to most effects
Tolerance to one opioid doesn’t necessarily mean tolerance to another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What are some important used of opioids

A

Relieve of mild to moderate pain
Relief of severe pain
Anxiety relief
Cough suppression
Euphoriant in terminal illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is morphine metabolised to

A

Morphine 6-glucuronide = pharmacologically active

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is drug dependence

A

When the administration of drug is sought compulsively
Continuous use despite the adverse psychological or physical effects produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What supports the dopaminergic pathway involved in drug addiction

A

Higher frequency mutation A1 of the D2 receptor gene in alcoholics and drug abusers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

How does nicotine cause dependence

A

Causes excitation of mesolimbic pathway and increased DA release in nucleus accumbens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What is the CNS effect of smoking

A

Activation of nicotinic Ach receptors = channel opening = neuronal excitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are the peripheral effects of nicotine

A

Effects on autonomic ganglia and peripheral sensory receptors in the heart and lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Describe the tolerance to nicotine

A

Rapid tolerance to the periphery caused by a desensitisation of nicotinic Ach receptors due to an increase in nicotinic Ach receptors in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What are pharmacological approaches to treatment of nicotine dependence

A

Nicotine replacement therapy
Champix
Clonidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

How can alcohol cause neurological syndromes

A

On chronic basis
Due to thiamine deficiency
Alcoholics absorb their energy from alcohol and not their diets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

How is drinking alcohol effective against atheroma formation

A

When consumed at sensible levels it increases plasma HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

How can ethanol consumption protect against ischaemic heart disease

A

Inhibits platelet aggregation if drank in moderation
Possible due to inhibiting arachidnonic formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

How is ethanol metabolised in the blood stream

A

Ethanol -> acetaldehyde -> acetic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What is the tissue between the air sacs of the lungs called

A

Interstitium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Describe the structure of type 1 epithelial cells

A

Flat cells with broad cytoplasmic flaps
Have a perinuclear zone
Basement membrane fusing the alveolar epithelium to capillary endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What is the function of type 1 epithelial cells

A

Site of gas exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What is the function of type 2 epithelial cells

A

Manufacture and release surfactant which reduces the surface tension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Which type of epithelial cell is capable of regeneration

A

Type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Why can type 1 cells not regenerate

A

No mitotic potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the major cellular host defence mechanism in the alveolar space

A

Macrophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

How can alveolar macrophages leave the lungs cells

A

Must migrate to the nearest bronchiole
Exit via:
- the mucocilary escalator
- interstitium
- blood vessels or lymph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

How does fibroblasts cause interstitial fibrosis

A

Fibroblasts not normal intestinal components
After disease, large amounts of collagen and elastin laid down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

How do fibroblasts contribute towards interstitial fibrosis

A

Not normal interstitial components
After disease insult, large amounts of collagen and elastin laid down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

How is a diagnosis of a pulmonary disease and disorders confirmed

A

Integration of pulmonary history and physical examination
Chest roentgenograms
Pulmonary function and blood gas laboratories

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Describe lung function in restrictive lung disease

A

FEV1 and FVC decrease to same extent
FEV1 is still 70-80% of FVC
Absolute values are lower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Describe lung function in airflow obstruction

A

FEV1 decreases
FVC may be reduced but to a lesser extent
FEV1 is therefore <65%of predicted FVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What is the purpose of bronchodilators

A

Oppose bronchoconstriction
Reduces resistance to air flow in respiratory tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What are the 5 major groups of bronchodilators

A

Short acting anticholinergic
Long acting cholinergic
Short acting B2 agonists
Long acting B2 agonists
Theophyllines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What is the mechanism of action for bronchodilators

A

Competitive antagonist of muscarinic Ach receptors
Block vagal control of smooth muscle tone
Reduce reflex bronchoconstriction in response to irritants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

How do anticholinergic effect goblet cells

A

Reduce mucus secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Why are anticholinergics not the first choice in asthma

A

Only reduce vagally mediated bronchoconstriction
No effect on inflammatory mediated bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What are the side effects on anticholinergic bronchodilators

A

Dry mouth
Urinary retention
Constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What is the mechanism of action for B2 agonists

A

Reduce intracellular calcium to reduce bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What is the difference between short acting and long acting B2 agonists

A

Short: acute symptoms and act within minutes, effects last 4-5 hours
Long: requires regular administration and effect achieved after several doses, effects last up to 12hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What are the side effects of B2 agonists as bronchodilators

A

Headache
Anxiety
Nausea
Tremor
Nervousness
Tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Why are B2 agonists bronchodilators typically administered by inhalation

A

Reduce chance of side effects due to non specificity:
Tachycardia, fine tremor, nervous tension and headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What are examples of short and long acting B2 agonist bronchodilators

A

Short: salbutamol
Long: salmeterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Describe the mechanism of action for Theophyllines

A

Inhibit phosphodiesterase = prevents cAMP breakdown
Promotes lowering of [intracellular Ca2+]
Prevents bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What is the cons of theophyllines

A

It is an irritant so must be injected slowly
Dose required is between 10-20mg/L nut adverse effects can occur at this range - severity increases with conc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What are the side effects of theophyllines

A

Peripheral: nausea, vomiting and diarrhoea
CNS: headache insomnia and irritability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What is the purpose of anti-inflammatories when treating respiratory disorders

A

Suppress inflammation
Reduce mucus secretion, oedema and reactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

How are glucocorticoid steroids beneficial in treating respiratory disorders

A

Reduce formation, release and action of inflammatory mediators
Inhibits virtually all aspects of the inflammatory cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Describe the mechanism of action for glucocorticoid steroids

A

Bind intracellular steroid receptors
Translocation of active receptor to nucleus = gene modulation
Downregulation of pro-inflammatory cytokines
Production of anti-inflammatory proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Why are glucocorticoid steroids the most important anti-asthma drug

A

Prevents exacerbations
Prevents remodelling i.e preserves lung function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Name an oral glucocorticoid steroid used in asthma treatment

A

Prednisolone

145
Q

Why are oral steroids avoided where possible

A

Risk of increased appetite/weight gain
Mood changes
Adrenal suppression
Osteoporosis

146
Q

Name an inhaled glucocorticoid steroid used in asthma treatment

A

Beclomethasone

147
Q

What are the side effects to inhaled steroids

A

Hoarseness and oral candidiasis
Short term effect on growth

148
Q

What histamine receptor is used in treating asthma

A

H1
Affects smooth muscle contraction

149
Q

Why are 2nd generation H1 antagonists better than 1st generation

A

Non-sedating
Do not cross the blood brain barrier
Inhibit smooth muscle contraction in respiratory tract
Reduce bronchorestrictor response to allergens and exercise

150
Q

Why can 1st gen H1 antagonists cause receptor depression

A

Bind to central and peripheral receptros
Can cross the blood brain barrier
Therefore dose must be limited

151
Q

Why do H1 antagonists produce anti-cholinergic effects

A

Potent muscarinic receptor antagonists

152
Q

What are the typical anticholinergic side effects

A

Dry skin, constipation, tachycardia and urinary retention

153
Q

What are the different mucoactive medications

A

Expectorants
Mucoregulators
Mucolytics
Mucokinetics

154
Q

What are expectorants

A

Hypertonic saline that increase secretion volume and/or hydration of mucus

155
Q

What are mucoregulators

A

Anticholinergic agents that decrease secretion volume

156
Q

What are Mucolytics

A

N-acetylcysteine that break disulphide bonds linking mucin polymers

157
Q

What are mucokinetics

A

Bronchodilators that improve cough clearance by increasing expiratory flow

158
Q

What is a cough

A

Forced expiratory blast stimulated by the sensory nerves in the lining of the respiratory system

159
Q

Describe the mechanism of a cough

A

Vocal cords close
Abdominals contract and intercostals brace
Generate positive pressure in thorax
Vocal chords open
Shear force clears airway

160
Q

What is sputum

A

The coughed up mixture of saliva and mucus

161
Q

Describe antitussives

A

Suppress cough w questionable efficacy

162
Q

Give an example of a non-narcotic antitussive

A

Dextromethorpan
Limited evidence for effectiveness

163
Q

Give an example of an effective antitussive

A

Codeine
Has intolerable side effects such as gastrointestinal discomfort and sedation

164
Q

What are the 2 types of glands

A

Exocrine and endocrine

165
Q

What is the master endocrine gland

A

Pituitary

166
Q

What is the supreme commander gland

A

Hypothalamus

167
Q

Describe the anatomy of the pituitary gland

A

Has 2 distinct lobes: posterior and anterior

168
Q

What is the role of the posterior lobe in the pituitary gland

A

Stores and secretes hormones synthesised in hypothalamus

169
Q

What is the role of the anterior lobe in the pituitary gland

A

Synthesise and secretes homes in response to hypothalamic regulation

170
Q

Describe the structure of the posterior pituitary gland

A

Consists mainly of axons extending from the supraoptic and paraventricular nuclei of the hypothalamus

171
Q

What is the role of the axons in the posterior pituitary gland

A

Release antidiuretic hormone and oxytocin into the capillaries of the hypophyseal circulation

172
Q

How are the hormones in the posterior pituitary gland stored

A

Neurosecretory vesicles

173
Q

Where is ADH synthesised

A

The supraoptic and paraventricular nuclei in the hypothalamus

174
Q

Where is ADH transported to once synthesised in the hypothalamus

A

Posterior pituitary gland via the neurohypophysial capillaries

175
Q

What factors control the release of ADH

A

Most influential: osmotic pressure and volume status

176
Q

Describe the mechanism of action of ADH

A

ADH bins to V2 receptors on the basolateral of principal cells
Promotes conversion of ATP -> cAMP via adenylate cyclase
Activates protein kinase A
Promotes fusion of aquaporin 2 into the apical luminal membrane

177
Q

What is the result of the aquaporin 2 fusing with the membrane

A

Enhances water permeability in distal convoluted and collecting duct resulting in concentrated urine

178
Q

What part of the nephron is impermeable to H2O

A

Ascending limb loop of Henle, DCT and collecting duct

179
Q

What is the purpose of anti diuretic hormone

A

Promotes membrane fusion on AQP2 concentrating urine

180
Q

Name an ADH hormone level stimulants

A

Opioids, anti-depressants, nicotine and MDMA

181
Q

Name an ADH hormone level depressant

A

Alcohol

182
Q

Describe the symptoms of ‘Syndrome of inappropriate ADH secretion’ (SIADH)

A

Excessive ADH secretion
High urine osmolality
Increased total body water
Hyponatremia
Hypoosmotic blood plasma
Hypervolemia

183
Q

What are a few causes of SIADH

A

Post-operative metabolic response to trauma and stress
Head trauma
Ectopic ADH production e.g tumours
Drugs

184
Q

What is the treatment for SIADH

A

ADH V2 antagonist
Tolvaptan

185
Q

Describe the symptoms of diabetes insipidus (DI)

A

Non functional ADH system
Excessive loss of water
Polyuria and polydipsia
Hypernatremia and hypotension

186
Q

Describe neurogenic DI

A

Failure of ADH secretion
Lesion of hypothalamus or pituitary

187
Q

Name a treatment for neurogenic DI

A

Synthetic ADH
Desmopressin

188
Q

Describe nephrogenic DI

A

Failure of principal cells to respond to ADH
V2 receptor mutation

189
Q

Name a treatment for nephrogenic DI

A

Restricted Na+ diet

190
Q

Where are the receptors for oxytocin located

A

Amygdala, nucleus accumbens and ventral pallidum

191
Q

How is autism and oxytocin potentially related

A

Lowered plasma oxytocin in children with ASD
Administration of oxytocin could potentially change brain patterns

192
Q

What hormones does the anterior pituitary release

A

Thyroid stimulation
Adrenocorticotrophic
Follicle stimulating
Lutenising
Growth
Prolactin

193
Q

Which hormones released by the anterior pituitary are direct acting

A

Growth and prolactin

194
Q

How is the synthesis of the homes released by the anterior pituitary controlled

A

Hypothalamic releasing factors

195
Q

How is T3 and T4 is released from the thyroid gland

A

Hypothalamus releases TSH releasing hormone
Stimulates the pituitary glands to release thyroid stimulating hormones
Stimulates the thyroid gland to release T3 and T4

196
Q

What is the role of the thyroid gland

A

Makes T3 and T4 as well as calcitonin

197
Q

What is the role of the colloid

A

Synthesise thyroglobulin

198
Q

What is role of thyroglobulin

A

Precursor to thyroid hormone production

199
Q

How is T3 and T4 produced

A

Thyroglobulin + iodide
Iodide comes from the bloodstream

200
Q

How is the production of T3 and T4 regulated

A

TSH that is released feeds back to the pituitary stop making more
Negative feedback

201
Q

Describe thyroxine (T4)

A

the most abundant hormone produced

202
Q

Describe triiodothyronine (T3)

A

The most biologically active hormone

203
Q

Describe the iodisation process

A

Incorporating iodine into tyrosine residues in thyroglobulin
Produces T1 and T2

204
Q

Describe the coupling process

A

Tyrosine residues bind
T1+T2 = T3
T2+T2 = T4

205
Q

What enzyme manages T3 and T4 levels

A

Thyroperoxidases

206
Q

Where does T4 and T3 bind to on their receptor

A

Ligand binding domain

207
Q

How does the DNA binding domain bind to DNA and begin transcription

A

Uses zinc fingers to bind DNA
Recruits RNA polymerase to transcribe new mRNA

208
Q

How is the hinge region helpful

A

Helps orientate DNA so that ligand binding domain isn’t in the way
Protects DNA binding domain and the nuclear localisation sequence in the N terminal while in the cytoplasm

209
Q

What is the sequence in the promoter region for thyroid hormones

A

Thyroid response element (TRE)

210
Q

What is Hashemites disease

A

Autoimmune response that destroys thyroid cells

211
Q

What is the treatment for Hashemites

A

Typically the administration of synthetic thyroid hormone
Don’t promote the body to make more - synthetic analogue instead

212
Q

What thyroid hormone is use to treat Hashemites

A

First line: synthetic T4
Patients with significant basal metabolic stress are replaced w a synthetic analogue

213
Q

Describe thryotoxicosis

A

Overactive thyroid
Higher metabolism rate
Increase in temperature
Tachycardia

214
Q

What is Graves’ disease

A

Autoimmune disease which promotes thyroid secretion

215
Q

What causes toxic modular goitre

A

Benign tumour or adenoma

216
Q

What are the 3 types of changes associated with a toxic modular goitre

A

Hypoplastic change
Dysplasia change
Metastatic change

217
Q

What is a hypoplastic change

A

When cellular function is maintain but an increased number of cells

218
Q

What is a dysplasia change

A

Function of the cell changes

219
Q

What is a metaplastic change

A

Swap the function for another function within that hormone gland

220
Q

What is the first line treatment for hyperthyroidism

A

Thiourelynes
Block TPO so can’t make T1 and T2

221
Q

What is another treatment for hyperthyroidism

A

Excess iodine which blocks the catalytic functions of TPO
Can be radioactive which destroys thyroid tissues

222
Q

Describe the mechanism of steroid hormone receptor signalling

A

Steroids diffuse into cell
Bind to intracellular receptors -> translocate to nucleus
Activated receptors bind to response elements in DNA
Modulate txn of specific genes
.mRNA is translated to protein
Protein exerts its effects on the cell

223
Q

Which part of the adrenal gland produced aldosterone/mineralcorticoids

A

Zona glomerulosa

224
Q

Which part of the adrenal gland produces cortisol/glucocorticoids

A

Zona fasiculata

225
Q

Which part of the adrenal gland produces androgens

A

Zona reticularis

226
Q

Which part of the adrenal gland produces nor/adrenaline

A

Medulla

227
Q

What is the effect of aldosterone on the distal tubule

A

Increases Na+ reabsorption into the blood
Increases K+ secretion into the urine

228
Q

What receptors does aldosterone act upon

A

Mineralcorticoid receptors specific to kidney

229
Q

How is aldosterone regulated directly

A

Stimulated by low plasma Na+ or high K+
Action on the Zona glomerulosa cells

230
Q

How is aldosterone regulated indirectly

A

Stimulated by angiotensin II

231
Q

How does angiotensin II stimulate water and salt retention

A

Increases aldosterone secretion from adrenal gland cortex
Increases ADH secretion from posterior pituitary gland
Increases H2O absorption from collecting duct

232
Q

Name a primary cause of hyperaldosteronism

A

Conn’s syndrome
Adrenal hyperplasia/tumour of z.glomerulosa

233
Q

Name a secondary case of hyperaldosterism

A

Chronic low blood pressure
Congestive heart failure = high renin - excess aldosterone

234
Q

What are some symptoms of hypoaldosterism

A

Hypernatremia: thirst and oedema
Hypertension: headache, confusion and fatigue
Hypokalemia: arrhythmias, constipation and weakness

235
Q

How is hyperaldosterism treated

A

MR antagonists: spironolactone

236
Q

What is a primary cause of hypoaldosterism

A

Addisons disease
Autoimmune disorder causing the destruction of z.glomerulosa cells

237
Q

What is a secondary cause of hypoaldosterism

A

Renin deficiency
Genetic predisposition

238
Q

What are some of the symptoms of hypoaldosterism

A

Hyponatremia: confusion, fatigue, seizure and coma
Hypotension: dizziness and vascular collapse
Hyperkalemia: arrhythmias, constipation and weakness

239
Q

How is hypoaldosterism treated

A

MR agonist: fludrocortisone

240
Q

Why is aldosterone itself not used in treating hypoaldosterism

A

Has a short half life

241
Q

What receptors does cortisol act upon

A

Glucocorticoid receptors

242
Q

What effects does cortisol have on the liver

A

Increases gluconeogenesis and prevents glycogenisis

243
Q

What effect does cortisol have on skeletal muscle

A

Increase in protein degradation
Increases amino acids for gluconeogenesis

244
Q

What effect does cortisol have on adipose tissues

A

Increased lipolysis
Increased free fatty acids and glycerols for gluconeogenesis

245
Q

What is the effect of cortisol on the bone

A

Matrix protein breakdown
Increases amino acids for gluconeogenesis

246
Q

What is the effect of cortisol on the pancreas

A

Inhibits insulin release
Hyperglycaemia

247
Q

What is cortisol effect on metabolism in general

A

Mobilisation of energy stores in times of stress

248
Q

What are the therapeutic exploitations of glucocorticoids

A

Effective anti-inflammatories and immunosuppressive agents

249
Q

Describe how cortisol boosts anti-inflammatory effects

A

Induces lipocortin which inhibits phospholipase A2
Decreases inflammatory mediators e.g prostaglandins
Decreases histamine release and proliferation/ repair of tissues
Decreases in thromboxane i.e increase in bruising

250
Q

Describe how cortisol has immunosuppressive effects

A

GR complexes bind directly to p65 subunit of NF-kB preventing activation of inflammatory genes
GR promotes IkBa synthesis - prevents p50/65 nuclear translocation
Prevents NFkB activation of anti inflammatory genes
Suppresses immune cell activation/replication

251
Q

What are the symptoms of Cushing syndrome

A

Lipolysis and fat redisposition - shoulder fat and moon face
Muscle protein degradation - weakness and skin transparency
Bone protein degradation - osteoporosis
Gluconeogenesis - diabetes mellitus

252
Q

What is the primary cause of Cushing’s syndrome

A

Adrenal hyperplasia or tumour of z.fasciculata

253
Q

What is a secondary cause for Cushings Syndrome

A

Chromic glucocorticoid therapy

254
Q

What os a treatment for Cushing’s syndrome

A

11B-hydroxylase antagonist e.g metyrapone
Decreases the amount of cortisol available for secretion

255
Q

How is cortisol regulated

A

HPA axis e.g stress circadian rhythm and feedback

256
Q

Describe Type 1 diabetes

A

Insulin deficiency disorder
Autoimmune pathogenesis
Requires insulin therapy

257
Q

Describe type 2 diabetes

A

Insulin insensitivity and inadequate compensatory insulin secretion
Metabolic pathogenesis i.e over eating
May progress to be insulin requiring

258
Q

Describe biguanides

A

E.g Metformin
Inhibit liver gluconeogenesis - decreases glucose entry into the blood
Can cause GI upset e.g diarrhoea and lactic acidosis

259
Q

Describe sulfonylureas

A

E.g gliclazide
Increases insulin supply
Bind to SU receptor to open K+ channels and depolarise islet B-cells to increase insulin secretion

Causes hypoglycaemia and modest weight gain

260
Q

Describe PPAR-ay agonists

A

E.g pioglitazone
Improve insulin sensitivity
Enhances peripheral lipogenesis and decreases lipolysis = decrease in plasma fatty acid levels
Causes fluid retention and cardiac failure
Weight gain and peripheral fractures

261
Q

Describe DPP-4 inhibitors

A

E.g sitagliptin
Increase insulin supply
Inhibits the degradation of natural GLP-1
Well tolerated

262
Q

Describe GLP-1 receptor agonists

A

Increase insulin supply
Stimulates insulin secretion
Inhibits glucagon secretion
Inhibits eating

Causes CV events in high CV risk people
Nausea and vomiting

263
Q

Describe SGLT2 inhibitors

A

Increase glucose loss from blood
Inhibit renal tubular resorption channel for glucose - causes urinary glucose loss
Urogenital infections and toe amputations
Reduce heart failure + protect kidneys

264
Q

What therapies are used for type 2 diabetes

A

Glucose lowering therapies

265
Q

What therapies are used for type 1 diabetes

A

Insulin therapy

266
Q

What are the 3 types of available insulin

A

Meal time insulin
Basal insulin
Insulin mixes

267
Q

Describe meal time insulin

A

Unmodidfed human insulin
Rapid acting insulin analogue

268
Q

Describe basal insulin

A

NPH insulin - protea mine complex suspension
Long acting insulin analogues

269
Q

Describe insulin mixes

A

Soluble + NPH insulin
Rapid acting and long acting analogues

270
Q

What is the possible insulin regime for type 2 diabetes

A

1 daily insulin:
NPH insulin i.e long acing insulin analogues

271
Q

What technical issues does insulin therapy have

A

Need to deliver SC
High variability between absorption profiles
Insulin given prospectively not regulated min by min

272
Q

What personal issues are there with insulin therpay

A

Nuisance of delivery systems i.e repetitive and a reminder of the condition
Consequences of erratic insulin profiles i.e unwanted eating habits and hypoglycaemia
Better glucose control gives weight gain

273
Q

What are the typical routes of administration for anti fungal agents

A

Topical for superficial infections
Systemic for both types on infections

274
Q

Name 2 ergosterol inhibitors

A

Azores and polyenes

275
Q

How do azoles work

A

Block 14-a demethylase cytochrome
Results in a lack of ergosterol in fungal membranes
Effects membrane associated functions in fungus

276
Q

How do polyenes work

A

Bind to sterols in membrane forming an ion channelS
Gi her affinity for fungi sterols than mammalian sterols

277
Q

Name an intracellular inhibitor

A

Mitotic inhibitors

278
Q

How to mitotic inhibitors work

A

Inhibits cells division by interfering w spindle formation

279
Q

What are the 3 main agents of echinocadins

A

Caspofungin
Anidulafungin
Micafungin

280
Q

Describe how echinocadins work

A

Non competitive inhibitors of 1,3-b- and 1,6-b-D glucan synthase
Important in the synthesis of an essential component of fungal cell wall
Changes in conc lead to osmotic instability and cell lysis

281
Q

Why do echinocadins not affect human cells

A

Human cells do not contain 1,3-b-glucan

282
Q

How well do fungal develop resistance against polyenes and azoles

A

Polyenes: very rare
Azoles: common and major clinical concern
Other: rarely

283
Q

What are the 2 sites of parasitic infection

A

Lumen of alimentary canal
Tissue of host

284
Q

Why is it easier to treat GI tract parasitic infections

A

Worms are localised in a limited compartment

285
Q

What agents are used in the treatment of worms

A

Interfere with metabolism
Cause paralysis rather than inhibitors of DNA synthesis

286
Q

What are the 3 classes of drugs used to treat worms

A

Mebendazole
Praziquantal
Piperazine

287
Q

How does mebendazole work to treat worms

A

Target microtubules of worm binding to b-tubulin
Prevents polymerisation
Prevents glucose uptake by worm

288
Q

What type of worm infections does mebendazole treat

A

Variety of worms
Mainly roundworm and threadworm

289
Q

How does praziquantal work to treat worm infections

A

Causes increased muscular activity in worms
Followed by contraction and spastic paralysis

290
Q

What does high doses of praziquantal do to worms

A

Damage the tegument of the worm as well
Effects due to increased Ca2+ permeability

291
Q

What types of worm infections does praziquantal treat

A

Schistosomes and tapeworms

292
Q

What could cause the adverse affects from praziquantal

A

Toxic products from dead worms rather than drugs

293
Q

How does piperazine work to treat worm infections

A

Reversible inhibits neuromuscular GABA transmission
Paralysed worm expelled alive by informal intestinal peristaltic activity

294
Q

What type of worm infections does piperazine treat

A

Common roundworm and threadworm

295
Q

Describe a virus replication cycle

A

Attachment to host cell
Un-coating of virus
Control of DNA, RNA and/or protein production
Production of viral subunits
Assembly of virions
Release of virions

296
Q

What is viral latency

A

Recurrence of infection

297
Q

What are a few reasons for viral latency

A

Non replicating cells
Joint replication processes
Limited immune detection

298
Q

Describe how antiviral resistance occurs

A

Rapid retaliation rates w a high rate of spontaneous mutation
Prevent binding of drug to active sites of key enzymes

299
Q

What are a few examples of herpesvirus

A

Simplex = cold sores
Varicella zoster = chicken pox
Epstein Barr = glandular fever

300
Q

When does the herpesvirus become latent

A

When it infects the sensory ganglia

301
Q

What is aciclovir

A

A synthetic guanosine analogue

302
Q

What type of herpesvirus is aciclovir most effective against

A

Simplex - high specificity
Varicella zoster - less susceptible
Cytomegalovirus - small and reproducible
EBV - slightly sensitive

303
Q

How does aciclovir become metabolic active

A

Utilises simplex virus specific thymidine kinase

304
Q

Describe aciclovir antiviral action

A

It’s a DNA chain terminator
Inhibitor of viral DNA polymerase

305
Q

How is the HIV virus transmitted

A

Congenitally, parenterally and by sexual contact

306
Q

What are the 2 forms of HIV

A

HIV-1: responsible for human AIDS
HIV-2: less virulent forms of immune suppression

307
Q

Describe the primary HIV infection

A

Asymptomatic
10-15% develop febrile illness
Acute retro viral syndrome

308
Q

Describe clinical stage I of HIV infection

A

Asymptomatic phase
Some develop PGL

309
Q

Describe clinical stage II of HIV infection

A

Progression to severe infections
Increase in opportunistic infections
Weight loss

310
Q

Describe clinical stage III of HIV infection

A

Increased weight loss
Oral candidiasis and other infections

311
Q

Describe clinical stage IV of HIV infection

A

HIV wasting syndrome
HIV encephalopathy
AIDS related complex (ARC)

312
Q

What are the target cells for HIV

A

Cytotoxic/helper T lymphocytes CD8+ and CD4+

313
Q

What receptor does HIV attach to

A

CD4 and CCR5 or CXCR4

314
Q

Describe Enfuvirtide in treating HIV

A

Fusion inhibitors - inhibits fusion of cellular and viral membranes
Most effective as combination therapy
Emergence in resistance in outer envelope glycoprotein gp41

315
Q

Describe maraviroc in treating HIV infections

A

CCR5 inhibitor - binds to CCR5 on CD4 cells preventing interaction of HIV-1 gp120
= no access into the cell

316
Q

What are the downfalls of Maraviroc

A

Does not prevent HIV-1 entry into CXCR4-tropic or dual tropic cells
Should be used on treatment history and tropism assay results

317
Q

Describe NRTI’s in treating HIV

A

Portent inhibitor of HIV replication
Active when phosphorylated intracellularly to its triphosphate
Inhibits viral reverse transcriptase

318
Q

What are the downfalls in using NRTIS in treating HIV

A

Inhibits mammalian y and b DNA polymerases increasing risk of toxicity in man
Life long therapy

319
Q

What are the indications and adverse effects to NRTIs

A

Indicated: patients w advanced HIV infection
Adverse effects: headache, nausea, anaemia, leukopenia and neutropenia

320
Q

What is the problem w NRTIs

A

Big problem with monotherapy - resistance
Combination therapy more effective

321
Q

What are NNRTIs

A

Structurally distinct from NRTIs
Bind to reverse transcriptase causing enzyme denaturation

322
Q

Describe how Ritonovir works in HIV treatment

A

Protease inhibitors that target virus specifc protease enzyme that’s required for post translation processing

323
Q

What are the downfalls for using protease inhibitors in HIV treatment

A

Drug-drug interaction problems
Resistance issues

324
Q

What is the preferred drug treatment for HIV

A

Highly active anti-retro viral therapy (HAART)
NRTI (x2) + NNRTI (x1) or PI (x1/2)

325
Q

Describe raltegravir as a HIV treatment

A

Integrase inhibitors
Inhibits integration of transcribed viral DNA into host cell chromosomes

326
Q

When are integrase inhibitors used

A

As combination therapy for:
- patients w resistant strains of HIV
- patients w ongoing viral replication whilst receiving A.Vs

327
Q

Describe inflammation

A

Protective response of vascularised tissues that brings the host defence in order to eliminate the offending agents

328
Q

What are the 5R’s of the inflammatory response

A

Recognition of the offending agent
Recruitment of leukocytes
Removal of offending substance
Regulation of response
Repair of the damaged tissue

329
Q

What are the 2 types of inflammation

A

Acute and chronic

330
Q

Describe acute inflammation

A

Rapid onset
Short duration
Mainly neutrophils
Prominent characteristic response

331
Q

What are the cardinal signs of acute inflammation

A

Redness
Heat
Swelling
Pain
Loss of function

332
Q

What are the 3 major components of acute inflammation

A

1- dilation of small vessels
2- increased vascular permeability of the microvasculature
3- emigration of leukocytes

333
Q

Describe chronic inflammation

A

Slow onset
Long duration
Monocytes/macrophages/lymphocytes
Less characteristic response

334
Q

Define selective toxicity

A

The drug is harmful to the infective agent but not to the host

335
Q

Define antibiotic

A

A medicine that inhibits the growth or destroys bacteria

336
Q

Define the 2 types of antibiotics

A

Bacteriostatic: inhibit multiplication
Bactericidal: kill bacteria

337
Q

What is the mechanism of action of penicillin

A

Beta-lac tam ring bind to DD-transpeptidase
Inhibits crosslinking
Prevent cell wall formation

338
Q

What penicillins are used to treat only gram positive infections

A

Natural penicillins

339
Q

What penicillins are used to treat only gram negative infections

A

Reverse spectrum penicillins

340
Q

What penicillins are used to treat both gram positive and negative infections

A

Broad spectrum penicillin
Extend penicillins

341
Q

What penicillins are used to treat only B-lactamase resistance infections

A

B-lactamase resistant penicillins

342
Q

Describe cephalosporins

A

Beta-lactam broad spectrum antibiotics
Used to treat septicaemia, pneumonia and meningitis

343
Q

What are the adverse effects of cephalosporins

A

Can cause nephrotoxicity and diarrhoea

344
Q

Describe carbapenems

A

Broad spectrum antibiotics
Contain B-lactam ring
Treat lower respiratory tract infections and sepsis

345
Q

Describe monobactams

A

Active against gram-negatives
B-lactam is peripheral not central

346
Q

What are the major estrogens produced by the body

A

Estradiol, estrone and estriol

347
Q

What does oestrogen drive

A

Follicular development

348
Q

Describe how oestrogen and progesterone are released from the ovary

A

GnRH released into bloodstream and travels to anterior pituitary gland
Anterior pituitary releases FSH and LH
FSH and LH bin receptors on target cells in ovary and release oestrogen and progesterone

349
Q

What does FSH stimulate the release of

A

Oestrogen

350
Q

How are the levels of progesterone and oestrogen regulated

A

Negative feedback to the hypothalamic-pituitary-ovarian axis
Oestrogen inhibits FSH
Progesterone inhibits GnRH, FSH and LH

351
Q

Describe the ovarian cycle

A

FSH is increasing due to low ovarian production
FSH aids follicular development
Follicles produce oestrogen
Positive feedback indicating the LH surge
LH surge induces ovulation
Remainder of ovualtory follicles are luteneised
Secretes progesterone and oestrogen

352
Q

What happens after ovulation if theres no fertilisation

A

Corpus luteum regression
Progesterone and oestrogen levels drop
Endometrium can’t be maintained
Releases GRH, FSH and LH again

353
Q

What happens after ovulation if there is fertilisation

A

Ovum secretes human chorionic gonadotropin (HCG)
Stimulates luteum to continue secreting progesterone
Maintains endometrium and pregnancy
Inhibits further secretion of GRH, FSH and LH

354
Q

What is targeted by ER and PR agonists in contraceptives

A

GnRH, FSH and LH
Prevents development of ovarian follicles
Blocks ovulation by blocking FSH peak
Makes cervical mucus less suitable for sperm passage

355
Q

What is targeted by PR antagonists in contraceptives

A

Inhibits LH
Thickens the mucus
Blocks ovualtion i.e LH surge
FSH peak can still occur

356
Q

What are the side effects of sex hormone agonists

A

Anabolic effects - weight gain and water retention
Skin changes and mild nausea
Venous thromboembolic disease
Myocardial infarction and stroke depression

357
Q

How are hormone antagonists used to treat cancer

A

Some tumours arise in hormone sensitive tissues and can be hormone dependent
Their growth may be inhibited by ER, PR and AR antagonist - agents that inhibit the synthesis of ER, PR or TR

358
Q

How does tamoxifen work in treating cancer

A

Competitive inhibitor of ER and binds forming a dimer
Translocation to nucleus where it binds to DNA
Forms unstable complex and can’t recruit RNA polymerase

Pharmacology (2 decks)

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